Wilderness Medicine: Expert Consult Premium Edition, 6th Edition

WILDERNESS MEDICINE

WILDERNESS MEDICINE Sixth Edition Paul S. Auerbach, MD, MS, FACEP, FAWM Redlich Family Professor of Surgery Division of Emergency Medicine Department of Surgery Stanford University School of Medicine Stanford, California

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

WILDERNESS MEDICINE

ISBN: 978-1-4377-1678-8

Copyright © 2012, 2007, 2001, 1995, 1989, 1983 by Mosby, an imprint of Elsevier Inc. Chapter 83 © 2012 by Michael E. Jacobs and Charles G. Hawley Chapter 3 all figures, tables, and photographs © Dr. Mary Ann Cooper Chapter 29 photographs © Dr. Grant S. Lipman, Elsevier granted non-exclusive license to publish Chapter 20 © Swaminatha Mahadevan No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of product liability, negligence, or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Wilderness medicine / [edited by] Paul S. Auerbach.—6th ed.     p. ; cm.   Includes bibliographical references and index.   ISBN 978-1-4377-1678-8 (hardcover : alk. paper)   I.  Auerbach, Paul S.   [DNLM:  1.  Wilderness Medicine.  2.  Emergency Treatment—methods.  3.  Environmental Exposure.  4.  Recreation.  5.  Rescue Work.  6.  Survival.  WB 107]   LC classification  not assigned   616.9′8—dc23                      2011032078 Acquisitions Editors: Dolores Meloni and Stefanie Jewell-Thomas Developmental Editor: Lucia Gunzel Publishing Services Manager: Anne Altepeter Associate Project Manager: Jessica Becher Design Direction: Steve Stave Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1 

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Contributors Javier A. Adachi, MD, FIDSA, FACP

Associate Professor, Department of Infectious Diseases, Infection Control, and Employee Health, The University of Texas MD Anderson Cancer Center; Adjunct Professor, The University of Texas Health Science Center at Houston, Medical School and School of Public Health; Adjunct Professor, Baylor College of Medicine, Houston, Texas; Visiting Professor, Universidad Peruana Cayetano Heredia, Lima, Peru

Martin E. Alexander, BScF, MSc, PhD, RPF

Adjunct Professor, Wildland Fire Science and Management, Department of Renewable Resources, Alberta School of Forest Science and Management, University of Alberta; Honorary Research Associate, Faculty of Forestry and Environmental Management, University of New Brunswick, Fredericton, New Brunswick, Canada; Senior Fire Behavior Research Officer (Retired), Canadian Forest Service, Northern Forestry Centre, Edmonton, Alberta, Canada

Robert C. Allen, DO, FACEP

Colonel, United States Air Force MC CFS (Retired), Contingency Operations Division, United States Air Force School of Aerospace Medicine, Brooks City, Texas

Susan Anderson, MD, MS

Clinical Associate Professor, Division of Infectious Diseases and Geographic Medicine, Stanford University, Stanford, California; Travel, Tropical, and Wilderness Medicine Consultant, Travel Medicine and Emergency/Urgent Care, Palo Alto Medical Foundation, Palo Alto, California

Aaron L. Baggish

Associate Director, Cardiovascular Performance Program, Division of Cardiology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts

Jennifer G. Baine, MD

Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Buddha Basnyat, MD, MSc, FACP, FRCP(E)

Medical Director, Nepal International Clinic, Himalayan Rescue Association; Principal Investigator, Oxford University Clinical Research Unit, Patan Academy of Health Sciences, Kathmandu, Nepal

Ryan P. Bayley, MD

Resident Physician, Emergency Medicine, New York-Presbyterian Weill Cornell Medical Center and Columbia University Medical Center, New York, New York

Greta J. Binford, PhD

Associate Professor of Biology, Lewis and Clark College, Portland, Oregon

Nicholas H. Bird, BA, MD, DABFM, DABPM

CEO and Chief Medical Officer, Divers Alert Network, Durham, North Carolina

Christopher J. Andrews, BE, MBBS, MEngSc, PhD, JD, EDIC, DipCSc, GDLP

Ryan Blumenthal, MBChB (Pret), MMed (Med Forens) Pret, FC for Path (SA), Dip For Med (SA)

E. Wayne Askew, PhD

Jolie Bookspan, MEd, PhD, FAWM

Mt Ommaney Family Clinic, Australia

Colonel, United States Army MSC (Retired), Professor and Chair, Division of Nutrition, University of Utah, Salt Lake City, Utah

Dale Atkins, BA

Forensic Pathologist, Department of Forensic Medicine, University of Pretoria, Pretoria, Gauteng, South Africa

Medical Director, Neck and Back Pain Sports Medicine, Academy of Functional Exercise Medicine, Temple University, Philadelphia, Pennsylvania

President, American Avalanche Association; Vice President, Avalanche Rescue Commission; International Commission for Alpine Rescue, North America Training and Education Manager, RECCO, AB, Boulder, Colorado

Ralph S. Bovard, MD, MPH, FACSM

Paul S. Auerbach, MD, MS, FACEP, FAWM

Warren D. Bowman, MD, FACP

Redlich Family Professor of Surgery, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Kira Bacal, MD, PhD, MPH, FACEP

Phase 2 Director, Medical Programme Directorate, University of Auckland, Auckland, New Zealand

Howard D. Backer, MD, MPH

Director, California Emergency Medical Services Authority

Department of Occupational and Environmental Medicine, HealthPartners, St. Paul, Minnesota

Clinical Associate Professor Emeritus, Department of Internal Medicine, University of Washington School of Medicine, Seattle, Washington; Staff Physician (Retired), Department of Internal Medicine, Division of Hematology-Oncology, The Billings Clinic, Billings, Montana

Leslie V. Boyer, MD

Director, Venom Immunochemistry, Pharmacology, and Emergency Response Institute; Associate Professor of Pathology, University of Arizona, Tucson, Arizona

v

CONTRIBUTORS

John E. Bradford, RN, MPAS, PA-C

Charles Clarke, MA, MBBCh, FRCP

Mark A. Brandenburg, MD

Kenneth S. Cohen, MA, MSTh

Peace Corps Medical Officer, United States Peace Corps, Malawi, Lilongwe, Malawi, Africa; Clinical Adjunct Professor, University of Utah Physician Assistant Program, Salt Lake City, Utah

Medical Director, Emergency Department, Bristow Medical Center, Bristow, Oklahoma; Medical Director, Emergency Medical Services, Tulsa Technology Center, Tulsa, Oklahoma

Beau Briese, MD

Resident Physician, Division of Emergency Medicine, Stanford/ Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California

Colin M. Bucks, MD

Clinical Instructor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

George H. Burgess

Florida Program for Shark Research, Florida Museum of Natural History, University of Florida, Gainesville, Florida

Sean P. Bush, MD, FACEP

Honorary Consultant Neurologist, National Hospital for Neurology and Neurosurgery, Queen Square, London, United Kingdom

Independent Scholar, Traditional Healer, Nederland, Colorado

Stephen D. Coleman, MD

Clinical Assistant Professor, Department of Anesthesia, Pain Management Division, Stanford University School of Medicine, Stanford, California

Bryan R. Collier, DO, FACS, CNSP

Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Shon Compton, MPAS, PA-C

Major, Specialty Corps (Retired), Chief Instructor, Center for Predeployment Medicine, United States Army Medical Department Center and School, Fort Sam Houston, Texas

Benjamin B. Constance, MD

Professor of Emergency Medicine, Loma Linda University School of Medicine, Loma Linda, California

Chief Resident Physician, Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University, Stanford, California

Frank K. Butler Jr., BS, MD

Donald C. Cooper, PhD, MBA, EMT-P

Dale J. Butterwick, ATC(C), BA, MSc

Jimmy L. Cooper, MD, FACEP

Chairman, Committee on Tactical Combat Casualty Care, Defense Health Board, Pensacola, Florida

Associate Professor, Faculty of Kinesiology, University of Calgary; Former President, Canadian Pro Rodeo Sport Medicine Team, Calgary, Alberta, Canada

Steven C. Carleton, MD, PhD

Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio

Betty Carlisle, MD

Adjunct Assistant Professor, Department of Public Health and Preventive Medicine, State University of New York Upstate Medical University; Staff Physician, Emergency Department, St. Joseph’s Hospital, Syracuse, New York

Scott P. Carroll, PhD

Department of Entomology, University of California, Davis, California

John W. Castellani, PhD

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Samuel N. Cheuvront, PhD

Research Physiologist, Division of Thermal and Mountain Medicine, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Richard F. Clark, MD

Professor of Clinical Medicine, Director, Division of Medical Toxicology, University of California, San Diego, San Diego, California

vi

State Fire Marshal, Department of Commerce, State of Ohio, Columbus, Ohio

Staff Physician, Department of Emergency Medicine, Director, Center for Predeployment Medicine, San Antonio, Texas

Mary Ann Cooper, MD, FAMS, FAAEM

Emerita Professor, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois

Kevin Coppock, BSc, MSc

Head of Mission, Northern Sudan, Médecins Sans Frontières, Khartoum, Sudan

Larry I. Crawshaw, PhD

Professor Emeritus, Department of Biology, Portland State University, Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon

Joy E. Crook, MD, MPH

Instructor, Department of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland

Gregory A. Cummins, DO, MS

Assistant Clinical Instructor, Department of Internal Medicine, Kansas University of Medicine and Biosciences; Hospitalist, Department of Medicine, North Kansas City Hospital, Kansas City, Missouri

Tracy A. Cushing, MD, MPH, FACEP, FAWM

Assistant Professor, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado; Attending Physician, Fellowship Director, Denver Health Wilderness Medicine Fellowship, Department of Emergency Medicine, Denver Health Medical Center, Denver, Colorado

Specialty Doctor, Emergency Department, Bristol Royal Infirmary, Bristol, United Kingdom

Daniel F. Danzl, MD

Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky

Ian Davis, MBBCH, BSc (Hons)

Herbert L. DuPont, MD

Professor and Director, Center for Infectious Diseases, University of Texas School of Public Health and Medical School; Chief of Internal Medicine, St. Luke’s Episcopal Hospital; Vice Chairman, Department of Medicine, Baylor College of Medicine, Houston, Texas

Blair Dillard Erb, BS, MD, FACP, FACC

Past President, Wilderness Medical Society, The Study Center, Townsend, Tennessee

Resident Medical Officer, Department of Accident and Emergency, Cirencester Hospital, Gloucestershire; Polar Medicine, Medical Cell, Royal Geographical Society, London; Chief Medical Officer, Polar Challenge, Venture Group, Cirencester, England, United Kingdom

Timothy B. Erickson, MD

Kathleen Mary Davis, BScF, MSc

Charles D. Ericsson, MD

Kevin Davison, ND, Lac

Peter J. Fagenholz, MD

Superintendent, Montezuma Castle and Tuzigoot National Monument, National Park Service, Camp Verde, Arizona

Director, Maui Prolotherapy Clinic, Hamakuapoko, Peahi, Haiku, Maui, Hawaii

Chad P. Dawson, BS, MPS, PhD

Professor, Forest and Natural Resources Management, State University of New York College of Environmental Science and Forestry, Syracuse, New York

Janice A. Degan, RN, MS

Senior Research Nurse, Venom Immunochemistry, Pharmacology, and Emergency Response Institute, Arizona Health Sciences Center, University of Arizona, Tucson, Arizona

Thomas G. DeLoughery, MD, FACP

Professor, Department of Emergency Medicine, Division of Medical Toxicology; Director, Center for Global Health, University of Illinois College of Medicine, Chicago, Illinois

Professor of Medicine, Head, Clinical Infectious Disease, Division of Infectious Disease, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas

Department of Surgery, Division of Trauma, Emergency Surgery, and Critical Care, Massachusetts General Hospital; Instructor in Surgery, Harvard Medical School, Boston, Massachusetts

Joanne N. Feldman, MD, MS

Clinical Faculty, Division of Emergency Medicine, University of California, Los Angeles, Los Angeles, California

D. Nelun Fernando, BA, MA, PhD

Department of Geography, Rutgers University, New Brunswick, New Jersey

Murray E. Fowler, BS, DVM

Professor of Medicine, Pathology, and Pediatrics, Head, Benign Hematology Section, Oregon Health and Science University, Portland, Oregon

Professor Emeritus, Veterinary Medicine and Epidemiology, University of California, Davis, California

Arlene E. Dent, MD, PhD

Assistant Professor, Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, Ohio

Clinical Associate Professor, Department of Dermatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina

Thomas F. Ditzler, PhD, MA, FRSPH, FRAI

Michael E. Franco, Major, MSM, MPAS, PA-C

Director of Research, Department of Psychiatry, Tripler Army Medical Center, Honolulu, Hawaii

Mark Donnelly, MD

Salem Emergency Department, Salem, Oregon

Howard J. Donner, MD

Wilderness Medicine Instructor, Mountain Medical Seminars, Bozeman, Montana; Adventure Training Coordinator, The Finer Points of Flying, San Francisco, California

Mark S. Fradin, MD

Chief, Plans and Operations, United States Army Environmental Management Systems Programs Office, United States Army Medical Department Center and School, Fort Sam Houston, Texas

Luanne Freer, MD, FACEP, FAWM

Medical Director, Medcor, Yellowstone National Park, Wyoming; Founder and Director, Everest Base Camp Medical Clinic, Himalayan Rescue Association, Kathmandu, Nepal

Eric Douglas, BA, EMT, DMT

Steven P. French, MD, BS, MS, IUCN, ASNE, SFW

Jennifer Dow, MD, FACEP, FAWM

Nathan K. Friedline, MD

Director, Education, Divers Alert Network, Durham, North Carolina

Medical Director, Denali National Park and Preserve; Medical Director, National Park Service, Alaska Region, Department of Emergency Medicine, Alaska Regional Hospital, Anchorage, Alaska

Co-founder and Research Director, Yellowstone Grizzly Foundation, Jackson Hole, Wyoming

Resident, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah; Captain, United States Army, 32nd Medical Brigade, Fort Sam Houston, Texas

vii

CONTRIBUTORS

Jon Dallimore, MB, BS, MSc, MRCGP, MCEM, FFTM RCPS (Glasg), DCH, DRCOG

CONTRIBUTORS

Raymond R. Gaeta, MD

Charles G. Hawley, BS

Tom Garrison, BS, MA, PhD

David M. Heimbach, MD

Associate Professor, Department of Anesthesiology, Medical Director, Pain Management Service, Stanford University School of Medicine, Stanford, California

Professor, Department of Oceanography, Orange Coast College, Costa Mesa, California; Adjunct Professor, Higher Education, University of Southern California, Los Angeles, California

Daniel Garza, MD

Assistant Professor, Department of Orthopaedic Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Alan Gianotti, MS, MD

Clinical Assistant Professor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

Gordon G. Giesbrecht, BPE, BTh, MPE, PhD

Professor of Thermophysiology, Health Leisure and Human Performance Research Institute, University of Manitoba; Professor, Department of Anesthesia, University of Manitoba, Winnipeg, Manitoba, Canada

Kimberlie A. Graeme, BS, MD

Division of Emergency Medicine, Naval Medical Center San Diego, San Diego, California

Colin K. Grissom, MD

Associate Professor of Medicine, University of Utah School of Medicine; Associate Medical Director, Shock Trauma Intensive Care Unit, Intermountain Medical Center, Murray, Utah

Kirby R. Gross, MD, FACS

Trauma Services, United States Army Medical Department, Walter Reed Army Medical Center, Washington, DC

Peter H. Hackett, MD

Clinical Professor of Surgery, Department of Emergency Medicine, Altitude Research Center, University of Colorado Denver School of Medicine, Denver, Colorado; Director, Institute for Altitude Medicine, Telluride, Colorado

N. Stuart Harris, MD

Chief, Division of Wilderness Medicine, Director, Wilderness Medicine Fellowship, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor of Surgery, Harvard Medical School, Boston, Massachusetts

Patricia R. Hastings, DO, MPH, FACEP, RN, NREMT

Colonel, Medical Corps, United States Army; MEDCOM Liaison, Department of Homeland Security, Washington, DC, Department of Emergency Medicine, Brooke Army Medical Center, San Antonio, Texas

Seth C. Hawkins, MD, FACEP, FAWM

Director, Mountain Emergency Physicians; Medical Director, Burke Emergency Medical Services Special Operations Team; Executive Director, Appalachian Center for Wilderness Medicine, Morganton, North Carolina; Assistant Professor, Emergency Medical Care Program, Western Carolina University, Cullowhee, North Carolina

viii

Vice President, West Marine, Safety at Sea Moderator, United States Sailing Technical Board Member, American Boat and Yacht Council, Santa Cruz, California

Professor of Surgery, University of Washington School of Medicine, Seattle, Washington

Carlton E. Heine, MD, PhD, FACEP, FAWM

Clinical Instructor, University of Washington School of Medicine, Seattle, Washington; Attending Physician, Emergency Department, Bartlett Regional Hospital, Juneau, Alaska

Lawrence E. Heiskell, MD, FACEP, FAAFP

International School of Tactical Medicine, Palm Springs, California

John C. Hendee, PhD

Emeritus Professor and Dean (Retired), University of Idaho, College of Natural Resources, Moscow, Idaho

Henry J. Herrmann, DMD, FAGD Dentist, Falls Church, Virginia

Ronald L. Holle, BS, MS

Meteorologist, Holle Meteorology and Photography, Oro Valley, Arizona

Renee Y. Hsia, MD, MSc

Assistant Professor, Department of Emergency Medicine, University of California, San Francisco; Attending Physician, Department of Emergency Services, San Francisco General Hospital, San Francisco, California

Franklin R. Hubbell, DO

Physician and Director, Urgent Care and Spine Center, Saco River Medical Group; Physician, Director of Education, Stonehearth Open Learning Opportunities Schools; Author, Wilderness Medicine Newsletter, TMC Books, Conway, New Hampshire

Stephen E. Hudson, CEO, NTC

National Training Coordinator, National Cave Rescue Commission, National Speleological Society, Huntsville, Alabama; President, Pigeon Mountain Industries, Lafayette, Georgia

Cynthia L. Idzik-Starr, DDS

Assistant Professor, Director of Urgent Care, Department of Oral and Maxillofacial Surgery, University of Maryland Dental School, Baltimore, Maryland

Christopher H.E. Imray, PhD, MB, BS, DiMM, Clin Med Sci, FRCS, FRCP

Professor of Surgery, Warwick Medical School, Department of Vascular Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, United Kingdom

Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, FIFEM

Professor Emeritus, Department of Emergency Medicine, The University of Arizona, Tucson, Arizona

United States Coast Guard Licensed Captain; Founder and Program Director, MedSail (Medicine for Mariners and Safety at Sea); Medical Director, Vineyard Medical Services, Martha’s Vineyard, Massachusetts

Ramin Jamshidi, MD

Fellow, Department of Pediatric Surgery, Children’s Hospital of Wisconsin; Clinical Instructor, Department of Surgery, Medical College of Wisconsin, Milwaukee, Wisconsin; Adjunct Professor, Physics Department, University of California, San Francisco, San Francisco, California

James M. Jeffers, BA, LLB, LLM, MPhil

PhD Candidate, Department of Geography, Rutgers University, New Brunswick, New Jersey

Jamie G. Jenkins, MD

Brian J. Krabak, MD, MBA

Clinical Associate Professor, Department of Rehabilitation, Orthopedics, and Sports Medicine; Team Physician, Seattle Children’s Sports Medicine, Seattle University Athletics, University of Washington; Team Physician, USA Swimming; Medical Director, RacingThePlanet: 4 Deserts Ultra Marathon Series, Seattle, Washington

Andrew C. Krakowski, MD

Pediatrician and Dermatologist, Rady Children’s Hospital of San Diego, University of California, San Diego, San Diego, California; Founder and Director, boonDOCS Wilderness and Travel Medicine, La Jolla, California

Peter Kummerfeldt, AD

President, OutdoorSafe, Former Survival Training Director, United States Air Force Academy, Colorado Springs, Colorado

Ultrasound Fellow, Department of Emergency Medicine, Washington Hospital Center, Georgetown University Hospital, Union Memorial Hospital, Washington, DC

Ashley R. Laird, MD

Kirsten Johnson, MD, MPH, CCFP-EM

Carolyn S. Langer, MD, JD, MPH

Assistant Professor, Department of Family Medicine; Director, University Humanitarian Studies Initiative; Affiliated Faculty, Institute for Health and Social Policy, McGill University, Montreal, Canada; Affiliated Faculty, Harvard Humanitarian Initiative, Harvard University, Cambridge, Massachusetts

Hemal K. Kanzaria, MD

Resident Physician, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California

Emergency Physician, Sonora Regional Medical Center, Sonora, California

Instructor, Harvard Massachusetts

School

of

Public

Health,

Boston,

Patrick H. LaValla

CEO, ERI International; Operations Chief, All Hands Consulting; Former President, National Association for Search and Rescue, Olympia, Washington

Jay Lemery, MD, FACEP, FAWM

Lee A. Kaplan, MD

Clinical Professor, Department of Dermatology, University of California, San Diego Health System, La Jolla, California

Assistant Professor, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital; President-Elect, Wilderness Medical Society; Visiting Scientist, François-Xavier Bagnoud Center for Health and Human Rights, Harvard School of Public Health, Boston, Massachusetts

Misha R. Kassel, MD

Lisa R. Leon, PhD

Stephanie Kayden, MD, MPH

Benjamin D. Levine, MD, FACC, FACSM

Clinical Instructor, Departments of Emergency Medicine and Orthopaedic Surgery, Stanford University School of Medicine, Stanford, California

Director, Harvard International Emergency Medicine Fellowship; Attending Physician, Brigham and Women’s Hospital; Instructor, Harvard Medical School; Faculty, Harvard Humanitarian Initiative, Boston, Massachusetts

James W. Kazura, MD

Professor of International Health and Medicine, Center for Global Health and Diseases, Case Western Reserve University School of Medicine, Cleveland, Ohio

Robert W. Kenefick, PhD

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Alexa B. Kimball, MD, MPH

Vice Chair, Department of Dermatology, Massachusetts General Hospital; Associate Professor, Harvard Medical School, Boston, Massachusetts

Judith R. Klein, MD, FACEP

Research Physiologist, Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts

Director, Institute for Exercise and Environmental Medicine; S. Finley Ewing Jr., Chair for Wellness, Texas Health Presbyterian Dallas; Harry S. Moss Heart Chair for Cardiovascular Research; Professor of Medicine and Cardiology, Distinguished Professorship in Exercise Science, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas

Matthew R. Lewin, MD, PhD, FACEP

Director, Center for Exploration and Travel Heath, California Academy of Sciences, San Francisco, California

James R. Liffrig, MD, MPH, FAAFP

Chair, Department of Family Medicine, Womack Army Medical Center, Fort Bragg, North Carolina; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland

Grant S. Lipman, MD, FACEP

Clinical Assistant Professor, Division of Emergency Medicine, Department of Surgery, Stanford University School of Medicine, Stanford, California

Assistant Professor, Department of Emergency Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California ix

CONTRIBUTORS

Michael Jacobs, MD, FAWM

CONTRIBUTORS

Joanne Liu, MDCM, FRCPC

Board of Directors, Médecins Sans Frontières-Switzerland, Assistant Professor, Sainte-Justine Hospital, Montreal, Canada

Vicki Mazzorana, MD, FACEP, FAAEM, FAWM

Andrew M. Luks, MD

Assistant Professor, Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington

Associate Clinical Professor, Department of Emergency Medicine, University of Nevada School of Medicine; Codirector, Wilderness Medicine Clerkship; Co-medical Director, Death Valley, Joshua Tree National Park, Mojave National Reserve; Ringside Physician, Nevada Athletic Commission, Las Vegas, Nevada

Binh T. Ly, MD, FACMT

Loui H. McCurley, RAT, TRS

Professor, Director, Medical Toxicology Fellowship, Division of Medical Toxicology; Director, Emergency Medicine Residency, Department of Emergency Medicine, University of California San Diego, California Poison Control System, San Diego, California

Edgar Maeyens Jr., MD

Board of Visitors, Nicholas School of the Environment, Duke University, Durham, North Carolina; Private Practice Dermatology, Dermatopathology and Mohs Surgery, Coos Bay, Oregon

Swaminatha V. Mahadevan, MD, FACEP, FAAEM

Associate Professor of Surgery and Associate Chief, Division of Emergency Medicine, Stanford University School of Medicine; Emergency Department Medical Director, Stanford University Medical Center, Stanford, California

Rick Marinelli, ND, MAcOM

Clinical Professor, National College of Natural Medicine, Doctoral Faculty, Division of Biomedicine, Oregon College of Oriental Medicine, Portland, Oregon

David S. Markenson, MD, FAAP, FACEP

Medical Director, Disaster Medicine and Regional Emergency Services, Westchester Medical Center, Maria Fareri Children’s Hospital; Professor of Pediatrics, New York Medical College; Director, Center for Disaster Medicine and Professor of Clinical Public Health, New York Medical College School of Health Sciences and Practice, Valhalla, New York

Millicent Marmer, BA, MS

Graduate Student, Alden March Bioethics Institute, Albany Medical College, Albany, New York

Armando Márquez Jr., MD, FACEP

Assistant Clinical Professor, Director, Emergency Medical Services, Department of Emergency Medicine, University of Illinois College of Medicine, Chicago, Illinois

Denise Martinez, MS, RD

Adjunct Faculty, Division of Nutrition, University of Utah, Salt Lake City, Utah

Nicholas P. Mason, MB, ChB, FRCA

Consultant in Intensive Care Medicine, Royal Gwent Hospital, Newport, United Kingdom

Michael J. Matteucci, MD, FAAEM

Assistant Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Director, Emergency Medicine Residency Program, Emergency Medicine Department, Naval Medical Center San Diego, San Diego, California

x

Technical Rescue Specialist, Alpine Rescue Team, Evergreen, Colorado; Technical Director, Vertical Rescue Solutions; Vice President, Pigeon Mountain Industries, Denver, Colorado

Marion C. McDevitt, DO, MPH

Associate Director, Wilderness Medicine Emergency Medical Services Fellowship; Associate Director, Global Health Fellowship; Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah

Marilyn McHarg, MSc (A), LLD (Hon)

Executive Director, Médecins Sans Frontières-Canada, Toronto, Ontario, Canada

Scott E. McIntosh, MD, MPH

Assistant Professor, Division of Emergency Medicine, University of Utah, Salt Lake City, Utah

Christopher M. McStay, MD, FACEP, FAWM

Assistant Professor of Emergency Medicine, Chief of Service, Bellevue Hospital Center Emergency Department, Department of Emergency Medicine, New York University School of Medicine, New York, New York

Timothy P. Mier, BA, EMT-P

Deputy Fire Marshal, Cuyahoga Falls Fire Department, Cuyahoga Falls, Ohio

Alicia B. Minns, MD

Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Division of Medical Toxicology, University of California, San Diego, San Diego, California

John Mioduszewski, BA, MA

Department of Geography, Rutgers University, New Brunswick, New Jersey

James K. Mitchell, PhD

Professor of Geography, Rutgers University, New Brunswick, New Jersey

James Moore, RN, BSc (Hons), Dip TravMed, MFTM, RCPS (Glasg), FRGS

Director, Travel Health Consultancy, Exeter, Devon, United Kingdom

Larry A. Moore, MD

Department of Emergency Medicine, Penrose-St. Francis Hospital, Wilderness Medicine Instructor, WildernessWise, Colorado Springs, Colorado

Barry Morenz, MD

Associate Professor of Psychiatry, Department of Psychiatry, College of Medicine, University of Arizona, Tucson, Arizona

Professor of Surgery and Biomedical Informatics, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Roger B. Mortimer, MD

Health Sciences Associate Clinical Professor, Department of Family and Community Medicine, University of California, San Francisco; Fresno Medical Education Program, Western Region Coordinator, National Cave Rescue Commission, Fresno, California

Michael J. Mosier, MD

Assistant Professor of Surgery, Loyola University Medical Center, Maywood, Illinois

Parveen K. Parmar, MD, MPH

Associate Director, International Emergency Medicine Fellowship, Brigham and Women’s Hospital; Associate Faculty, Harvard Humanitarian Initiative, Harvard Medical School, Boston, Massachusetts

Naresh J. Patel, DO

Private Practice, Fort Wayne Allergy and Asthma Consultants, Fort Wayne, Indiana

Sheral S. Patel, MD, FAAP

Consultant, Pediatrics and Pediatric Infectious Diseases, Hartford, Connecticut

Martin I. Radwin, MD

Robert W. Mutch, BA, MScF, DF (Honorary) Consultant, Fire Management Applications, Darby, Montana

Department of Medicine, Granger Medical Clinic, Chief of Gastrointestinal Endoscopy, Department of Medicine, Pioneer Valley Hospital, Salt Lake City, Utah

Kei Nagashima, MBSS, DMSci

Sheila B. Reed, MS

Professor, Laboratory of Integrative Physiology (Body Temperature and Fluid Laboratory), School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Mayumi Nakamura, PhD

Consultant, Disaster Risk Reduction and Development, Middleton, Wisconsin

William P. Riordan Jr., MD, MS†

Visiting Researcher, Faculty of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Assistant Professor of Surgery, Division of Trauma and Surgical Critical Care, Vanderbilt University Medical Center, Nashville, Tennessee

Eric K. Noji, MD, MPH

Robert C. Roach, PhD

Chairman and CEO, Noji Global Health and Security LLC, Director (Retired), International Emergency and Refugee Health Program, Centers for Disease Control and Prevention, Washington, DC

Robert L. Norris Jr., MD

Professor of Surgery, Stanford University School of Medicine; Chief, Division of Emergency Medicine, Stanford University Medical Center, Stanford, California

Director, Altitude Research Center; Co-Chair, International Hypoxia Symposia, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, Colorado

David A. Robinson, PhD

Professor and New Jersey State Climatologist, Department of Geography, Rutgers University, New Brunswick, New Jersey

Eloy Rodriguez, PhD

Command Surgeon, United States Army Training and Doctrine Command, Fort Monroe, Virginia

James A. Perkins Endowed Professor of Environmental and Toxicology Studies, Institute of Comparative Environmental Toxicology, Department of Plant Biology, Cornell University, Ithaca, New York

Lesley J. Ogden, MD, MBA, FACEP

Nancy V. Rodway, MD, MPH, MS

Karen K. O’Brien, MD

Staff Physician and Assistant Emergency Room Director, Department of Emergency Medicine, Samaritan North Lincoln Hos­ pital, Lincoln City, Oregon; Clinical Faculty, Department of Emergency Medicine, Western University of Health Sciences, Pomona, California; Affiliate Assistant Professor, School of Medicine, Oregon Health and Science University, Portland, Oregon

Bohdan T. Olesnicky, MD

Medical Director of Occupational Medicine and Ambulatory Care, Lake Health Hospital System, Painesville, Ohio; Adjunct Faculty, Department of Occupational Medicine, Ohio State University College of Medicine, Columbus, Ohio

Richard S. Salkowe, DPM, FACFAS, FAWM

PhD Candidate, Department of Geography, Environmental Science, and Policy, University of South Florida, Tampa, Florida

SWAT Team Physician, Palm Springs Police Department, Palm Springs, California; Partner, Global Protection Medical Group, Indian Wells, California; Director of EMS, Eisenhower Medical Center, Rancho Mirage, California

Sandra M. Schneider, MD

Sheryl Olson, BSN, RN, FAWM, CCRN

Robert B. Schoene, MD, FACP

Outdoor Survival and Navigation Instructor, Flight Nurse, Wilderness Safety Instructor, Colorado Springs, Colorado

Edward J. Otten, MD

Professor of Emergency Medicine and Pediatrics, Director, Division of Toxicology, University of Cincinnati, Cincinnati, Ohio

Professor and Chair Emeritus, Department of Emergency Medicine, University of Rochester, Rochester, New York

Clinical Professor of Medicine, Division of Pulmonary and Critical Care Medicine, University of Washington School of Medicine, Seattle, Washington, Bozeman Deaconess Hospital, Bozeman, Montana

Justin Sempsrott, MD, EMT

Emergency Medicine Resident, University of Nevada School of Medicine, Las Vegas, Nevada †

Deceased.

xi

CONTRIBUTORS

John A. Morris Jr., MD, FACS

CONTRIBUTORS

Jamie R. Shandro, MD, MPH

Assistant Professor, Division of Emergency Medicine, University of Washington School of Medicine, Seattle, Washington

Charley Shimanski

Education Director and Past President, Mountain Rescue Association; Senior Vice President, Disaster Services, American Red Cross, Washington, DC

Uta S. Shimizu, MD

Clinical Instructor, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California

David R. Shlim, MD

Jackson Hole Travel and Tropical Medicine, Jackson, Wyoming

Joshua D. Shofner, MD

Resident, Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts

Julie A. Switzer, MD

Assistant Professor, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, Minnesota; Director, Geriatric Orthopaedic Trauma Program, Regions Hospital, St. Paul, Minnesota

Robert I. Tilling, BA, MS, PhD

Senior Research Volcanologist, Volcano Science Center, U.S. Geological Survey, Menlo Park, California

Ken Tokizawa, PhD

Assistant Professor, Faculty of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan

Joseph E. Tonna, MD

Division of Emergency Medicine, Stanford/Kaiser Emergency Medicine Residency Program, Stanford University School of Medicine, Stanford, California

David A. Townes, MD, MPH, DTM&H

Eunice Singletary, MD, FACEP

Clinical Associate Professor, Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia

Associate Professor of Medicine, Division of Emergency Medicine; Adjunct Associate Professor of Global Health, Department of Global Health, University of Washington School of Medicine, Seattle, Washington

Kieran Smart, MBChB, MSc, MPH, MRCGP

Stephen J. Traub, MD

Physician, Florida FL-3 Disaster Medical Assistance Team, Florida State Medical Response Team Region 4; Advisor, Space Medicine Associates; Adjunct Clinical Assistant Professor, Department of Community Health and Family Medicine, University of Florida College of Medicine, Gainesville, Florida

Jennifer Cohen Smith, MD

Medical Toxicologist, Banner Good Samaritan Medical Center, Phoenix, Arizona

Will Smith, MD, EMT-P

Clinical Faculty, Division of Emergency Medicine, WWAMI, University of Washington School of Medicine, Seattle, Washington; Medical Director, Teton County Search and Rescue, Jackson Hole Fire/EMS, Grand Teton National Park; President and Medical Director, Wilderness and Emergency Medicine Consulting, LLC; Faculty, Student/Resident Rotation Coordinator, Department of Emergency Medicine, St. John’s Medical Center, Jackson, Wyoming

Matthew C. Spitzer, MD, DTMH

Chairman, Department of Emergency Medicine, Mayo Clinic Arizona, Phoenix, Arizona; Assistant Professor of Emergency Medicine, Mayo Medical School, Rochester, Minnesota

Yuki Uchida, MS

PhD Student, Laboratory of Integrative Physiology (Body Temperature and Fluid Lab), Graduate School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan

Sydney J. Vail, MD, FACS

Director of Trauma Surgery, Medical Director, Tactical Medicine Program, Trauma Center, Maricopa Medical Center, Phoenix, Arizona

Karen B. Van Hoesen, MD

Clinical Professor, Department of Emergency Medicine, University of California, San Diego; Director, University of California San Diego Diving Medicine Center; Director, Undersea and Hyperbaric Medicine Fellowship, University of California San Diego, San Diego, California

President, Doctors Without Borders/Médecins Sans Frontières, Member, International Council and International Council Board, Médecins Sans Frontières; Assistant Clinical Professor of Medicine, Director, Predoctoral Education, Center for Family and Community Medicine, College of Physicians and Surgeons of Columbia University, New York, New York

Michael VanRooyen, MD, MPH, FACEP

Alan M. Steinman, MD, MPH, FACPM

Raghu Venugopal, MD, MPH, FRCPC

Rear Admiral (Retired), United States Public Health Service, Director of Health and Safety, United States Coast Guard, Olympia, Washington

Robert C. Stoffel

CEO, Emergency Response International; Prime Survival Training Contractor, Department of Homeland Security; Customs and Border Protection, United States Coast Guard Aviation Survival Technician Program, Cashmere, Washington

Jeffrey Suchard, MD

Professor of Clinical Emergency Medicine, Director of Medical Toxicology, Department of Emergency Medicine, University of California, Irvine Medical Center, Orange, California xii

Chief, International Division, Department of Emergency Medicine, Brigham and Women’s Hospital; Director, Harvard Humanitarian Initiative, Harvard University; Associate Professor, Department of Emergency Medicine, Harvard Medical School, Boston, Massachusetts

Assistant Professor of Medicine, University of Toronto; Attending Physician, Department of Emergency Medicine, University Health Network, Toronto, Ontario, Canada

Brandee L. Waite, MD

Medical Director, Racing The Planet: 100, Ultra Marathon Series; Assistant Professor, Physical Medicine and Rehabilitation, Sports Medicine, University of California, Davis Medical Center, Sacramento, California

John Walden, MD, DTM&H

Professor and Chairman, Department of Family and Community Health, Marshall University Joan C. Edwards School of Medicine, Huntington, West Virginia

Emeritus Professor of Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom

Eric A. Weiss, MD, FACEP

Associate Professor of Surgery, Director, Wilderness Medicine Fellowship, Division of Emergency Medicine, Stanford University School of Medicine; Medical Director, Office of Emergency Management, Stanford University Medical Center, Lucile Packard Children’s Hospital, Stanford, California

Jan West, PhD

Visiting Professor of Biology, Soka University of America, Aliso Viejo, California

James A. Wilkerson III, MD

Merced Pathology Medical Group (Retired), Merced, California

Tamae Yoda, PhD

Associate Professor, Department of Interdisciplinary Studies, Faculty of International Liberal Arts, Dokkyo University, Soka, Saitama, Japan

Lynn E. Yonge, MD, FAAFP, FAWM

Chairman, Environmental Council, Wilderness Medical Society, Director, Wilderness Medicine Training, Outward Bound, Assistant Clinical Professor, The University of South Alabama College of Medicine, Mobile, Alabama

Ken Zafren, MD, FAAEM, FACEP, FAWM

Clinical Associate Professor of Surgery, Division of Emergency Medicine, Stanford University School of Medicine, Stanford, California; Staff Emergency Physician, Alaska Native Medical Center, Alaska Mountain Rescue Group, Anchorage, Alaska; Vice President, International Commission for Mountain Emergency Medicine; Associate Medical Director, Himalayan Rescue Association, Kathmandu, Nepal.

xiii

CONTRIBUTORS

David A. Warrell, MA, DM, DSc, FRCP, FRCPE, FMedSci, HonFZS, FRGS

Foreword Two hours into my first trans-Pacific flight to Hong Kong (on my way to Nepal), a flight attendant put out a call to see if there was a physician on board. I raised my hand and was taken to see a 22-year-old American soldier who was suffering a moderately severe allergic reaction to peanuts. The young man was flushed, had a diffuse urticarial rash, and felt some swelling in his throat. He was so itchy he could not sit still. The reaction had been going on for 45 minutes. As I looked him over, the captain of the plane came down the aisle to talk to me. “We’re as close as we’re going to be to Anchorage,” he said. “We can dump the entire trans-Pacific load of fuel and land there, if you say so.” I greeted this with disbelief. A few hours into my first trip to Asia, and suddenly I was in charge of the plane. I did not want to land in Anchorage if we did not have to (apart from not wanting to dump 40,000 gallons of fuel into the ocean). I asked the flight attendants to bring me the first-aid kit from the plane. I would give the soldier a shot of epinephrine and an antihistamine tablet, and we could keep going. “We don’t carry a first-aid kit,” came the reply. “We have a few bandages, that’s it.” I looked at the soldier. I did not think he was in danger of dying, but it would be a long flight for him with itchy skin and a swollen face. On the other hand, hundreds of people would be delayed a day or more, at a cost of hundreds of thousands of dollars, if we diverted to Anchorage. It occurred to me that someone on a Boeing 747 with 400 passengers might be carrying a bee sting kit. I asked the flight attendant to make an announcement, and three people raised their hands. I accepted one of the kits, injected the soldier, gave him some diphenhydramine, and watched him quickly improve. I told the captain that we could continue flying to Hong Kong. Solving problems with what you have at hand is one of the main themes of wilderness medicine, a discipline that had yet to evolve in 1979 when I was on that flight. Ten days later, I was trekking on my way to the Himalayan Rescue Association Aid Post at Pheriche, a yak-herding village at 14,000 feet, near the base of Mt Everest. Eating dinner at a teahouse next to the Thyangboche monastery, I was asked if I could help an 84-yearold Sherpa man just up the valley in Pangboche. He had fallen down his stairs and sustained a scalp laceration the day before. I was not carrying suture supplies, but I had just visited the Kunde Hospital and was familiar with the staff, so I wrote a note to request instruments and suture material. A Sherpa runner carried the note and would return with the supplies the next morning. In the morning, I walked a couple of hours to Pangboche, where I was led to the house of the man who had fallen down. He lay inside, moaning, and his hair was densely matted with blood. We carried him outside into the sun, where it was warm enough to work and there was good light. I put the instruments in a pot of water and boiled them on the hearth inside. I had no gloves and no sterile field. I poured povidone-iodine into the bowl that held the instruments and used the bowl as my sterile field, reaching into the disinfectant each time I needed to use an instrument. This kept both my hands and the instruments relatively sterile as I worked. The laceration was truly major. It split the old man’s right eyebrow and extended across his forehead and over the crown of his head to the back of his neck. A huge skin flap had been created, so I lifted it up and irrigated underneath it with copious quantities of water I had boiled earlier. I began to sew. The man moaned and muttered as I worked. I asked one of the Sherpas what he was saying. “He’s saying, ‘Leave me alone. I just want to die.’ ”

I finished the repair and placed a padded dressing on his head. I gave instructions to his son and continued my journey to the Pheriche aid post. Three days later in Pheriche, the defining case in my wilderness medicine education arrived on the back of a yak. The patient being carried down the valley was a young New Zealand nurse named Barbara. She had not been feeling well for 2 days at 16,000 feet and was no longer able to descend under her own power. Barbara was alert and oriented, although she appeared very tired. She denied having a headache, nausea, or shortness of breath over the past 2 days, and she had just descended 2000 feet. I gave her a cup of tea. She drank half the cup and then lay down and fell asleep. I sat in a chair across the room and watched her. I half-convinced myself that she looked a little blue, then talked myself out of it. She had just descended a considerable distance, with only mild symptoms of possible altitude illness. She could not have high-altitude cerebral edema (HACE). I continued this internal debate for about an hour, until I felt like I needed to know if she was okay. I touched her shoulder and spoke her name. She did not respond. I shook her gently, and she shifted slightly and made unintelligible sounds. I shook her more vigorously, but she was unable to wake up. She was no longer just sleeping—she was unconscious. There was no radio at the aid post. I sent a written note to the park ranger in Namche, requesting a helicopter rescue for early the next morning. I gave her intravenous dexamethasone and put an oxygen mask over her mouth and nose running at 2 liters per minute, trying to conserve the only two small bottles of oxygen that we had on hand. A little while later, she suddenly stirred and vomited all over her sleeping bag. Over the course of the night, she deteriorated steadily. I observed the effects of every additional drop of fluid that leaked into her brain. She became decerebrate, then flaccid, then unresponsive to deep pain. She was clearly dying. It was now just a matter of whether the helicopter would arrive in time. I felt very alone, wondering if there was anything more that I could do. The night had been completely clear when I had stepped outside before taking a short nap. When I awoke at 6:00 A.M., it was snowing. I did not think a helicopter could fly through the mountains in a snowstorm. I had kept up my hope for rescue all night long, but at that moment I began to feel that she might not make it. When that thought hit me, I found myself emotionally unprepared to watch her die. Alone in a remote aid post, with one Sherpa helper and the patient’s best friend, the circumstances were too intimate, the patient too like myself. I realized what it meant to do medicine in a wilderness setting. You are on your own. There is no one to call, no one to help. You just have to do the best you can with whatever limited resources you have. At 10:00 A.M., a Sherpa arrived carrying a portable radio. This enabled me to tell the park ranger how desperate the situation had become. His response was not encouraging. He informed me that he had been unable to reach Kathmandu by radio to request a helicopter. Later in the day, he was finally able to contact Kathmandu, but the trekking company refused to guarantee payment for a helicopter evacuation. The park ranger offered to guarantee the money himself. It got worse from there. A helicopter was ready at the airport, but the pilot had gone home for the day. When they tried to telephone him, they found that the phone lines had just gone dead. By this point, Barbara was completely unresponsive to deep pain and barely breathing at a rate of 4 times per minute. She had even lost her corneal reflexes. xv

FOREWORD

At least it had stopped snowing. I sat near the radio, waiting. The park ranger called again. “Maybe we should just try to organize the helicopter for tomorrow,” he told me. “She’s going to die this afternoon if we don’t rescue her,” I replied. “If you can’t get a helicopter this afternoon, there won’t be any point in sending one tomorrow.” “Got that,” said the ranger. Another hour went by. Finally, I heard the ranger’s voice. “Pheriche, Pheriche, Pheriche. This is Namche. The pilot has landed here and set off fuel. He’s on his way up the valley, but the weather is bad and he wants the patient ready to go.” I pulled out the intravenous line, and we secured Barbara in her sleeping bag. Her friend would fly out with her. I stepped outside the clinic and looked down the valley. Clouds whipped past the peaks. I spotted the Alouette III helicopter emerging from the clouds. I had never before been involved in a helicopter rescue, and the miraculous appearance of the aircraft seemed like an angel descending from heaven. The helicopter flew past the clinic, made an abrupt turn, and landed. The pilot shut down the rotors, but left the engine running. He waved impatiently for us to bring the patient. We carried her outside with the help of some trekkers and slid her onto the floor in the back of the helicopter, which immediately took off. We turned our faces away from the dust as the chopper disappeared down the valley, back into the clouds. It was 3 days before we got word about Barbara. She had arrived in the emergency room at Patan Hospital in Kathmandu an hour and a half after leaving us, having descended 10,000 feet. On arrival at the hospital, she was breathing 18 times per minute and was already responding to pain. Twenty-four hours later, she was sitting up in bed and eating. Thirty years later, I recognize that the key things I have learned about wilderness medicine were introduced during my experience of caring for Barbara. I was on my own, with no expert to whom I could turn for advice. I had to care for a patient in ways that I had never done in a hospital setting. I had to clean her up, turn her, catheterize her—all by candlelight, in addition to trying to figure out how to medically treat and evacuate her. Although her presentation of HACE remains the most atypical I have ever encountered, I still had to make a diagnosis and act on it, with no further tests or opinions to rely on. As I reflect back on these events, I still recall the depth of my fear that she would die despite my efforts. I have since witnessed on a number of occasions that this is a not-uncommon feeling among rescuers, who often feel devastated when the person they have tried to rescue ends up dying. Barbara’s illness taught me the value of personal experience. After this episode, the lectures I gave every day that season at the aid post on the prevention of altitude illness carried a sense of personal authority that I could not otherwise have evoked. Symptoms can be subtle. Altitude illness really can be fatal. Descent really is lifesaving. My career in medicine ran parallel to the development of the field of wilderness medicine. In the mid-1970s, physicians and mountain guides began to meet to discuss what was then called “mountain medicine.” The topics included altitude illness, first aid, frostbite, hypothermia, and evacuation. Lectures and handson workshops were included. Gradually the gatherings expanded to include topics of hiking and rafting and the skills that supported those activities, such as water disinfection, treatment of traveler’s diarrhea, and heat and cold injury. Because we were no longer talking only about the mountains, this new field was dubbed wilderness medicine. Lecturers shared their anecdotal experiences and opinions, but soon they mined the research literature and carried out investigations of their own. In 1983, the first edition of Wilderness Medicine was published. It was also in 1983 that I moved to Kathmandu to begin a 15-year stint working at the CIWEC Clinic Travel Medicine Center and started carrying out my own research into the diseases and injuries that affect travelers in Nepal. Wilderness Medicine now appears in its sixth edition. Rather than wilderness medicine defining what should be in the textbook, the textbook has helped define what is in the field of wilderness medicine. Instead of focusing solely on traditional xvi

areas, the editor has opted for inclusiveness, covering topics that include such stalwarts as lightning and frostbite, but also volcanic eruptions, combat casualty care, alligator and crocodile attacks, global humanitarian medicine, and space travel. Despite this wide range of knowledge, the specialty of wilderness medicine still has a common denominator: when something bad happens in the field, immediacy and bonding lead to an increased emotional requirement from the rescuers. In addition to diagnosis and treatment of the patient, one is confronted with limited resources and the compounding factors of weather, terrain, and isolation. Not infrequently, rescuers have to place themselves in harm’s way. At the very least, they may have to endure their own discomfort and exhaustion. Although these factors create a different dynamic of medical care, ultimately the goal is the same—to ease or prevent suffering in the patient. The quest for adventure may take travelers to countries with little or no available medical care. Many adventurers think only of their personal medical situation or of the risks that they are taking in a remote environment. They may give little or no thought to the thousands of people along their routes who can live entire lives without access to even basic medical care. The plight of the world’s poorest people may only briefly come to light at those times when a major disaster strikes. Wilderness medicine aficionados have frequently been rescuers in these extreme situations. Their experiences have sometimes taught the physicians what it really means to try to practice medicine on behalf of people who have no resources. They often return with a newly discovered desire to share medical knowledge and skills around the planet on an ongoing basis. They have come to recognize that all human beings are the same in wanting to be happy and free from suffering. Seen in this light, there is no difference between a mountaineer with altitude illness, the traveler with diarrhea, a Tibetan refugee with frostbite, the woman in an African village in the midst of a difficult birth, or a child shivering with the fever of malaria. My initial attraction to high-altitude medicine had far-reaching consequences in my personal life that I could never have foreseen. After three trekking seasons in the mountains, I moved to Kathmandu, and within a year I had volunteered to be the doctor for a Tibetan Buddhist monastery. The head of the monastery, Chokyi Nyima Rinpoche, became my teacher and close personal friend. By applying his teachings on Buddhist philosophy to my medical practice, I became more the physician I wanted to be— calmer, kinder, clear thinking, and willing to help. Our friendship led to collaboration on a book about how to train in compassion. I strongly believe that there is a way to connect wilderness medicine to conventional medicine, and even further, to our personal lives. This advice can be condensed into three key principles. First, there is competence. We should be advocates of learning and apprenticeship in the backcountry and not be satisfied with merely attaining just enough fitness to be guided on an adventure. Although one can take pleasure from achieving a distinct goal, one’s satisfaction is greatly enhanced by the cultivation of skills gained through lectures, practice in the field, and extensive personal experience. When one starts to plan a journey or an adventure, one needs to do research and fully understand the limitations imposed by that activity. Are there hazards of weather and terrain that could result in being stranded for long periods? Is there the possibility of rescue? Where is the closest medical care? To what degree are we prepared to accept the situation? Commitment means accepting the risks and limitations of a given adventure before facing the challenge, so that one can deal with it realistically. Ideally one would like to avoid having to say, “If I had known it was going to be like this, I would never have gone.” Finally, no matter what happens, one should always make decisions with full consideration of compassion. This could involve abandoning one’s own goals to help someone else or modifying the trip so that everyone can succeed. There is a famous Tibetan Buddhist saying that is true in all aspects of our lives, including our wilderness adventures:

Adventures in the wilderness, by occasionally taking us close to our limits, can teach us a great deal about our true nature. A well-known mountaineer, after living through a major rescue drama on Mt Everest, once said, “The person I wanted to be met the person I actually was.” In such defining moments, I have observed that those who abandoned their own ambitions in order to help others have always ended up happier than those who pursued only their own goals.

The wilderness is a proving ground that draws us in with its physical splendor, then tests us with hardship. We are often changed by these encounters. Whether we perceive these changes as positive or not may depend less on whether we have succeeded in our adventurous goals and more on how we learned to conduct ourselves in pursuit of those goals. The elderly Sherpa with the head laceration healed without infection and lived for 3 more years, before dying of old age. David R. Shlim, MD Author, Medicine and Compassion: A Tibetan Lama’s Guidance for Caregivers Jackson Hole, Wyoming

xvii

FOREWORD

All the joy the world contains Has come through wishing happiness for others. All the misery the world contains Has come through wanting pleasure for oneself.

Preface The sixth edition of Wilderness Medicine arrives at an exciting juncture for the field and its practitioners. Except at the time of the origin of the practice of medicine, when one might argue that perhaps all of medicine was “wilderness medicine,” there has never been greater need for people to heal in austere settings. With each natural disaster, adventure into uncharted territory, and global humanitarian relief effort, medical professionals and amateurs alike must make diagnoses with their eyes, ears, fingertips, and noses; better understand the unique physiology and pathophysiology of extreme environments; and recognize the limitations of technology in the deepest jungles and on the most remote mountaintops. More than any other specialty of medicine, wilderness medicine engages humans with Planet Earth, as it constantly calls the question, “What can we do to help?” We should help our fellow humans, while we always seek to preserve the planet. On the eve of the sixth edition, it is fair for an editor to reminisce. I suspect that many readers of this book were not born when the first edition of Wilderness Medicine (then titled Management of Wilderness and Environmental Emergencies) was published. I owe so much to the contributors to each and every edition, who in the beginning ranged from savvy clinicians and hardy explorers to youthful (and upstart) innovators. Without the collaboration of my best friend, Edward Geehr, and inspiration from the legendary professors Charlie Houston and Dave Sabiston, this book would have never exited my typewriter. In the beginning, it was no more complicated than the fact that Ed and I loved the outdoors. We had been medical students together at Duke, where we camped and hit the beach, and then enjoyed what little free time we had as interns at Dartmouth hiking and cross-country skiing. During medical school, I had been an extern on the prairie for the Indian Health Service at Fort Belknap in Montana and Ed an instructor in the mountains of New Hampshire for Outward Bound. When we were emergency medicine residents at the University of California, Los Angeles, we attended one particular mountain medicine symposium at the Yosemite Institute and listened to Charlie Houston, Herb Hultgren, John Dill, and other experts spin tales of intertwined adventure and medicine. There was no book for physicians that covered what we had heard and what more we wished to learn, so we proposed the first edition of what became Wilderness Medicine. After more than a few turndowns, the book was published as a title in the Nursing Division at Macmillan, because even though we were young and unknown, an acquisitions editor believed in us. We endured a tempestuous relationship with our senior editor, so we eagerly moved to Mosby for the second edition. The book has remained here through a series of mergers with Saunders and Elsevier. It has been a blessing to have a publisher with a vision for the vitality and relevance of wilderness medicine, and the imagination to understand that this field crosses into uncharted territory. In this edition, Dolores Meloni, Lucia Gunzel, and Jessica Becher have put forth their wonderful Elsevier spirit. My lifelong wilderness medicine buddies are too numerous to count, sustaining me for more than three decades. Each generation has raised the bar. With every edition, we used the book to push the envelope. As the content of Wilderness Medicine expanded, so did the training, practice, research, and education. It was not my intention to define the specialty, but it happened. Somewhere around the third edition, numerous aspects of a thriving specialty emerged, eminently capable leaders arose, and I could put the cart behind the horse. Now, we run to catch up, and I suspect that it will be that way forever. As change abounds, we daily appreciate novel interrelationships that are integral to a complete understanding of wilderness

medicine. High altitude is not just about hypoxia. It is about exercise physiology, genetics, ventilatory response during sleep, and much more. Understanding frostbite requires superb knowledge of anatomy, cell membrane function, reperfusion injury, and much more. To comprehend the field management of trauma, one must integrate all of the complexities related to hemorrhage, shock, hypoxia, and pain. The entire field of wilderness medicine does much more than overlap with military medicine, disaster medicine, sports medicine, environmental medicine, and travel medicine—it defines many of their most important features. Wilderness medicine is much more holistic than I would ever have imagined. Yet as robust as it has become, it will continue to expand, because we have only scratched the surface and our need is so great to know more. In recognition of venues in which wilderness medicine has been applied, to support a continuing effort to deliver credible information about the wilderness environment, and based upon requests from readers, much has been added to this sixth edition. Some of the chapters, such as Expedition Medicine, Global Humanitarian Medicine and Disaster Relief, and Ultrasound and Telemedicine in the Wilderness, are completely new, whereas others are refinements derived from wanting to leave no stone unturned. Because wilderness medicine volunteers are so capable under difficult circumstances, such as while providing disaster or global humanitarian relief, I have invited experts to broaden the coverage and better meet the information needs of the readers. Wilderness Medicine is affected by an accelerating sea change in the publishing world. Electronic publishing—words, images, and multimedia presentations—will one day render paper pages obsolete, except for collectors. Information is available instantly and disseminates at light speed, so the obligations of authors and editors have multiplied and deepened. This edition of Wilderness Medicine occurs at a watershed, when the contributors have provided much more material than can be economically offered in printed volumes. As a result, the traditional book contains the information one must be able to retrieve even when the power fails (… and if you are willing to carry 20 pounds of textbook with you); the entire electronic offering with its additional features will be there when your Internet connection is good or the power for your tablet or e-reader is plentiful. For authors, all of this takes a bit of acclimation. For readers, I suspect the transition will be welcome. There is much discussion these days about the future of medicine and in particular, if it is headed in a good direction. The camaraderie of the wilderness medicine community negates any doubts about whether or not medicine is still a desirable career path. In the days immediately after the January 2010 earthquake in Haiti, I stood side by side in Port-au-Prince with wilderness medicine colleagues from around the globe—pediatric surgeons from Switzerland, logistics experts from Norway, mountaineers from the United States, ocean divers from Spain— to put our collective skills to the most difficult challenge of our careers. Time and time again, military medical personnel make essential use of research and practice advances generated by wilderness medicine specialists that decrease morbidity and improve survival in extreme environmental settings. During global humanitarian relief efforts, when there are scarce resources, physicians, nurses, and other health care professionals who have learned how to make do with what is at hand through wilderness medicine education programs are vital to their adopted communities. The doctor who accompanies climbers to the base camp at Mt Everest also builds clinics in rural Nepal, and a nurse who leads adventure treks is moved to staff a refugee camp in the Sudan. Wilderness medicine resides at the core of what it means to be a healer. xix

PREFACE

Wilderness is at the center of wilderness medicine. To a certain degree and appropriately so, wilderness will always remain enigmatic and mysterious. Its verdant landscapes and abundant wildlife should be approached with the explicit understanding that human intrusion on its current scale is a recent phenomenon. The best that our collective environmental efforts have been able to do for wilderness is limit its destruction. We speak and write of managing wilderness, but that activity really means that we are trying to protect it from humansponsored consumption and devastation. Humans are a force of nature, so if wilderness is to cease shrinking and unimpeded fulfill its destiny, without wholesale alteration of patterns and disruption of natural cycles, then our behaviors must change. Today wilderness is considered austere because it is remote and not defined by modern technology. Our appreciation for it grows greater because breathtaking scenery is becoming more elusive. If we are not proactive, then tomorrow’s wilderness will be desolate because it has become used up and bleak. For heaven’s sake, we cannot let that happen. For the rest of my career, I am going to try to give something back. My wife, Sherry, and I began doing that with three wonderful children—Brian, Lauren, and Danny. By helping to establish a specialty, a research tradition, the Wilderness Medical Society, a peer-reviewed journal, education programs, affinity groups, clubs, and an ethos of service and multiple goals to which wilderness medicine enthusiasts can aspire, this book has accomplished its mission. Wilderness medicine in the modern

xx

age has passed its infancy and is now into childhood. There is still so much to be done. Let us together go forward with integrity and optimism.

Paul S. Auerbach, MD, MS, FACEP, FAWM

Photo credits for cover images and part openers Cover: Photographs on the cover are provided courtesy of fine art landscape photographer Elizabeth Carmel from Truckee, California. Her wonderful images may be viewed at www.ElizabethCarmel.com and www.TheCarmelGallery.com. (All images copyright ElizabethCarmel.com.) Back Cover: For cover photos and other outdoor images, visit www.TheCarmelGallery.com. Part 1: Upper: Courtesy Paul S. Auerbach, MD; Middle and Lower: Courtesy Mathias Schar, MD Part 2: Upper: Courtesy Mathias Schar, MD; Lower: Courtesy Paul S. Auerbach, MD Part 3: Upper: Courtesy R.W. Halsey, California Chaparral Field Institute; Middle: Courtesy NASA; Lower: Courtesy Michael Poland, U.S. Geological Survey Part 4: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Sheri Trbovich and Weber County Sheriff’s Department; Lower: Courtesy Jack Putnam, Maridocs Part 5: Upper: Courtesy Will Smith; Middle: Courtesy Kris H. Green; Lower: Courtesy Mathias Schar, MD Part 6: Upper: Courtesy Timothy Floyd; Middle: Courtesy Jan Ove Rein; Lower: Courtesy Michael Cardwell Part 7: Upper: Provided by K. Davison and R. Marinelli; Middle: Courtesy asimulator via flickr.com; Lower: Courtesy Daniel Ryan Part 8: Upper: Courtesy Brenda Tiernan, RN; Middle and Lower: Courtesy Paul S. Auerbach, MD Part 9: Upper and Lower: Courtesy Carl Roessler; Middle: Courtesy Marty Snyderman Part 10: Upper: Courtesy Paul S. Auerbach, MD; Middle: Courtesy Francesco Zizola, Médecins Sans Frontiéres; Lower: Courtesy N. Stuart Harris, MD Part 11: Upper: Courtesy N. Stuart Harris, MD; Middle: Courtesy Mathias Schar, MD; Lower: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Part 12: Upper: Courtesy Corbis; Middle: Courtesy Craig Gray; Lower: Courtesy Paul S. Auerbach, MD Part 13: Upper: Courtesy Arius Hopman; Middle: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal; Lower: Courtesy Paul S. Auerbach, MD Index: Courtesy Mingmar Sherpa, Peak Promotion Pvt. Ltd., Kathmandu, Nepal Preface: Courtesy Chuck Liddy, The News & Observer, 2010

xxv

CHAPTER 1 

High-Altitude Medicine and Physiology PETER H. HACKETT AND ROBERT C. ROACH

The Population More than 40 million tourists visit recreation areas above 2400 m (7874 feet) in the American West each year. Hundreds of thousands visit central and south Asia, Africa, and South America, many traveling to altitudes above 4000 m (13,123 feet). In addition, millions live in large cities above 3000 m (9843 feet) in South America and Asia. The population in the Rocky Mountains of North America has doubled in the past decade; 700,000 live above 2500 m (8202 feet) in Colorado alone. Increasingly, physicians and other health care providers are confronted with questions of prevention and treatment of high-altitude medical problems (Box 1-1), as well as the effects of altitude on preexisting medical conditions. Despite advances in high-altitude medicine, significant morbidity and mortality persist (Table 1-1). Clearly, better education of the population at risk and those advising them is essential. Altitude illness should be considered a public health problem. In this chapter, we emphasize clinical issues likely to be encountered in lowlanders visiting high-altitude locations by reviewing basic phy­siology of ascent and the pathophysiology, recognition, and management of medical problems for both visitors and residents of high altitudes (see Box 1-1).

Definitions HIGH ALTITUDE (1500 to 3500 M [4921 to 11,483 FEET]) The onset of physiologic effects of diminished partial pressure of inspired oxygen (PIO2) includes decreased exercise performance and increased ventilation (lower PaCO2) (Box 1-2). Minor impairment exists in arterial oxygen transport (arterial oxygen saturation [SaO2] at least 90%), but PaO2 is significantly diminished. Because of the large number of people who ascend rapidly to 2500 to 3500 m (8202 to 11,483 feet), high-altitude illness is common in this range (Table 1-2; see Table 1-1).

VERY HIGH ALTITUDE (3500 to 5500 M [11,483 to 18,045 FEET]) Maximum arterial oxygen saturation falls below 90% as PaO2 falls below 50 mm Hg (Figure 1-1; see Table 1-2). Extreme hypoxemia may occur during exercise, sleep, and high-altitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.

EXTREME ALTITUDE (HIGHER THAN 5500 M [18,045 FEET]) Marked hypoxemia, hypocapnia, and alkalosis characterize extreme altitude. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no permanent human habitation is above 5500 m (18,045 feet). A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude illness.

The Environment of High Altitude Barometric pressure falls with increasing altitude in a logarithmic fashion (Table 1-3). Therefore the partial pressure of oxygen 2

(21% of barometric pressure) also decreases, resulting in the primary insult of high altitude: hypoxia. At approximately 5800 m (19,029 feet), barometric pressure is one-half that at sea level, and on the summit of Mt Everest (8848 m [29,029 feet]) the inspired pressure of oxygen is approximately 28% that at sea level (see Figure 1-1 and Table 1-3). The relationship of barometric pressure to altitude changes with distance from the equator. Thus, polar regions afford greater hypoxia at high altitude in addition to extreme cold. West565 has calculated that barometric pressure on the summit of Mt Everest (27 degrees N latitude) would be about 222 mm Hg instead of 253 mm Hg if Mt Everest were located at the latitude of Mt McKinley (62 degrees N). Such a difference, he claims, would be sufficient to render impossible an ascent without supplemental oxygen. In addition to the role of latitude, fluctuations related to season, weather, and temperature affect the pressure-altitude relationship. Pressure is lower in winter than in summer. A lowpressure trough can reduce pressure 10 mm Hg in one night on Mt McKinley, making climbers awaken “physiologically higher” by 200 m (656 feet). The degree of hypoxia is thus directly related to barometric pressure, not solely to geographic altitude.565 Temperature decreases with altitude (average of 6.5° C [11.7° F] per 1000 m [3281 feet]), and the effects of cold and hypoxia are generally additive in provoking both cold injuries and highaltitude pulmonary edema.419,559 Ultraviolet light penetration increases approximately 4% per 300-m (984-foot) gain in altitude, increasing the risks for sunburn, skin cancer, and snowblindness. Reflection of sunlight in glacial cirques and on flat glaciers can cause intense radiation of heat in the absence of wind. We have observed temperatures of 40° to 42° C (104° to 107.6° F) in tents on both Mt Everest and Mt McKinley. Heat problems, primarily heat exhaustion, are often unrecognized in this usually cold environment. Physiologists have not yet examined the consequences of heat stress or rapid, extreme changes in environmental temperature combined with the hypoxia of high altitude. Above the snow line is the “high-altitude desert,” where water can be obtained only by melting snow or ice. This factor, combined with increased water loss through the lungs from increased respiration and through the skin, commonly results in dehydration that may be debilitating. Thus, the high-altitude environment imposes multiple stresses, some of which may contribute to or be confused with the effects of hypoxia.

Acclimatization to High Altitude Although rapid exposure from sea level to the altitude at the summit of Mt Everest (8848 m [29,029 feet]) causes loss of consciousness in a few minutes and death shortly thereafter, climbers can ascend Mt Everest over a period of weeks, without supplemental oxygen, because of a process termed acclimatization. A complex series of physiologic adjustments increases oxygen delivery to cells and also improves their hypoxic tolerance. The severity of hypoxic stress, rate of onset, and individual physiology determine whether the body successfully acclimatizes or is overwhelmed. Recently, a revolution has taken place in our understanding of the molecular mechanisms of human responses to hypoxia. At the center of this rapidly changing field is hypoxia-inducible factor (HIF), a transcription factor that modulates the expression

BOX 1-2  Glossary of Physiologic Terms

Lowlanders on Ascent to Altitude • Acute hypoxia • High-altitude headache • Acute mountain sickness • High-altitude cerebral edema • Cerebrovascular syndromes • High-altitude pulmonary edema • Symptomatic pulmonary hypertension • High-altitude deterioration • Organic brain syndrome (extreme altitude) • Peripheral edema • Retinopathy • Disordered sleep • Sleep periodic breathing • High-altitude pharyngitis, bronchitis, and cough • Ultraviolet keratitis (snowblindness) • Exacerbation of preexisting conditions

PB P O2 PIO2 PAO2 PACO2 PaO2 PaCO2 SaO2 RQ Alveolar gas equation

Barometric pressure* Partial pressure of oxygen Inspired PO2 (0.21 × [PB − 47 mm Hg] (47 mm Hg = vapor pressure of H2O at 37° C [98.6° F]) PO2 in alveolus PCO2 in alveolus PO2 in arterial blood PCO2 in arterial blood Arterial oxygen saturation (HbO2 ÷ total Hb × 100) Respiratory quotient (CO2 produced ÷ O2 consumed) PAO2 = PIO2 − (PACO2/RQ)

*Pressures are expressed as mm Hg (1 mm Hg = 1 Torr).

on repeated exposure if rate of ascent and altitude gained are similar, supporting the notion of important genetic factors. Successful initial acclimatization protects against altitude illness and improves sleep. Longer-term acclimatization (weeks) primarily improves aerobic exercise ability. These adjustments disappear at a similar rate on descent to low altitude. A few days at low altitude may be sufficient to render a person susceptible to altitude illness, especially high-altitude pulmonary edema (HAPE), on reascent. The improved ability to do physical work at high altitude, however, persists for weeks.317 Persons who live at high altitude during growth and development appear to realize the maximum benefit of acclimatization changes; for example, their exercise performance matches that of persons at sea level.365

Life or Long-Term Residents of Altitude • Chronic mountain sickness (chronic mountain polycythemia) • Symptomatic high-altitude pulmonary hypertension with or without right heart failure • Problems of pregnancy: preeclampsia, hypertension, and low-birth-weight infants • Exacerbation of lung disease and congenital heart disease

of hundreds of genes, including those involved in apoptosis, angiogenesis, metabolism, cell proliferation, and permeability processes.90,423,484-487,503,504 In chronic hypoxia, HIF activation by hypoxia has the positive effect of elevating oxygen delivery by boosting hemoglobin mass. But HIF also plays a role in carotid body sensitivity to hypoxia, which in turn largely determines the ventilatory response to hypoxia. As a master regulator of the hypoxia response in humans, HIF has some beneficial and harmful effects at different stages in the time course of human exposure to hypoxia, and in different cells in the body. See Figure 1-2 for an overview of some of the hundreds of processes in which the response to hypoxia is modulated by HIF. Individuals vary in their ability to acclimatize, no doubt reflecting certain genetic polymorphisms, including HIF. Some adjust quickly, without discomfort, whereas acute mountain sickness (AMS) develops in others, who go on to recover. A small percentage fails to acclimatize even with gradual exposure over weeks. The tendency to acclimatize well or to become ill is consistent

VENTILATION By reducing alveolar carbon dioxide, increased ventilation raises alveolar oxygen, improving oxygen delivery (Figure 1-3; see Figure 1-1). This response starts as low as 1500 m (4921 feet) (PIO2 = 124.3 mm Hg; see Table 1-3) and within the first few minutes to hours of high-altitude exposure. The carotid body, sensing a decrease in PaO2, through a HIF-mediated process, signals the central respiratory center in the medulla to increase ventilation.153,281 This carotid body function (hypoxic ventilatory response [HVR]) is genetically determined562 but influenced by a number of extrinsic factors. Respiratory depressants such as alcohol and soporifics, as well as fragmented sleep, depress HVR. Agents that increase general metabolism, such as caffeine and coca, as well as specific respiratory stimulants, such as progesterone277 and almitrine,192 increase HVR. (Acetazolamide, a respiratory stimulant, acts on the central respiratory center rather than

TABLE 1-1  Incidence of Altitude Illness in Various Groups

Study Group

Number at Risk per Year

Western state visitors

30 million

Mt Everest trekkers

12,000

Mt McKinley climbers Mt Rainier climbers Mt Rosa, Swiss Alps

1200 10,000 †

Indian soldiers Aconcagua climbers Kilimanjaro hikers

Unknown 4200 2500

Maximum Altitude Reached (m [ft])

Average Rate of Ascent*

~2000 (6562) ~2500 (8202) ~≥3000 (9843) 3000-5200 (9843-17,060)

3500 (11,483)

1-2

5500(18,045)

3000-5300 (9843-17,388) 3000 (9843) 2850 (9350) 4559 (14,957) 3000-5500 (9843-18,045) 3300-5800 (10,827-19,029) 2700-4700 (8858-15,420)

6194 4392 2850 4559 5500 6962 5895

1-2 (fly in) 10-13 (walk in) 3-7 1-2 1-2 2-3 1-2 2-8 2-6

Sleeping Altitude (m [ft])

(20,322) (14,409) (9350) (14,957) (18,045) (22,841) (19,341)

Percent With AMS 18-20 22 27-42 47 23 30-50 30 67 7 27 † 39 (LLS >4) 50-83

Percent With HAPE and/or HACE

Reference

0.01

214

1.6 0.05 2-3 — — 5 2.3-15.5 2.2 †

376 181 286 323 99, 323, 475 499, 500 405 106, 242

AMS, Acute mountain sickness; HAPE, high-altitude pulmonary edema; HACE, high-altitude cerebral edema; LLS, Lake Louise score. *Days to sleeping altitude from low altitude. †Reliable estimate unavailable.

3

CHAPTER 1  High-Altitude Medicine and Physiology

BOX 1-1  Medical Problems of High Altitude

PART 1  MOUNTAIN MEDICINE

TABLE 1-2  Arterial Blood Gases and Altitude* Population

Altitude Meters †

Altitude residents Acute exposure

Subacute exposure

1646 2810‡ 3660‡ 4700‡ 5340‡ 6140‡ 6500§ 7000§ 8000§ 8400|| 8848§ 8848¶

Feet

PB (mm Hg)

5400 9219 12,008 15,420 17,520 20,144 21,325 22,966 26,247 27,559 29,029 29,029

630 543 489 429 401 356 346 324 284 272 253 253

PaO2 (mm Hg)

SaO2 (%)

PaCO2 (mm Hg)

73.0 60.0 47.6 44.6 43.1 35.0 41.1

(65.0-83.0) (47.4-73.6) (42.2-53.0) (36.4-47.5) (37.6-50.4) (26.9-40.1) ± 3.3

95.1 91.0 84.5 78.0 76.2 65.6 75.2

35.6 (30.7-41.8) 33.9 (31.3-36.5) 29.5 (23.5-34.3) 27.1 (22.9-34.0) 25.7 (21.7-29.7) 22.0 (19.2-24.8) 20 ± 2.8

36.6 24.6 30.3 30.6

± ± ± ±

67.8 ± 5 54 58 ± 4.5

2.2 5.3 2.1 1.4

(93.0-97.0) (86.6-95.2) (80.5-89.0) (70.8-85.0) (65.4-81.6) (55.5-73.0) ±6

12.5 ± 1.1 13.3 11.2 ± 1.7 11.9 ± 1.4

PB, Barometric pressure; PaCO2, arterial partial pressure of carbon dioxide; PaO2, arterial partial pressure of oxygen; SaO2, arterial oxygen saturation. *Data are mean values and (range) or ± SD, where available. All values are for subjects age 20 to 40 years who were acclimatizing well. † Data from reference 302. ‡ Data from reference 343. § Data for chronic exposure during Operation Everest II from reference 526. || Data from near the summit of Mt Everest from reference 172. ¶ Data from the simulated summit of Mt Everest from reference 430.

SaO2

160

100

140

90

PIO2

120

80

100 80

70

PaO2

60

SaO2 (%)

Partial pressure oxygen (mm Hg)

on the carotid body.) Physical conditioning apparently has no effect on HVR. Numerous studies have shown that a good ventilatory response enhances acclimatization and performance and that a very low HVR may contribute to illness433 (see Acute Mountain Sickness and High-Altitude Pulmonary Edema, later). However, over a normal range of values, HVR is not a reliable predictor of susceptibility to altitude illness. Other factors influence ventilation on ascent to high altitude. As ventilation increases, hypocapnia produces alkalosis, which acts as a braking mechanism on the central respiratory center and limits a further increase in ventilation. To compensate for the alkalosis, within 24 to 48 hours of ascent the kidneys excrete bicarbonate, decreasing the pH toward normal; ventilation increases as the braking effect of the alkalosis is removed. Ventilation continues to increase slowly, reaching a maximum only after 4 to 7 days at the same altitude (see Figure 1-3). The plasma bicarbonate concentration continues to drop and ventilation to increase with each successive increase in altitude. Persons with

60

40 20 0

2000

4000

6000

50 8000 10,000

Altitude (m) FIGURE 1-1  Increasing altitude results in decreasing inspired PO2 (PIO2), arterial PO2 (PaO2), and arterial oxygen saturation (SaO2). Note that the difference between PIO2 and PaO2 narrows at high altitude because of increased ventilation and that SaO2 is well maintained while awake until over 3000 m (9843 feet). (Data from Morris A: Clinical pulmonary function tests: A manual of uniform lab procedures, Salt Lake City, 1984, Intermountain Thoracic Society; and Sutton JR, Reeves JT, Wagner PD, et al: Operation Everest II: Oxygen transport during exercise at extreme simulated altitude, J Appl Physiol 64:1309, 1988.)

4

lower oxygen saturation at altitude have higher serum bicarbonate values; whether the kidneys might be limiting acclimatization or whether this reflects poor respiratory drive is not clear.102 This process is greatly facilitated by acetazolamide (see Acetazolamide Prophylaxis, later). The paramount importance of hyperventilation is readily apparent from the following calculation: the alveolar PO2 on the summit of Mt Everest (about 33 mm Hg) would be reached at only 5000 m (16,404 feet) if alveolar PCO2 stayed at 40 mm Hg, limiting an ascent without supplemental oxygen to near this altitude. Table 1-2 gives the measured arterial blood gas levels resulting from acclimatization to various altitudes.

CIRCULATION The circulatory pump is the next step in the transfer of oxygen, moving oxygenated blood from the lungs to the tissues. Systemic Circulation Increased sympathetic activity on ascent causes an initial mild increase in blood pressure, moderate increases in heart rate and cardiac output, and increase in venous tone. Stroke volume is low because of decreased plasma volume, which drops as much as 12% over the first 24 hours577 as a result of the bicarbonate diuresis, a fluid shift from the intravascular space, and suppression of aldosterone.35 Resting heart rate returns to near sea level values with acclimatization, except at extremely high altitude. Maximum heart rate follows the decline in maximal oxygen uptake with increasing altitude. As the limits of hypoxic acclimatization are approached, maximum and resting heart rates converge. During Operation Everest II (OEII), cardiac function was appropriate for the level of work performed and cardiac output was not a limiting factor for performance.417,518 Interestingly, myocardial ischemia at high altitude has not been reported in healthy persons, despite extreme hypoxemia. This is partly because of reduction in myocardial oxygen demand from reduced maximal heart rate and cardiac output. Pulmonary capillary wedge pressure is low, and catheter studies have shown no evidence of left ventricular dysfunction or abnormal filling pressures in humans at rest.174,236 On echocardiography, the left ventricle is smaller than normal because of decreased stroke volume, whereas the right ventricle may become enlarged.518 The abrupt increase in pulmonary artery pressure can cause a change in left ventricular diastolic function, but because of compensatory increased atrial contraction, no overt diastolic dysfunction results.7 In trained athletes doing an ultramarathon, the strenuous exercise at high altitude did not result in left ventricular damage; however, wheezing, reversible pulmonary hypertension, and right ventricular dysfunction occurred in one-third of those completing the race and resolved within 24 hours.107

Pressure, Estimated Partial Pressure of Inspired Oxygen, and the Equivalent Oxygen Fraction at Sea Level*

m

ft

PB

PIO2

FIO2 at SL

Sea level 1000 1219 1500 1524 1829 2000 2134 2438 2500 2743 3000 3048 3353 3500 3658 3962 4000 4267 4500 4572 4877 5000 5182 5486 5500 5791 6000 6096 6401 6500 6706 7000 7010 7315 7500 7620 7925 8000 8230 8500 8534 8839 8848 9000 9144 9500 10,000

Sea level 3281 4000 4921 5000 6000 6562 7000 8000 8202 9000 9843 10,000 11,000 11,483 12,000 13,000 13,123 14,000 14,764 15,000 16,000 16,404 17,000 18,000 18,045 19,000 19,685 20,000 21,000 21,325 22,000 22,966 23,000 24,000 24,606 25,000 26,000 26,247 27,000 27,887 28,000 29,000 29,029 29,528 30,000 31,168 32,808

759.6 678.7 661.8 640.8 639.0 616.7 604.5 595.1 574.1 569.9 553.7 536.9 533.8 514.5 505.4 495.8 477.6 475.4 460.0 446.9 442.9 426.3 419.7 410.2 394.6 393.9 379.5 369.4 364.9 350.7 346.2 337.0 324.2 323.8 310.9 303.4 298.6 286.6 283.7 275.0 265.1 263.8 253.0 252.7 247.5 242.6 230.9 215.2

149.1 132.2 128.7 124.3 123.9 119.2 116.7 114.7 110.3 109.4 106.0 102.5 101.9 97.9 95.9 93.9 90.1 89.7 86.4 83.7 82.9 79.4 78.0 76.0 72.8 72.6 69.6 67.5 66.5 63.6 62.6 60.7 58.0 57.9 55.2 53.7 52.6 50.1 49.5 47.7 45.6 45.4 43.1 43.1 42.0 40.9 38.5 35.2

0.209 0.185 0.180 0.174 0.174 0.167 0.164 0.161 0.155 0.154 0.149 0.144 0.143 0.137 0.135 0.132 0.126 0.126 0.121 0.117 0.116 0.111 0.109 0.107 0.102 0.102 0.098 0.095 0.093 0.089 0.088 0.085 0.081 0.081 0.077 0.075 0.074 0.070 0.069 0.067 0.064 0.064 0.060 0.060 0.059 0.057 0.054 0.049

Exp, Exponent; FIO2, fraction of inspired oxygen; PB, barometric pressure; PIO2, partial pressure of inspired oxygen; SL, sea level. *Barometric pressure is approximated by the equation PB = Exp (6.6328 − {0.1112 × altitude − [0.00149 × (altitude2)]}), where altitude = terrestrial altitude in meters/1000 or km. PIO2 is calculated as the PB − 47 (where 47 = water vapor pressure at body temperature) × fraction of O2 in inspired air. The equivalent FIO2 at sea level for a given altitude is calculated as PIO2 ÷ (760 − 47). Substituting ambient PB for 760 in the equation allows similar calculations for FIO2 at different altitudes.

Pulmonary Circulation On ascent to high altitude, a prompt but variable increase in pulmonary vascular resistance from hypoxic pulmonary vasoconstriction increases pulmonary artery pressure. Mild pulmonary hypertension is greatly augmented by exercise, with pulmonary pressure reaching near-systemic values,174 especially in persons with a previous history of high-altitude pulmonary edema.32,110 During OEII, Groves and colleagues174 demonstrated that even with a mean pulmonary artery pressure of 60 mm Hg, cardiac output remained appropriate and right atrial pressure did not rise above sea level values. Thus, right ventricular function was intact

in spite of extreme hypoxemia and pulmonary hypertension in these well-acclimatized subjects. Administration of oxygen does not completely restore pulmonary artery pressure to sea level values,324 likely because of vascular remodeling with medial hypertrophy. See Stenmark and associates509 for an excellent review of molecular and cellular mechanisms of the pulmonary vascular response to hypoxia, including remodeling. Pulmonary vascular resistance returns to normal within a few weeks after descent to low altitude. Cerebral Circulation Cerebral oxygen delivery, the product of arterial oxygen content and cerebral blood flow (CBF), depends on the net balance between hypoxic vasodilation and hypocapnia-induced vasoconstriction. CBF increases, despite hypocapnia, when PaO2 is less than 60 mm Hg (altitude greater than 2800 m [9186 feet]). In a classic study, CBF increased 24% on abrupt ascent to 3810 m (12,500 feet) and returned to normal over 3 to 5 days.491 These findings have been confirmed by positron emission tomography and brain magnetic resonance imaging (MRI) studies showing both elevations in CBF in hypoxia in humans and striking heterogeneity of the CBF, with CBF rising up to 33% in the hypothalamus and 20% in the thalamus, with other areas without significant changes.66,396 Cerebral autoregulation, the process by which cerebral perfusion is maintained as blood pressure varies, is impaired in hypoxia. Interestingly, this occurs both in newcomers, with acute246,296,521,547 and prolonged hypoxia,522 and in natives to high altitude.246 This observation raises questions about the importance of this process in AMS and acclimatization, because it appears to be a uniform response in all humans made hypoxemic. Overall, global cerebral metabolism seems well maintained with moderate hypoxia.103,356

BLOOD Hematopoietic Responses to Altitude Ever since the observation in 1890 by Viault550 that hemoglobin concentration was higher than normal in animals living in the Andes, scientists have regarded the hematopoietic response to increasing altitude as an important component of the acclimatization process. On the other hand, hemoglobin values apparently have no relationship to susceptibility to high-altitude illness. In response to hypoxemia, erythropoietin is secreted by the kidneys and stimulates bone marrow production of red blood cells.483 The hormone is detectable within 2 hours of ascent, nucleated immature red blood cells can be found on a peripheral blood smear within days, and new red blood cells are in circulation within 4 to 5 days. Over a period of weeks to months, red blood cell mass increases in proportion to the degree of hypoxemia. Iron supplementation can be important; women who take supplemental iron at high altitude approach the hematocrit values of men at altitude202 (Figure 1-4). The increase in hemoglobin seen 1 to 2 days after ascent is due to hemoconcentration secondary to decreased plasma volume, rather than a true increase in red blood cell mass. This results in a higher hemoglobin concentration at the cost of decreased blood volume, a trade-off that might impair exercise performance. Longer-term acclimatization leads to an increase in plasma volume as well as in red blood cell mass, thereby increasing total blood volume. Overshoot of the hematopoietic response causes excessive polycythemia, which may impair oxygen transport because of increased blood viscosity. Although the “ideal” hematocrit at high altitude is not established, phlebotomy is often recommended when hematocrit values exceed 60% to 65%. During the American Medical Research Expedition to Mt Everest (AMREE), hematocrit was reduced by hemodilution from 58% ± 1.3% to 50.5% ± 1.5% at 5400 m (17,717 feet) with no decrement in maximum oxygen uptake and increased cerebral functioning.465 Oxyhemoglobin Dissociation Curve The oxygen dissociation curve (ODC) plays a crucial role in oxygen transport. The sigmoidal shape of the curve allows wellmaintained SaO2 up to 3000 m (9843 feet), despite significant 5

CHAPTER 1  High-Altitude Medicine and Physiology

TABLE 1-3  Altitude Conversion: Barometric

PART 1  MOUNTAIN MEDICINE

Ub Ub

A Normoxia

PHD2

HIF-1α

Fe2+ 2-OG Ascorbate

PHD1 O2

Ub

PHD3

HIF-1α

HIF-1α

OH OH OAc

OH OH OAc

VHL

VHL

B Hypoxia HIF-1α HIF-1α

Ub Ub

Ub

26s Proteasome

Proteolytic degradation

HIF-1α HIF-1α p300/CBP HIF-1α

Nucleus

HIF-1β

HIF-1β HRE

Angiogenesis Erythropoiesis Apoptosis

Cell proliferation and survival

HIF-1 target genes

Proteolysis pH regulation Glucose metabolism

FIGURE 1-2  Regulation of oxygen sensing by hypoxia-inducible factor (HIF). The HIF is produced constitutively, but in normoxia the α subunit is degraded by the proteasome in an oxygen-dependent manner. Hypoxic conditions prevent hydroxylation of the α subunit, enabling the active HIF transcription complex to form at the hypoxia-response element (HRE) associated with HIF-regulated genes. A range of cell functions are regulated by the target genes, as indicated. CBP, CREB binding protein; OAc, acetylation of HIF-1α; 2-OG, 2-oxoglutarate; PHD, prolyl hydroxylase; Ub, ubiquitin; VHL, von Hippel–Lindau tumor suppressor. (Reprinted from Carroll VA, Ashcroft M: Targeting the molecular basis for tumour hypoxia, Expert Rev Mol Med 7:1, 2005.)

decreases in PaO2 (see Figure 1-1). Above 3000 m (9843 feet), small changes in PaO2 cause large changes in SaO2 (Figure 1-5). Because PaO2 determines diffusion of oxygen from capillary to cell, small changes in PaO2 can have clinically significant effects. This is often confusing for clinicians because SaO2 appears relatively well preserved. At high altitude, small changes in PaO2 lead to lower O2 uptake that can have a large effect on systemic hypoxemia, and thus on clinical status, while the SaO2 may appear relatively unchanged. In 1936, Ansel Keys and colleagues266 demonstrated an in vitro right shift in position of the ODC at high altitude, favoring release of oxygen from blood to tissues. This change, due to increased 2,3-diphosphoglycerate, is proportional to the severity of hypoxemia. In vivo, however, the alkalosis at moderate altitude offsets this, and no net change occurs. In contrast, the marked alkalosis of extreme hyperventilation, as measured on the summit and simulated summit of Mt Everest (PaCO2 8 to 10 mm Hg, pH greater than 7.5), shifts the ODC to the left, facilitating oxygen-hemoglobin binding in the lung that raises SaO2 and is advantageous.462 Persons with a very left-shifted ODC, caused by an abnormal hemoglobin (Andrew-Minneapolis), when taken to moderate (3100 m [10,171 feet]) altitude, had less tachycardia and dyspnea and remarkably had no decrease in exercise performance.208 Highaltitude adapted animals also have a left-shifted ODC.

TISSUE CHANGES The next link in the oxygen transport chain is tissue oxygen transfer, which depends on capillary perfusion, diffusion distance, and driving pressure of oxygen from the capillary to the cell. Banchero20 has shown that capillary density in dog skeletal muscle doubled in 3 weeks at a barometric pressure of 435 mm Hg. A recent study in humans noted no change in 6

capillary density or in gene expression thought to enhance muscle vascularity.316 Ou and Tenney395 revealed a 40% increase in mitochondrial number but no change in mitochondrial size, whereas the study of Oelz and colleagues392 showed that highaltitude climbers had normal mitochondrial density. A significant drop in muscle size is often noted after high-altitude expeditions because of net energy deficit,316,319 resulting in increased capillary density and ratio of mitochondrial volume to contractile protein fraction as a result of the atrophy. Although there is no de novo synthesis of capillaries or mitochondria, the net result is a shortening of diffusion distance for oxygen.316,319

SLEEP AT HIGH ALTITUDE Disturbed sleep is common at high altitude. There are multiple causes. Reflecting the great interest in sleep, more than 160 papers in the last 10 years have addressed sleep at altitude. The interested reader is referred to recent reviews.67,308,551,561,569 Nearly all subjects complain of disturbed sleep at high altitude, with severity increasing with the altitude. At moderate altitude, sleep architecture is changed, with a reduction in stages 3 and 4 sleep, stage 1 time increased, and little change in stage 2. Overall, there is a shift from deeper sleep to lighter sleep. In addition, more time is spent awake, with significantly increased arousals. Clinicians have reported either slightly less rapid eye movement (REM) time or no change in REM compared with what occurs at low altitude. REM sleep may improve over time at altitude.268 The subjective complaints of poor sleep are out of proportion to the small reduction (if any) in total sleep time and appear to be due to sleep fragmentation. With more extreme hypoxia, sleep time was dramatically shortened and arousals increased, without a change in ratio of sleep stages but with a reduction in REM sleep.10 The mechanisms of this change in sleep architecture and

~10% decrease

80 10 8 40

PACO2 (mm Hg)

~ No change

12

SaO2 (%)

· VE (L/min, BTPS)

100

CHAPTER 1  High-Altitude Medicine and Physiology

14

60

40

35

B

20

30 25

A

0 0

100

20

40

60

80

100

120

SaO2 (%)

PaO2 (mm Hg) FIGURE 1-5  Oxygen-hemoglobin dissociation curve showing effect of 10-mm Hg decrement in arterial partial pressure of oxygen (PaO2) on arterial oxygen saturation (SaO2) at sea level (A) and near 4400 m (14,436 feet) (B). Note the much larger drop in SaO2 at high altitude. (Modified from Severinghaus JW, Chiodi H, Eger EI, et al: Cerebral blood flow in man at high altitude: Role of cerebrospinal fluid pH in normalization of flow in chronic hypoxia, Circ Res 19:274, 1966.)

90

80 0 1 Denver

2

3

4

5 Placebo

Days at 4300 m FIGURE 1-3  Change in minute ventilation ( V E ), end-tidal carbon dioxide (PACO2), and arterial oxygen saturation (SaO2) during 5 days’ acclimatization to 4300 m (14,108 feet). BTPS, Body temperature pressure saturated. (Modified from Huang SY, Alexander JK, Grover RF, et al: Hypocapnia and sustained hypoxia blunt ventilation on arrival at high altitude, J Appl Physiol 56:602, 1984.)

50

Hematocrit (%)

100 80 SaO2 (%) 60 40

Acetazolamide

Men Women (+Fe)

48 46

Women (−Fe) 44 42 40

Respiratory pattern

Sea level 1

20

40

60

Days at 4300 m

FIGURE 1-4  Hematocrit changes on ascent to altitude in men and in women with and without supplemental iron. (Modified from Hannon JP, Chinn KS, Shields JL: Effects of acute high altitude exposure on body fluids, Fed Proc 28:1178, 1969.)

fragmentation are poorly understood. Periodic breathing appears to play only a minor role in altering sleep architecture at high altitude.461 The arousals have been linked to periodic breathing in some studies but not in others. Other factors might include change in circadian rhythm and perhaps body temperature.98 Obesity may explain susceptibility to both deranged sleep and sleep-disordered breathing in some individuals.155 Recent studies

Respiratory pattern 100 80 60 40

SaO2 (%)

FIGURE 1-6  Respiratory patterns and arterial oxygen saturation (SaO2) with placebo and acetazolamide in two sleep studies of a subject at 4200 m (13,780 feet). Note pattern of hyperpnea followed by apnea during placebo treatment, which is changed with acetazolamide. (Modified from Hackett PH, Roach RC, Harrison GL, et al: Respiratory stimulants and sleep periodic breathing at high altitude: Almitrine versus acetazolamide, Am Rev Respir Dis 135:896, 1987.)

of infants and children590 and athletes in simulated altitude devices used for training also revealed deranged sleep quality in these groups.269,270,401 Although deranged sleep is a frequent complaint in high-altitude visitors, it seems to have little relation to susceptibility to altitude illness or other serious problems. Symptomatic treatment that avoids respiratory depression is safe (see Treatment under Acute Mountain Sickness, later). Periodic Breathing Periodic breathing is most common in early and light sleep, may occur during wakefulness when drowsy, and does not occur in REM sleep. The pattern is characterized by hyperpnea followed by apnea (Figure 1-6) and is caused by a battle for control of 7

100

SaO2 (%)

80 60 40 Arrival Acclimatized

20

0

50

100 150 200 250 300 350 400 450 500 Time asleep (min)

FIGURE 1-7  Sleep oxygenation improves with acclimatization to same altitude. Top line is maximum, and bottom line is minimum arterial oxygen saturation (SaO2) in an acclimatized person. Shaded area is maximum and minimum SaO2 values for new arrival at 5360 m (17,585 feet). (Modified from Sutton JR, Gray GW, Houston CS, et al: Effects of acclimatization on sleep hypoxemia at altitude. In West JB, Lahiri S, editors: High altitude man, Bethesda, Md, 1984, American Physiological Society, pp 141-146.)

breathing between peripheral chemoreceptors (carotid body) and the central respiratory center. Respiratory alkalosis during hyperpnea acts on the central respiratory center, causing apnea. During apnea, SaO2 decreases, carbon dioxide increases, and the carotid body is stimulated, causing a recurrent hyperpnea and apnea cycle. The apnea is central, not associated with snoring, and occurs with absence of rib cage movement. Persons with high hypoxic ventilatory response have more periodic breathing,55 with mild oscillations in SaO2,282 whereas persons with low hypoxic ventilatory response have more regular breathing overall but may suffer periods of apnea with extreme hypoxemia distinct from periodic breathing.192 As acclimatization progresses, periodic breathing lessens but does not disappear, especially over 5000 m (16,404 feet), and sleep SaO2 increases (Figure 1-7; see Figure 1-6).10,55,524 Periodic breathing has not been implicated in the etiology of highaltitude illness, but nocturnal oxygen desaturation has been implicated.55,133,150 Eichenberger and colleagues130 have also reported greater periodic breathing in persons with HAPE, secondary to lower SaO2. As with fragmented sleep, intensity of periodic breathing is quite variable. Total sleep time with periodic breathing can vary from 1% to over 90%.598 Most studies report no association between periodic breathing and AMS.55 This may relate to the fact that persons with periodic breathing tend to have higher HVR and greater average ventilation and oxygenation.561 Pharmaceutical Aids Acetazolamide, 125 mg at bedtime, diminishes periodic breathing and awakenings, improves oxygenation and sleep quality, and is a safe and superior agent to use as a sleeping aid (see Figure 1-6). It has the added benefit of diminishing symptoms of AMS. Other agents include diphenhydramine (Benadryl, 50 to 75 mg) or the short-acting benzodiazepines such as triazolam (Halcion, 0.125 to 0.25 mg) and temazepam (Restoril, 15 mg).308 Although caution is warranted for any agent that might reduce ventilation at high altitude, some studies have suggested that benzodiazepines in low doses are generally safe in this situation.124,164,384 Another option is to use both acetazolamide and a benzodiazepine. Bradwell and colleagues63 showed that acetazolamide (500 mg slow-release orally) given with temazepam (10 mg orally) improved sleep and maintained SaO2, counteracting a 20% decrease in SaO2 when temazepam was given alone. The nonbenzodiazepine hypnotic zolpidem (Ambien, 10 mg) was shown to improve sleep at 4000 m (13,123 feet) without adversely affecting ventilation.45

EXERCISE Maximal oxygen consumption drops dramatically on ascent to  2 max ) falls from high altitude.151,434 Maximal oxygen uptake ( VO 8

sea level by approximately 10% for each 1000 m (3281 feet) of altitude gained above 1500 m (4921 feet). Persons with the  2 max values have the largest decrement in highest sea level VO  2 max at high altitude, but overall performance at high altitude VO  2 max .392,428,566 In fact, is not consistently related to sea level VO many of the world’s elite mountaineers have quite average  2 max values, in contrast with other endurance athletes.392 VO Acclimatization at moderate altitudes enhances submaximal  2 max (Figure 1-8).151 endurance time but does not enhance VO Oxygen transport during exercise at high altitude becomes increasingly dependent on the ventilatory pump. The marked rise in ventilation produces a sensation of breathlessness, even at low work levels. The following quotation is from a high-altitude mountaineer: After every few steps, we huddle over our ice axes, mouths agape, struggling for sufficient breath to keep our muscles going. I have the feeling I am about to burst apart. As we get higher, it becomes necessary to lie down to recover our breath.347 In contrast to the increase in ventilation with exercise, at increasing altitudes in OEII, cardiac function and cardiac output were maintained at or near sea level values for a given oxygen consumption (workload).417 Recent work has attributed the  2 max to the lower PIO2, impairment altitude-induced drop in VO of pulmonary gas exchange, and reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third  2 max .76 However, mechanisms to explain the of the loss in VO impairment of gas exchange and the lower blood flow remain elusive. Wagner556 proposes that the pressure gradient for diffusion of oxygen from capillaries to the working muscle cells may be inadequate. Another concept is that increased cerebral hypoxia from exercise-induced desaturation is the limiting factor.91,241,356,519,520 Mountaineers, for example, become lightheaded and their vision dims when they move too quickly at extreme altitude (Figure 1-9).564 Training at High Altitude Optimal training for increased performance at high altitude depends on the altitude of residence and the athletic event. For aerobic activities (events lasting more than 3 or 4 minutes) at altitudes above 2000 m (6562 feet), acclimatization for 10 to 20 days is necessary to maximize performance.104 For events

180 Endurance time · VO2max

160 Sea level performance (%)

PART 1  MOUNTAIN MEDICINE

SLEEP SATURATION AT 5360 m

140 120 100 80 60 40 0

2

4

6

8

10

12

Days at altitude FIGURE 1-8  On ascent to altitude, maximum oxygen consumption  2max ) decreases and remains suppressed. In contrast, endurance ( VO  2max ) time (minutes to exhaustion at 75% of altitude-specific VO increases with acclimatization. (Modified from Maher JT, Jones LG, Hartley LH: Effects of high altitude exposure on submaximal endurance capacity of men, J Appl Physiol 37:895, 1974.)

Alveolar

Arterial

PO2 (torr)

30

20

Mixed venous

Assumed critical PO2

NEUROLOGIC SYNDROMES

Loss of consciousness · VO2max

10 Man on summit PB 253 torr DMO2 100 mL/min/torr 0 0

200

400

600

800

1000

1200

Oxygen uptake (mL O2/min) FIGURE 1-9  Calculated changes in the PO2 of alveolar gas and arterial and mixed venous blood as oxygen uptake is increased for a climber on the summit of Mt Everest. Unconsciousness develops at a mixed venous PO2 of 15 mm Hg. PB, Barometric pressure; DMO2, muscle dif 2max , maximum oxygen consumption. (Modified fusing capacity; VO from West JB: Climbing Mt. Everest without oxygen: An analysis of maximal exercise during extreme hypoxia, Respir Physiol 52:265, 1983.)

occurring above 4000 m (13,123 feet), acclimatization at an intermediate altitude is recommended. Highly anaerobic events at intermediate altitudes require only arrival at the time of the event, although mountain sickness may become a problem. The benefits of training at high altitude for subsequent performance at or near sea level depend on choosing the training altitude that maximizes the benefits and minimizes the “detraining” inevitable when maximal oxygen uptake is limited (altitude greater than 1500 to 2000 m [4921 to 6562 feet]). Hence, data from training above 2400 m (7874 feet) have shown no increase in subsequent sea level performance. Also, intermittent exposures to hypoxia seem to have no benefit.251,540 Runners returning to sea level after 10 days’ training at 2000 m (6562 feet) had faster running times and an increase in aerobic power, plasma volume, and hemoglobin concentration.19 Today the “live high–train low” approach pioneered by Levine and Stray-Gundersen294,513 has been adopted by many endurance athletes. The optimal dose for specific sports is still being worked out,570 but overall, endurance athletes believe and the science supports a small, but significant improvement in sea level performance after participating in a live high–train low training camp.514 The benefit appears to be due to enhanced erythropoietin production and increased red cell mass, which requires adequate iron stores and thus usually iron supplementation.328,443,512 Some individuals do not respond to live high–train low, perhaps related to genetic polymorphisms and the inability to increase erythropoietin levels sufficiently to raise red cell mass and thus increase oxygen-carrying capacity.79,247

High-Altitude Syndromes High-altitude syndromes are illnesses attributed directly to hypobaric hypoxia, even if exact mechanisms are unclear. Clinically and pathophysiologically these syndromes overlap. Rapidity of onset of hypoxia is crucial; for example, sudden exposure to extreme altitude may result in death from acute hypoxia (asphyxia), whereas more gradual ascent to the same altitude may result in AMS or no illness at all. Where symptoms of acute hypoxia end and AMS begins is vague, as reflected in the classic

Neurologic syndromes reflect both nervous system sensitivity to hypoxia and effects of compensatory mechanisms. Although brain adenosine triphosphate (ATP) production and overall metabolism remain intact during moderate hypoxia, impaired synthesis of neurotransmitters can produce cerebral symptoms such as lassitude, malaise, and cognitive defects. Compensatory cerebral vasodilation at altitude appears to be the trigger for altitude headache and contributes to development of AMS and HACE. However, much of the pathophysiology of AMS and HACE remains a mystery. Focal neurologic deficits without cerebral edema are also difficult to explain; cerebral artery spasm and watershed hypoxia have both been invoked. Understanding the exact etiology of these neurologic syndromes will parallel advances in neuroscience; the emphasis in altitude illness is finally and appropriately on the brain.438

ACUTE CEREBRAL HYPOXIA Acute, profound hypoxia, although of greatest interest in aviation medicine, may also occur on terra firma when ascent is too rapid or when hypoxia abruptly worsens. Carbon monoxide poisoning, pulmonary edema, sudden overexertion, sleep apnea, or a failed oxygen delivery system may rapidly exaggerate hypoxemia. Unacclimatized persons will lose consciousness from acute hypoxia at SaO2 of 40% to 60% or a PaO2 of less than about 30 mm Hg or mixed venous PO2 of 15 mm Hg. Tissandier, the sole survivor of the flight of the balloon Zenith in 1875, gave a graphic description of the effects of acute hypoxia: But soon I was keeping absolutely motionless, without suspecting that perhaps I had already lost use of my movements. Towards 7500 m [24,606 feet], the numbness one experiences is extraordinary. The body and the mind weaken little by little, gradually, unconsciously, without one’s knowledge. One does not suffer at all; on the contrary. One experiences inner joy, as if it were an effect of the inundating flood of light. One becomes indifferent; one no longer thinks of the perilous situation or of the danger; one rises and is happy to rise. Vertigo of the lofty regions is not a vain word. But as far as I can judge by my personal impression, this vertigo appears at the last moment; it immediately precedes annihilation—sudden, unexpected, irresistible. I wanted to seize the oxygen tube, but could not raise my arm. My mind, however, was still very lucid. I was still looking at the barometer; my eyes were fixed on the needle which soon reached the pressure number of 280, beyond which it passed. I wanted to cry out “We are at 8,000 meters.” But my tongue was paralyzed. Suddenly I closed my eyes and fell inert, completely losing consciousness.54 The ascent to over 8000 m (26,247 feet) took 3 hours, and the descent less than 1 hour. When the balloon landed, Tissandier’s two companions were dead. The prodigious work that Paul Bert conducted in an altitude chamber during the 1870s showed that lack of oxygen, rather than an effect of isolated hypobaria, explained the symptoms experienced during rapid ascent to extreme altitude. There exists a parallelism to the smallest details between two animals, one of which is subjected in normal air to a 9

CHAPTER 1  High-Altitude Medicine and Physiology

experiments of Bert.54 In terms of altitude illness, the general concept of a spectrum of illness with a common underlying pathogenesis is well accepted and provides a useful framework for discussion. For the neurologic syndromes, the spectrum progresses from high-altitude headache to AMS to high-altitude cerebral edema (HACE). In the lungs, the spectrum includes pulmonary hypertension, interstitial edema, and HAPE. These problems all occur within the first few days of ascent to a higher altitude, have many common features, and respond to descent and/or oxygen. Longer-term problems of altitude exposure include high-altitude deterioration in sojourners and chronic mountain sickness in high-altitude residents.

40

PART 1  MOUNTAIN MEDICINE

progressive diminution of pressure to the point of death, while the other breathes, also to the point of death, under normal pressure, an air that grows weaker and weaker in oxygen. Both will die after having presented the same symptoms.54 Bert goes on to describe the symptoms of acute exposure to hypoxia: It is the nervous system which reacts first. The sensation of fatigue, the weakening of the sense perceptions, the cerebral symptoms, vertigo, sleepiness, hallucinations, buzzing in the ears, dizziness, pricklings … are the signs of insufficient oxygenation of central and peripheral nervous organs. … The symptoms … disappear very quickly when the balloon descends from the higher altitudes, very quickly also … the normal proportion of oxygen reappears in the blood. There is an unfailing connection here.54 Bert was also able to both prevent and immediately resolve symptoms by breathing oxygen. Modern studies of acute hypoxic exposure use the measurement of time of useful consciousness; that is, the time until a subject can no longer take corrective measures, such as putting on an oxygen mask. With exposure to 8500 m (27,887 feet), that time is 60 seconds during moderate activity and 90 seconds at rest. Acute hypoxia can be quickly reversed by immediate administration of oxygen, rapid pressurization or descent, or correction of an underlying cause, such as relief of apnea, removal of a carbon monoxide source, repair of an oxygen delivery system, or cessation of overexertion. Hyperventilation increases time of useful consciousness during severe hypoxia.

HIGH-ALTITUDE HEADACHE The term high-altitude headache (HAH) has been used in the literature for decades, and studies directed toward the pathophysiology and treatment of HAH have been reported. Obviously these are to an extent also studies of AMS. Headache lends itself to investigation better than do some other symptoms, because headache scores have been well validated.244 Headache is generally the first unpleasant symptom consequent to altitude exposure and is sometimes the only symptom.214 It may or may not be the harbinger of AMS, which is defined as the presence of headache plus at least one of four other symptoms, in the setting of an acute altitude gain.435 One could even argue that it is the headache itself that causes other symptoms such as anorexia, nausea, lassitude, and insomnia, as is commonly seen in migraine or tension headaches, and that mild AMS is essentially due to headache. The International Headache Society206 has defined high-altitude headache as headache with at least two of the following characteristics: (1) bilateral; (2) frontal or frontotemporal; (3) dull or pressing quality; (4) mild or moderate intensity; and (5) aggravated by exertion, movement, straining, coughing, or bending. In addition, the headache must occur with an ascent to altitude greater than 2500 m (8202 feet), develop within 24 hours after ascent, and resolve within 8 hours after descent. Recent studies have attempted to characterize the clinical features and incidence of headache at altitude (Table 1-4). Silber and co-workers496 found that 50 of 60 trekkers (83%) in Nepal up to 5100 m (16,732 feet) developed at least one headache when over 3000 m (9843 feet). Older persons were less susceptible; women and those with headaches in daily life had more severe headaches, but no more headaches than others. Of those with headache, 52% did not have AMS by the Lake Louise criteria. The clinical features were widely variable. In general, the headaches were bilateral, generalized, dull, exacerbated by exertion or movement, often occurring at night, and resolved within 24 hours. Thus the headaches had some features of increased intracranial pressure (ICP). Persons with history of migraine did not have a higher incidence of headache. Various medications alleviated the headaches, especially mild ones, 70% of the time. Serrano-Duenas489 also described in detail HAH in 98 climbers in the Andes. Persons with history of primary headache were excluded. He found the following characteristics: holocranial, 65.6%; pulsatile-burst type quality, 75.3%; oscillating evolution, 10

TABLE 1-4  Clinical Characteristics of Headache Characteristic Location Global Frontal Hemi-cranial Occipital Change side Quality Pulsatile-burst Pressing/tightening Burning Dull Evolution Oscillate Disappear Diminish Increase Equal Break out in Elements Worsening Exercise Sudden movements Valsalva maneuver Light Elements Relieving Rest Analgesics Darkness Activity Concurrent Symptoms Anorexia Irritability Nausea Vomiting Apathy Gastric Malaise Somnolence Dysphasia Feelings Pessimism Anxiety Fear Isolation Strangeness

Percent Reporting 65.6 18.9 8.7 3.6 3.2 75.3 14.8 5.1 4.8 36.7 18.1 17.8 10.4 10.4 6.6 49.5 30.2 13.8 6.5 41.8 39 10.2 9 26.8 26.5 16.3 9.7 7.1 6.1 5.7 1.8 33.2 29.5 23.4 11.2 2.7

Modified from Serrano-Duenas M: High-altitude headache: A prospective study of its clinical characteristics, Cephalalgia 25:1110, 2005.

36.7%; increasing with exercise, 49.5%; relieved by rest, 41.8%; concurrent symptoms referred to: anorexia, 26.8%, irritability, 26.5%, and finally pessimism and anxiety feelings, 33.2% and 29.5%, respectively. Headaches were worse after a night’s sleep, more common in men, were of moderate intensity, and responded to analgesics. In general, the literature suggests that HAH can be prevented by the use of nonsteroidal antiinflammatory drugs65,72,157 and acetaminophen204 as well as the drugs commonly used for prophylaxis of AMS, acetazolamide and dexamethasone. Some agents appear more effective than do others, with ibuprofen and aspirin apparently superior to naproxen.65,70,73 A serotonin agonist (sumatriptan, a 5-HT1 [serotonin type 1] receptor agonist) was reported to be effective for HAH prevention and/or treatment in some studies,69,243,544 but not in others.28 Flunarizine, a specific calcium antagonist used for treatment of migraine, was not effective in one study.44 Interestingly, oxygen is often immediately effective for HAH (within 20 minutes) in subjects with and without AMS, indicating a rapidly reversible mechanism of the headache.26,191 The response to many different agents might reflect multiple components of the pathophysiology, or merely the nonspecific nature of analgesics. As Sanchez del Rio and Moskowitz463 have

Hypothalamus Brainstem

Autonomic response

CNS processing

High-altitude headache

Lower threshold for pain Trigeminovascular system activation

Hypoxia

eNOS upregulation

ACUTE MOUNTAIN SICKNESS Epidemiology and Risk Factors Although the syndrome of AMS has been recognized for centuries, modern rapid transport and proliferation of participants in mountain sports have increased the number of victims and therefore public awareness (see Table 1-1). The incidence and severity of AMS depend on the rate of ascent and the altitude attained (especially the sleeping altitude), duration of altitude exposure, level of exertion, recent altitude exposure, and inherent physiologic (genetic) susceptibility.440,475 For example, AMS is more common on Mt Rainier because of the rapid ascent, whereas high-altitude pulmonary or cerebral edema is uncommon because of the short stay (less than 36 hours). Persons with a demonstrated susceptibility to AMS had twice the incidence of AMS compared with nonsusceptibles, and this was independent of rate of ascent.475 The basis for inherent susceptibility is still unknown, but obviously depends on genetic factors. Acclimatization induced by recent altitude exposure can be protective; 4 days or more in the previous 2 months above 3000 m (9843 feet) reduced susceptibility to AMS on ascent to 4559 m (14,957 feet) by one-half, which was as effective as slow ascent475 (Figure 1-11). It also appears that protective effects of acclimatization persist after descent to low altitude. AMS was essentially absent in those who acclimatized to high altitude, returned to low altitude for 7 days, and were then reexposed to 4300 m (14,108 feet) in a hypobaric chamber.317 In addition, ventilation, SaO2, and exercise performance at altitude were maintained for at least 7 days,46,317,377 with some enhanced physical performance retained for several weeks.59,60,141,273,274 Recent epidemiologic studies suggest that protection from AMS may persist for months.475,586 Retention of the HVR might explain these results;305,433 yet studies showed that HVR returned to preascent values 7 days after descent.377 Compared with persons living at a lower altitude, residents at 900 m (2953 feet) or above reduced the incidence of AMS from 27% to 8% when ascending to between 2000 and 3000 m (6562 and 9843 feet) in Colorado.214 Age has an influence on incidence, with those over 50 years old somewhat less vulnerable.439,496 In a large study in Colorado, those over 60 had one-half the

incidence of AMS as those under 60 years of age. In contrast, a study of 827 mountaineers in Europe showed no influence of age on susceptibility.475 Perhaps different populations and physical activity explain the differing results. No study has ever shown older people to be more susceptible. Children from 3 months to puberty studied in Colorado had the same incidence as did young adults.534,592 A small study of tourists in Chile, however, found lower oxygen saturation and higher AMS in the 6- to 48-month age-group at 4440 m (14,567 feet).369 The largest study of children to date, of Han Chinese after ascent to Tibet, showed essentially the same incidence of AMS in 464 children as in 5335 adults, 34% and 38%, respectively.580 Women apparently have the same442,464,475 or a slightly greater incidence of AMS,214,546 but may be less susceptible to pulmonary edema.99,506 There appears to be no relation between AMS and the menstrual cycle.424 Most studies show no relation between physical fitness and susceptibility to AMS. However, obesity seems to increase the odds of developing AMS.154,214 Neither smoking nor the use of oral contraceptives increases risk for AMS.214,259,391 In summary, the most important variables related to AMS susceptibly are genetic predisposition, altitude of residence, altitude reached, rate of ascent, and prior recent altitude exposure. 70% 60%

Prevalence of AMS

pointed out, different inciting factors for headache may result in a final common pathway, such that the response to different therapies is not necessarily related to the initial cause of the headache. They have provided a useful multifactorial concept of the pathogenesis of HAH, based on current understanding of headaches in general.463 They suggest that the trigeminovascular system is activated at altitude by both mechanical and chemical stimuli (vasodilation, nitric oxide [NO] and other noxious agents), and in addition, the threshold for pain is likely altered at high altitude (Figure 1-10).463 If AMS and especially HACE ensue, then altered intracranial dynamics may also play a role, via compression or distension of pain-sensitive structures. A recent study provided evidence against sustained trigeminovascular activity,14 but more study will hopefully bring better understanding of the pathophysiology of these often debilitating headaches, and new treatments as well.

↑ NO

Nonsusceptible Susceptible

50% 40% 30% 20% 10% 0% Either ascent Ascent <4 days >3 days or and preexposure preexposure <5 days ≥5 days Rate of ascent and pre-exposure

Ascent >3 days and preexposure ≥5 days

FIGURE 1-11  The prevalence of acute mountain sickness (AMS) and 95% confidence intervals in nonsusceptible (blue bars) and susceptible (red bars) mountaineers in relation to the state of acclimatization defined as slow ascent (more than 3 days), fast ascent (3 days or less), preexposed (5 days or more above 3000 m [9843 feet] in the preceding 2 months), and not preexposed (4 days or less above 3000 m [9843 feet] in the preceding 2 months). (Reprinted from Schneider M, Bernasch D, Weymann J, et al: Acute mountain sickness: Influence of susceptibility, preexposure, and ascent rate, Med Sci Sports Exerc 34:1886, 2002.)

11

CHAPTER 1  High-Altitude Medicine and Physiology

FIGURE 1-10  Proposed pathophysiology of high-altitude headache. CNS, Central nervous system; eNOS, endothelial nitric oxide synthase; NO, nitric oxide. (Modified from Sanchez del Rio M, Moskowitz MA: High altitude headache. In Roach RC, Wagner PD, Hackett PH, editors: Hypoxia: Into the next millennium, New York, 1999, Plenum/Kluwer Academic Publishing, pp 145-153.)

PART 1  MOUNTAIN MEDICINE

TABLE 1-5  Clinical Characteristics of High-Altitude Illnesses Clinical Classification HAH

Mild AMS

Moderate to Severe AMS

HACE

Symptoms

Headache only

Headache plus one or more symptoms (nausea/vomiting, fatigue/lassitude, dizziness or difficulty sleeping) Symptoms of moderate to severe intensity

±Headache Worsening of symptoms seen in moderate to severe AMS

LL-AMS score* Physical signs

1-3, headache only None

Headache plus one more symptom (nausea/ vomiting, fatigue/ lassitude, dizziness or difficulty sleeping) All symptoms of mild severity 2-4 None

Findings

None

None

Pathophysiology

Unknown; cerebral vasodilation, trigeminovascular system?†

Unknown; same as HAH?

Antidiuresis Slightly increased body temperature Slight desaturation Widened A-a gradient Elevated ICP White matter edema (CT, MRI) Vasogenic edema; cytotoxic edema?

5-15 None

Ataxia Altered mental status HAPE common: positive chest radiograph, rales, dyspnea at rest Elevated ICP White matter edema (CT, MRI) Advanced vasogenic cerebral edema; cytotoxic edema?

AMS, Acute mountain sickness; CT, computed tomography; HACE, high-altitude cerebral edema; HAH, high-altitude headache; HAPE, high-altitude pulmonary edema; ICP, intracranial pressure; MRI, magnetic resonance imaging. *The self-reported Lake Louise AMS score. † See Figures 1-10 and 1-12.

Diagnosis Diagnosis of AMS is based on the setting, symptoms, physical findings, and exclusion of other illnesses. The setting is generally rapid ascent of unacclimatized persons to 2500 m (8202 feet) or higher from altitudes below 1000 m (3281 feet). For partially acclimatized persons, abrupt ascent to a higher altitude, overexertion, use of respiratory depressants, and perhaps onset of infectious illness376 are common contributing factors. The cardinal symptom of early AMS is headache, followed in incidence by fatigue, dizziness, and anorexia.214,500 The headache is usually throbbing, bitemporal, typically worse during the night and on awakening, and made worse by the Valsalva maneuver or stooping over (see High Altitude Headache, earlier). A good appetite is unusual, and nausea is common. These initial symptoms are strikingly similar to an alcohol hangover. Frequent awakening may fragment sleep, and periodic breathing often produces a feeling of suffocation. Although sleep disorder is nearly universal at high altitude, also affecting those without AMS, these symptoms may be exaggerated during AMS. Affected persons commonly complain of a deep inner chill, unlike mere exposure to cold temperature, accompanied by facial pallor. Other symptoms may include vomiting, dyspnea on exertion, and irritability. Lassitude can be disabling, with the victim too apathetic to contribute to his or her own basic needs. Pulmonary symptoms vary considerably. Everyone experiences dyspnea on exertion at high altitude; dyspnea at rest is distinctly abnormal, however, and presages HAPE rather than AMS. Cough is also extremely common at high altitude and not associated with AMS. Recent work suggests that altitude hypoxia actually lowers the cough threshold, as measured with an inhaled citric acid stimulus.333 However, any pulmonary symptom mandates careful examination for pulmonary edema. Specific physical findings are lacking in mild AMS. A higher heart rate has been noted in those with AMS,34,391 but Singh and associates500 noted bradycardia (heart rate less than 66 beats/min) in two-thirds of 1975 soldiers with AMS. Blood pressure is normal, but postural hypotension may be present. Occasionally, localized rales may be present,323 but this has also been observed in those without AMS.187 A slight increased body temperature with AMS may be present but is not diagnostic.321 Peripheral oxygen saturation as measured by pulse oximetry correlated poorly with presence of AMS during rapid ascent391,439,450 but was related to AMS during trekking.39 SaO2 at altitude on Denali was predictive of developing AMS on further ascent.436 Overall, pulse oximetry is 12

of limited usefulness in diagnosing AMS. Funduscopic examination reveals venous tortuosity and dilation; retinal hemorrhages may or may not be present and are not diagnostic. They are more common in AMS than non-AMS subjects at 4243 m (13,921 feet).187 Absence of the normal altitude diuresis, evidenced by lack of increased urine output and retention of fluid, is an early finding in AMS, although not always present.35,188,442,500,528 More obvious physical findings develop if AMS progresses to HACE. AMS displays no neurologic findings, whereas HACE is an encephalopathy (see High-Altitude Cerebral Edema, later). It is clinically useful to classify AMS as mild or moderate to severe on the basis of symptoms (Table 1-5). Importantly, AMS can herald the beginning of life-threatening cerebral edema. Differential Diagnosis Given the nonspecific nature of the symptoms, AMS is commonly confused with other conditions (Box 1-3). AMS is most commonly misdiagnosed as a viral flulike illness, hangover, exhaustion, dehydration, or medication or drug effect. Unlike an infectious illness, uncomplicated AMS is not associated with fever and myalgias. Hangover is excluded by the history. Exhaustion may cause lassitude, weakness, irritability, and headache and may therefore be difficult to distinguish from AMS. Dehydration, which causes weakness, decreased urine output, headache, and nausea, is commonly confused with AMS. Response to fluids BOX 1-3  Differential Diagnosis of High-Altitude

Illnesses

Acute mountain sickness and high-altitude cerebral edema

High-altitude pulmonary   edema

Dehydration, exhaustion, viral or bacterial infection, alcohol hangover, hypothermia, carbon monoxide poisoning, migraine, hyponatremia, hypoglycemia, diabetic ketoacidosis, CNS infection, transient ischemic attack, arteriovenous malformation, stroke, seizures, brain tumors, ingestion of toxins or drugs, acute psychosis Asthma, bronchitis, pneumonia, mucus plugging (secondary to previous), hyperventilation syndrome, pulmonary embolus, heart failure, myocardial infarction

CNS, Central nervous system.

↓O2 vasodilation

Acute hypoxic ventilatory ↓CO2 response vasoconstriction ←→

Ca2+

sensitivity NO→impaired →relaxation/vasodilation

↑Ca2+ No release

Endothelium Elastic lamina Smooth muscle

Other molecules that may be involved: Acetylcholine Substance P Prostaglandins

Microhemorrhage

↑K+

Raised hydrostatic pressure

Venous

Capillary and blood-brain barrier

Arteriole

CHAPTER 1  High-Altitude Medicine and Physiology

Artery

NO

HIF-1α not broken down

Hypoxemia

Raised venous pressure

Free radical formation

Basement membrane damage Na+/K+ Upregulation ATPase failure of VEGF →intracellular Edema→↑ICP edema Adenosine →hypoxic vasodilation

Headache

Capillary basement membrane damage and angiogenesis Mechanical mediator PO2/PCO2 mediator Chemical mediator

Vasodilation→pain Pain fibers of trigeminal nerve→trigeminovascular system

FIGURE 1-12  Proposed pathophysiology of acute mountain sickness. HIF, Hypoxia-inducible factor; ICP, intracranial pressure; NO, nitric oxide; VEGF, vascular endothelial growth factor. (Modified from Wilson MH, Newman S, Imray CH: The cerebral effects of ascent to high altitudes, Lancet Neurol 8:175, 2009.)

helps to differentiate the two. AMS is not improved by fluid administration alone, and body hydration does not influence susceptibility to AMS (contrary to conventional wisdom).11 Hypothermia may manifest as ataxia and mental changes. Sleeping medication can cause ataxia and mental changes, but soporifics may also precipitate high-altitude illness because of increased hypoxemia during sleep. Migraine may be very difficult to distinguish from AMS. A trial of oxygen breathing or descent can be helpful to discriminate these other conditions from AMS. Pathophysiology The basic cause of AMS is hypoxemia, but the syndrome is different from acute hypoxia. Because symptoms are somewhat worse with hypobaric hypoxia than with normobaric hypoxia, hypobaria apparently also plays a minor role, most likely through its effect on fluid retention.240,261,303,304,441 Because of a time lag in onset of symptoms after ascent and lack of immediate or complete reversal of all symptoms with oxygen, AMS is thought to be secondary to the body’s responses to modest hypoxia. In addition, even though an altitude of 2500 to 2700 m (8202 to 8858 feet) presents only a minor decrement in arterial oxygen transport (SaO2 is still above 90%), AMS is common and some individuals may become desperately ill. Some aspects of AMS pathophysiology are clear. Findings documented in mild to moderate AMS include relative hypoventilation,336,366 impaired gas exchange (interstitial edema),171,286 fluid retention and redistribution,35,442,528 and increased sympathetic

drive.31,34 In mild to moderate AMS, limited data show that ICP or cerebrospinal fluid (CSF) pressure is not elevated at rest.17,205,579 In contrast, increased ICP and cerebral edema are documented in severe AMS, reflecting the continuum from advanced AMS to HACE.220,276,337,500,573 The known, well-established findings in AMS are reviewed extensively elsewhere.179,233,240 The remainder of this section focuses on remaining questions and new work in the quest to find the cause of AMS. We proposed more than a decade ago that moderate to severe AMS was caused by brain swelling leading to elevated ICP via a compromised buffering capacity. This hypothesis has not yet been directly tested. We now examine the data on brain swelling, ICP, and cranial buffering capacity in AMS. Brain Swelling in AMS.  For decades, clinicians have postulated that AMS is a mild form of cerebral edema. Although this appears true for moderate to severe AMS, it now seems unlikely that mild AMS, or the headache alone, is due to edema (see High-Altitude Headache, earlier). Persons with moderate to severe AMS or HACE display elevated ICP and white matter edema on brain imaging in most but not all studies,144 whereas those with mild AMS do not.* Recent MRI studies have demonstrated that brain swelling occurs in all subjects ascending rapidly to moderate altitude, regardless

*References 197, 220, 276, 295, 337, 500.

13

PART 1  MOUNTAIN MEDICINE

of the presence of AMS, and is due to both vasodilation and minor vasogenic edema. In addition, there may be an intracellular fluid shift as evidenced by low apparent diffusion coefficient. Although this was greater in those with AMS, the volumetric changes were minor and unlikely to result in increased ICP without contributing factors.144,239,252,372,481 In summary, no gross elevation in brain volume has been found yet in mild AMS or headache alone, but elevated brain volume is almost universally observed in moderate to severe AMS and HACE. Intracranial Pressure and AMS.  A fascinating story was recently reported in which a neurosurgeon measured ICP changes from a self-implanted ICP monitoring bolt in himself and in two others.572 They demonstrated that ICP remained normal at rest at all altitudes (studied from sea level to 5030 m [16,503 feet]); however, in the single subject with AMS, there was a dramatic increase in ICP even on minimal exertion. This study is consistent with recent indirect assessment of elevated ICP in AMS based on optic nerve sheath diameter.138,523 In addition, a study that measured opening lumbar pressure revealed significant elevations in AMS subjects compared with control or after AMS resolved.500 In contrast, one recent study in normobaric hypoxia reported no elevation of ICP in AMS when measured indirectly by repeat lumbar puncture.252 The evidence that ICP is elevated in mild AMS is limited and not compelling. Stronger evidence suggests that perhaps intracranial compliance is altered,275 and that although ICP might not be elevated at rest, it rises abruptly with isometric maneuvers such as lifting a pack, with Valsalva, or even with turning the head, which slightly elevates venous pressure.205,572 Altered compliance is consistent with the tight-fit hypothesis (see below). The Tight-Fit Hypothesis and AMS.  Ross457 hypothesized in 1985 that persons with smaller intracranial and intraspinal CSF capacity would be disposed to develop AMS, because they would not tolerate brain swelling as well as those with more “room” in the craniospinal axis. It is displacement of CSF through the foramen magnum into the spinal canal that is the first compensatory response to increased brain volume, followed by increased CSF absorption and decreased CSF formation. Studies have shown that the increase in ICP for a given increase in brain volume is directly related to the “tightness” of the brain in the cranium (the brain volume: intracranial volume ratio) and to the volume of the spinal canal.492 Thus, the greater the initial CSF volume, the more accommodation that can take place in response to brain edema. Increases in volume are “buffered” by CSF dynamics. In light of our present understanding of increased brain volume on ascent to altitude, his hypothesis is still very attractive. Preliminary data that showed a relationship of preascent ventricular size or brain volume: cranial vault ratios and susceptibility to AMS support this hypothesis,182,252,572,593 as do the studies showing elevated ICP in moderate to severe AMS.220,276,337,500,573 The idea deserves further study. New Concepts.  New, potentially important work is under way to understand the potential role of inflammatory mediators, free radicals, and even HIF-modulated reactions in the pathophysiology of AMS.14,16 Progress is hampered by the technical difficulty of some of these approaches, by lack of an animal model, and by the unresolved status of the basic pathophysiology. A potentially unifying hypothesis, with several novel ideas, is presented in Figure 1-12. In this schema, mechanical factors increase intravascular pressure and hence can cause vasogenic edema and vessel wall damage. This pressure can act in the artery (increased hydrostatic pressure associated with increased flow) or vein (if there is venous outflow obstruction, as in benign intracranial hypertension, for example). The partial pressures of oxygen and carbon dioxide are thought to have direct vasoactive properties, with hypoxemia causing vasodilation and hypocarbia causing vasoconstriction. A balance between these is mediated by the hypoxic and CO2 ventilatory responses. Cytotoxic edema is attributed to direct hypoxia-induced Na+/K+ ATPase failure. Many chemical mediators have been implicated. Free radical formation could directly damage the blood–brain barrier, causing vasogenic edema. Accumulation of HIF-1α and subsequent upregulation of 14

vascular endothelial growth factor (VEGF) could contribute to further blood–brain barrier damage and edema. Neuronally mediated adenosine release also causes vasodilation. Vessel dilation has been implicated in activating the trigeminovascular system, causing headache. An important element of HACE is microhemorrhage formation, caused by vessel damage from chemical mediators or cytokines or by damage through increased hydrostatic pressure.253 Natural Course of Acute Mountain Sickness The natural history of AMS varies with initial altitude, rate of ascent, and clinical severity. Symptoms can start within 2 hours after arrival and rarely if ever start after 36 hours at a given altitude. AMS usually resolves over the next 24 to 48 hours. The more rapid the ascent, and the higher the altitude, the more likely that symptoms will appear sooner and be worse. Singh and associates500 followed the illness in soldiers airlifted to altitudes of 3300 to 5500 m (10,827 to 18,045 feet). Incapacitating illness lasted 2 to 5 days, but 40% still had symptoms after 1 week and 13% after 1 month. Nine soldiers failed to acclimatize in 6 months and were considered unfit for duty at high altitude.500 Chinese investigators report that a percentage of lowland Han Chinese stationed on the Tibet Plateau cannot tolerate the altitude because of persistent symptoms and must be relocated to the plains.583 Persistent anorexia, nausea, and headache may afflict climbers at extreme altitude for weeks and can be considered a form of persistent AMS. The natural history of AMS in tourists who sleep at more moderate altitudes is much more benign. Duration of symptoms at 2700 m was 15 hours, with a range of 6 to 94 hours.361 Most individuals treat or tolerate their symptoms as the illness resolves over 1 to 3 days while acclimatization improves, but some persons with AMS seek medical treatment or are forced to descend if symptoms persist. A small percentage of those with AMS (3.4% at 4243 m [13,921 feet]) go on to develop cerebral edema, especially if ascent continues in spite of illness. Although 50% of persons with HAPE have AMS, no study has documented how many with AMS develop HAPE. Treatment Management of AMS is based on severity of illness at presentation, logistics, terrain, and experience of the caregiver. Early diagnosis is key, because treatment in the early stages of illness is easier and more successful (Box 1-4). Proceeding to a higher sleeping altitude in the presence of symptoms is contraindicated. The victim must be carefully monitored for progression of illness. If symptoms worsen despite 24 hours of acclimatization or treatment, descent is indicated. The two indications for immediate descent are neurologic findings (ataxia or change in consciousness) and pulmonary edema. Mild AMS can be treated by halting the ascent and waiting for acclimatization to improve, which can take from 12 hours to 3 or 4 days. Acetazolamide (250 mg twice a day orally, or as a single dose) speeds acclimatization and thus terminates the illness if given early.171,326 Symptomatic therapy includes analgesics such as aspirin (500 or 650 mg), acetaminophen (650 to 1000 mg), ibuprofen65 or other nonsteroidal antiinflammatory drugs, or codeine (30 mg) for headache. Ondansetron 4 mg orally disintegrating tablets every 4 hours as necessary is useful for nausea and vomiting. Persons with AMS should avoid alcohol and other respiratory depressants because of possible exaggerated hypoxemia during sleep. Descent to an altitude lower than where symptoms began effectively reverses AMS. Although descent should be as far as necessary for improvement, 500 to 1000 m (1640 to 3281 feet) is usually sufficient. Exertion should be minimized. Oxygen, if available, is particularly effective (and supply is conserved) if given in low flow (0.5 to 1 L/min by mask or cannula) during the night. Hyperbaric chambers, which simulate descent, have been used to treat AMS and aid acclimatization. They are effective and require no supplemental oxygen. Lightweight (less than 7 kg) fabric pressure bags inflated by manual air pumps are now being used on mountaineering expeditions and in mountain clinics (Figure 1-13). An inflation of 2 psi is roughly equivalent to a drop in altitude of 1600 m (5249 feet); the exact equivalent depends on initial altitude.257,437 A few hours of pressurization

High-Altitude Headache and Mild Acute Mountain Sickness • Stop ascent, rest, acclimatize at same altitude • Symptomatic treatment as necessary with analgesics and antiemetics • Consider acetazolamide, 125 to 250 mg bid, to speed acclimatization • OR descend 500 m (1640 feet) or more Moderate to Severe Acute Mountain Sickness • Low-flow oxygen, if available • Acetazolamide, 125 to 250 mg bid, with or without dexamethasone, 4 mg PO, IM, or IV q6h • Hyperbaric therapy • OR immediate descent High-Altitude Cerebral Edema • Immediate descent or evacuation • Oxygen, 2 to 4 L/min • Dexamethasone, 8 mg PO, IM, or IV, then 4 mg q6h • Hyperbaric therapy High-Altitude Pulmonary Edema • Minimize exertion and keep warm • Immediate descent or hyperbaric therapy • Oxygen, 4 to 6 L/min until improving, then 2 to 4 L/min • If above unavailable, one of the following: • Nifedipine, 30 mg extended release q12h • Sildenafil 50 mg q8h • Tadalafil 10 mg q12h • Consider inhaled β-agonist Periodic Breathing • Acetazolamide, 62.5 to 125 mg at bedtime as needed

hydrochlorothiazide, and other diuretics have not yet been evaluated for treatment (see Prevention, later). The steroid betamethasone was initially reported by Singh and co-workers500 to improve symptoms of soldiers with severe AMS. Subsequent studies have found dexamethasone to be effective for treatment of all degrees of AMS.140,196,262 Hackett and colleagues196 used 4 mg orally or intramuscularly every 6 hours, and Ferrazinni and associates140 gave 8 mg initially, followed by 4 mg every 6 hours. Both studies reported marked improvement within 12 hours, which was the first postdrug assessment, but clinical experience suggests improvement of AMS within 4 hours. There were no significant side effects. Symptoms increased when dexamethasone was discontinued after 24 hours.196 Clinicians debate whether the use of dexamethasone should also mandate descent. Is it safe to continue to ascend after treatment with dexamethasone or while taking the medication? In reality, people do, and problems seem to be few. In our opinion, dexamethasone use should be limited to less than 72 hours to minimize side effects. This generally is sufficient time to descend, or to better acclimatize, with or without acetazolamide. The mechanism of action of dexamethasone is unknown; it does not affect oxygen saturation, fluid balance, or periodic breathing.295 The drug blocks the action of VEGF,476 diminishes the interaction of endothelium and leukocytes (thus reducing inflammation),167 and may also reduce cerebral blood flow.250 Dexamethasone seems to not improve acclimatization, because some symptoms recur when the drug is withdrawn. Therefore an argument could be made for using dexamethasone to relieve symptoms and acetazolamide to speed acclimatization.52 Prevention Prevention strategy is based on risk assessment311 (Table 1-6). Graded ascent is the surest and safest method of prevention, although particularly susceptible individuals may still become ill. TABLE 1-6  Risk Categories for Acute Mountain

Sickness

IM, Intramuscularly; IV, intravenously; PO, orally.

result in symptomatic improvement and can be an effective temporizing measure while awaiting descent or the benefit of medical therapy.257,375,398,444,532 Long-term (12 hours or more) use of these portable devices is necessary to resolve AMS completely. Acetazolamide is of unquestionable prophylactic value and is now commonly and successfully used to treat AMS as well, although data supporting this are minimal.171,326 Singh and colleagues500 successfully used furosemide (80 mg twice a day for 2 days) to treat 446 soldiers with all degrees of AMS; it has not since been studied for treatment. Furosemide induced a brisk diuresis, relieved pulmonary congestion, and improved headache and other neurologic symptoms.500 Spironolactone,

Risk Category Low

Moderate

High

FIGURE 1-13  A fabric hyperbaric pressure bag being used on Mt Everest for treatment of severe altitude illness. Two psi pressure is equivalent to a drop of approximately 1600 m (5249 feet) in altitude.

Description Individuals with no prior history of altitude illness and ascending to <2800 m (9186 feet) Individuals taking >2 days to arrive at 2500-3000 m (8202-9843 feet) with subsequent increases in sleeping elevation <500 m (1640 ft)/day and an extra day for acclimatization every 1000 m (3281 feet) Individuals with prior history of AMS and ascending to 2500-2800 m (8202-9186 feet) in 1 day No history of AMS and ascending to >2800 m (9186 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) at altitudes above 3000 m (9843 feet) but with an extra day for acclimatization every 1000 m (3281 feet) History of AMS and ascending to >2800 m (3281 feet) in 1 day All individuals with a prior history of HAPE or HACE All individuals ascending to >3500 m (11,483 feet) in 1 day All individuals ascending >500 m (1640 ft)/day (increase in sleeping elevation) above >3000 m (9843 feet) without extra days for acclimatization Very rapid ascents (e.g., <7-day ascents of Mt Kilimanjaro)

Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness, Wilderness Environ Med 21:146, 2010. AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema. Notes: Altitudes listed in the table refer to the altitude at which the person sleeps. Ascent is assumed to start from elevations <1200 m (3937 feet). The risk categories described above pertain to unacclimatized individuals.

15

CHAPTER 1  High-Altitude Medicine and Physiology

BOX 1-4  Field Treatment of High-Altitude Illness

PART 1  MOUNTAIN MEDICINE

Carbonic anhydrase

CO2 + H2O <==> H2CO3 <==> H+ + HCO3 FIGURE 1-14  Action of acetazolamide to block carbonic anhydrase (shown in a molecular ribbon diagram) and thus slow the hydration of carbon dioxide.

Current recommendations are to avoid abrupt ascent from low altitude to sleeping altitudes greater than 2800 m (9186 feet) in 1 day, to spend 2 to 3 nights at 2500 to 3000 m (8202 to 9843 feet) before going higher, to not advance sleeping altitude more than 500 m (1640 ft)/day, and to take an extra night for acclimatization every 1000 m if continuing ascent.311 However, a recent study on Aconcagua reinforced the notion that individual susceptibility is a key factor, and that persons who are resistant to AMS can proceed much more quickly on the mountain safely.405 Day trips to higher altitude, with a return to lower altitude for sleep, aid acclimatization. Alcohol and sedative-hypnotics are best avoided on the first 2 nights at high altitude. Whether a diet high in carbohydrates reduces AMS symptoms is controversial.96,203,530 Exertion early in altitude exposure contributes to altitude illness,440 whereas limited exercise seems to aid acclimatization. Because altitude exposure in the previous weeks is protective, a faster rate of ascent may then be possible.475,586 Acetazolamide Prophylaxis.  Acetazolamide is the drug of choice for prophylaxis of AMS. A carbonic anhydrase inhibitor, acetazolamide slows the hydration of carbon dioxide (Figure 1-14).

The effects are protean, involving particularly red blood cells, the brain, lungs, and kidneys. By inhibiting renal carbonic anhydrase, acetazolamide reduces reabsorption of bicarbonate and sodium and thus causes a bicarbonate diuresis and metabolic acidosis, beginning within 1 hour after ingestion. This rapidly enhances ventilatory acclimatization, increasing oxygenation. Importantly, the drug maintains oxygenation during sleep and prevents periods of extreme hypoxemia (see Figure 1-6).192,525,529 Because of acetazolamide’s diuretic action, it counteracts the fluid retention of AMS. It also diminishes nocturnal antidiuretic hormone secretion86 and decreases CSF production and volume and possibly CSF pressure.488 Acetazolamide also impacts brain aquaporin channels, possibly preventing water transport into the brain.533 Which of these effects is most important in preventing AMS is unclear. Numerous studies taken together indicate that acetazolamide is approximately 75% effective in preventing AMS in persons rapidly transported to altitudes of 3000 to 4500 m (9843 to 14,764 feet).132 Acetazolamide prophylaxis should be considered for persons with moderate to severe risk, as indicated in Tables 1-6 and 1-7. The ideal dose of acetazolamide for prevention is debated. Many studies have shown that 250 mg twice a day or 3 times a day was effective, as well as 500 mg in sustained action capsule taken every 24 hours.* To reduce the side effects, especially paresthesias, clinicians have more recently been using smaller doses (125 mg twice a day),348 and a number of studies now support this.37,77,548 Renal carbonic anhydrase is blocked with 5 mg/kg/ day, and this may be the maximum dose required, both in children and adults. Duration of medication use varies; the standard advice is to start 24 hours before ascent. Most clinicians recommend continuing for at least the first 2 days at high altitude, and longer if there is continuing gain in altitude. Acetazolamide can also be taken episodically, to speed acclimatization at any point while gaining altitude or to treat mild AMS. There is no rebound when discontinued. Although the danger of altitude illness passes after a few days of acclimatization, acetazolamide may still be useful to promote more effective sleep. Acetazolamide has side effects, most notably peripheral paresthesias and polyuria, and less commonly nausea, drowsiness, impotence, and myopia. Because it inhibits the instant hydration of carbon dioxide on the tongue, acetazolamide allows carbon dioxide to be tasted and can ruin the flavor of carbonated beverages, including beer. The issue of sulfonamide allergy and acetazolamide was recently reviewed.263 As a nonantibiotic sulfonamide drug, acetazolamide is usually tolerated well by persons with a history of sulfa antibiotic allergy; approximately 10% may have an allergic reaction.517 In persons without a history *References 83, 156, 170, 186, 286, 421, 575.

TABLE 1-7  Recommended Dosages for Medications Used in the Prevention and Treatment of Altitude Illness Medication

Indication

Route

Dosage

Acetazolamide

AMS, HACE prevention

Oral

AMS treatment*

Oral

AMS, HACE prevention

Oral

AMS, HACE treatment

Oral, IV, IM

HAPE HAPE HAPE HAPE HAPE

Oral Oral Oral Oral Inhaled

125 mg twice per day Pediatric dose: 2.5 mg/kg q12h 250 mg twice per day Pediatric dose: 2.5 mg/kg q12h 2 mg q6h or 4 mg q12h Pediatrics: should not be used for prophylaxis AMS: 4 mg q6h HACE: 8 mg once then 4 mg q6h Pediatric dose: 0.15 mg/kg/dose q6h up to 4 mg 30 mg SR version q12h 30 mg SR version q12h 10 mg twice per day 50 mg q8h 125 mcg twice per day*

Dexamethasone

Nifedipine Tadalafil Sildenafil Salmeterol

prevention treatment prevention prevention prevention

Modified from Luks AM, McIntosh SE, Grissom CK, et al: Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness, Wilderness Environ Med 21:146, 2010. AMS, Acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema; IM, intramuscular; IV, intravenous; SR, sustained release. *Should not be used as monotherapy and should only be used in conjunction with oral medications.

16

Dexamethasone Prophylaxis.  Dexamethasone effectively prevents AMS. Two mg every 6 hours or 4 mg every 12 hours was sufficient for sedentary subjects,250 but for exercising subjects at or above 4000 m (13,123 feet), this was insufficient,51,196,446 and 4 mg every 6 hours was necessary to prevent AMS.447 The initial chamber study in 1984 was with sedentary subjects.250 The drug reduced the incidence of AMS from 78% to 20%, comparable with previous studies with acetazolamide. Dexamethasone was not as effective in exercising subjects on Pike’s Peak,446 but subsequent work has shown effectiveness comparable with acetazolamide.42,132,295,360,594 The combination of acetazolamide and dexamethasone proved superior to dexamethasone alone.594 Because of potential serious side effects and the rebound phenomenon, dexamethasone is best reserved for treatment rather than for prevention of AMS, or used for prophylaxis when necessary in persons intolerant of or allergic to acetazolamide. Other Agents for AMS Prevention.  Studies with Ginkgo biloba have had inconsistent results. Four studies had positive results, ranging from 100% to 50% reduction in AMS when given either 5 days or 1 day before ascent.158,318,368,451 Three studies were negative, two of which were follow-up studies by investigators with positive results previously.83,156,288 Conflicting results can possibly be explained by differences in dosing, duration of pretreatment, and varying rates of ascent, but most likely, they are due to differences in preparations of ginkgo.289 Ginkgo biloba is a complicated plant extract whose active ingredient in terms of preventing AMS is unknown. Even in the “standardized” preparations (24% flavonoids and 6% terpene ginkolides), the amounts of specific chemicals can vary considerably. Until the active ingredient is discovered and standardized, results with ginkgo will continue to be mixed. Meanwhile, because the product is very safe, nonprescription, inexpensive, and can be helpful, it is reasonable to consider its use. Acetazolamide, however, is likely the superior agent. Spironolactone,245,285 naproxen, calcium channel blockers, antacids, and medroxyprogesterone acetate have shown ineffectiveness for AMS prevention. Bailey and Davies15 tested an antioxidant “cocktail” for prevention of AMS. They reasoned that free-radicalmediated damage to the blood–brain barrier might play a role in the pathophysiology. They preloaded nine subjects with daily L-ascorbic acid, DL-α-tocopherol acetate and α-lipoic acid, and nine subjects with placebo for 3 weeks, and then during a 10-day trek to the Mt Everest base camp. Those on antioxidants had a slightly lower AMS score and higher arterial oxygen saturation and better appetite.15 A recent study failed to confirm any benefit of antioxidant therapy for preventing AMS.18 In spite of these marginal findings in field studies, some clinicians propose that regional changes in redox state in the brain can lead to focal blood–brain barrier disruption and vasogenic edema. See Bärtsch and associates25 for a detailed discussion of the antioxidant hypothesis.

HIGH-ALTITUDE CEREBRAL EDEMA HACE is an uncommon but deadly condition, usually occurring in those with AMS or HAPE. Although HACE is most common over 3000 m (9843 feet), it has been reported at altitudes as low as 2100 m (6890 feet).115 Reliable estimates of incidence range from 0.5% to 1% in unselect high-altitude visitors,33,186 but was 3.4% in those who had developed AMS.186 In Chinese railway workers at 4500 to 4900 m (14,764 to 16,076 feet), incidence was 0.5%. HACE occurs in 13% to 20% of persons with HAPE152,211,232 and in up to 50% of those who die from HAPE. In addition, HAPE is very common in those diagnosed with HACE; one series

from Colorado reported that 11 of 13 with a primary diagnosis of HACE also had HAPE. Pure cerebral edema, without pulmonary edema, appears to be uncommon at lower altitudes, but accounted for 54 of 66 HACE cases in Tibet.582 The mean altitude at onset was 4730 m (15,518 feet)in one survey, but was lower (3920 m [12,861 feet]) when associated with HAPE.233 Data are insufficient to draw any conclusions regarding effects of gender, age, preexisting illness, or genetics on susceptibility to HACE. Clinically and pathophysiologically, advanced AMS and HACE are similar, so that a distinction between them is inherently blurred. See our review190 and the recent series reported by Wu and associates582 for a more complete discussion. Clinical Presentation HACE is an encephalopathy, whereas AMS is not. The hallmarks of HACE are ataxic gait, severe lassitude, and altered consciousness, including confusion, impaired mentation, drowsiness, stupor, and coma. Headache, nausea, and vomiting are frequent, but not always present. Hallucinations, cranial nerve palsy, hemiparesis, hemiplegia, seizures, and focal neurologic signs have also been reported.118,199,220,500,582 Seizures are distinctly uncommon. Retinal hemorrhages are common but not diagnostic. The progression from mild AMS to unconsciousness may be as fast as 12 hours but usually requires 1 to 3 days; HACE can develop more quickly in persons with HAPE. Arterial blood gas study or pulse oximetry often reveals exaggerated hypoxemia. Clinical examination and chest radiography may reveal pulmonary edema. Laboratory studies and lumbar puncture are useful only to rule out other conditions. Computed tomography (CT) may show compression of sulci and flattening of gyri, and attenuation of signal more in the white matter than gray matter. MRI is more revealing, with a characteristic high T2 signal in the white matter, especially the splenium of the corpus callosum, and most evident on diffusion-weighted images.197,578,582 The following case report from Mt McKinley illustrates a typical clinical course of HACE in conjunction with HAPE. CLINICAL PRESENTATION H.E. was a 26-year-old German lumberjack with extensive mountaineering experience. He ascended to 5200 m (17,060 feet) from 2000 m (6562 feet) in 4 days and attempted the summit (6194 m [20,322 feet]) on the fifth day. At 5800 m (19,029 feet) he turned back because of severe fatigue, headache, and malaise. He returned alone to 5200 m (17,060 feet), stumbling on the way because of loss of coordination. He had no appetite and crawled into his sleeping bag too weak, tired, and disoriented to undress. He recalled no pulmonary symptoms. In the morning H.E. was unarousable, slightly cyanotic, and noted to have Cheyne-Stokes respirations. After 10 minutes on high-flow oxygen, H.E. began to regain consciousness, although he was completely disoriented and unable to move. A rescue team lowered him down a steep slope, and on arrival at 4400 m (14,436 feet) 4 hours later, he was conscious but still disoriented, able to move extremities but unable to stand. Respiratory rate was 60 breaths/min, and heart rate was 112 beats/min. Papilledema and a few rales were present. SaO2 was 54% on room air (normal is 85% to 90%). On a nonrebreather mask with 14 L/min oxygen, the SaO2 increased to 88% and the respiratory rate decreased to 40 breaths/min. Eight milligrams of dexamethasone were administered intramuscularly at 4:20 PM and continued orally, 4 mg every 6 hours. At 5:20 PM, H.E. began to respond to commands. The next morning H.E. was still ataxic but was able to stand, take fluids, and eat heartily. He was evacuated by air to Anchorage (sea level) at 12:00 PM. On admission to the hospital at 3:30 PM, roughly 36 hours after regaining consciousness, H.E. was somewhat confused and mildly ataxic. Arterial blood gas studies on room air showed a PO2 of 58 mm Hg, pH of 7.5, and PCO2 of 27 mm Hg. Bilateral pulmonary infiltrates were present on the chest radiograph. Magnetic resonance imaging of the brain revealed white matter edema, primarily of the corpus callosum (Figures 1-15 and 1-16). On discharge the next morning, H.E. was oriented, bright, and cheerful and had very minor ataxia and clear lung fields. 17

CHAPTER 1  High-Altitude Medicine and Physiology

of allergy to sulfa antibiotic, the incidence of hypersensitivity reaction to a sulfonamide nonantibiotic was 1.6%.517 The same analysis concluded that persons who are penicillin allergic are actually more likely to react to drugs like acetazolamide than those who are sulfa allergic. Nonetheless, it is wise to be cautious in persons with a history of allergy, especially anaphylaxis to either sulfa or penicillin. Many experts recommend a trial dose of the medication well before the altitude sojourn, to determine if the drug is tolerated well. Although the usual allergic reaction is a rash starting a few days after ingestion, anaphylaxis to acetazolamide does rarely happen.

PART 1  MOUNTAIN MEDICINE

Pathophysiology

FIGURE 1-15  Magnetic resonance image of a patient with highaltitude cerebral edema. Increased T2 signal in splenium of corpus callosum (arrow) indicates edema. (Reprinted from Hackett PH, Yarnell PR, Hill R, et al: High-altitude cerebral edema evaluated with magnetic resonance imaging: Clinical correlation and pathophysiology, JAMA 280:1920, 1998.)

The pathophysiology of HACE is a progression of the same mechanism as advanced AMS (see Acute Mountain Sickness, Pathophysiology, and Figure 1-12) and appears to be vasogenic edema. In cases similar to this, lumbar punctures have revealed elevated CSF pressures, often more than 300 mm H2O,220,573 evidence of cerebral edema on CT scan and MRI,197,272 and gross cerebral edema on necropsy.117,118 Small petechial hemorrhages were also consistently found on autopsy, and venous sinus thromboses were occasionally seen.117,118 Well-documented cases have often included pulmonary edema that was not clinically apparent. Whereas the brain edema of reversible HACE is most likely vasogenic, as the spectrum shifts to severe, end-stage HACE, then gray matter (presumably cytotoxic) edema develops as well, culminating in brain herniation and death. As Klatzo271 has pointed out, as vasogenic edema progresses, the distance between brain cells and their capillaries increases, so that nutrients and oxygen eventually fail to diffuse and the cells are rendered is­ chemic, leading to intracellular (cytotoxic) edema. Raised ICP produces many of its effects by decreasing cerebral blood flow, and brain tissue also becomes ischemic on this basis.344 Focal neurologic signs caused by brainstem distortion and by extraaxial compression, as in third and sixth cranial nerve palsies, may develop,452 making cerebral edema difficult to differentiate from primary cerebrovascular events. The most common clinical presentation, however, is change in consciousness associated with ataxia, without focal signs.582,589

1

2

3

4

5

6

FIGURE 1-16  Magnetic resonance imaging (MRI) scans of patient with high-altitude cerebral edema (HACE). A fluid-attenuated inversion recovery (FLAIR) (1) shows an areal lesion of the corpus callosum—confirmed by diffusion-weighted imaging (DWI) (2), with increased values in apparent diffusion coefficient (ADC) (3), indicating increased water diffusivity compatible with vasogenic edema; in combination, the characteristic MRI pattern consistent with HACE (1 to 3) that persists 6 weeks after the event. A novel finding relates to the multiple patchy hypointensities that correspond to multiple microhemorrhages (arrows) displayed on the T2* images (4 to 6). The right frontal meningioma (visible on FLAIR [1]; [arrowhead]) is an incidental finding. (Reprinted from Kallenberg K, Dehnert C, Dorfler A, et al: Microhemorrhages in nonfatal high-altitude cerebral edema, J Cereb Blood Flow Metab 28:1635, 2008.)

18

STROKE

Given the sporadic nature and generally remote location of this disorder, it is not surprising that there are no controlled trials regarding treatment of HACE. All experts agree that successful treatment requires early recognition. At the first sign of ataxia or change in consciousness, descent should be started, dexamethasone (4 to 8 mg intravenously, intramuscularly, or orally initially, followed by 4 mg every 6 hours) administered, and oxygen (2 to 4 L/min by vented mask or nasal cannula) applied if available (see Box 1-4). Oxygen can be titrated to maintain SaO2 at greater than 90% if oximetry is available. Comatose patients require additional airway management and bladder drainage. Attempting to decrease ICP by endotracheal intubation and hyperventilation is a reasonable approach, although these patients are already alkalotic and overhyperventilation could result in disastrous cerebral ischemia. Loop diuretics such as furosemide (40 to 80 mg) or bumetanide (1 to 2 mg) may reduce brain hydration, and have been used successfully,116,500 but an adequate intravascular volume to maintain perfusion pressure is critical. Hypertonic solutions of saline, mannitol, or oral glycerol have been suggested, but rarely used in the field. Controlled studies are lacking, but empirically the response to corticosteroids and oxygen seems excellent if they are given early in the course of the illness and disappointing if they are not started until the victim is unconscious. Coma may persist for days, even after evacuation to low altitude, but other causes of coma must be considered and ruled out by appropriate evaluation.220 The average duration of hospital stay in one series of patients with severe HACE was 5.6 days, and average time to full recovery was 2.4 weeks, with a range of 1 day to 6 weeks.197 Two patients of the 44 in the series by Dickinson118 remained in coma for 3 weeks. Sequelae lasting weeks are common;197,220 longer-term follow-up has been limited, but presumed permanent impairment has been reported.190,220 In the Chinese series of 66 patients, HACE was diagnosed early, and descent was uniformly successful. Ataxia resolved in all but one within 7 days, and only one patient had long-term sequelae, clonic convulsions affecting the left hand.582 Prevention of HACE is the same as for AMS and HAPE.

The occurrence of stroke in a young, fit person at high altitude is uncommon but tragic. A number of case reports have described climbers with resultant permanent dysfunction.85,219,505 Indian soldiers at extreme altitude have a high incidence of stroke.249 Cerebral venous thrombosis manifests more insidiously, and diagnosis is often delayed.* Factors contributing to stroke may include polycythemia, dehydration, increased ICP if AMS is present, increased cerebrovenous pressure, cerebrovascular spasm, and familial thrombophilia.38 Stroke may be confused with HACE. Neurologic symptoms, especially focal abnormalities without AMS or HAPE that persist despite treatment with oxygen, corticosteroids, and descent, suggest a cerebrovascular event and mandate careful evaluation with a complete neurologic workup.

FOCAL NEUROLOGIC CONDITIONS WITHOUT AMS OR CEREBRAL EDEMA Various localizing neurologic signs, transient in nature and not necessarily occurring in the setting of AMS, suggest migraine, cerebrovascular spasm, transient ischemic attack (TIA), local hypoxia without loss of perfusion (watershed effect), or focal edema.41 Cortical blindness is one such condition. Hackett and colleagues194 reported six cases of transient blindness in climbers or trekkers with intact pupillary reflexes, which indicated that the condition was due to a cortical process. Treatment with breathing of either carbon dioxide (a potent cerebral vasodilator) or oxygen resulted in prompt relief, suggesting that the blindness was due to inadequate regional circulation or oxygenation. Descent effected relief more slowly. Other conditions that could be attributed to spasm or “TIA” have included transient hemiplegia or hemiparesis, transient global amnesia, unilateral paresthesias, aphasia, and scotoma.* The true mechanism of these focal findings is unknown and may be multifactorial. Young, healthy altitude sojourners are unlikely to have TIA syndrome from cerebrovascular disease. Other neurologic complications at altitude include globus pallidum lesions, which were considered complications of AMS or HACE and reported to lead to Parkinson’s disease.248,355,495,527,543 Although these deficits were related to high altitude, whether altitude illness was truly the proximate cause of these lesions is unclear. The globus pallidum is sensitive to hypoxia, especially from carbon monoxide poisoning, and can also be damaged by ischemia.

*References 36, 41, 57, 78, 299, 576, 597.

CLINICAL PRESENTATION E.H., a 42-year-old male climber on a Mt Everest expedition, awoke at 8000 m (26,247 feet) with dense paralysis of the right arm and weakness of the right leg. On descent the paresis cleared, but at base camp (5000 m [16,404]) severe vertigo developed, along with extreme ataxia and weakness. Neurologic consultation on return to the United States resulted in a diagnosis of multiple small cerebral infarcts, but none was visible on CT scan of the brain. The hematocrit value 3 weeks after descent from the mountain was 70%. Over the next 4 years signs gradually improved, but mild ataxia, nystagmus, and dyslexia persist. The focal and persistent nature of the cerebral symptoms and signs, although multiple, indicates a cerebrovascular, rather than an intracranial, pressure etiology. The hematocrit value on the mountain was greater than 70%, high enough for increased viscosity and microcirculatory sludging to contribute to ischemia and infarction. No familial thrombophilia was detected. Treatment of stroke is supportive. Oxygen and corticosteroids may be worthwhile to treat any AMS or HACE component. Immediate evacuation to a hospital is indicated. Persons with TIAs at high altitude should probably be started on aspirin therapy and proceed to a lower altitude. Oxygen may quickly abort cerebrovascular spasms and will improve watershed hypoxic events. When oxygen is not available, rebreathing to raise alveolar PCO2 may be helpful by increasing cerebral blood flow.

COGNITIVE CHANGES AT HIGH ALTITUDE If cerebral oxygen consumption is constant, what causes the well-documented, albeit mild, cognitive changes at high altitude? The cognitive changes may be related to specific neurotransmitters. For example, tryptophan hydroxylase in the serotonin synthesis pathway has a high requirement for oxygen (Michaelis constant [Km] = 37 mm Hg).95,160 Tyrosine hydroxylase, in the dopamine pathway, is also oxygen sensitive. Gibson and Blass160 suggested that a decrease in acetylcholine activity during hypoxia might explain the lassitude. In a fascinating study, Banderet and Lieberman21 showed that increased dietary tyrosine reduced mood changes and symptoms of environmental stress in subjects at simulated altitude. Further work with neurotransmitter agonists and antagonists will help shed light on their role in cognitive dysfunction at altitude and could lead to new pharmacologic approaches to improve neurologic function.

HIGH-ALTITUDE PULMONARY EDEMA The most common cause of death related to high altitude, HAPE is completely and easily reversed if recognized early and treated properly. Undoubtedly HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of “pneumonia” within days of arriving at high altitude. The death of Dr. Jacottet, “a robust, broad-shouldered young man,” on Mt Blanc in 1891 (he refused descent so that he could *References 177, 256, 460, 505, 538, 597.

19

CHAPTER 1  High-Altitude Medicine and Physiology

Treatment

PART 1  MOUNTAIN MEDICINE

“observe the acclimatization process” in himself) may have provided the first autopsy of HAPE. Angelo Mosso wrote, From Dr. Wizard’s post-mortem examination . . . the more immediate cause of death was therefore probably a suffocative catarrh accompanied by acute edema of the lungs. . . . I have gone into the particulars of this sorrowful incident because a case of inflammation of the lungs also occurred during our expedition, on the summit of Monte Rosa, from which, however, the sufferer fortunately recovered.374 On an expedition to K2 (Karakorum Range, Pakistan) in 1902, Alistair Crowley101 described a climber “suffering from edema of both lungs and his mind was gone.” In the Andes, physicians were familiar with pulmonary edema peculiar to high altitude,238,301 but it was not until Hultgren and Spickard226 and Houston218 offered their observations that the English-speaking world became aware of high-altitude pulmonary edema (see Rennie422 for a review). Hultgren and colleagues237 then published hemodynamic measurements in persons with HAPE, demonstrating that it was a noncardiogenic edema. Since that time, many studies and reviews have been published, and HAPE is still the subject of intense investigation. The reader is referred to recent reviews.* Individual susceptibility, rate of ascent, altitude reached, degree of cold,419 physical exertion, and certain underlying medical conditions are all factors determining the prevalence of HAPE. The incidence varies from approximately 1 in 10,000 skiers at moderate altitude in Colorado to 1 in 50 climbers on Mt McKinley (6194 m [20,322 feet]) and up to 6% of mountaineers in the Alps ascending rapidly to 4559 m (14,957 feet).29 Hultgren and associates235 reported 150 cases of HAPE over 39 months at a Colorado ski resort at 2928 m (9606 feet). Some regiments in the Indian Army had a much higher incidence of HAPE (15%) because of very rapid deployment to the extreme altitude of 5500 m (18,045 feet)501 (see Table 1-1). Wu and colleagues582 reported HAPE in 0.5% of Chinese railway workers at 4000 to 4900 m (13,123 to 16,076 feet). Persons with previous HAPE had a 60% attack rate when they went to 4559 m (14,957 feet) in 36 hours, but with slower ascent, some of the same individuals climbed over 7000 m (22,966 feet) without illness.24,30 HAPE appears to be less common in women.99,232,506 Whether all persons are capable of developing HAPE (with a very rapid ascent to a sufficiently high altitude and with heavy exercise) is arguable.32 Likewise, some studies suggest that many persons contract subclinical extravascular lung water,100 whereas others contradict this.111 Even well-acclimatized individuals with a sudden push to a higher altitude can succumb to HAPE.100 Nonetheless, a population of HAPE-susceptible persons with unique physiologic characteristics has been described (see HAPE Susceptibility, later). These individuals represent the small percentage of people who develop HAPE when others in the same circumstances do not. HAPE in children is associated as well with antecedent viral infections, trisomy 21, and underlying congenital cardiovascular malformations, such as unilateral absence of the pulmonary artery.105 CLINICAL PRESENTATION D.L., a 34-year-old man, was in excellent physical condition and had been on numerous high-altitude backpacking trips, occasionally suffering mild symptoms of AMS. He drove from sea level to the trailhead and hiked to 3050 m (10,007 feet) sleeping altitude the first night of his trip in the Sierra Nevada. He proceeded to 3700 m (12,139 feet) the next day, noticing more dyspnea on exertion when walking uphill, a longer time than usual to recover when he rested, and a dry cough. He complained of headache, shivering, dyspnea, and insomnia the second night. The third day the group descended to 3500 m (11,483 feet) and rested, primarily for D.L.’s benefit. That night, D.L. was unable to eat, noted severe dyspnea, and suffered

*References 32, 109, 307, 320, 467, 472, 477, 515.

20

coughing spasms and headache. On the fourth morning D.L. was too exhausted and weak to get out of his sleeping bag. His companions noted that he was breathless, cyanotic, and ataxic but had clear mental status. A few hours later he was transported by helicopter to a hospital at 1200 m (3937 feet). On admission he was cyanotic, his oral temperature was 37.8° C (100° F), blood pressure 130/76 mm Hg, heart rate 96 beats/min, and respiratory frequency 20 breaths/min. Bilateral basilar rales to the scapulae were noted. Findings of cardiac examination were reported as normal. Romberg and finger-to-nose tests revealed 1+ ataxia. Arterial blood gas studies on room air revealed PO2 24 mm Hg, PCO2 28 mm Hg, and pH 7.45. The chest radiograph showed extensive bilateral patchy infiltrates (Figure 1-17, C ). D.L. was treated with bed rest and supplemental oxygen. On discharge to his sea level home 3 days later, the pulmonary infiltrates and rales had cleared, although blood gas values were still abnormal: PO2 76 mm Hg, PCO2 30 mm Hg, and pH 7.45. He had an uneventful, complete recovery at home. D.L. was advised to ascend more slowly in the future, staging his ascent with nights spent at 1500 m (4921 feet) and 2500 m (8202 feet). He was taught the early signs and symptoms of HAPE and advised on pharmacologic prophylaxis. This case illustrates typical aspects of HAPE. Victims are frequently young, fit males who ascend rapidly from sea level and may not have previously suffered HAPE even with repeated altitude exposures; the particular ascent may have been faster than previously. HAPE usually occurs within the first 2 to 4 days of ascent to higher altitudes (above 2500 m [8202 feet]), most commonly on the second night.180 Decreased exercise performance and increased recovery time from exercise are the earliest indications of HAPE. The victim suffers fatigue, weakness, and dyspnea on exertion, especially when walking uphill; he or she often ascribes these nonspecific symptoms to various other causes. Signs of AMS are present about 50% of the time.232 A persistent dry cough develops. Nail beds and lips become cyanotic. The condition typically worsens at night, and tachycardia and tachypnea develop at rest. Increasing respiratory distress heralds to the victim the development of a serious condition. In contrast to the usual 1- to 3-day gradual onset, HAPE may strike abruptly, especially in a sedentary person who may not notice the early stages.552 Orthopnea is uncommon (7%). Pink or blood-tinged, frothy sputum is a very late finding. Hemoptysis was present in 6% of victims in one series.235 Severe hypoxemia may produce cerebral edema with mental changes, ataxia, decreased level of consciousness, and coma. Hultgren and colleagues235 reported an incidence of HACE of 14% in those with HAPE at ski resorts. On admission to the hospital, the victim does not generally appear as ill as expected based on arterial blood gas and radiographic findings. Elevated temperature up to 38.5° C (101.3° F) is common. Tachycardia correlates with respiratory rate and severity of illness.237 Rales may be unilateral or bilateral and usually originate from the right middle lobe. Concomitant respiratory infection is sometimes present. Pulmonary edema may manifest with predominantly neurologic manifestations and minimal pulmonary symptoms and findings, most likely in persons with low HVR. Cerebral edema, especially with coma, may obscure the diagnosis of HAPE.189 Pulse oximetry or chest radiography confirms the diagnosis. Differential diagnosis includes pneumonia, bronchitis, mucus plugging, pulmonary embolism or infarct, heart failure, acute myocardial infarction, and sometimes asthma (see Box 1-3). Complications include infection, cerebral edema, pulmonary embolism or thrombosis, and such injuries as frostbite or trauma secondary to incapacitation.24,189,233 Hemodynamics Hemodynamic measurements by catheter show elevated pulmonary artery pressure and pulmonary vascular resistance, low to normal pulmonary wedge pressure, and low to normal cardiac output and systemic arterial blood pressure.234,403 Echocardiography demonstrates high pulmonary artery pressure, tricuspid regurgitation, normal left ventricular systolic function, somewhat

CHAPTER 1  High-Altitude Medicine and Physiology

A

B

C

D

FIGURE 1-17  A, Typical radiograph of high-altitude pulmonary edema (HAPE) in a 29-year-old female skier at 2450 m (8038 feet). B, The same patient 1 day after descent and oxygen administration, showing rapid clearing. C, Bilateral pulmonary infiltrates on radiograph of a patient with severe HAPE after descent (case presented in text). D, Ventilation and perfusion scans in a person with congenital absence of right pulmonary artery after recovery from HAPE.

abnormal diastolic function,7 and variable right-sided heart findings of increased atrial and ventricular size.193,393 The electrocardiogram (ECG) usually reveals sinus tachycardia. Changes consistent with acute pulmonary hypertension, such as right axis deviation, right bundle branch block, voltage for right ventricular hypertrophy, and P-wave abnormalities, have been described.24,232 Atrial flutter has been reported, but ventricular arrhythmias have not. Laboratory Studies Kobayashi and colleagues272 reported clinical laboratory values in 27 patients with HAPE that showed mild elevations of hematocrit and hemoglobin, probably secondary to intravascular volume depletion and perhaps plasma leakage into the lungs. Elevation of peripheral white blood cell count is common but is rarely above 14,000 cells/mL3. Serum concentration of creatine

phosphokinase (CPK) is increased, mostly due to skeletal muscle damage, although in two patients, CPK isoenzymes showed brain fraction levels of 1% of total, which may have indicated brain damage.272 An unpublished study in Colorado has found normal brain natriuretic peptide (BNP) values in patients with HAPE (S. Gallagher, personal communication). Arterial blood gases consistently reveal respiratory alkalosis and marked hypoxemia, more severe than expected for the patient’s clinical condition. Because respiratory or primary metabolic acidosis has not been reported, arterial blood gas studies are unnecessary if noninvasive pulse oximetry is available to measure arterial oxygenation. At 4200 m (13,780 feet) on Mt McKinley, the mean value of PaO2 in HAPE was 28±4 mm Hg. Values as low as 24 mm Hg in HAPE are not unusual. Arterial oxygen saturation values in HAPE subjects at 4300 m (14,108 feet) ranged from 40% to 70%, with a mean of 56% ± 8%.480 At 2928 m (9606 feet), mean 21

PART 1  MOUNTAIN MEDICINE

SaO2 was 74%.235 Arterial acid–base values may be misleading in patients taking acetazolamide, because this drug produces significant metabolic acidosis. Radiographic Findings The radiographic findings in HAPE have been described in original reports.237,330,554,555 Findings are consistent with noncardiogenic pulmonary edema, with generally normal heart size and left atrial size, and no evidence of pulmonary venous prominence, such as Kerley lines. The pulmonary arteries increase in diameter.555 Infiltrates are commonly described as fluffy and patchy with areas of aeration between infiltrates and in a peripheral rather than central location. Infiltrates may be unilateral or bilateral, with a predilection for the right middle lung field, which corresponds to the usual area of rales. Pleural effusion is rare. Radiographic findings generally correlate with illness severity and degree of hypoxemia. A small right hemithorax, absence of pulmonary vascular markings on the right, and edema confined to the left lung are criteria for diagnosis of unilateral absent pulmonary artery.185 Radiographic findings of HAPE are presented in Figure 1-17. Clearing of infiltrates is generally rapid once treatment is initiated. Depending on severity, complete clearing may take from 1 to several days. Infiltrates are likely to persist longer if the patient remains at high altitude, even if confined to bed and receiving oxygen therapy. Radiographs taken within 24 to 48 hours of return to low altitude may still be able to confirm diagnosis of HAPE. Recently, an ultrasound technique known as “comet-tail” scoring, previously validated in cardiogenic pulmonary edema, has been used to evaluate extravascular lung water at high altitude, which in the right setting might indicate clinical or subclinical pulmonary edema. The comet-tail artifacts are created by microreflections of the ultrasound beam within interlobular septa thickened by the presence of increased lymphatic fluid consistent with interstitial and/or alveolar edema. Eleven patients at 4240 m (13,911 feet) with a clinical diagnosis of HAPE underwent chest ultrasound examinations using this technique.137 Seven patients with no evidence of HAPE or other altitude illness served as control subjects. HAPE patients had much higher comet-tail scores and lower oxygen saturation than did control subjects, and scores decreased as HAPE cleared. The comet-tail technique seemed to be able to recognize and monitor the degree of pulmonary edema in HAPE. Although an ultrasound machine is rarely available in the wilderness, this technique might prove to be a valuable research tool, and it offers easy repeated measurements while avoiding radiation.313 Recently, investigators successfully used a satellite telemedical connection with a remote expert to guide thoracic ultrasound examinations at Advanced Base Camp on Mt Everest; high-quality images were obtained that verified increases in lung water.394 Another group, also in Nepal, used the technique while trekking up to 4700 m (15,420 feet) and found a high prevalence of extravascular lung water, but no association with estimated pulmonary artery pressure.409 This technique may lend itself well to answering the question of whether the oft-reported increase in extravascular lung water on ascent to high altitude and in AMS is actually a precursor to HAPE. Pathologic Findings More than 20 autopsy reports of persons who died of HAPE have been published.* Of those whose cranium was opened, more than one-half had cerebral edema. All lungs showed extensive and severe edema, with bloody, foamy fluid in the airways. Lung weights were two to four times normal. The left side of the heart was normal. The right atrium and main pulmonary artery were often distended. Proteinaceous exudate with hyaline membranes was characteristic. All lungs had areas of inflammation with neutrophil accumulation. The diagnosis of bronchopneumonia was common, although bacteria were not noted. Pulmonary veins, the left ventricle, and the left atrium were generally not dilated, in contrast to the right ventricle and atrium. Most reports mention *References 12, 117, 380, 500, 501, 573.

22

capillary and arteriolar thrombi and alveolar fibrin deposits, as well as microvascular and gross pulmonary hemorrhage and infarcts. The autopsy findings thus suggest a protein-rich, permeability type of edema with thrombi or emboli. Confirmation of HAPE as a permeability edema was obtained by analysis of alveolar lavage fluid by Schoene and associates.478,480 These clinicians found a 100-fold increase in lavage fluid protein levels in patients with HAPE compared with well control subjects and patients with AMS.480 The lavage fluid also had a low percentage of neutrophils, in contrast to findings in adult respiratory distress syndrome. Further evidence for a permeability edema was a 1:1 ratio of aspirated edema fluid protein to plasma protein level found by Hackett and colleagues.184 In addition, the lavage fluid contained vasoactive eicosanoids and complement proteins, indicative of endothelium–leukocyte interactions. More recent research using repeated bronchoalveolar lavage as HAPE was developing found that inflammation was absent early on, suggesting that inflammation is a response to the alveolar damage, rather than an initiating event.531 Mechanisms of High-Altitude Pulmonary Edema An acceptable explanation for HAPE must take into account three well-established facts: excessive pulmonary hypertension, highprotein permeability leak, and normal function of the left side of the heart. A mechanism consistent with these facts is failure of capillaries secondary to overperfusion and capillary hypertension (Figure 1-18). Role of Pulmonary Hypertension.  Excessive pulmonary artery pressure (PAP) is the sine qua non of HAPE; no HAPE has been reported without pulmonary hypertension. All persons ascending to high altitude or otherwise enduring hypoxia, however, have some elevation of PAP. The hypoxic pulmonary vasoconstrictor response (HPVR) is thought to be useful in humans at sea level because it helps match perfusion with ventilation. When local areas of the lungs are poorly ventilated because of infection or atelectasis, for example, the HPVR Altitude hypoxia HVR, sleep, and exercise ↓ PaO2

Uneven HPV

↑ Sympathetic activity

Exercise PHTN

Pulmonary and peripheral venous constriction

Overperfusion

↑ Pcap

↑ Pulmonary blood volume

Capillary stress failure

Capillary leak

↓ Alveolar Na and H2O clearance

High-altitude pulmonary edema FIGURE 1-18  Proposed pathophysiology of high-altitude pulmonary edema. HPV, Hypoxic pulmonary vasoconstriction; HVR, hypoxic ventilatory response; PaO2, arterial partial pressure of oxygen; Pcap, capillary pressure; PHT, pulmonary hypertension.

Overperfusion and Capillary Leak.  To explain how pulmonary hypertension might lead to edema, Hultgren suggested that in those who develop HAPE, the hypoxic pulmonary vasoconstriction is uneven and the delicate microcirculation in an unconstricted (relatively dilated) area is subjected to high pressure and flow, leading to leakage (edema). The unevenness could be due to anatomic characteristics, such as distribution of muscularized arterioles, or to functional factors, such as loss of HPVR in severely hypoxic regions.227 Uneven perfusion is suggested clinically by the typical patchy radiographic appearance and is supported by lung scans and MRI imaging during acute hypoxia showing uneven perfusion in persons with a history of HAPE.215,553 Persons born without a right pulmonary artery are highly susceptible to HAPE (see Figure 1-17, D),185 supporting the concept of overperfusion of a restricted vascular bed as a cause of edema, because the entire cardiac output flows into one lung. Other causes of overperfusion of the pulmonary circulation that predispose to HAPE include left-to-right shunts such as atrial septal defect, ventricular septal defect, and patent ductus arteriosus. Rapid reversibility of the illness and response to vasodilators are also consistent with this mechanism. When hydrostatic pressure is reduced, alveolar fluid is quickly reabsorbed. Other factors contributing to increased hydrostatic pressure, such as exercise or high salt load with subsequent hypervolemia, also may play a role in HAPE. The authors have several times observed onset of HAPE after large salt intake. Some studies have also suggested roles for pulmonary venous constriction, which would contribute to increased capillary hydrostatic pressure.193,325 The end result of overperfusion and increased capillary pressure325 is distension, increased filtration of fluid, and even rupture of the capillary–alveolar membrane, termed “stress failure,”567,568 with subsequent leakage of cells and proteins. Alveolar Fluid Balance.  Fluid filtration into the interstitial and alveolar space, reabsorption back across the epithelial membrane, and clearance of interstitial fluid by lymph result in a dynamic balance that generally prevents alveolar flooding. On ascent to altitude, the hydrostatic pressure gradient for filtration is increased. As might be expected, multiple lines of evidence suggest that extravascular lung water is increased at altitude.100,169,409,557 Despite this, frank alveolar flooding is uncommon. This may well be due to differences in hydrostatic pressure in persons resistant and susceptible to HAPE. However, persons who contract HAPE appear to also have impaired ability to clear alveolar fluid. On a constitutive (genetic) basis, HAPE subjects have lower activity of the epithelial sodium channel and therefore reduced ability to transport sodium across the epithelium back into the interstitial space.329,466,468 (It is the sodium gradient across the epithelium that determines movement of water from alveoli.) In addition, epithelial sodium transport is diminished by hypoxia per se, so that those with already impaired function become more impaired at altitude. How large a role this mechanism plays in HAPE is uncertain216 (see Figure 1-18). Control of Ventilation.  As in AMS, persons with HAPE had a lower HVR than did persons who acclimatized well,195,336 but not

all persons with a low HVR become ill. Thus, low HVR appears to play a permissive, rather than causative, role in HAPE, whereas a brisk HVR appears to be protective. Persons who hypoventilate are more hypoxemic and presumably suffer greater pulmonary hypertension. Possibly more important, low HVR may permit episodes of extreme hypoxemia during sleep (see Figure 1-7).180,195 In addition, a low HVR may allow further ventilatory depression through central nervous system (CNS) suppression (hypoxic ventilatory depression). Such persons, when given oxygen, show a “paradoxical” increase in ventilation.195 Despite correlation of HAPE with low HVR, its value as a sea level predictor is poor.110 HAPE Susceptibility Persons susceptible to HAPE (HAPE-s) show at sea level abnormal rise of PAP and pulmonary vascular resistance during hypoxic challenge at rest and during exercise and even during exercise in normoxia, suggesting overreactivity of the pulmonary circulation to both hypoxia and exercise.131,175,258 Part of this reactivity may be related to greater alveolar hypoxemia secondary to lower HVR,195,212,338 but other factors have been uncovered. Microneurographic recordings from the peroneal nerve during hypoxia established a direct link in HAPE-s between the rise in PAP and greater sympathetic activation,126 indicating that sympathetic overactivation might contribute to HAPE. Smaller and less distensible lungs have been noted in HAPE-s, which might limit the ability to accommodate increased flow by vascular recruitment and thus result in a higher vascular resistance.131,212,508 Another characteristic of HAPE-s is abnormal endothelial function, as evidenced by reduced NO synthesis during hypoxia50,74,474 and during HAPE,125 and higher levels of endothelin, a potent pulmonary vasoconstrictor.470,509 The importance of reduced NO is reinforced by studies showing improvement in pulmonary hemodynamics when either NO or a phosphodiesterase (PDE)-5 inhibitor was given to HAPE subjects9,159,322,474 (Figure 1-19). As mentioned previously, HAPE-s also are characterized by impairment of respiratory transepithelial sodium and water transport, making it more difficult to reabsorb alveolar fluid.469,473 Patent foramen ovale (PFO) also has been observed to be more common among HAPE-susceptible than among HAPEresistant adult mountaineers.6,311 Since the initial report of Levine and co-workers,293 the association of PFO and HAPE has been confirmed, but cause and effect have not been established.6 Allemann and associates6 performed a case-control study of 16 HAPE-susceptible participants and 19 mountaineers resistant to HAPE. Presence of PFO was determined by transesophageal echocardiography and estimated pulmonary artery pressure by Doppler echocardiography at low (550 m [1804 feet]) and high altitude (4559 m [14,957 feet]). The frequency of PFO was more than four times higher in HAPE-susceptible than in HAPE-resistant participants, both at low altitude (56% versus 11%) and high altitude (69% versus 16%). At high altitude, SaO2 before the onset of pulmonary edema was significantly lower in HAPE-susceptible participants than in the control group (73% versus 83%). Also, in the HAPE-susceptible group, participants with a large PFO had more severe arterial hypoxemia (65% versus 77%) than did those with smaller or no PFO. The authors speculated that at high altitude a large PFO may contribute to exaggerated arterial

Nitric oxide—overview Hypoxia

eNOS

L-arginine

NO

cGMP

Vascular muscle relaxation

PDE-5 inhibitor

Degradation by PDE-5

FIGURE 1-19  The nitric oxide pathway and action of phosphodiesterase-5 inhibitors. In the presence of an inhibitor  c-GMP, the second messenger of nitric oxide is not degraded, and vasodilation is therefore enhanced. c-GMP, guanosine monophosphate; eNOS, endothelial nitric oxide synthase NO, nitric oxide; PDE, phosphodiesterase.

23

CHAPTER 1  High-Altitude Medicine and Physiology

directs blood away from those areas to well-ventilated regions. In the setting of global hypoxia, as occurs with ascent to high altitude, HPVR is presumably diffuse and all areas of the lung constrict, causing a restricted vascular bed and an increase in PAP, which is of little if any value for ventilation–perfusion matching at high altitude. The degree of HPVR varies widely among individuals (as well as among species), and is most likely an inherent trait. HAPE-susceptible persons have a greater increase in PAP than do persons who are not susceptible (see HAPE Susceptibility, later). Although other factors, such as the vigor of the ventilatory response and subsequent alveolar PO2, may help determine the ultimate degree of pulmonary hypertension, HPVR appears to be the dominant factor. Because all persons with HAPE have excessive pulmonary hypertension, but not all those with excessive pulmonary hypertension have HAPE, it appears that pulmonary hypertension is necessary but in and of itself is not the cause of HAPE.

PART 1  MOUNTAIN MEDICINE

hypoxemia and facilitate HAPE.6 Others pointed out, however, that the greater hypoxemia may have been due to subclinical pulmonary edema,139 or that a PFO was a marker of a reactive pulmonary vascular bed.108 HAPE-s are known to have exaggerated pulmonary pressure response to exercise at sea level, for example, which could maintain an open shunt. Because occurrence of PFO is so common in the general population, more compelling evidence is required before suggesting that PFO is a predisposing factor to HAPE, and that those with PFO should consider closure of the defect before significant altitude exposure, or as a result of an episode of HAPE, as some have recommended.82 Genetics of HAPE The first major genetic studies in lowlanders visiting high altitudes have focused on HAPE because it is the most fully understood pathophysiologic process occurring in lowlanders visiting high altitudes.* Although many characteristics of HAPE-susceptible persons are apparently genetically determined, actual genetic studies are conflicting and difficult to interpret. Good evidence for a genetic component to HAPE susceptibility comes from study of major human leukocyte antigen (HLA) alleles in 28 male and 2 female subjects with a history of HAPE compared with HLA alleles in 100 healthy volunteers.201 The HLA-DR6 and HLA-DQ4 antigens were associated with HAPE, and HLA-DR6 with pulmonary hypertension. These findings suggest that immunogenetic susceptibility may underlie development of HAPE, at least in some cases. Given the importance of endothelial function in HAPE, investigators have looked at gene polymorphisms for endothelial nitric oxide synthase (eNOS). Two recent studies have established a link between HAPE-s and the Glu298Asp alleles of the eNOS gene in Japanese and Indian subjects.2,123 An additional study of NOS3-related gene polymorphisms that could explain decreased NO synthesis found no relation to HAPE-s.563 This may be explained by racial differences or by the specific processes encoded by the different gene fragments. The insertion–deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has also garnered attention, because the renin-aldosterone-angiotensin system is known to be activated in HAPE,34 and the ACE gene has also been linked to performance at altitude.362 The insertion–deletion polymorphism was not associated with HAPE susceptibility in populations of Indians, Japanese, and whites.112,217,280 However, one variant of the angiotensin receptor gene was correlated with HAPE susceptibility in Japanese.217 In summary, gene polymorphisms coding for the angiotensin receptor and endothelial NO distinguish HAPE-s from HAPEresistant subjects. In the near future, single nucleotide polymorphism scanning techniques as well as RNA gene expression techniques will be used to explore the genetic contributions to high-altitude physiology and pathophysiology. The search continues for a genetic basis for HAPE susceptibility.† Treatment Treatment choices for HAPE depend on severity of illness and logistics. As with all high-altitude illnesses, early recognition is key to successful outcome (see Box 1-4). In the wilderness, where oxygen and medical expertise may be unavailable, persons with HAPE need to be urgently evacuated to lower altitude. However, because of augmented pulmonary hypertension and greater hypoxemia with exercise, exertion must be minimized. Early HAPE responds rapidly to descent of only 500 to 1000 m (1640 to 3281 feet), and the victim may be able to reascend slowly 2 or 3 days later. In high-altitude locations with oxygen supplies, bed rest with supplemental oxygen may suffice, but severe HAPE may require high-flow oxygen (4 L/min or more) for more than 24 hours. Hyperbaric therapy with a fabric pressure bag (2 psi) is equivalent to low-flow oxygen and can help conserve oxygen supplies.437 Oxygen immediately increases arterial oxygenation and reduces pulmonary artery pressure, heart rate, respiratory rate, *References 3, 200, 306, 363, 412, 413, 458, 502, 510, 536, 558, 596. † References 3, 122, 200, 306, 363, 373, 412, 413, 458, 502, 510, 536, 558, 596.

24

and symptoms. When descent is not possible, oxygen (or a hyperbaric bag) can be lifesaving. Rescue groups should make delivery of oxygen to the victim, by airdrop if necessary, the highest priority if descent is slow or delayed. If oxygen is not available, immediate descent is lifesaving. Waiting for a helicopter or rescue team has too often proved fatal. Because cold stress elevates PAP, the victim should be kept warm.80 The use of a mask providing resistance on expiration (expiratory positive airway pressure [EPAP]) was shown to improve gas exchange in HAPE, and this or continuous positive airway pressure (CPAP) may be useful as a temporizing measure.479 The same is accomplished with pursed-lip breathing. An unusual case report suggested that a climber may have saved his partner’s life by postural drainage to expel airway fluid.56 Drugs are of limited necessity in HAPE, because oxygen and descent are so effective.311 Medications that reduce pulmonary blood volume, PAP, and pulmonary vascular resistance are physiologically rational to use when oxygen is not available or descent delayed. Singh and associates500 reported good results with furosemide (80 mg every 12 hours), and greater diuresis and clinical improvement occurred when 15 mg parenteral morphine was given with the first dose of furosemide. Their use, however, has been eclipsed by recent results with vasodilators. The calcium channel blocker nifedipine (30 mg slow release every 12 to 24 hours) was effective in reducing pulmonary vascular resistance and PAP during HAPE and slightly improved arterial oxygenation.30 Clinical improvement, however, was not dramatic. Nifedipine is well tolerated and unlikely to cause significant hypotension in healthy persons and avoids the danger of CNS depression from morphine and possible hypovolemia from diuretics. Clinical improvement is much better, however, with oxygen and descent than with any medication. NO, a potent pulmonary vasodilator, improves hemodynamics in HAPE but is rarely available, and in any event is usually given with oxygen. The PDE-5 inhibitors, which increase cyclic guanosine monophosphate (c-GMP) to produce pulmonary vasodilation during hypoxia159,425,427 (see Figure 1-19), have shown value for prevention of HAPE322 but have not yet been studied for treatment. Whether these agents will prove to be more effective than nifedipine for treatment is unknown. A theoretic advantage is that the PDE-5 inhibitors produce less systemic vasodilation. Nifedipine, and perhaps other vasodilators, might be useful adjunctive therapy but is not a substitute for definitive treatment (see Box 1-4 and Table 1-7).178,311 β-Agonists may also have an adjunctive role but should not be considered for monotherapy.311 After evacuation of the victim to a lower altitude, hospitalization may be warranted for severe cases. Treatment consists of bed rest and oxygen sufficient to maintain SaO2 greater than 90%; medications are rarely necessary. Rapid recovery is the rule.599 Antibiotics are indicated for infection when present. Occasionally pulmonary artery catheterization or Doppler echocardiography is necessary to differentiate cardiogenic from high-altitude pulmonary edema. Endotracheal intubation and mechanical ventilation are rarely needed. A HAPE victim demonstrating unusual susceptibility, such as onset of HAPE despite adequate acclimatization or onset below 2750 m (9022 feet), might require further investigation, such as echocardiography, to rule out an intracardiac shunt or preexisting pulmonary hypertension. In children, undiagnosed congenital heart disease is worth considering105 (Figure 1-20). Hospitalization until blood gas values are completely normal is not warranted; all persons returning from high altitude are at least partially acclimatized to hypoxemia, and hypocapnic alkalosis persists for days after descent. Distinct clinical improvement, radiographic improvement over 24 to 48 hours, and PaO2 of 60 mm Hg or SaO2 greater than 90% are adequate discharge criteria. Patients are advised to resume normal activities gradually and are warned that 1 to 2 weeks may be required to recover complete strength. Physicians should recommend preventive measures, including graded ascent with adequate time for acclimatization, and should provide instruction on use of acetazolamide, nifedipine, or PDE-5 inhibitors for future ascents. An episode of HAPE is not a contraindication to subsequent high-altitude exposure, but education to ensure proper preventive measures and recognition of early symptoms is critical.

FIGURE 1-20  Chest radiograph of severe high-altitude pulmonary edema (HAPE) in a 4-year-old girl with a small previously undiagnosed patent ductus arteriosus that predisposed her to HAPE.

Prevention The preventive measures previously described for AMS also apply to HAPE: graded ascent, time for acclimatization, low sleeping altitudes, and avoidance of alcohol and sleeping pills.311 Exertion may contribute to onset of HAPE, especially at moderate altitude. Reports from North America at 2500 to 3800 m (8202 to 12,467 feet) have included hikers, climbers, and skiers, all of whom were exercising vigorously. Menon and colleagues346 clearly showed that sedentary men taken abruptly to higher altitude were just as likely to become victims of HAPE. Prudence dictates not overexerting for the first 2 days at altitude. Considerable clinical experience suggests that acetazolamide prevents HAPE in persons with a history of recurrent episodes. Recent animal work showing that acetazolamide blocks hypoxic pulmonary hypertension supports this practice49,213 as does the fact that acetazolamide speeds acclimatization. Nifedipine (20 mg slow release every 8 hours) prevented HAPE in subjects with a history of repeated episodes.30 The drug should be carried by such individuals and started at the first signs of HAPE or, for an abrupt ascent, started when leaving low altitude. The PDE-5 inhibitors sildenafil and tadalafil effectively block hypoxic pulmonary hypertension and therefore will prevent HAPE.320 Tadalafil 10 mg every 12 hours prevented HAPE with rapid ascent in HAPEsusceptible subjects.322The optimal dose has not been established; regimens for sildenafil have varied from a single dose of 50 or 100 mg just before exposure for acute studies159,425 to 40 mg 3 times a day for 2 to 6 days at altitude,404,427 and for tadalafil 10 mg every 12 hours was effective.145,322 Most recently, and rather surprisingly, dexamethasone was also found effective in preventing HAPE in susceptible subjects. Maggiorini and co-workers322 gave 8 mg dexamethasone every 12 hours, starting 2 days before exposure, and found it as effective as tadalafil in reducing PAP and preventing HAPE. Dexamethasone has many actions in the lungs; which particular action(s) explains this observed effect is unknown.32 As these studies demonstrate, any agent that blocks hypoxic pulmonary hypertension will block onset of HAPE, reinforcing the concept of pulmonary hypertension as the sine qua non of high altitude pulmonary edema. Problems of Lifelong or Long-Term Residents of High Altitude Reentry Pulmonary Edema.  In some persons who have lived for years at high altitude, HAPE develops on reascent from a trip to low altitude.128 Clinicians have suggested that the incidence of HAPE on reascent of altitude residents may be higher than that during initial ascent by flatlanders,34,229 but data on true incidence are difficult to obtain. Children and adolescents are more susceptible than adults.128 Hultgren228 found HAPE prevalence in Peruvian natives of 6.4 per 100 exposures in the 1- to 20-year age-group, and 0.4 per 100 exposures in persons over 21 years.

Chronic Mountain Sickness.  In 1928 Carlos Monge359 described a syndrome in Andean high-altitude natives that was characterized by headaches, insomnia, lethargy, plethoric appearance, and polycythemia greater than expected for the altitude. Known variously as Monge’s disease, chronic mountain polycythemia, or chronic mountain sickness, the condition has now been recognized in all high-altitude areas of the world.279,358,402 Lowlanders who relocate to high altitude and native residents are susceptible. Chinese investigators reported that 13% of lowland Chinese males and 1.6% of females who had relocated to Tibet developed excessive polycythemia (hemoglobin level greater than 20 g/dL).588 The incidence in Leadville, Colorado, is also high in men over 40 years of age and distinctly low in women.278 The increased hematopoiesis is apparently related to greater hypoxic stress, which may be due to a number of causes, such as lung disease, sleep apnea syndromes, and idiopathic hypoventilation. A diagnosis of “pure” chronic mountain polycythemia excludes lung disease and is characterized by relative alveolar hypoventilation, excessive nocturnal hypoxemia, and respiratory insensitivity to hypoxia.292,358 Some studies suggest that even for the degree of hypoxemia, the red blood cell mass is excessive, implying excessive amounts or overactivity of erythropoietin.574 The new international guidelines propose a hemoglobin value greater than 21 g/dL for males and 19 g/dL for females as essential for the diagnosis, as well as residence above 2500 m (8202 feet) and absence of lung disease.292 The reader is referred to recent reviews for in-depth information.357,418,420,584 In addition, an international consensus group has recently published papers on the definition and scoring of chronic mountain sickness.291 Therapy of CMS is routinely successful. Descent to a lower altitude is the definitive treatment. The syndrome reappears after return to high altitude. Supplemental oxygen during sleep is valuable. Phlebotomy is a common practice and provides sub­ jective improvement, although without significant objective changes.574 The respiratory stimulants medroxyprogesterone acetate (20 to 60 mg/day)277 and acetazolamide (250 or 500 mg/ day)429 have also been shown to reduce hematocrit value by improving oxygenation. Acetazolamide (250 mg) increased nocturnal arterial O2 saturation by 5%, decreased mean nocturnal heart rate by 11%, the number of apnea/hypopnea episodes during sleep by 74%, and hematocrit by 7%.429 The response to acetazolamide emphasizes the contribution of hypoventilation and nocturnal desaturation to chronic mountain sickness. Another approach was based on the knowledge that ACE inhibitors blunt hypoxia-mediated erythropoietin release. Plata and associates406 showed that 5 mg/day of enalapril for 2 years reduced hemoglobin concentration, packed cell volume, proteinuria, and need for phlebotomy. Pulmonary hypertension and right heart failure may also occur in persons with CMS. Symptomatic High-Altitude Pulmonary Hypertension.  Children living at high altitude may be at risk for symptomatic highaltitude pulmonary hypertension (SHAPH).388 This problem has been identified in South America, North America, and Asia, with a predilection in populations not genetically adapted to altitude. Other names for this affliction previously have included “pediatric high-altitude heart disease” and “subacute infantile mountain sickness.” The underlying pathophysiology is pulmonary 25

CHAPTER 1  High-Altitude Medicine and Physiology

The phenomenon has been observed most often in Peru, where high-altitude residents can return from sea level to high altitude quite rapidly. Cases have also been reported throughout Colorado,482 but reports are conspicuously rare from Nepal and Tibet,581 perhaps because Himalayan highlanders are better adapted or because very rapid return back to high altitude has not been readily available,587 although that is changing. Wu581 reported a 37-year-old Tibetan man with chronic mountain sickness who developed reentry HAPE and suggested that similar cases may have been missed previously. Severinghaus490 has postulated that increased muscularization of pulmonary arterioles that develops with chronic high-altitude exposure generates an inordinately high PAP on reascent, causing the edema. Whether uneven pulmonary vasoconstriction is present has not been investigated. Changes in fluid balance with descent and reascent might also play a role.581

PART 1  MOUNTAIN MEDICINE

hypertension resulting in hypertrophy and dilation of the right ventricle with eventual right-sided congestive heart failure. Clinically these children have poor growth, fatigue, irritability, dyspnea, and cyanosis or pallor. On physical examination, as the illness advances, hepatomegaly and leg edema signal right-sided heart failure. Blood gases or pulse oximetry reveal exaggerated hypoxemia. Chest radiograph shows cardiomegaly and enlarged main pulmonary artery and sometimes infiltrates. Echocardiography usually confirms the diagnosis, although ECG and cardiac catheterization can also be useful. Right ventricular hypertrophy, right atrial dilation, and persistence of PFO and patent ductus arteriosus may also be noted. Definitive treatment is relocation to a lower altitude. Other but inferior therapies include supplemental oxygen, diuretics, and pulmonary vasodilators such as calcium channel blockers, PDE-5 inhibitors, and NO and prostaglandin inhibitors.292

CHILDREN AT HIGH ALTITUDE Children born at high altitude in North America appear to have a higher incidence of complications in the neonatal period than do their lower-altitude counterparts.386 In populations better adapted to high altitude over many generations, neonatal transition has not been as well scrutinized, but there does appear to be some morbidity.388,571 High-altitude residence does not clearly impact eventual stature, but growth and development are slowed. In the developing world, confounding factors such as nutrition and socioeconomic status make these issues difficult to assess. Children residing at high altitude are more likely to develop pulmonary edema on return to their homes from a low-altitude sojourn than are lowland children on induction to high altitude. Some of these children may have preexisting pulmonary hypertension of various etiologies.105 Lowland children traveling to high altitude are just as likely to suffer AMS as are adults.408 No data indicate that children are more susceptible to altitude illness, although diagnosis can be more difficult in preverbal children.591 Despite this somewhat reassuring fact, very conservative recommendations are made regarding taking children to high altitude; it should be made clear that these opinions are not based on science.40,407 Durmowicz and colleagues128 showed that children with respiratory infections were more susceptible to HAPE, as are children with Down syndrome, past repair of congenital shunts, following chemotherapy, and other problems. Children can be given acetazolamide or dexamethasone as necessary for AMS/HACE.129 The dosage of acetazolamide for prevention or treatment of AMS in children is 5 mg/kg/day in divided doses (see Table 1-7). See Pollard and associates408 for an excellent consensus document on children at altitude, and excellent recent reviews.129,388,591 Healthy newborn term infants born to lowland mothers should probably avoid sleeping altitudes greater than 2500 m (8202 feet) for the first 4 to 6 weeks of life because of concern regarding cardiopulmonary transition rather than for altitude illness.387 Infants with viral infections, neonatal intensive care unit stay, transient oxygen treatment, Down syndrome, or any pulmonary condition or cardiac defect should be carefully evaluated by a physician regarding altitude exposure. For all infants going to altitude, pulse oximetry monitoring should be considered. Parents need to be aware of potential problems at altitude, including symptoms of AMS unique to infants.387

Other Medical Concerns at High Altitude CARBON MONOXIDE Carbon monoxide poisoning is a danger at high altitude, where field shelters are designed to be small and windproof. Cooking inside closed tents and snow shelters during storms is a particular hazard.* The effects of carbon monoxide and high-altitude hypoxia are additive. A reduction in oxyhemoglobin caused by *References 146, 264, 290, 453, 535, 542.

26

carbon monoxide increases hypoxic stress, rendering a person at a “physiologically higher” altitude, which may precipitate AMS. Because of preexisting hypoxemia, smaller amounts of carboxyhemoglobin produce symptoms of carbon monoxide poisoning. These two problems may coexist. Immediate removal of the victim from the source of carbon monoxide and forced hyperventilation, preferably with supplemental oxygen, rapidly reverse carbon monoxide poisoning.

HIGH-ALTITUDE DETERIORATION The world’s highest human habitation is at approximately 5500 m (18,045 feet). Above this altitude, deterioration outstrips the ability to acclimatize.265 The deterioration is more rapid the higher one goes above the maximum point of acclimatization. Above 8000 m (26,247 feet), deterioration is so rapid that without supplemental oxygen, death can occur in a matter of days. Life-preserving tasks such as melting snow for water may become too difficult, and death may result from dehydration, starvation, hypothermia, and especially neurologic and psychiatric dysfunction.142 Loss of body weight due to anorexia and malabsorption is a prominent feature during expeditions to extreme high altitude. Pugh410 reported 14 to 20 kg (30.9 to 44 lb) body-weight losses in climbers on the 1953 British Mt Everest Expedition. Nearly 30 years later, with improvement in food and cooking techniques, climbers on the American Medical Research Expedition to Mt Everest still lost an average of 6 kg (13.2 lb).61 This was due in part to 49% decrease in fat absorption and 24% decrease in carbohydrate absorption. During OEII, in which the “climbers” were allowed to eat foods of their choosing ad libitum, they still suffered large weight losses: 8 kg (17.6 lb) overall, including 3 kg (6.6 lb) of fat and 5 kg (11 lb) of lean body weight (muscle).221,455 At 4300 m (14,108 feet), weight loss was attenuated by adjusting caloric intake to match caloric expenditure.75 In fact, recent work supports hypoxic exposure as a treatment for obesity.298,381,414,593 Thus, significant weight loss with prolonged exposure to high altitude may be overcome with adequate caloric intake, but decreased appetite is a problem.260,541 At very high altitudes, an increase in caloric intake may not be sufficient to completely counteract the severe anorexia and weight loss because other mechanisms may come into play. At extreme altitude, Ryn459 reported an incidence of acute organic brain syndrome in 35% of climbers going above 7,000 m (22,966 feet), in association with high-altitude deterioration. This syndrome, which features impaired judgment or even psychosis, could directly threaten survival.

HIGH-ALTITUDE SYNCOPE Syncope within the first 24 hours of arrival occurs occasionally at moderate altitude382,383 but is not observed in mountaineers at higher altitudes; it is a problem of acute induction to altitude.370 The mechanism is an unstable cardiovascular control system, and it is considered a form of neurohumoral (or neurocardiogenic) syncope.149 An unstable state of cerebral autoregulation may also play a role.595 These events appear to be random and seldom occur a second time. Preexisting cardiovascular disease is not a factor in most cases. Postprandial state and alcohol ingestion seem to be contributing factors. Altitude syncope has no direct relation to high-altitude illness.41

ALCOHOL AT HIGH ALTITUDE Two questions regarding alcohol are frequently asked: (1) does alcohol affect acclimatization, and (2) does altitude potentiate the effects of alcohol? Epidemiologic research indicated that 64% of tourists ingested alcohol during the first few days at 2800 m (9186 feet).214 The effect of alcohol on altitude tolerance and acclimatization might therefore be of considerable relevance. Roeggla and co-workers449 determined arterial blood gases 1 hour after ingestion of 50 g of alcohol (equivalent to 1 L of beer) at 171 m (561 feet) and again after 4 hours at 3000 m (9843 feet). A placebo-controlled, double-blinded paired design was used. For the 10 subjects, alcohol had no effect on ventilation at the low altitude, but at high altitude it depressed ventilation, as gauged

THROMBOSIS: COAGULATION AND PLATELET CHANGES Autopsy findings in deaths due to altitude illness of widespread thrombi in the brain and lungs, as well as the impression that thrombosis is greater at altitude,249 have led to many investigations of the clotting mechanism at high altitude. For a review, see Grover and Bärtsch.173 Although changes in platelets and coagulation have been observed in rabbits, mice, rats, calves, and humans on ascent to high altitude,207 these are generally in vitro and with very rapid ascent. In vivo studies using more realistic ascent profiles up to 4500 m (14,764 feet) in the mountains, and higher in chambers, have generally not found changes in coagulation and fibrinolysis,173 but this is still an area of active study.62,549 Although the increased incidence of thrombosis in soldiers and others at extreme altitude can be attributed to dehydration, polycythemia, and forced inactivity, there is some

evidence of enhanced fibrin formation with stay of a few weeks over 5000 m (16,404 feet).449 In addition, unexplained thrombosis is reported at moderate altitude of 4000 to 5000 m (13,123 to 16,404 feet)81,136 and at extreme altitude.8,267 As for thrombosis in HAPE, Singh and colleagues498 reported increased fibrinogen levels and prolonged clot lysis times during HAPE, attributed to a breakdown of fibrinolysis. These authors also reported thrombotic, occlusive hypertensive pulmonary vascular disease in soldiers who had recently arrived at extreme altitude.497 A series of experiments by Bärtsch and colleagues,27,173 however, carefully examined this issue in well subjects and in those with AMS and HAPE. They concluded that HAPE is not preceded by a prothrombotic state and that only in “advanced HAPE” is there fibrin generation, which abates rapidly with oxygen treatment. They considered the coagulation and platelet activation as an epiphenomenon rather than as an inciting pathophysiologic factor and likely due to inflammation from structural damage to the capillaries or the extreme hypoxemia. A difficult clinical question is whether ascent to altitude might result in thrombosis in persons with familial thrombophilia, such as factor V Leiden, a common anomaly, or protein C deficiency, antiphospholipid syndrome, or others. Such cases have been reported,8,38,58,255,267,379 although cause and effect cannot be established with certainty. In addition, persons with a past history of deep vein thrombosis or pulmonary embolism wonder if they are at increased risk at high altitude, as do women on hormonal contraceptives. Unfortunately, the literature does not provide guidance for these individuals. Some experts empirically recommend daily aspirin during altitude exposure for such patients, and this seems to be a safe suggestion. Others have raised the possibility that aspirin therapy might cause or exacerbate retinal hemorrhages at high altitude. Although no study has investigated this at altitude, research from patients with diabetic retinopathy has shown no danger of increased hemorrhages from aspirin.22 In addition, a retinal hemorrhage in a climber was treated with aspirin, and the hemorrhage resolved.284

PERIPHERAL EDEMA Edema of the face, hands, and ankles at high altitude is common, especially in females. Incidence of edema in at least one area of the body in trekkers at 4200 m (13,780 feet) was 18% overall, 28% in females, 14% in males, 7% in asymptomatic trekkers, and 27% in those with AMS.187 Although not a serious clinical problem, edema can be bothersome. The presence of peripheral edema demands examination for pulmonary and cerebral edema. In the absence of AMS, peripheral edema is effectively treated with a diuretic. Treatment of accompanying AMS by descent or medical therapy also results in diuresis and resolution of peripheral edema. The mechanism is presumably similar to fluid retention in AMS but may also be merely due to exercise.350

IMMUNOSUPPRESSION Mountaineers have observed that infections are common at high altitude, slow to resolve, and often resistant to antibiotics.376 On the American Medical Research Expedition to Mt Everest in 1981, serious skin and soft tissue infections developed. “Nearly every accidental wound, no matter how small, suppurated for a period of time and subsequently healed slowly.”465 A suppurative hand wound and septic olecranon bursitis did not respond to antibiotics but did respond to descent to 4300 m (14,108 feet) from the 5300 m (17,388 feet) base camp. Nine of 21 persons had significant infections not related to the respiratory tract. Most highaltitude expeditions report similar problems. Data from OEII indicated that healthy individuals are more susceptible to infections at high altitude because of impaired T lymphocyte function; this is consistent with previous Russian studies in humans and animals.345 In contrast, B cells and active immunity are not impaired. Therefore resistance to viruses may not be impaired, whereas susceptibility to bacterial infection is increased. The degree of immunosuppression is similar to that seen with trauma, burns, emotional depression, and space flight. The mechanism may be related, at least in part, to release of 27

CHAPTER 1  High-Altitude Medicine and Physiology

by decreased PaO2 (from 69 to 64 mm Hg) and increased PCO2 (from 32.5 to 34 mm Hg). Whether this degree of ventilatory depression would contribute to acute mountain sickness and whether repeated doses would have greater effect was not tested. Nonetheless, the authors argue that alcohol might impede ventilatory acclimatization and should be used with caution at high altitude. Conventional wisdom proffers an additive effect of altitude and alcohol on brain function. McFarland,341 who was concerned about the interaction in aviators, wrote, “…the alcohol in two or three cocktails would have the physiologic action of four or five drinks at altitudes of approximately 10,000 to 12,000 feet.” Also, “Airmen should be informed that the effects of alcohol are similar to those of oxygen want and that the combined effects on the brain and the CNS are significant at altitudes even as low as 8,000 to 10,000 feet.”341 His original observations were made on two subjects in the Andes in 1936. He found that blood alcohol levels rose more rapidly and reached higher values at altitude but noted no interactive effect of alcohol and altitudes of 3810 and 5335 m (12,500 and 17,503 feet).342 Most subsequent studies refuted the increased blood alcohol concentration data except at the highest altitudes, over 5450 m (17,881 feet). Higgins and associates, 209,210 in a series of chamber studies, found blood alcohol levels were similar at 392 and 3660 m (1286 and 12,008 feet), and they noted no synergistic effects of alcohol and altitude. Lategola and colleagues287 found that blood alcohol uptake curves were the same at sea level and 3660 m (12,008 feet), and that performance on math tests showed no interaction between alcohol and altitude. In another study of 25 men, performance scores were similar at sea level and at a simulated 3810 m (12,500 feet) altitude, with blood alcohol level of 88 mg%.93 Performance was not affected by hypoxia, only by alcohol, and older subjects were more affected. When more demanding tasks were tested, Collins92 found that a blood alcohol level of 91 mg% affected performance, as did an altitude of 3660 m (12,008 feet) during night sessions when the subjects were sleep deprived, but there was no significant altitude–alcohol interaction. In the one study in which Collins and co-workers94 were able to discern some altitude effect, there was a simple additive interaction of altitude (hypoxic gas breathing) and alcohol. He concluded that performance decrements due to alcohol may be increased by altitudes of 3660 m (12,000 feet) if subjects are negatively affected by that altitude without alcohol. All of these aviation-oriented studies used acute hypoxia equivalent to no more than 3500 m (11,483 feet). Perhaps the highest altitude (without supplemental oxygen) at which alcohol was studied was 4350 m (14,272 feet), on the summit of Mt Evans in Colorado. Freedman and associates148 found that alcohol affected auditory evoked potentials the same as in Denver; that is, no influence of altitude was detectable. In summary, the limited data on blood gases at altitude after alcohol ingestion support the popular notion that alcohol could slow ventilatory acclimatization and therefore might contribute to AMS. Considerable data at least up to 3660 m (12,000 feet), however, refute the belief that altitude potentiates the effect of alcohol. How altitude and alcohol might interact during various stages of acclimatization in individuals at higher altitudes is still unknown.

PART 1  MOUNTAIN MEDICINE

adrenocorticotropic hormone, cortisone, and β-endorphins, all of which modulate the immune response.135,354 Intense ultraviolet exposure has also been shown to impair immunity. Persons with serious infections at high altitude may need oxygen or descent for effective treatment. Impaired immunity because of altitude should be anticipated in situations where infection could be a complication, such as trauma, burns, and surgical and invasive procedures.

HIGH-ALTITUDE PHARYNGITIS, BRONCHITIS, AND COUGH Sore throat, chronic cough, and bronchitis are nearly universal in persons who spend more than 2 weeks at an extreme altitude (over 5500 m [18,045 feet]).84,300,333,370 All 21 members of the 1981 American Medical Research Expedition to Mt Everest suffered these problems.465 Only two of eight subjects in OEII (where the temperature was greater than 21° C [69.8° F] and relative humidity was greater than 80%) developed cough, and only above 6500 m (21,325 feet). Only four had sore throat. Acute hypoxia directly lowers the cough threshold, thus exacerbating high-altitude cough.334 Other factors are at play.332 In the field, these problems usually appear without fever or chills, myalgia, lymphadenop­ athy, exudate, or other signs of infection. The increase in ventilation, especially with exercise, forces obligate mouth breathing at altitude, bypassing the warming and moisturizing action of the nasal mucous membranes and sinuses. Movement of large volumes of dry, cold air across the pharyngeal mucosa can cause marked dehydration, irritation, and pain, similar to pharyngitis. Vasomotor rhinitis, quite common in cold temperatures, aggravates this condition by necessitating mouth breathing during sleep. For this reason, decongestant nasal spray is one of the most coveted items in an expedition medical kit. Other countermeasures include forced hydration, hard candies, lozenges, and steam inhalation. High-altitude bronchitis can be disabling because of severe coughing spasms. Cough fractures of one or more ribs are not rare.300 Purulent sputum is common. Response to antibiotics is poor; most victims resign themselves to taking medications such as codeine and do not expect a cure until descent. Bronchitis developed in 13 of 19 climbers above 4300 m (14,108 feet) on Aconcagua.415 Mean sputum production was 6 teaspoons per day. All reported that onset was after a period of excessive hyperventilation associated with strenuous activity. Although an infectious etiology is possible, experimental evidence suggests that respiratory heat loss results in purulent sputum and sufficient airway irritation to cause persistent cough.340 This is supported by the beneficial effect of steam inhalation and lack of response to antibiotics. Many climbers find that a thin balaclava, porous enough for breathing, traps some moisture and heat and effectively prevents or ameliorates the problem. Many climbers with high-altitude cough use inhaled fluticasone and salmeterol or similar inhaled agents and report success; studies of these medications are underway. Differential diagnosis of persistent cough in these conditions can be difficult.162

HIGH-ALTITUDE RETINOPATHY AND ULTRAVIOLET KERATITIS See Chapter 28.

Common Medical Conditions and High Altitude Persons with certain preexisting illnesses might risk adverse effects on ascent to high altitude, due either to exacerbation of illnesses or to illnesses that impact acclimatization and susceptibility to altitude illness. Certain populations also require special consideration, such as the very young, the pregnant and older adults. This section presents an overview of current knowledge regarding these issues. Despite the importance of the interaction of altitude and common medical conditions, research has so far been limited. See the original review by Hackett183 and updated recent reviews for more detailed discussions.315,349,448,585 28

BOX 1-5  Advisability of Exposure to High and Very

High Altitude for Common Conditions (Without Supplemental Oxygen)

Probably No Extra Risk • Young and old • Fit and unfit • Mild obesity • Diabetes • After coronary artery bypass grafting (without angina) • Mild chronic obstructive pulmonary disease (COPD) • Asthma • Low-risk pregnancy • Controlled hypertension • Controlled seizure disorder • Psychiatric disorders • Neoplastic diseases • Inflammatory conditions Caution • Infants <6 weeks old • Moderate COPD • Asymptomatic pulmonary hypertension • Compensated congestive heart failure (CHF) • Morbid obesity • Sleep apnea syndromes • Troublesome arrhythmias • Stable angina/coronary artery disease • High-risk pregnancy • Sickle cell trait • Cerebrovascular diseases • Space-occupying brain lesions • Any cause for restricted pulmonary circulation • Seizure disorder (not on medication) • Radial keratotomy • Recent myocardial infarction or stroke Contraindicated • Sickle cell anemia (with history of crises) • Severe COPD • Symptomatic pulmonary hypertension • Uncompensated CHF • Unstable coronary or cerebrovascular disease

Conditions that can be aggravated by high-altitude exposure are listed in Box 1-5.

RESPIRATORY DISEASES Chronic Lung Disease Although oxygen saturation remains above 90% in a normally acclimatizing, healthy, and awake person until over 3000 m (9843 feet) (see Figure 1-1), persons with hypoxemic lung disease reach this threshold at a lower altitude that depends on the baseline blood oxygen values. As a result, these persons might have altitude-related problems at lower altitudes than would healthy individuals. Improved airflow will result from decreased air density at high altitude, but hypoxemia, pulmonary hypertension, disordered control of ventilation, and sleep-disordered breathing could all become worse. Unfortunately, few data are available to guide the clinician advising such a person undertaking a trip to altitude.89,314,516 Most literature addresses prediction of blood gas values at 2500 m (8202 feet), the maximum allowable cabin altitude in commercial aircraft. Ascent to terrestrial high altitude, of course, involves much longer time periods and often at higher altitudes. Thus, the clinical usefulness of these studies is limited. Hypoxic gas breathing at sea level, as in the High Altitude Simulation Test, can predict oxygenation at high altitude, but this does

Cystic Fibrosis Children with cystic fibrosis have been reported to do poorly at high altitude,507 and hypoxic testing has also tried to predict the need for supplemental oxygen upon ascent in this condition.143,254,390,454 As with COPD, such tests are not particularly useful and tend to underestimate the oxygen requirements, because they are done only during rest and while awake. Supplemental oxygen should be available for these children, and oxygen saturation monitoring might be desirable in certain circumstances. The physician should be liberal with the use of antibiotics and adjunctive therapy for exacerbations at high altitude, given the likely danger of greater hypoxemia and greater difficulty treating

infections at high altitude. Cystic fibrosis encompasses a wide range of pulmonary impairment; one patient with mild disease was able to hike to 5600 m (18,373 feet).89 Asthma The available literature suggests that asthmatics, both residents and sojourners, do well at moderate altitude, primarily because of decreased allergens and pollution.88,89,224,560,585 Indeed, high altitude as a treatment for asthma has been popular in Europe for many decades. The effect is comparable with high doses of inhaled corticosteroids.89 However, because altitude exposure often includes exercise (and cold), asthmatics with exerciseinduced bronchospasm (EIB), rather than allergic asthma, might have problems at altitude. Matsuda and colleagues335 investigated the effect of altitude on 20 asthmatic children with EIB in a hypobaric chamber simulating 1500 m (4921 feet), with the temperature and humidity held constant. Except for the increased respiratory rate during exercise, as expected, all other physiologic variables were unchanged compared with those at sea level. The authors concluded that the modest altitude of 1500 m (4921 feet) does not exacerbate exercise-induced asthma. Berntsen and coworkers53 reported similar results at 2500 m (8202 feet). Durand and associates, 127 however, found that 50% of highly trained ski mountaineers in the Alps developed EIB during racing, and that only one-fourth had been previously diagnosed with EIB. Whether this occurs with such frequency in nonelite athletes at lesser exercise intensities requires investigation. Given the frequency of exercise dyspnea at high altitude, EIB should always be considered by the clinician. Golan and colleagues163 screened travelers and found 147 asthmatics who trekked to high altitude. Risk factors for an asthma attack at altitude were use of inhaled bronchodilators more than 3 times a week before travel and intensive physical exertion during the trek. A small but careful study was done with 11 asthmatics who were in stable condition with normal respiratory function at sea level. Cogo and colleagues87 tested both methacholine challenge and hyperosmolar aerosol at sea level and multiple altitudes up to 5050 m (16,568 feet). At no altitude was there an increase in bronchial responsiveness, and at the highest altitude, there was a decrease. They concluded that the positive aspects of high altitude prevailed over potential negative factors for asthmatics and attributed the benefit to the increase in circulating catecholamines found in their subjects. In the presence of bronchoconstriction at high altitude, however, hypoxemia is likely to be greater than at low altitude, and for this reason there could be an association between asthma and HAPE or AMS. Reassuringly, no such relationship has yet been reported.224,511 Mirrakhlmov353 investigated the effect of acetazolamide in 16 asthmatic patients taken to 3200 m (10,499 feet). Acetazolamide showed the same benefits as in nonasthmatics, with higher oxygen saturation and fewer AMS symptoms compared with the placebo control group. Seven of the eight asthmatics in the control group developed symptoms of AMS, a rather high incidence, but without a nonasthmatic control group for comparison, it is not known whether this incidence was abnormal. Persons with asthma ascending to high altitude should be advised to be at maximum function before ascent, to continue on their usual medications, including corticosteroids, and to have corticosteroids and bronchodilators with them in the event of an exacerbation.88 Because airway heat loss can be a trigger for bronchospasm, the use of an airway warming mask might be helpful but is unproved.456 In summary, the available data, although limited, suggest that high altitude does not exacerbate asthma, and it actually improves allergic asthma. Further work needs to determine if asthma might have any influence on susceptibility to AMS and HAPE; anecdotally, this does not seem to be the case. Although it seems likely that a severe asthma attack at high altitude would be more dangerous than at low altitude, no data are available to answer this question. Although caution and adequate preparation are necessary, asthma is not a contraindication to high-altitude travel. Pulmonary Vascular Disorders Because of the danger of HAPE, pulmonary hypertension (PHT) of any etiology is at least a relative contraindication to 29

CHAPTER 1  High-Altitude Medicine and Physiology

not always correlate with symptoms and is inconvenient.121 Sea level PO2 values of 68 and 72 mm Hg successfully classified more than 90% of the subjects with a PaO2 greater than 55 mm Hg at simulated altitudes of 1525 m (5003 feet) and 2440 m (8005 feet), respectively.165,166 Such predictions have been further refined with the addition of spirometry.120 A PaO2 of 55 mm Hg results in saturation of 90% at high altitude, where there is slight alkalosis. These data suggested that persons with PaO2 values lower than these at sea level might require supplemental oxygen at modest altitudes. The British Thoracic Society states that patients with resting SaO2 less than 92% at sea level should use supplemental oxygen during airplane flight, and presumably on ascent to altitude. However, in the only clinical studies to date, patients with moderate chronic obstructive pulmonary disease (COPD) did quite well at altitude.168,339 Graham and Houston168 found that eight subjects with COPD taken to 1920 m (6299 feet) had only minor symptoms on ascent, despite the fact that mean PaO2 declined from 66 mm Hg at sea level to 51 mm Hg while at rest and from 63 to 47 mm Hg with exercise. The patients did acclimatize with a drop in PCO2 and a corresponding increase in PaO2 over 4 days, the same response as seen in healthy persons. Matthys and associates339 studied 10 patients at simulated altitude of 2500 m (8202 feet). Mean PAP increased from 21 to 25 mm Hg, PaO2 decreased from 68 to 51 mm Hg at rest, and the only symptom was an increase in fatigue. The authors concluded that travel to this moderate altitude is safe for such patients. They speculated that these persons might have been partially acclimatized because of their hypoxic lung disease and were therefore less likely to develop AMS. Unfortunately, no further investigations with sicker patients or at higher altitudes have yet been reported. Persons with COPD who become hypoxic and uncomfortable at altitude should be treated with oxygen therapy. Oxygen should also be considered for those predicted to become severely hypoxemic.47 See Luks310 for a helpful discussion on determining need for oxygen in these patients. To adjust oxygen therapy at altitude for persons already on supplemental oxygen, FIO2 is increased by the ratio of higher to lower barometric pressure (see Table 1-3). Oxygen also improved hemodynamics (lowered blood pressure) and decreased pulsus paradoxus and pulse pressure in COPD patients at a simulated altitude of 2438 m (8000 feet).48 With the advent of simple and inexpensive pulse oximetry, patients can be counseled to monitor their oxygen saturation, determine the need for oxygen, and titrate their own oxygen use. All patients with lung disease contemplating a trip to high altitude should be aware of oxygen availability at their destination, as well as medical services. Nearly all resorts worldwide, for example, have oxygen concentrators or compressed gas cylinders that can be obtained for use in hotels or other accommodations. In North America, home oxygen companies honor prescriptions from physicians in any state, and oxygen is quite easily obtained. Interestingly, reports of persons with COPD developing altitude illness are absent from the literature. On the other hand, the issue has not been specifically addressed. Any degree of pulmonary hypertension might be expected to increase the likelihood of HAPE, and although this has been clearly demonstrated in other conditions (see High-Altitude Pulmonary Edema, earlier), it has not yet been reported with pulmonary hypertension associated with COPD. No research has yet addressed the use of medications such as acetazolamide or medroxyprogesterone in these patients to determine if respiratory stimulants might improve altitude tolerance.

PART 1  MOUNTAIN MEDICINE

high-altitude exposure. In addition, hypoxic pulmonary vasoconstriction will most likely exaggerate preexisting pulmonary hypertension, leading to greater symptoms.183,309 Many patients with pulmonary hypertension may not be diagnosed as such, and the clinician must have an awareness of conditions associated with PHT, including trisomy 21, congenital heart disease, unilateral absent pulmonary artery, granulomatous mediastinitis, and restrictive lung diseases, all of which have been associated with high-altitude pulmonary edema.185,312,431,539 Other conditions warranting caution include bronchopulmonary dysplasia, recurrent pulmonary emboli, mitral stenosis, kyphoscoliosis, and scleroderma with CREST syndrome. As Hultgren has observed, however, some patients with PHT are able to tolerate high altitude,231 and hypoxic gas breathing can be used to identify an individual’s response to hypoxia if clinically indicated.309 Persons with PHT who must travel to high altitude might benefit from calcium channel blockers, isoproterenol, and especially low-flow oxygen.309 A report by Naeije and associates378 highlighted the increased susceptibility to HAPE in those with pulmonary hypertension; a lowland woman with pulmonary hypertension secondary to fenfluramine developed two episodes of HAPE. The first episode was at 2300 m (7546 feet) and the second one at only 1850 m (6070 feet), with skiing up to 2350 m (7710 feet). Whether pulmonary hypertension is primary or secondary, patients should be made aware of the potential hazards of high altitude, including right heart failure and HAPE. Despite lack of firm data to guide clinicians, a reasonable approach is that persons with mean PAP greater than 35 mm Hg or systolic PAP greater than 50 mm Hg at baseline should probably avoid travel to altitudes greater than 2500 m (8202 feet). If such travel is undertaken, supplemental oxygen during the sojourn should be recommended. Patients with milder degrees of pulmonary hypertension may travel to altitudes less than 3000 m (9843 feet) but should consider prophylactic measures, including pulmonary vasodilators or supplemental oxygen.309

(p <0.01 between altitudes) with ratios of central to obstructive events of 0.1, 0.8, 1.0, 1.9, and 1.9 (p <0.01 between altitudes), respectively. Tracking performance during simulated driving was significantly impaired at 2590 m (8497 feet) compared with 490 m (1608 feet). Systolic blood pressure and cardiac arrhythmias were increased at altitude. In a report linking obesity–hypoventilation syndrome, OSA, and reduced peripheral chemosensitivity to hypoxia, Richalet and co-workers426 studied a 24-year-old man with Down syndrome who developed HAPE at 2000 m (6562 feet); he did not have pulmonary hypertension. These studies were all in patients without treatment and suggest that a trade-off of OSA for CSA is not a benefit in terms of oxygenation or adverse events, and that patients with OSA or CSA must be cautious when traveling to high altitude. In contrast, patients with sleep apnea treated at altitude with CPAP, oxygen, or acetazolamide (for central events) apparently do well. Patz and associates400 showed that CPAP pressure did not vary significantly in seven patients traveling between 3048 m (10,000 feet) and sea level. Average CPAP 95th percentile absolute pressure and mean CPAP absolute pressure were stable, using a ResMed Autoset autotitrating CPAP unit. Others have suggested that the hypobaria of high altitude can decrease the delivered pressure of CPAP machines that do not have pressurecompensating features, but such machines are no longer in use. For those not being treated with CPAP, but who exhibit hypoxemia during sleep at low altitude, the physician should provide supplemental nocturnal oxygen during an altitude sojourn. Because central apnea events are easily treated with acetazolamide, patients with sleep apnea going to altitude should be considered for acetazolamide therapy, regardless of CPAP use.1,161 See Table 1-8 for recommendations regarding sleep apnea and other ventilatory disorders.

Sleep Apnea, Sleep-Disordered Breathing Persons with snoring, sleep apnea syndrome, and sleep-disordered breathing who become mildly hypoxemic at sea level may become severely hypoxemic at high altitude. This could contribute to high-altitude illness and aggravate attendant problems such as polycythemia, pulmonary hypertension, systemic hypertension, cardiac arrhythmia, or insomnia. On the other hand, changes in ventilatory control and breathing secondary to altitude hypoxia might conceivably improve certain apnea syndromes. In general, the limited research available has shown that obstructive sleep apnea (OSA) tends to improve at altitude, but that central sleep apnea (CSA) can either develop or become worse. Burgess and colleagues68 demonstrated a decrease in obstructive events but a “conversion” to severe central events in five men with moderate OSA studied without CPAP. The obstructive respiratory disturbance index fell from 25.5/hr at 60 m (197 feet) to 0.5/hr at 2750 m (9022 feet), while the central respiratory disturbance index rose from 0.4/hr at 60 m (197 feet) to 78.8/hr at 2750 m (9022 feet). Mean sleep SaO2 fell from 94% at 60 m (197 feet) to 85% at 2750 m (9022 feet) simulated altitude.68 They attributed the decrease in OSA to increased upper airway tone and increased respiratory rate, and the increased CSA to hypocapnia during non-REM sleep. Similarly, a small study in Colorado showed that the apnea–hypopnea index decreased in patients with OSA not on CPAP living at high altitude when they went to lower altitudes, due primarily to a decrease in central events, while OSA events persisted.399 These observations were confirmed in a detailed study of 34 patients with OSA with median apnea–hypopnea index of 47.5 events per hour, residing above 600 m (1969 feet). They did the following: patients spent 1 day in Zurich (490 m [1608 feet]) and 4 days in the Swiss Alps at 1860 m (6102 feet) and 2590 m (8497 feet) (2 days each), during which their CPAP was discontinued.389 Daily evaluations included polysomnography, symptom questionnaires, physical examination, and driving simulator tests. Median oxygen saturations at 490 m (1608 feet) and in the first and second nights at 1860 and 2590 m (6102 and 8497 feet), respectively, were 94%, 90%, 90%, 86% and 87% (p <0.01 between altitudes). Corresponding median apnea–hypopnea index values were 47.5, 85.1, 74.6, 90.0, and 90.9 events per hour

Hypertension In healthy persons rapidly ascending to high altitude, the change in blood pressure, if any, is variable, depending on magnitude of hypoxic stress, cold, diet, exercise, and genetic factors. Most studies report a slight increase in blood pressure, associated with increased catecholamine activity and increased sympathetic activity.416 One well-controlled study showed an increase in blood pressure at 3500 m (11,483 feet) from a mean of 105/66 mm Hg at sea level to 119/77 mm Hg at 3 days, 111/75 mm Hg at 3 weeks, and back to 102/65 mm Hg on return to sea level.331 Pugh411 reported transient increases in blood pressure in athletes at the Olympics in Mexico City. Certain individuals, however, appear to have a pathologic response on induction to high altitude. For example, arterial hypertension develops in 10% of lowland Chinese who move to Tibet.494 The authors consider this a form of altitude maladaptation and treat the condition by returning the affected individuals to low altitude. After a period of at least 2 months, however, downregulation of adrenergic receptors results in attenuation of the initial blood pressure response. This mechanism is thought to be the reason that longterm residents of high altitude have lower blood pressure than do their sea level counterparts.230,445 Apparently for the same reason, chronic altitude exposure has also been shown to inhibit progression of hypertension.352 As for the effect of short-term altitude exposure on preexisting hypertension, studies have generated mixed results. In general, the response in hypertensives is similar to those without hypertension (i.e., a small increase in blood pressure, with an exaggerated response in some individuals). The greater the hypoxic stress (the higher the altitude), the greater the change in blood pressures. Altitudes less than 3000 m (9843 feet) seem to result in little if any change.439 Palatini and colleagues397 studied 12 normotensives and 12 untreated mild hypertensives with 24-hour ambulatory blood pressure monitoring at sea level, after 12 hours at 1210 m (3970 feet), and after 1.5 to 3 hours at 3000 m (9843 feet). The authors concluded that the increase of blood pressure in both normotensives and hypertensives was not important at 1200 m (3970 feet) but could become so at 3000 m (9843 feet). However, individual variability was great; the maximum change

30

CARDIOVASCULAR CONDITIONS

for Ventilatory Disorders

Obesity Hypoventilation • Counsel against high-altitude travel. • If high-altitude travel cannot be avoided, administer supplemental oxygen for daytime and nighttime use. • Counsel patients about the risks for and symptoms of AMS, and achieve prophylaxis with acetazolamide 125 mg or 250 mg bid. • In patients with preexisting CPAP prescription, travel to altitude with CPAP unit. Obstructive and Central Sleep Apnea • Travel to altitude with CPAP machine. • Consider acetazolamide 125-250 mg bid, or single dose at bedtime. • Continue preexisting nocturnal oxygen therapy; if so, acetazolamide not indicated. • Evaluate patients with daytime hypoxemia for PHT and, if present, achieve prophylaxis with nifedipine SR 30 mg bid. • Optimize heart-failure regimen for patients with central sleep apnea due to cardiomyopathy. Prior Carotid Artery Surgery • Avoid high-altitude travel in patients with preceding bilateral carotid body resection. • If travel cannot be avoided, administer supplemental oxygen. • Assess hypoxic ventilatory response in patients with prior history of carotid endarterectomy, and administer supplemental oxygen if response is suppressed. Neuromuscular Disorders • Screen for sleep-disordered breathing and, if present, treat with bilevel positive airway pressure at altitude. • Screen for baseline hypoventilation and, if present, travel to high altitude with bilevel positive airway pressure. • Administer nocturnal supplemental oxygen in patients with history of nocturnal desaturation. • Screen kyphoscoliosis patients for pulmonary hypertension and, if present, administer supplemental oxygen and prophylax with nifedipine SR 30 mg bid. • Counsel patients with bilateral diaphragmatic paralysis against high-altitude travel. If travel cannot be avoided, administer bilevel positive airway pressure. Modified from Luks AM, Swenson ER: Travel to high altitude with pre-existing lung disease, Eur Respir J 29:770, 2007. AMS, Acute mountain sickness; CPAP, continuous positive airway pressure, PHT, pulmonary hypertension.

was 17.4 mm Hg for systolic and 16.3 mm Hg for diastolic blood pressures. Two other studies were able to demonstrate a slightly greater blood pressure response in hypertensives compared with normotensives on ascent to 2572 m (8438 feet) and 3460 m (11,352 feet).113,471 Again, these authors also noted important individual variation, with some subjects increasing their systolic blood pressure by as much as 25 mm Hg at rest and 40 mm Hg during exercise, compared with sea level measurements. The important question of whether the blood pressure would continue to increase over the first 2 weeks at high altitude, as it does in normotensives, has not yet been addressed. At a more modest altitude, Halhuber and co-workers198 claimed a significant reduction in the blood pressure of 593 persons with hypertension after 14 days at 1700 to 2000 m (5577 to 6562 feet) in the Alps. A similar study of hypertensives at higher altitude will hopefully be accomplished. Patients receiving antihypertensive treatment should continue their medications while at high altitude. Because some persons may unpredictably become markedly hypertensive acutely,231 blood pressure monitoring should be considered, especially in those with labile hypertension or those who become symptomatic at altitude. Hypertension in short-term high-altitude sojourners for the most part should be considered transient and should not be treated, because it rarely reaches dangerously high levels and will resolve on descent. Given the large number of

hypertensive patients visiting ski resorts and trekking at high altitude, however, the occasional person with an exaggerated response will require treatment.231 Because the mechanism appears to be increased α-adrenergic activity, an α-blocker might be the best choice of therapy for these individuals. A preliminary report also suggested that nifedipine might be useful and superior to atenolol.114 The best medication, dosage, and duration still need to be determined. There is no evidence to date to suggest that hypertensive patients are more likely to develop high-altitude illnesses. Although requiring some caution, hypertension does not seem to be a contraindication to high-altitude exposure. Arteriosclerotic Heart Disease Lifelong residence at high altitude appears to offer some protection from coronary artery disease (CAD) and the attendant acute coronary artery events,351 perhaps in part because of increased myocardial vascularity. Other factors that might explain this finding, such as genetics, fitness, and diet have not been adequately evaluated. The effect of acute, transient exposure to high altitude on the healthy heart also appears to be benign. Various avenues of research have indicated that the healthy heart tolerates even extreme hypoxia quite well, all the way to the summit of Mt Everest (PaO2 less than 30 mm Hg). Numerous ECGs, echocardiograms, heart catheterizations, and exercise tests have failed to demonstrate any evidence of cardiac ischemia or cardiac dysfunction in healthy persons at high altitudes. This could partly be due to the marked reduction in maximal exercise with increasing altitude, which reduces maximal heart rate and myocardial oxygen demand, and also due to increased coronary blood flow. A person with CAD, however, may not have the same adaptive capacities. For example, diseased coronary arteries might have limited ability to vasodilate and might actually constrict, because of unopposed sympathetic activation.297 What then are the risks, and what should be the advice for persons with CAD considering a visit to high altitude? Surprisingly little literature is available to help the physician advise such persons. Does high altitude provoke acute coronary events or sudden death? In the United States., no evidence from state or county mortality statistics suggests an increased prevalence of acute coronary events in visitors to high-altitude locations. In Europe, Halhuber and associates198 reported an incidence of only 0.2% for myocardial infarction in 434 patients with CAD taken to altitudes between 1700 and 3200 m (5577 and 10,499 feet) for 4 weeks in the Alps. They also reported a very low incidence of sudden death in 151,000 vacationers in the Alps, 69,000 of whom were over age 40 years. In contrast are data from Austria claiming a higher rate of sudden cardiac death in the mountains, compared with the overall risk for sudden cardiac death.71 However, the altitudes were rather low (1000 to 2100 m [3281 to 6890 feet]), and no increased risk was evident in men who participated regularly in sports. The authors suggested that abrupt onset of exercise in sedentary men combined with altitude stress might induce cardiac sudden death, but whether altitude contributed at all is unclear. In summary, limited data suggest no increased risk for sudden cardiac death or myocardial infarction at altitudes up to 2500 m (8202 feet). Another important question is whether altitude will exacerbate stable ischemia. The slight increase in heart rate and blood pressure on initial ascent to altitude might exacerbate angina in persons with CAD, as described by Hultgren.231 One study evaluated nine men with stable exercise-induced angina by exercise treadmill test at 1600 m (5249 feet) (Denver) and within the first hour of arrival at 3100 m (10,171 feet).371 Cardiac work was slightly higher for a given workload at high altitude compared with low altitude, and as a result, the onset of angina was at a slightly lower workload. They found that a heart rate of 70% to 85% of the rate that produced ischemia at low altitude was associated with angina-free exercise at 3100 m (10,171 feet), and they suggested that angina patients at altitude adjust their activity level based on heart rate, at least on the day of arrival.371 Brammel and colleagues64 reported similar results and also suggested that those with angina need to reduce their activity at high altitude to avoid angina episodes. In a more recent study, Levine and co-workers297 investigated 20 men who were much older than those in the previous investigations (mean age 68 ± 3 years) and 31

CHAPTER 1  High-Altitude Medicine and Physiology

TABLE 1-8  Summary of Recommendations

PART 1  MOUNTAIN MEDICINE

performed symptom-limited exercise tests. With acute exposure to 2500 m (8202 feet), the double product (heart rate times systolic blood pressure) required to induce 1 mm ST depression was decreased about 5%, but after 5 days of acclimatization at 2500 m (8202 feet), this value was unchanged from sea-level. The degree of ischemia (maximal ST segment depression) was the same at sea level, with acute altitude exposure, and after 5 days at 2500 m (8202 feet). Also, no new wall motion abnormalities on echocardiography were seen at high altitude. Only one subject exhibited increased angina at altitude, and one person with severe coronary artery disease developed a myocardial infarction after maximal exercise at 2500 m (8202 feet). The authors concluded that coronary artery disease patients who are well compensated at sea level do well at a moderate altitude after a few days of acclimatization, but that acutely angina threshold may be lower and activity should be reduced.297 Finally, a study of 97 older adults visiting 2500 m (8202 feet), many with CAD and abnormal ECGs, found no new ECG changes and no events suggestive of ischemia. In contrast with the Levine study, these subjects did not do exhaustive exercise tests, but merely their usual activities, which included walking in the mountains.439 Taken altogether, these various investigations indicate that persons with CAD, including older adults, generally do well at the modest altitude of 2500 m (8202 feet), but that reducing their activities the first few days at altitude is wise. To address the question of whether altitude might provoke cardiac arrhythmia, Levine associates,297 in their study mentioned above, found that premature ventricular contractions (PVCs) increased 63% on acute ascent but returned to baseline after 5 days of acclimatization. A simultaneous rise in urine norepinephrine in these subjects indicated that sympathetic activation was the cause of the increased ectopy. They observed no increase in higher-grade ectopy, however, and no changes in signal-averaged ECG suggestive of a change in fibrillation threshold; in other words, the PVCs appeared benign. Halhuber and colleagues198 also found increased ectopy in their subjects and also no serious adverse events. In addition, Alexander5 described asymptomatic PVCs and ventricular bigeminy in himself while trekking to 5900 m (19,357 feet). Subsequent evaluation found no evidence of heart disease, and the event prompted him to thoroughly review the subjects of altitude, age, and arrhythmia. Although no dangerous arrhythmias have ever been reported in high-altitude studies, persons with troublesome or high-grade arrhythmias have not been evaluated upon ascent to high altitude. The available evidence would suggest that patients whose arrhythmias are well controlled on medication should continue the medication at altitude, whereas those with poorly controlled arrhythmias might do better to avoid visiting high altitude. In terms of advising persons with CAD or high likelihood of CAD about altitude exposure, the stress of high altitude on the coronary circulation appears to be minimal at rest but significant in conjunction with exercise. Ideally no one with known CAD or even risk factors for CAD should undertake unaccustomed exercise at any altitude, and especially at high altitude. Therefore advising an exercise program at sea level before exercising at altitude is prudent. The same technique of risk stratification that is commonly used at sea level can be applied for providing advice for high altitude.225 Using the standard recommendations, asymptomatic males over age 50 with no risk factors require no testing. For asymptomatic males over age 50 with risk factors, an exercise test is recommended to determine risk status before exercising at high altitude, and then further evaluation as indicated. Patients with previous myocardial infarction, bypass surgery, or angioplasty are considered high risk only if they have a strongly positive exercise treadmill test. Patients with multiplevessel bypass grafts who were asymptomatic and with normal exercise tests at sea level have successfully visited altitudes over 5000 m (16,404 feet). High-risk patients may require coronary angiography to establish appropriate management. Alexander4 has proposed different criteria for those with CAD at high risk at altitude: an ejection fraction of less than 35% at rest, a fall in exercise systolic blood pressure, ST-segment depression greater than 2 mm at peak heart rate, and high-grade ventricular ectopy. For these persons, he recommends ascent to no more than 2500 m (8202 feet) and proximity to medical care. Both sets of 32

recommendations, while reasonable, need to be validated with outcome studies. Heart Failure Although information on the effect of high altitude on heart failure is scant, physicians in resort areas have noted a tendency toward acute decompensation in those with a history of heart failure within 24 hours of arrival. Those with CAD and low ejection fractions (less than 45%), but without active heart failure, actually did quite well, as gauged by exercise tests during acute exposure to 2500 m (8202 feet).134 Compared with 23 control subjects, the decrement in exercise performance was similar, and no complications or signs of ischemia developed. Although these results are encouraging for such patients, they made no observations past the first few hours at altitude. One concern is that persons with heart failure might be more likely to retain fluid at altitude, especially if AMS were to develop, and that this could aggravate heart failure. Supporting this notion, Alexander4 found that ejection fraction declined at altitude during an exercise study in patients with angina, with an increase in end-diastolic and systolic volume as measured by two-dimensional echocardiography. Ventricular contractility was not depressed, however, and these changes were attributed to fluid overload. Patients with heart failure need to be informed about possible consequences of high-altitude exposure. In particular, they need to avoid acute mountain sickness, which is associated with fluid retention, continue their regular medications, and be prepared to increase their diuretic should symptoms of failure exacerbate. Acetazolamide prophylaxis may be useful to consider in terms of speeding acclimatization, inducing diuresis, and preventing AMS, but its efficacy in these patients remains untested.

OBESITY The interaction of obesity and altitude has recently received much attention. A small study suggested increased susceptibility to AMS in mildly obese men,154 possibly because of lower nocturnal oxygen saturation that was present despite greater than normal hypoxic and hypercapnic chemosensitivity.155 Another larger study examined men with metabolic syndrome (obesity, hypertension, diabetes, and hyperlipidemia) with a 3-week stay at 1700 m (5577 feet) and found normal altitude responses and a loss of body fat.176 In fact, recent work supports hypoxic exposure as a treatment for obesity.298,381,414,493 However, obese men and women (mean body mass index 47.1 kg/m2) who were permanent residents at a mean altitude of 2448 m (8031 feet) had a 96% incidence of systolic pulmonary artery hypertension (>30 mm Hg), which was related to alveolar hypoventilation.545 These residents with obesity–hypoventilation syndrome are at increased risk for developing right heart failure. Tourists with obesity–hypoventilation are at risk for AMS and HAPE.314,426 Because of the high risk for altitude illness or aggravation of pulmonary hypertension and decompensation of the right ventricle, these patients should probably avoid high-altitude travel. See recommendations in Table 1-8.

SICKLE CELL DISEASE Sickle cell crisis is a well-recognized complication of high-altitude exposure.147 Even the modest altitude of a pressurized aircraft (1500 to 2000 m [4921 to 6562 feet]) causes 20% of persons with hemoglobin SC and sickle-thalassemia genetic configuration to have a vasoocclusive crisis.327 High-altitude exposure may precipitate the first vasoocclusive crisis in persons previously unaware of their condition. Persons with sickle cell anemia and a history of vasoocclusive crises are advised to avoid altitudes over 1800 m (5906 feet) unless they are taking supplemental oxygen. Persons with sickle cell disease who live at high altitude in Saudi Arabia have twice the incidence of crises, hospitalizations, and complications as do Saudis at low altitude. Splenic infarction syndrome has been reported more commonly in persons with sickle cell trait than in those with sickle cell anemia, probably because sickle cell disease produces autosplenectomy early in life. Frequent reports in the literature emphasize the need to consider splenic syndrome caused by sickle cell trait in any

person with left upper quadrant pain, even at an altitude of only 1500 m (4921 feet).283,327 A number of authors have suggested that nonblack persons with the trait may be at greater risk for splenic syndrome at high altitude than are black persons.283 Treatment of splenic syndrome consists of intravenous hydration, oxygen, and travel to a lower altitude.537 The overall incidence of problems in persons with the trait is low, however, and no special precaution other than recognition of the splenic syndrome is recommended. The U.S. Army, for example, does not consider soldiers with the trait unfit for duty at high altitude.119

PREGNANCY In high-altitude natives, pregnancy-associated hypertension is four times more common than in low-altitude pregnancies, preeclampsia is more common, and full-term infants are small for gestational age.364,367 These problems raise the issue of whether short-term altitude exposure may also pose a risk. So far, there is no evidence that these problems or others, such as spontaneous abortion, abruptio placentae, or placenta previa, can result from a sojourn to high altitude.385 Unfortunately, however, few data exist on the influence of a high-altitude visit during pregnancy on the mother and the fetus. For moderate altitude, the research to date has been reassuring.222,223 Artal and associates13 studied seven sedentary women at 34 weeks’ gestation. Maximal and submaximal exercise tests were completed at sea level and 1829 m (6000 feet) after 2 to 4 days of acclimatization. They reported the expected decrease in maximal aerobic work but found no difference from sea level in fetal heart rate responses or in maternal lactate, epinephrine, and norepinephrine levels. Although this study was in a small number of subjects, the authors concluded that it is safe for third-trimester women to engage in brief bouts of exercise at moderate altitude. A similar conclusion was reached in a study of 12 pregnant subjects who exercised after ascent to 2225 m (7300 feet). The authors did not discover any abnormal fetal heart rate responses and considered exercise at altitude benign for both mother and fetus.43 Huch222 also concluded that short-term exposure to altitude with exercise was safe during pregnancy. In summary, available data, though limited, indicate that short-term exposure to altitudes up to

2500 m (8202 feet) with exercise is safe for a lowland woman with a normal pregnancy. Another avenue of research has been alteration of blood gases during pregnancy. Human and animal studies with acute hypoxic challenge, as well as oxygen-breathing studies, have drawn two conclusions: (1) that a compromised placental–fetal circulation could be unmasked at high altitude, and (2) that a fetus with a normal placental–fetal circulation seems to tolerate a level of acute hypoxia far exceeding that incurred by moderate altitude exposure.23,97,432 Based on available research, it seems prudent to recommend that only women with normal, low-risk pregnancies undertake sojourns to altitude. For these women, exposure to an altitude at which SaO2 will remain above 85% most of the time (up to 3000 m altitude) appears to pose no risk for harm. However, further study is needed to place these recommendations on a more solid scientific footing. Ultrasound or other assessment may be useful to rule out the more common complications before travel. It is not the altitude per se that determines whether the fetus becomes stressed, but rather it is maternal (and fetal) arterial oxygen transport. A woman with high-altitude pulmonary edema at 2500 m (8202 feet), for example, is much more hypoxemic than is a healthy woman at 5,000 m (16,404 feet). Therefore a strategy for preventing altitude illness, especially pulmonary edema, must be explained and implemented. Similarly, elevated carboxyhemoglobin from smoking, lung disease, and other problems of oxygen transport will render the pregnant patient at altitude more hypoxemic and physiologically at a higher altitude. Consideration of a high-altitude sojourn in the developing world or in a wilderness setting raises other issues that may be more important than the modest hypoxia. These include remoteness from medical care should a problem arise, quality of available medical care, use of medications for such important risks as malaria and traveler’s diarrhea (many of which are contraindicated in pregnancy), and the risks for trauma.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 2 



AVALANCHES COLIN K. GRISSOM, MARTIN I. RADWIN, DALE ATKINS, AND SCOTT E. MCINTOSH

An avalanche is a mass of snow that slides down a mountainside. In the United States, approximately 100,000 avalanches occur annually, of which about 100 cause injuries, death, or the destruction of property. According to a database of reported incidents from 1999-2000 to 2008-2009, about 350 people per year are caught or otherwise involved in avalanches.3 Of these, approximately 90 individuals are partly or wholly buried, 40 sustain injury, and 28 are killed. Average annual property damage varies tremendously, depending on the severity of the winter. From 1999 to 2009, damages as a result of avalanches ranged from a low of $30,000 to a high of $16.5 million (median = $265,000).4 This chapter describes the properties of the mountain snowpack that contribute to avalanche formation; avalanche safety techniques; rescue; and victim physiology and treatment.

Properties of Snow SNOW CLIMATES Snow cover is variable on both the broad geographic scale (i.e., Antarctic snow is quite different from snow found in the Cascade

Mountains of North America, which is quite different from the snow in the Southern Rocky Mountains of the United States) and the microscale (i.e., snow conditions may vary greatly from one side of a rock or tree to the other). All snow crystals are made of the same substance (i.e., water molecules), but local and regional environmental conditions control the type and character of the snow that is found at a given location. To better understand the geographic differences that affect avalanche initiation, it is helpful to consider some basic climate conditions. The character of the snow and the avalanche propensity in different mountain ranges around the world can be described as one of three types—maritime, continental, or transitional—on the basis of the average snow conditions of that particular region. Heavy snowfall and relatively mild temperatures characterize the maritime snow climate. The snow cover is deep and the new snow is dense as a result of moist ocean storms coming ashore at lower altitudes. Rain is common, and it is a significant cause of avalanches when it falls on deep fresh snow. Arctic air intrusions are uncommon but can occur each winter. In general, the

For online-only figures, please go to www.expertconsult.com

33

PART 1  MOUNTAIN MEDICINE

TABLE 2-1  Characteristics of Maritime, Transitional

(Intermountain), and Continental Snow Climates on the Basis of 15-Year Means

Type Maritime Transitional Continental

Total Precipitation (mm)

Air Temperature in ° C (° F)

Snow Depth (cm)

New Snow Density (kg/m3)

1286 854 550

−1.3° (29.7°) −4.7° (23.5°) −7.3° (18.9°)

186 170 113

120 (12%) 90 (9%) 70 (7%)

Data from Armstrong R, Armstrong B: Snow and avalanche climates of the Western United States: A comparison of maritime, intermountain and continental conditions. In Proceedings of the Davos Symposium. Davos, Switzerland, 1986, Swiss Avalanche Institute.

snowpack gains strength quickly with time in this snow climate. In North America, examples of maritime ranges include the Sierras, Cascade Mountains, and Coast Range of British Columbia. Far removed from coastal areas, the continental snow climate is characterized by low snowfall, cold temperatures, and higher altitudes. Snowfall is light and of low density, and wind is a key instigator of avalanches. Avalanche cycles are often the result of buried structural weaknesses that occur in shallow snowpacks and that may cause avalanche danger to persist for days, weeks, or even months. Avalanches that are released from these old, persistent, weak layers are a distinguishing trait of a continental climate. In this climate, especially during the early months of the winter, the shallow snow cover loses strength with time. Continental ranges include the Canadian Rocky Mountains, Southern Rocky Mountains, and Brooks Range. In between the maritime and continental regions is a transitional snow climate that, in North America, is often referred to as the “intermountain” snow climate. Many mountain regions in this class tend to exhibit intermediate features that reflect both of the other types of climates (Table 2-1). Examples of these mountain ranges include the Wasatch Range in Utah, Teton Range in Wyoming, and Columbia Mountains of British Columbia.

PHYSICAL PROPERTIES Although snow cover appears to be nothing more than a thick homogeneous blanket that covers the ground, it is in fact one of the most complex materials found in nature. It often exists concurrently in solid, liquid, and gaseous phases. Snow is highly variable; it may go through significant changes during relatively short periods as a result of environmental factors. At any single site, the seasonal snow cover varies from top to bottom and results in a complex layered structure, the study of which is referred to as stratigraphy. Individual layers may be quite thick or very thin, and they may vary greatly in strength and in their ability to adhere to one another. In general, thicker layers represent consistent conditions during one storm, when new snow crystals that fall are of the same type, when wind speed and direction vary little, and when temperature and precipitation are fairly constant. Thinner layers that are perhaps only millimeters in thickness often reflect conditions between storms. Examples include a melt-freeze crust or sun crust that is formed during fair weather or a hard wind crust that is formed during a period of strong winds. A brittle buried surface hoar layer represents what were once delicate feather-shaped crystals of surface hoar on the surface of the snow that were deposited from the moist atmosphere onto the cold snow surface during a clear night. These crystals are very fragile and weak; after they are buried by subsequent snowfalls, they may be a persistent and major contributor to avalanche formation. One property of snow is strength or hardness, which is of great importance in terms of avalanche formation. Snow can vary from light and fluffy, easy to shovel, and especially delightful to ski through to heavy and dense, impossible to penetrate with a shovel, and firm enough to make it very difficult for a skier to carve a turn. The arrangement of the ice skeleton (i.e., the lattice 34

of ice crystals within the snowpack) and the changing density (i.e., the mass per unit volume, which is typically represented as kg/m3) produce this wide range of conditions. In the case of snow, density is determined by the volume mixture of ice crystals and air. In general, the denser the snow layer, the harder and stronger it becomes, as long as it is not melting. The density of new snow can have a wide range of values. This depends on how closely the new snow crystals pack together, which is controlled by the shapes of the crystals. The initial crystals that fall from the atmosphere have a variety of shapes, and some pack more closely together than do others (Figure 2-1). For example, needles pack more closely than stellars; thus the density of snow made of compressed needles may be three to four times greater than that of snow composed of stellars. Wind can alter the shapes of new snow crystals and break them into much smaller pieces that pack very closely together to form wind slabs. Such slabs may possess a density that is five to ten times that of new stellars falling in the absence of wind. Because these processes occur at different times and locations at the surface of the snow cover and are buried by subsequent snowfalls, a varied heterogeneous layered structure results. Thus minor variations in atmospheric conditions can have an important influence on the properties of snow on the ground. After snow has been deposited on the surface, snow density increases as the snow layer compacts vertically as a result of the effects of gravity, weather, and crystal metamorphosis (i.e., settlement). Because an increase in density often equals an increase in strength, the rate at which this change occurs is important with respect to avalanche potential. Snow is composed predominantly of air pockets within an ice skeleton of crystals, and it is therefore highly compressible. In a typical layer of new snow, 85% to 95% of the volume is comprised of air pockets, and it can settle under its own weight. Individual ice crystals can move and slide past each other, and, because the force of gravity causes them to move slowly downward, the layer shrinks. A heavier snow layer or a warmer temperature speeds settlement. At the same time, the complex and intricate shapes that characterize the new snow crystals begin to change. They become more rounded and suitable for closer packing. Intricate crystals (e.g., stellars) possess a shape that is naturally unstable and that changes quickly. New snow crystals have a large surface area– to–volume ratio and are composed of a crystalline solid that is close to its melting point. In this regard, snow crystals are unique among the materials that are found in nature. Surface energy physics dictate that this unstable condition will lead to a change in the crystalline shape toward an energy equilibrium; in other words, the warmer the temperature, the faster the change. Under very cold conditions, the original shapes of the snow crystals are sometimes still recognizable after they have been in the snow cover for several days or even after a week or two. However, as temperatures warm and approach the melting point, such shapes disappear within a few hours to a day. Changes in the shape or texture of snow crystals are examples of metamorphism, which in geologic terms defines changes that result from the effects of temperature and pressure. As the crystal shapes simplify, they

F1

Plate

F6

Capped column

F2

Stellar crystal

F7

Irregular crystal

F3

Column

F8

Graupel

F4

Needle

F9

Ice pellet

F5

Spacial dentrite

F0

Hail

FIGURE 2-1  International classification of solid precipitation. (From the International Association of Scientific Hydrology, with permission.)

KINETIC METAMORPHISM

Ice grain

Water vapor Ice grain

Low temperature

Heat flow High temperature

FIGURE 2-4  In the temperature-gradient process, ice sublimates from the top of one grain, moves upward as water vapor, and then is deposited on the bottom surface of the grain above. If conditions allow this process to continue long enough, all of the original grains are lost as the recrystallization produces a layer of new crystals.

CHAPTER 2  AVALANCHES

can pack more closely together, thereby enhancing further settlement and strength (Figure 2-2, online). New snow metamorphic changes generally occur within hours to a few days. However, the structure of a seasonal snow cover changes over a period of weeks to months via other processes. Settlement, which may initially have been rapid, continues at a much slower rate. Other factors begin to exert dominant influences on metamorphism throughout the snowpack. These factors include the difference in temperature measured upward or downward in the snow layer, which is called the temperature gradient. Averaged diurnally, snow temperatures are generally coldest near the surface and warmest near the ground at the base of the snow cover, which creates a temperature gradient across a snow layer that is sandwiched between cold winter air and the relatively warm ground (Figure 2-3, online). The effect of temperature gradients is an ongoing dynamic process that can cross ice, large empty spaces filled with air, and dense snow. Warm air contains more water vapor than does cold air; this holds true for air that is trapped within the snow cover. The greater the amount of water vapor, the greater the pressure; therefore both a pressure gradient and temperature gradient exist through the snow cover. When a pressure difference exists, the difference naturally tends to equalize, just as adjacent high and low atmospheric pressure centers cause the movement of air masses. Pressure differences within snow cause vapor to move upward through the snow layers. The air within the layers of the snow cover (i.e., in the pore spaces between grains) is saturated with water vapor, with a relative humidity of 100%. When air moves from a warmer to a colder layer, the amount of water vapor that can be supported in the pore spaces diminishes. Some vapor changes to ice and is deposited on the surrounding ice grains. We witness a similar process when warm, moist air in a heated room comes in contact with a cold windowpane. The invisible water vapor is cooled to its freezing point, and some of the vapor changes state and is deposited as frost on the window. Figure 2-4 shows how the texture of the snow layer changes during this temperature-gradient process. Water molecules sublimate from the upper surfaces of a grain. The vapor moves upward along the temperature (and vapor) gradient and is deposited as a solid ice molecule on the underside of a colder grain above. This process will continue as long as a strong temperature gradient exists. If the gradient continues long enough, all grains in the snow layer are transformed from solid to vapor and back to solid again; in other words, they recrystallize. The new crystals are completely different in texture and shape from their initial form. They become loose, coarse crystals with faceting, straight sides, and sharp angles (also known as faceted crystals or sugar snow), and they may eventually evolve into a large, striated, hollow-cup form. Examples of these crystals are shown in Figure 2-5. This process is called temperature-gradient metamorphism

A

B FIGURE 2-5  A, Mature depth-hoar grains. Facets and angles are visible. Grain size, 3 to 5 mm (0.12 to 0.20 inch). B, Advanced temperature-gradient grains attain a hollow cup-shaped form. Size, 4 mm (0.16 inch). (Courtesy Doug Driskell.)

or kinetic metamorphism. Well-developed crystals that typically form at the basal layer of the snow cover are commonly known as depth hoar. Depth hoar and faceted crystals are of particular importance to avalanche formation, because these crystals are very weak, with little or no cohesion (bonding) at the grain contacts. They can form the weak layer that fails under a slab and causes an avalanche.

KINETIC METAMORPHISM In the presence of a strong temperature gradient (e.g., ≥1° C [1.8° F] per 10 cm [3.9 inches]), kinetic metamorphism can occur anywhere within a snowpack. Typically, temperature gradients are described as extending upward from the warm ground toward the colder snow surface; however, very strong temperature gradients on the order of 2° C (1.8° F) per centimeter or more (20° C [18° F] per 10 cm [3.9 inches]) can extend for a couple of centimeters from a warm melt-freeze crust into colder snow. Strong temperature gradients can exist in the upper 10 to 30 cm (3.9 to 11.8 inches) of the snowpack, which is often related to the effects of alternating incoming solar radiation (short-wave radiation) and outgoing radiational cooling (longwave radiation) resulting in near-surface facets. These coarse and poorly bonded loose crystals, which are typically 1 to 3 mm (0.04 to 0.12 inch) in size, have straight sides and sharp angles. Backcountry skiers often describe this snow as “recycled powder,” because it often forms on colder and northerly facing slopes with prolonged periods of cold and clear conditions. A temperature gradient forms because radiational cooling (which occurs often— but not exclusively—on clear nights) causes the surface snow to become very cold relative to the snow 10 to 30 cm (3.9 to 11.8 inches) below the surface, which changes more slowly and which may still be under the effects of daytime warming. In the colder temperatures of continental snow climates, strong temperature gradients often exist just above the warm ground and can persist for months when the snow cover remains shallow (typically <1 m [3.3 feet] deep). The persistent gradient and warm basal snow layer temperature can cause very large 35

PART 1  MOUNTAIN MEDICINE

and complex faceted grains to form as well-developed depth hoar. These large, cup-shaped crystals, which are typically 4 to 10 mm [0.16 to 0.39 inch] in size, are characterized by straight sides, sharp angles, and multiple layers of faceted faces. The grains can be described as looking like etched crystal glass, and their organized striations can make them sparkle. The strong temperature gradients that drive kinetic metamorphism are aided by low-density new snow, because the larger pore spaces allow for the easier migration of water vapor. Typical faceted crystals or grains, which were previously referred to as temperature-gradient snow, are commonly called squares. Depth hoar is reserved for well-developed, cup-shaped, and large faceted crystals. Any faceted layer in the snow cover can lead to a persistent weak layer, especially layers of larger grains, which are slower and more resistant to change or to gaining strength.

EQUILIBRIUM METAMORPHISM In the absence of a strong temperature gradient, a totally different type of snow texture develops. When the gradient is less than about 1° C (1.8° F) per 10 cm (3.9 inches), there are still vapor pressure differences, but upward movement of vapor through the snow layers occurs at a much slower rate. As a result, water vapor that is deposited on a colder grain tends to cover the total grain in a more homogeneous manner rather than showing the preferential deposition that is characteristic of faceted crystals. This process produces a grain with a smooth surface of a more rounded or oblong shape. Over time, vapor is deposited at the grain contacts (concavities) as well as over the remaining surface of the grain (convexities). Connecting bonds that are formed at the grain contacts give the snow layer strength over time (Figure 2-6, online). Bond growth, which is called sintering, yields a cohesive texture, which is in contrast to the cohesionless texture of depth hoar and other forms of faceted crystals. This type of grain has been referred to by various terms: equilibrium snow, equitemperature snow, equilibrium metamorphism, or simply rounds. These grains can generally be described as fine and well-sintered (bonded) snow. Such bonded and interconnected grains are shown in Figure 2-7. Weak temperature gradients and high-density new snow force water vapor molecules to form bonds and thus drives equilibrium metamorphism. The preceding paragraphs described the big picture in terms of what happens to snow layers after they have been buried by subsequent snowfalls. If the temperature layer is below freezing and no melting is taking place, one of the two processes described previously is occurring, or perhaps a transition exists between the two. Within the total snow cover, these metamorphic processes may occur simultaneously, but only one can take place within a given layer at a given time, depending upon the strength or weakness of the temperature gradient. Both processes accelerate with warmer snow temperature, because more water vapor is involved.

FIGURE 2-7  Bonded or sintered grains that result from equitem­ perature metamorphism. Grain size, 0.5 to 1 mm (0.02 to 0.04 inch). (Courtesy Doug Driskell.)

36

FIGURE 2-8  Loose snow or point-release avalanche. (Courtesy U.S. Department of Agriculture Forest Service.)

AVALANCHE TYPES There are two basic types of avalanche release. The first is a point-release avalanche or a loose snow avalanche (Figure 2-8). A loose snow avalanche involves cohesionless snow; it is initiated at a point, and it spreads out laterally as it moves down the slope to form a characteristic inverted “V” shape. A single grain or a clump of grains slips out of place and dislodges those below on the slope, which in turn dislodge others. The avalanche continues as long as the snow is cohesionless and the slope is steep enough. In dry snow, this type of avalanche usually involves only small amounts of near-surface snow. However, in wet snow, which is caused by warm air temperatures or rain, these avalanches can be very large and destructive. The second type of avalanche, the slab avalanche, requires a cohesive layer of stronger snow over a layer of weaker snow. The cohesive blanket of snow breaks away simultaneously over a broad area (Figure 2-9). A slab release can involve a range of snow thicknesses, from the near-surface layers to the entire snow cover down to the ground. Slab avalanches can occur in dry or wet snow. In contrast with a loose snow avalanche, a slab avalanche has the potential to involve very large amounts of snow. Because dry slab avalanches are responsible for 95% of U.S. fatal accidents, these avalanches receive the interest of researchers.4 The majority of the information in this chapter deals with

MECHANICAL PROPERTIES: HOW SNOW DEFORMS ON A SLOPE Almost all physical properties of snow can be easily seen or measured in the field. A snow pit provides a wealth of information about these properties, layer by layer, throughout the thickness of the snow cover; however even detailed knowledge of these properties does not provide all of the information that is necessary to evaluate avalanche potential. The current mechanical state of the snow cover must be considered. Unfortunately, for the average person, these properties are virtually impossible to directly measure. Mechanical deformation occurs within the snow cover just before its failure and the start of a slab avalanche. Snow cover has a tendency to settle simply from its own weight. When this occurs on level ground, the settlement is perpendicular to the ground, and the snow layer increases in density and gains in strength. The situation is not so simple when snow rests on a slope. The force of gravity is divided into two components: one that tends to cause the snow layer to shrink in thickness and a new component that acts parallel to the slope, which tends to pull the snow down the slope. Down-slope movement within the snow cover occurs at all times, even on gentle slopes. The speed of movement is slow, generally on the order of a few millimeters per day, but it can be up to millimeters per hour within new snow on steep slopes or with warming temperatures. The evidence of these forces is often clearly visible in the bending of trees and damage to structures built on snow-covered slopes. Although the movement is slow, when deep snow pushes against a rigid structure, the forces are significant, and even large buildings can be pushed off of their foundations. Snow deforms in a highly variable fashion, and is described as a viscoelastic material. Sometimes it deforms as if it were a liquid (viscous), and at other times it responds more like a solid (elastic). Viscous deformation implies continuous and irreversible flow. Elastic deformation implies that, after the force that is causing the deformation is removed, some part of the initial deformation is recovered. The elasticity of snow is not so obvious, primarily because the amount of rebound is very small as compared with those of more familiar materials.

FIGURE 2-9  Slab avalanche. (From the U.S. Department of Agriculture Forest Service; Williams K, Armstrong B: The snowy torrents, Jackson, Wyo, 1984, Teton Bookshop, with permission. Top courtesy Alexis Kelner.)

dry slab avalanches or dry loose snow avalanches. Because wet snow avalanches have received little research, relatively little is known about the processes that cause these avalanches. Recent research reaffirms the challenges to “observe, measure, and quantify the characteristics leading to wet snow avalanches.”32

SLAB AVALANCHE FORMATION To understand the conditions of snow cover that contribute to dry slab avalanche formation, it is essential to reemphasize that snow cover develops layer by layer. The layered structure is directly tied to the two ingredients that are essential to the formation of slab avalanches: the cohesive layer of snow and the weak layer beneath. If the snow cover is homogeneous from the ground to the surface, slab avalanche danger is low, regardless

Moderate to heavily rimed crystals

SLAB

a We

SLAB

SLAB

tr

bs

u ks

ate

Lightly rimed crystals

Warm, dense

Deposited by strong winds

a We

te

tra

bs

u ks

Cold, light

Deposited by light winds

st

ub

s ak

e rat

We

FIGURE 2-10  Snow-layer combinations that often contribute to avalanche formation.

37

CHAPTER 2  AVALANCHES

of the snow type. If the entire snow cover is sintered, dense, and strong, stability is very high. Even if the entire snow cover is composed of depth hoar, there is still no hazard from slab avalanches, because the cohesionless character precludes formation of a slab, which is one of the essential ingredients. Loose snow avalanches may still occur in this situation on steep slopes. The combination of a basal layer of depth hoar with a cohesive layer above provides the ingredients for slab avalanche danger. For successful evaluation of slab avalanche potential, information is needed about the entire snowpack and not just its surface. A hard wind slab at the surface may intuitively appear strong and safe. However, when it rests on a weaker layer that may be well below the surface, it may fail under the weight of a skier and be released as a slab avalanche. Many snow structure combinations can contribute to slab avalanche formation, but the prerequisite conditions are a cohesive layer over a weak layer sitting on a bed surface. Figure 2-10 describes other combinations that result in brittle or cohesive layers of snow on a weak layer.

PART 1  MOUNTAIN MEDICINE

Force

Snow

Viscous deformation

Elastic fracture FIGURE 2-11  Depending on prevailing conditions, snow may deform and stretch in a viscous or flowing manner, or it may respond more like a solid and thus fracture.

With regard to avalanche formation, it is important to know when snow acts primarily as an elastic material and when it responds more like a viscous substance. These conditions are shown in Figure 2-11. Laboratory experiments have shown that conditions of warm temperatures and the slow application of force favor viscous deformation. One sees examples of this as snow slowly deforms and bends over the edge of a roof or sags from a tree branch. In such cases, the snow deforms but does not crack or break. By contrast, when temperatures are very cold or when force is applied rapidly, snow reacts like an elastic material. If enough force is applied, it fractures. We think of such a substance as brittle; release of stored elastic energy causes fractures to move through the material. In the case of snow cover on a steep slope, forces associated with accumulating snow or the weight of a skier may increase until the snow fails. At that point, stored elastic energy is released and is made available to drive brittle fractures over great distances through the snow slab. The slab avalanche provides the best example of elastic deformation in snow cover. Although the deformation cannot actually be seen, evidence of the resultant brittle failure is clearly present in the form of the sharp, linear fracture line and crown face of the slab release (Figure 2-12). The crown face is almost always perpendicular to the bed surface, which is evidence that snow has failed in a brittle manner. To fully understand the slab avalanche condition or the stability of the snow cover, its mechanical state must be considered. Snow is always deforming in a down-slope fashion, but, throughout most of the winter, the strength of the snow is sufficient to prevent an avalanche. The snow cover is layered, and some layers are weaker than others. During periods of snowfall, blowing snow, or both, an additional load or weight is being applied to the snow in the starting zone, the snow is creeping

FIGURE 2-12  The consistent 90-degree angle between the crown face and the bed surface of the avalanche shows that slab avalanches result from an elastic fracture. (Courtesy A. Judson.)

38

faster, and these new stresses are beginning to approach the strength of the weakest layers. The weakest layer has a weakest point somewhere within its continuous structure. If the stresses caused by the load of the new snow or the weight of a skier reach the level at which they equal the strength of the weakest point, the snow fails completely at that point (Figure 2-13); this means that the strength at that point immediately goes to zero. This is analogous to what would happen if someone on a tugof-war team were to let go of the rope. If the remainder of the team was strong enough to make up for the lost member, not much would change immediately. The same situation exists with snow cover. If the surrounding snow has sufficient strength to make up for the fact that the strength at the weakest point has now gone to zero, nothing happens beyond perhaps a localized movement or collapse in the snow, which is often heard as a “whumpf” sound. If the surrounding snow is not capable of compensating, the area of snow next to the initial weak point fails, then at the next, and so forth, until a propagating chain reaction begins. As the initial crack forms in the now unstable snow, the elastic energy is released, which in turn drives the crack further and releases more elastic energy. The ability of snow to store elastic energy is essentially what allows large slab avalanches to occur. As long as the snow properties are similar across the avalanche starting zone, the crack will continue to propagate, thereby allowing entire basins that are many acres in area to be set in motion within a few seconds.

Avalanche Dynamics The topic of avalanche dynamics includes how avalanches move, how fast they move, and how far and with how much destructive power they travel. The science of avalanche dynamics is not well advanced, although much has been learned during the past few decades. Measured data for avalanche velocity and impact pressure are still lacking. Although any environmental measurement presents its own set of problems, it is clear that opportunities for making measurements inside a moving avalanche are extremely limited. Although avalanche paths exist in a variety of sizes and shapes, they all have three distinct parts with respect to dynamics (Figure 2-14). In the starting zone, which is usually the steepest part of the path, the avalanche breaks away, accelerates down the slope, and picks up additional snow. From the starting zone, the avalanche proceeds to the track, where it remains essentially constant and picks up little or no additional snow as it moves; the average slope angle becomes less steep, and frequently the snow cover is more stable than in the starting zone; however a significant amount of snow can be entrained into the avalanche from the track.40 Small avalanches often stop in the track. Larger avalanches travel down the track and into the runout zone, where the avalanche motion ends. Most avalanches stop quickly, within seconds, although very large avalanches tend to slowly decelerate across a gradual slope, such as an alluvial fan. As a general rule, the slope angle of starting zones is 30 to 45 degrees, the track is 20 to 30 degrees, and the runout zone is less than 20 degrees. Avalanches may appear to be turbulent rivers of snow with fluid-like characteristics; however avalanches are granular flows that move much more like a sliding block than water. Few actual measurements of avalanche velocities have been made, but enough data have been obtained to provide some typical values for the various avalanche types. For the highly turbulent dry powder avalanches, the velocities are commonly in the range of 34 to 45 m/s (75 to 100 mph), with rare examples in the range of 67 to 89 m/s (150 to 200 mph). Such speeds are possible for powder avalanches because large amounts of air in the moving snow greatly reduce the forces that result from internal friction. As the snow in the starting zone becomes dense, the terrain becomes less steep and movement becomes more flow-like, with typical velocities slowing to the range of 22 to 34 m/s (50 to 75 mph). During spring conditions, when the snow contains large amounts of liquid water, speeds may reach only about 11 m/s (25 mph). In most cases, the avalanche simply follows a path down the steepest route on the slope while being guided or channeled by

CHAPTER 2  AVALANCHES

A

B

C

FIGURE 2-13  Slab avalanche released by a skier. A skier is descending a slope (A) and causes the release of a slab of avalanche (B), but is able to ski off to the side to escape (C). (Courtesy R. Ludwig.)

terrain features. However the higher-speed avalanche may deviate from this path. Terrain features (e.g., the sidewalls of a gully) that would normally direct the flow of the avalanche around a bend may be overridden by a high-velocity powder avalanche (Figure 2-15). The slower-moving avalanches, which travel near the ground, tend to follow terrain features, thereby giving them somewhat predictable courses. Because avalanches can travel at very high speeds, the resultant impact pressures can be significant. Smaller and medium-size

events with impact pressures of 1 to 15 kilopascals have the potential to heavily damage wood-frame structures. Extremely large avalanches with impact pressures of more than 150 kilopascals possess the force to uproot mature forests and even to destroy structures that are made of concrete. Some reports of avalanche damage describe circumstances that cannot be easily explained simply by the impact of large amounts of fast-moving dense snow. Some observers have noted that as an avalanche passed, some buildings seemingly exploded, 39

PART 1  MOUNTAIN MEDICINE

of snow crystals can increase the air density by a factor of three or more. A powder cloud that is traveling at a moderate dry avalanche speed of 27 m/s (60 mph) could have the impact force of a 80-m/s (180-mph) wind, which is well beyond the destructive capacity of a hurricane.

Identifying Avalanche Terrain Starting zone

The essential ingredients of an avalanche—snow and a steepenough slope—are such that any mountain or even a small hillside can produce an avalanche if conditions are exactly right. To be a consistent producer of avalanches, a mountain and its weather must work in harmony. Track

SLOPE ANGLE

Runout zone

FIGURE 2-14  The three parts of an avalanche path: the starting zone, the track, and the runout zone. (Courtesy B. Armstrong.)

perhaps from some form of vacuum created by the fast-moving snow. Other reports have indicated that a structure was destroyed by the “air blast” preceding the avalanche, because there was no evidence of large amounts of avalanche debris in the area. This damage more likely resulted from the powder cloud, which may be composed of only a few inches of settled snow, yet which contributes significantly to the total impact force. The presence

Avalanches occur with greatest frequency on slopes of 30 to 45 degrees. These are the angles at which the balance between strength (i.e., the bonding of the snow trying to hold it in place) and stress (i.e., the force of gravity trying to pull it loose) is most critical. The easiest way to create high stress is to increase the slope angle; gravity works that much harder to stretch the snow out and to rip it from its underpinnings. A slope of 45 degrees produces many more avalanches than a slope of 30 degrees. On even steeper slopes (i.e., >45 degrees), the force of gravity wins; snow generally rolls or sloughs off, thus preventing the buildup of deep snowpacks. Exceptions exist, especially in maritime snow climates or when strong winds plaster damp snow onto steep slopes. Dry snow avalanches have occurred on slopes of 22 to 25 degrees, which is the angle of repose for granular round substances like sand; however these are rare, because snow grains are seldom round and seldom touch without forming bonds. Although an avalanche release requires a steep slope, it is possible to trigger an avalanche from shallow and even flat slopes at the bottom of steep slopes. A collapse in a persistent weak layer in these areas could send fractures upslope, thus releasing the avalanche. This is analogous to pulling a log out from the bottom of a wood pile. When snow is thoroughly saturated with water, a slush mixture is formed, and an avalanche can release on low-angle terrain. For example, a wet snow avalanche in Japan occurred on a beginner slope at a ski area. The slope was only 10 degrees, but the avalanche was large enough to kill seven skiers. This extreme situation applies only to a water-saturated snowpack, which behaves more like a liquid than a solid.

ORIENTATION

FIGURE 2-15  The large powder cloud associated with a fast-moving dry snow avalanche. (Courtesy R. Armstrong.)

40

Avalanches occur on slopes facing every point of the compass. Steep slopes are equally likely to face east, west, north, or south. In the northern hemisphere, certain factors cause more avalanches to occur on slopes that are facing north, northeast, and east than on those facing south through west; these relate to slope orientation with respect to sun and wind. In the southern hemisphere, more avalanches occur on east, southeast, and south-facing slopes. The sun angle in northern hemisphere winters causes south slopes to get much more sunshine and heating than do north slopes, which frequently leads to radically different snow covers. North slopes have deeper and colder snow covers, often with a substantial layer of depth hoar near the ground. South slopes usually carry a shallower and warmer snow cover that is laced with multiple ice layers that are formed on warm days between storms. Most ski areas are built on predominantly north-facing slopes to take advantage of deeper and longer-lasting snow cover. At high latitudes (e.g., in Alaska), the winter sun is so low on the horizon and the heat input to south slopes is so small that there are few differences in the snow covers of north and south slopes. The effect of the prevailing west wind at mid latitudes is important. Storms most often move west to east, and storm winds are most frequently from the western quadrant (i.e., southwest, west, or northwest). Storm winds pick up fallen snow and redeposit it on slopes that are facing away from the wind (i.e., northeast, east, and southeast slopes). These are the slopes that are most often overburdened with wind-drifted snow. The net

AVALANCHE TERRAIN PATHS The frequency with which a path produces avalanches depends on a number of factors, with slope steepness being a major one. The easiest way to create high stress is to increase the slope angle; gravity works that much harder to stretch out the snow and to rip it from its underpinnings. A slope of 45 degrees produces many more avalanches than does one of 30 degrees, however, specific terrain features are also important. Broad slopes that are curved into a bowl shape and narrow slopes that are confined to a gully efficiently collect snow. Those that have a curved horizontal profile, such as a bowl or gully, trap blowing snow that is coming from several directions; the snow drifts over the top and settles as a deep pillow. Alternatively, the plane-surfaced slope collects snow efficiently only if it is being blown directly from behind. A side wind scours the slope more than it loads the slope. The surface conditions of a starting zone often dictate the size and type of avalanche. A particularly rough ground surface (e.g., a boulder field) does not usually produce avalanches early in the winter, because it takes considerable snowfall to cover the ground anchors. After most of the rocks are covered, avalanches pull out in sections, with the area between two exposed rocks running one time and the area between another two other rocks running another. A smooth rock face or a grassy slope provides a surface that is usually too slick for snow to grip; therefore fulldepth avalanches are distinctly possible. If the avalanche does not run during the winter, it is likely to run to ground in the spring after melt water percolates through the snow and lubricates the ground surface.

VEGETATION Vegetation has a mixed effect on avalanche releases. Bushes provide anchoring support until they become totally covered; at that point, they may provide weak points in the snow cover, because air circulates around the bush and provides an ideal habitat for the growth of depth hoar. It is common to see that the fracture line of an avalanche has run from a rock to a tree to a bush, because these are all places of healthy depth hoar growth. A dense stand of trees can easily provide enough anchors to prevent avalanches. The reforestation of slopes that are devoid of trees as a result of logging, fire, or avalanche is an effective means of avalanche control. Scattered trees on a gladed slope offer little if any support to hold snow in place. Isolated trees may do more harm than good by providing concentrated weak points on the slope.

Factors That Contribute to Avalanche Formation The factors that contribute to avalanche release are terrain, weather, and snowpack. Terrain factors are fixed, but the states of the weather and of the snowpack change daily or even hourly. Precipitation, wind, temperature, snow depth, snow surface, weak layers, and settlement are all factors that determine whether an avalanche will occur.

SNOWFALL New snowfall is the event that leads to most avalanches. More than 80% of all avalanches run during or just after a storm. Fresh snowfall adds weight to existing snow cover. If the snow cover is not strong enough to absorb this extra weight, avalanche releases occur. The size of the avalanche is usually related to the amount of new snow. Snowfalls of less than 15 cm (6 inches) seldom produce avalanches. Snows of 15 to 30 cm (6 to 12 inches) usually produce a few small slides, and some of these harm skiers who release them. Snows of 30 to 60 cm (1 to 2 feet) produce avalanches of larger size that present considerable

threats to skiers and that pose closure problems for highways and railways. Snows of 60 to 120 cm (2 to 4 feet) are much more dangerous, and snowfalls of more than 120 cm (4 feet) produce major avalanches that are capable of large-scale destruction. These predictions are guidelines that are based on data and experience and must be considered with other factors to arrive at the true hazard. For example, a snowfall of 10 inches (25 cm) whipped by strong winds may be serious; a fall of 60 cm (2 feet) of feather-light snow in the absence of wind may produce no avalanches.

SNOWFALL INTENSITY The rate at which snowfall accumulates is almost as important as the amount of snow. A snowfall of 90 cm (3 feet) in one day is far more hazardous than the same amount of snow falling over the course of 3 days. As a viscoelastic material, snow can absorb slow loading by deforming or compressing. Under a rapid load, the snow cannot deform quickly enough and is more likely to crack, which is how slab avalanches begin. A snowfall rate of 2.5 cm (1 inch) or more per hour that is sustained for 10 hours or more is generally a red flag with regard to avalanche danger; the danger worsens if the snowfall is accompanied by wind.

RAIN The age of the surface snow is an important factor with regard to changes in stability when rain falls. Within hours of light rain falling on fresh or recent snow (i.e., from within several days), avalanching can occur for reasons that are not well understood. The rain somehow causes a loss of strength in the new snow. Significant rain (usually about 2.5 cm [1 inch]) falling on an old snow surface (i.e., several days old or older) produces few or no avalanches. Despite the apparent addition of weight caused by rain (2.5 cm [1 inch] of rain is the equivalent in weight to 25 to 30 cm [10 to 12 inches] of snow), the rain tends to drain down through the older snow grains and invariably freezes into an ice crust, which adds strength to the snow cover. At a later time, the smooth crust could become a sliding layer beneath new snowfall. Heavy rain (usually >2.5 cm [1 inch]) greatly weakens the snow cover. It adds weight to the snowpack, but it adds no internal strength of its own (in the form of a skeleton of ice, as new snow would create); it dissolves bonds between snow grains as it percolates through the top snow layers, thus reducing strength even further.

NEW SNOW DENSITY AND CRYSTAL TYPE A layer of fresh snow contains only a small amount of solid material (ice); the majority of the volume is occupied by air. It is convenient to refer to snow density as a percentage of the volume occupied by ice. New snow densities usually range from 7% to 12%, depending on the snow climate. In the high elevations of Colorado, 7% is an average value; in the more maritime climates of the Sierras and the Cascades, 12% is a typical value. Density becomes an important factor in avalanche formation when it varies from average values. Avalanche danger increases when heavier, more-dense snow falls on lighter, less-dense snow, which can occur from storm to storm or even within a single storm (sometimes called an upside-down storm). Wet snowfalls or falls of heavily rimed crystals (e.g., graupel) may have densities of 20% or more. Graupel is a type of snowflake that has been transformed into a pellet of soft ice because of riming inside a cloud. A layer of heavier-than-normal snow presents a danger because of excess weight. Snowfall that is much lighter than normal (e.g., 2% to 4%) can also present a dangerous situation. If the low-density layer quickly becomes buried by snowfall of normal or high density, a weak layer has been introduced into the snowpack. By virtue of low density, the weak layer has a marginal ability to withstand the weight of layers above, thereby making it susceptible to collapse. Storms that begin with low temperatures but then warm up produce an unstable layer of weak, light snow beneath a stronger, heavier layer, thereby acting as a slab and thus as one of the necessary ingredients for an avalanche. 41

CHAPTER 2  AVALANCHES

effect of sun and wind is to cause more avalanches on northfacing through east-facing slopes.

PART 1  MOUNTAIN MEDICINE

Density is closely linked to crystal type. Snowfalls that consist of graupel, fine needles, and columns can accumulate at high densities. Snowfalls of plates, stellars, and dendritic forms account for most of the lower densities.

WIND SPEED AND DIRECTION Wind can transport snow into avalanche starting zones at rates that are much greater than can snow falling from clouds. Wind drives fallen snow into drifts and cornices from which avalanches begin. Winds pick up snow from exposed windward slopes and drive it onto adjacent leeward slopes, where it is deposited into sheltered hollows and gullies; this can quickly turn a 1-foot snowfall into a 3-foot drift in a starting zone. The rate at which blowing snow collects in bowls and gullies can be impressive. In one test at Berthoud Pass, Colorado, the wind deposited snow in a gully at a rate of 45 cm (18 inches) per hour. A speed of 7 m/s (15 mph) is sufficient to pick up freshly fallen snow. Higher speeds are required to dislodge older snow. Speeds of 9 to 22 m/s (20 to 50 mph) are the most efficient for transporting snow into avalanche starting zones. Speeds of more than 22 m/s (50 mph) can create spectacular banners of snow streaming from high peaks, but much of this snow is lost to sublimation in the air or is deposited far down the slope away from the avalanche starting zone. Winds also increase the avalanche potential, because blowing snow is denser after deposition than before transport. This is because snow grains are subjected to harsh treatment in their travels; each collision with another grain knocks off arms and rounds sharp angles, thereby reducing the grain’s size and allowing the pieces to settle and pack together into a denser layer. The net result of wind is to fill avalanche starting zones with additional, heavier, and more cohesive snow than if the wind had not blown.

TEMPERATURE The role of temperature in snow metamorphism occurs over a period of days, weeks, and even months. The influence of temperature on the mechanical state of the snow cover is more acute, with changes occurring in minutes to hours. The actual effect of temperature is not always easy to interpret; whereas an increase in temperature may contribute to the stabilization of the snow cover in one situation, it might at another time lead to avalanche activity. In several situations, an increase in temperature clearly produces an increase in avalanche potential. In general, these conditions include a rise in temperature during a storm or immediately after a storm or a prolonged period of warm, fair weather such as occurs with spring conditions. In the first example, the temperature at the beginning of a snowfall may be well below freezing, but, as the storm progresses, the temperature increases. As a result, the initial layers of new snow are light, fluffy, low density, and relatively low in strength, whereas the later layers are warmer, denser, and stiffer. Thus, the essential ingredient for a slab avalanche is provided within the new snow layers of the storm: a cohesive slab resting on a weak layer. If the temperature continues to rise, the falling snow turns to rain; this situation is not uncommon in lower-elevation coastal mountain ranges. When this happens, avalanches are almost certain; as the rain falls, additional weight is added to the avalanche slope, but no additional strength is provided as it is whenever a new layer of snow accumulates. The second example may occur after an overnight snowstorm that does not produce an avalanche on the slope of interest. By morning, the precipitation stops, and clear skies allow the morning sun to shine directly on the slopes. The sun rapidly warms the cold, low-density, new snow, which begins to deform and creep down slope. The new snow layer settles, becomes denser, and gains strength. At the same time, it is stretched downhill, and some of the bonds between the grains are pulled apart; thus the snow layer becomes weaker. If more bonds are broken by stretching than are formed by settlement, there is not enough strength to hold the snow on the slope, and an avalanche occurs. 42

In these first two examples, the complete snow cover generally remains at temperatures that are below freezing. A third example occurs when a substantial amount of the winter’s snow cover is warmed to the melting point. During winter, sun angles are low, days are short, and air temperatures are cold enough that the small amount of heat gained by the snow cover during the day is lost during the long cold night. As spring approaches, this pattern changes, and eventually enough heat is available at the snow surface during the day to cause some melt. This melt layer refreezes again that night, but the next day more heat may be available, so eventually a substantial amount of melting occurs and melt water begins to move down through the snow cover. As melt water percolates slowly downward, it melts the bonds that attach the snow grains, and the strength of the layers decreases. At first the near-surface layers are affected, with the midday melt reaching only as far as the uppermost few inches and with little or no increase in avalanche hazard. If warm weather continues, the melt layer becomes thicker, and the potential for wet snow avalanches increases. The conditions that are most favorable for wet slab avalanches occur when the snow structure provides the necessary layering. When melt water encounters an ice layer or an impermeable crust—or, in some cases, a layer of weak depth hoar—wet slab avalanches are likely to occur.

DEPTH OF SNOW COVER Of the snowpack factors that contribute to avalanche formation, the depth of the snow cover is the most basic. When the early winter snowpack covers natural anchors (e.g., rocks, bushes), the start of the avalanche season is at hand. However a word of caution is necessary for backcountry travelers in the weak, depth-hoar–prone, continental snow climate. The early winter avalanche danger starts not when the natural anchors are covered but when the snow fills in the spaces between the obvious anchors. North-facing slopes are usually covered before other slopes. A scan of the terrain usually suffices to discern this clue, but another method can be used to determine the time of the first significant avalanches. Long-term studies show a relationship between snow depth at a study site and avalanche activity. For example, along Red Mountain Pass, Colorado, it is unlikely that an avalanche large enough to reach the highway will run until close to 90  cm (3 feet) of snow covers the ground at the University of Colorado’s snow study site. At Alta, Utah, when 130  cm (52 inches) of snowpack has built up, the first avalanche to cover the road leading from Salt Lake City can be expected.

WEAK LAYERS Any layer that is susceptible to failure and fracture as a result of the overburden of additional weight is a weak link. Of the snowpack contributory factors, this is the most important, because a weak layer is essential to every avalanche. Fracture in the weak layer propagates along what is called the failure plane, sliding surface, or bed surface. The most troubling layers are called persistent weak layers, which are usually made of snow crystals and include larger faceted snow, depth hoar, and surface hoar. These crystals are slow to change shape and gain strength, so they may persist for days, weeks, months, or even all season. One common weak layer is an old snow surface that offers a poor bond for new snow. Another weak layer that forms on the snow surface is hoar frost or surface hoar (see Physical Properties, earlier). On clear and calm nights, this hoar forms a layer of feathery, sparkling flakes that grow on the snow surface. The layer can be a major contributor to avalanche formation when it is buried by snowfall as a result of its frequent persistence in the snowpack. Many avalanches have been known to release from a buried layer of surface hoar, and sometimes this layer is more than 1 month old and 180 cm (6 feet) or more below the surface. A weak layer that is almost always found deep within the snowpacks that blanket the Colorado Rocky Mountains (continental snowpack) is large temperature-gradient snow (facets) or depth hoar. One way to decide whether a temperature-gradient layer is near its collapse point is to test the strength of the

Safe Travel in Avalanche Terrain The first major decision that is often faced in backcountry situations is whether to avoid or confront a potential avalanche hazard. A group that is touring with no particular goal in mind will probably not challenge avalanches. For this group, education to recognize and avoid avalanche terrain is sufficient. At the other extreme, mountaineering expeditions that have specific goals and that are willing to wait out dangerous periods or take severe risks to accomplish their objective need considerably more information. Traveling safely in avalanche terrain requires special preparations, including education and the carrying of safety and rescue equipment. The group should have the skills required to anticipate and react to an avalanche.

IDENTIFYING AVALANCHE TERRAIN Because most avalanches release on slopes of 30 to 45 degrees, judging angle is a prime skill for the recognition of potential avalanche areas. An inclinometer can be used to measure slope angles. Some compasses are also equipped for this purpose; a second needle and a graduated scale in degrees can be used to measure slope angles. A ski pole may be used to judge approximate slope angle. When dangled by its strap, the pole becomes a plumb line from which the slope angle can be “eyeballed.” Evidence of fresh avalanche activity (i.e., the presence of fracture lines and the rubble of avalanche snow on the slope or at the bottom) identifies avalanche slopes. Other clues are swaths of missing trees or trees that are bent downhill or damaged, especially with the uphill branches removed. Above the tree line, steep bowls and gullies are almost always capable of producing avalanches.

ROUTE FINDING Good route-finding techniques are necessary for safe travel in avalanche terrain (Figure 2-16). Route finding in avalanche country should not only avoid avalanches but should also be efficient and take into account the abilities and desires of the group to choose a route that is not overly technical, tiresome, or

time consuming. The safest way to avoid avalanches is to travel above or below and at a distance from them. When taking a route above avalanche terrain, the traveler should choose a ridgeline that is above the avalanche starting zones. It is safest to travel the windward side of the ridge. The snow cover is usually thinner and wind packed, with rocks sticking through; this does not make for the most pleasant skiing, but it is safe. Cornice collapses present a very real hazard; they should be avoided by staying on the roughened snow toward the windward side. When ascending a potential avalanche path, a safe route (e.g., a dense forested area that is well anchored, a low-angle approach) should be selected. Skiers who are taking a route in the valley below avalanche terrain should not linger in the runouts of avalanche paths. Although it is unlikely that a skier who is traveling along the valley could trigger an avalanche high up on the slope, it is possible to trigger an avalanche from below if one is traveling close to the compression zone, thereby initiating a fracture that propagates upward. Slopes of 30 degrees or more should be approached with caution. By climbing, descending, and traversing only in gentle terrain, avalanche risk can be avoided.

CROSSING AVALANCHE SLOPES Travel through avalanche country always involves risk, but certain travel techniques can minimize that risk. Proper travel techniques might not prevent an avalanche release but can improve the odds of survival. The timing of a trip has a lot to do with safety. Most avalanches occur during and just after storms. Waiting a full day after a storm has ended can allow the snowpack to react to the new snow load and to gain strength. Before crossing or venturing onto a potential avalanche slope, the skier, hiker, or snowmobiler should tighten up clothing; zip up zippers; and put on a hat, gloves, and goggles. Backpacks should be worn normally, because they may afford protection from back trauma and because the items necessary for survival after a rescue can be stored inside. If the use of a large mountaineering pack will cause a person to be top heavy and more likely to fall, another route should be considered. The skier should remove pole wrist straps and ski runaway straps, because poles and skis attached to the victim hinder extremity motions and only serve to drag the victim under. A person who is wearing a rescue beacon should always be certain that it is transmitting. When crossing potential avalanche slopes, it is always better to cross as high or as low as possible and to avoid the middle. All persons should traverse in the same track. This not only reduces the amount of work required but also disturbs less snow, which lowers the chance of avalanche release. Should the slope fracture when individuals are crossing high, most of the sliding snow will be below, and the chance of staying on the surface of the moving avalanche will be greater. Invariably the person who is highest on the slope runs the least risk of being buried. A person who must climb or descend an avalanche path should keep close to its sides. Should the slope fracture, escaping to the side improves the chance of survival. Only one person at a time should cross, climb, or descend an avalanche slope; all other members should watch from a safe location. Two commonsense principles lie behind this advice. First, only one group member is exposed to the hazard, thereby leaving the others available as rescuers. Second, less weight is put on the snow. Snowmobilers all too often fall prey to multivictim accidents, because an additional rider will drive up a steep slope to help a friend who is stuck near the starting zone. Skiers, snowboarders, climbers, and snowmobilers should never drop their guard on an avalanche slope. They should stop only at the edge of the slope or beneath a point of protection (e.g., a rock outcropping); they should not stop in the middle of a slope or in the runout zone. It is not uncommon for the second, third, or even tenth person traversing or traveling down a slope to trigger the avalanche. Trouble should always be anticipated, and an escape route (e.g., getting to the side, grabbing a tree) should be kept in mind. 43

CHAPTER 2  AVALANCHES

overlying layers and the support provided by specific stability testing performed near the edge of the slope. This is no easy task, and results may be unreliable as a result of the spatial variability of weaknesses on the slope. In addition, most fieldstability tests do not test for deep instabilities in the snowpack. Another method is to try jumping on your skis while standing on a shallow test slope of similar aspect. Collapse is a good indication that comparable snow cover on a steeper slope will produce an avalanche. Often skiers and climbers cause inadvertent collapses while skiing or walking on a depth-hoar– riddled snowpack. The resulting “whumpf” sound is a warning of weak snow below. In recent years, attention to the frequency of faceted snow layers near the surface of the snowpack and their relation to avalanches—particularly in the deeper snow cover of the transitional (intermountain) snow climate—have been well studied. Several mechanisms involved in the evolution of these layers may account for the majority of avalanches in this region, because significant depth hoar-related avalanches are less common. Graupel, which are pellet-like heavily rimed crystals, can act as ball bearings after they are buried in the snowpack; they can be responsible for the layer that is involved in avalanche initiation. Finally, a weak layer can be created within the snow cover when surface melting or rain causes water to percolate into the snow and then fan out on an impermeable layer, thereby lubricating that layer and destroying its shear strength. This phenomenon can be seen during the winter months in the maritime snow climate of the West Coast mountains. Combining the constellation of contributory factors on a dayby-day basis is the avalanche forecaster’s art. Every avalanche must have a weak layer on which to release, so knowledge of snow stratigraphy or layering and what level of applied load will cause a layer to fail form the essence of forecasting.

PART 1  MOUNTAIN MEDICINE

Poor route

Poor route

Good route

Good route

B

A

Gentle slopes d oo

te

rou

G

Poor route Poor route

Steep slopes

Good route

C

D

FIGURE 2-16  Four ski-touring areas showing the safer routes (green dashed lines) and the more hazardous routes (red dashed lines). Arrows indicate areas of wind loading. (From the U.S. Department of Agriculture Forest Service: Avalanche handbook, agricultural handbook 489, Washington DC, 1976, U.S. Government Printing Office, with permission. Courtesy Alexis Kelner.)

STABILITY EVALUATION TESTS People who are traveling on snow-covered slopes should perform hands-on tests of snow strength and instability. Testing the strength of snow helps with the location of weak layers, and checking for instability demonstrates how well the layers are adhering to one another. Several simple but meaningful tests can be performed without digging holes in the snow, although much more information can be learned by digging snow pits. A fast and simple test to find significant weak layers is to push a ski pole into the snow; this should be done handle-end first if the snow is dense. This helps the individual to feel the major layering of the snowpack. For example, the skier may feel the layer of new snow, and stronger or weaker layers in the middle of the pack can be appreciated by the ease of the push. 44

Hard-snow layers and ice lenses may resist penetration altogether, but these can sometimes be felt as resistance by pulling out the pole slowly along the side of the hole. This test reveals only the gross layers within the reach of the pole; thin weak layers, such as buried surface hoar or a poor bond between any two layers, cannot be detected. Thus, although the ski-pole test has limited value, it can provide useful information that must then be correlated with other testing. The simple but very meaningful ski cut test reveals how a similar slope may react to the additional weight of a skier, snowboarder, or snowmobiler. On a small slope that is not too steep (and therefore probably not avalanche prone), the skier can try a ski cut by skiing along a shallow traverse and then setting the ski edges in a hard check. Any cracks or collapse noises indicate instability and that slopes of similar aspect and elevation, if

CHAPTER 2  AVALANCHES

steeper, would have probably avalanched. Ski cuts can be made on steeper suspect slopes by starting a diagonal straight path from an area of safety in a continuous cut to another planned area of safety on the other side of the slope. This can be a dangerous maneuver, but the momentum—even if an avalanche is initiated—increases the chances of escaping off of the starting zone to a safe position. An experienced snowmobiler can perform a similar test by riding his or her machine across the test slope. A much better way to directly observe and test snowpack layers is to dig a hasty snow pit. In a spot as near as possible to a suspected avalanche slope, without putting the traveler at risk, a pit 120 to 150 cm (4 to 5 feet) deep and 90 cm (3 feet) wide should be dug. With the shovel, the uphill wall is shaved until it is smooth and vertical. Now the layers of snow can be observed and felt. The tester can see where the new snow touches the layer beneath, poke the pit wall with a finger to test hardness, and brush the pit wall with a brush to see which layers are soft and fall away and which are hard and stay in place after being brushed. Buried surface hoar, faceted grains, graupel, and crusts are better appreciated; in shallow snowpacks, basal depth hoar can also be easily reached and evaluated. The shovel shear test (ST) is a simple and quick test that is used to locate weak layers (especially very thin layers); however, its small sample size and subjective nature make it less reliable for determining the stability of the snowpack. A column of snow is isolated from the vertical pit wall. Both the sides and the back of the column are cut with a saw (a shovel or a ski will suffice) so that the column is free standing. The dimensions are a shovel’s width on all sides. The tester inserts the shovel blade at the back of the column and gently pulls forward on the handle. A cohesive layer of the column will shear on a weak layer and make a clean break; the poorer the bond, the easier the shear. The following five-point scale is used to rate the shear: (1) “very easy” (STV) if it breaks as the column is being cut or as the shovel is being inserted; (2) “easy” (STE) if a gentle pull on the shovel does the job; (3) “moderate” (STM) if a slightly stronger pry with the shovel is required; (4) “hard” (STH) if a solid tug is required; and (5) “no shear” (STN) if no shear failure is observed. Generally, “very easy” and “easy” shears indicate unconditionally weak snow, “moderate” means conditionally weak, and “hard” and “no shear” mean strong. The value of the ST is that it can find thin weak layers that are undetectable by any other method, even on flat areas. The ST’s major shortcoming is that it is not a true test of stability, because it does not indicate the amount of weight or compression required to cause shear failure. The compression test (CT) is an effective way to find weak layers near the surface (≈1 m [3.3 feet]), and it works well in soft, new snow. The test also gives a good indication of snow stability, because it stresses the weak layer. The CT involves isolating a block similar to that created for the ST on sloping terrain. Using the shovel blade turned upside down and held on the top of the column, successive taps are made on the shovel: 10 from the wrist using the fingertips, 10 from the elbow using the fingertips, and finally 10 from the shoulder using the palm or the fist. The number of taps required to produce a shear is recorded. For example, a shear after 5 taps from the elbow would be recorded as CT15. The interpretation of the stability of the weak layer that is discovered is defined as “easy” (taps 1 through 10), “moderate” (taps 11 through 20), or “hard” (taps 21 through 30). The CT evaluates the ability of weak layers in the upper snowpack to fail in shear and can be performed quickly, thereby allowing for multiple assessments of different aspects and elevations during backcountry travel (Figure 2-17). Most tests, like the ST and the CT, assess fracture initiation (i.e., the additional force or stress needed to start fractures), but they do not assess fracture propagation (i.e., the propensity for fractures to spread through a weak layer in the snowpack). Without assessing for fracture propagation, tests may conceal the real problem layer in a weak snowpack. In a stable snowpack, a fracture may be easy to initiate, but no avalanche may result, because fracture does not propagate across the weak layer. In an unstable snowpack, a fracture may be easy or difficult to initiate; however, after it has been initiated, the fracture can propagate across the weak layer, thereby resulting in an avalanche.

Tapping

30 cm

30 cm k ea r W ye la

Snow pit

FIGURE 2-17  Photo and schematic of a shovel compression test. (With permission from The American Avalanche Association. Top courtesy Doug Richmond.)

To better assess fracture initiation, propagation, and instability, many backcountry travelers and avalanche professionals use the Rutschblock test (RB). This test is calibrated to the skier’s weight and to the stress that he or she would put on the snow. Again, a snow pit is dug with a vertical uphill wall, but the pit must be about 240 cm (8 feet) wide. By cutting into the pit wall, the skier isolates a block of snow that is about 210 cm (7 feet) wide (i.e., a ski length) and that goes back 120 cm (4 feet; i.e., a ski-pole length) into the pit wall. Both the sides and the back are cut with a shovel or a ski so that the block is freestanding. (The test receives a score of RB1 if the snow fails while the individual is isolating the block.) While wearing skis, the skier climbs around and well uphill from the isolated block and carefully approaches it from above. With skis across the fall line, the skier gently steps onto the block—first with the downhill ski and then with the uphill ski—so that he or she is standing on the isolated block of snow. If the slab of snow fails at this time, the score is RB2. Gently flexing the knees applies a little more pressure (RB3). The tester then jumps and lands in the same compacted spot (RB4). The jump is then repeated (RB5). If no failure occurs, the skier moves to about the middle of the block and repeats the flexing and jumping (RB6). If no reasonably smooth failure is produced at this time, the test is considered an RB7. The results are interpreted as “extremely unstable” if the block fails while the skier is cutting it, approaching it from above, or merely standing on it (RB1 or RB2); “unstable” if it fails with a 45

PART 1  MOUNTAIN MEDICINE

knee flex or one gentle jump (RB3 or RB4); “moderately stable” if it fails after repeated jumps (RB5); and “very stable” if it never fails but merely crumbles (RB6 or RB7). These are objective results that help answer the bigger question of whether the snowpack will slide and that help the mountain traveler to decide how much risk to take. The limitations include the time required to isolate the block; the inability to test deep, weak layers; the spatial variability of the results; and the problem of relying on it as a one-step stability evaluation. A new test that was developed during the late 2000s is the extended column test (ECT), which does a remarkable job of effectively discriminating between unstable and stable slopes by extending the size of the column beyond the size of the loading area. Similar to the loading of the CT, stress can be transmitted across the slab. If conditions are unstable, fracture will propagate across the column’s weak layer. To prepare an ECT, a snow pit is dug with a vertical uphill wall and isolates a column that is 90 cm (3 feet) across the slope by 30 cm (1 foot) up the slope. The column is then loaded from one side with the use of the same successive tap technique as is used in the CT. The result reporting emphasizes what happened to the snow column (i.e., whether a fracture propagated across the column or not). The coding is recorded as ECTPV (“very easy”) if the fracture propagates across the entire column during isolation. Like the CT, the number of taps is reported as ECTP## when a fracture initiates and propagates across the entire column. If a fracture initiates on ## tap but does not propagate across the entire column or if more than one additional tap is required after initiation to cause complete propagation, the result is noted as ECTN##. If no fracture occurs, the result is noted as ECTX. Interpreting stability from a single snow pit or stability test is dangerous as a result of spatial variability. The snow cover is not homogenous in its stability; rather it has a patchwork-quilt–like pattern of stronger and weaker snow. Even within a known combination of an unstable slab and a weak layer, there are variations along the slope where one can trigger or not trigger an avalanche (i.e., the false-stable rate). The implications of spatial variability are significant. On a suspected avalanche slope, explosives set in an area of strength will not result in an avalanche. A ski area might then assume incorrectly that the snow is stable and safe only to have a skier hit a weak spot and trigger an avalanche. Likewise, a backcountry skier might dig a snow pit and find strong snow only to trigger an avalanche on the entire slope after skiing a few turns. All tests are prone to misleading results. Research has shown that the CT and RT tests, which are favored by most avalanche professionals, have a relatively high false-stable rate (i.e., a stable test result on an unstable slope) of about 10% to 20%.6,28,38 On paper, being right 80% to 90% of the time may sound encouraging. However, in practice, the false-stable rate is still too high, because the consequences of an error can be fatal. The falsestable rate of 3% with the ETC is more encouraging, but researchers caution that more studies are needed.39 For backcountry travelers and avalanche workers, the falsestable rate should prompt users to dig multiple snow pits and perform multiple stability tests on the same slope. As an exercise in probability, a false-stable rate of 10% implies that digging two snow pits on the same slope decreases the chances from getting a false-stable rate in both pits to 1 in 100. Three pits drop the chances to 1 in 1000. One should always use a variety of tests and combine those results with direct observations of avalanche, snowpack, and weather conditions. More detailed descriptions and guidelines regarding the performance of all presently recommended stability tests can be found in Snow, Weather and Avalanches: Observation Guidelines for Avalanche Programs in the United States (Pagosa Springs, Colorado, 2009, The American Avalanche Association).

AVALANCHE RESCUE EQUIPMENT Shovel The first piece of safety equipment that the skier or climber should own is a shovel, which can be used to dig snow pits for 46

stability evaluation and snow caves for overnight shelter. A shovel is also needed for digging in avalanche debris, because such snow is far too hard for digging with the hands or with skis. The shovel should be sturdy and strong enough to dig in avalanche debris yet light and small enough to fit into a pack. There is no excuse for not carrying a shovel. Collapsible shovels made of aluminum or high-strength plastic are available in mountaineering stores. Probe Several pieces of equipment are designed specifically for finding buried avalanche victims. The first is a collapsible probe pole. Organized rescue teams keep rigid poles in 3- to 4-m (10- to 12-foot) lengths as part of their rescue caches. The recreationist can buy probe poles of tubular aluminum or carbon fiber that come in 45-cm (18-inch) sections that fit together to make a fulllength probe. Ski poles with removable grips and baskets can be screwed together to make an avalanche probe. Survivors of an accident use probes to search for buried victims by either spot probing in likely burial areas or to confirm transceiver location before shoveling. Avalanche Rescue Beacon Avalanche rescue beacons (transceivers) are the best personal rescue devices for quickly finding buried companions. When used properly, they are a fast and effective way to locate buried avalanche victims. In the United States and worldwide, these devices have become standard issue for ski-area patrollers involved in avalanche work and for helicopter skiing guides and clients. They are also commonly used by highway departments, search and rescue organizations, and anyone traveling into avalanche terrain. Since beacons were introduced in the United States, they have saved several lives each winter. All transceivers act as electromagnetic transmitters that emit a signal on a world-standard frequency of 457 kHz. A buried victim’s unit emits this signal, and the rescuers’ units receive the signal. The signal carries 30 to 50 m (100 to 150 feet) and, after it is picked up, it guides searchers specifically to the buried unit. Beacon technology is evolving rapidly, and the transceivers that are on the market are continually improving. Two major categories of transceiver have emerged: (1) analog, which processes the receiving signal in a basic electromagnetic convergence of induction pulses to allow for a stronger (visual and audible) signal as the receiving beacon approaches the sending beacon; and (2) digital, which uses a computer chip to microprocess the receiving analog signal and to then display a digital readout of the distance, strength (audible and visual), and, in some units (i.e., dual and triple antennae), the general direction to the buried unit. The newest transceivers are triple-antennae devices that not only give data about distance, direction, and signal strength but that can also identify multiple burials and their approximate location in relation to each other. The tripleantennae transceivers also reduce false signals, which can often be a confusing issue with single and dual devices, in the final few meters of the search. Transceivers are audio-magnetic-induction devices and not radio devices; the directional arrows point only along a flux line of the sending unit’s magnetic field. Likewise the displayed distance represents the distance along a flux line rather than a direct distance to the sending unit. In this regard, the closer the distance displayed, the closer the flux line from the sending unit. Both analog and digital beacons operate on the same internationally standardized frequency and therefore are compatible with one another. However, slightly different search techniques may be necessary to use each type most efficiently, and special training and practice are required before the user attains proficiency. Experience has shown that digital units have a faster learning curve, and these are routinely used by helicopter skiing services and backcountry guides for clients with limited experience. Merely possessing a beacon does not ensure its lifesaving capability. Experience in the United States and from European studies shows that the chances of surviving a full avalanche burial with a beacon and companion rescue are still less than 50%.12,27

Avalanche Airbag The purpose of the avalanche airbag is not to quicken rescue but to prevent burial. German industrialist Peter Aschauer introduced the backpack-integrated avalanche airbag system (ABS) in 1985 (Figure 2-19). It was designed specifically for guides and ski patrollers, but it rapidly became popular in Europe for use by recreationalists who were venturing into avalanche terrain. Accident data have been compiled since the beginning of its use

by the Swiss Federal Institute for Snow and Avalanche Research in Davos, Switzerland.44 The first documented case of survival with the use of an ABS was in February 1991. Since then (as of 2009), 253 ABS-equipped persons have been caught in avalanches; 226 victims survived with deployed airbags, and there were only three deaths among those victims whose airbag deployed. Two deaths occurred among victims whose airbag deployed and who were buried, even though their airbags were visible on the surface. In a third case of death in a victim whose airbag deployed, the victim and airbag were completely buried by a second avalanche. In another 27 victims the airbags failed to work properly or the user did not or could not deploy the airbag, and among these victims seven deaths occurred. Thus, among 253 avalanche victims wearing an ABS system, there were 10 deaths total. The airbag works as a result of inverse segregation (Figure 2-20). An avalanche in motion is composed of many different-sized

BOX 2-1  Avalanche Transceiver Search Initial Search 1. Safely access the slide path and debris area, and have everyone switch their transceivers to “receive” and turn the volume to “high.” 2. If enough people are available, post a lookout to warn others about possible additional slides. 3. Should a second slide occur, have rescuers immediately switch their transceivers to “transmit.” 4. Have rescuers space themselves no more than 30 m (100 feet) apart and walk abreast along the slope. 5. If a single rescuer is searching within a wide path, he or she should zigzag across the rescue zone and limit the distance between crossings to 30 m (100 feet). 6. For multiple victims, when a signal is picked up, have one or two rescuers continue to focus on that victim while the remainder of the group carries out the search for additional victims. 7. For a single victim, when a signal is picked up, have one or two rescuers continue to locate the victim while the remainder of the group prepares shovels, probes, and medical supplies for the rescue. Locating the Victim With practice, the induction line search is more efficient than the conventional grid search for getting close to the sending beacon, but the conventional grid search is still necessary to fine search for the buried victim. A probe pole can be used to pinpoint the victim’s exact location. The induction line search is very similar to the flux line search that is used by digital transceivers. Users should always study the owner’s manual to learn the best techniques for the specific brand of avalanche rescue beacon that they are using. Induction Line Search (Preferred Method) When an induction line search is used, the rescuer may initially follow a line that leads away from the victim (see Figure 2-18, A and B). Remember to lower the transceiver volume if it is too loud, because the ear detects signal strength variations better at lower volume settings. 1. After picking up a signal during the initial search, hold the transceiver horizontally (parallel with the ground), with the front of the transceiver pointing forward (see Figure 2-18, C). 2. Holding the transceiver in this position, turn until the signal is maximal (maximum volume), then walk five to seven steps (about 5 m [16.4 feet]), stop, and turn again to locate the maximum signal (see Figure 2-18). When locating the maximum signal, do not turn yourself (or the transceiver) more than 90 degrees in either direction. If you rotate more than 90 degrees to locate the maximum signal, you will become turned around and follow the induction line in the reverse direction. 3. Walk another five steps, as just described, and then stop and orient the transceiver toward the maximum signal. Reduce the volume. 4. Continue repeating these steps. You should be walking in a curved path along the induction line toward the victim (see Figure 2-18, B).

5. When the signal is loud at the minimum volume setting, you should be very close to the victim and can begin the grid search. Grid Search 1. When a signal is picked up, stand and rotate the transceiver, which is held horizontally (parallel with the ground) to obtain the maximum signal (loudest volume). Maintain the transceiver in this orientation during the remainder of the search. 2. Turn the volume control down until you can just hear the signal. Walk in a straight line, down the fall line from where the signal was first detected. (If the signal fades immediately, walk up the fall line.) If you are headed in the right direction, the signal will increase; turn the volume control down until the signal fades. Take an extra couple of steps to be sure that the signal truly fades. If the signal increases, continue until it fades. 3. When the signal fades, mark the point, and then turn 180 degrees and walk back toward the starting position. The   signal will increase in volume and then fade again; take two additional steps to confirm the fade. Walk back to the middle   of the two fade points; this spot may or may not be the point   of loudest volume and maximum signal. If you experience two maximum signals, go to the midpoint between the two maximums. 4. At this point, turn 90 degrees in one direction or the other. From that position, reorient the transceiver (held parallel with the ground) to locate the maximum signal. After orienting the transceiver to the maximum signal, reduce the volume, and begin walking forward. If the signal fades, turn around 180 degrees, and begin walking again. 5. As the signal volume increases, repeat steps 3 and 4 until you have reached the lowest volume control setting on the transceiver. (Be sure to always take an extra step or two to confirm the fade point.) This time, when you return to the middle of the fade points, you should be very close to the buried victim and can now begin pinpointing him or her. a. While stationary, orient the transceiver to receive the maximum signal (loudest volume). At this point, turn the volume control all the way down. b. With the transceiver just above the surface of the snow, continue doing the grid search pattern two to four more times. Always sweep the transceiver a couple of feet beyond the fade point to confirm the fade point. c. Find the signal position halfway between the fade points (i.e., at the loudest signal). At this point, you should be very close to the victim’s position, and you can begin to mechanically probe. Speed is essential. With practice, the transceiver will be accurate to less than one-fourth of the burial depth. For example, a 4-foot burial should result in about a 1-foot square at the surface. d. Depending on the brand, pinpointing with a digital transceiver will involve the use of a slight variation or a combination of the induction line and grid techniques. Be sure to study the owner’s manual.

47

CHAPTER 2  AVALANCHES

Frequent practice is required to master a transceiver-guided search, which may not be as straightforward as the directions suggest. Skilled practitioners can find a buried unit in less than 5 minutes after they pick up the signal. Because speed is essential in avalanche rescue, beacons can certainly be lifesavers. The best-proved rescue equipment is a transceiver for a quick find, a collapsible probe or pole to confirm and pinpoint the spot, and a shovel for a quick recovery (Box 2-1 and Figure 2-18).

PART 1  MOUNTAIN MEDICINE

min weak

–

–

E

+

+ 5m – –

–

–

max strong

min weak max strong

W

–

A

S

B

C

FIGURE 2-18  Induction (“tangent”) line search method. A, The arrangement of the electromagnetic flux lines (induction lines) emitted from a buried victim. The signal received by the searching transceiver along the transmitted flux line is strongest when it is oriented in parallel, and it is weakest when it is oriented perpendicularly. B, The searcher moves in short (3 to 5 m [9.8 to 16.4 feet]) “tangents” and then orients the transceiver to the strongest signal. In this way, the receiving transceiver follows a flux line toward the victim. The sensitivity (loudness) of the beacon should be adjusted downward as the victim is approached so that the searcher can discern the strongest signal before proceeding in a new direction. C, The “pinpoint” search is performed when the buried subject is within 3 m (9.8 feet); this typically occurs when the transceiver is at its loudest with the sensitivity turned all the way down. It is a “grid” search on a much smaller scale that is carried out close to the snow surface. The loudest signal is found along one axis (E to W) and followed by the perpendicular axis (N to S) to the likely burial position. A probe is then used to confirm the victim’s location and depth. (From Auerbach PS, Donner HJ, Weiss EA: Field guide to wilderness medicine, St Louis, 1999, Mosby, with permission.)

particles of snow. Gravity causes granular flows to segregate, with smaller particles sinking to the lower portion of the flow and larger particles rising to the surface. The process of inverse segregation depends primarily on the relative sizes of the particles in a granular flow. A person who is carried in the flow of an avalanche is not necessarily a large-enough particle to remain on the surface as compared with a particulate slab. However, the airbag (150 L [5.3 feet3] when inflated) apparently makes the user a large enough particle, which allows for a greater separation effect. Buoyancy plays no role in the efficiency of this system. Since 1995, the ABS has undergone continued and significant improvements with regard to device sizes and cartridge weight. The airbag is integrated into a special backpack, and the user deploys it by pulling a ripcord-like handle. This releases a

A

Inverse segregation

B FIGURE 2-19  A, A small-size Avalanche ABS backpack with deployed airbags. The airbags are stowed in the outside pockets of the backpack. B, Integrated into a backpack, the Avalanche ABS is deployed by pulling the white “T” handle. (Courtesy Peter Aschauer, GmbH.)

48

FIGURE 2-20  Inverse segregation. The physical unmixing of flowing particles is based on size, which distributes larger particles in the upper layers and forms the basis for successful functioning of the Avalanche ABS.

AvaLung In 1996, Dr. Thomas Crowley received a patent for an emergency breathing device to extract air from the snow surrounding a buried avalanche victim after testing a homemade prototype on himself. Black Diamond Equipment, Ltd., in Salt Lake City, Utah, performed the research and development on the device and secured distribution rights in 2000 for the original external vest format of the AvaLung. The company redesigned the device in 2002 for easier and more comfortable use when worn outside of the clothing like a bandoleer (Figure 2-21). The most recent version, which is the most popular, is incorporated into varioussized backpacks with a stowable mouthpiece kept in the shoulder strap (Figure 2-22, online). The AvaLung functions mainly by separating inhaled from exhaled air in the surrounding snowpack with a goal of prolonging survival time by slowing the process of asphyxiation. Ambient air is 21% oxygen and has virtually no carbon dioxide. Expired air is 16% oxygen and 5% carbon dioxide. The AvaLung prevents FIGURE 2-21  The AvaLung is a breathing device that is intended to prolong survival during avalanche burial by diverting expired air away from inspired air drawn from the snowpack and that is worn over all other clothing. The white arrows show the flow of inspiratory air, and the red arrows show the flow of expiratory air. The subject breathes in and out through the mouthpiece (A). Inhaled air enters from the snowpack through the one-way inspiratory valve on the side of the housing inside the mesh-protected harness on the chest (B). Expired air leaves the lungs via the mouthpiece and travels down the respiratory tubing to the housing and then passes through an expiratory one-way valve located at the bottom of the housing (B). It then travels via respiratory tubing inside the harness around to the back (C). (A courtesy Jill Rhead; B courtesy Black Diamond Equipment, Ltd.)

rebreathing of expired air, which is one cause of asphyxiation during avalanche burial, by diverting expired air away from inspired air that is drawn from the snowpack23 (see Avalanche Victim Physiology and Medical Treatment after Rescue, later; see Figure 2-22, online). Survival after complete avalanche burial with use of the AvaLung has occurred in a number of cases.34 The AvaLung system has been proved effective in numerous simulated burials by allowing subjects to breathe for 1 hour in tightly packed snow, including dense, wet snow. In addition, several known cases have occurred in which burial time was fairly short. In a dramatic hallmark case, a helicopter skier survived a 120-cm (4-foot) burial of 35 to 45 minutes by breathing with an AvaLung. Two others were buried in the avalanche a few feet apart at about the same depth but were not wearing the device. Rescue times were similar for the three victims, none of which had suffered any trauma. The two skiers that were not wearing the AvaLung died of asphyxiation.15 The ABS and the AvaLung are designed to help avalanche victims, and they are adjuncts to the basic companion rescue equipment which includes a transceiver, probe, and shovel. These devices should never be used to justify the taking of additional risks. Because surviving any avalanche is uncertain, no equipment should ever replace good judgment.

Avalanche Rescue SELF-RESCUE Escaping to the Side The moment that the snow around a person begins to move, there is a split second during which that person can make a decision or make a move. The person should shout to alert companions and then close the mouth and breathe through the nose to prevent inhaling a mouthful of snow. If the individual is wearing an AvaLung, the mouthpiece should be quickly placed in the mouth, which also helps to prevent oropharyngeal snow impaction. If he or she is using an ABS, every effort should be made to activate the ripcord. Whether on foot, skis, or snowmobile, the person should first try to escape to the side of the avalanche or try to grab onto a tree. Staying on one’s feet or snow machine gives the individual some control and keeps his or her head up. Escaping to the side gets the person out altogether or to a place where the forces and speeds are less. Turning the skis or the snow machine downhill in an effort to outrun the avalanche is a bad move: the avalanche invariably overtakes its victims. Swimming For years, the command to swim if caught in an avalanche was dogma. However, during recent years, the effectiveness of

A

B

C d

mon

ck

Bla

Dia

49

CHAPTER 2  AVALANCHES

cartridge of nitrogen gas that escapes at high velocity and that draws in outside air through jets that inflate two 75-L (2.6-foot3) airbags in 2 to 3 seconds with the use of the Venturi effect. In an initial study, Brugger and Falk13 found that the ABS reduces the likelihood of avalanche burial from 39% to 16.2% and that it lowers mortality from 23% to 2.5%. In a more recent analysis by Brugger and colleagues,12 use of the ABS reduced mortality in an avalanche to 2.9% as compared with 18.9% without the ABS in complete or partially buried avalanche burial victims. This dramatic reduction in mortality occurs because the ABS device prevents burial, and very few (i.e., ≈4% to 5%) partly buried or unburied victims die in avalanches. Commercial sales of the ABS system in the United States were delayed until recently because of problems with obtaining certification for the nitrogen-gas cartridges; however, the device is now readily available for sale in the United States. Two American companies have started to produce airbags with different configurations. Both use a single 150-L (5.3 feet3) airbag; one airbag is integrated into a backpack, whereas the other is incorporated into a vest and deployed as a balloon in a horseshoe shape around the back of the victim’s head toward the anterior chest. A third airbag device from Switzerland makes use of a continuous balloon that arches over and along the upper side of a backpack to surround the victim’s head. The latter two systems have the theoretic advantage of preventing head trauma, and both may allow for a greater chance of a head-up partial burial. Unlike the ABS, none of these three new systems has been independently tested by the Swiss Federal Institute for Snow and Avalanche Research or has a documented history of use in avalanche accidents. Only the German ABS has been rigorously tested, with extensive experience. The new airbag designs are too recent for the making of any sound recommendations at this time.

PART 1  MOUNTAIN MEDICINE

swimming has been called into question. It is the process of inverse segregation (see Avalanche Airbag, earlier) rather than swimming that keeps the victim on or near the surface. However many survivors claim that “swimming” (i.e., struggling with the arms and legs flailing) kept them on or close to the surface. It is possible that these motions may create a large particle effect and that inverse segregation applies. The most important thing to do when caught and being tumbled violently and unable to swim with the avalanche is to get a hand or both hands in front of the face to create an air pocket. This is especially important, because the avalanche may stop abruptly, at which time no arm movement will be possible. Without an air pocket, very few buried victims survive. Cumbersome or heavy gear and ski poles should already have been discarded, and, with any luck, the avalanche will strip away the skis. Although skiers should try to discard their gear, snowmobile riders should try to stay on their snow machines. Once they are off their machine, riders are twice as likely to be buried as are their machines. Reaching the Surface Anyone who is caught in an avalanche should fight for his or her life. Creating an air pocket is the key to survival, but some victims, sensing themselves to be near the surface, have thrust a hand or a foot toward the surface. Any clue on the surface that gives the rescuers something to see greatly improves an individual’s odds of survival.

COMPANION RESCUE Marking the Last-Seen Area A companion or eyewitness to an accident needs to act quickly and positively. The rescuer’s actions over the next several minutes may mean the difference between life and death for the victim. First, the victim’s last-seen area (LSA) should be fixed and marked with a piece of equipment or clothing, a tree branch, or anything that can be seen from a distance down slope. It is usually safe to enter the bed surface of an avalanche that has recently run. It is dangerous when the fracture line has broken at mid slope, which leaves a large mass of snow still hanging above the fracture. If the victim was seen riding the avalanche before the LSA, a line of trajectory can be visualized that could narrow down likely areas of burial. Persons equipped with transceivers can go to the LSA to begin their search (see Beacon Search, later). Those without transceivers face a very difficult situation.

SEARCHING FOR CLUES The fall line (i.e., the line of trajectory) should be searched below the LSA in the flow line for any clues of the victim. Shallow probes should be made into likely burial spots with an avalanche probe, a ski, a ski pole, or a tree limb (i.e., spot probing). Likely spots are the uphill and downhill sides of trees and rocks and benches or bends in the slope where snow avalanche debris piles up. The toe of the debris should be searched thoroughly; many victims are found in this area. Rescue Beacons If the group was using beacons, all companions must immediately switch their units to receive mode. While making the fast visual search for clues, companions should at the same time search the debris using their transceivers as described in Box 2-1. When a signal is detected, companions must narrow the search area quickly. If they are skilled with a transceiver, companions can pinpoint the burial site in a few minutes and should confirm the location with a probe that is then left in place. Shoveling Techniques Unfortunately, shoveling will take much longer than the transceiver search, and, depending on the number of rescuers and the technique used, this aspect of the rescue could be the difference between life and death. Recent attention regarding efficient shoveling techniques during avalanche rescue has emerged. It is clear that unburying 50

Snow shoveled to side Burial depth

1.5 x burial depth FIGURE 2-23  Strategic shoveling technique for one or two rescuers. (Courtesy Dale Atkins and the National Ski Patrol, Lakewood, Colo.)

an avalanche victim is the most time-consuming component of the rescue, and inefficiencies have been identified. Strategic Shoveling During companion rescue, where typically only one to three shovelers might be available and where the debris is often softer, the strategic shoveling technique16 increases digging efficiency (Figure 2-23). There are several important things to consider when shoveling when only a few diggers are available: avoid standing over the buried victim, begin digging down slope from the probe, lift snow as little as possible by throwing it to the side, and move snow only once. With the probe left in place, the shovelers begin digging down slope about one to oneand-one-half times the burial depth as determined by the probe. Quickly dig a waist-deep starter hole about one wingspan wide (i.e., the distance between the fingertips when the arms are held out to the sides). If two shovelers are digging, they should work in tandem and side by side rather than one digging behind the other. Throw the snow to the sides. Move to the starter hole, and continue digging downward and forward. As depth increases, snow can be cleared to the back rather than lifted and tossed to the sides. When close to the victim, use a scraping action to clear snow. Use the first body part to estimate the location of the head, and then use the hands to clear away snow from the victim’s face and airway, and continue to clear snow off his or her chest. The most important feature of efficient shoveling is to create a ramp or platform in the snow that leads to the probe (and the victim) instead of digging a hole down around the probe. In this way, extrication and resuscitation of the victim are made easier by having a flat surface available, the air pocket is not compromised, there is space to work on the victim, and raising up the victim is not necessary. V-Shaped Conveyor Belt With an organized rescue, the debris is often much harder as a result of age hardening than what is experienced by companion rescuers, but typically more shovelers are available. In this situation, the V-shaped conveyor belt method18 works effectively to clear snow quickly (Figure 2-24). Starting down slope from the probe, rescuers are arranged in a wedge-shape or inverted-“V” pattern. The lead shoveler chops out blocks of snow and scoops the snow down slope. The other shovelers use paddling-like motions to clear out snow through the center of the “V” to create a platform. When getting close to the buried victim, an additional shoveler may join the lead to increase the working space. Shovelers may rotate clockwise every 5 minutes to decrease fatigue. After the victim is reached, locate his or her head and chest, and use the hands to clear the airway. Teaching efficient shoveling techniques should be included in all avalanche rescue courses, and it should be practiced as often as transceiver searches to reduce the total time to extrication. Going for Help A difficult question during rescues is when to seek outside help. If the accident occurs in or near a ski area and there are several

CHAPTER 2  AVALANCHES

80 cm

A

D

B

C

E F

FIGURE 2-24  V-shaped conveyor belt shoveling approach. A, Positioning of rescuers, with a quick measurement of the distance between shovelers. B, Working in sectors on the snow conveyor belt; snow is transported with paddling motions. C, Clockwise rotation is initiated by the front person; job rotation maintains a high level of motivation and minimizes early fatigue. D, The buried victim is first seen. More rescuers are needed at the front, and the snow conveyor belt only needs to be kept partially running. E, Careful work occurs near the buried victim, while some shovelers aggressively cut the side walls to adapt the tip of the V to the real position of the victim. F, Interface to organized rescue. More space is shoveled only after medical treatment of the victim has begun. (Courtesy Manuel Genswein. From Genswein M, Eide R: V-shaped conveyor belt approach to snow transport, The Avalanche Review 20:20, 2008, with permission.)

companions, one person can be sent to notify the ski patrol immediately. If only one or two companions are present, the correct choice is more difficult. The best advice is to search the surface quickly but thoroughly for clues before anyone leaves to notify the patrol. Cell phones have been the most effective and efficient method of calling for help, because contact can be made without losing manpower for continued companion rescue; however, cell phones do not work in all mountain areas. If a voice connection cannot be made, try sending a text message. In the United States, the Next Generation 911 system is being implemented to support text messages, images, and video. If the avalanche occurs in the backcountry far from any organized rescue team, all companions should remain at the site. The guiding principle in backcountry rescues is that companions search until they cannot or should not continue. When deciding when to stop searching, the safety of companions must be weighed against the decreasing survival chances of the buried victim.

ORGANIZED RESCUE Incident Command System In 2003, Presidential Homeland Security Directive 5 required that all emergencies be managed with the Incident Command System (ICS; visit www.fema.gov for more information). To meet this mandate, members of organized rescue teams should have an

awareness of ICS. ICS only changes how incidents are managed; it does not change how avalanche rescuers do their jobs. No matter how an incident is managed, all avalanche search and rescue operations have four key functional components that are often being organized and managed simultaneously. One component is search, the goal of which is quickly finding and extricating any buried victims. The first team dispatched to the avalanche, which is known as the immediate search team, should consist of skilled and swift-traveling rescuers that are competent not only in avalanche rescue but also in route finding and hazard evaluation. Basic search and rescue tools are transceivers, probes, shovels, avalanche rescue dogs, the RECCO system (described later in this chapter), and basic first-aid equipment. The immediate search team performs the initial search and looks for clues with the hope of making a quick find. If they have no luck, the team determines the most likely burial areas. The person who is reporting the avalanche should meet rescuers at the accident site, or the reporting person should be returned to the same vantage point from which the accident was witnessed to best guide rescuers to locate LSAs. Arriving rescuers will meet the site leader and continue the immediate search until sufficient clues can steer rescuers to positioning probe lines. The second component is emergency care to provide medical care for victims who are found. One or two small teams are dispatched with resuscitation, medical, and simple evacuation equipment. Ideally, the medical team should be sent within minutes of fielding the first search teams to ensure that necessary 51

Probing Probing avalanche debris is a simple but slow method of searching for buried victims. For more than 40 years, the traditional probe line (closed course probing) used by rescue teams was composed of about a dozen rescuers standing elbow to elbow with a probe pole that was 3 to 3.5 m (10 to 12 feet) long. The rescuers probe once between their feet, with each probe entering the snow about 75 cm (30 inches) from the neighbors on either side; the line then advances 70 cm (28 inches), and the rescuers probe again. Open course probing involves the rescuers being an arm’s length apart and probing twice (once in front of each foot) before stepping forward. The probability of detection (POD) with these methods was thought to be about 70%. If the probe line missed the victim on the first pass—which tended to happen—then the area was probed again and again. Behind the probe line, shovelers stood ready to check out any possible strike. The line did not stop in such an event but continued to march forward with a methodic “probe down, probe up, step forward” cadence. In 2004, Ballard and colleagues5 developed a computer program that simulated a human body in an avalanche and compared the POD for any probe-grid spacing. The results showed the POD for the traditional probe line to be 59% as opposed to the 70% as previously believed. At a grid spacing of less than 50 cm (20 inches), the search time increased faster than the POD. Thus, a grid spacing of 50 cm by 50 cm (20 inches by 20 inches) was optimal, yielding the best combination of POD and search time. For a three-holes-per-step probe, probers stand with their arms out, wrist to wrist. Probers first probe between their feet, and then they probe 50 cm (20 inches) to the right and 50 cm (20 inches) to the left (Figure 2-25). At a command from the leader, the line advances 50 cm (20 inches [i.e., one step]). This method gives an 88% chance of finding the victim on the first pass, with an estimated time to discovery that is nearly identical to that of traditional spacing. Ski patrols and mountain rescue teams that have adopted the three-holes-per-step style of probe with a 50 cm by 50 cm (20 inches by 20 inches) grid have noted improved efficiency and effectiveness of the probe line. Because these rescuers insert more probes per rescuer, it is possible to have fewer rescuers on a probe line, and short probe lines are easier to manage and work faster than do long probe lines. Five rescuers doing three holes per step at 50-cm intervals form a slightly longer probe line than do nine rescuers using the traditional method. To ensure proper spacing, it is most helpful to use a guidon cord with marked 50-cm intervals. Suspended between two rescuers, the lightweight guidon cord positions rescuers and probes at the correct spots, thereby allowing the

50 cm

PART 1  MOUNTAIN MEDICINE

medical and evacuation equipment reach the site in a timely fashion. The third component is transportation, which includes travel for additional rescuers to and from the accident site and for the evacuation of victims. The transportation effort must begin immediately so that rescuers and equipment can be moved efficiently and quickly. Likewise, coordination of helicopters, snow machines, and rescuers is essential to a fast and safe evacuation. The fourth component is support, which sustains the entire operation, especially when a rescue is prolonged. This support may include additional rescuers to take over for cold and tired searchers, hot food and drinks, tents, warm clothing, and lights for nighttime searching.

50 cm 50 cm

FIGURE 2-25  Three-probe spacing for 50-cm by 50-cm three-holeper-step probe method.

52

TABLE 2-2  Type of Rescue for Buried Avalanche

Victims in Direct Contact With Snow on the Basis of a Sample of 300 Burials in the United States From the Winter of 1999-2000 to the Winter of 2008-2009

Type of Rescue, 1999-2000 to 2008-2009

Found alive Found dead

Self-Rescue

Companions

11 (10%) —

84 (78%) 73 (38%)

Rescue Teams 13 (12%) 119 (62%)

Total 108 192

Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.

line to move smoothly and efficiently without interruption. When a guidon cord is not used, the probe line must be frequently stopped and reassessed to ensure proper spacing. If the victim is missed on the first pass, the second pass increases the POD to 99%. Rescue teams use probe lines to find most avalanche victims who are not equipped with transceivers or RECCO reflectors, or when an avalanche rescue dog fails to locate the victim. However, these search methods should all be used concurrently. Because probe lines are time intensive, few victims are found alive using this technique alone (Tables 2-2 and 2-3). Avalanche Rescue Dogs Trained search dogs, which are traditionally used in Europe early during avalanche rescues, are capable of locating buried victims very quickly. However, in the United States, few live rescues have occurred, because the dogs are often brought to the scene only after extended periods of burial. In the March 1982 avalanche disaster in Alpine Meadows, California, a dog made the first live recovery of an avalanche victim in the United States. Since then, dogs have made additional live recoveries. Unfortunately no live dog rescue has been reported in the last 10 years; since 1950, there have only been six reported live recoveries, with four occurring at ski areas. The number of trained certified search dogs has increased substantially. Search and rescue teams and law-enforcement agencies work closely with search-dog handlers, and trained avalanche dogs are now common fixtures at ski areas in the western United States. A trained avalanche dog moving rapidly over avalanche debris and using its sensitive nose to scan for human scent (i.e., rafts or shed dead skin cells) diffusing upward

TABLE 2-3  Method of Locating (First Contact)

Buried Avalanche Victims on the Basis of a Sample of 274 Avalanche Burials in the United States From the Winter of 1999-2000 to the Winter of 2008-2009

Method Attached object or body part Spot probe Coarse or fine probe Transceiver Avalanche dog Voice Other (e.g., digging, RECCO) Found after a long time span Not found, not recovered Inside vehicle Inside structure Total

Found Alive

Found Dead

Total

38 3 1 39 0 7 2 — — 1 1 92

18 15 40 58 30 0 8 9 3 0 1 182

56 18 41 97 30 7 10 9 3 1 2 274

Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.

CHAPTER 2  AVALANCHES

A

B

FIGURE 2-26  A, The RECCO reflector is a thin circuit card that is covered in soft plastic. It does not need batteries and does not need to be turned on or off. The reflector can be attached to jackets, pants, boots, and helmets. B, The RECCO detector consists of a transmitter and a receiver. It can also be used from a helicopter. (Courtesy RECCO AB, Sweden.)

through the snowpack can search more effectively in 30 minutes than can 20 searchers in 4 hours with the use of course probing. Dogs are not infallible, and their ability to find buried human scent may be affected by several factors, such as the length of burial, weather, snow density, and contamination of the debris field with spit, urine, cigarettes, or gasoline from snowmobiles or generators. Dogs have found bodies buried 10 m (30 feet) deep, but have also passed over persons buried only 2 m (6 feet) deep.

electronic cameras, radios, and even turned-off avalanche rescue beacons, so RECCO should be used by rescue teams together with avalanche rescue dogs, rescue beacons, and probers as part of the first response to any avalanche rescue. A detector operator can search as quickly as if he or she were using an avalanche beacon. In North America, more than 130 ski areas, mountain rescue teams, and National Parks have detectors. Worldwide, more than 600 ski resorts and helicopter rescue teams make use of them.

RECCO RECCO (www.recco.com) is an electronic rescue system that enables organized rescue teams to find victims who are equipped with reflectors (Figure 2-26). The system consists of two parts: a detector that is used by the rescue teams (either on the ground or from helicopters) and the reflector that is worn by the recreationist. About the size and weight of a notebook computer, the detector is easily transported to the accident site. The detector transmits a directional radar signal. When it hits the reflector, the signal’s frequency is doubled and reflected back to the detector, and the rescuer can follow the signal to the buried person. The reflectors are small and passive (i.e., no batteries) electronic transponders that are fitted into outerwear, ski and snowboard boots, and helmets. The system will detect some electronic equipment (with diminished range), such as cell phones,

Avalanche Guard When considering the need for an avalanche guard, if the threat of a second avalanche exists, one person should stand in a safe location to shout out a warning. This gives the searchers a few seconds to flee to the safety of a predefined escape route. Rescues are often carried out under dangerous conditions, and self-preservation should be the primary consideration.

The Avalanche Victim After reaching a 20-year low in the late 1980s, avalanche deaths in the United States soared during the 1990s (Figure 2-27) and spiked in the winter of 2007-2008 with 36 deaths, which was the highest number killed during the modern era (i.e., after 1950). Figure 2-27 also presents the 5-year moving average. After the end

Avalanche deaths (number of persons)

40 U.S. fatalities U.S. 5-year moving average

35 30 25 20 15 10 5 0 1950

1955

1960

1965

1970

1975

1980

1985

1990

1995

2000

2005

Winter season by fall and spring year 1950-1951 to 2008-2009

FIGURE 2-27  Avalanche deaths in the United States in the modern era (i.e., after 1950) by winter, by season, and showing a 5-year moving average. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)

53

PART 1  MOUNTAIN MEDICINE

Snowmobilers Backcountry skiers Climbers Out-of-bounds skiers Backcountry snowboarders Snowshoers Out-of-bounds snowboarders In-area skiers/snowboarders Hikers Hunters Residents Avalanche forecasters Roof shovelers Avalanche course students Highway workers Ski patrolers

Recreation

Nonrecreation

0

20

40

60

80

100

120

Number of fatalities

FIGURE 2-28  U.S. avalanche fatalities by activity, the winter of 1999-2000 to the winter of 2008-2009. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)

of the 1980s, the average number of fatalities per winter rose from 11 to 30, but this number decreased slightly during the mid 2000s. However, in recent years, the 5-year average has begun to edge back upward to 28 deaths per winter. As more people head into the winter backcountry, avalanches continue to be deadly. In the United States, since 1950, avalanches have claimed 854 lives, and 33% (280) of the victims died between 1999 and 2009 in 232 fatal avalanche accidents. During the prior 10 years, avalanches killed 220 people. The mean age for all victims is 33 years (median, 31 years). The average age for men is 33 years, and the average age for women is 36 years. From 1999 to 2009, nearly all avalanche victims (96%) were pursuing some form of recreation at the time of the accident. Figure 2-28 shows the activity groups of the victims. Snowmobilers constitute the largest single group of avalanche victims, primarily because snow machines with powerful engines and better tracks can climb steep avalanche-prone terrain, thereby exposing riders to greater avalanche risk. A snowmobiler can cover a much greater area in a given time than can a skier or snowboarder, which also exposes them to a greater risk of being caught in an avalanche. When the skier and snowboarder categories are combined, these riders are not far behind the snowmobilers (109 vs. 114 deaths). Backcountry and “out of bounds” skiers and snowboarders venture into areas that are not parts of a ski resort and thus not managed for avalanches in any way. The backcountry-skier category includes ski mountaineers, helicopter skiers, and snowcat skiers. Out-of-bounds skiers and snowboarders refer to those who leave the ski area boundary or enter into “closed” areas within the ski area. In-area skiers and boarders are those who are caught and killed on open terrain within the ski area boundary that is managed for avalanches. In-area avalanche fatalities are rare. However, three fatalities occurred in in-area spaces in three different states during a 2-week period of the 2008-2009 season. The slopes had been managed to mitigate avalanches, but the avalanches occurred nonetheless, and they were attributed to an extremely unstable snowpack. Among nonrecreation groups, avalanches strike houses (residents), highways (motorists and plow drivers), and workplaces (ski patrollers, avalanche forecasters, and roof shovelers). Since 1999, 14 states have registered avalanche fatalities (Figure 2-29, online); however, since 1980, avalanche deaths have also occurred in Arizona, Maine, and New Mexico. 54

STATISTICS OF AVALANCHE BURIALS The factors that affect a buried victim’s chances of survival are the length of time buried, depth of burial, clues on the surface, available rescue equipment, competence of the rescuers, presence of injury, body position, snow density, and presence and size of an air pocket. A victim who is uninjured and able to fight on the downhill ride usually has a better chance of being only partly buried, or, if completely buried, a better chance of creating an air pocket for breathing. A victim who is severely injured or rendered unconscious will more likely be rolled, flipped, and twisted during the slide. Being trapped in an avalanche is a lifeand-death struggle. Avalanches kill in two ways. First, traumatic injury may occur as the victim tumbles down the avalanche path. Trees, rocks, cliffs, and the wrenching action of snow in motion can produce blunt or penetrating trauma. Up to one-quarter of all avalanche deaths are caused by trauma, especially to the head and neck. Second, snow burial causes asphyxiation in at least three-quarters of avalanche deaths from either airway obstruction or hypercapnia and hypoxemia as a result of rebreathing expired air. A very small percentage of avalanche victims succumb to hypothermia (see Avalanche Victim Physiology and Medical Treatment After Rescue, later). A victim who is swept down in the churning maelstrom of snow has a difficult time breathing. Inhaled snow clogs the mouth and nose; if the victim is buried with the airway already blocked, asphyxiation will occur more quickly. Snow that was light and airy when a skier carved turns becomes viselike in its new form. Where the snow might have been 80% air to begin with, it might be less than 50% air after an avalanche, and it is much less permeable to airflow, thereby making it harder for the victim to breathe. Snow sets up hard and solid after an avalanche. It is almost impossible for victims to dig themselves out, even if they are buried less than a foot deep. Hard debris also makes recovery very difficult, so a sturdy shovel is essential. The pressure of the snow in a burial of several feet is sometimes so great that the victim is unable to expand the chest to draw a breath.42 Warm exhaled breath freezes on the snow around the face, eventually forming an ice lens that cuts off all airflow. This process usually takes longer to develop than do snow-clogged airways, but the result is still death by asphyxiation.

90

Alive % Dead % Survival %

80 70 60 50 40 30 20 10 0 1

2

3

4

5

6

7

Burial depth (feet) FIGURE 2-30  Percent survival versus depth of burial for U.S. avalanche fatalities and survivors in direct contact with the snow (i.e., not in a structure or vehicle) from the winter of 1999-2000 to the winter of 2008-2009. (Data from Dale Atkins and the Colorado Avalanche Information Center. http://avalanche.state.co.us/acc/accidents_stats.php.)

Statistics regarding survival are derived from a large number of avalanche burials (Figures 2-30 and 2-31). When compiling these figures, only persons who were totally buried in direct contact with the snow were included. Victims who were buried in the wreckage of buildings or in vehicles are not included, because they can be shielded from the snow in situations in which sizable air pockets may be present. Under such favorable circumstances, some victims have been able to live for days. In 1982, Anna Conrad lived for 5 days in Alpine Meadows, California, in the rubble of a demolished building; this is the longest avalanche victim survival on record in the United States. A completely buried victim has a poor chance of survival, which is related to both time and depth of burial, as shown in Figure 2-30. Survival diminishes with increasing burial depth,

Survival probability (%)

100 Swiss data 1981 to 1998 (N = 638)4 Swiss data 1981 to 1991 (N = 422)9

80 60 40 20 0 0

20 40 60 80 100 120 140 160 180 200 220 240 Time buried under avalanche (min)

FIGURE 2-31  The solid blue line indicates data from Switzerland for survival probability for completely buried avalanche victims in open areas from 1981 to 1998 (n = 638) in relation to time (minutes) buried under the snow. The median extrication time was 37 minutes. The dashed red line represents survival probability for completely buried avalanche victims in open areas (n = 422) on the basis of the Swiss data for 1981 to 1991. (Data from Falk M, Brugger H, Adler-Kastner L: Avalanche survival chances, Nature 386:21, 1994. From Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche victims, Resuscitation 51:7, 2001, with permission.)

because it takes longer to uncover a victim who is buried deeper. To date, no one in the United States who has been buried deeper than 3 m (10 feet) has been recovered alive; however, in Europe, two victims survived burials of 6 to 7 m (20 to 23 feet).45 Burial depth is important in avalanche survival, but time is the true enemy of the buried victim. Figure 2-31 shows survival probability function calculated from European data, which have become a classic demonstration of decreasing survival chances with increasing burial time. During the first 15 minutes, most people (≈90%) are found alive. At 30 minutes, an equal number are found dead and alive. After 30 minutes, more are found dead than alive, and the survival rate continues to diminish with longer burial time. Speed is essential to the search. Buried victims can live for several hours beneath the snow under favorable circumstances, and rescuers should therefore never abandon a search prematurely. A miner in Colorado who was buried by an avalanche near a mine portal was able to dig himself free using his hard hat from nearly 1.8  m (6 feet) of debris after approximately 22 hours. In 2003, two snowshoe hikers caught near Washington’s Mt. Baker survived burials of 23 and 24 hours. Such long survival times are a reminder that no rescue should be abandoned prematurely on the assumption that the victim is dead.

RESCUE STATISTICS A buried victim’s chance of survival directly relates not only to the depth and length of time of burial but also to the type of rescue. Table 2-2 shows the statistics for survival as a function of the rescuer. Buried victims rescued by companions or groups nearby have a much better chance of survival than those who are rescued by organized rescue teams. Companions can potentially rescue a victim in minutes, whereas it may take hours to mount an organized rescue. Of people who are found alive, 78% were rescued by companions, and 12% were found by an organized rescue team. Table 2-3 compares the results of rescue by different techniques. Sixty-eight percent of victims (38 of 56) buried with a body part (e.g., a hand) or an attached object (e.g., a ski tip) protruding from the snow were found alive. In most cases, this was simply good luck, but, in some cases, it was the result of actively fighting with the avalanche or of thrusting a hand upward when the avalanche stopped. Either way, this statistic shows the advantages of a shallow burial: less time required to search, shorter digging time, and the possibility of attached objects or body parts being visible on top of the debris. Of the fatalities in this category, many of the individuals were skiing or snowboarding alone with no companion present to identify the hand or ski tip and provide rescue. Organized probe lines have found more victims than any other method, but, because of the time required, most victims (88%) are recovered after they are already dead. During the past 10 years, the avalanche transceiver has been used to find more victims than any other method; it is the best method for finding the completely buried victim if it is carried and used correctly. The bad news is that the mortality rate over the last 10 years was 60% (see Table 2-3). Unfortunately most companions cannot use a transceiver fast enough to save a life. However, even in textbook rescues (i.e., the signal was quickly located and the victim is dug free in a short time), many victims did not survive. Organized probe lines are an effective way to find a buried victim, but, because this method requires many rescuers and much time, most victims (i.e., 98%) are recovered dead. Despite the sound-insulating properties of snow, seven victims who were shallowly buried were able to yell and be heard by rescuers (i.e., voice contact; see Table 2-3). These statistics point out the extreme importance of rescue skills. Organized rescue teams (e.g., ski patrollers, mountain rescuers) must be highly practiced. They must have adequate training, manpower, and equipment to perform a hasty search and probe the likely burial areas in a minimal amount of time. For backcountry rescues, the buried victim’s companions remain the best hope for survival. The need to seek outside rescue units practically ensures a body recovery mission. 55

CHAPTER 2  AVALANCHES

100

PART 1  MOUNTAIN MEDICINE

TABLE 2-4  Injuries Among Survivors of Avalanche

Accidents (Partial and Total Burials)

Total injuries Major orthopedic injuries Hypothermia requiring hospital treatment Skin and soft-tissue injuries Craniofacial injuries Chest injuries Abdominal injuries

Utah

Europe

9 (total of 91 avalanche accidents) 3 (33%) 2 (22%)

351 (total of 1447 avalanche accidents) 95 (27%) 74 (21%)

1 (11%) — 3 (33%) —

84 83 7 4

(25%) (24%) (2%) (1%)

From Grossman MD, Saffle JR, Thomas F, et al: Avalanche trauma, J Trauma 29:1705, 1989.

Avalanche Victim Physiology and Medical Treatment After Rescue AVALANCHE VICTIM MORBIDITY AND MORTALITY Asphyxiation is the most common cause of death during avalanche burial. More than 75% of avalanche deaths result from asphyxiation; less than 25% result from trauma, and very few result from hypothermia.8,25,30,31,42,45 These statistics vary with geographic location and the terrain over which the avalanche slides. Because asphyxiation is the major cause of death during avalanche burial, time to extrication is a major determinant of survival. Fully buried avalanche victims have a more than 90% chance of survival if they are extricated within 15 minutes, but this chance drops to only 30% after about 35 minutes (see Figure 2-31),11,17 thus emphasizing the need for a swift companion rescue at the avalanche site. Survival beyond 30 minutes of burial requires an air pocket for breathing. If the air pocket is large enough, avalanche victims may survive for hours and develop severe hypothermia. Traumatic injury to avalanche victims depends on the terrain over which the avalanche occurred. If the victim is carried through trees or over rock bands, then trauma is more likely and may result in death. Grossman and colleagues,25 with the use of data that included both partial and complete burials in Utah and Europe, reported that traumatic injuries occurred among 25% of survivors of avalanche accidents. The most common traumatic injuries were major orthopedic, soft-tissue, and craniofacial injuries (Table 2-4). Hohlrieder and colleagues26 reviewed the injuries of 105 avalanche victims in Austria and noted mostly no or only minor injuries (Table 2-5). They also noted a high incidence of

TABLE 2-5  Pattern of Injury Among

105 Avalanche Victims

Trauma Cerebral trauma Chest trauma: all   Chest trauma: sternum or rib fracture (n = 16)   Chest trauma: pneumothorax or hemothorax (n = 6) Spine fracture: all   Spine fracture: cervical (n = 3)   Spine fracture: thoracic (n = 1)   Spine fracture: lumbar (n = 3) Abdominal trauma Pelvic fracture Extremity trauma: all   Extremity trauma: lower-leg fracture (n = 8)   Extremity trauma: shoulder dislocation (n = 6)   Extremity trauma: femur fracture (n = 4)

Frequency (n) 2 18

7

1 1 20

From Hohlrieder M, Brugger H, Schubert HM, et al: Pattern and severity of injury in avalanche victims, High Alt Med Biol 8:56, 2007.

56

lower-leg fractures and shoulder dislocations, which were thought to be caused by the attached skis and poles causing additional mechanical leverage on the extremities. Spine fractures were found in 7% of the cohort. Johnson and colleagues29 reviewed autopsy reports from 28 avalanche deaths in Utah over a 7-year period. Among 22 avalanche victims who died from asphyxiation, one-half experienced mild or moderate traumatic brain injury, which the authors argued could cause a depressed level of consciousness and contribute to death from asphyxiation. All six of the avalanche deaths that were the result of trauma involved severe traumatic brain injury. In another review of 56 avalanche fatalities in Utah, all three deaths that were due solely to trauma involved evidence of head injury.31 Although these studies demonstrate the role of head injury in avalanches, Hohlrieder and colleagues26 noted that the only two solely traumatic deaths in their series were caused by isolated fracture and dislocation of the cervical spine. This reveals the force that an avalanche applies to the human body and the vulnerability of the cervical spine in an avalanche, because repeated hyperflexion and hyperextension can occur. In addition, it emphasizes the need for proper cervical spine stabilization during the rescue and resuscitation period. Avalanche victims can sustain virtually any trauma type to any body part during their slide. The head and neck are especially vulnerable to the enormous forces, and these areas appear to be the cause of much of the traumatic mortality during avalanche accidents.

RESPIRATORY PHYSIOLOGY OF AVALANCHE BURIAL Asphyxiation occurs during avalanche burial because inhaled snow occludes the upper airway or because expired air is rebreathed. Acute upper airway obstruction that results in asphyxiation is one of the causes of asphyxiation during the first 15 to 30 minutes of avalanche burial. Asphyxiation caused by rebreathing expired air may also occur during this time if there is no air pocket for breathing, or it may be delayed if an air pocket is present. Inspired air contains 21% oxygen and less than 0.03% carbon dioxide; expired air contains about 16% oxygen and 5% carbon dioxide. Rebreathing expired air in an enclosed space results in progressive hypoxia and hypercapnia that eventually causes death from asphyxiation. The larger the air pocket, the greater the surface area for the diffusion of expired air into the snowpack and for the diffusion of ambient air from the snowpack into the air pocket and thus a longer survival time before death occurs as a result of asphyxiation. An ice mask is formed when water in the warm, humid, expired air freezes on the snow surface in front of the face. Because this barrier is impermeable to air, it accelerates asphyxiation by preventing diffusion of expired air away from the air pocket in front of the mouth. The physiology of asphyxiation from breathing with an air pocket in the snow was demonstrated in a study by Brugger and colleagues.14 Subjects sat outside a snow mound and breathed through an air-tight mask connected by respiratory tubing to 1- or 2-L (0.9- or 1.8-quart) air pockets in the snow. The snow had a density similar to that of avalanche debris (i.e., 150 to 600  kg/m3 or 15% to 60% water). The initial fraction of inspired oxygen (FIO2) in the air pocket was 21%, and the initial fraction of inspired carbon dioxide (FICO2) was near 0%. As expired air was rebreathed in the air pocket over about 30 minutes, the FIO2 decreased to about 10% and the FICO2 increased to about 6% (Figure 2-32, online). These changes in the oxygen and carbon dioxide levels in the air pocket resulted in decreased arterial oxygen saturation as measured by a pulse oximeter and increased end-tidal partial pressure of carbon dioxide. Most subjects were not able to complete the entire 30 minutes of the study and had to stop as a result of dyspnea, hypercapnia, and hypoxia. Hypoxemia and hypercapnia occur as expired air is rebreathed. A smaller air pocket or denser snow causes the more rapid development of hypoxia and hypercapnia. Larger air pockets and less-dense snow allow for more mixing of expired air with ambient air in the snowpack and result in longer survival times before hypoxia and hypercapnia become severe enough to cause death from asphyxiation. Brugger and

MEDICAL TREATMENT AND RESUSCITATION OF AVALANCHE BURIAL VICTIMS The key points regarding assessment and treatment of an extricated avalanche burial victim are presented in an algorithm in Figure 2-34. An initial impression of the level of consciousness is made as the head is exposed and cleared of snow. Opening the airway and ensuring adequate breathing are the primary medical interventions. Every effort should be made to clear the airway of snow as soon as possible and to provide assisted ventilation if breathing is absent or ineffective. These measures should be instituted as soon as possible and not be delayed until the entire body is extricated. If traumatic injury to the spinal column is suspected or if there is evidence of head or facial trauma, then the spinal column is immobilized as the airway is opened, adequate breathing ensured, and oxygen provided. When the avalanche burial victim is unconscious, maintaining the airway may be challenging because of space limitations of the opening of the snow leading to the victim. If endotracheal intubation is required for the unconscious apneic patient who is not yet fully extricated from snow burial, then the inverse intubation technique may be required.36 With this technique, the laryngoscope is held in the right hand while straddling the victim’s body and facing the head and face. While facing the victim, insert the laryngoscope blade into the oropharynx with the right hand so that the larynx and cords can be visualized by leaning over and looking into the victim’s mouth; the endotracheal tube is then passed through the vocal cords with the left hand. After an adequate airway and breathing are established and supplemental oxygen is provided, circulation is assessed. The conscious patient is assumed to have a perfusing rhythm, and further treatment is directed at treating mild hypothermia and traumatic injuries. A patient who is found unconscious but with a pulse may have moderate or severe hypothermia and should be handled gently to avoid precipitating ventricular fibrillation. The medical treatment of this patient is focused on ensuring adequate oxygenation and ventilation, either noninvasively with a bag-valve-mask device or by endotracheal intubation if clinically indicated, and on immobilizing the spinal column for transport and treatment of any obvious signs of trauma. Intravenous access may be obtained and warmed isotonic fluids infused. Treatment of hypothermia is described later in this chapter.

Extrication from avalanche burial

CHAPTER 2  AVALANCHES

colleagues11 suggest that equilibrium may occur when FIO2 and FICO2 in an air pocket reach a plateau within a physiologically tolerable range, and the avalanche victim may then survive prolonged burial. This may occur even with small air pockets, which has been observed when extricating avalanche burial survivors of up to 2 hours’ duration. Radwin and colleagues35 demonstrated that there is sufficient ambient air in densely packed snow to permit normal oxygenation and ventilation as long as all expired air is diverted out of the snowpack. They studied subjects who were totally buried in dense snow who inhaled air directly from the snowpack (density, 300 to 680 kg/m3 or 30% to 68% water) through a two-way nonrebreathing valve attached to respiratory tubing that diverted all expired air to the snow surface. Subjects maintained normal oxygenation and ventilation for up to 90 minutes. This study demonstrated that there is sufficient air for breathing in snow with a density similar to that of avalanche debris as long as expired air is not rebreathed. This is the principle behind the AvaLung (see Avalanche Rescue Equipment, earlier), which has been designed to prolong survival during avalanche burial; Figure 2-21 describes its operation. Although the device prevents the formation of an ice mask, the expired air permeates around the buried person’s body and through the snow, and it eventually contaminates inspired air. Grissom and colleagues23 compared breathing with this device while buried in dense snow and breathing without the device but with a 500-cc (0.45-quart) air pocket in the snow. Mean burial time was 58 minutes when breathing with the device and 10 minutes when breathing with a 500-cc air pocket in the snow. Development of hypoxia and hypercapnia was significantly delayed by breathing with the device (Figure 2-33, online). The AvaLung has resulted in survival during actual avalanche burials.34

Yes

Conscious?

Treat for hypothermia I (core temperature >32° C) or hypothermia II (28 to 32° C): clear the airway, provide oxygen, dry warm insulation, hot drink containing sugar if awake, medical transport to closest appropriate facility.

No

Yes

Breathing?

Treat for hypothermia II (core temperature 28 to 32° C) or hypothermia III (24 to 28° C): clear the airway, provide oxygen, assist ventilations, consider intubation and ventilation with heated and humidified oxygen, dry warm insulation, heated IV fluid, medical transport to tertiary care facility.

No

Yes

Obvious fatal injuries?

Cease efforts

No Clear the airway, assist ventilation, provide oxygen, intubate, warm IV fluids, handle gently. Check for pulse after ventilating and oxygenating. If no pulse start CPR. Check ECG.

Rhythm asystole?

No

If rhythm is VF defibrillate once if core temperature <30° C and hold ACLS drugs until rewarmed. Treat for hypothermia III or IV as indicated below.

Yes Burial >1 hour?

No

Yes Core temperature <30° C?

No

Yes Airway patent during burial?

No

Death from asphyxiation likely. Resuscitation per ACLS protocol. Cease efforts when clinically indicated. May continue resuscitation and transport to the nearest appropriate medical facility. A K+ of greater than 12 mEq/L suggests that resuscitation may be futile and death has occurred from asphyxiation.

Yes

Treat for hypothermia III or IV (core temperature <28° C): intubation, assisted ventilation with warmed humidified oxygen, monitor ECG, CPR, warmed IV fluids, dry insulation, medical transport to a facility capable of extracorporeal rewarming. FIGURE 2-34  Assessment and medical care of extricated avalanche burial victims.

If a pulse is not present after opening the airway and ventilating the patient, cardiopulmonary resuscitation (CPR) is begun. However, before CPR is initiated, careful evaluation for the presence of a pulse should occur. Avalanche burial victims are hypothermic, which causes peripheral vasoconstriction and makes pulses difficult to palpate. In addition, moderate to severe hypothermia causes depression of respiration and bradycardia. Before initiating CPR, palpation for a pulse should be done for a period that is long enough to ensure that spontaneous circulation is not present, which may take 30 seconds or more in a wilderness setting. American Heart Association CPR guidelines 57

victims who are extricated from burials of more than 1 hour who have no signs of life but who are severely hypothermic (i.e., who have a core temperature of <30° C [86° F]) and who have a patent airway may be considered for ongoing resuscitation and transport to a medical facility that is capable of extracorporeal rewarming (Figure 2-35). Avalanche burial victims who are extricated in cardiac arrest after more than 1 hour of burial and who have an obstructed airway have most likely died from asphyxiation, and continuing resuscitation efforts until rewarming occurs is unlikely to result in survival. In a study by Locher and Walpoth,30 none of 13 avalanche victims who were found in cardiac arrest after burials of 30 to 165 minutes’ duration survived. These results suggest that cardiac arrest was the result of asphyxiation rather than hypothermia. An air pocket for breathing and a patent airway must be present for an avalanche burial victim to survive long enough to develop severe hypothermia. If an air pocket for breathing is not present or if the airway is obstructed, the avalanche victim who is extricated from snow burial in cardiac arrest has most likely died from trauma or asphyxiation. This is not meant to discourage initial attempts at resuscitation but rather to suggest that prolonged CPR may be a futile exercise. It is always warranted to initially start CPR to see if return of circulation can be achieved in a reasonable time. This is because the rescuer can never know when the avalanche burial victim went into cardiac arrest; it may have been minutes or hours before extrication. The case of an 11-year-old boy in Utah who was extricated in cardiac arrest after 40 minutes of full burial demonstrates why it is important to immediately start CPR. Return of circulation was achieved 5 minutes after the initiation of CPR, and the boy went on to full recovery. When laboratory testing equipment is available, serum potassium level can be measured and used as a prognostic indicator for avalanche burial victims in cardiac arrest.2,7,37 In an adult hypothermic avalanche burial victim in cardiac arrest, a serum potassium level of greater than 10 mmol/L may, in combination with other factors, indicate that resuscitation efforts will not be successful. If the serum potassium is greater than 12 mmol/L in an adult or a child, resuscitation efforts should be terminated.7

38.0 Extrication 37.5 Afterdrop Rewarming Temperature (° C)

PART 1  MOUNTAIN MEDICINE

suggest checking for a pulse for at most 10 seconds,1 which may not be long enough to confirm that there are no signs of life in an extricated avalanche burial victim. CPR initiated on a severely hypothermic patient who actually has a perfusing rhythm may cause ventricular fibrillation. The State of Alaska Cold Injuries Guidelines recommend checking for a pulse for 60 seconds, then providing assisted ventilations, and then checking again for another 60 seconds before starting chest compressions.43 We suggest that a defined timeline for palpating a pulse may not be appropriate for all situations and that the rescuer should take enough time to confirm that there are no signs of life before beginning chest compressions. In a pulseless avalanche burial victim, electrocardiographic monitoring should be used to assess cardiac rhythm, or, alternatively, an automatic external defibrillator may be applied. In the moderate or severely hypothermic patient in ventricular fibrillation with a core body temperature of less than 30° C (86° F), defibrillation should be performed according to published guidelines,1,2 with the caveat that, after multiple unsuccessful defibrillations, further defibrillation may be deferred until rewarming is underway as chest compressions continue. Drugs may be administered as part of advanced cardiac life support in accordance with published guidelines.2 The likelihood of the successful resuscitation of an avalanche burial victim who is in cardiac arrest at the time of extrication depends on whether cardiac arrest occurred from asphyxiation or from hypothermia. Factors that may be used to indicate the likelihood of survival in an extricated avalanche burial victim are the length of time of burial, airway patency, core temperature, and serum potassium level.2,7 For burials of less than 1 hour with a core body temperature of more than 30° C (86° F) where the airway is obstructed, resuscitation is unlikely to be successful, because death has most likely occurred as a result of asphyxiation. If the airway is patent with burial duration of less than 1 hour, there is a greater chance of successful resuscitation. Even if the airway is occluded, resuscitation should always be attempted for a limited time period if feasible for safety reasons. Avalanche

37.0

36.5

36.0

35.5

Esophageal core temperature Rectal core temperature

35.0 –60

–50

–40

–30

–20

–10

0

10

20

30

40

50

60

Time relative to extrication (min) FIGURE 2-35  Esophageal ( ; Tes) and rectal ( ; Tre) core temperatures in ° C ± standard deviation during snow burial and after extrication during passive rewarming. Time zero is relative to extrication from snow burial. At extrication from snow burial, both Tes and Tre show an afterdrop, but the afterdrop of Tes is attenuated and the Tes shows rewarming of the core as insulation is provided to the shivering subject. Tre lags behind Tes during rewarming, which represents temperature gradients from the body core to the body shell as rewarming occurs. These findings suggest that core cooling rates during avalanche burial will cause only mild hypothermia during burials of up to about 1 hour in duration, but significant afterdrop can occur among avalanche burial victims after they are extricated from snow burial. Insulation should be provided as quickly as possible. Avalanche burial victims who are awake and shivering after extrication from snow burial can be rewarmed in the field by spontaneous endogenous rewarming (i.e., providing insulation and allowing shivering to occur to rewarm the avalanche burial survivor). (From Grissom CK, Harmston CH, McAlpine JC, et al: Spontaneous endogenous rewarming of mild hypothermia after snow burial, Wilderness Environ Med 21:229, 2010.)

58

In avalanche burial victims who are extricated alive, hypothermia is the major medical problem that requires treatment.8-10 Clinical definitions of hypothermia severity correlated with core body temperature are shown in Table 2-6. As the patient is extricated from snow burial, warm dry insulation is provided during packaging, and wet clothing is removed as soon as is practical. If the patient is unconscious, moderate or severe hypothermia is suspected, and handling should be gentle to avoid precipitating ventricular fibrillation. When treatment of moderate or severe hypothermia is clinically indicated, intravenous access is obtained, and warmed (42° C [107.6° F]) isotonic fluid is infused. If the patient is unconscious, endotracheal intubation is appropriate to provide adequate oxygenation and ventilation with heated (40° to 45° C [104° to 113° F]) humidified oxygen. The goal of treating moderate to severe hypothermia before reaching the hospital is to limit temperature afterdrop during medical transport to the location at which definitive rewarming can occur. The shivering patient with mild hypothermia can rewarm in the field if dry insulation is provided.19 If the patient is conscious and alert, warm fluids that contain sugar may be given by mouth. If possible, patients with mild hypothermia should remain supine until rewarming has occurred to prevent a greater temperature afterdrop from ambulation. Optimally the severity of hypothermia is determined by a core body temperature measurement in the field, preferably with the use of an esophageal probe, but tympanic membrane sensors or rectal probes may also be used. If core body temperature cannot be measured in the field, the severity of hypothermia may be estimated with the use of Swiss hypothermia stages I through IV as determined by the clinical presentation (see Table 2-6).9 Severity of hypothermia may also be estimated from the time that the victim was buried and the average rate of core temperature cooling during burial. Grissom and colleagues22 measured core temperature cooling rate during snow burial in a controlled experiment. Among subjects who were buried in dense snow for up to 60 minutes wearing a lightweight clothing insulation system while breathing with an artificial device (i.e., the AvaLung), core body temperature cooling rate was about 1.3° C (2.3° F) per hour. Retrospective studies of core temperature on hospital arrival by Locher and Walpoth30 suggest that the average core temperature cooling rate is 3° C (5.4° F) per hour (range, 0.75° to 4.75° C [1.4° F to 8.6° F] per hour in survivors), which is greater than the 1.3° C (2.3° F) per hour that was estimated by Grissom and colleagues.24 The higher rate of cooling reported by Locher and Walpoth is based on a known time of burial and known arrival time at the hospital where core body temperature was recorded, and does not differentiate between core temperature cooling rate during snow burial and cooling rate during medical transport. Burial cooling rates are accelerated by hypercapnia that occurs during snow burial. Grissom and colleagues21 found that cooling

TABLE 2-6  Hypothermia Clinical Prehospital

Evaluation: Swiss Society of Mountain Medicine Definitions

Hypothermia I: Patient alert and shivering (core temperature ≈35-32° C [95-90° F]) Hypothermia II: Patient drowsy and not shivering (core temperature ≈32-28° C [90-82° F]) Hypothermia III: Patient unconscious (core temperature ≈28-24° C [82-75° F]) Hypothermia IV: Patient not breathing (core temperature <24° C [75° F]) Data from Brugger H, Durrer B, Adler-Kastner L: On-site triage of avalanche victims with asystole by the emergency doctor, Resuscitation 31:11, 1996; and Brugger H, Durrer B, Adler-Kastner L, et al: Field management of avalanche victims, Resuscitation 51:7, 2001.

rates measured in hypercapnic as compared with normocapnic buried subjects were 1.28° C and 0.97° C, (34.3° F and 33.7° F) respectively. In addition, minute ventilation, respiratory heat loss, total metabolic rate, and respiratory muscle metabolic rate were greater for the hypercapnic subjects. The same study group also reports that the afterdrop cooling rate increases transiently after extrication from snow burial.20 The afterdrop cooling rate accelerated fourfold for a mean of 12 minutes after extrication in subjects who were buried in snow for 60 minutes. An accelerated cooling rate during and after extrication places avalanche burial victims at greater risk for complications caused by hypothermia. Every effort should be made by rescue personnel to prevent further heat loss in avalanche burial victims starting as soon as possible during extrication from the snow. Core temperature cooling rate during avalanche burial may also be estimated from anecdotal reports of prolonged survival during avalanche burial. In one case, a 25-year-old male snowboarder with a large air pocket in front of his body survived 20 hours of avalanche burial.41 At the time of extrication, he had a tympanic core body temperature of 25.6° C (78.1° F) in snow at 5° C (23° F) and was spontaneously breathing; he had a Glasgow Coma Scale score of 8, heart rate of 35 beats/min, and a palpable pulse. Core body temperature cooling rate in this anecdotal report was about 0.6° C (1.1° F) per hour. The large air pocket probably allowed for adequate diffusion of expired air away from inspired air and prevented asphyxiation. In that same rescue, the survivor’s companion was found dead from asphyxiation after 20 hours of burial with a tympanic core body temperature of 6° C (42.8° F), which is an average core body temperature cooling rate of about 1.5° C (2.7° F) per hour. The highest reported rate of core body temperature cooling in an avalanche burial victim is 9° C per hour, which was reported for a 29-year-old male who was buried for 100 minutes and extricated alive with an epitympanic core temperature of 22° C.33 He was intubated and ventilated, but went into ventricular fibrillation during helicopter transport and was transported with ongoing CPR (except for 15 minutes during the initial helicopter evacuation from the scene to a local hospital). He was in cardiopulmonary arrest for 150 minutes before defibrillation on the fifth attempt resulted in return of spontaneous circulation after cardiopulmonary bypass rewarming. He made a full recovery. These anecdotal reports demonstrate that core body temperature cooling rates during avalanche burial may vary significantly and that survival after a long-duration avalanche burial or after cardiac arrest after extrication from avalanche burial is possible.

Summary Asphyxiation is the major cause of death during avalanche burial, and it is time dependent. Avalanche burial victims who are extricated within 15 minutes have a greater than 90% chance of survival, but this decreases to about a 30% chance of survival if they are extricated after 30 minutes, thus emphasizing the need for companion rescue with use of avalanche transceivers and shovels. Survival beyond 30 minutes of burial depends on the presence of an air pocket for breathing. The larger the size of the air pocket, the longer that survival is possible during the burial; this is because asphyxiation during avalanche burial is caused by rebreathing expired air that contains 16% oxygen and 5% carbon dioxide. A larger air pocket provides more surface area for diffusion of expired air away from an avalanche burial victim, thus allowing more ambient air from the snowpack to diffuse into the air pocket for inspiration. Opening the airway, ensuring adequate ventilation, and providing supplemental oxygen are the primary medical interventions for an extricated avalanche burial victim. If the victim is conscious, mild hypothermia is most likely, and treatment consists of proving warm, dry insulation and warm, sugar-containing liquids. Rewarming will occur through shivering. Avalanche burial victims who are not shivering have progressed to moderate or severe hypothermia and require medical transport to a hospital for definitive rewarming. Unconscious avalanche burial victims who are breathing may require endotracheal intubation for airway control and assisted ventilation, and are most likely moderately to severely hypothermic. Victims who are extricated in asystolic cardiac arrest have 59

CHAPTER 2  AVALANCHES

HYPOTHERMIA IN THE AVALANCHE BURIAL VICTIM

most likely died from asphyxiation; however if the burial time is greater than 1 hour and the core body temperature is less than 30° C (86° F), these individuals may be severely hypothermic and resuscitation efforts may be continued while they are transported to a medical facility that is capable of extracorporeal rewarming. Head and cervical spine trauma should be anticipated, although any injury pattern can occur. Many victims have no traumatic injuries.

Acknowledgments. The authors thank Betsy R. Armstrong, Richard L. Armstrong, and Knox Williams for their contributions to previous editions of this text.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 3 

Lightning Injuries MARY ANN COOPER, RONALD L. HOLLE, CHRISTOPHER J. ANDREWS, AND RYAN BLUMENTHAL

Historical Overview* Lightning has caused injuries to humans since humans evolved on Earth. It has played a major part in nearly every ancient religion and culture. Priests, some of whom were the earliest astronomers, also became proficient at weather prediction, interpreting changes in weather as omens of good or bad fortune, sometimes to the advantage of their political mentors. To this day, it continues to engender stories, perceptions, and myths and is a popular topic for the press and science and weather documentaries.114,234 Lightning was often depicted in the art of ancient cultures and religions and has long been feared as an atmospheric flash of supernatural origins. A roll seal from Akkadian times (2200 BC) portrays a goddess holding sheaves of lightning bolts in each hand. Next to her, a weather god drives a chariot and creates lightning bolts by flicking a whip at his horses, while priests offer libations. A relief found on a castle gate in northern Syria (900 BC) depicts the weather god Teshub holding a three-pronged thunderbolt (Figure 3-1, online). Beginning around 700 BC, Greek artists began to incorporate lightning symbols representing Zeus’s tool of warning or favor. Zeus, as the king of the gods, could control the weather. Early Greeks believed that lightning was his weapon and that when lightning struck Earth, it was a direct sign of Zeus’s presence or influence. The ancient Greek poet, Hesiod, called him the “cloudgatherer” and the “thunderer.” Zeus was also concerned with hospitality. If you treated a guest or stranger badly, you could outrage Zeus and not be treated so favorably (Figure 3-2). *References 72, 114, 234, 274.

FIGURE 3-2  Zeus, king of gods who hurls the lightning.

60

Because lightning was a manifestation of the gods, any spot struck by lightning was regarded as sacred. Temples often were erected at these sites, where the gods were worshipped in an attempt to appease them. Roman mythology saw lightning as more ominous than did the Greeks, with Jupiter using thunderbolts as tools of vengeance and condemnation. Romans killed by lightning strikes were considered damned by Jupiter and denied burial rituals. Several Roman emperors wore laurel wreaths or sealskin to ward off lightning strikes. Important matters of state were often decided on observations of lightning and other natural phenomena. Both Seneca and Titus Lucretius discussed lightning in their treatises on natural events, and Plutarch noted that sleeping persons, having no spirit of life, were immune to lightning strikes. The Navajo Indians of North America have a story about the hero Twins who used “the lightning that strikes straight” and “the lightning that strikes crooked” to kill several mythic beasts that were plaguing the People (Navajo) and in the process created the Grand Canyon. Bantu tribesmen in Africa believed that lightning was due to the flashing feathers of a mystic bird whose flapping wings produced the sound of thunder. Umpundulo is the name of the lightning bird-god (Figure 3-3, online). They hold that lightning has great power in their healing rituals. Even today, their medicine men go out in storms and bid lightning to strike far away. Sand paintings show the lightning bolt as a wink in the thunderbird’s eye. Lightning is associated with wind, rain, and crop growth. The art of native Australians incorporates lightning symbols, where the lightning spirit is depicted as having axes, attached to his joints, that beat together to make thunder. Lightning also played a role in Buddhist symbolism. Early statues of Buddha show him carrying a thunderbolt with arrows at each end. Although lightning is most frequently rendered as fire, it has also been represented as stone axes hurled from the heavens. In the pantheistic Hindu religion, Indra (Figure 3-4, online) was the god of heaven, lightning, rain, storms, and thunder. The Maruts used thunderbolts as weapons. The Yakuts of eastern Asia regard rounded stones found in fields hit by lightning as thunder axes and often use the powdered stones in medicines and potions. In Chinese mythology, the goddess of lightning, Tien Mu, used mirrors to direct bolts of lightning. She was one of the deities of the “Ministry of Thunderstorms” of ancient Chinese religion. Scandinavian mythology alludes to Thor (Figure 3-5, online), the thunderer, who was the foe of all demons. Thor tossed lightning bolts at his enemies, and Thursday is named for him. For the Vikings, lightning was produced by Thor as his hammer struck an anvil while riding his chariot across the clouds. Throughout early Europe, church bell ringers would make as much noise as possible, hoping to scare away the storms from

For online-only figures and videos, please go to www.expertconsult.com

Common Modern Myths, Superstitions, and Misconceptions* The Roman author Pliny noted that a man who heard thunder was safe from the lightning stroke. This implies that the person who hears the thunder is far enough away from the lightning strike to survive it, although today we know the person may still be injured. Persons so close that they cannot hear the thunder are much more likely to be injured. Persons who receive ground current are more likely to report both seeing the flash and hearing the stroke, indicating that the main stroke was some distance away. Many myths about lightning, including the notion that lightning strikes are invariably fatal, persist (Box 3-1). According to an American study of cases reported in the lightning literature since 1900, lightning strike carries a mortality rate of 30% and a morbidity rate of 70%.64 A slightly different statistical interpretation of the same data yielded a mortality figure of 20%.18 Because literature reports are usually biased toward severe or interesting cases, case reviews tend to overestimate mortality rate. In reality, mortality rate may be as low as 5% to 10%.54 Most people suspect that the major cause of death is from burns. However, the only cause of immediate death is from cardiac arrest.64 Persons who are stunned or lose consciousness without cardiopulmonary arrest are highly unlikely to die, although they may still have serious and long-term sequelae.67,74,212,232 Delayed causes of death include suicide induced by depression and disability wrought by lightning.67 Most people “have enough sense to come out of the rain” and seek shelter when storm clouds roll overhead. Unfortunately, a large number of injuries occur as the storm is approaching because people misjudge it, do not pay attention to warning signs, or want to finish one more thing before seeking shelter.66,135 Lightning may travel nearly horizontally as far as 10 miles or more in nearly any direction from a thunderstorm and seem to occur “out of a clear blue sky,” or at least when the day is still *References 66, 72, 234, 274.

sunny where the person is located. At least 10% of cloud-toground strikes occur when no rain is occurring at the time and location of the strike. The faster the storm is traveling and the more violent it is, the more likely a fatal strike will occur. Another dangerous time is at the end of a thunderstorm, when people go out to begin activities before the danger has passed. Lightning casualties have decreased dramatically in the last few decades,138,143,217 but people continue to be injured when they could easily be in safe shelters only a few feet away from where they were hit. “When thunder roars, go indoors” is the teaching mantra of the National Weather Service’s (NWS’s) Lightning Awareness Week for individuals and small groups (http://www. lightningsafety.noaa.gov).217 Although one might suppose seeing lightning is a reliable warning, this is not always the case. On the great plains of the United States, lightning may be seen up to one-hundred miles away, but in the woods of Maine, it may not be seen at all before people are in danger. Thus, seeing lightning is too variable to use reliably because it may overestimate or underestimate the risk. Thunder is a much more reliable tool for estimating distance and danger, because it is seldom audible more than 10 miles away. Unfortunately, in special cases, such as in a city, heavy traffic areas, or a noisy sports stadium, it may be less audible. The flash-to-bang method is now used less often than it was a decade ago, because of uncertainty in linking flashes to thunder, as well as confusion in how to calculate the distance. The “30-30 rule,” a modification of the flash-to-bang method, was adopted in the mid-1990s as a catchy teaching tool.27,217 The first 30 stood for counting the seconds from seeing lightning to hearing its thunder at the beginning of a storm. If the count was 30 or less, the person was in danger and should be seeking safer shelter. It soon became apparent that the recommendation should be that the person actually be in safe shelter at that point. This part of the rule was replaced by “When thunder roars, go indoors.”217 The second 30 is still useful and indicates the number of minutes at the end of the storm after seeing the last lightning or hearing the last thunder that one should wait before once again going outside and resuming activity. Although the “30-30 rule” has been abandoned for individuals, it is useful for some larger venues such as industrial sites.216,217 One of the most dangerous and consistent places of injury is standing near a tree or other tall object. Tent poles, regardless of their construction, can be a source of lightning injury. Standing in an isolated flat area (larger than 15 to 30 m [49 to 98 feet] in diameter) is a recipe for disaster. Lighting injuries may occasionally occur indoors, particularly from contact injury or side flashes from plumbing fixtures, computers, hard-wired telephones or electronic game devices, and other appliances.8,95,96 With a hard-wired phone, persons may suffer acoustic damage,17,209 neurocognitive deficits, death, or other lightning-related problems, because the phone system in most houses is not grounded to the house’s electrical system and so acts as a conduit for lightning either to come into the home or to exit from it. Cell phones, on the other hand, offer complete protection from the indoor electrical effects.* Because of the nearly universal use of cell phones, more injuries have been reported to people using them. It has been mistakenly concluded that they “attract” lightning (Figure 3-7, online). However, injury occurs because mobile phones, iPods, and similar devices distract people from paying attention to the weather, as well as other dangers, when they are outside, delaying them from seeking safe shelter, not because the devices have any effect on thunderstorms or lightning.† Although small sheds, such as hikers’ lean-tos, or sun, rain, bus, or golf shelters, may be protected or “hardened” against lightning strike under the National Fire Protection Association (NFPA) lightning codes (NFPA780), this is no guarantee of safety to persons sheltering within them.171,215,216 Personal safety is not guaranteed by structural protection. Grounding of the building is no guarantee of safety. In fact, it is likely that using these *References 3, 14, 104, 126, 127, 206, 217. † References 3, 14, 104, 126, 127, 206, 217.

61

CHAPTER 3  Lightning Injuries

holy dwellings whose steeples were struck frequently by lightning. French peasants carry a pierre de tonnerre, or lightning stone, to ward off lightning strikes. Even Santa Claus gets into the act with his reindeer Donner (thunder) and Blitzen (lightning). People in both developed and Third World countries often regard lightning and thunder with a great deal of fear as mys­ terious, uncontrollable, and unmanageable. Cambodians, for instance, believe that by doing good deeds, they can avoid lightning strikes and that people with moles on their calves are susceptible to lightning strikes, as are people who have broken promises. To resuscitate a victim, Cambodian villagers may drape the person’s body with a white cloth, or jump over it three times, or place the victim in a bed and light a fire under the bed. In South Africa, there is a belief that lightning can be “sent” to steal something, or from a traditional healer to someone else. In the Venda and Tsonga cultures of South Africa, families may petrol bomb the house of an enemy who they believed called down lightning on a relative who was struck. In Africa in the 1990s, when only the members of one soccer team were injured, it was ascribed to witchcraft on the part of the other team. Other African beliefs state that burying a hippopotamus hide 2.4 m (8 feet) under ground will protect their area. Wearing red is believed to be protective, but mirrors are felt to attract lightning, not only in Africa but in other cultures, including the United States. South Africans believe that the Syringa tree (Figure 3-6, online) attracts lightning. So strong is this belief that some farmers will cut down every Syringa tree on their farm. Even in “civilized” Western societies, lightning can take on mystical significance. When lightning struck an English cathedral just before enthronement of a controversial bishop in the late 20th century, some regarded it as an omen. Bullock,35,36 in a modern article, advances a case that the conversion of Saul on the road to Damascus was a result of a lightning strike.

PART 1  MOUNTAIN MEDICINE

BOX 3-1  The Most Common Myths and Facts No Truth • Lightning injuries are always fatal.9,15,18,64 • Lightning is spelled with an E as in “lightening.” • The cause of death from lightning injury is burns.9,15,18,64 • Burns are a major component of lightning injury.9,15,18,64 • Nothing is left of a person after a lightning strike except a pile of ashes.64,65 • Lightning victims have “entry” and “exit” points.18,65 • Lightning victims have internal burns.65 • One can predict the degree of injury from the voltage, amperage, or polarity of the strike. • Metal (on the body or not) attracts lightning. • Lightning does not hit outside the rainstorm.217 • It is safe to wait until the rain arrives to evacuate.217 • It is safe to finish the game if lightning is nearby.135,217 • As soon as the rainstorm passes and rain stops falling, it is safe to resume activity.135,217 • If you can see blue sky, lightning danger is minimal. • Lightning never strikes the same place twice. • It is safe to seek shelter and dryness under a tree.217 • Tall objects provide a 45-degree “cone of protection.” • The majority of persons injured are golfers.135,217 • Lightning injuries cannot occur inside a building. • Rubber tires (shoes, raincoats, sitting on a backpack) protect a person from lightning.217 • Cell phones, iPods, and other electronics attract lightning.* • Golf, picnic, bus, rain, beach, and other shelters are safe.171,217 • Grounding a building or shelter makes it safe for people from lightning injury.171 • Grounding a building makes it safe from structural damage.171,216,234 • Lightning victims remain electrified and dangerous to touch. • Lightning victims are easier to resuscitate than are other cardiac arrest victims.266 • If there are no outward signs of lightning injury, the damage cannot be serious.66,67 • Lightning victims usually require treatments similar to those for high-voltage electrical injuries with aggressive fluid resuscitation, alkalinization, and fasciotomies.65,71 • Lightning survivors have few permanent problems.67,74,212,232

Some Truth • Lightning always hits the highest object. • The “pointier” an object, the more likely it will be hit. True • No place outside is safe near thunderstorms.217 • It is better to be “proactive” rather than “reactive” with lightning injury avoidance.217 • The top activities and places for lightning casualties in the United States are all outdoors:217 • Near trees (or other tall object) • Open fields and elevated locations • Water-related activities (e.g., swimming, boating, fishing) • Safe shelter is a typical house or other fully enclosed and substantially constructed building with properly earthed plumbing and wiring.217 • Another safe shelter is a fully enclosed solid metal-topped vehicle such as a car or bus.217 • Open picnic, bus, golf, and rain shelters, as well as tents and other camping cover, offer absolutely no protection from lightning and may actually increase the risk for injury.171,216,217 • Having and following a lightning safety plan can decrease the number of lightning deaths and injuries.217 • There is nothing that a person can do that will substantially decrease his or her lightning injury risk if “caught” in a thunderstorm. • The lightning crouch does not significantly decrease the chance of injury or death.217,242 • Sitting on a backpack or sleeping pad does nothing to decrease an injury. • Lying flat on the ground increases injury by increasing ground current effect.72 • The primary cause of death is cardiac and respiratory arrest at the time of the injury.64 • Ninety percent of lightning victims survive, but often with disability.67 • Lightning victims are safe to touch and do not retain an electrical charge.216,217 • Automated external defibrillators (AEDs) have been useful in some resuscitations.78,158,218 • Cell phones, iPods, and other small electronic devices do not attract lightning.† • Lightning can strike the same place more than once. • Lightning has no E in it.

*References 3, 14, 104, 126, 127, 206, 217. † References 3, 14, 104, 126, 127, 191, 206, 217.

shelters can actually increase a person’s risk for injury for reasons including side flash and ground current. One should think of these shelters as capacitors with air insulation between the capacitor plates (roof and the floor). It is easy to see why someone standing inside decreases the amount of energy needed to “discharge” the capacitor and send lightning energy through the person. Similarly, sheltering within a shallow cave on a mountainside may protect from rain but may be very dangerous from a lightning standpoint. The “crispy critter” myth is the belief that someone struck by lightning bursts into flames or is reduced to a pile of ashes.59 In reality, lightning often flashes over the outside of a victim, sometimes blowing off the clothes but leaving few external signs of injury and few, if any, burns. Less than one-third of lightning survivors have any signs of burns or marks to their skin. Two other myths held by the public and many physicians are that “If you’re not killed by lightning, you’ll be OK” and “If there are no outward signs of lightning injury, the damage can’t be serious” (Box 3-2).66 Medical literature, because of lack of follow-up or longitudinal reports, implies that there are few permanent sequelae of lightning injury. Several permanent sequelae may 62

occur.* In addition, many lightning victims with significant sequelae have no evidence acutely of burns. Peripheral neuropathy, chronic pain syndromes, and neuropsychological symptoms, including severe short-term memory difficulty, difficulty processing new information, attention deficit, depression, and post-traumatic stress disorder, may be debilitating.221,229-233,235,237 A myth still prevalent is that the lightning victim retains the charge and is dangerous to touch because he or she is still “electrified.” A person does not retain a charge like a battery. This myth has led to unnecessary deaths by delayed resuscitation efforts.66 Medical literature and practice are plagued by myths that grew out of misread, misquoted, or misinterpreted data and continue to be propagated without further investigation. Not the least of these is the tenet that lightning victims who have resuscitation for several hours may still successfully recover. This belief seems to be grounded in the old idea of suspended animation—the concept that lightning is capable of shutting off systemic and cerebral metabolism, allowing rescuers a longer period in which *References 16, 62, 65, 67, 74, 212, 223, 232, 272, 280.

These apply to electrical injury as well as lightning injury. Behavior of Current in the Body • Current seeks Earth. • Current seeks the path of lowest resistance. • Nerve tissue is a good conductor, or alternatively, current is preferentially conducted by nerve tissue. • When a person touches a source of potential, current flows through the skin to other parts of the skin in contact with the same conductor (i.e., current passage is local only). The Severity of Electric Shock Myth: If the following are absent, the shock cannot be severe and no deleterious effect can result: • Being thrown (i.e., if a person is not thrown, the shock is not severe). • Burns (i.e., if burns are not present, the shock is not severe). • If the only surface change is a blister, the shock was not severe. • Entry and exit wounds • Must be present • Demonstrate the current path • If not present, indicate no shock occurred. • Fuses being blown (i.e., if a fuse does not blow, the shock is not severe enough to harm a victim). • Low voltage cannot harm. • Electroconvulsive therapy does not give long-term post– electric-shock symptoms (also false), so any other electric shock cannot be harmful. Investigations • If computed tomography (CT) and magnetic resonance imaging (MRI) scans are normal, there are no injuries. • Negative investigations (e.g., nerve conduction study, electroencephalogram, CT, MRI) mean a victim has not sustained an electric shock. • Neuropsychological testing is objective and easily interpreted. • Burns of electrical origin can be distinguished on histologic examination. Remote Symptoms • Remote symptoms do not exist. • Remote symptoms are proportional to the size of the shock. • Symptoms of the shock that are not present immediately after the shock are not related to it. • A person getting remote symptoms was psychologically vulnerable all the time. Miscellaneous • Litigation increases the potency of the claimed symptoms. Corollary: resolving litigation terminates symptoms. • Medical specialists understand electricity or lightning. • Electrical experts can predict lightning or electrical injury. • A diagnosis of depression, post-traumatic stress disorder, adjustment disorder, and so on, negate an electrical injury causation. • Residual current devices (RCDs) eliminate the possibility of all shocks. Corollary: a shock occurring when an RCD breaks the circuit cannot be severe.

to resuscitate the patient without anoxic injury. This concept, credited to Taussig,266 actually appeared some time before her article. In addition, the case recounted by Taussig that is the basis for this myth, when searched to its source, was a case report by Morikawa and Steichen.210 The case shows a somewhat longer resuscitation period than usual, but not as miraculous as reported in Taussig’s paper or as propagated in subsequent references to her paper. In a study of lightning survivors, Andrews, Colquhoun, and Darveniza13 have shown prolongation of the QT interval, bringing up the theoretic possibility of torsades de pointes as a mechanism

for the suspended animation reports. There is evidence from animal experiments to support the teaching that respiratory arrest may persist longer than does cardiac arrest.9,80,81 One study, in which Australian sheep were hit with simulated lightning strokes, showed histologic evidence of damage to the respiratory centers located beneath the fourth ventricle.9 Prolonged assisted ventilation may in some cases be successful after cardiac activity has returned, but this is obviously difficult to test in any clinical study.69,70,225 Another series of animal experiments with hairless rats has shown that it is possible to obtain the skin changes (keraunographic markings), primary and secondary cardiac arrest with prolonged respiratory arrest, and temporary lower extremity paralysis with simulated lightning strike.80,81 Several booklets listing precautions for personal lightning protection appeared in the late 1700s and early 1800s. One of the superstitions listed was that humans, by their presence, could attract lightning to a nearby object. A book of the times, Catechism of Thunderstorms, illustrated other myths. Lightning was said to follow the draft of warm air behind a horse-drawn cart, so that coachmen were cautioned to walk their horses slowly through a storm. Historically, many remedies for resuscitation of lightning victims have been offered. On July 15, 1889, Alfred West testified in a New York court that he was revived by “drawing out the electricity” when his feet were placed in warm water while his rescuer pulled on Mr. West’s toes with one hand and milked a cow with the other.29 Other early attempts at resuscitation included friction to bare skin, dousing the victim with a bucket of cold water, and chest compression. An early attempt at cardiopulmonary resuscitation was given in 1807 when mouth-to-mouth ventilation was used for lightning victims, and it was proposed that gentle electric shocks from galvanic batteries passed through the chest might be successful in resuscitating a victim of lightning.40 Before that, Benjamin Franklin110 had purposely electrocuted a chicken during a lightning experiment and reported successful, albeit temporary, resuscitation with mouth-to-beak ventilation. A myth in current treatment is that lightning injuries should be treated like other high-voltage electrical injuries. The injuries seen with lightning are very different from high-voltage injuries and should be treated differently if iatrogenic morbidity and mortality are to be avoided.15,65 “Lightning never strikes the same place twice.” In reality, the Empire State Building and the Willis Tower are hit dozens of times a year, as are mountaintops and radio-television towers. If the circumstances facilitating the original lightning strike are still in effect in an area, the laws of nature will encourage further lightning strikes.

OTHER MYTHS* • Victims may have “internal burns.” False. There may be cellular damage and certainly nervous system damage but rarely, if ever, internal burns such as those suffered with high-voltage electrical injuries. However, some physicians use this euphemism with patients to explain their pain and neurologic injuries. • Wearing a raincoat or rubber-soled shoes, sitting on a foam pad or backpack, or the like will protect a person or decrease the severity of the injury. False. If lightning has burned its way a mile or more through the air, which is an excellent insulator, it is foolish to believe that a fraction of an inch of rubber or that a few inches of any material will serve as an adequate insulator. • The rubber tires on an automobile are what protects a person from lightning injury. False. See the preceding myth. Electrical energy travels along the outside of a metal conductor (the car body) and dissipates through the rainwater to the ground or flashes off the axles or bumper of the car (Figure 3-8).

*References 66, 234.

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CHAPTER 3  Lightning Injuries

BOX 3-2  Myths Commonly Cited as Facts in Litigation

PART 1  MOUNTAIN MEDICINE

attract lightning. Tall objects tend to be made of metal, but their height, isolation, and pointiness, not their composition, are factors. • Carrying an umbrella increases the risk. The lightning “crouch” can be used to protect someone “caught” in a thunderstorm. Both false: Compared with the mile or two that lightning has already traveled to reach the person, increasing or decreasing their height by a foot or so has minor effect. • Lightning may occur without thunder. False. Whenever there is lightning, there is thunder, and vice versa. Sometimes it will appear that there is lightning without thunder because thunder is seldom heard more than 16 km (10 miles) from the lightning stroke. It can also be blocked by buildings, mountains, and noisy activities, and from perception because of distraction by mobile phones or other electronic devices. Survivors who are very close to a strike may not hear or remember the thunder.

Incidence of Injury LIGHTNING ACROSS THE UNITED STATES The distribution of lightning across the United States is well known because of the operation of real-time lightning detection networks for the past two decades.86,94 About 25 million cloudto-ground flashes occur each year in the lower 48 states.226 In addition to the strike points of the first return strokes, 45% of flashes have a subsequent return stroke that terminates at a different location on the ground.271 As a result, about 37 million ground terminations are directly impacted by cloud-to-ground lightning over the United States each year. The variability from year to year over the entire country is only a few percent due to the compensating effects of a variety of meteorologic regimes over the course of a year. On a shorter time scale, more than 50,000 flashes per hour sometimes occur on summer afternoons across the United States. Existing technology detects over 90% of all cloud-to-ground flashes within the contiguous United States.86 The most recent 11-year climatology of cloud-to-ground lightning from the National Lightning Detection Network shows that three locations along the east and west coasts of peninsular Florida have the largest density of flashes per area during the entire year (Figure 3-9). Flash density decreases northward and westward from Florida, although there are many variations that depend on the well-identified meteorologic factors of strongly heated land surfaces producing strong upward motions in the atmosphere because of coastal sea breezes during most summer afternoons. This acts on deep moisture in the lower levels of the atmosphere. Similar important features occur along the coast of the Gulf of Mexico. In the mountainous western states, strong upward atmospheric motions are produced during many summer days along with large changes in elevation.194

FIGURE 3-8  Simulated lightning in a high-voltage laboratory travels across the external metal body of the car, escaping through the axle, hubcaps, or other metal closer to ground (arrow). The Faraday cage effect of the metal body of the car protects the person from injury but does not protect the tires or wiring system of the vehicle.

• Lightning always hits the highest object. False. Lightning only “sees” objects about 30 to 50 m (98 to 164 feet) from its tip. In addition, several pictures exist of lightning hitting halfway down a flagpole or striking in a parking lot next to light poles. Someone standing in the middle of a football field will not be protected by the goalposts if lightning is coming down over his or her head. Similarly, there are many photographs of lightning branching to meet the earth in several places. • Metal attracts lightning; wearing metal increases the risk or “attracts” lightning. False. The only factors that affect where lightning will strike are the following: • Height of an object • Isolation of an object from taller objects • “Pointiness” of an object (not a factor for people) Metal objects, such as fences and bleachers, conduct electricity and lightning after they have been hit, but they do not attract lightning. Metal objects worn by the victim may heat and cause secondary injury but do nothing to

FIGURE 3-9  Cloud-to-ground flashes per square kilometer per year in the United States from a network of lightning detection sensors from 1997 to 2007. (Courtesy Vaisala, Inc, Tucson, Ariz.)

N W

E S

64

Avg flash density fl/sq km/year 14 and up 10 to 14 8 to 10 6 to 8 5 to 6 4 to 5

3 to 4 2 to 3 1 to 2 0.5 to 1 0.1 to 0.5 0+ to 0.1

CHAPTER 3  Lightning Injuries

30

–30

–180 Orbits 17,371 Areas 808,854 Flashes 4,345,364 Groups 20,727,622 Events 42,265,608 (Created: 02/15/100)

–90 <10 >10

0

90

180

>25 >50 >100 >150 >200 >300 >400 >500 >750 >1000

Flash scale April 12, 1995 – December 31, 1999

NASA/MSFC

FIGURE 3-10  Total flashes per square kilometer per year for the world from April 12, 1995, to December 31, 1999 from the Optical Transient Detector. (http://thunder.nsstc.nasa.gov/data/OTDsummaries/gifs/mission_world.gif )

LIGHTNING AROUND THE WORLD Over 60 cloud-to-ground lightning detection systems using commercial instrumentation in the very low frequency (VLF) and low frequency (LF) range have been installed in more than 45 countries on every continent except Antarctica.86 Some have operated for longer than two decades. However, the only formally published compilation of flash data from more than one country at a time is for the United States and Canada.226 The ability to detect the full horizontal and sometimes vertical extent of flashes in cloud has been developed in recent years.86,193 These cloud lightning or total lightning flashes are detected in the VHF range over regions as large as metropolitan areas. Total lightning networks detect three to five cloud flashes for every cloud-to-ground flash, although some storms have much higher ratios. The longest detected cloud flash stretched horizontally across 190 km (118 miles) over the Dallas-Fort Worth area and was connected with two cloud-to-ground flashes during its 2-second lifetime.92 Cloud flashes do not directly affect people on the ground. However, their association with cloud-to-ground flashes helps to understand the location and timing of ground strikes. No maps of total lightning have been developed to date, although there is a general view of worldwide total lightning detected by the satellite-borne Optical Transient Detector and Lightning Imaging Sensor that measure both cloud-to-ground and cloud flashes as shown in Figure 3-10.59 The highest rates of all types of lightning occur over tropical and subtropical continents. Maxima have been found in central Africa and northwest South America.2 Lightning frequencies in these areas far exceed those over Florida and the Gulf Coast. The uncertainty concerning the portion of these maxima that are cloud-to-ground flashes is being resolved by the recent deployment of the Global Lightning Dataset GLD360.93

TIME OF U.S. LIGHTNING* During the year, lightning is by far most common during summer months. Two-thirds of U.S. cloud-to-ground flashes occur in June, July, and August (Figure 3-11, online). The maximum during the warmer months of the year, especially in the southeastern states,

*References 141, 191, 194, 277.

is due primarily to daytime heating of the lower and middle levels of the atmosphere. An equally critical ingredient is the large amount of moisture in the lower and middle levels of the atmosphere that provides fuel for the daily thunderstorm cycle. The concentration of U.S. cloud-to-ground lightning in June, July, and August is present over nearly all of the United States.141 During the day, cloud-to-ground lightning is most common in the afternoon (Figure 3-12, online). Nearly one-half of all lightning occurs between noon and 18:00 local standard time (LST). Lightning is at a maximum in the afternoon because updrafts necessary for thunderstorm formation are strongest during the warmest times of the day when surface temperatures are highest, resulting in the greatest vertical instability. Other factors can extend the maximum into the evening hours, especially in the plains and southeastern states, because of outflows and other propagating features that usually originate with the afternoon convection.

U.S. LIGHTNING CASUALTIES Each month, NWS offices compile a list of damaging or notable weather phenomena that occurred in the office’s area of responsibility. These lists are combined into a monthly national report issued by the National Oceanic and Atmospheric Administration (NOAA) titled Storm Data. During the last 20 years, U.S. lightning fatalities have averaged 51 per year. Lightning deaths have equaled or exceeded those from tornadoes in 11 years and equaled or exceeded those from hurricanes in 18 of the 20 years (Figure 3-13). Flood deaths exceeded lightning fatalities during 16 of these 20 years. Males (84%) make up a much higher number of fatalities in the United States than females.87 This male majority has been found in every region of the world over the last two centuries, although some subsets can have less dominance of males than this typical value. The most common situation is for one victim to be involved in a lightning incident. The largest single death total in one U.S. event resulted from a 1963 airliner crash that killed 81, and the largest U.S. injury total was 90 at a Michigan campground. Although single-incident cases dominate the more developed countries’ data sets, very large numbers of deaths and injuries often occur in developing countries.140 Lightning-related casualties and damages are often less spectacular and more dispersed in time and space than are those from other storm phenomena. As a result, lightning deaths, 65

PART 1  MOUNTAIN MEDICINE

+

150 125 100 75 50 25 0 1989

1991

1993

1997

1995

1999

2001

2003

2005

2007 2008

Lightning Tornado Flood Hurricane FIGURE 3-13  U.S. storm-related fatalities from 1989 through 2008 from the National Oceanic and Atmospheric Administration publication Storm Data. The + sign indicates that hurricane Katrina had 1016 fatalities in 2005.

injuries, and damages have been found to be underreported in Storm Data.19,144,196,258 The following factors contribute to this underreporting: most casualties occur to one person or object at a time, Storm Data collection is not entirely consistent among offices, there are some differences in the definitions of lightning versus secondary lightning-related deaths, and there is inconsistency in listing medical diagnoses.1,19,239,258 Nonfatal injuries are underreported to a greater extent than are fatalities. A thorough search of Colorado hospital and emergency department visits found a ratio of 10 injuries to every death.53 Although this ratio of injuries to fatalities is generally applicable, there may be additional injuries that are not reported. Damage reports in Storm Data are an extremely small portion of the estimated total damages, direct or indirect, of several billion dollars per year in the United States.19,144 Despite its underreporting and sometimes incomplete nature, Storm Data has been a consistent national database for lightning impacts since 1959 and is likely the best system in the world for such information. Data drive change. It would be highly desirable for similar data to be collected and made available in many other areas of the world, both to have a baseline of damage and injuries to measure changes and to spur governments and other organizations to address injury prevention.

DISTRIBUTION OF U.S. LIGHTNING DEATHS BY STATE Lightning casualty deaths in the United States by state for the decade from 1999 to 2009 are shown in Figures 3-14 and 3-15. The general pattern is somewhat similar to the distribution of lightning in Figure 3-9. In general, there are more fatalities in the Southeast, but the more populous states also have larger totals. Note that Florida has had more than twice as many deaths as Colorado, the next state in terms of frequency. Fatality information is used for these maps, rather than injuries, because of the greater uncertainty due to injury underreporting, as mentioned previously. The lightning hazard is shown more clearly when population is taken into account in Figure 3-15. There are two maxima with this approach, one in the southeast and the other in the northern Rocky Mountain states. Most populous states, such as Illinois, no longer have high ranks. The only states in the top 10 of both lightning fatality and fatality rates are Florida, Colorado, Alabama, and South Carolina. Similar tabulations were recently made by Ashley and Gilson,19 and earlier maps for single U.S. states are listed by Curran and colleagues.87 Outside the United States, the distributions of fatalities by political boundaries have been developed for Canada,207

FATALITIES 2000-2009 0

0

2

0

7

3

1

3 9

27

8 7

66

9 3

7

27

9

11

14

10

5

10 0

24

17

11

6 11

1

5 4

13

13

4

12 4

3

Source: Storm Data Alaska: 0 Hawaii: 0 American Samoa: 1 D.C.: 0 Guam: 1 Puerto Rico: 3 Virgin Islands: 1

8

4

2 1

2 0

3

20

14

70

Rank 1-10 11-20 21-30 31-52

FIGURE 3-14  Rank and number of lightning fatalities in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)

CHAPTER 3  Lightning Injuries

FIGURE 3-15  Rank of population-weighted lightning fatality rate in each state from 2000 to 2009 from Storm Data. (Modified from Curran EB, Holle RL, López RE: Lightning casualties and damages in the United States from 1959 to 1994, J Climate 13:3448, 2000.)

FATALITY RATE 2000-2009

Source: Storm Data Ranks include 50 states, D.C., and Puerto Rico

Singapore,228 Australia,61 and France.116 Many additional studies have included national casualty totals, but not maps, over periods from several to many years.138

time series in the plains and Midwest.87 At night between 18:00 and 06:00, the relatively few fatalities occur mostly in the plains, upper Midwest and some populous eastern states, because of outflows and other propagating features that usually begin with afternoon convection. More than one-half of the deaths after midnight occurred when people were in a house set on fire by lightning,139 whereas some fatalities were campers.

TIME OF U.S. FATALITIES During the course of the year, lightning fatalities are nearly symmetric around the most frequent month of July (Figure 3-16, online). This annual casualty cycle is quite similar to the cloud-toground lightning variation by month in Figure 3-11, online. Because summer dominates the sample size, summer fatality maps are very similar to Figures 3-11 and 3-12, online for the entire year.87 On the West Coast, fatality rates are highest during autumn and winter, and these rates are also higher in the southern states than elsewhere in months other than summer. Outside the United States and away from the tropics, summer also accounts for the largest number of fatalities, such as that shown by the January peak in Australia because of the reversal of seasons from the northern hemisphere.61 In the equatorial location of Singapore, fatality maxima in November and April are similar to the annual maxima in local thunderstorms.228 During the hours of the day, most lightning fatalities occur during the afternoon (Figure 3-17, online). About two-thirds of U.S. fatalities occur between noon and 18:00 LST.87 There is a somewhat faster rise up to the maximum then a slower decrease afterward. This general cycle is very similar to cloud-to-ground lightning in Figure 3-12, online. However, there is a somewhat narrower concentration of fatalities in the afternoon in the Rockies, southeast, and northeast compared with the broader

FIGURE 3-18  Annual reported U.S. lightning fatalities from 1900 to 2007. (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)

Rank 1-10 11-20 21-30 31-52

TRENDS IN U.S. LIGHTNING FATALITIES During the early years of the 20th century, U.S. lightning deaths were much more frequent than at present (Figure 3-18). Not all states participated in lightning fatality data collection systems in the early years of the period shown in Figure 3-18. However, once all states reported, the peak was reached in 1921, when 459 lightning fatalities were reported.195 Since then, there has been a steady decline in the number of fatalities listed in Storm Data. In recent years, there have been less than 50 fatalities annually. The steady downward trend is made more noticeable by population weighting, shown in Figure 3-19. Although the U.S. population has increased greatly since 1900, the weighted rate has decreased from as high as 6 fatalities per million people per year in the early 20th century to about 0.3 in recent years. Paralleling this decrease is a shift from a mainly rural to a mostly urban population in the United States during the same years (see Figure 3-19). Other significant factors that contribute to this downward trend are improved grounding of home and building electrical and plumbing systems, ready access to fully enclosed metal-topped vehicles, improved medical treatment, and greater

500

300 200 100 0

19 00 19 07 19 14 19 21 19 28 19 35 19 42 19 49 19 56 19 63 19 70 19 77 19 84 19 91 19 98 20 05

Reported fatalities

400

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Deaths per million Percent rural

Deaths per million

6 5

70 60 50

4 3

40

2

30

1

20

0 1900

10 1920

1940

1960

1980

Percent rural to total population

7

2000

meteorologic and lightning awareness and warnings. The potential effects of changing fatality data collection rules and methods are difficult to identify but may account for some variations in all data sets. The net effect of these changes is apparent in a comparison of fatality data from the 1890s to 1990s in Figure 3-20.195 Agricultural cases have decreased from 26% to 10%, while indoor cases went from 40% to 5%. The latter may be due to the introduction of grounding into buildings, often on a farm or ranch, which has greatly reduced the lighting threat in recent years. There has been a large increase in recreational and sports incidents during that century and in the general category of outdoors, often in the yard of a dwelling and other everyday situations.

WORLDWIDE LIGHTNING FATALITIES

Lightning deaths (per million)

The weighted U.S. lightning fatality rate dropped during the 20th century by more than a factor of 10, from 6 deaths per million in some early years to under 0.3 in most recent years, as shown in Figure 3-19. Three apparently dominant factors are reduction in the rural population involved in labor-intensive agriculture, substantial grounding of most buildings where people live and work, and ready availability of fully enclosed metal-topped vehicles. Other more developed countries, such as Australia, Canada, England and Wales, France, Japan, and Sweden, have seen very similar reductions. All show current rates of less than 0.5, although some had rates exceeding 2 a century ago in areas where the lightning frequency is not as high as in the United States.138 Many people continue to participate in labor-intensive agriculture and live in ungrounded buildings in areas of the world where lightning frequency is high.163,164 The rates a century ago in the United States and other more developed countries can be considered for estimating fatalities and injuries in locations where lightning injury statistics are not readily available. Populous regions of Africa, South America, and Southeast Asia have as many as 4 billion people who are vulnerable to the lightning

Australia Canada India Japan

Agriculture

0

FIGURE 3-19  Annual lightning fatalities weighted by population ( ) from 1900 to 2007 for the United States and rural percentage ( ). (Modified from López RE, Holle RL: Changes in the number of lightning deaths in the United States during the twentieth century, J Climate 11:2070, 1998.)

10 9 8 7 6 5 4 3 2 1 0

1890s 0

25%

Indoors

25%

Outdoors

50%

75%

Recreation

100%

Small Sports structures

75%

100%

1990s FIGURE 3-20  Types of U.S. lightning fatalities from 1891 to 1894 compared with 1991 to 1994. (From Holle RL: Lightning-caused recreation deaths and injuries. Preprints, 14th Symposium on Education, January 9-13, San Diego, Cali. Boston, 2005, American Meteorological Society.)

threat, although urbanization makes it difficult to know the number of agriculturally dependent people living in unsafe structures. If the annual rate of 6 fatalities per million is used for 4 billion people, a total of 24,000 lightning deaths per year is obtained. If there are 10 injuries for every death,54 then 240,000 injuries occur per year in these areas. Holle138 lists all known published estimates of the lightning totals and converts them to fatality rates per population. Some of the countries indeed reach the rate of 6 per million per year, whereas other less developed countries have much lower rates (Figure 3-21). There is such a dearth of reliable data in regions such as Africa and Southeast Asia that it is very difficult to know whether these estimates are generally correct. However, a study of lightning casualties in and near dwellings and other buildings showed that large losses of life occur in schools, huts, and agricultural field shelters in these regions.139 Also in these countries, people spend less time inside the safety of fully enclosed metal-topped vehicles while working or traveling between school, work, and home than in more developed regions.137 Better systematic and reliable lightning fatality collection in these regions is needed to determine the validity of the global estimate of 24,000 deaths and 240,000 injuries per year from lightning.

Forensic Investigation An unwitnessed lightning event can be one of the most difficult clinical presentations to diagnose.50,111 The forensic examination of a critical lightning event can be divided into the following five stages:33,197,253,282 1. Case history 2. Scene investigation 3. Physical and/or autopsy examination 4. Special investigations 5. Collation

Singapore S. Africa U.S. Zimbabwe

1900-9 1910-9 1920-9 1930-9 1940-9 1950-9 1960-9 1970-9 1980-9 1990-9

68

50%

FIGURE 3-21  Lightning deaths per million people per year for eight countries outside Europe by decade during the 20th century. Note that the 1990s Zimbabwe value is 17.8. (From Holle RL: Annual rates of lightning fatalities by country. Preprints, International lightning detection conference, April 21-23, 2008, Tucson, Ariz., Vaisala.).

If a witness is available, it is important to ascertain the following: • Was there a storm? • Was there lightning? • Did the witness actually see the lightning strike the victim? • Was death immediate or not? • Where was the deceased at the time of the strike (e.g., under a tree, on an open golf course)? • Was any attempted resuscitation applied? • What was the activity of the deceased before death? • A meticulous description of the lightning event must be given. • How many people were involved? • Were there any survivors? If so, where are they? • What was the medical history of the deceased? Specifically, were there any cardiac problems? • A history of electrical storm activity should be ascertained from the weather service, because lightning network detection and location systems should be able to assist with the exact time and location of the strike.103

SCENE INVESTIGATION Attending a critical lightning incident is a very specialized activity that crosses many disciplines. Insurance investigators, electrical engineers, scene reconstruction experts, and/or investigating officers will be called to review the scene of a lightning strike. Signs of lightning strike on the scene can be subtle or blatant.154 Lightning scene investigation can be divided into the following: • Environmental signs of direct lightning strike • Structural signs of direct lightning strike • Trace evidence signs of direct lightning strike Environmental Signs of Direct Lightning Strike • At the scene there may be damage to nearby trees, such as splitting or removal of bark. • Arc marks may be present on the walls or nearby structures. • The ground may display a fern pattern.

A

CHAPTER 3  Lightning Injuries

CASE HISTORY

FIGURE 3-22  Damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural damage to the clubhouse. (Copyright Ian R. Jandrell.)

• Soil may show fulgurite formation—bore or tube-like structures formed in sand or rock by lightning. • Often a crater will be exposed in the earth, with rock and sand being flung far afield. Craters of up to 2 meters (6.6 feet) in diameter have been reported. • To preserve the case history for scientific purposes, a relevant academic institution or other expert in the field should if possible be advised of the incident, more specifically should there be any suggestion of litigation by a surviving party. Structural Signs of Direct Lightning Strike Jandrell and associates described the effects of direct lightning strike to housing structures in southern Africa.118,203,204 Figure 3-22 shows damage to the roof of a clubhouse from direct lightning strike. The damage was extensive and included structural and internal damage (Figure 3-23). Figure 3-24 shows damage to curtaining material covering the window. Thatched structures have been known to ignite as a result of lightning strike. Thatch is very combustible, so inhabitants are at greater risk for severe injury and burns.118,139

B

FIGURE 3-23  Damage to the ceiling (A) and internal wall (B) of the clubhouse in Figure 3-22 with resultant damage to the electrical and electronic devices connected to the electrical system. (Copyright Ian R. Jandrell.)

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PART 1  MOUNTAIN MEDICINE

Trace Evidence Signs of Direct Lightning Strike This can be very difficult to prove. Cindering on clothing or arc marks on metallic structures may be seen. In “zincification” and/ or “cuprification” metal with a lower melting point vaporizes, leaving the other metal behind. Magnetization of metallic objects has been mentioned in the literature, although current thinking is that this could possibly be a myth. Reports of metallic chains being magnetized and “sticking” to metallic postmortem trays have yet to be verified.

PHYSICAL AND/OR AUTOPSY EXAMINATION A complete postmortem examination should be performed. • The external examination should include a meticulous description of clothing and any evidence of resuscitation (Figures 3-25 and 3-26; Figure 3-25, online). • Metal objects may have burned underlying skin or may have been marked by the heat of electrical arcing. Figure 3-27 shows damage to clothing and underlying burns. Figure 3-28 shows permanent tattooing from a metal necklace burned into skin in a nonfatal injury.159

FIGURE 3-24  Damage to curtaining material covering a window of the clubhouse in Figure 3-22. (Copyright Ian R. Jandrell.)

A

B

FIGURE 3-26  Damage to the socks of a fatally injured farmer. (Copyright Mary Ann Cooper.)

A

B

FIGURE 3-27  A, Melting of synthetic clothing material from lightning damage. B, Underlying damage to skin from zipper and melted material. (Copyright Ryan Blumenthal.)

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CHAPTER 3  Lightning Injuries

A FIGURE 3-28  Metal necklace burned into skin by lightning with permanent tattooing (nonfatal injury). (Copyright Mary Ann Cooper; courtesy R. Washington.)

• Metal objects may show signs of fusing, zincification, or cuprification. Always check for magnetization. Metallic objects, such as tooth fillings, spectacles, belt, buckles, coins, and pacemakers, should be specifically described. • The type, pattern, and distribution of any cutaneous thermal injuries, including clusters of punctuate burns, blisters, or charred burns, should be noted. Figure 3-29 shows damage to a hiking shoe with underlying damage to the skin of the foot.15 • Determine if there has been rupture of tympanic membranes. Barotrauma has been cited as one of the injuring mechanisms of lightning. Pneumomediastinum has been cited in the literature.124 Burst eardrums and pneumomediastinum are signs suggestive of barotrauma. • Singed or scorched hair should be noted. • Ocular injuries, such as retinal detachment, should be determined. Cataracts may be difficult to demonstrate postmortem. • Unique arborescent or fern-like injuries (Lichtenberg figures) (Figure 3-30) should be noted. • Determine if there are lightning wounds on the bases of the feet—the “tiptoe” sign typically on the base of the foot.213 • The procedure for internal examination is identical to that for any forensic autopsy. • In female victims, ascertain whether or not the victim was pregnant, and if so, carefully examine the fetus macroscopically and microscopically for any injuries.112

SPECIAL PROCEDURES • Diagrams: Where possible, diagrams of the pattern and distribution of the lightning injury to the body should be constructed to provide graphic documentation of the nature and extent of the electrothermal injury patterns. • Photographs: Close-up and distance photographs should be taken to document all injuries. • Radiographs: Radiographic examination may be helpful. Certain fractures, dislocations, and subluxations may be missed at autopsy examination.155 Computed tomography (CT) or magnetic resonance imaging (MRI) might add to the body of knowledge that constitutes postmortem, noninvasive, and virtual analyses. Certain keraunopathologic findings, such as pneumomediastinum, may be missed at autopsy examination.124 • Histologic examination:155,159 The skin burn wounds should always be microscopically examined for signs of electrothermal injury patterns such as vacuolation in the epidermis, eosinophilia, and elongation and streaming of the nuclei of the lower epidermis. Histologic staining of the heart with hematoxylin and eosin may prove useful. The heart should also be carefully examined under the

B FIGURE 3-29  The heat from a lightning strike caused water in the wet boot to instantaneously turn to steam, exploding the boot off the foot (A) and causing burns (B). (Courtesy Sheryl Olson, RN.)

microscope for signs such as “waviness” of the myofibers,155 necrosis, and contraction bands.286 Special staining of the heart with Mallory, Weigert elastic, Movat pentachrome, acid fuchsin orange, and immunohistochemical staining with monoclonal anti–complement C9 antibodies may help in the diagnosis of myofiber breakup—an antemortem change that may be a distinct finding in electrothermal injury cases.105 Any neuropathologic condition should also be specifically investigated and commented on. • Toxicologic studies: Ethanol, recreational drugs, and carbon monoxide levels would be justified as the minimum toxicologic investigations required in such cases. From a mitigating-circumstance point of view, ethanol and recreational drugs are always important to know. Carbon monoxide levels will be valuable, especially if there is a thermal component to the injuries.

FIGURE 3-30  Lichtenberg figures in a teenager who survived. (Courtesy/copyright Mary Ann Cooper.)

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• Collection of evidence: Collect and preserve evidence or specimens, because equivocal cases may require electrical testing of equipment by an electrical expert. Nearby damaged electrical equipment should be sent to an electrical engineer for testing. Unwitnessed lightning cases are typically complex, and unusual situations may arise from time to time. The approach to all these cases should be multidisciplinary. Only by means of a careful forensic investigation, with strict adherence to guidelines, will the truth be revealed. This becomes even more important in determining whether or not a lightning strike was the cause of a later medical condition.

COLLATION If the fresh facts which come to our knowledge all fit themselves into the scheme, then our hypothesis may gradually become a solution. SHERLOCK HOLMES

The Adventures of Wisteria Lodge

Data become information, which becomes knowledge, which becomes scientific opinion. Scientific opinion depends on experience, cognitive ability, and facts. At the end of the investigation, one should collate one’s findings with the known physics and effects of lightning.234

Early Scientific Studies and Invention of the Lightning Rod* The study of electrical phenomena is often traced to the publication of Gilbert’s De Magnete in London in 1600. Experiments in France and Germany and by members of the Royal Society of London led to invention of the Leyden jar in 1745. Benjamin Franklin is generally regarded as the father of electric science and during his lifetime was known as the American Newton. The reason he was accepted into the French and English courts around the time of the American Revolution was not because he was an ambassador from America but because he was considered to be one of the foremost scientists of his time. Franklin was elected to every major scientific society at the time and received medals of honor from France and England for his scientific contributions.60,234 Before his work, it was thought that two distinct types of electric phenomena existed. Franklin’s work111 unified these two aspects and is responsible for renaming them positive and negative. He went on to prove that lightning was an electrical phenomenon and that thunderclouds are electrically charged, as demonstrated by the famous kite and key experiment.110 Because of the damage he saw to buildings, he invented the lightning rod and announced its use in 1753 in Poor Richard’s Almanack: It has pleased God in his Goodness to Mankind, at length to discover to them the Means of securing their Habitation and other Buildings from Mischief by Thunder and Lightning. The Method is this: Provide a small Iron Rod (It may be made of the Rod-iron used by the Nailers) but of such a Length, that one End being three or four Feet in the moist Ground, the other may be six or eight Feet above the highest Part of the Building. To the upper End of the Rod fasten a Foot of brass Wire the Size of a common Knitting-needle, sharpened to a fine Point; the Rod may be secured to the House by a few small Staples. If the House or Barn be long, there may be a Rod and Point at each End, and a middling Wire along the Ridge from one to the other. A House thus furnished will not be damaged by Lightning, it being attracted to the Points, and passing thro the Metal into the Ground without hurting any Thing. Vessels also, having a sharp pointed rod fix’d on the Tops of their Masts, with a Wire from the Foot of the Rod reaching down, round one of *References 60, 110, 111, 234.

72

the Shrouds, to the Water, will not be hurt by Lightning. In the 1750s and 1760s, the use of lightning rods became prevalent in the United States for the protection of buildings and ships. Some scientists in Europe urged installation of lightning rods on government buildings, churches, and other tall buildings. Religious advocates at the time, unfortunately, maintained that it would be blasphemy to install such devices on church steeples, which received “divine protection.” Some groups chose to store munitions in churches, leading on more than one occasion to significant destruction and loss of life when the buildings were struck by lightning. Part of the delay in installing lightning rods in England has been attributed to distrust of scientific theories originating in the upstart, newly independent United States. Years and numerous unsuccessful trials with English designs were required before the Franklin rod became accepted on Her Majesty’s ships and buildings.40 At one time (and still believed by some laymen today), lightning rods were theorized to diffuse electric charge, neutralizing storm clouds and averting lightning. This may have been an outgrowth of the observation of St Elmo’s fire, an aura appearing around the tip of lightning rods, noses of airplanes, and ships’ masts during a thunderstorm, caused by an electron discharge that results from the strong electromagnetic field induced around the glowing object. Properly installed lightning rods and lightning protection systems neither “diffuse” nor “attract” lightning, but rather protect a building by allowing the current from a lightning strike to be harmlessly directed through the system to the ground.34,215,217 Lightning otherwise can travel into or through the building and cause extensive damage (see Figures 3-22 to 3-24) Around the late 1800s and 1900s, it was not uncommon for charlatans to take advantage of the fear of lightning and the danger of lightning-caused fires. They drove from farm to farm, offering to “discharge” the lightning rods on buildings for a fee. The first Lightning Rod Conference was held in London in 1882. Recommendations from this conference were published that year and again in 1905. Several countries developed codes of practice for lightning protection (Germany, 1924; United States, 1929; Britain, 1943; British colonies, 1965).87 In the past decade, NFPA 780 (U.S. National Fire Protection Act) has been accepted worldwide as a reliable standard.215 Building codes and industrial standards may require particular structures to have lightning protection systems.34,215 Including a system in the initial design and construction is always easier and less expensive than modifying a completed building. Other factors to be considered include relative frequency of strikes in an area; height, construction, and design of the building; and degree of protection desired, depending on whether the building is a storage shed, house, school, hospital, or munitions factory. In instances not covered by code, a lightning protection system, despite high exposure to lightning, may not be worth the expense, such as for a mountain cabin that is seldom visited.170,216 Today the most important economic impacts from lightning include electrical utility interruption; interruptions at airports and other outdoor locations; loss or corruption of financial, security, and other databases and control systems; and down time of industrial equipment. Lightning may pose significant danger not just to individuals, but to larger groups, such as when hundreds of miners are trapped deep underground after lightning has made elevators, ventilation systems, and water pumps nonoperational.216 At home the most reliable way to protect electronic equipment is to unplug it from the wall before the arrival of a thunder­ storm. Surge protectors, which may be effective for minor household electrical surges, are seldom effective with lightning, despite manufacturers’ claims. The best source of information on lightning risk for people is the NWS Lightning Safety website (http://www.lightningsafety.noaa.gov) and for more general risk, the National Lightning Safety Institute (http:// www.lightningsafety.com).132,216,217

CHAPTER 3  Lightning Injuries

High-altitude winds

40,000

30,000

–36

Snow

–16 Snow

25,000 20,000

10,000

18

air

Freezing

W ar m

15,000

–3

32

level

Rain

46

Temperature (° F)

Altitude (feet)

35,000

–60

Ice

63

5000

A

Heavy surface rain

B

Downward leader

Return stroke

Upward streamer

C

D

E

F

FIGURE 3-31  A, Air rises and condenses into a cumulonimbus cloud. B, Typical anvil-shaped thundercloud. C, Water droplets within the cloud accumulate and layer charges. D, Stepped downward leader initiates the lightning strike. E, Positive upward streamer releases from the ground to meet the stepped leader. F, Return stroke travels back up the channel made by the stepped leader.

Physics of Lightning Stroke* LIGHTNING DISCHARGE The study of lightning discharge and formation is complex and has led to development of a separate specialization within physics and meteorology Here we describe the simplified and most common mechanisms of thundercloud formation and lightning strike. Thunderstorms can be formed by a number of methods to produce the necessary vertical updrafts. These ingredients are afternoon heating of warm moist air, large-scale upward motions (Figure 3-31, A), sea and lake breezes, lifting of deep layers of the atmosphere by mountains, and cold fronts.141,269 As warm air rises, turbulence and induced friction cause a complex redistribution of charges within the cloud (Figure 3-31, B). Although the ground temperature may be very warm to hot, thunderstorms are tall enough that their highest parts are colder than freezing. In fact, all lightning comes from clouds that have ice aloft at temperatures colder than freezing. At temperatures colder than freezing, water droplets and ice particles of several types within the cloud acquire and increase their individual charges as they interact and transfer charge. The varying sizes and shapes of the frozen snow and ice crystals, supercooled water droplets, and hail are moving vertically at different speeds because of their different fall speeds. The result is separation of charge into several layers. A large potential difference develops *Reference 230.

between layers as a result of the interaction of charged water and ice particles, updrafts that vary in time and space, and internal and external electric fields within the cloud. Lower layers of the cumulonimbus generally become negatively charged relative to the earth. The earth, which normally is negatively charged relative to the atmosphere, has a strong positive induced charge as the negatively charged thunderstorm passes overhead. The induced positive charge tends to flow as an upward current from trees, tall buildings, poles, people, or sometimes very small objects or flat open ground beneath the overhead thunderstorm cloud and may move up in upwardpropagating leaders.234 Normally the discharge of the potential difference is discouraged by the strong insulating nature of air. However, when the potential difference between charges within the clouds or between the cumulonimbus cloud and the ground becomes too strong, the molecular structure of the intervening air may break down under the influence of the electric field that has developed, and the charge is then dissipated as lightning. A downward stroke begins as a relatively weak and slow downward leader from the cloud (Figure 3-31, C ). Although the tip of the leader may be luminous, the stepped leader itself is barely discernible with the unassisted eye. Recent very high-speed video has shown this bright tip and more faint trailing leader as it travels to the ground.249,251 The leader travels at about one-third the speed of light (1 × 108 m/sec), and the potential difference between the leader’s lower tip and the earth ranges from 10 to 200 million volts. The leader ionizes a pathway that contains superheated ions, both positive and negative, and forms a plasma column of very low resistance. The leader travels in relatively short 73

PART 1  MOUNTAIN MEDICINE

branched steps downward about 50 m (164 feet), and then retreats upward. The next time the leader goes downward toward the ground, it fills the original ionized path but branches at the end to go down another 50 m (164 feet) and then retreats again. This up-and-down multiple-branching process continues until the leader comes to within 30 to 50 m (98 to 164 feet) of the ground. Because lightning follows this ionized path, its lower tip only can sense the existence of nearby objects within a radius of about 30 to 50 m (98 to 164 feet), meaning that lightning will not be affected by the existence of a hill or tower farther away. For human safety, being within 50 m (164 feet) of the lowest tip of a cloud-to-ground lightning flash as it comes to ground is very unsafe.

DIAMETER AND TEMPERATURE OF LIGHTNING* Although many techniques have been used to measure the diameter and temperature of lightning, all measurement techniques have artifact problems. Visual measurements of the lightning stroke using standard photography usually show the diameter of the main body of the stroke to be about 2 to 3 cm (0.8 to 1.2 inches). The diameter of the channel is sometimes measured indirectly, using measurements of holes and strips of damage that lightning produces when it hits aircraft wings, buildings, or trees. Measurements vary from 0.003 to 8 cm (0.001 to 3.15 inches), depending on the material that was destroyed. Hard metallic structures sustain smaller punctures than relatively softer objects such as trees. The ionized sheath around the tip of the bright leader stroke has not been measured but is estimated to have a diameter of 3 to 20 m (9.8 to 6.6 feet). The temperature of the lightning stroke varies with the diameter of the stroke and has been calculated to be about 8000° C (14,400° F). Other estimates of the temperature are as high as 50,000° C (90,000° F). After a few milliseconds the temperature falls to 2000° to 3000° C (3600° to 5400° F), similar to the temperature of a high-voltage electric arc.

FORMS OF LIGHTNING Lightning can be divided into cloud-to-ground and cloud (intracloud) flashes (Figure 3-32). Cloud-to-ground flashes contain one or more return strokes. The flickering often seen in a cloudto-ground flash is due to the return strokes, which average three to four per flash. Cloud-to-ground flashes contact the surface of the earth at one or more locations, because one of the subsequent return strokes often takes a different path to the surface, *Reference 230.

FIGURE 3-32  Cloud-to-ground flash (right) and cloud flash (center). (Copyright Ronald L. Holle.)

74

up to a few kilometers from the first return stroke; the average is 1.47 ground contact points per flash.262 The term total lightning describes the sum of cloud-to-ground and cloud flashes. An extremely small portion (less than 0.01 of 1%) of all lightning travels from ground to cloud, when this is induced by the special circumstances of high towers or mountains. Cloud flashes can travel between clouds, within clouds, from cloud to cloud, and in all combinations of these paths. The same flash can simultaneously strike ground at one or more locations and travel a long distance in cloud (see Figure 3-32). There are several times as many cloud flashes as those that reach the ground. Cloud flashes have been measured to exceed 190 km (118 miles) in horizontal length and last up to 2 seconds.92 From the point of view of a person on the ground, cloud flashes may appear to travel in long streaks across the sky, or the channels may be obscured and visible only by the brightening within clouds along their paths. Such cloud flashes are seen more often in regions with low cloud bases in humid areas. This effect was one of the reasons for the phenomenon to be originally called “lightening.” The most unusual and least understood type of lightning is ball lightning. It is usually described as an orange, blue, or white globe between the size of a softball and a basketball. It has been observed to enter planes, ships, or houses and travel down narrow spaces such as hallways. Ball lightning very infrequently injures people and objects and often exits through a door, chimney, or window.257 It may explode with a loud bang or exhibit other bizarre behavior. Cloud-to-ground lightning flashes usually lower negative charge to the ground.234 The less frequent (5% to 10%) positive cloud-to-ground flashes tend to occur during the winter, at the end of thunderstorms, on the U.S. high plains, and in relatively shallow thunderstorms. Positive flashes usually have one return stroke. It is not known if positive cloud-to-ground flashes cause a different injury profile, although they have a tendency to have long continuing current that may impart more energy to a person than do the usually shorter-pulsing negative cloud-to-ground flashes.

THUNDER Thunder is formed when shock waves result from the almost explosive expansion of air heated and ionized by the lightning channel. Understanding some basic features of thunder is important because of its usefulness in many lightning safety recommendations.114,217 The following are accepted features of thunder: • Cloud-to-ground lightning flashes produce the loudest thunder. • Thunder is seldom heard more than 16 km (10 miles) away, except under extremely quiet conditions. • The time interval between the perception of lightning and the first sound of thunder can be used to estimate the distance from the lightning channel, at a rate of 3 sec/km (5 sec/mile). • Wind, rain, man-made noise such as traffic, and vegetation, as well as intervening buildings, hills, and mountains, reduce the audibility of thunder. • The pitch of thunder deepens as the rumble persists, because only lower frequency sounds remain at greater distances. • Atmospheric turbulence reduces the audibility of thunder. The thunderclap from a close lightning flash is heard as a sharp crack. Distant thunder rumbles as the sound waves are refracted and modified by the thunderstorm’s turbulence.269 Because there is a large difference between the speed of light and the speed of sound, the distance to lightning can be estimated by a person on the ground. The estimation is made by the flash-to-bang method of counting the seconds between seeing a flash and hearing thunder from the same flash, when the two can be matched. The time interval between lightning and thunder is 3 sec/km (5 sec/mile). For example, if the difference is 30 seconds between when a flash is seen until its thunder is heard, the flash is 10 km (6.2 miles) away. This time interval is part of the basis for the 30-30 rule described in Precautions for Avoiding Lightning Injury.

BOX 3-3  Mechanisms of Lightning Injury

CONCEPTS IN ELECTRICAL MECHANISMS— DIFFERENCES BETWEEN LIGHTNING AND INDUSTRIAL ELECTRICITY

Electrothermal Effects 1. Direct strike 2. Contact potential 3. Side flash, sometimes called “splash” (1 to 3 may include surface arcs over the body surface) 4. Step voltage (also termed “Earth potential rise” or “ground current”) a. Transmitted through the ground b. Surface arcing 5. Upward streamer current1,53 (also called “fifth mechanism”)

A voltage can be applied to a body. It can be regarded as the pressure applied to a body to force it to conduct electric current, like water pressure applied at one end of a pipe to cause water flow. It is an external force, and after it is applied, a current (measured in amperes) flows through the conductor (i.e., body), like water in the pipe. The amount of current is inversely proportional to the resistance of the body. That is, for a given applied voltage, the higher the resistance of the body, the smaller the resulting current. For technical or generated electrical injuries, the voltage is externally selected, and the resistance of a body is a given. The current is the result. Resistance is a given property of a body. A piece of metal has a predictable and exact resistance, for our purposes invariable. It might be thought of as analogous to the diameter of the water pipe, or friction within the pipe. It is the property that determines how easy it is to force current through the body. Resistances of various tissues have been measured and characterized as properties. If it is assumed that resistance is predictable, then resistance, voltage, and current can be linearly related, making modeling, and therefore prediction, possible. Voltage, current, and resistance are related by Ohm’s law (Voltage = Resistance × Current). However, tissue resistance is not constant but affected by a number of factors that do not depart from principles of linear analysis. Alterations in tissue resistance are predictable, so analysis can proceed on a “piecewise linear” basis. Unlike generated electricity that is voltage driven, lightning is a “current” phenomenon. If a current is forced to flow through a body of a given resistance, as is the case with lightning, a voltage directly proportional to the resistance of the body can be measured across the body. That is, for a given current forced through a body, the higher its resistance, the higher will be the measured voltage. The relationship is, once again, governed by Ohm’s law. The terms voltage and potential tend to be used interchangeably. In the case of lightning, current and resistance are the external variables. The resulting voltage is derived. The remaining concept is that of an electric field. When a voltage is applied to a distance (for instance, the “gap” between a cloud and the ground), an electric field results. Air generally has a high resistance and is a very good insulator, conducting very little current under normal circumstances. The electric field is defined as the voltage across the gap divided by the width of the gap. If the magnitude of the field is increased, it reaches a size where the intervening insulator will “break down.” Before this point, a degree of current will be conducted under the influence of the field. After this point, entirely new processes come into play, causing the physical structure of the conducting medium to be disrupted, resulting in an avalanche of current—“breakdown.” The actual moment that this event occurs varies with the voltage applied and the width of the gap. The voltage that is necessary to flash over an air gap is about 4000 V/cm (10,000 V/inch), depending on humidity and other factors, and is also referred to as the “dielectric” constant of air. A large noisy flashover (thunder) may be observed if the gap is sufficiently large. By definition, fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured by an electric field, explaining why lightning injury is a primarily a neurologic injury rather than a burn injury as one might otherwise expect from the high voltages associated with lightning.

CHAPTER 3  Lightning Injuries

Mechanisms of Injury by Lightning*

Blunt Force Trauma Effects 6. Barotrauma 7. Concussive injury 8. Musculoskeletal injury from muscle contraction, falls

Lightning is dangerous to humans because of the effects caused by electricity, heat, and concussive force. In addition, lightning may injure indirectly via forest fires, house fires, explosions, or falling objects. Only injuries directly caused by lightning are

discussed here. The later discussion on pathophysiology states that when lightning current is injected into an individual, the current is initially transmitted directly through the individual. Then, as internal structures (capacitances) charge, flashover occurs over the surface of the individual, and internal current reduces dramatically.225 Lightning current may initially be inflicted on a person in one of several ways, described in more detail later (Box 3-3 and Figure 3-33). In each of these mechanisms, the following processes can occur:169 1. The internal current phase may be the most causative for development of cardiac and respiratory arrest, particularly if the pathway directly includes the heart. 2. As the body’s electric potential builds up in response to the internal current, it produces an electric field over the surface of the body. At a certain level (about one-half the air breakdown field of 4000 V/cm [10,000 V/inch]), current can emerge or escape the body at various points on the body’s surface. Because of the very fast rise time and high current associated with lightning, this occurs after only a few microseconds. In wood, current travels over the surface of wood or internally to it, but not both.89 The consistency and resistance of wood are much closer to the human body than one would initially expect. Metal pieces inserted into wood enhanced “swapping” from internal to external flow. It is unknown if metal pieces on the body may trigger, enhance, or reroute surface discharges and flashovers. However, there is no evidence that metal “attracts” a lightning attachment, regardless of where it may be on or near the body, including whether one is using a mobile phone or other personal digital device* 3. As the current continues to increase, the surface flashover bridges the strike point and the ground. At this level, most of the lightning current flows as an arc current through the air outside the body (flashover effect). Only a very tiny fraction flows through the body at this point and may be too little to cause cardiac and respiratory arrest. A direct strike occurs when the lightning stroke attaches directly to the victim (see Figure 3-33, A). This is most likely in the open when a person has been unable to find a more safe location and probably occurs no more often than in 3% to 5% of injuries. Even though it seems intuitive that direct strike might be the most likely to cause fatalities, there are no studies on the relative fatality rate for each strike mechanism. This low rate of occurrence is estimated on the basis of the examination of thousands of cases by the authors (Figure 3-34).77 Contact, or touch potential, injury occurs when the person is touching or holding onto an object to which lightning attaches. A voltage gradient is set up on that object from strike point to ground, and the individual in contact with the object is subject

*References 4, 6, 7, 15, 25, 43, 53, 68-73, 77.

*References 3, 14, 104, 126, 127, 206, 217.

MECHANISMS OF INJURY

75

PART 1  MOUNTAIN MEDICINE

Contact voltage

Side flash

A

Direct strike

B

C

Upward streamer Ground current

D2

Step voltage

Step voltage

D1 D3

E

FIGURE 3-33  Illustrations of mechanisms of injury. A, Direct. B, Contact. C, Side splash/flash. D1, Ground current through the earth. D2, Ground arcing. D3, Ground arcing cave. E, Upward streamer.

76

Upward streamer 10–15% Side splash/flash 30–35%

Ground current 50–55%

FIGURE 3-34  This chart shows the frequencies of primary lightning fatality mechanisms. (From Cooper MA, Holle RL: Mechanisms of lightning injury should affect lightning safety messages, 2010, University of Illinois at Chicago.)

to the voltage between his or her contact point and the earth (see Figure 3-33, B). A current therefore flows through them. Contact injury probably occurs in about 3% to 5% of injuries. A more frequent cause of injury, perhaps as much as 30% to 35%, is a side flash, also termed “splash.” Side flashes occur when lightning that has hit an object such as a tree or building travels partly down that object before a portion “jumps” to a nearby victim (see Figure 3-33, C). Standing under or close to trees and other tall objects is a very common way in which people are splashed and is the reason safety instructions stress keeping away from trees or other tall or overhanging objects. Current divides itself between the two paths in inverse proportion to their resistances. The resistance of the “jump” path represents an additional path separate from the path to the earth through the originally stricken object. Side flash may also occur from person to person. Earth potential rise (EPR) occurs because the earth, modeled ideally as a perfect conductor, is not so in reality. When lightning current is injected into the earth, it travels through the earth just as it would in any other conductor. Earth has a finite resistance, and so voltages are set up in the ground, decreasing in size with distance from the strike point. The voltage (or potential) of the earth is raised, hence the term EPR. EPR may account for 50% or more of lightning injuries. There are several consequences of EPR. If a person is standing in an area where EPR is active, that is, near the base of a strike, a voltage will appear between their feet and current will flow via the legs into the lower part of the body. This is more significant between the front and back legs of animals, where the path may involve the heart (see Figure 3-33, Dl and D2). A special case occurs on those relatively rare occasions when a person is injured inside a building as lightning hits nearby and is transmitted through the land line of the telephone, pipes of plumbing and faucet handles, or electrical wiring as one uses a computer or attempts to dispatch an ambulance.8,16,95 This is caused, for example, when the person, along with the environment around the person, is raised in potential via EPR. If the telephone line is not locally earthed (grounded), it is at the same voltage as the environment. The fact that the line is earthed remotely away from the local EPR environment causes the person to be subjected to a shock with current flowing between the local Earth at high potential and the distant unaffected Earth. This highlights that local electrical apparatus, including telephones, should be well grounded locally. The grounds of all local structures (power, telephone, plumbing, structural steel) should have a common grounding point (i.e., be bonded) to eliminate any voltage differences developing between separated ground points for each system. For the special case of indoor or telephone

injury, EPR may account for 80% or more of the injuries. It should be noted that all of these refer to hard-wired phones. Cell phones, not being hard wired or distantly grounded, provide no connection or EPR effect to a person during a lightning strike. Static electrical discharges may occur when a person reaches for a car door or stands close to a metal window or door frame in a thunderstorm, because the surrounding electric field induces static electrical charges. These are not lightning injuries. Although people may be startled when this happens, these discharges are unlikely to be any more dangerous than static discharges experienced in the winter months from shuffling across the carpet and reaching for a door handle. Kitagawa and colleagues169 have identified further subdivisions of the EPR phenomenon. They note that not only can EPR occur as discussed, but it can also occur in a manner similar to the surface flashes over a body, with arcs developing over a ground surface (Figure 3-35). Despite modeling that assumes the contrary for mathematical reasons, the grounding Earth is not homogeneous and provides arc generation points. Ground current effects are possibly more likely to be temporary and less likely to produce fatalities. However, multiple victims and injuries are frequent. Large groups have been injured on baseball fields, at racetracks, while hiking, and during military maneuvers.40,41,188 Shocks via telephones can produce significant long-term problems, and the majority of these are via EPR.16,95,212 Irregularities occur on mountainsides. If the terrain is markedly irregular, spreading lightning current may reach the surface. A surface arc discharge may develop together with flow of the conduction current in the ground. Because arcs carry considerable energy, a person exposed to a surface arc discharge is more likely to have a more severe effect, including thermal injuries, temporary

A

B FIGURE 3-35  A, Lightning injury and ground current effect to a golfing green—photographed a few days after the strike when the grass had died. B, Laboratory lightning onto a pool surface.

77

CHAPTER 3  Lightning Injuries

Contact Direct Blunt injury strike injury 3–5% 3–5% ?

PART 1  MOUNTAIN MEDICINE

FIGURE 3-36  Example of contact injury.

paralysis, or even death. This mechanism of injury makes it particularly dangerous for someone on a mountainside to shelter inside a shallow cave or under a small cliff or outcropping of terrain where surface arcing is much more likely to occur, injuring the person just as they feel some degree of safety has been achieved (see Figure 3-33, D3). All these factors point to the danger of being anywhere outside in the presence of lightning. The danger of upward streamers has been documented.4,41,68 Injury may occur when a victim serves as the conduit for one of the usually multiple upward leaders induced by a downward stepped leader and its field (see Figure 3-33, E). Streamers occur even when there is no attachment between them and the stepped leader. Although one might think that these are weak in energy compared with the full lightning strike, they may carry several hundred amperes of current to be transmitted through the victim. Upward streamer injury is probably a much underestimated mechanism of injury and may account for as much as 10% to 15% of injury cases, but needs substantial additional study and documentation. Finally, persons may suffer from (nonelectrical) blunt injury, either by being close to the concussive force of the shock wave produced as lightning strikes nearby or if ground current or some other mechanism induces an opisthotonic contraction. Victims have been witnessed to have been thrown tens of yards by either mechanism. In addition, some have theorized that a person struck by lightning may suffer from explosive and implosive forces created by the thunderclap, with resulting contusions and pressure injuries, including tympanic membrane rupture (barotrauma—see Lightning Explosive Barotrauma, later). Another mechanism of blunt injury is blast injury resulting from vaporization of water on the body surface from a surface flashover spark. Lightning blast injury to the skull, brain, and viscera has been elegantly demonstrated in animals.224 Many cases of multiple injuries are likely a combination of many of these effects, with the majority of them from EPR and upward streamers, sometimes complicated by side flashes if people or animals are standing too close together (Figures 3-36 and 3-37).

medical literature. Figure 3-38 shows 20 kV applied to a 1.8-m (6-foot) man, causing current to ground. This produces an internal electric field strength of approximately 10 kV/m. When a child chews on an electric cord and suffers a lip burn, the field strength is approximately the same: 110 V applied to 1 cm of a child’s lip generates a field strength of 11 kV/m. Even though no one would classify the child’s injury as “high” voltage, it is a high electric field strength and produces the same tissue destruction in a small localized area, much as would a high-voltage injury. Electric fields operate over a space. The longer or wider the space, the more effect. Because nerves are by far the longest cells in the body, they are preferentially injured, explaining why lightning injury is a primarily a neurologic injury. Although Lee184 has discussed the importance of internal electric field calculations in describing electroporation damage, this has not been studied for lightning injury. A similar inconsistency involves the breakdown strength of air (the force needed to cause a spark of electricity to cross a gap), which is roughly 4000 V/cm, or 10,000 V/inch. Most people are familiar with the shock experienced from walking across a carpet in the winter, although few appreciate this phenomenon would be classified as “high-voltage” injury by the 500- to 1000-V criterion used in medical literature. Thus terms used in the medical literature to categorize electrical injuries, such as high versus low voltage and exit versus entry in alternating current injuries, as well as the simplistic application of Kouwenhoven’s six factors, do not reflect either medical or engineering reality and are poor predictors of injury.

LIGHTNING INJURY PHYSICS It is necessary to distinguish between lightning and generatorproduced high-voltage electrical injuries, in that there are significant differences between the mechanisms of injuries and their treatment.65 Although lightning is an electrical phenomenon and is governed by the laws of physics, it accounts for a unique spectrum of induced signs and symptoms that are best understood relative to specific physical properties of lightning.

FREQUENCY, VOLTAGE, AMPERAGE, AND RESISTANCE Lightning is neither a direct nor an alternating current. At best description, lightning is a unidirectional massive current impulse. The cloud-to-ground impulse results from breakdown of a large electric field between cloud and ground, measured in millions of volts. Once connection is made with the ground, the voltage difference between cloud and ground disappears and a large current flows impulsively in a very short time. The study of massive electrical discharges of such short duration, particularly

Pathophysiology of Lightning Injury* ELECTRICAL INJURY PHYSICS REVISITED Kouwenhoven determined six factors that affect the type and severity of injury encountered with electrical accidents: frequency, duration of exposure, voltage, amperage, resistance of the tissues, and pathway of the current. However, several inconsistencies appear when these are applied too literally. Electric field strength, not listed as one of the factors, is a more useful and accurate concept in explaining and predicting injuries from technical or man-made electricity than are the classic Kouwenhoven factors that have traditionally been cited in the

*References 15, 64, 72, 153.

78

FIGURE 3-37  Example of side flash or “splash.”

Energy ( heat ) = Current 2 × Resistance × Time

20 kV

6 feet

= Electric field approx. 10 kV/m 20 kV 2m

A

= 10 kV/m

PATHWAY, DURATION OF CURRENT, FLASHOVER EFFECT, AND TIME

110 V

1 cm

1 cm = 11 kV/m

B

where a current flows through a resistance for a time T. As resistance goes up, so does the heat generated by passage of the same current. In humans, when low energy levels are encountered, much of the electric energy may be dissipated by the skin, so that superficial burns are often not accompanied by internal injuries. Although lightning occasionally creates what appear to be discrete entry and exit wounds, these are rare. Lightning more commonly causes only superficial streaking burns. Burns are discussed later and are a most important distinction between lightning and technical electric shocks. The exception to this is when there occurs long continuing current. This is a prolonged stroke lasting up to 0.5 second that delivers a tremendous amount of energy, capable of exploding trees and setting fires. Other poorly understood factors may contribute to the formation of deep burns, although deep burns similar to those of high-voltage electrical injuries generally are quite rare with lightning.

110 v/1 cm = 11 kV/m

C FIGURE 3-38  A, If 20 kV is applied to a 1.8-m (6-foot) man source to ground, an electric field strength of approximately 10 kV/m is produced. B, When a child chews on the end of an extension cord, the applied voltage of 110 V across 1 cm produces an electric field strength of 11 kV/m—higher than the classic “high-voltage” injury.  C, This explains the deep full-thickness burns the child receives, which one would not predict given the “low-voltage” source.

It takes a finite amount of time for the skin to break down when exposed to heat or energy. Generally lightning is not present long enough to cause this skin breakdown. Probably a large portion travels along the outside of the skin as “flashover.” There is some experimental evidence that a portion of the current may enter the cranial orifices—the eyes, ears, nose, and mouth.10 This pathway would help explain the myriad eye and ear symptoms that have been reported with lightning injury. Andrews further examined the functional consequences of lightning on cardiorespiratory function and concluded that entry of current into cranial orifices leads to passage of current directly to the brainstem. In a sheep study, he was able to demonstrate specific damage to neurons at the floor of the fourth ventricle in the location of the medullary respiratory control centers. It is postulated that current travels via cerebrospinal fluid (CSF) and blood vessel pathways to impinge directly on the myocardium. Andrews also showed histologic damage to the myocardium, consistent with a number of autopsy reports of inferior myocardial necrosis.9,17 An alternative hypothesis can be tested with mathematical modeling.15 Certain assumptions are made in any model, usually based on principles accepted in the literature.31 Figure 3-39, A shows a model for skin resistance, and its connection to the internal body milieu is shown in Figure 3-39, B. Note that the internal body structures are regarded as purely resistive, whereas the skin contains significant elements of capacitance.31 In the model, the sequence of events during the strike starts with the postulate that the stroke attached initially to the head of the victim. From our knowledge now that “direct strike” occurs in probably only 3% to 5% of lightning injuries, it seems that this is an uncommon point of attachment, but the model is still useful in illustrating lightning energy flow. For a small fraction of time, current flows internally as the skin capacitance elements become charged. At a voltage taken as 5 kV, the skin was assumed to break down. (A lightning stroke is modeled as a current wave, building to a maximum value in around 8 msec, although this may be “modulated lightning,” that is, lightning that has passed through other structures, such as wiring. Others have measured the rise time of direct lightning as 1.2 to 1.5 msec.) Once the internal current increased, the voltage across the body to the earth built up, and external flashover across the body occurred when the field reached the breakdown strength of air. 79

CHAPTER 3  Lightning Injuries

their effects on the human body, is not well advanced. Lightning is said to be a “current” phenomenon rather than a “voltage” phenomenon. Examining the particular voltage in these equations becomes difficult because the voltage between cloud and ground disappears after lightning attachment, and equations such as Ohm’s law (V = I × R) and power calculation (P = V × I) cannot be accurately applied. Thus we must resort to alternative formulations of the equations. The energy dissipated in a given tissue is determined by the current flowing through the tissue and its resistance by:

PART 1  MOUNTAIN MEDICINE

10 k

0.25 µ 10 k

10 kΩ

200 0.25 µF

200 0.25 µ

Key

A

300

300

10 k

0.25 µ

300

10 k

0.25 µ

B FIGURE 3-39  A, Electrical model for human skin impedance. B, Model of human body for the purpose of examining current flow during lightning strike.

The results of mathematical modeling of these events are shown in Figure 3-40, and the relative magnitudes of the various voltage components can be seen with their time scale. On this time scale, the times to breakdown are short and most events occur early in the course of the stroke. In summary, in this model, lightning applies a current to the human body. This current initially is transmitted internally, following which skin breaks down. Ultimately, external flashover occurs. Andrews9 draws support for this model from measurements made in the experimental application of lightning impulses to sheep. Further modeling of step voltage injury verified that, for the erect human, this mechanism is less dangerous than is a direct strike, although this has not been corroborated in clinical studies.169 Experimental evidence suggests that “a fast flashover appreciably diminishes the energy dissipation within the body and results in survival.”225 In addition, Ishikawa obtained experimental results with rabbits similar to the human data found by Cooper’s study.64,153 Cooper has carried her studies to animals in developing a model of lightning injury and has successfully shown primary cardiac arrhythmias, prolonged ventilatory arrest, secondary cardiac arrest, keraunographic skin changes, and temporary lower extremity paralysis.80-82 As current flashes over the outside of the body, it may vaporize moisture on the skin and blast apart clothes and shoes, leaving the victim nearly naked, as noted by Hegner128 in 1917: The clothing may not be affected in any way. It may be stripped or burned in part or entirely shredded to ribbons. Either warp or woof may be destroyed leaving the outer garments and the skin intact.… Metallic objects in or on the clothing are bent, broken, more or less fused or not affected. The shoes most constantly show the effects of the current. People are usually standing when struck, the current then enters or leaves the body through the feet. The shoes, especially when dry or only partially damp, interpose a substance of increased resistance. One or both shoes may be affected. They may be gently removed, or violently thrown many feet, be punctured or have a large hole torn in any part, shredded, split, reduced to lint or disappear entirely. 80

The soles may disappear with or without the heels. Any of the foregoing may occur and the person not injured or only slightly shocked. The amount of damage to clothing or the surface of the body is not an index to the severity of injuries sustained within a human. Either may be disproportionately great or small. However, in unwitnessed situations, Cooper and others have found that forensic evidence of damage to shoes and clothing may be the most important and reliable indicator in determining whether lightning caused a person’s death, in addition to ruptured tympanic membrane when no other cause is apparent.32,162,279 The factor that seems most important in separating the effects of lightning from high-voltage electrical injuries is the duration of exposure to the current, both because lightning is not present long enough to cause tissue breakdown in the classic burn sense and because of the results of the mathematical modeling describing the path of the energy and how long it is in contact with the body.

ESTIMATES OF STREAMER CURRENTS A fifth mechanism of current impingement on an individual has been described.4-6,68 This mechanism recognizes that as a stepped leader steps toward the earth from a cloud, an upward leader will emanate from several objects that are possible points of attachment. Of these, a return stroke will evolve perhaps from only one. Alternatively stated, there will be several upward leaders that dissipate without attachment. The current needed to establish and maintain any upward leader nonetheless must be supplied from the earth, and if a person is the source of an upward leader, then current must flow through the person as a first approximation. Becerra and Cooray25 have studied the amount of current to which a victim of upward leader current may be exposed. They identify two processes that are important to model. First, current flows through a victim to establish the upward streamer and the space charge around the victim’s head, under the influence of the electric field resulting from the stepped leader’s downward

Response

No flashover 5 MV

G4

VAC VAB

4 MV

CHAPTER 3  Lightning Injuries

A

5 kV

F

5 kA VAF VEB,DB

IFH

1.11.7

50

G1 500 kV

Time (µsec)

H

5 kA peak 8/20 µsec wave

With flashover E

D VAB

500 kV

IFH

800A

G2

5 kV

150

VDB 340 nsec

B

Physical Earth

<<5 kV

VAF

G3

5 kV

True Earth

C

Time

FIGURE 3-40  Model of human body adapted for the circumstance of direct lightning strike. Responses of the body model are shown for cases of direct strike with and without subsequent flashover.

path. Second, once a leader other than the leader affecting the person makes connection with the stepped leader, then the electric field collapses rapidly. In that case, the charge in the unattached upward leader rapidly returns to the earth. The first process is relatively prolonged and regular, and the second is rapid and impulsive. In an analysis using a human model and a 30-kA lightning strike grounding just beyond the striking distance, current rises to approximately 20 A over 150 µsec. At the very start of this rise, there is an extremely short pulse of about 5 A. This represents a body charging component before the propagation current for the actual streamer. This is a significant current; however, the duration is extremely short. In fact, the flow of any substantial current internally occurs for less than 10 µsec before the current escapes externally and flashover occurs. The fatal effect of this current, conducted internally within a victim for such a short time, theoretically depends on its timing to the vulnerable period of the cardiac cycle. For an 80-kA return stroke, the peak current is approximately 80 A, again significant. Once the aborted leader collapses, there is a current pulse of opposite polarity. This is exquisitely short. Little is known about the collapse of an aborted leader, and assumptions are made regarding the time constant of the collapse. This ranges from 0.1 to 1 µsec. Cases are examined for a 30-kA and an 80-kA return stroke. The peak current can be large, depending on the size of the stroke and the time constant. The least is computed at about -600 kA, with the least energy deposited being .22 kJ. Again, these are highly significant currents that are large enough to produce significant injury and death.

BEHAVIOR OF ELECTRIC CURRENT IN TISSUE High- or low-voltage electric current may be carried through tissue in a direct conduction fashion, obeying simple linear equations such as Ohm’s law. The result is heating of tissues under Joule’s law, with thermally induced cellular death and dysfunction. Simple passage of current may interfere with neural and muscular function.184

Earlier in the previous century, electrical injury was thought to occur not only because of thermal effects but also because of some mysterious cellular effects.29,157 Unfortunately, the technology was not available to investigate these effects, and this idea was largely forgotten until the past few decades. Cell wall integrity, enzyme reactions, protein shape and structure, and cell membrane “gates” and pumps all operate by changes on the order of microvolts. It is not beyond the realm of imagination that passage of an electric current too small to produce significant thermal damage may cause irreversible changes in these functions, leading to cell death or dysfunction.184 Induction of electric charges by external electromagnetic fields has been shown to force water molecules into cell walls (electroporation), causing fatal “pores.” Cells can die from exhausting their energy and resources attempting to maintain intracellular integrity. Although electroporation has been demonstrated in the laboratory for electrical injuries, it has never been documented for lightning injury with lightning’s very different properties and effects on the body.184

MAGNETIC FIELD EFFECTS* It has been stated that some effects of lightning might be magnetically mediated. A case cited in support of this contention was of a golfer under a tree in the company of three other persons. It was stated that death occurred without evidence of current entering or leaving the index case. On the other hand, one accompanying golfer showed evidence of current traversal but survived. It is stated that three methods of shock may have existed—direct strike, side flash, and ground potential—but no evidence of any was seen. It was considered that contact potential was not relevant. In this case, with persons under a tree, it would seem possible to explain deleterious effects without resorting to a magnetic hypothesis, but the hypothesis bears examination if only because it is a recurrent question. *References 7, 53.

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In the case under consideration, the stroke was considered as a line current 1 m (3.3 feet) distant from the victim, and calculation of peak fields and their effects were given. In considering the contention, it is useful to consider the stroke as a single line current as referenced; however, one must also gain a feeling for how far from a victim such a stroke will act. If the stroke is close to a victim, then attachment to the victim takes place and electrical effects apply as described earlier. If further away, the magnetic field is operative without attachment and magnetic effects need to be examined. Ground potential also exists at this 1-m (3.3-foot) distance. It is necessary to find the minimum distance away from a victim that a stroke can reach ground without attachment to the victim. This gives the worst case distance from a victim (the worst case being the closest) at which a pure magnetic field acts without attachment. The standard striking distance formula gives such a distance.91 The formula is as follows: d s = 10 I 0.65 where ds (m) is the striking distance and I is the stroke current in kiloamperes. This represents the distance at the last turn of the downward stepped leader, such that if an object lies inside this distance, attachment of the leader to the object will take place. For illustrative purposes, let a stroke have a peak current of 18,000A (the 50th percentile) so that ds is 65.5 m. Pure magnetic effects are applicable at this distance and beyond. Inside this distance, the victim will be subject to electrical current effects. By comparison, the ground potential between two points 1 m (3.3 feet) apart at 60 m (197 feet) from a stroke of 18 kA is about 60 V, assuming Earth resistivity of 100 ohm-meters. In examining the magnetic fields involved at this distance, assume an 18-kA stroke at a distance of 65 m (213 feet) from an individual. The peak magnetic B field (the “magnetic induction” formally quantifying the force on a moving charge in its influence) is: µ0 I peak B peak = 2π d s At 65 m (213 feet), the peak B field is 88 µT. For comparison, the earth’s magnetic field is about 1 µT, and the magnetic fields causing concern for power-line fields are in the 1 to 100 µT range. The magnetic fields used in MRI scanning are around 2,000,000 to 5,000,000 times these levels. As with other exposures, effects from chronic exposures may be quite a bit different from acute or momentary exposures. Power-line fields, for instance, are arguably dangerous only if chronic. If one is concerned about a lightning stroke magnetic field, it would be wise to be concerned about MRI fields as well, where, to this date, no effect has been found in practice. Certainly, the time-varying nature of any B field is important, both in terms of the rate of change of the field and of movement of a conductor within this field. If one assumes that the above B field is generated in about 2 µsec, then the time rate of change for the B field is about 22 T/sec. Andrews applied this field to a model heart and found an entirely noninjurious current resulting. It is concluded that magnetic field danger in normal circumstances does not seem to exist.7 Certainly special circumstances might exist, such as the presence of a pacemaker or the presence of an arrhythmic pathway, but in normal terms, magnetic effects would not seem to be clinically significant during occurrences of lightning strike.

BOX 3-4  Lightning Injuries Immediate • Cardiac arrest and cardiac injuries • Pulmonary injuries • Neurologic signs • Seizures • Deafness • Confusion, amnesia • Blindness • Dizziness • Contusion from shock wave • Chest pain, muscle aches • Tympanic membrane rupture • Headache, nausea, postconcussion syndrome Delayed • Neurologic symptoms and signs • Neuropsychological changes • Memory deficits • Attention deficit • Coding and retrieval problems • Distractibility • Personality changes • Irritability • Chronic pain • Seizures

INITIAL PRESENTATION MODEL* Minor Injury These victims are awake and may report symptoms such as dysesthesia in an extremity, a feeling of having been hit on the head or having been in an explosion. They may or may not have perceived lightning or thunder. They often suffer confusion, amnesia, temporary deafness or blindness, or temporary unconsciousness at the scene.65 They seldom demonstrate cutaneous burns or paralysis but may complain of confusion and amnesia lasting from hours to days. Paresthesias, muscle pain, and headaches may last for days to months. Victims may suffer tympanic membrane rupture from the explosive force of the lightning shock wave. Vital signs are usually stable, although occasionally, victims demonstrate transient mild hypertension. They may experience soreness for a few days, but recovery is usually gradual and may or may not be complete. Permanent neurocognitive damage may occur. Some victims may suffer post-traumatic stress disorder and other psychological sequelae.

There have been at least two useful categorizations of lightning injuries by severity of injury: one starts from initial presentation and one is based on neurologic outcome (Box 3-4).

Moderate Injury Moderately injured victims may be disoriented, combative, or comatose. They often exhibit keraunoparalysis: motor paralysis, particularly of the lower extremities, with mottled skin and diminished or absent pulses. Nonpalpable peripheral pulses may indicate arterial spasm and sympathetic instability, which should be differentiated from hypotension. If true hypotension occurs and persists, the victim should be scrutinized for fractures and other signs of blunt injury. Spinal shock from cervical or other spinal fractures, although rare with lightning, may also account for hypotension. Occasionally victims have suffered temporary cardiopulmonary standstill, although it is seldom documented. Spontaneous recovery of the pulse is attributed to the heart’s inherent automaticity. However, respiratory arrest that often occurs with lightning injury may be prolonged and lead to secondary cardiac arrest from hypoxia or some other yet-to-be-elucidated cause. Seizures may also occur.

*References 15, 46, 65, 72.

*Reference 15, 72.

Injuries from Lightning*

82

Severe Injury Victims with severe injury may be in cardiac arrest with either ventricular standstill or fibrillation when first examined. Cardiac resuscitation may not be successful if the victim has suffered a prolonged period of cardiac and central nervous system (CNS) ischemia. Direct brain damage may occur from the lightning strike or blast effect. Tympanic membrane rupture with hemotympanum and CSF otorrhea is more common in this group. The prognosis is usually poor in the severely injured group, complicated by any delay in initiating cardiopulmonary resuscitation with resultant anoxic injury to the brain and other organ systems. There are anecdotal reports of successful resuscitation of these victims with automated external defibrillators (AEDs).218

NEUROLOGIC OUTCOME MODEL* Cherington proposed the classification, focusing on neurologic complications consisting of four groups based on time of onset, duration of symptoms, and severity of the clinical situation. Immediate and Transient Symptoms These may include loss of consciousness, amnesia, confusion, headache, paresthesia, and weakness. Many patients experience a temporary paralysis of their limbs called keraunoparalysis, a term introduced by the French neurologist Charcot. Keraunoparalysis is a brief paralytic state with loss of sensation that affects lower limbs more than upper limbs. Muscle strength and sensation usually return to normal within one to a few hours. The paralysis is accompanied by pallor, severe vasoconstriction, and hypertension. Some have suggested that this peculiar state is caused by transient outpouring of catecholamines.

TABLE 3-1  Lightning Injuries Compared With

High-Voltage Electrical Injuries

Factor

Lightning

High Voltage

Energy level Time of exposure Pathway Burns Renal

30 million volts, 50,000 Å Brief, instantaneous

Usually much lower* Seconds

Fasciotomy

Flashover, orifice Superficial, minor Rare myoglobinuria or hemoglobinuria Rarely if ever necessary

Blunt injury

Explosive thunder effect

Deep, internal Deep, major injury Myoglobinuric renal failure common Common, early, and extensive Falls, being thrown

*Range is 500 V up to millions of volts in transmission lines.

DIFFERENCES BETWEEN INJURIES FROM HIGH-VOLTAGE ELECTRICITY AND LIGHTNING* There are marked differences in injuries caused by high-voltage electrical accidents and lightning (Table 3-1). Exposure to highvoltage generated electricity tends to be more prolonged, particularly if the victim “freezes” to the circuit. In this context, “long” may mean only a few to several seconds of contact. With skin breakdown, electrical energy surges through the tissues with little resistance to flow, causing massive internal thermal injuries that sometimes necessitate major amputations. Myoglobin release may be pronounced, and renal failure may occur. In addition, compartment syndromes requiring fasciotomy may occur. Burns may be severe. Lightning contact with the body is almost instantaneous, often leading to flashover with very little energy going through the body, if at all, particularly because the vast majority of lightning injuries are indirect, as with side flash and ground current. Burns and deep injury are uncommon. Fluid restriction and expectant care are usually the rule. Lighting injury is primarily a neurologic injury, not a burn injury.

CARDIOPULMONARY ARREST AND CARDIAC INJURIES†

Lightning-Linked Secondary Trauma From Falls or Blast Lightning can cause trauma secondarily when the patient is thrown or falls. Injuries include epidural, subdural, and subarachnoid hemorrhages. Blunt and blast effects can damage the brain and other organs and cause tympanic membrane rupture, the most common blast effect seen in patients with lightning strike.

Cardiac Arrest The most common cause of death in a lightning victim is cardiopulmonary arrest. In fact, a victim is highly unlikely (P <.0001) to die unless cardiopulmonary arrest is suffered as an immediate effect of the strike.64 In the past, nearly 75% of persons who suffered cardiopulmonary arrest from lightning injuries died, many because cardiopulmonary resuscitation was not attempted. Primary and secondary cardiac arrests had previously been hypothesized and confirmed with animal studies.9,80-82,266 Injury first occurs with immediate asystolic cardiac arrest and respiratory standstill. Because of the heart’s automaticity, contractions generally resume within a short time. Unfortunately, respiratory arrest caused by unknown factors may last far longer than cardiac arrest. Unless the victim receives immediate ventilatory assistance, attendant hypoxia may induce arrhythmias and secondary cardiac arrest. Alternatively, the respiratory arrest and secondary cardiac arrest may be from more severe injury and not cause and effect. The course has been verified experimentally in sheep, with initial asystole followed by resumption of a short run of bradycardia, then tachycardia, followed by atrioventricular block or bradycardia, and finally with second asystolic arrest.9 Prolonged respiratory arrest has also been confirmed in hairless rats.82,174 It is unknown whether cardiac arrest and arrhythmias induced by lightning are a result of damage to central cardiac and res­ piratory centers in the brain, to the carotid body and other pacemakers along the cardiac control paths, to feedback control

*References 45, 46, 58.

*References 15, 65. † References 23, 64, 71, 78, 79, 85, 173, 286.

Immediate and Prolonged or Permanent Patients have structural lesions that may be seen on imaging studies or on postmortem examination. The great majority of these neurologic complications involve the CNS, including posthypoxic ischemic encephalopathy, intracranial hemorrhage, cerebral infarction, cerebellar syndromes, and spinal cord injuries. Possible Delayed Neurologic Syndromes Delayed neurologic disorders attributed to lightning include motor neuron disease and movement disorders. These sequelae have followed lightning strikes by days to years, although the cause-and-effect relationship between lightning and all subsequent delayed neurologic complications is open to question.

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CHAPTER 3  Lightning Injuries

Burns are uncommon in lightning victims. First- and seconddegree burns not prominent on admission may evolve over the first several hours. Rarely, third-degree burns may occur. Tympanic membrane rupture should be anticipated and, along with hemotympanum, may indicate a basilar skull fracture. Whereas the clinical condition often improves within the first few hours, victims are prone to have permanent sequelae, such as sleep disorders, irritability, difficulty with fine psychomotor function and attention, chronic pain and dysesthesia, generalized weakness or easy fatigability, sympathetic nervous system dysfunction, chronic headaches, and sometimes post-traumatic stress syndrome. A few cases of atrophic spinal paralysis have been reported.

PART 1  MOUNTAIN MEDICINE

mechanisms within the autonomic nervous system, to the heart, or to a combination of these.70,82 Certainly, clinical evidence of general damage to autonomic nervous system regulation has been well documented and confirmed in the animal laboratory.82 Asystole and ventricular fibrillation has each been reported with lightning strike.10,113 As noted in the animal studies, asystole seems to be both the first and last responses to the strike, as the secondary agonal arrest rhythm of ventricular fibrillation deteriorates. Other Cardiac Injuries An immediate prolongation of the QT interval has been shown with consequent predisposition to arrhythmias.13 An associated enzyme rise has been noted in some.108 The QT interval changes may have implications for the cessation of metabolism hypothesis if torsades de pointes is involved.13 The electrocardiogram (ECG) pattern after initial shock may show tachycardia or bradycardia and may show the pattern of myocardial infarction. In the long term, arrhythmias—tachycardia, bradycardia, premature contractions, and atrial fibrillation—have all been reported.79,99,187,259 Postural tachycardia also has been reported, implicating the autonomic nervous system.122 Although the initial ECG may be unreliable for reasons given below, it is not uncommon to find ECG ST changes consistent with ischemia and damage in subepicardial, posterior, inferior, or anterior patterns.18,187 Creatine phosphokinase MB-isoenzyme elevation has been reported. The first report of troponin level elevations and cellular damage in a lightning survivor was published by a high-altitude pulmonary physiologist who suffered injury while climbing in the Alps, using himself as a control.24 Saglam and co-workers250 present a typical case of infarct changes with normal coronary angiography. They summarize the widespread cardiac consequences of lightning strike: “the victim may develop hypertension, tachycardia, nonspecific electrocardiographic changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with the release of creatine phosphokinase–myocardial band fraction.” Unfortunately, their case of a “13-year-old boy with myocardial infarction secondary to an indirect lightning strike” resulted in early death, so the progress of the changes was not able to be reported. Others tend to show resolution of infarct changes.117,248 All that is stated in the articles is that the ECG pattern resolves; no indication is given if there is permanent scarring associated with an infarct. ECG changes may not occur until the second day, making the initial ECG a poor screening tool for ischemia. Several clinicians stress that cardiac symptoms may not be apparent on initial presentation. Premature ventricular contractions were reported in one patient nearly 1 week after presentation. Whereas most ECG changes resolve within a few days, some may persist for months. Several reports of cardiomyopathy have appeared. Rivera and associates241 refer to “stunned myocardium” and document a 42-year-old victim with severe cardiogenic shock and left ventricular dysfunction. This was demonstrated clinically with ECG changes and scan changes. The victim recovered fully with no long-term disability. They concluded that “the exact mechanism of abnormal contractility in the absence of direct electrofulguration is unknown but may be explained by release of oxygen-free radicals, proteolysis of the contractile apparatus, and cytosolic overload of intracellular calcium, followed by reduced myofilament sensitivity to calcium.” Takotsubo-shaped hypokinesis with aneurysmal dilation (transient left ventricular apical ballooning syndrome) has been described with associated cardiomyopathy.125 This is noted in the setting of ECG changes mimicking myocardial infarction, but with minimal enzyme release.100,117 Recovery from dramatic dysfunction is complete over days to weeks. Some clinicians have theorized that vascular spasm is a cause of cardiac damage not dissimilar to keraunoparalysis.228 However, ECG changes are not always consistent with cardiac vascular supply patterns. Areas of focal cardiac necrosis have been reported in autopsies, and histologic changes have been shown in sheep hearts.10 84

PULMONARY INJURIES Pulmonary edema may accompany severe cardiac damage. Pulmonary contusion, with hemoptysis and pulmonary hemorrhage, may result from blunt injury or direct lung damage.260 Blunt thoracic trauma may also cause pneumomediastinum.124

NEUROLOGIC INJURIES* Although cardiac arrest may be the only immediate cause of death, lightning injury is primarily a neurologic injury with damage possible to central, peripheral, and sympathetic nervous systems. Injury to the nervous system far and away causes the greatest number of long-term problems to survivors. Tools commonly used in evaluation and treatment include functional scans, such as single photon emission computed tomography (often positive); positron emission tomography; anatomic scans, such as CT and MRI (usually negative); neuropsychological assessment; cognitive retraining; pharmacotherapy; and psychotherapy. Electroencephalography is often mentioned in the literature but is seldom helpful.17,65 Central Nervous System Injury† Gross structural changes to the brain, such as coagulation of brain substance, formation of epidural and subdural hematomas, paralysis of the respiratory center, and intraventricular hemorrhage, have been reported but are all rare and may be more from blunt trauma than from electrical injury. Autopsy findings include meningeal and parenchymal blood extravasation, petechiae, dural tears, scalp hematomas, and skull fractures.269 Although MRI or CT may show diffuse edema, intracranial hemorrhage, or other injuries, they are more commonly normal.57,58 There have been reports of hemorrhage on MRI findings in a few acutely injured victims.57,227,275 In animals, direct cellular damage to the respiratory center beneath the fourth ventricle, as well as to the anterior surface of the brainstem, has been shown.9 Lightning energy has been theorized to enter through the orifices of the head, pass through the pituitary and hypothalamus and also through the CSF into the retropharyngeal area, so that signs and symptoms of endocrine dysfunction, respiratory or cardiac arrest, and sleep disturbances could be reasonably expected to occur. Seizures may accompany initial cardiorespiratory arrest as a result of hypoxia or intracranial damage. Electroencephalographs may show epileptogenic foci in the acute phase. These patterns may be focal or diffuse, varying with the site and type of injury. However, most patients do not experience seizures during hospitalization. Some victims, however, including children, develop delayed seizures, some of which manifest as “absence spells,” memory losses, or blackouts that are often diagnosed as “pseudoseizures.” Obviously the victim of prolonged cardiopulmonary arrest may have anoxic brain injury that is not specific to lightning injury. Whether by this mechanism or others, cell loss and/or infarction of various areas (e.g., cerebellum,21 cerebrum) has been reported. In Cooper’s study64 of severely injured victims, nearly twothirds had some degree of lower extremity paralysis (keraunoparalysis), usually demarcating around the waist or pelvis, and about one-third of victims had upper extremity paralysis. The affected extremities appear cold, clammy, mottled, insensate, and pulseless.15 This is probably the result of sympathetic instability and intense vascular spasm, similar in appearance to Raynaud’s phenomenon. It usually clears after several hours.15,65 Fasciotomies are seldom indicated for lightning injuries, because signs of compartment syndrome or distal ischemia usually clear with patient observation. Pulses can sometimes be elicited with Doppler examination. Atrophic spinal paralysis has been reported, as have persistent paresis, paresthesias, incoordination, delayed and acute cerebellar ataxia, hemiplegia, aphasia, quadriplegia

*References 21, 46-49, 55, 57, 67, 161, 168. † References 21, 46-49, 55-58, 67, 168.

Peripheral Nerve Injury‡ The peripheral nervous system may be affected. Pain and paresthesias are prominent features of the injury, particularly in the line of presumed current passage, although this is difficult to ascertain from external burns or other injury. Symptoms may be delayed by weeks to months. Almost any peripheral nerve can be involved. Autonomic Dystrophy§ Chronic pain syndromes may occur. Autonomic dystrophy, also called sympathetic dystrophy or sympathetically mediated pain syndrome, may occur. Such chronic pain syndromes are now subsumed under the classification of the complex regional pain syndromes, which are of type 1 (reflex sympathetic dystrophy) or 2 (previously causalgia). The complex regional pain syndromes are long-term neurologic sequelae that may be caused by even minor injuries to nerves and are characterized by pain, edema, autonomic dysfunction, trophic changes (including atrophy secondary to disuse from pain), and movement disorder. Post-Traumatic Headache¶ Many victims of lightning injury exhibit severe, unrelenting headaches for the first several months after lightning injury, along with other symptoms, including gastrointestinal distress, that resemble postconcussion symptoms. Acupuncture may be effective. Many victims complain of nausea and unexpected, frequent vomiting spells early in their recovery period. Dizziness and tinnitus from eighth cranial nerve injury are also common complaints, especially with telephone-transmitted lightning strikes.16,67,72,278,281

*References 45-48, 129, 227, 229-232, 237, 254, 263, 267, 272, 281. † References 62, 130, 161, 233, 254, 255. ‡ Reference 276. § References 62, 129, 130, 161, 233, 254, 255. ¶ References 71, 270.

BURNS* Most people assume that because of the tremendous energy discharge involved, a lightning victim will be flash-cooked.40,66 Fortunately, the physics of lightning flashover, as well as the fact that the vast majority of injuries are from indirect strikes, saves most victims from suffering more than minor burns. Less than one-third of lightning survivors have any signs of burns or skin marks. Although extensive third- and fourth-degree burns may occur in combination with skeletal disruption, these are quite rare. The incredibly short period of exposure may explain the lack of significant burn injury in most cases. As shown in mathematical models, a portion of the lightning current may travel through the tissues.9 If the electric field in the tissue becomes too large, electrons can be freed from their atoms. Referred to as dielectric breakdown, this can cause a large increase in the flow of current and become manifest as an electric arc. This may occur internal or external to the body, the latter when the breakdown strength of air (2 × 106 V/m) is exceeded. Arc-like burns can result. This happens more often with high-voltage electrical injury but may occasionally occur with lightning. Discrete entry and exit points are uncommon with lightning. The burns most commonly seen may be divided into five categories: linear burns; punctate, full-thickness burns; feathering or flowers; thermal burns from ignited clothing or heated metal; and combinations. Linear burns (Figure 3-41) often begin at the victim’s head and progress down the chest, where they split and continue down both legs. The burns generally are 1 to 4 cm (0.5 to 1.5 inches) wide and tend to follow areas of heavy sweat concentration, such as beneath breasts, down the midchest, and in the midaxillary line.65 Linear burns are usually first- and seconddegree burns that may be present initially or develop as late as several hours after the lightning strike. They are not primary lightning injuries but more likely steam burns secondary to vaporization of sweat or rainwater on the victim’s skin as flashover and current flow occurs around the body. In patients wearing thin or cotton clothing, the steam tends to escape through the clothing with less damage than in areas where the clothing is bunched (axilla, antecubital fossa [see Figure 3-41, C], groin) or under nonporous material, such as leather jackets or belts (Figure 3-42). Punctate burns (Figure 3-43) are discrete circular burns that individually range from a few millimeters to a centimeter (0.5 inch) in diameter and may be multiple and closely spaced. They may be full thickness and resemble cigarette or cinder burns and are usually too small to require grafting. Particularly useful for forensic investigation is explosion of clothing, such as occurs with vapor explosion of wet socks in shoes. This may blast shoes off with subsequent contusion and avulsion injuries to parts of the foot (see Figure 3-41, H). Examination of clothing may show singeing of fibers at the edge of the damage (see Figures 3-26 and 3-43, B) and absence of the very fine fibers on material, such as cotton, because they were vaporized and/or burned away. With a handheld 10× magnifier, plasticized or polyester materials may show frank melting. Even in cotton clothing with no apparent damage to the material, examination of the threads used in joining pieces together at the seams will often show a tiny droplet of plastic, because thread contains a polyester or nylon core for strength and durability. Feathering burns (Figure 3-44; see Figure 3-30) are pathognomonic of lightning and are known by such names as Lichtenberg’s flowers, filigree burns, arborescent burns, ferning, and keraunographic markings.† These markings are not true burns but usually appear as transient pink to brownish, sometimes lightly palpable, arborescent marks that follow neither the vascular pattern nor nerve pathways. The pattern found is similar to that on a photographic plate exposed to a strong electric field and has been compared with fractals.131 Sometimes the most superficial skin over the areas will slough or flake off after a few *References 22, 63, 71, 72, 131, 152, 202, 213, 214, 257, 261, 273. † References 51, 52, 63, 98, 149, 179, 198, 238, 273.

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CHAPTER 3  Lightning Injuries

(immediate or delayed), and one report of progressive muscle atrophy of the upper extremities. Nearly 72% of victims in Cooper’s study64 suffered loss of consciousness. Nearly three-fourths of these also suffered cardiopulmonary arrest.64 Those with cranial burns were two to three times more likely to suffer immediate cardiopulmonary arrest and had a three to four times greater probability of death.64 Persons who are stunned or lose consciousness without cardiopulmonary arrest are highly unlikely to die, although they may still suffer serious sequelae.64 Whether or not victims have suffered loss of consciousness, they almost universally demonstrate anterograde amnesia and confusion, which may last for several days. Retrograde amnesia is less common. Although the victim may carry on a conversation and remember his or her actions before the strike, he or she is often unable to assimilate new experiences for several days, even when there is no external evidence of lightning burns on the head or neck. Survivors may have persistent sleep disturbances, difficulty with fine mental and motor functions, dysesthesias, headaches, mood abnormalities, emotional lability, storm phobias, decreased exercise tolerance, and post-traumatic stress disorder.67 Early on, their symptoms resemble postconcussion syndrome. The basal ganglia and cerebellum may be affected.45-48,57,58,221,227 This agrees with older reports of localization. CNS damage may also eventually manifest as parkinsonism, extrapyramidal syndrome, or other involuntary movement disorders or signs of intracranial hematomata and hemorrhage; infarction; hypoxia; edema; cerebellar signs of infarction, dysfunction, and atrophy; and centrally derived pain and psychological syndromes.* Spinal cord injury developing over months following the injury has been reported.182,183 Paresthesias are frequently seen, often mirroring the area of keraunoparalysis. There is also evidence of autonomic neuropathy.†

PART 1  MOUNTAIN MEDICINE

A

C

B

D

E

G

H

F

I

J

FIGURE 3-41  Linear burns from a fatal 1977 lightning injury to 22-year-old baseball player. Most of these marks did not appear until a few hours to a few days (those with small eschar) after the injury. A, The mark that matured on the back of the head by the third day. B, The linear marks continuing down the side of the neck. C and D, Continuing marks down the anterior and lateral torso. Note that these are the normal “sweat lines” that a baseball player in July would develop. Also note the burn to the antecubital fossa where sweat would accumulate under the baseball jersey as the player stood crouched and ready to catch near second base. Note that all of these burns are partial thickness with sparse blistering. E, More extensive burns where a metal belt buckle or athletic supporter may have been causing secondary thermal burns or electrical discharge to the skin from the metal. F to H, Damage to the right leg and foot. Note the parallel marks on the foreleg, which would correspond to sweat accumulation or wetness in the ribbing of the athletic socks. Note also the mark on the heel, which may have been from the metal heel cup in the shoe or contusion from the shoe being ripped off by the vapor explosion of the flashover. The socks were destroyed or exploded off below the ankles, and the shoes were never found. Blunt injury from the explosion caused nonburned ripping of the fifth toe web as well (H). I and J, Damage to the left lower leg and foot. (Copyright Mary Ann Cooper.)

A

B

FIGURE 3-42  Steam burns on a motorcyclist who was wearing a leather jacket, belt, and pants. This man was injured 3 weeks after and only a few miles away from the man in Figure 3-41. A, Note the more extensive burn to the back where the steam was held against the skin longer by the leather jacket than would occur with more porous clothing. B, More linear burns where the jacket was not as close to the skin. Note that the burns take a right angle under the belt at the waist before splitting at the groin and continuing laterally down the leg. Old scarring on the right knee was from a previous airplane crash and not part of the lightning injury. (Copyright Mary Ann Cooper.)

86

BLUNT, CONCUSSIVE, AND EXPLOSIVE INJURIES

B FIGURE 3-43  A, Punctate burns to the shoulder and arm of a 12-yearold girl who was at a campfire with friends. B, Note singeing of the cotton T-shirt that she was wearing at the time over the area of the right arm burn. (Copyright Mary Ann Cooper.)

The recipient of a lightning strike may be injured directly from the explosive force of lightning or from a fall (as from a horse or mountain ledge, out of a vehicle, or being hurled by endogenous opisthotonic force). Back and spinal injuries unrelated to the electrical effects of lightning injury may occur from these mechanisms. A variety of fractures, including skull, ribs, extremities, and spine, have been reported in lightning victims.165,190 Unfortunately, these are often missed, particularly in the workups of persons with chronic pain. Rarely a burst-like injury of soft tissue occurs and discloses extensive underlying injuries, especially in the feet, where boots or socks may explode as a result of vapor expansion (see Figures 3-29 and 3-41, H). Tympanic membrane rupture is common. Abdominal injuries due to blasts are well described and include gastrointestinal perforation and an abdominal compartment syndrome.20,166 Hemoglobinuria and myoglobinuria are seldom reported. When they occur, they are usually transient. Myoglobinuric renal failure has not been reported in the literature, although one case has been verbally relayed to the first author. Persistent hypotension should alert the physician to blunt injuries to the chest, spine, lungs, heart, and intestines that may lead to complications of prolonged coma, pulmonary contusions,260 heart failure, and ischemic bowel. Several victims have complained of jaw pain. A number have suffered loss of teeth or fillings or necrosis of the jaw and teeth, and many describe a metallic taste in the mouth for months after the acute injury. At least one was found to have a styloid process fracture. Many recovering victims believe that premature arthritis may be a result of their injury.

EYE INJURIES*

A

Ocular injuries may be due to direct thermal or electrical damage, intense light, contusion from the shock wave, or combinations of these factors. Although cataracts most commonly develop within the first few days, they may occur late and are often bilateral.† Whereas the cataracts may be the typical anterior midperipheral type, posterior subcapsular opacities and vacuolization seem to occur more often with lightning injuries.38 Corneal lesions, hyphema, uveitis, macular holes, iridocyclitis, vitreous hemorrhage, choroidal rupture, chorioretinitis, retinal detachment, macular degeneration, optic atrophy, diplopia, loss of accommodation, and decreased color sense have also been reported. Autonomic disturbances of the eye, including mydriasis, Horner’s syndrome, anisocoria, and loss of light reflexes, may be transient or permanent. Transient bilateral blindness of unknown etiology is not uncommon. Intense photophobia may be present as the victim recovers. An interesting paper conjectures that the

B FIGURE 3-44  A, Feathering marks. B, Ferning developed after the victim received a side flash lightning strike. (A courtesy Mary Ann Cooper; B courtesy Sheryl Olson, RN.)

*References 38, 42, 95-97, 102, 121, 123, 151, 160, 172, 208, 219, 220, 240, 261, 285. † References 38, 95-97, 102, 121, 123, 172, 208, 240, 261.

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CHAPTER 3  Lightning Injuries

A

days. Although many pictures exist of these marks, they have never been described histologically. The most current theory is that they represent blood cells forcefully extravasated into the superficial layers of the skin from contracting capillaries, much like a superficial bruise, which is consistent with their rapid resolution and pattern of color changes. Experimentally, they follow the flashover current lines seen in Cooper’s animal model.80,81 Burns may be caused by metal worn close to the skin.72,159 Figure 3-41, E shows a burn resulting from a metal belt buckle or athletic supporter worn by a young man who was struck while playing softball. Figure 3-28 shows a necklace burned into the skin with permanent tattooing. Another theory for these burns involves discharge of current from metal to underlying skin. On rare occasions, clothing is ignited by lightning, causing severe thermal burns.15,65 Victims of lightning may exhibit various combinations of burns, as demonstrated in Figure 3-41.

PART 1  MOUNTAIN MEDICINE

conversion of St Paul on the Damascus Road and his subsequent blindness were due to lightning.35,36 Dilated or unreactive pupils should never be used as a prognostic sign or as a criterion for brain death in a lightning victim until all anatomic and functional lesions have been excluded.44

EAR INJURIES* Between 30% and 50% of more severely injured lightning victims may have rupture of one or both tympanic membranes from the shock-wave effect, concomitant basilar skull fracture, or direct burn damage because of current flow into this orifice.18,64 Otorrhea of CSF or hemotympanum rarely occur. Disruption of the ossicles and mastoid has been reported. Many cases of permanent deafness are noted in older literature but are seldom found today. Facial palsies, both acute and delayed, may occur from direct nerve damage by lightning. Balance problems and tinnitus are common, probably from eighth cranial nerve injury, and nystagmus and ataxia may occur. Temporary deafness is not uncommon.161 It has been postulated that the intense noise and shock wave accompanying thunder may be responsible for sensorineural hearing loss. Otologic injury from hard-wired telephone–transmitted lightning strikes is common but probably occurs less often now with the advent of mobile phones.8,16,17

FETAL SURVIVAL† The fetus of a pregnant woman struck by lightning has an unpredictable prognosis. Of 11 cases reported, nearly one-half of the pregnancies ended in full-term live births, with no recognizable abnormality in the child. Approximately one-fourth resulted in live births with subsequent neonatal death; the remainder were stillbirths or deaths in utero. There has been one report of ruptured uterus after lightning strike.

HEMATOLOGIC ABNORMALITIES Several unusual hematologic complications have been attributed to lightning injuries in isolated case reports. These include disseminated intravascular coagulation, transiently positive Coombs’ test, and Di Guglielmo’s syndrome, a type of erythroleukemia characterized by erythroblastosis, thrombocytopenia, and hepatosplenomegaly. Although there have been anecdotal reports of increased hypersensitivity, development of allergies, and increased risk for cancer in lightning victims, perhaps indicating an immunologic component to lightning injury, these have not been studied or validated with controlled longitudinal studies.

ENDOCRINE AND SEXUAL DYSFUNCTION Decreased libido for both men and women and impotence for men are common complaints. Sexual dysfunction may be due to neural, spinal cord, endocrine, autonomic, or neuropsychological injury, side effects of therapeutic drugs, and possibly other causes and should not be discounted. A report of male hypersexuality after a lightning strike has not been authenticated but can also be explained from a specific brain injury mechanism. Some victims have reported amenorrhea or menstrual irregularities lasting up to 2 years.

PSYCHOLOGICAL AND NEUROCOGNITIVE DYSFUNCTION‡ It is not uncommon for a person hit by lightning to rest at home for a few days, assuming that he or she is supposed to feel “bad” after being hit by lightning. The victim may not see a physician until family members insist or symptoms worsen or do not abate. Neurocognitive deficits may not become apparent until a victim attempts skilled mental functions. Often the person will attempt *References 26, 28, 39, 113, 115, 120, 160, 178, 209, 222, 223, 236, 265, 278. † References 64, 106, 112. ‡ References 47, 48, 72, 229-232, 235, 272, 283, 284.

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to return to work after the injury, but because of decreased work tolerance, short-term memory problems, easy fatigability, and difficulty assimilating new information, he or she will be unable to continue in the prestrike occupation. Chronic pain syndromes are cited as commonly overlooked diagnoses in psychiatric and functional terms.129,130 Although some medical clinicians have been historically suspicious of victims’ complaints of psychological and neurocognitive dysfunction, evaluation of many such patients appears to have confirmed a vast commonality of psychological symptoms. This should begin to reverse a regrettable tendency, both medically and legally, to discount complaints as evidence of malingering, excessive reaction, conversion reaction, personality problems, or manifestations of “weak” coping strategies. The syndrome is described first from a clinical viewpoint and then discussed in light of the extant literature. Functional Issues • Memory disturbance: Individuals show marked diminution of short-term memory ability. They require shopping lists and reminder lists. Memory for recent names and places is diminished to the point of disability. Individuals tend to selfisolate, stop mixing socially, and avoid going into new circumstances.67 • Concentration disturbance (adult attention deficit disorder): Individuals show deficits in their working memory, are unable to focus attention for more than a short period, and are easily distracted. In particular, reading and understanding are poor. Job training is detrimentally affected. This is worsened by sleep disturbance. • Cognitive function: Individuals report diminished mental agility. The keeping of accounts is a noteworthy example. Calculation and estimation become erratic and affect work performance. Ability at mental manipulation and problem solving is markedly decreased. • Higher executive functioning: Individuals are neither able to coordinate multiple tasks simultaneously nor able to follow orders for complex tasks they used to perform easily before the injury. One victim described it as if “the office manager of my brain had quit.” Behavioral Issues • Emotional lability and aggression: Individuals find that they are more aggressive than before. They are easily frustrated and are liable to have outbursts of temper. The strains on a partnership are significant, and marital and relationship dysfunction is common. An increased state of arousal and anxiety may further complicate distractibility as well as proper recognition and assimilation of new learning. • Sleep disturbance: Easy fatigability, sleep disturbance, or hypersomnolence (usually early on) is common and may last for years. Flashbacks and nightmares may be experienced. • Phobic behavior: Avoidance of the precipitant circumstances is demonstrated, in some cases to phobic proportion tantamount to post-traumatic stress disorder. • Depression: Depression is almost always present in classic biologic form and should be anticipated. Although the aforementioned symptoms can certainly arise secondary to a depressive state, it would also be reasonable for a victim to react with depression to the decrements in work power and lifestyle engendered by chronic pain, sleep deprivation, or decreased personal performance. A third reasonable possibility is concurrent neuropsychological syndrome and biologic endogenous depression. Antidepressant medication may be useful. Formal neuropsychological testing may be used to attempt to validate the injury, quantify a functional baseline, and design cognitive therapy. Very few studies have formally examined the syndrome.232,272 Primeau and co-workers point to research difficulties, including sample bias and heterogeneity, methodology (cross-sectional rather than longitudinal or prospective), and the essential difficulties of determining premorbid status or current independent psychiatric status. It is also noted that the magnitude of insult does not correlate with psychological disability.67 Duration, type, and severity of the syndrome are therefore unpredictable.

Recognition and Treatment of Lightning Injuries* DIAGNOSIS Diagnosis of lightning injury may be difficult. History of a thunderstorm, witnesses who can report having seen the strike, and typical physical findings in the victim make diagnosis easier but are not always present. Lightning can strike on a relatively sunny day, thunder may not be appreciated, and sometimes the victim is alone when injured. A diligent historical effort and careful physical examination at the earliest opportunity may help determine the true cause. Any person found with linear burns, mental status changes, *References 65, 67.

ruptured tympanic membrane, and clothes exploded off should be treated as a victim of lightning strike. Diagnosis is made doubly difficult because burns, which most people expect to accompany lightning injuries, are often absent. Feathering marks, also called Lichtenberg’s flowers, are pathognomonic of lightning strike but are rare.* Another sign and/or symptom complex includes linear or punctate burns, tympanic membrane rupture, confusion, and outdoor location. Because there have been several cases of side flash or contact injury from indoor plumbing and telephones, the physician should suspect lightning strike in persons found confused and unconscious indoors after or during a thunderstorm.8,15,16,65 Documentation of lightning activity to support legal or insurance claims is available from commercial sources.

INITIAL FIRST AID AND TRIAGE OF VICTIMS† Ensuring scene safety is paramount. Rescuers are at risk if thunderstorms are in the area.268 As in any other emergency, the first steps are the CAB: compression (circulation), airway, and breathing. If the victim has suffered a cardiac arrest, cardiopulmonary resuscitation should be started immediately and a rescue vehicle called for transportation. AEDs have been helpful in some cases.218 If the strike occurs far from civilization and evacuation is improbable, the victim will probably die unless pulse and respirations resume spontaneously in a short period of time. The heart may resume activity but may slip into secondary arrest. It is unknown whether the secondary cardiac arrest is due to primary brain damage, hypoxia from prolonged respiratory arrest, primary cardiac damage, autonomic nervous system damage, or a number of other mechanisms that could be hypothesized. If no pulse is obtained within 20 to 30 minutes of starting resuscitation, it is reasonable to stop further resuscitation efforts. If a pulse is obtained, ventilation should be continued until spontaneous adequate respirations resume, the victim is pronounced dead, continued resuscitation is deemed unfeasible because of rescuers’ exhaustion, or there is danger to rescuers’ survival. When lightning strike involves multiple victims, resources and rescuers may not meet the demand and triage must be instituted. Normally, the rules of triage in multiple-casualty situations dictate bypassing dead persons for those who are moderately or severely injured and can benefit from resuscitation efforts. However, “resuscitate the dead” is the rule in lightning incidents, because victims who show some return of consciousness or who have spontaneous breathing are already on the way to recovery. The most vigorous attempts at cardiopulmonary resuscitation should be directed to the victims who appear to be dead because they may ultimately recover if properly resuscitated. Survivors should be routinely stabilized and transported to the hospital for more thorough evaluation. The probability that lightning victims can recover after prolonged cardiopulmonary resuscitation is low. There is no evidence to suggest that survival after a longer period than normal without resuscitation is possible in the setting of lightning injury. Often in a remote setting, the rescuer is emotionally tied to the victim by age and friendship and may tend to continue resuscitation past the point of futility. In pronouncing a victim dead, the rescuer must ensure that other problems such as hypothermia are not contributing to the victim’s response to resuscitation efforts. Other stabilization procedures, including splinting of fractures, airway control or intubation, spinal precautions, and institution of intravenous fluids and oxygen, should be accomplished whenever indicated and feasible before transport.

HISTORY AND PHYSICAL EXAMINATION An eyewitness report is helpful because victims are often confused and amnestic.64,65 History that includes a description of the event and the victim’s behavior following the strike may be helpful. *References 51, 52, 63, 98, 238, 273. † References 15, 65, 78, 79.

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Disturbances of verbal memory, attention, concentration, and new learning are very frequently identified.232 This commonality among victims is noteworthy. Primeau and co-workers also draw attention to the similarity of some facets of the disorder and those of other etiologies. They generally find the head injury model a useful one that can guide treatment. Other syndromes to which the lightning and electrical injury syndrome show similarities include post-traumatic stress disorder, depression, anxiety, and obsessional and adjustment disorders. Features of these are seen to be present, although the syndrome is not simply an example of these dysfunctions per se. The authors have considered somatoform disorders as a cause, noting the tendency to be preoccupied with the injury and to overattribute subsequent symptoms to the lightning injury. This may be due in part to physicians’ general lack of knowledge of the problems and the lack of longitudinal controlled studies, so that victims do not know what to expect in the future. Conversion reaction may also be considered, although it cannot account for the symptomatology of lightning and electrical disability.67 Good neuropsychological testing can detect this facet. One difficulty with neurocognitive testing is use and interpretation of the Minnesota Multiphasic Personality Inventory (MMPI). Although it was not developed to characterize patients with chronic problems, particularly those with chronic pain, the MMPI has been applied to them, often resulting in erroneous conclusion of conversion reaction or preoccupation with physical complaints. It should surprise no one that anyone suffering from chronic pain and neurologic injury that hampers their normal preinjury activities will rank higher on the “preoccupation with physical complaints” and “conversion” scales than will uninjured normal individuals. Andrews and Darveniza16 recognized three postinjury syndromes and correlated these with the postinjury periods of 1 week, 1 week to 3 months, and 3 months to 3 years. Primeau and co-workers add a fourth, which is persons experiencing longer and perhaps lifetime dysfunction.120,232 Cherington46,58 has further classified lightning injury by its permanent sequelae. The first 12 months after injury are crucial to recovery. It is during this period that the most recovery is seen, with possible mild improvement up to 3 years after injury. Beyond this time, chronic dysfunction may be assumed, although it is also at this time that the survivor may decide to move on with life, accept limitations, and even sometimes be able to successfully pursue a new career. Van Zomeren and co-workers272 provide one of the few thorough examinations of the syndrome in lightning-injured patients. Fatigue and energy loss were the main complaints; poor concentration, irritability, and emotional lability were other common themes confirmed. Impairment of memory, attention, and visual reaction times were documented. Depression and “convincing signs of post-traumatic stress disorder” were seen. The syndrome was highly differentiable from normal (P <.001), and no parallel model was available for comparison. They stated that the lasting complaints and mild cognitive impairments could not be explained on the basis of anxiety reactions or depression. They summarized their findings under the heading of “vegetative dystonia.”

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After scene safety as been secured, the victim should be undressed to search for hidden signs of injury. Special note should be taken of vital signs, temperature, and level of consciousness. Because many victims are struck during a thunderstorm, they may be wet and cold. Hypothermia should be anticipated and treated appropriately (see Chapter 5). The awake patient should be assessed for orientation and short-term memory. A cursory mental status examination of the lightning victim may reveal good ability to carry on a “social conversation” that easily hides deficits in fine neurocognitive skills. It is easier to detect deficits when the victim cannot assimilate information, perseverates, or asks repetitive questions. Continuing confusion or a deteriorating level of consciousness mandates CT or MRI of the brain to rule out intracranial injury. Examination of the victim’s eyes should be done to establish pupillary reactivity and ocular injury. Lack of pupillary reaction or pupillary dilation should not be taken as a sole indicator of death. Tympanic membrane rupture is an important indicator of lightning strike. Ossicular disruption may be one explanation for a victim’s lack of appropriate response to verbal stimuli. Although the pulmonary system may be affected by cardiac arrest, pulmonary edema, or adult respiratory distress syndrome, it is uncommon to witness these initially. The cardiovascular examination should include distal pulses in all extremities, appreciation of arrhythmias, and evaluation of cardiac damage, including ECG changes. Cardiac enzyme elevations have rarely been reported with lightning injury. The victim’s abdominal examination occasionally demonstrates absent bowel sounds, which suggests ileus or indicates acute traumatic injury, such as contusion of the liver, bowel, or spleen. The examiner should document any skin changes. The victim’s skin may show mottling, especially below the waist. Burns are not universally present or may take a period of hours to evolve. Notation of pulses, color, and movement and sensory examination of the victim’s extremities are important. Keraunoparalysis is common but usually improves in a few hours. The physical findings and mental state of minimally and moderately injured victims tend to change considerably over the first few hours; careful observation and documentation delineate the course so that therapy can be modified. The minimally injured victim can almost always be discharged to a responsible person or requires only overnight observation, whereas the severely injured person may require intensive care with mechanical ventilation, antiarrhythmic medications, and invasive interventions and monitoring techniques.

LABORATORY TESTS AND RADIOGRAPHIC EXAMINATION Minimum laboratory examination includes urinalysis (including a dipstick for myoglobin on fresh urine). The more severely injured victim may require tests such as complete blood count, electrolytes, blood urea nitrogen, and creatinine and testing for cardiac damage. If the victim is to be placed on a ventilator, measurement of arterial blood gas levels will be necessary; if intracranial pressure monitoring is used, determination of serum osmolality may be required. An ECG is desirable for most lightning victims. Although several types of acute arrhythmias have been reported, they are uncommon. QT prolongation is an abnormality sometimes associated with lightning injury. Radiographs and other imaging studies may be obtained, depending on the presentation and history. Cervical spine imaging should be performed if there is evidence of cranial burns, contusions, loss of consciousness, or change in mentation that would make the physical examination unreliable, or if there is any suspicion of a fall or being thrown. The victim who is unconscious, confused, or has a deteriorating level of consciousness requires a CT or MRI scan of the brain to identify trauma or ischemic injury. Other studies to rule out fractures, dislocations, and other bony injuries may be obtained as clinically indicated. 90

TREATMENT* Fluid Therapy Intravenous access is required for the victim who shows unstable vital signs, unconsciousness, or disorientation. If the victim is hypotensive, fluid resuscitation with normal saline or Ringer’s lactate solution may be indicated but with the caution that cerebral edema may develop. Fluid restriction in normotensive or hypertensive victims is recommended because of this risk. In seriously injured or unstable patients, intensive care unit types of monitoring, including arterial or central venous pressure, may be indicated. Careful intake and output measurements are necessary in the severely injured patient and require placement of an indwelling urinary catheter. Myoglobinuria, unless caused by blunt injury or other mechanism, is rarely attributed to lightning injury alone. When it occurs, it is usually transient, so that mannitol-induced diuresis, alkalinization, and aggressive fluid loading used with high-voltage electrical injuries are rarely necessary. However, if burns are severe and extensive, which is rarely the case, fluid resuscitation may be required. Fasciotomy Not Needed Intense vascular spasm with lightning is usually transient and caused by sympathetic instability. The presence of keraunoparalysis, paralyzed and pulseless extremities seen with lightning injuries, should not be treated like similar-appearing traumatized extremities caused by high-voltage electrical injury.15,65,202 Steady improvement in the mottled, cool extremity, with return of pulses in a few hours, is the rule rather than the exception. Fasciotomies are rarely indicated unless the extremity shows no signs of recovery and raised intracompartmental tissue pressures are documented. Antibiotics and Tetanus Prophylaxis Prophylactic antibiotics are not indicated. Antibiotic therapy should only follow culture and identification of pathogens except in obvious cases involving open fractures or cranial fractures that violate the dura. Appropriate tetanus prophylaxis should be given if burns or lacerations are present. Cardiovascular Therapy† Management of cardiac arrest is standard, including the use of an AED if available. In the victim who is not in cardiac arrest, vasospasm may make peripheral pulses difficult to palpate. Usually femoral, brachial, or carotid pulses may be appreciated. Doppler examination may help to locate peripheral pulses and record blood pressure. If a victim remains hypotensive, fluid resuscitation may be necessary to establish adequate blood pressure and tissue perfusion. Causes of hypotension include major fractures, blood loss from abdominal or chest injuries, spinal shock, cardiogenic shock, and occasionally deep burns similar to high-voltage electrical burns. As soon as an adequate central blood pressure is obtained, fluids should probably be restricted because of the incidence of cranial injuries, cerebral edema, and postarrest anoxic brain injury. Mechanical ventilation is required for the victim who is without spontaneous or adequate respirations until the person resumes adequate ventilation, brain death is declared, or the physician and family decide to cease efforts. Cardiac monitoring and serial isoenzyme and troponin measurements are indicated if there is any sign of cardiac ischemia or arrhythmia or if the victim complains of chest pain. Injury patterns, as well as arrhythmias, have been reported.65 The indications for antiarrhythmic drugs and pressor agents are the same as those for a suspected myocardial infarction.65 Transient hypertension may be so short-lived as to require no acute therapy. However, several cases of hypertension have occurred 12 to 72 hours after lightning strike and seemed to respond well to antihypertensive medications. No systematic *Reference 64. † References 78, 79, 106, 173, 187.

Central Nervous System Injury* Every lightning victim should have a screening neurologic examination. If there is a history of loss of consciousness or if the victim exhibits confusion, hospital admission is warranted. The victim with tympanic membrane rupture, cranial burns, or loss of consciousness, or who shows decreasing level of consciousness, should undergo cervical spine imaging, brain CT, and possibly brain MRI. Cerebral edema may be managed with mannitol, furosemide, fluid restriction, cerebral pressure monitoring, and other standard therapies. Although hypothermia was reported to contribute to complete recovery in one victim with prolonged cardiac arrest before resuscitation efforts, there is no evidence that this would benefit all victims.167 Early seizures are probably due to anoxia. If there is evidence of CNS damage or if seizures continue after adequate oxygenation and perfusion have been restored, standard pharmacologic intervention with diazepam, fosphenytoin, phenobarbital, and/or other anticonvulsants should be considered. The response to specific drugs has not been studied. If paralysis does not improve, causes other than lightning, including blunt injury from a fall, may be responsible. Spinal artery syndrome has been reported, perhaps caused by arterial spasm or undiagnosed fractures. A physical therapy program should be initiated before discharge. Unfortunately, neuropathy and autonomic pain syndromes may develop in many survivors. These may respond to chronic pain management therapies, such as combinations of nonsteroidal antiinflammatory drugs, antiepileptic agents, antidepressants, and ganglionic blocks.15,16,129,130,232 Acupuncture may be helpful for resistant post-traumatic headaches that often accompany lightning injury. In recent years, neuropsychological deficits from lightning have become better appreciated.12,172,229-232,272 Heightened anxiety states, hyperirritability, memory deficits, attention deficit, aphasia, sleep disturbance, post-traumatic stress disorder, and other evidence of brain damage should be assessed.16 Some of these deficits are much like those suffered by victims of blunt head trauma. A rehabilitation program should be instituted early for these patients to return them to as functional a state as possible.47,231,284,285 Often, the victim’s family and co-workers have difficulty understanding the change in personality that affects many of these victims. Neuropsychological testing to define the injury, establish a baseline, and plan appropriate cognitive therapy may be helpful. It is unknown if certain personality types may predispose victims to more pronounced neuropsychological symptoms. In some cases, the feeling of isolation and change that victims sometimes experience can lead to depression, substance abuse, and suicidal ideation. Because of unfamiliarity with lightning injuries and their sequelae, many physicians are ill equipped to manage long-term care of lightning victims or may be so skeptical that the victim and family become frustrated and angry with their care. Burns† Lightning burns may be apparent at the time of admission but more commonly develop within the first few hours. They occur in less than one-half of lightning survivors and are generally superficial, unlike high-voltage electrical burns, and seldom cause massive muscle destruction. Myoglobinuria is infrequently seen, so vigorous fluid therapy and mannitol diuresis are not usually indicated. In the rare instance of myoglobinuria, intravenous mannitol and urine alkalinization with bicarbonate may be used. Overzealous hydration with resultant cerebral edema from the presumption of similarity to high-voltage injuries has probably harmed more lightning victims than has myoglobinuric renal failure.

*References 15, 45, 46, 49, 55, 57, 58, 66, 67, 283, 284. † References 22, 63, 71, 72, 98, 131, 152, 202, 213, 214, 256, 257, 261, 273.

Lightning burns are generally so superficial that they do not require treatment with topical agents. In the unusual instance of deep injury, topical therapy is standard. The findings that lightning burns are superficial and do not require active surgical intervention is reinforced by Matthews and Fahey.202 Their paper provides a useful guide to the remote need for surgical intervention in lightning injury. Eye Injuries* Eye injuries are myriad. Visual acuity should be measured and the victim’s eyes thoroughly examined. Cataracts may develop in the first few weeks or months. Eye injuries should be treated in standard fashion and may require referral to an ophthalmologist. Case reports of successful treatment of optic neuritis with highdose corticosteroids similar to those used with spinal cord injury have been reported, but because there were no controls, it is not known if recovery would have occurred without their use. Ear Injuries† Loss of hearing mandates otologic evaluation. Blast as well as direct injury may occur. Simple tympanic membrane rupture is usually handled conservatively with observation until the victim’s tissues heal. Sensorineural damage to the auditory nerve, resulting in hearing changes, dizziness, and permanent tinnitus and facial nerve palsies, is not uncommon. Ossicular disruption or more severe damage may necessitate surgical repair. Otorrhea and hemotympanum suggest basilar skull fracture. Complaints of pain around the angle of the victim’s jaw may indicate occult fracture of the styloid process and other musculoskeletal damage. Pregnant Victims‡ If a pregnant woman is struck, fetal viability should be assessed, including fetal heart tones, ultrasonography to observe fetal activity, and other standard methods. Other Considerations Gastric irritation is sometimes seen.109 A nasogastric tube is appropriate if ileus or hematemesis occurs. An abdominal CT scan may be indicated in comatose patients who remain hypotensive, because intestinal contusions and hemorrhage have been reported. It is common for survivors to report continuing nausea for several weeks to months. Endocrine dysfunction, perhaps as a result of pituitary or hypothalamic damage, including amenorrhea, impotence, and decreased libido, has occurred in some victims. Spinal cord or sympathetic nervous system injury or postinjury depression, as well as side effects of medications, may also cause impotence, decreased libido, and sexual dysfunction after lightning injury. Pronouncing the Victim Dead§ Dilated pupils should not be taken as a sole sign of brain death in the lightning victim. It is always necessary to exclude other causes of dysfunction and eliminate them before death is declared. Hypothermia with lightning injury may cloud end-of-life decisions. If the victim has not regained a pulse after 20 to 30 minutes of resuscitation, it is reasonable to cease cardiopulmonary resuscitation. Long-Term Care¶ In the long run, there is no specific treatment for lightning injury. It should be remembered that lightning is a nervous system injury that can involve chronic pain, neuropathy, and brain injury, sometimes complicated by initially unrecognized musculoskeletal injury. Most symptoms can be treated in standard fashion, including cognitive therapy, pain management, job retraining, and counseling as indicated by the survivor’s signs and symptoms. *References 38, 42, 95-97, 102, 121, 123, 151, 160, 172, 208, 219, 220, 240, 261, 285. † References 10, 26, 28, 39, 113, 115, 120, 160, 178, 209, 222, 223, 236, 265, 278. ‡ References 106, 112. § References 37, 44, 72, 78, 79. ¶ References 47, 83, 84, 183, 231, 256, 283, 284.

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study of antihypertensive agents has been undertaken for lightning survivors.

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As with any serious illness, the caregiver and family may be the unsung heroes and need support, recognition, and counseling. Referral to Support Groups and Other Information Sources Lightning Strike and Electric Shock Survivors International (LSESSI), a support group founded in the late-1980s, has numerous materials for survivors and their families. LSESSI is located at PO Box 1156, Jacksonville, NC 28541-1156 (Tel: 910-346-4708, http://www.lightning-strike.org).83,84,189 Other useful websites are http://www.uic.edu/labs/lightninginjury and http://www. lightningsafety.noaa.gov.

Precautions for Avoiding Lightning Injury LIGHTNING SAFETY GUIDELINES* Most lightning casualties in the United States involve only one person at a time. The possibility for multiple injuries exists where large crowds gather for fireworks, holiday beach outings, sporting events, concerts, and other similar situations. Lightning injury prevention behavior should be proactive, rather than reactive, after the threat becomes imminent. Clearly defined education is important to help make proper decisions at the critical times when lightning threatens. Prevention is more important than cure, as is apparent from the impacts of lightning injuries described in the medical discussions of this chapter. There are about 25 million cloud-to-ground lightning flashes in the United States every year, and one-half of them have a subsequent return stroke coming to ground at a different location up to a few kilometers from the first stroke.262 As a result, it is impractical for the NWS to warn of every potentially dangerous lightning flash, so the key to safety is individual education and responsibility.† Only one-quarter of U.S. lightning fatalities are associated with tornado or severe thunderstorm warnings issued by the NWS.19 As a result of this situation, a broad collection of lightning safety guidelines for minimizing the lightning risk is available from a multiagency group coordinated by the NWS at http:// www.lightningsafety.noaa.gov. Cloud-to-ground lightning data from the National Lightning Detection Network have shown that lightning deaths and injuries occur in generally equal portions before, during, and after the strongest lightning activity in a thunderstorm.147,185 Weak thunderstorms are as likely to result in casualties as are moderate or strong storms.146,185 A detailed study by Lengyel and associates185 found that nearly one-half of lightning victims had enough warning to reach safety from nearby lightning before they became a lightning casualty, so that anticipation would have been beneficial. A multidisciplinary group of lightning safety experts met in 1998 to develop guidelines that had not been adjusted in any meaningful way for several decades.147,288 Development of national lightning detection networks and availability of other meteorologic data sets had caused major rethinking of existing guidelines. Since then, most of the 1998 guidelines have been supported, others have been evaluated, and some have been adjusted further or placed into a more limited context. At this point, most pre-1998 recommendations are recognized as based on false assumptions and have become obsolete. The following sections describe the stages of a lightning safety approach and how the plan varies according to the circumstance and size of the group.

LIGHTNING SAFETY PLAN‡ For a person who is watching the sky and has prepared by being aware of the forecast, lightning rarely appears so suddenly that precautions could not have been taken to minimize the risk. *References 27, 72, 74, 88, 101, 142, 147, 186, 217, 244-247, 276, 288. † References 61, 74, 147, 185, 186, 276, 288. ‡ References 27, 74, 88, 101, 147, 217, 244-246, 276, 288.

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Thunderstorms take tens of minutes to develop or move into an area, so the only surprise is because it was not anticipated correctly. The surprise is avoided by a series of steps in a lightning safety plan. The plan includes knowing the safest place to reach, how long it takes to reach it, how far in advance action should be taken, who makes the decision, and backup plans when the people or situations change. The National Collegiate Athletic Association (NCAA) website has a succinct version at http:// www.ncaapublications.com/productdownloads/MD10.pdf.27 Before working in the open or going on a recreational trip, be aware of weather forecasts and conditions. If thunderstorms are forecast later in the day, pay attention to updated forecasts by using NOAA weather radio, cell phone alerts, websites, and tailored information from private weather providers. Because access is available for much of the United States via mobile methods, there should be fewer surprises with regard to storms that are growing or moving into an area. Users, however, should be aware that many sources of lightning data, particularly free sources, may be delayed by several minutes or more. Unless users ensure that lightning data are real time, they may be lulled into a false sense of security and not take timely safety precautions. Thunderstorm and tornado warnings issued by the NWS indicate that thunderstorms are almost certain to occur in the area, and most likely in surrounding counties. However, most lightning does not occur within a warning area, but in less intense yet frequent nonsevere thunderstorms that also contain the lightning danger.19 Most lightning occurs in the summer months of June, July, and August, as shown in Figure 3-16, online.141 Further, most lightning occurs between noon and 6 PM, as shown in Figure 3-2. These general figures make it much more apparent when to avoid long, risky exposure to lightning. Storms start before noon on some days, such as over the high mountains of Colorado, where a few flashes are not uncommon by 10 AM on active days. In such a location, starting hikes very early in the morning helps to eliminate the lightning threat, but beginning in late morning on active thunderstorm days, there is increased vulnerability to lightning.136,287 Similarly, lightning may linger into the summer evening in almost all regions of the country, when sports and recreation users are more likely to be outdoors on every day of the week.27

APPROACHING THUNDERSTORM Pay more attention to lightning than rain. About 10% of all cloudto-ground lightning strikes occur without rain at the location of the lightning ground strike, so waiting for rain to arrive does not provide absolute protection from lightning as a thunderstorm approaches. Thunder can be heard up to about 10 miles away in quiet conditions, but not nearly that far in the presence of wind, traffic, and when inside a structure. A simple rule at the start of a storm is, “When thunder roars, go indoors.”132,216,244-247 This rule removes any doubt about whether it is time to take action and is effective as a thunderstorm approaches. Although there is some overwarning because of distant lightning that may not reach a location, it is an effective and easy way to manage the lightning threat. For a more objective approach, use the 30-30 rule developed at the 1998 lightning safety meeting.* The first 30 refers to the time in seconds between seeing lightning and hearing thunder from that flash (the second 30 refers to the wait time; see next section). If the time interval from flash to bang is 30 seconds or less, people are in danger from lightning and should actively seek a designated safe place. This count of 30 seconds indicates that lightning is no more than 10 km (6.2 miles) away, using the speed of the sound of thunder of 5 sec/mile. Ten kilometers (6.2 miles) includes about 80% of all subsequent cloud-to-ground lightning flashes in a storm.148 Variations of the 30-second rule are widely used at military and civilian airports for radii between 8 and 16 km (5 and 10 miles), where validated and accurate cloud-to-ground lightning detection systems are used. In such *References 27, 74, 101, 145, 147, 199, 276, 288.

CHAPTER 3  Lightning Injuries

situations, too many warnings from a large radius around a point result in a lack of trust in the method, whereas too small a radius misses too many storms and leads to more injuries. Comparison of the two methods indicates that “When thunder roars, go indoors” is a useful approach for everyday use. The first 30 of the 30-30 rule corresponds to a 10-km (6.2-mile) radius and is more objective than the previous phrase. It may be adjusted based on local preferences to balance down time with operational efficiency at a facility such as an airport or mine. With either approach, when the rule indicates that lightning is a threat, attention should focus on the lightning rather than the rain. Outdoor activity should be stopped with immediate evacuation to a designated safe place.

END OF THUNDERSTORM Do not underestimate the danger of lightning at the end of a thunderstorm. As many people are killed or injured by lightning at the end as at the start or during the middle of a storm.148,185 A number of people are killed every year when going outside into the backyard of a home too soon because of impatience or crossing a field or parking lot before the storm is finished.137,139 The second 30 of the 30-30 rule says to wait 30 minutes after the last lightning is seen or thunder is heard before resuming outdoor activities.27,74,101,147,288 At night, flashes may be visible low on the horizon inside tall thunderstorms up to 80 km (50 miles) away, but these are not of much concern unless the lightning channel itself is visible to the ground. Since the 1998 meeting, it has become apparent that 30 minutes is longer than is needed in most situations because the lightning threat is minimal after 15 minutes.148 But in a large group situation where a long evacuation time is needed, the full 30 minutes is needed to avoid returning people to a field or stadium too soon, then sending them to safety again a few minutes later when the lightning threat returns. In one’s own backyard, a person can wait 15 minutes after lightning and thunder and be quite safe, although a lingering flash can cause a return to a dwelling in a matter of a few seconds if necessary. In practice, most airports and other industrial situations use a wait time of 15 minutes, although local high levels of safety concerns may make 30 minutes more desirable. Less than a 10-minute wait time is not desirable. There are exceptions to all rules when a large overhead thunderstorm lingers for hours over a location.156 In such a situation, the policy is difficult to balance between efficiency and safety of outside workers.

SAFE PLACES INSIDE There are two reliable places to be safe from lightning. One safe place is inside a large substantial building and the other is inside a fully enclosed metal-topped vehicle. Buildings Large substantial buildings where people live and work are very safe from lightning in more developed countries. Although such structures are often hit directly by lightning, fatalities inside them are extremely rare, considering the amount of time spent by people inside them. In a study of U.S. dwellings and buildings, the only lightning-caused fatalities among many hundreds of cases were to older adults, very young persons, or persons with physical or intellectual disabilities who were unable to leave the dwelling when a fire broke out, usually at night.139 There were no fatalities inside offices, schools, or other large buildings. As a result, adequate safety is attained by directing people to go inside a large substantial building, including a dwelling, rather than staying outside.216 The protection in modern buildings is provided by grounded wiring and plumbing, as well as metal structural members inside the buildings that carry the charge of a strike to the structure around people and into the ground. Contact with conducting paths of wiring, plumbing, corded telephones, and large openings such as garages and doors can result in injuries. Such contact needs to be avoided during the presence of lightning to avoid potentially serious injury, but these are not known to lead to fatalities in well-constructed and grounded buildings.

FIGURE 3-45  Lightning-unsafe picnic shelter in Tucson, Arizona. Note warning sign on roof, which states: “WARNING: This structure is unsafe for shelter during lightning storms. Seek suitable shelter elsewhere.”

Unsafe indoor locations are small structures such as those used as golf, beach, sun, rain, school, agricultural, or bus shelters (Figure 3-45). All of them are to be considered unsafe and must be abandoned for a larger safe building. It is possible to make such small structures safe, but their protection must be designed and installed by a knowledgeable lightning protection specialist.171 Also on this list of unsafe structures are all tents that provide rain protection but are invisible to lightning.135 Pads on the ground inside a tent are of no value in lightning protection, and the composition of the tent structure and poles provides no protection. In less developed countries, these dwellings and workplaces may be thatched-roofed huts that provide no protection from lightning because they are often ungrounded and made with nonconducting material.139 Note that it is possible to provide low-cost lightning protection for such unsafe structures by using simple towers and natural local materials for grounding; however, these must be designed and installed by knowledgeable lightning protection specialists to be sure of their efficacy.180 Vehicles* Fully enclosed metal-topped vehicles are safe from lightning and should be used as a safe place when no large substantial building is available. In a study of hundreds of vehicle incidents, there were injuries to vehicle occupants in less than one-half of the cases; the majority said the experience was frightening but they were amazed to be unscathed. There have been no documented “electrical” injuries to occupants, with the exception of those involving direct wiring, such as the older handheld police radios.137 The only unambiguous fatality was due to an older adult who was startled or incapacitated by a nearby flash and drove into oncoming traffic. Damage to the vehicles ranged from minor, such as antennas vaporizing, to a few cases of major engine failure and electrical fires; nevertheless, all passengers escaped such vehicles. Unsafe vehicles are those without the safety of fully enclosed metal surroundings that act in a manner consistent with a Faraday cage.76 Safety is provided from a direct vehicle strike by the lightning energy traveling across the outside shell of the metal vehicle and around anyone inside, with subsequent arcing to the ground through bumpers or axles. This path may account for the mistaken impression that tires are the safety feature; they are sometimes blown apart by current passing through the vehicle’s metal frame (nearest to the ground) through the tires. Unsafe vehicles have cloth tops (convertibles) or fiberglass or plastic bodies. Others include golf carts and four-wheelers with open sides. Strikes to such vehicles have no defined path to ground, *References 137, 156, 216, 288.

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and it is not safe for people to be inside them. Although it is possible to design lightning protection for unsafe golf carts and other open-sided vehicles, there is no such commercially available product; such an approach requires an exacting configuration and correct behavior of people inside them.90 Another very serious cause of injury is the step voltage when people are on the ground while working on a vehicle during a thunderstorm. Any place outside such a vehicle is as unsafe as anywhere else outside.137 Particularly dangerous is step voltage, when a person is in contact with both the vehicle and the ground. This situation occurs when stepping into or out from a vehicle when lightning strikes the vehicle, because the step potential between the energized vehicle and the ground is very large. Conversely, a nearby ground strike will travel to a person with one foot on the ground and the other in contact with an unaffected vehicle. Other situations outside a vehicle include frequent cases on parking lots, waiting for buses, and law enforcement and other people near but not inside disabled vehicles. Finally, a fully enclosed metal-topped vehicle can be used as a safe place at a school or sports event. If flashes are going to strike the ground at such a venue, it is an easy choice to be inside such a vehicle rather than outside at the same location.

ALWAYS UNSAFE OUTSIDE* There are no reliable places outside to be safe from lightning. Earlier recommendations had not sufficiently emphasized the nearly complete safety of being inside a large safe building or fully enclosed metal-topped vehicle, as described in the previous two sections. Some recommendations continue to emphasize the speculative safety approaches outside, at the expense of pointing out the reliable safety that is often present in more developed countries in nearby substantial buildings and fully enclosed metal-topped vehicles. One of the most important misconceptions of such outdoor safety advice is the expectation that the direct strike is the most common mechanism of lightning injury and that avoiding such a direct strike resolves the danger. As described elsewhere in this chapter, it is estimated that only about 3% to 5% of lightning injuries and deaths are due to direct strikes. The result of this mistaken direct-strike approach is the recommendation that lowering one’s height is sufficient, rather than recognizing the other more likely mechanisms and having reliable safety plans and evacuation. The reliable lightning safety approach is to recognize the lightning threat early and go to the known safe places of buildings and vehicles described above. The sooner a person reaches the safety of one of these locations, the sooner the lightning threat is ameliorated. As a result, the everyday lightning situation encountered by an individual is to anticipate the lightning threat, know where the safe building or vehicle is located, how long it will take to reach that location, and complete the plan by reaching it before lightning arrives. Lightning is not predictable in its path to ground, and what it strikes is not predictable to any certainty. Case reports have indicated that the prior advice of seeking a small tree among larger ones is unreliable. Recent very high-speed video shows lightning traveling toward ground in multiple branches. The first branch that contacts the surface of the earth is the only important one, whereas the rest dissipate in the air. Which branch reaches the surface appears to be random within the flash.251 Roeder242 examined the relative values of common outdoor lightning avoidance advice according to the five mechanisms of lightning injury described elsewhere in this chapter. It was found that if every precaution were followed, and some are quite difficult, only a 50% reduction in risk is achieved. The other 50% of the time results in an injury or fatality, which is unacceptable. As mentioned, one of the least effective approaches is to stress the direct strike by lowering one’s height, because the directstrike situation is scarce. More implications of this analysis will be described in the next section. The recommendation is *Reference 212.

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reinforced that reliable safety is achieved by reaching the safe building or vehicle in a timely manner. The Difficulty of Wilderness Situations No action will achieve certain safety from lightning in the wilderness away from a substantial building or fully enclosed metaltopped vehicle. The two approaches to lightning safety in the wilderness are to avoid the risk in the first place and to accept that a lightning risk exists. The amount of time spent by hikers and climbers in multiday situations is quite small. The more common situation is a hike or climb lasting 1 day or less, often during a weekend day.135 For this common situation, the first approach of avoiding the risk is most manageable, because a vehicle or sometimes a large building is available at the trailhead. Pay close attention to the forecast for the day, and avoid the daytime period when lightning is most prevalent. Over high mountains of the West, for example, storms start as early as 1000 or 1100 LST, so hikers should be off the higher parts of the mountain by that time. Otherwise, postpone the hike to another day. Such an approach does not preclude hiking on most days, because a study over Colorado’s Rocky Mountains203 showed that no location had lightning on more than one-third of summer days, and almost none during spring and fall months.141,194 The choice exists, then, to manage the risk by choosing the time and place of a day hike. Once the hike is under way, pay attention to building clouds that indicate future lightning, stop the hike or climb, and return to safety when the situation arises (see Approaching Thunderstorm and End of Thunderstorm). The pressure of a schedule or other factors may be such that a wilderness activity will take place in spite of the possibility of a very real lightning threat. Then a hiker or climber has accepted the personal risk in the same manner as risks from dangerous animals, falls, or other natural hazards. A portable device has been developed for lightning safety involving a triangle of tall rods, but it has not been made commercially available.90 Roeder242 analyzed the relative risk when no acceptable buildings or vehicles are nearby. The five mechanisms of lightning injury were considered to identify actions that are to be taken, such as crouching (minimal value) and staying away from tall objects. The results of the Roeder analysis show a reduction in risk to about one-half of the full lightning exposure. In other words, following all precautions does not prevent half of the lightning risk. Because the steps must be performed correctly, remembered under duress, and reduce the risk for death or injury by only half, they are not to be considered when lightning safety can be attained at a safe building or vehicle.

LARGE GROUP SAFETY An individual can respond to the lightning threat quickly by going inside a large substantial building or fully enclosed metaltopped vehicle. In less than a minute in the backyard of a dwelling, for example, quick action places the person in safety. When the threat is over, using a rule such as 15 minutes for the cessation of lightning and thunder, an individual can return to the backyard. If the lightning threat returns, a person can quickly go back into the dwelling or a safe vehicle until the threat is over. For larger crowds, all of these steps are more difficult. Steps include accepting that the lightning threat is important, knowing how to identify the lightning threat, where the safe locations are located, how long it will take to reach them, when the threat is over, and who makes these decisions.27,74,88,147,199,216,276 In the case of a neighborhood youth soccer game, for example, safety can be reached in minutes in nearby fully enclosed metaltopped vehicles. When game officials or others make the decision to go to safety, players and spectators need to go immediately to the cars, vans, or buses. Note that small venues may have rest rooms or concession stands that are likely to be unsafe from lightning, and people in those locations need to be informed to abandon them for the safety of vehicles in parking lots around the field (see Buildings section of Safe Places Inside). At a somewhat larger school sporting event, including practices, there are likely to be nearby lightning-safe large buildings. Sports and custodial staff need to be informed to leave doors unlocked or

the all-clear signal is appropriate. Nothing is more ineffective and reduces confidence more in the evacuation process than sending people back to their seats, making them return to a safe place again a short time afterward, only to return once again to their seats. For a large stadium or golf tournament, for example, at least 30 minutes should be used for the wait time, and still longer times may be needed to avoid the back-and-forth crowd movement. At a fireworks show, people may be unwilling to leave a favored spot on a field, so crowd control and security specialists may be needed to address the situation. However, in many cases after the first suspension of a concert, for example, some of the crowd does not return, so the problem may be somewhat reduced. Instead of moving a large group from one place to another, it is possible, and usually much less expensive than managers might expect, to provide safety in place. The approach is to place large, properly grounded poles and overhead wires that divert the flash from striking a crowd by using these down-conducting paths into the ground.11 The principles are the same as those routinely applied in lightning protection of buildings, towers, utility poles and lines, and many other aspects of modern infrastructure. This approach has long been used for the space shuttles and other critical government activities and structures. There are large benefits to installing such a system, such as no evacuation, no need for safe places to be identified, and no uncertainty in the process and its execution. However, people must stay at the correct locations within the protection provided by such a system and trust that it will work as intended. Flags or banners at the top of the protection poles can make the installation as unobtrusive as possible for the crowd and media at such an installation (Figure 3-46).

A

B

C FIGURE 3-46  A, Natural protection zone of a stand. B, The effect of flagpoles implementing Franklin rods. C, The added effect of a catenary added to a stand. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)

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be available to open doors when players and spectators need to go inside. When the crowd is large at a sporting or other outdoor event, the situation becomes more complex. Advance planning is essential. The first step is convincing a venue owner or manager in advance of the potential lightning risk. Many lightning threats are accompanied by rain, strong winds, hail, and other significant weather, so that placing lightning into the context of the thunderstorm threat may be more acceptable. In the United States, the lightning threat at collegiate football games was examined by Gratz and Noble,119 who found that a single game’s threat is not large but the large number of games per year makes a lightning incident at a football game inevitable over a period of years. A case study of an individual game’s response to the lightning threat is presented by Holle and Krider.142 Edwards and Lemon101 emphasized the potential for major storm-related disruptions at auto, dog, and horse races; professional and collegiate sporting events; and outdoor concerts but have often been met with silence or limited positive responses. Among the situations examined by Edwards and Lemon101 are recent close calls of tornadoes passing near large crowds. Fortunately there has been a positive lightning recommendation by the NCAA for NCAA schools.27 Although not all institutions follow the recommendations, it has become common for all types of U.S. collegiate sporting events to be delayed or suspended because of this policy, as well as many more games at the high school and other levels. In fact, there have been almost no lightning casualties in the last few years in the United States at organized sports events. It is a useful tactic in convincing venue operators that they should follow the lead of the NCAA in accepting the lightning risk. This recommendation applies equally to practices and rehearsals. Once there is acceptance of the lightning threat, a method of identifying the existence of lightning is needed. For a large crowd, the sound of thunder is probably not applicable. Reliable, proved, and accurate cloudto-ground lightning data are now available on cell phones, websites, and other portable devices that are objective measures of lightning. Any purchaser or monitor of these, however, should make sure that lightning data are real time. Currently, many sources of lightning data, particularly free sources, may be delayed by several minutes or more, depending on the supplier. Rules need to be established for how close is close enough at a particular stadium or event site. Stadium managers need to know how long a lead time is needed to evacuate people to safety. Once that time is decided, it determines the distance to lightning for action to be taken as it approaches. The rule needs to be followed objectively on days when the threat exists. When an announcement is made of a lightning threat, the plan goes into action. At a football game, for example, players and coaches may try to stay on the field, which gives the impression that the situation is not really important. In every case, the game or performance area needs to be empty and nothing shown on video screens except the current safety announcement, so that the event no longer provides an attraction to the crowd. In many stadiums, there is adequate room beneath the stands.142 At other locations, a nearby gymnasium or warehouse may be the best alternative, so plans need to include permission to enter those buildings. In the case of a golf tournament, the first concern of organizers is for player and sponsor safety; they can be sent quickly to a safe building or vehicle. However, spectators need a much longer time to reach the safety of their vehicles and may need to walk several miles. While at the safe location, information needs to be given to the audience and participants concerning the status of warnings. This can be difficult in many situations, and warning horns or message boards may be the best approach. Informing people waiting in diverse locations involves complete and active planning in advance on the part of the venue operator. The safe location also needs to be comfortable enough for the crowd to accept a long wait. Appropriate signage or inclusion of lightning safety information in event programs may also be useful in communicating safety information. The all-clear at the end of the lightning threat needs to be identified as objectively as is the beginning (see End of Thunderstorm). As crowds become larger, a very long wait time until

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Covered stand

FIGURE 3-47  Protected zones on a pathway from light poles of varying height. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)

Protection in Situ* The Franklin rod is often the basis of lightning protection schemes. Many existing structures can be turned into such rods with ease without detracting from appearances. Examples are given below. It is emphasized that these are illustrative only, and proper design is needed when these are being implemented. Figure 3-47 shows a pathway with light poles of a given height. Spacing of these poles may be selected to protect the pathway, depending on the height of the poles and width of the path. Figure 3-46, A shows the “natural” protected zone around a temporary stand that might form an evacuation region if other risks are accepted. Franklin rods (see Figure 3-46, B) added along the back of the stand extend this zone and also add some in situ

FIGURE 3-49  Effect of existing covered stands and lighting stanchions. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)

protection. Useful Franklin rods are formed by flagpoles that have the required “look.” A horizontal wire at a given height above a stand also provides in situ protection (see Figure 3-46, C ). These can be made all but invisible, especially to media cameras. Alternatively, they can carry banners, lights, or media cameras. Figure 3-48 shows horizontal wires providing protection to a group of stands. The width of the protective corridor depends on the height of the catenary, and the position of the corridor can be altered as a design parameter for effectiveness. Figure 3-49 shows a stadium for a field game like baseball, where an existing stand provides some protection, as do lighting pylons. The addition of overhead wires can complete the coverage. Figure 3-50 shows the main stadium stylistically and shows how open stands at either end of the stadium can be protected by fine wires, which are all but invisible.

Controversies in Lightning Injury* Much remains to be learned about lighting injury, and knowledge at present remains partial.

Covered stand Open stand

Open stand

Open field—overhead is a network of cables along which cameras travel—providing adequate protection.

Covered stand

FIGURE 3-48  Use of catenaries to protect several stands. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)

FIGURE 3-50  Open field—a properly installed network of overhead cables that can double for moveable cameras can also provide adequate protection. (Redrawn from Crowd protection strategies: Experience from the Sydney Olympic Games, 2000. Presented at International Conference on Lightning and Static Electricity, Blackpool, UK, 2003.)

*Reference 10.

*References 69, 70.

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This is especially evident when expert and legal assessments are made of victims. For example, the area of the psychological effects of lightning injuries is under active research and still needs clarification. The effects are well documented in the literature. Nonetheless, psychiatric and psychological standards (e.g., the Diagnostic and Statistical Manual of Mental Disorders and other standard teaching and textbooks) have not yet incorporated the syndrome into their formularies. This highlights the fact that victims represent a numerically small group in routine practice, and most practitioners are rarely aware of the literature on the subject. Consequently, we see established practitioners struggling for a diagnosis and trying to fit the “new” syndrome into existing categories.

RESEARCH METHODOLOGY PROBLEMS Cooper69,70 draws attention to further features of what is not yet known in lightning injury and documents methodology difficulties. She states that without knowledge of the basic physiology, only general symptomatic aftercare can be rendered. It may be more desirable to have specific treatments or even early interventions that might stop or change the course of the injury cascade that is precipitated by the initial injury. Research on lightning injuries is difficult (Box 3-5). There are no public health regulations that require reporting of lightning injuries, so cases are difficult to collect and survivors are difficult to locate in any systematic fashion.54,143,205 Although it may be convenient to use select populations, such as the membership of LSESSI, as a study group, people who join support groups differ from those who do not. They represent only a subset of survivors and may have systematic biases developed from the services and materials that LSESSI supplies to its members.69,70,189 In addition, limited research can be done with them because of ethical limitations on human research, national dispersion, and lack of funding for the research, among other difficulties. To sort out lightning electrical effect from other etiologies, it is necessary to obtain relatively recently injured patients (no more than 6 to 12 months) with a “clean” history. There must be no *References 69, 75. BOX 3-5  Research Problems Human Research • Recruitment of cases • Study biases • Dispersion of subjects • Cases must be free from • Diabetes and other neuropathic illnesses • Drug history • Psychiatric history • Blunt head trauma Animal Research • Expensive—both animals and equipment • Large number of animals for some studies • Difficult signal processing problems • Monitoring equipment design • Shock timing control considerations • Definition of dose • Standardization of dose • Flashover effect Molecular Biology • Cell culture, blood levels of indicators of injury, and so on • Requires specialized techniques • Bioengineering, collaboration • Expensive

past history of alcohol or drug abuse, head injury, psychiatric problems, or concurrent medical problems that cause neuropathic pain or psychiatric symptoms and no blast effect during the injury that would confound investigation of the electrical effects of lightning. Unfortunately, this further narrows the available pool. Difficulties therefore compel selection of other models, raising problems of applicability. Because it is difficult to recruit volunteers to stand in a thunderstorm, animal work is a reasonable alternative. Kitagawa, Ishikawa, Ohashi, and Andrews have all done credible research using animals.9,10,153,169,225 Cooper and colleagues80-82 have built a reasonable rat model, inducing most of the clinical signs that are seen in humans. Unfortunately, such research is expensive, time consuming, and sometimes requires large numbers of animals to show significant differences. Most problematic is the delivery of a “standardized dose” that can reliably reproduce a specific pattern of injury. Many hurdles must be overcome in research equipment design, anesthetic choice, and animal care, as well as shock timing and delivery, given instrumentation requirements. Monitoring equipment must be electrically isolated from the animal and shocking platform, or the connections may preferentially transmit the lightning shock to the equipment, not the animal, clouding the experiment and destroying the equipment. Some anesthetics are neuroprotective, whereas others affect cardiac function. Temperature control in anesthetized rats is a significant issue. Animals that are studied for neurocognitive injury using water maze and other behavioral models need a standardized quiet environment, which is not always possible in the cramped quarters of most animal facilities. In survival or cardiac studies, timing of the shock to either target or avoid the “vulnerable period” must be done on a statistically predictive basis, because direct sensing of the specific targeted cardiac cycle would again result in damage to the equipment.

AREAS OF SPECIFIC CONTROVERSY Survival Statistics Box 3-6 lists factors concerning the unknown issues as to why the vast majority of casualties survive.54 It is possible that characteristics of a lightning strike or possibly the mechanism by which the current impinges on the individual may be different for lightning fatalities. It is possible that timing of the lightning strike may be the important factor, particularly if it hits during a more vulnerable portion of the cardiac cycle. Although it is possible, it is unlikely that the physical characteristics of people differ sufficiently to cause a difference in mortality. Remote and Psychological Symptoms A further area of active research is the etiologic origin of symptoms not directly in the line of passage of current. This is as much for electrical injuries as for lightning injuries.211 Even when there is no indication of current near the brain or evidence of blast/blunt injury, neuropsychological testing consistently suggests an organic origin to the deficits. Imaging, imperfect as it is, suggests unspecified organic impairment. The exact nature of the impairment, its relation to functional pathologic conditions, and its origin remain obscure. BOX 3-6  Why Do 70% to 90% of Victims Survive? • Lightning characteristics (possible factor) • “Type” of lightning • “Dose” of lightning delivered • Timing of hit during cardiac cycle or other factors • Pathway of lightning • Other meteorologic conditions (possible factor) • Physical characteristics of those “hit” (possible factor) • Comorbidities • Rescue/resuscitation efforts • Where people were/what they were doing (possible factor)

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PROBLEMS WITH EXPERT REPORTING*

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BOX 3-7  Possible Injuring Forces • Blunt trauma—explosive injury • Structural changes—direct damage • Pathway of the injury • Orifice entry • Flashover—how much goes through versus around • Neurochemical changes • Autonomic nervous system effects • Electrical effects • Electroporation • Cellular level mechanical effects • Cellular level enzymatic effects • Subcellular organelle damage

Increasing awareness of the role of the spinal cord in nociception and existence of proximally directed neural pathways may provide a fruitful connection. Release of humoral transmitters may play a role. The importance of premorbid personality predisposition is unknown. It has been noted by some that the neuropsychological constellation bears resemblance to the psychological effects of other syndromes, like head injury and the response to autoimmune disorders. It is possible the symptom complex that is seen represents a “final common pathway” of brain injury due to many etiologies. Psychiatric insights, for example the effect of cortisol on hippocampal changes in depression, may offer insight into depression following lightning and electrical injury. There is a tantalizing observation allied to this of hippocampal neuron loss in electrical injury, regardless of cranial or peripheral application of current.181 Box 3-7 lists other possible factors yet to be verified. Technical Matters The degree of lightning injury, or “dose,” may vary considerably with the mechanisms of injury (e.g., direct, splash, contact), few of which have been modeled or quantified. Other technical factors regarding interaction of a lightning stroke with the body, such as the effect of multiple return strokes, are poorly known. Although flashover is known to occur, the course of energy going through the victims versus around them and the duration of energy flow initially or with return strokes is unknown. Although these factors have been calculated based on engineering assumptions, actual measurements have never been done on research subjects or simulated subjects to test the assumptions. Medical Resources Because common imaging techniques like CT and MRI are anatomic tests, results are limited by resolution achieved by the equipment. As anatomic tests, they do not show functional deficits in how the brain, heart, nerves, or other structures behave when injured. Although it has been hypothesized that deficits are at a cellular, subcellular, synapse, or enzymatic level, this has not been actually investigated or measured, either clinically or in an experimental model. Lee has corroborated electroporation of muscle cell walls with high-voltage electrical injury, but the physics of such injury are quite different from lightning physics, and certain important symptoms are also different.65,69,184 Electroporation has not been investigated in the lightning model or investigated in nerve or brain cells that are more affected clinically than is muscle tissue. Our knowledge of very short (submillisecond) impulses and their effects on the body is poor, and it is not a priori obvious that results attributed to longer durations of exposure (electrical) are immediately transferable to short (lightning) durations.

SAFETY CONTROVERSIES Predictability of Lightning Atmospheric physicists, electrical engineers, meteorologists, and other lightning experts have spent their careers working to 98

describe the characteristics of lightning, how it forms, and how it acts. However, one must always remember that, however learned and mathematical, these are descriptions and not “rules” that lightning must follow. Lightning, at best, is capricious in its behavior. We do not have complete knowledge of why lightning acts the way it does. At best, we can describe the conditions under which lightning is likely to form. The common thunderstorm cell is much smaller than expected and arises, moves on, and resolves over a period less than an hour. That is why when a huge downpour occurs with lots of lightning, all one need do is seek shelter for 20 to 30 minutes as the cell passes by, the rain decreases, and perhaps sunlight even shows. When conditions are right, multiple smaller cells of varying intensity can stack and follow each other so closely that the storm seems continuous. Sometimes, very intense storms, including huge tornadoes, can arise. The NWS is charged with providing severe weather warnings to minimize property and personal injury. Life is a calculated risk. There are always tradeoffs between absolute safety, convenience, and getting on with your life and work. The weather, like life, is somewhat unpredictable. One of the controversies is the compromise between absolute safety that results from issuing many warnings that later turn out to be “false” and lesser guarantees of safety with fewer but more reliable warnings. People learn not to pay attention when too many warnings turn out to be false. An additional complication is that because of the small areas in which thunderstorm cells arise, it is impossible for regional forecasts to cover all of them. Individuals should be aware of the general weather forecasts and incorporate their own knowledge of local weather patterns, along with an eye to the sky, when fast-changing weather is predicted, to notice quick development of nearby storms that may contain dangerous lightning. Preplanning, alertness, and knowing the lightning safety rules, primarily “When thunder roars, go indoors,” can save lives.216 Lightning Exposure Prudent outdoors people educate themselves and plan for foreseeable risks, whether they be grizzly bears, mosquitoes, hypothermia, falls, or weather problems such as flash floods, unexpected early or late snows, or lightning. In leaving civilization behind, they realize that they are giving up 5-minute response times for emergency medical services, easy food sources, warm showers, and other benefits. Unfortunately, some risks have no halfway measures that will significantly improve safety. Lightning is one of those. At the current time there is an outcry for advice on improving lightning safety for wilderness situations. However, NO place outdoors is safe when thunderstorms are in the area. Avoidance of the risk is the only prudent recourse. One must look at the risk–benefit ratio in considering any other response. During the vast majority of their lives, most people are within a very short distance of safety from lightning. Many routine outdoor adventures are on frequently hiked paths, common ascents of mountains, and gatherings at tent-only campgrounds and scenic overlooks. Planning to avoid being in these areas during times of high risk (afternoons) can minimize but not entirely exclude the chance of injury. In addition to avoidance of risk, the other part of the “When thunder roars, go indoors” rule is seeking safe shelter. Modified metal shipping (Figure 3-51) containers are used in many countries in industrial, heavy construction, and mining sites and are moved as needed by truck or heavy lift helicopter. These could be used in many wilderness situations to provide lightning-safe shelters within easy hiking distance of common paths, particularly in areas such as summer camps and parks. Development of inexpensive shelters that could be backpacked in by a scout group and set up as a summer project is potentially possible but fraught with design, testing, maintenance, and liability issues, particularly in the United States. Other considerations would be location, accessibility, expense, signage, ownership, vandalism, and permits, not to mention resistance from some at altering the environment for what may not be perceived as major risk.

Research LIGHTNING SAFETY RESEARCH There is a variety of unresolved issues relating to improving lightning safety recommendations. The topic includes a mixture of scientific, social, economic, and demographic variables that are often very difficult to identify. Although the phenomenon of lightning has become better understood in the last decade or two, many features of how lightning results in fatalities and injuries remain elusive. The mechanisms of lightning injury have been categorized more completely than before, as described in this chapter, and identifying this mixture of mechanisms has made a difference in lightning safety advice. Most importantly, the commonly held perception of a direct strike is now thought to represent only 5% or less of lightning injury. However, the estimates in Cooper70 and related publications are based on subjective experience of researchers studying large numbers of cases, showing the need to better identify the ratio of mechanisms causing lightning injury. The issue of the upward leader with regard to human injury is in need of more study. Roeder243 provides a set of questions and comments on research needed to improve lightning safety. The requirements can be divided into several main groups from Table 3-1:243 safety of buildings and vehicles, determining the range to be safe from lightning, and demographics. Building and Vehicle Safety Lightning safety recommendations now state that safety is reached inside large well-constructed buildings or fully enclosed metaltopped vehicles.* Although fatalities in these locations are rare in more developed countries, injuries continue to occur, and their circumstances are not well understood or identified. Smaller structures are always problematic, so recommendations stress staying away from them, although it is possible to make them safe in certain situations.171 A related issue is how much time people spend outdoors in more developed countries. People may now spend more of their time inside safe buildings and vehicles than in the past. Although these social data are extremely difficult to quantify, knowing this information may explain a portion of the steady decrease in lightning fatality rates in all of the more developed countries studied in recent years.138,143 In less developed regions, safe buildings and vehicles are not available to many people much of the time. Lack of such a safe place nearby is an unknown, but likely, contributor to the higher lightning fatally rate in such regions compared with more developed countries.138 Safe Distance to Lightning Real-time cloud-to-ground lightning data have been available across the United States since 1989, and monthly maps have been *References 27, 74, 88, 139, 147, 199, 216, 276.

Demographics Lightning fatality and injury rates are quite well known in more developed countries, as described earlier in this chapter. The global impact of lightning, however, is not well specified. Lightning casualty data are beginning to be collected systematically in some very populous countries, but data collection methods are in early stages and will need to be established over longer periods.239 Global lightning impacts were first estimated in Holle and López143 to be 24,000 deaths and 240,000 injuries per year around the world. This estimate is based on minimal or no data from Africa, Southeast Asia, and India, where lightning casualty rates appear to be quite high and flash densities are coincidentally often large. Availability of safe or unsafe buildings and vehicles is important in understanding the data that may be collected in less developed areas of the world. It is important that related casualty data be collected concerning activity, location, gender, age, nearby structures, and other issues related to fatality and injury data, in order to separate the influences that have been outlined here and in Roeder’s work.243 Such information can then be used to develop relevant safety recommendations and strategies.

Lightning Detection and Data Applications DETECTION Cloud-to-ground lightning over the United States has been detected and located in real time since the late 1970s. Pulses from lightning in the VLF and LF range that propagate along the earth are used to detect and locate return strokes in cloud-toground flashes. Such sensors can also locate distant lightning in the VLF because signals propagate thousands of kilometers between the earth and ionosphere.86 The U.S. National Lightning Detection Network (NLDN) has gone through several stages of improvements to combine direction finding and time-of-arrival location methods. Networks with some or most of the NLDN capabilities operate in real time in more than 40 countries; most are owned and operated by national meteorologic services or electric utilities. The NLDN has been operating continuously since 1989 and has become the benchmark for cloud-to-ground lightning detection; it has typical 99

CHAPTER 3  Lightning Injuries

FIGURE 3-51  Metal shipping container modified for use as a safe shelter in mining areas of New Guinea, Tanzania, and Peru. (Courtesy Richard Kithil, National Lightning Safety Institute.)

compiled.85,141 Similar regional or national lightning detection network data are also available to a varying extent in many other regions of the world, and a global lightning data set is becoming accessible everywhere.93 These data sets have been considered in some situations for determining the distance between flashes and the time of day and year when flashes occur.148 The linkage to specific applications is less developed than these and other major advances in detection.156 How long a lead time is needed for the general public, for airports, for sports events, and other applications? The lead time includes identifying the safe places that are nearby and a plan to reach them. What amount of risk is acceptable for each application? For example, a munitions depot has no tolerance for any direct lightning strike, whereas other situations accept more lightning exposure in exchange for economic efficiency. The role of cloud lightning in the warning process is also less well understood. Does an overhead flash without a cloud-toground flash demand the same response? What are the safe distances to anvil lightning? With the development of total lightning detection, it is becoming possible to address these questions in a more systematic way than could be accomplished earlier.94 Thunder distancing is often recommended for safety when lightning detection network data are not available. Few if any studies of thunder have been made in the last few decades, so the audibility of thunder is not well understood from the practical point of view of lightning safety. The issues involved are the normal distance that thunder can be heard, the effect of nearby noise on that distance, the role of cloud lightning in producing thunder to its use in warnings, and the relationship of hearing thunder to the actual lightning threat.243

PART 1  MOUNTAIN MEDICINE

distances between sensors of 300 to 350 km. The NLDN has been calibrated by rocket-triggered lightning, tower strikes, and camera studies to determine location accuracy over the contiguous United States of 300 to 500 m and flash detection efficiency exceeding 90%.30,86,107 The NLDN also provides polarity and peak current and measures the quality of each flash location. Approximately 70% of the multiple-return strokes within a cloudto-ground flash are also located by the NLDN, and a small fraction of cloud flashes contain pulses that are strong enough to be detected and located.86 Direction finding and time-of-arrival methods have been recently combined into an advanced method that allows global coverage to detect lightning over extremely long distances.93 The new global data set, known as the Global Lightning Dataset GLD360, achieves 70% cloud-to-ground flash detection efficiency with a horizontal location accuracy of 5 to 10 km (3.1 to 6.2 miles). Several lightning detection satellites have made twice-daily or regional passes for a few years at a time; the new GOES-R lightning sensor scheduled for launch in 2015 will cover much of the western hemisphere at an expected 8-km (5-mile) resolution. In addition to cloud-to-ground lightning detection networks, detailed cloud lightning can be detected by regional VHF networks that use direction finding and/or time-of-arrival techniques over line-of-sight distances.92,134,175-177,192,264 These networks track the horizontal branching associated with cloud-to-ground flashes, and some provide vertical resolution. Such cloud lightning networks have closer spacing between sensors than the NLDN, because they use line-of-sight detection in the VHF frequency range. Growth of both larger global and smaller regional networks has occurred beyond the medium-area coverage of wide-area VLF/LF networks. These technologies indicate the need for different techniques or frequency ranges to meet differing demands for lightning information.86

APPLICATIONS The first operational U.S. lightning detection network was developed for early recognition of lightning-caused fires. Eventually, large networks were established to detect cloud-to-ground lightning across the western United States, Canada, and Alaska. Cloud-to-ground lightning is the largest cause of transients, faults, and outages in electric power transmission and distribution systems in lightning-prone areas. As a result, this was the other early application of such wide-area networks.86 In these situations, each flash or stroke is carefully identified as the cause, for example, of a power-line fault on a transmission or distribution line. It should be noted that the initial motivation leading to development of real-time lightning detection was concern about lightning during ground activities and launches at Kennedy Space Center in the 1970s.86 A very broad array of applications of lightning detection data has developed over the last three decades. There are more than 2200 published papers on the applications and operations of real-time lightning detection networks in the United States and elsewhere. The applications can be separated into four categories, those of the direct threat from lightning and lightning as an indicator, substitute, or covariate. Direct Threat The direct threats to forest and utility concerns are described in the previous section. In addition, archived and real-time lightning data are used in many forensic and insurance applications. Other direct threats include munitions, ground safety in aviation and defense operations, recreational and workplace safety, spacecraft launches, and many other situations. However, the linkage of lightning network data with human casualties has not often been made, and more research is needed.133,148,156,185 Indicator Climatologies of lightning have been developed over a variety of regions and time periods.141 Such annual, monthly, or hourly maps can also be divided according to the type of meteorologic regime at the time to provide information about where thunderstorms and associated impacts are most likely. Lightning 100

climatologies have been found to be easier to compile than are many other data sets, such as radar reflectivity, because VLF and LF lightning detection is unaffected by terrain. In remote regions where conventional radar and surface observations are not available, tracking of thunderstorms and assessing topical and nontropical cyclone status are important challenges in weather prediction for civilian and defense purposes. Thunderstorms over the ocean represent a threat to aircraft routing and ocean shipping and are usually beyond the range of ground-based meteorologic radars. Current research with longrange lightning data has indicated the presence of sporadic cloud-to-ground lightning in the inner cores of tropical cyclones that may be useful for assessing their intensity changes. There are many other ways that meteorologists use lightning data to indicate the state of the atmosphere. These include identifying the difference between showers and thunderstorms; deciding when convection has become strong enough to produce the first flash in a developing thunderstorm; identifying storm orientation, size, and shape; the location of frontal boundaries; and when excessively high lightning rates are occurring in a thunderstorm that may indicate significant weather of many types. Isolated versus organized thunderstorms can sometimes be assessed better with lightning data than with radar and/or satellite information. Lightning data can also be used to indicate the location and timing of a developing low over the oceans, as well as the presence of very cold air aloft. In addition, some winter storms have distinct bands of ice and snow that include lightning where the heaviest precipitation may be falling. Substitute In many situations, such as over oceans and less developed countries, the desired meteorologic data are not available to identify the situation that may lead to significant or severe weather. For example, over the oceans beyond radar range of about 300 km (186 miles), aircraft can use lightning as a radar substitute to identify turbulence for air traffic management. Similarly, meteorologic radar information is lacking in mountainous areas of the United States below mountain tops due to blockage of the radar beam, so lightning can identify thunderstorms in rugged terrain. Rainfall can also be estimated to some extent with lightning information in regions, times, or areas when radar, rain gauge, or other information is missing during flash floods, tropical cyclones, and other severe weather. National meteorologic agencies also use lightning data along borders of neighboring countries without accessible radar data. Lightning data have proved valuable in geophysical research concerning the natural versus man-made production of nitrogen oxides. Covariate When radar, satellite, and surface data are available, real-time lightning detection data can be used to identify trends that occur simultaneously or earlier or later than other data, as well as spatially displaced from other information. Examples include lightning jumps combined with radar in severe weather situations, and hurricane eyewall outbreaks as the storm changes intensity. More complex methods are also being actively pursued with respect to the assimilation of lightning network information into numeric weather prediction models to help initialize them by better locating convection. There is also promise that lightning can be combined with radar or satellite data to more accurately locate heavy and excessive rainfall, because VLF and LF lightning network data do not suffer from terrain effects. Changes of cloudto-ground lightning polarity and rate changes, as well as ratios of cloud to cloud-to-ground lightning, are areas that require large, accurate, and complex data sets and statistical analyses over multiple regions but hold promise for many applications.

Lightning Explosive Barotrauma Lightning is a multiphysics phenomenon requiring a multidisciplinary approach. Current lightning injury models suggest that lightning injury is chiefly electrical and/or thermal in nature. Although electrothermal phenomena explain the vast majority of injuries observed in lightning strike victims, including cardiac and at least some of the neurologic injuries, review of the lightning

The return stroke heats the channel created by the preceding stepped or dart leader from nearly 10,000 K to near 30,000 K or more in several microseconds or less. Such a channel overpressure will result in an expansion of the luminous channel and the formation of a shock wave that propagates outward and eventually beyond the luminous channel, which attains pressure equilibrium with the surrounding atmosphere within tens of microseconds. The shock wave differs from the acoustic wave (thunder) in that it compresses and heats the air and, as a result, propagates at supersonic speeds. The initial propagation speed of the shock wave is probably about 10 times the speed of sound. After the bulk (probably 99%) of the energy delivered to the shock wave has been expended in performing thermodynamic work on the surrounding atmosphere, the shock wave is transformed, within a few meters or less from the lightning channel, into an acoustic wave that propagates at the velocity of sound. Thus, the heated-channel thundergeneration mechanism involves the production and evolution of the shock wave, which is typically characterized by its pressure as a function or radial coordinate at different instants of time. A further review of the lightning literature reports that thunder consists of a roughly cylindric initial pressure shock wave in excess of 10  atm at the lightning channel. The shock wave rapidly decays to a sound wave within meters. The pressure wave—shock propagation—sometimes may cause exterior

and interior damage to structures. There have been anecdotal reports of popping of nail-supported drywall away from horizontal and vertical wooden studs inside houses and broken glass windows. It is not uncommon for a lightning flash to enter an unprotected building through a water pipe or wiring. The sometimes explosive effect may rip a hole in the wall where the flash passed through a ventilator, splinter the ceiling, or blow off roof tiles. A case is on record where a lightning flash entered a small double-storied house and caused complete collapse of one of the walls.200 There are multiple well-documented reports of trees being split asunder, blast holes in the ground, and flying masonry.5 Physics of Lightning by D.J. Malan,200 under the heading Explosive Effect, notes: Should the heavy current of a lightning flash pass through a confined space, the heated air is not free to expand and will exert a pressure on the walls of the cavity. The larger the cavity, the smaller the excess pressure, since only part of the air in a large cavity will be heated. When a lightning flash is incident on rocky soil the electric current tends to follow the interstices between the rocks or cracks, which are filled with moist soil. Rocks may be split asunder or thrown aside with explosive violence. Muller Hillebrand carried out detailed studies of the effects produced by lightning on the rocky soils of Sweden. On one occasion investigated, lightning struck a pine tree and from there plowed branching furrows in the ground. The total length of the furrows was 250 m (820 feet), and in one spot there was a craterlike hole 2 m (6.6 feet) in diameter and 75 cm (29.6 inches) deep. Rocks of up to one-half a ton in weight were dislodged, and trees were uprooted. The total volume of stones and Earth cast aside amounted to 25 m3 or the equivalent of 70 tons. He estimated that about 200 kg (441 lb) of high-explosive trinitrotoluene (TNT) would have been required to produce the same effect as a lightning flash. Luckily, few lightning strikes are sufficiently forceful to produce such devastating effects.200 Review of the otorhinologic medical literature sometimes describes the tympanic membrane following lightning strike as “a large tympanic membrane perforation with ossicular chain disruption.”* Proposed mechanisms of injury have included concussive “blast” effect on the ear, “direct” effect of electrical conduction, “splash” effect, “cylindric shock wave of electrons,” and/ or direct “thermal burn.”236 More research is needed to investigate if there is significant concussive blast effect or lightning explosive barotrauma immediately surrounding a lightning channel that could add to our understanding of some of these curious lightning injury patterns that have not been explained in the past. *References 26, 28, 113, 115, 160, 222, 236, 265, 279.

VIDEO RESOURCES Video 3-1: A slow-motion montage of cloud-to-cloud lightning. (Aquavision TV Productions, used with permission. http://www.aquavision.co.za.)

REFERENCES *References 5, 26, 28, 113, 115, 124, 160, 165, 190, 237, 278, 281.

Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 3  Lightning Injuries

literature shows an interesting injury phenomenon that is difficult to explain with the current electrical and thermal injury models and that has become a topic of controversy.32,279 The phenomenon includes torn and tattered clothing, fractures, rupture of shoes, traumatic perforation of tympanic membranes, lung contusion and hemorrhage, and even pneumomediastinum.* These findings are similar to injuries seen in individuals who have been exposed to a bomb explosion and suggest explosive barotrauma as a mechanism of injury.165,203 To be injured by a blast, one has to be in the immediate vicinity (about a meter or so) of the explosion. About 690 kPa (100 psi) is the minimum threshold for serious damage to humans.252 Blast lung, bowel contusion, and tympanic membrane rupture, all of which may be found in some cases of lightning injury, are typically found in cases of direct transmission of a detonation shock wave.201 It is customary to use Marshall’s triad when considering the pathology of trauma of bomb explosions. The triad includes punctate bruises, abrasions, and small punctate lacerations, all of which are typically found in an explosive bomb blast. Although many similarities exist between injury patterns seen in lightning and concussive injuries, Marshall’s triad findings are not typically found in lightning strike injuries. A blast consists of a wave of compression passing through the air. The velocity of the shock wave depends on the distance from the epicenter, being many times the speed of sound at the start, but rapidly decreasing as it spreads out. The magnitude of the blast varies with the energy released and also the distance from the epicenter, the intensity obeying the inverse square law. Rakov and Uman234 describe something similar in their book, Lightning: Physics and Effects, explaining little-appreciated forces that can occur with lightning:

CHAPTER 4 

Thermoregulation LARRY I. CRAWSHAW, KEI NAGASHIMA, TAMAE YODA, MAYUMI NAKAMURA, KEN TOKIZAWA, AND YUKI UCHIDA

A warm body has long been recognized as one of the primary conditions of life. Although humans have physiologic, intellectual, and cultural capabilities that equip them to maintain viable body temperatures under many climatic conditions, thermal extremes, heavy exercise, and injury can rapidly lead to dangerous internal temperatures. For a physician who is operating in primitive circumstances, maintaining or restoring a patient’s body temperature can require quick action and ingenuity, both of which are aided by an understanding of the physiology of temperature regulation. Because the thermal environment can be extremely complicated and the thermoregulatory system of humans is complex, making decisions about body temperature maintenance in the field can be difficult. This chapter is designed to aid in the decision process by providing a basic understanding of the relationships among the ambient thermal environment, the thermal characteristics of the body, and the thermoregulatory system. First, some overall concepts of temperature regulation as well as a way to conceptualize the system will be reviewed. Second, the range of normal body temperatures will be covered, along with the consequences of higher and lower body temperatures. Third, methods and potential pitfalls of monitoring body temperature will be outlined, after which the physical factors that affect heat flow will be covered. Fourth, the neuronal systems involved in processing thermal information (i.e., sensation, integration, and output) will be reviewed, followed by a detailed description of the effector organ responses involved in the maintenance of thermal homeostasis. Last, modifications of thermoregulatory responses, induced alterations of the regulated temperature, and changes in the responsiveness as well as in the capabilities of the thermoregulatory system will be noted. Note that, when values are given for “a person,” they refer to a 70-kg (154-lb) man.

Conceptualizing the Thermoregulatory System Humans are homeotherms and as such are capable of maintaining a relatively constant body temperature across a wide range of ambient temperatures. Such constancy is attained through the use of behavioral processes that involve maintaining or searching for a preferable environment and autonomic processes such as vasodilation of the skin blood vessels and sweating in the heat and shivering in the cold. These processes are controlled via a negative feedback system with a primary feed-forward input from skin sensors that monitor ambient temperature (Figure 4-1).89 The feed-forward input from the skin allows for the elicitation of thermoregulatory responses without a change in core body temperature. Thus, the primary regulated variable, core temperature, can remain relatively constant under widely varying environmental conditions. Without the feed-forward element, if a hot or cold stress were encountered, large amounts of heat would be gained or lost before deep body sensors were sufficiently affected to elicit restorative responses. In addition, when greater thermal stresses were encountered, greater deviations in core temperature would be necessary to elicit sufficient restorative responses. Figure 4-2 illustrates some of the concepts that relate to the thermoregulatory system and that will be discussed in this chapter. Under normal conditions, body temperature is relatively constant under a range of ambient temperatures, as is depicted by trace “a.” The breadth of this range of ambient temperature is called the range of normothermia. The midpoint of this range can be conveniently called the regulated temperature, which is 104

shown by the dot in trace “a.” Toward the upper and lower ends of trace “a,” the core temperature inflects up and down. These inflections represent ambient temperature extremes at which the regulation begins to fail. Altered core temperatures can also accrue when there are alterations in the regulated temperature. Such alterations could be caused by the presence of bacterial toxins (e.g., fever) or starvation, which would cause increases (trace “b”) or decreases (trace “c”) in the regulated temperature. In addition, under various conditions, the effector responses can become compromised, which leads to decreases in the ability to defend against low temperatures (dashed line at “d”), which could indicate a problem with metabolic stores, or high temperatures (dashed line at “e”), which may indicate dehydration. Of course, various combinations of regulatory changes and altered effector responsiveness occur in conjunction with many threatening situations.

Basics of Core Temperature Typical measurements of core temperature provide a good estimate of the temperature of critical internal organs and are quite stable across individuals. In a study that involved 700 observations of 148 healthy individuals,113 90% of the early-morning oral core-temperature measurements were between 36.0° C (96.9° F) and 37.1° C (98.9° F). Core temperature is vigorously defended by the body. At low temperatures, regional heterothermy that results from peripheral vasoconstriction forms an important aspect of this defense. The lowered skin temperature decreases the thermal gradient from the skin to the environment and thus decreases heat loss. At cooler temperatures, there can be a large amount of peripheral tissue that is well below core temperature, which leads to a major decrease in the overall heat content of the body. A nude human resting at 35° C (95° F) or 20° C (68° F) exhibits similar temperatures at various locations within the core. However, because of decreased temperatures in the outer shell, a person resting at 20° C will have a total heat content that is about 200 kcal lower than when resting at 35° C.168 If the peripheral vessels were suddenly dilated, an immediate drop in core temperature of about 3.5° C (6.3° F) would result. In a hypothermic individual, the discrepancy between core and shell temperatures could be considerably greater and could result in a dangerous postdilation drop in core temperature. A method for making a rough estimate of the potential drop in core temperature after peripheral vessel dilation is given in Estimating Mean Body Temperature, later. A different type of heterothermy may be present in hyperthermic humans. As the brain temperature reaches high levels, blood flow that normally moves outward from the intracranium to the face via the ophthalmic vein is redirected and flows from the face inward.75 This results in the brain being cooled by blood that has passed through areas that have been cooled by facial sweating and leads to a brain temperature that is lower than that of the remainder of the core. Although brain cooling is clearly documented and accepted in many mammals,5 there has been some controversy about its importance in humans.15,24 Nevertheless, there is unanimous agreement that the head is an extremely important area for heat loss.15,25 Thus, for hyperthermic patients, it is important to optimize the heat loss from that region and, when necessary, to augment cranial heat dissipation by fanning and moistening. A variety of conditions can lead to an abnormal core temperature. Under some circumstances, the regulator may be defending an altered core temperature for reasons that will be described

For online-only figures, please go to www.expertconsult.com

Sensor Feed-forward signal

(Effectors)

Feedback signal

Regulated variable (Tcore)

Controlled system

Controller

(Body mass) Sensor

FIGURE 4-1  A negative feedback system with feed-forward input from the main disturbance (ambient temperature), which decreases variation of the main regulated variable (core temperature). (From Kanosue K, Crawshaw LI, Nagashima K, et al: Concepts to utilize in describing thermoregulation and neurophysiological evidence for how the system works, Eur J Appl Physiol 109:5, 2010.)

later in this chapter. Alternatively, the thermal load posed by the environment or by heavy exercise may be too great for the capacity of the effectors. Finally, the regulator could be deranged as a result of substance abuse, extreme temperatures, side effects of prescription drugs, or other factors. When interpreting a particular core temperature, it is important to evaluate all of these alternatives. Accidents in the wilderness often involve the compromise of many aspects of thermal balance, and an altered body temperature is very likely.

Consequences of Altered Core Temperature When tissue temperatures change, there are immediate and important effects on metabolism as well as on other physiologic mechanisms. With a 10° C (18° F) increase in temperature, the metabolism of typical human tissue increases by a factor (Q10) of about 2.7. The metabolic rate of the entire organism—apart from thermoregulatory responses—responds similarly. For temperature differences other than 10° C (18° F), these effects can be calculated with the following equation:168

Core temperature

°C °F 39 (102)

37 (98)

b

36 (96)

a e

d

Monitoring the Temperature of the Core and Other Sites The overall status of the thermoregulatory system is determined by measuring the core temperature. This can be done at a number of sites with several types of instruments (i.e., thermometers). In the following paragraphs, the relative merits of locations and instruments are discussed.

MONITORING THE CORE TEMPERATURE

R 2 = R 1 × Q10 ([ T2 − T1 ] /10 )

38 (100)

where R2 and R1 are the two rates of physiologic response; T2 and T1 are the two temperatures; and Q10 is the increase in rate caused by a 10° C (18° F) increase in temperature. Within the normal range of body temperatures, higher temperatures favor speed at the expense of tissue resources, whereas lower temperatures conserve resources. Although both high and low temperature extremes pose a threat to humans, increased temperatures greatly accelerate the development of serious complications and pose a much more immediate danger. A deviation of about 2° C (3.6° F) above or below normal core temperature is well tolerated by the various regulatory systems of the body, but a discrepancy of 3° C (5.4° F) begins to disrupt these systems, including those involved in temperature regulation. At this level of deviation, if there is no intervention, physiologic problems compound very rapidly. A core temperature of 34° to 36° C (93.2° to 96.9° F) disrupts many important physiologic functions, which, taken together, may significantly affect patient outcome. Such mild hypothermia impairs recovery from surgical procedures as a result of such things as impaired peripheral blood flow and oxygen availability, increased possibility of cardiovascular complications, decreased antibody and cellular immune defenses, impaired coagulation, and increased metabolic expenditure for heat production.47,57,103,107 In most situations, it is very important to maintain the patient at normothermic levels. Traumatic brain injury can be present in wilderness accidents, and it may be accompanied by hyperthermia. Heightened temperatures can exacerbate cerebral inflammation and lead to increased neuronal damage.185 There is current interest in invoking mild hypothermia to minimize damage to the central nervous system after neurologic injury.139 However, when this approach is used, care must be taken to deal with the side effects mentioned previously.148

c

35 (95)

A history of clinical thermometry is available111 as are good overviews of the assessment of core temperature.10,32,201 Sites for taking the temperature, in order of increasing invasiveness, include the forehead, axilla, oral cavity, tympanum, rectum, esophagus, bladder, and pulmonary artery. There is no clear-cut choice regarding the best site to monitor; particular situations demand different techniques. Thermometers that have been employed clinically include mercury-in-glass thermometers (which are now obsolete), electronic thermometers, tympanic radiation thermometers, and liquid crystal thermometers. Whatever instrument is used should have an accuracy of ±0.1° C (0.2° F). The handheld electronic thermometer is a good choice for field emergencies.

MEASURING INSTRUMENTS Ambient temperature FIGURE 4-2  A stylized diagram that represents body temperature at different ambient temperatures. The relatively flat portions of the three traces a, b, and c represent the range of normothermia. Trace a represents regulation under normal conditions; traces b and c represent increased and decreased levels of regulation, respectively. Inflections at the trace extremes depict the ambient temperatures at which the effector responses are unable to compensate for the increased ambient thermal stress. The dashed traces d and e correspond with situations in which the effectors for cold defense and heat loss are compromised. (Modified from Kanosue K, Crawshaw LI, Nagashima K, et al: Concepts to utilize in describing thermoregulation and neurophysiological evidence for how the system works, Eur J Appl Physiol 109:5, 2010.)

The handheld electronic thermometer has replaced the mercuryin-glass thermometer, and it has been widely used for many years. Electronic thermometers can make use of either thermistors or thermocouples as sensors; they have the requisite degree of accuracy, and they are very flexible in application. Although an equilibration time of 1 minute is specified for the typical probe, this is largely because of the need for a stiff casing for ease of insertion; smaller probes are available that can equilibrate in seconds. The digital display of these instruments reduces errors, and the probes can be left in place for continuous monitoring. A quality instrument with a wide range of interchangeable probes is important. Even then, these devices are subject to the usual problems inherent with electronic instruments and rarely 105

CHAPTER 4  Thermoregulation

Disturbance (Ta)

PART 2  COLD AND HEAT

have a range low enough to monitor skin temperature in cold environments. A second electronic thermometer with a wide temperature range is important for measuring skin temperature and as a backup for the standard clinical thermometer. Alternate probes and spare batteries for both instruments are essential. Tympanic infrared radiometers are often used in hospital settings. However, even in this relatively predictable environment, some controversy exists regarding their ability to accurately assess core temperature. These instruments monitor the electromagnetic radiation that emanates from the ear canal; various manufacturers make use of different and complicated electronic circuitry to produce a temperature display. An advantage is that the reading takes only a few seconds,32 but questions remain regarding the overall accuracy of the measurement displayed. In a laboratory situation in which the auditory canal is plugged with a sponge and the probe measures only radiation that emanates from the tympanum, infrared tympanic thermometry provides an excellent estimate of the core temperature.174 In clinical settings, the results are less consistent. In one study, infrared tympanic thermometry produced core temperatures that were much more variable than rectal temperatures. Even after correcting for the higher rectal values (0.5° C [0.9° F]), tympanic measurements still inaccurately displayed one-third of the temperatures that were more than 37.7° C (99° F). An extended training program did not significantly alter the accuracy of the readings.147 In one instance, a child who arrived at an emergency department presented with tachycardia and skin vasoconstriction. Separate tympanic infrared thermometers gave core temperatures of 36.4° and 37.6° C (97.5° and 99.7° F); the rectal temperature was determined to be 42.2° C (108° F).158 Alternatively, in a hospital setting with a trained operator and immobile patients, two brands of infrared tympanic thermometers produced readings that were closer to pulmonary artery readings than those obtained from the axilla or the rectum.155 The potential benefits of a continuous and easily applied core temperature monitor have led to repeated attempts to validate liquid-crystal thermometers, which are typically placed on the head or neck surface. Unfortunately, the temperature readings produced by this method are not reliable.10,111 Because these measurements are compromised by the thermoregulatory vascular changes associated with heat conservation and heat dissipation and by changes in ambient temperature,80 they are particularly unsuited for field emergency measurements.

MEASUREMENT SITES Although the deep internal temperatures of normothermic humans are reasonably similar, no specific anatomic site represents the “official” core temperature. The temperature at each location is a consequence of a combination of the local metabolic rate, local perfusion rate, proximity to the outer shell, and proximity to other locations that have differing rates of meta­ bolism and perfusion. Nevertheless, because of the generally high overall rates of tissue perfusion in mammals, deep core temperatures rarely differ by more than 0.5° C (0.9° F). The temperature of the pulmonary artery is a good reference temperature for the overall status of the thermal core. At steady state, accepted sites for assessing core temperature differ with regard to varying amounts from this temperature. Esophageal and tympanic temperatures are essentially the same as the temperature of the pulmonary artery,155,166 whereas rectal temperature averages about 0.4° C (0.7° F) higher, and axillary and oral tem­ peratures are about 0.2° C (0.4° F) and 0.4° C (0.7° F) lower, respectively.10,110,155 Although esophageal temperature is somewhat difficult to obtain, this is the site that is most likely to accurately reflect the temperature of the pulmonary artery. Measurement at this location accurately follows changes in core temperature and is reasonably noninvasive. For placement, the probe is lubricated, and a small amount of local anesthetic is applied. It is then passed via a nasal passage into the distal portion of the esophagus to the level of the heart. The probe can be moved up and down slightly to obtain the highest temperature. Although this procedure is routinely used in physiology experiments, it is somewhat 106

unpleasant for conscious patients. Esophageal temperature is affected by swallowing for about 30 seconds. Tympanic temperature as an estimation of core temperature has long been controversial. Because the tympanic membrane is highly vascular and supplied by branches of the external and internal carotid arteries, it should be an ideal site. Nevertheless, over the years many studies have indicated that tympanic temperature is affected by ambient temperature and local facial cooling.166 Conditions under which these complications can be avoided have now been clarified: (1) if the ear canal is insulated; (2) if the thermocouple is made of fine wire and insulated except at the active junction; and (3) if the thermocouple is in direct contact with the tympanum (which causes the patient to “hear” a continuous and low-pitched sound), then alterations in core temperature are detected more rapidly than by an esophageal probe, are not affected by facial skin temperature, and are otherwise identical to esophageal temperature.166 In fact, if these conditions are adhered to during facial fanning, tympanic temperature provides a better estimate of brain temperature than do measurements made in the esophagus or the rectum.115 Accurate results were also obtained when an insulated probe was used in conjunction with an optical sensor to detect infrared radiation from the tympanum.174 Whether the conditions met in these carefully controlled studies can be duplicated in the field is unknown. In steady-state conditions, rectal temperature is a good index of core temperature, and it can also be used to estimate brain temperature.204 However, when the heat content of the body or of the internal thermal compartments is in flux, rectal temperature changes more slowly than temperatures measured in other commonly used sites.155 There is a thermal gradient along the rectum, so all measurements should be made at a standard depth; 4  cm is recommended.10 The higher temperatures recorded in this region may be caused by a combination of low perfusion rates, digestive reactions, and bacterial activity, but there is not clear evidence of this.111 For assessing core temperature during outdoor exercise in the heat, the National Athletic Trainers’ Association recommends that only rectal temperature be used.29 Oral temperature is an excellent index of core temperature, provided that the mouth is kept closed. The sublingual pocket is well perfused by blood flow, and responds quite rapidly to alterations in core temperature. Mastication, smoking, fluid intake, and mouth breathing can affect sublingual temperature; these should be avoided during the period that immediately precedes the measurement.10,110,111 The use of an electronic thermometer with a rapidly responding sensor makes this measurement considerably more accurate and rapid than when it is performed with a mercury-in-glass thermometer. Although axillary temperature does reflect core temperature, it has a number of negative characteristics and should be used only as a last resort. The axillary temperature is affected by local blood flow as well as by thermal and nonthermal sweating.10 Changes in core temperature are slow to affect the axillary temperature, and there is high interpatient variability.155 However, this measurement has proved to be particularly useful for assessing core temperature in infants.10,111

ESTIMATING MEAN BODY TEMPERATURE Mean body temperature (MBT) provides a mass-weighted average of body tissue temperature and thus can be related to the heat content of the entire body. For a severely hypothermic patient, MBT provides a way to gauge the potential fall in core temperature (afterdrop) after vessel dilation caused by rapid surface warming. Traditionally, estimates of MBT have been made with the use of a formula that combines mean skin temperature and core temperature. Recently, the validity of such estimates was evaluated for patients undergoing various procedures, including cardiac surgery during extracorporeal circulation; these studies included core temperatures as low as 18.5° C (65.3° F).106 “Peripheral compartment temperatures were estimated using fourth-order regression and integration over volume from 18 intramuscular needle thermocouples, 9 skin temperatures, and ‘deep’ hand and foot temperatures.”106 The authors concluded

TABLE 4-1  Thermal Characteristics of Select

Substances

MBT = 0.64 ( Core temperature ) + 0.36 ( Mean skin temperature ) Ramanathan151 found that a rough but reasonably accurate estimate of mean skin temperature could be provided by the temperature of the medial thigh, and that a very accurate estimate of mean skin temperature could be made by measuring and weighting the temperature of four skin sites as follows: 0.3 Chest + 0.3 Arm + 0.2 Thigh + 0.2 Leg

Physical Factors That Govern Heat Exchange: The Heat Balance Equation The physical laws that govern heat transfer determine the net energy flux into or out of the body.* The heat balance equation is a convenient method for partitioning and quantifying the flow of energy between the environment and the body. A high rate of metabolic heat production is critical for maintaining a constant body temperature in mammals. This is represented by total heat production (Htot) on the left side of the following equation. For a person whose body is at thermal equilibrium, the equation is balanced and given as follows: H tot = ± H d ± H c ± H r ± H e where Htot is the total metabolic heat production; Hd is the conductive heat exchange; Hc is the convective heat exchange; Hr is the radiative heat exchange; and He is the evaporative heat exchange. Htot is always positive. The various modes of heat exchange from the right side of the equation can be positive or negative, depending on the situation. Positive values refer to net heat loss from the body. If the equation does not balance, the body either loses or gains heat. When the sum of the net heat exchange through the various channels exceeds Htot, heat content of the body will decrease, and mean body temperature will fall. Alternatively, if Htot is greater than the net heat exchange, heat content of the body will increase, and mean body temperature will rise.

CONDUCTIVE HEAT EXCHANGE Heat transfer between objects that are in direct contact is called conduction (Hd). The direction of heat flow is always from the higher to the lower temperature. Because conduction involves a direct interaction (i.e., contact) between molecules, this type of heat transfer is minimal except under certain circumstances, such as when sitting on a cold rock with a little insulation. Under such conditions, the heat lost to the rock would be similar to that lost from the remainder of the body surface by radiation and convection. Adequate insulation should be placed under patients who are in contact with hot or cold substrates.125 The equation that governs heat exchange by conduction is kA ( Tsk − Ta ) Hd = L where k is thermal conductivity; A is the area of contact; Tsk is the skin temperature; Ta is the ambient temperature; and L is the distance between the two surfaces. The thermal conductivity of a number of substances is given in Table 4-1. Note that water has 25 times the conductivity of air but only one fifth that of granite. Muscle tissue has about twice the conductivity of fat tissue. The conduction of heat through a tissue is called thermal diffusivity. This expression is obtained by dividing the thermal conductivity by the product of the density and the specific heat. The specific heats of various substances are also given in Table 4-1. Water and muscle tissue, which consists mostly of water, have particularly high values. However, specific heats can be misleading, so the volumetric heat *References 37, 69, 124, 133, 168.

Substance Air Water Granite Muscle tissue Fat tissue

Conductivity (cal • s−1 • cm−1 • ° C−1)

Specific Heat (cal • g−1 • ° C−1)

Volumetric Heat Capacity (cal • L−1 • ° C−1)

0.000057 0.0014 0.007 0.0011 0.00051

0.24 1.0 0.2 0.8 0.5

0.29 1000 540 850 460

Data from Schmidt-Nielsen K: Animal physiology: Adaptation and environment, ed 4, Cambridge, 1990, Cambridge University Press; Cossins AR, Bowler K: Temperature biology of animals, New York, 1987, Chapman & Hall; and Hodgman CD, editor: Handbook of chemistry and physics: A ready-reference book of chemical and physical data, ed 43, Cleveland, 1962, Chemical Rubber.

capacities are also listed in Table 4-1. Although the specific heat of water is four times that of air, it takes about 3500 times as much heat to raise the temperature of a given volume of water by 1° C (1.8° F) as it does to accomplish the same feat with a similar volume of air. For someone in the water, the consequence of these properties is that skin temperature is within 1° C (1.8° F) of water temperature, and heat transfer to or from the environment is greatly facilitated. In cool water during rest, skin blood flow is minimized as a result of peripheral vasoconstriction. Heat loss is importantly determined by the subcutaneous fat layer; an average-size fat person with 36% body fat by weight begins shivering at a water temperature of about 27° C (81° F), whereas a lean person with less than 10% body fat starts shivering at about 33° C (91° F).135

CONVECTIVE HEAT EXCHANGE Convection (Hc) can be seen as the facilitation of conduction caused by the movement of molecules in a gas or liquid. This movement decreases the functional value of L, which is the denominator in the conduction equation. Convection can be either forced or natural (free). Forced convection results from gas or liquid movement caused by the application of an external force, such as the movement of a fan or the pumping of a heart. Natural convection results from density changes that are produced by heating or cooling molecules adjacent to the body. These density changes cause the molecules to move with respect to the body surface. For humans, natural convection predominates at air speeds of less than 0.2 m/sec (0.7 ft/sec), whereas forced convection is more important at greater air speeds.124 The relationships that define heat exchange as a result of convection can be complicated. They depend on surface temperature profiles, surface shape, flow dynamics, density, conductivity, and specific heat. Any factor that impedes the movement of the boundary layer (i.e., the molecules immediately adjacent to the body) greatly retards convective heat transfer. Brengelmann and Brown16 have noted that, under relatively neutral conditions (Ta = 29° C [84.2° F], wind velocity = 0.9 m/sec [3 ft/sec]), about 40% of heat loss from a nude human is mediated by convection. Increases in air or fluid velocity greatly increase convective heat transfer. Fanning a minimally clothed patient will greatly augment heat loss in a cool environment.

RADIATIVE HEAT EXCHANGE All objects at temperatures of more than absolute zero emit electromagnetic radiation. This energy transfer occurs through space and does not require an intervening medium. In any given situation, the object is both transmitting and receiving infrared thermal radiation. In some cases, the object also receives solar radiation. The net heat transfer depends on the absolute temperatures, nature of the surfaces involved, and solar input. Surfaces that are effective absorbers of radiation are also effective emitters of radiation. The idealized “black body” illustrates this property; such bodies absorb all and reflect none of the incident radiation. Conversely, poor absorbers (e.g., a polished silver surface) are also poor emitters. Heat transfer that results from 107

CHAPTER 4  Thermoregulation

that the estimation of MBT from Burton’s original formula23 “is generally accurate and precise.”106 That formula is as follows:

PART 2  COLD AND HEAT

infrared (first-term) and solar (second-term) radiation is given by the following equation: H r = σe sk e a ( Tsk 4 − Ta 4 ) + a(1 + r )s where Hr is the radiative heat exchange; s is the Stefan-Boltzmann proportionality constant; esk is the emissivity of the skin; ea is the emissivity of the environment; Tsk is the skin temperature (given in K); Ta is the ambient temperature (given in K); a is the absorptance; r is the reflectance; and s is the solar radiation. For temperatures in the physiologic range and where (Tsk − Ta) is less than 20° C (68.0° F), several authors have noted that infrared radiation heat exchange is roughly proportional to Tsk − Ta.14,168 Also of note is that the spectrum of emitted radiation depends on the temperature of the object. At physiologic temperatures, the predominant wavelengths of emitted radiation are longer (infrared), whereas, at higher temperatures (e.g., like that of the sun’s surface), the predominant wavelengths are shorter (visible radiation) and can be detected by the human eye. This difference leads to some important consequences. The middle infrared radiation that is emitted by mammals is maximal, regardless of skin pigmentation or the color of clothing. However, solar radiation peaks in the visible portion of the spectrum and is differentially absorbed. In other words, dark clothes absorb more heat from solar radiation than do light clothes, but both types emit similar amounts of radiation energy. Incident radiation can vary drastically under different environmental conditions and may severely tax the body’s ability to respond. Heat input from solar radiation on a cloudless day may exceed by several times the heat produced by basal metabolism; on a cloudless night, there is a significant net loss of radiation to the sky. Under the relatively thermoneutral conditions noted earlier by Brengelmann and Brown,16 radiant heat loss accounts for about 45% of the total.

Evaporative Heat Exchange When water changes state, a large amount of energy is either absorbed or given off. Evaporation of 1 g (0.035 oz) of water at 35° C (95.0° F), which is the usual skin temperature of a person who is sweating,168 requires the input of 0.58 kcal of thermal energy. In the field, the preferred cooling measure is to splash water on the patient, and this is coupled with air fanning.66 Heat absorbed by the evaporation of 100 cc of water will lower body temperature by about 1° C (1.8° F). In a neutral thermal environment, sweating does not occur, and evaporation accounts for only 15% of the total heat loss. Of this, slightly more than onehalf is the result of evaporation from the respiratory tract, with the remainder coming from water that passively diffuses through the skin and evaporates.16 Although it is unusual, the evaporation term (He) of the heat balance equation can become negative, which means that heat is being introduced into the body. This occurs during airway rewarming, when water-saturated oxygen is introduced into the respiratory system at about 43° C (109.4° F). Because the victim’s body is considerably colder than 43° C, water condenses in the airways. For every gram of liquid water that is formed, the body heat content increases by 0.58 kcal.

Thermoregulatory Network A regulatory system requires sensing the controlled variable, comparing it with an ideal value, and producing an appropriate output signal. In the following sections, the role of the nervous system in maintenance of a stable body temperature is outlined.

PERIPHERAL THERMAL SENSORS The entire outer surface of the body is well supplied with sensitive thermoreceptive structures. Because one destination of the output of these transducers is the sensory cortex, many properties of the receptors can be gleaned from direct experience. Afferent thermal information produces both hot and cold sensations, and it is particularly rate sensitive. In addition to cortical input that arrives via the medial lemniscus and the ventrobasal thalamus, the brain receives a large amount of thermal information from 108

pathways that synapse in the reticular area.20 Although cortical thermal input is part of the sensory information that is used to reconstruct the external thermal environment, reticular inputs are more important to the behavioral and autonomic regulation of body temperature.43 This distinction was pointed out by Cabanac,26 who found that internal body temperature determined whether a particular surface temperature was perceived as pleasant or unpleasant. However, altered body temperature did not affect the discriminative (cortically mediated) aspects of the thermal stimulus; subjects had no problem correctly identifying the actual peripheral temperature. This study also confirms the intimate relationship between the thermoregulatory network and the pleasure–pain system.142 The structure, location, and properties of peripheral thermoreceptors are well documented. Thermal sensors are free nerve endings, and they are categorized as either warm or cold. Cold receptors are found immediately beneath the epidermis, whereas warm receptors are located slightly deeper in the dermis. The hallmark of both types of receptors is their extremely high rate sensitivity (Figure 4-3, online). Although the static firing rate of cold receptors is usually less than 10 impulses per second, under conditions of rapid temperature change, firing rates are often higher by an order of magnitude. Cold receptors are excited by cooling and inhibited by warming, and they have static maxima at about 25° C (77.0° F); these receptors are active from about 10° C (50.0° F) to 40° C (104.0° F). Warm receptors are excited by warming and inhibited by cooling, and they have static maxima at more than 40° C; they are active from about 30° C (86.0° F) to 45° C (113.0° F). At both ends of the spectrum, more extreme temperatures activate neuronal responses that are phenomenologically reported as “cold pain” and “warm pain.”72 Recent work with the use of cloning and ion-channel characterization has elucidated peripheral temperature transduction mechanisms. A family of related temperature-activated transient receptor potential (TRP) ion channels is highly sensitive to temperature. The cloned receptors TRPV3 and TRPV4 respond over a range similar to that of the warm receptors just described, whereas TRPM8 responds similarly to the cool receptors. TRPM8 also responds to menthol, eucalyptol, and icillin.117,146 TRPV1, TRPV2, and TRPA1 respond similarly to the heat-pain–sensitive and cold-pain–sensitive neurons. The heat-pain channels (vanilloid receptor 1 [VR1]) also respond to low pH, ethanol, and capsaicin, which is the active ingredient in chili peppers.144 Alternatively, TRPM2, TRPM4, and TRPM5 respond to warm temperatures and involve insulin secretion187 and taste.183 However, they are not regarded as warm receptors for thermal sensation, because sensory neurons have none of those receptors. In addition to TRP channels, TREK-1 and TRAAK channels may also be related to control of warm and cold perception.137 Psychophysical and physiologic studies indicate that thermal receptors are not uniformly distributed across the body surface and that there are far more cold receptors.72 Cold receptors are abundant in the face and trunk areas, especially in the lips; however, they are less numerous in the feet and lower legs. The face and fingers have a greater number of warm spots.153,181 Threshold temperature for the perception of thermal sensation follows the anatomic distribution and is not uniform across the body. The face, particularly near the mouth, is exquisitely sensitive, whereas the extremities, by comparison, have poor sensitivity. Other regions of the body are intermediate in sensitivity.179 Because peripheral thermal input is intimately involved in regulation of body temperature, heating and cooling different body sites can differentially affect the magnitude of the restorative physiologic response produced. In one study, cooling the forehead was found to be more than three times as effective (per unit area) for decreasing ongoing sweating as was cooling the lower leg.41 A separate study evaluated regional trunk and appendage sensitivity to cooling by assessing the magnitude of the gasping response that occurs at the onset of immersion. In this case, exposing various parts of the body to water at 15° C (59.0° F) indicated that the upper torso had the greatest cold receptor density or sensitivity (or both). The lower torso was somewhat less sensitive, with the arms and legs exhibiting similar but considerably lower sensitivity.22

Many sites within the body are capable of eliciting generalized thermoregulatory responses. Such areas include the abdominal viscera, spinal cord, hypothalamus, and lower portions of the brainstem.12,69 The genesis of input to the regulator that results from heating or cooling these areas is poorly understood. Some of the effects may result from modulation of synaptic connections rather than from stimulation of specific thermodetectors per se. Input from central detectors is not rate sensitive; rather, it is a direct reflection of the absolute temperature. The area with the highest thermal sensitivity and that has received the greatest amount of experimental attention is the preoptic area/anterior hypothalamus (POAH). Heating or cooling this portion of the brainstem elicits the entire array of autonomic and behavioral heat loss and heat gain responses, respectively.68 Neurons in this portion of the brain exhibit both warm sensitivity and cold sensitivity.12 Recent work on hypothalamic slice preparations with the use of synaptic blockers has indicated that warm sensitivity may be an inherent property of some of the POAH neurons, whereas cold sensitivity in this area of the brain requires synaptic input.12,45 Figure 4-4, online illustrates the effects of temperature on the firing rates of three representative types of hypothalamic neurons. The high level of temperature sensitivity shown by one of the cells (labeled “C”) results from the temperature-dependent characteristic of the prepotential. Voltage-clamp experiments indicate that the altered rate of depolarization is most likely the result of an effect on hyperpolarizing (K+) conductances.64 Work involving the use of hypothalamic slices has also established that about one-half of the thermosensitive neurons also respond to nonthermal stimuli such as osmotic pressure, glucose concentration, and steroid hormone concentration. Such neurons could form the basis for the interactions between the homeostatic systems that are described later in this chapter. Figure 4-5, online illustrates the response of a warm-sensitive POAH neuron in a slice preparation. This cell is excited by increased temperature, low glucose, or increased osmotic pressure.13 TRPV protein expression has been detected in the POAH; thus, it was proposed that the TRPV channels may underlie the thermosensitivity found in POAH neurons144 and that both TRPV1 and TRPV2 channels may be active within the physiologic range of temperature.93,149 However, a large body of evidence is at odds with the proposal of TRPV1 as a thermosensor.157 Furthermore, TRPV channels respond to warming with persistent inward cationic currents, and this would produce a change in the resting membrane potential. In the POAH, both warm-sensitive neurons and temperature-insensitive neurons show identical membrane potential responses to temperature change.203 In addition, several in vivo studies have shown that TRPV1, TRPV3, and TRPV4—all of which are expressed in the hypothalamus—are not likely to be involved in thermoregulation in either the heat or the cold.31,107,118 It is more likely that POAH warm sensitivity is caused by brief ionic currents that determine the rate of change in depolarizing the prepotentials that occur between two successive action potentials.64

REGULATOR As mentioned previously, the brain is capable of accurately regulating body temperature under a wide range of conditions. Although almost all portions of the central nervous system can potentially be involved, the most critical neuroanatomic structures for thermoregulation include the spinal cord, brainstem, hypothalamus, and septum. The preoptic area and anterior hypothalamus are particularly important for both integration and sensing of internal temperature.68,70 Recent advances in neurophysiologic and neuroanatomic techniques have been used to extend our understanding of the systems involved in regulation of body temperature; a number of excellent sources document this progress.11,122,200 Notable advances include demonstration of the relative independence of populations of neurons that control separate effector systems91,202 and elucidation of a pathway that conveys cold-sensitive afferent (feed-forward) information to the hypothalamus.131

A schematic model for regulation of body temperature is presented in Figure 4-6. Credit for much of the information and organization in the figure comes from the authors listed in the figure legend as well as from many others in the field. For ease of understanding, many aspects of the system’s complexity have been simplified or modified. Among the many inputs to this system that are not shown include those mentioned in the section about central thermoreceptors (e.g., glucose concentration, osmotic pressure) as well as factors that are covered later in this chapter (e.g., time of day, hormone levels, pyrogen titer, oxygen concentration of the blood). In addition, central thermoreceptors from many locations in the body provide input to this system. The key sensing elements of Figure 4-6 involve the peripheral warm and cold receptors and the central thermodetectors, the latter of which are depicted by solid cell bodies and bold axons. Peripheral input originates in the skin and enters the central nervous system via the spinal or trigeminal dorsal horns; this information ascends to both the midbrain and the thalamus. The thalamic neurons that receive thermal information project to the sensory cortex and subserve sensory integration and localization of peripheral thermal information. They are also likely involved to some degree in learned behavioral thermoregulatory responses. Thermal afferent pathways reaching the midbrain are involved in the feed-forward aspect of regulation.131 Axons of the cell bodies in the midbrain synapse on cells in the midline subregion of the preoptic area. These preoptic cells receive excitatory input from peripheral warm and cold sensors, but they inhibit the cells upon which they synapse. The systems that subserve heat loss and cold defense act as if they reciprocally inhibit each other and receive output from a unitary integrating system. However, as mentioned previously, the systems are actually functionally separate to a large degree. In the schema of Figure 4-6, both systems depend on inherently warm-sensitive cells that have a high spontaneous firing rate at normal body temperatures. These cells inhibit the succeeding neurons, but the connections are such that, in a cold environment or when the body temperature is below normal, cold defense responses are disinhibited and heat loss responses are further suppressed. The opposite would occur in a warm environment or when the body becomes excessively hot. The output of these systems under different conditions is illustrated in the panels below the neuroanatomic diagram of Figure 4-6. The middle panel illustrates the situation for a person with a body temperature of 37° C (98.6° F) in a thermoneutral environment. At 37° C (98.6° F), both systems are inhibited, and there is no effector response. If the body cools or becomes warmer, the inherently temperature-sensitive neurons disinhibit either the cold defense or the heat-loss system. The panel on the left illustrates the action of the feed-forward cold neurons in a cold environment. Although the inherently thermosensitive neurons do not change their firing rate as a result of a local temperature that stays constant, input from the peripheral cold-sensitive pathway disinhibits the cold defense system. A similar situation—but in reverse—occurs when a person encounters a warm environment; that situation is depicted in the right panel. The error signal or output driving force is shown as the difference between the horizontal dashed line and the effector output at a given body temperature. The system is extremely accurate, and the error signal created by peripheral feed-forward input is usually just sufficient to counteract the sensed disturbance and to maintain body temperature at a constant level. In addition to autonomic responses that are organized and transmitted from the brainstem (e.g., sweating, shivering), various complex whole-animal responses are also activated by the thermoregulatory system. Postural reflexes (e.g., huddling, sprawling) and complex learned behavioral thermoregulatory responses are initiated by cold and warm error signals. Although the mechanism is not understood, appropriate behavior reduces the error signal and activates the reward system, which likely culminates in the release of dopamine in the nucleus accumbens of the septum via cell bodies located in the ventral midbrain.81 109

CHAPTER 4  Thermoregulation

CENTRAL THERMAL SENSORS

Preoptic area/ anterior hypothalamus

GABA

ac

G L U G A B A

+

+

−

Thalamocortical relay

− − − oc

Midbrain Lateral parabrachial nucleus

+

Reward system activated when thermal deficit decreased

+

GLU

Rostral ventro– medial medulla Rostral raphé pallidus

G L U

+

Postural reflexes Sprawl Huddle

− G A B A

Learned behavioral responses— integrate cortical, limbic, and brainstem information

+

To final autonomic organization and output

Collateral fibers ascending to midbrain Dorsal horn– spinal column Input from cutaneous temperature receptors

FIGURE 4-6  A simplified schematic diagram of the basic parts of the nervous system responsible for regulating internal body temperature. Details of how this system functions are given in the text. ac, Anterior commissure; GLU, glutaminergic synapse; GABA, GABAergic synapse; oc, optic chiasm. (Anatomic, neurophysiologic, and conceptual concepts represented in this image are from Boulant JA: Neuronal basis of Hammel’s model for set-point thermoregulation, J Appl Physiol 100:1347, 2006; Hammel HT: Regulation of internal body temperature, Annu Rev Physiol 30:641, 1968; and Morrison SF, Nakamura K, Madden CJ: Central control of thermogenesis in mammals, Exp Physiol 93:773, 2008. These articles should be consulted for a more rigorous explanation of the details of the thermoregulatory system.)

Sweat Vasodilation

+

Cold skin

Increase metabolic heat production Vasoconstriction

To thalamus

+

Heat loss Cold defense

Warm skin

+ Effector output

PART 2  COLD AND HEAT

Cerebral cortex Sensory integration and localization of peripheral thermal information

Dorsomedial hypothalamus

0

0 35

37

39

Cold environment

0 35

37

39

Core temperature (° C) Neutral environment

35

39

Warm environment

Effector Responses VASCULAR ADJUSTMENTS Excellent overviews of the role of the vasculature in coping with thermal stresses are available.16,33 One function of the circulatory system is to maintain a relatively homogeneous internal body temperature. Heat from metabolically active organs is convectively distributed to portions of the body where less heat is produced. More commonly appreciated are alterations of blood flow patterns that increase or decrease the overall thermal conductivity of the body during exposure to hot or cold environments, respectively. Some of these alterations in conductivity result from the preferential shunting of peripheral blood flow superficial or deep relative to the subcutaneous fat layer. Indeed, fat has about one-half the tissue conductivity of muscle. Nevertheless, shunting blood away from major portions of the body is at least as important for determining overall conductivity as is the conductive property of the tissue itself. For example, during immersion in cold water, muscle accounts for about 90% of the total tissue insulation of the forearm.48 Thus directing blood away from poorly insulated (and more highly conductive) regions reduces heat loss and preserves core temperature. In addition to capillaries, microcirculatory units contain arterioles, metarterioles, and arteriovenous anastomoses. Flow through all of these vessels is under the control of smooth muscle. The smooth muscle of precapillary sphincters is largely 110

37

influenced by local factors such as the partial pressures of oxygen and carbon dioxide, whereas the other vessels are well supplied with receptors that respond to both neuronal and endocrine inputs. Glabrous skin (i.e., the palms, lips, and soles) contains numerous arteriovenous anastomoses and is innervated only by sympathetic vasoconstrictor fibers. Nonglabrous (i.e., hairy) skin is innervated by sympathetic vasoconstrictor and vasodilator fibers and contains few arteriovenous anastomoses. The vasoconstrictor system acts primarily through α-1 and α-2 adreno­ ceptors. By contrast, the active vasodilator system makes use of acetylcholine. This was verified by experiments that involved intradermal injection of botulinum toxin, which blocks the release of acetylcholine.96 However, in the same experiments, involvement of an unidentified cotransmitter was also suggested. Vasoactive intestinal polypeptide is a likely candidate, because nitric oxide is an important end product for inducing active vasodilation.6 About 90% of the elevation in skin blood flow during heat stress is a result of input from the active vasodilator system, and, of this, about 30% is the result of nitric oxide.6 Thermoregulatory skin blood flow can reach up to 8 L/min and involve 60% of the cardiac output.33 Operation of the vasomotor effector system is affected by excessive exposure to ultraviolet B radiation. Moderate sunburn impairs the vasoconstrictor response to cold; an associated uncontrolled increase in thermal conduction is still present 1 week after exposure, although the original erythema will have disappeared.140

Vascular changes are bioenergetically the least costly thermoregulatory autonomic effector response. Because of the high sensitivity of the vasomotor system, ambient temperatures between the thresholds for sweating and shivering are often referred to as being in the zone of vasomotor regulation. If a particular vascular bed is kept at a relatively constant temperature, output from the central nervous regulator can be assessed. Under these conditions in dogs, manipulations of hypothalamic temperature confirm a high level of vasomotor activity between the thresholds for the activation of panting and shivering.71 In humans, forearm blood flow increases rapidly as core temperature rises; a sixfold increase in blood flow can occur with a core temperature that has risen to only 38° C (100° F).191 Within the vasomotor zone (i.e., skin temperatures of 33° to 35° C [91.5° to 95.1° F]), core and skin temperatures linearly combine to control skin blood flow. Skin blood flow responds accurately and rapidly to changes in skin temperature, which leads to a very stable core temperature.17 Although most peripheral arterioles are well supplied with adrenergic receptors, output from the thermoregulatory centers is not homogeneously distributed. Extensive nervous inputs from the thermoregulator occur only in the lips, ears, and distal extremities; thus immersing the feet in cold water leads to marked vasoconstriction in the hands and forearms but not in the abdomen or upper arms.63

LOCAL MODULATION Local temperature has a great effect on the vasomotor status of the peripheral vessels, and, in some cases, may be largely responsible for the observed thermal conductivities. Local heating produces a biphasic response. Initial dilation occurs in a few minutes and depends on release of various factors from the nerve ending. The VR1 receptors mentioned previously are involved in this response. The longer-lasting second phase of dilation is not dependent on local nerve endings, and involves nitric oxide. Local cooling can decrease superficial cutaneous blood flow to almost zero.33 Although vascular beds on the skin surface constrict in response to cooling, other vascular beds dilate when cooled.51 The specific response to cold shown by cutaneous vessels follows from the observed distribution and properties of the α-adrenergic vascular receptors. Although in most of the vasculature α1-receptors predominate, in the superficial cutaneous areas, α2-receptors constitute a clear majority. The usual predominance of α1-receptors is found in the deeper blood vessels. Local temperature affects the α2- and α1-receptors in a reciprocal manner. Although cooling augments the response of the α2-receptors, it either inhibits or does not affect the response of the α1-receptors. Thus cooling the skin not only constricts the superficial vessels but also concomitantly dilates many underlying vessels. The ensuing flow pattern increases tissue insulation and augments countercurrent exchange between incoming cool blood and outgoing warm blood.51,53 Although initial work was done on canine vessels, subsequent studies that involved α-adrenergic agonists and antagonists have demonstrated that a similar mechanism exists in human fingers.49,52 The responsiveness of cutaneous blood vessels is diminished in people with type 2 diabetes mellitus. The increased incidence of this disorder among the general population presages a greater number of patients exhibiting severe hyperthermia.33

Evaporative Responses At high workloads and at environmental temperatures approaching 37° C (98.6° F), the only way to maintain thermal balance is to augment evaporative cooling by mobilizing the eccrine sweat glands. This sympathetic and cholinergically innervated organ system is spread over the entire body surface, but it is more profuse in some areas than in others. A person who is acclimatized to heat can produce several liters of sweat per hour.76 High rates of sweating occur on the forehead, neck, anterior and posterior portions of the trunk, and dorsal surfaces of the hands and forearms. Low rates occur on the medial femoral regions, lateral trunk areas, and

palms and soles.133 Sweat is secreted in these latter two areas in response to emotional rather than thermal inputs.16 Sweating is cholinergically mediated, and can be completely abolished by atropine. Sweat gland activity interacts with the regional vasculature; metabolic products of active sweat glands increase blood flow in areas of active sweating. In well-hydrated individuals, the degree of anhidrosis is correlated with the severity of generalized autonomic failure.63,109 Several reviews discuss the many aspects of sweating disorders.34,109

CENTRAL SIGNAL By controlling the local milieu at different skin sites, it has been possible to separate the central thermoregulatory drive to sweat glands from local effects on the glands themselves. The central thermoregulatory system provides a proportional output that is influenced by both internal and whole-body skin temperatures. Per degree increase above thermoneutral values, internal temperature is about 10 times as important as is mean skin temperature for eliciting an output to the sweat glands.126,128

LOCAL MODULATION Local effects are also important for determining the output of sweat glands. Temperature exerts a multiplicative effect on sweat secretion; the Q10 for this augmentation is about 3.70. In addition, skin wetness has an important local effect on sweat glands. The wetter the skin, the greater the suppression of sweating.127 Moderate sunburn disrupts evaporative cooling. This effect is locally mediated and involves decreases in both responsiveness and capacity of the sweat glands.141

Metabolic Responses Heat is an inevitable by-product of the inefficiencies of the body’s metabolic reactions. When oxidizing foodstuffs to carbon dioxide and water during adenosine triphosphate (ATP) production and transferring the ATP produced to the functional systems of the cells, about 75% of the original chemical potential energy appears as heat. With the exception of excreted or that used to perform physical work, the remaining 25% of the original energy is also converted to heat when ATP is used in the numerous metabolic reactions of the body.169 Mammals—as compared with poikilotherms such as reptiles or fish—use much more ATP to maintain ionic and electrochemical balances of the cells178 and for many other functions. This leads to greatly increased metabolic heat production, which forms the basis for homeothermy. It also creates the need to maintain a substantial thermal gradient between the body and the environment to dissipate the high levels of heat that are produced. An increased rate of metabolism above basal levels is critical for maintenance of body temperature in cold environments. The elevated heat production is derived from shivering and non­ shivering responses. Shivering consists of simultaneous rhythmic excitation of agonistic and antagonistic skeletal muscles. Under normal circumstances, carbohydrate oxidation provides the major substrate for shivering. In glycogen-depleted individuals, shivering levels are maintained by the greatly increased oxidation of lipid and protein reserves.67 Nonshivering heat production is associated with the presence of uncoupling protein 1 in brown adipose tissue. Uncoupling protein 1 is a transmembrane protein that is located in the mitochondrial inner membrane, which, on activation by the sympathetic nervous system, allows for protons to reenter the mitochondrial matrix without passing through ATP synthase. Because the energy released during substrate oxidation is not conserved as ATP, heat is generated. Although brown adipose tissue was believed to be of little importance in adult humans, recent research has indicated the presence of potentially significant amounts of active brown adipose tissue in adults.44,162 There is evidence that both epinephrine and thyroid hormones are released in humans after cold exposure.56 Because these hormones augment overall tissue metabolism, they are components of the response to cold environments. In the absence of thyroid hormone, metabolic heat production is reduced by 111

CHAPTER 4  Thermoregulation

CENTRAL SIGNAL

PART 2  COLD AND HEAT

30% or more. Thyroid hormone acts by both accelerating ATP turnover and reducing efficiency of ATP synthesis.175 Basal metabolic rate, when calculated on a weight-specific basis, decreases with body size. This relationship holds within as well as across species. Because drug potency as determined by the rate of inactivation is most closely related to metabolic rate, when drug dosing is extrapolated to persons of different sizes, it should not be done on a per-kilogram or per-pound basis unless the weights are similar. Basal metabolic rate relates to size according to the following equation:168  2 = ( 0.676 )M b 0.75 VO  2 is oxygen consumption in L/hr and Mb is body mass where VO in kg.

CENTRAL SIGNAL Of the various thermoregulatory outputs, metabolism is the easiest to evaluate quantitatively; the most complete documentation is available for this response, and most models of the thermoregulatory system are based on this information. Experiments on medium-size mammals have allowed for separate thermal manipulation of various parts of the brain, body core, and skin. This work has made it clear that the thermoregulatory centers act as a proportional controller and that skin temperature provides a feed-forward input to the system.68,84 Thus greater decreases in either core or skin temperature or both below neutral values elicit proportionally larger compensatory increases in metabolism. In addition to an impaired ability to generate metabolic heat, hypothyroidism is also associated with a decrease in regulated core temperature of about 1° C (1.8° F).196 Evidence indicates that humans have a control system similar to that of medium-sized mammals. In a summary of their data and of that collected previously, Hong and Nadel77 noted that central output for shivering is augmented by increased rate of skin cooling. They also concluded that a given decrease in core temperature elicits 10 to 20 times the metabolic response of an equivalent decrease in mean skin temperature. Exercise is not incompatible with shivering, but increased levels of exercise exert increasing degrees of suppression on the shivering response, possibly as a consequence of an increased arousal response.77

LOCAL MODULATION Although the central and local effects of decreased core temperature on shivering have not been directly partitioned, both inputs are important. Slight decreases in core temperature create large compensatory responses, as delineated previously. However, even moderate hypothermia decreases the metabolic response to cold, and, at about 30° C (86.0° F), the shivering response is lost.16 This decrement must involve nervous system malfunction, because the muscles themselves are quite responsive below this temperature. For example, limb muscles and diaphragm muscles develop peak tensions that are not greatly affected by temperatures down to 25° C (77.1° F), and fatigue resistance is considerably increased at 25° C (77.1° F).150,170 Likewise, altering the skin and superficial muscle temperature of the anterior thigh through a range of temperatures between 12° and 40° C (between 53.6° and 104.0° F) for 30 minutes had little effect on subsequent isometric peak torque production during isometric knee extensions to exhaustion. Time to fatigue was longer at the coolest temperature.186

Behavioral Responses In most wilderness situations, a variety of ambient temperatures is available, and external insulation is easily adjusted. Under these conditions, the choice of thermal microenvironment and clothing provides a far higher gain than any of the autonomic effector systems discussed previously. Whole-body adjustments are achieved by all motile animals, and are particularly well developed in vertebrates.40 In addition to moving the body, the somatic effectors are important for optimizing autonomic responses to thermal stress. Thus spreading out the arms and legs during heat stress increases the surface area available for the 112

autonomic augmentation of conductive, convective, evaporative, and radiative heat losses. Cabanac26 found that internal body temperature determined whether a particular surface temperature was perceived as pleasant or unpleasant. When subjects were hypothermic, a warm stimulus applied to the hand was experienced as pleasant and a cold stimulus as unpleasant. The opposite responses were observed in hyperthermic subjects. An overall sensation of thermal pleasantness is obtained when environmental conditions are appropriate for maintaining a normal body temperature with no fluid or energy expenditure. However, altered body temperature did not affect the discriminative (cortically mediated) aspects of the thermal stimuli; subjects had no problem correctly identifying the actual peripheral temperature. This study also confirmed the intimate relationship between the thermoregulatory network and the pleasure–pain system.142

CENTRAL SIGNAL As compared with the knowledge about autonomic thermoregulation, we know little about the neural mechanisms that underlie behavioral thermoregulation. As noted in previous sections, the preoptic area plays a key role in autonomic thermoregulation. Animals with lesions of the POAH are severely compromised with regard to their ability to use autonomic thermoregulatory effectors; however, their ability to behaviorally thermoregulate is relatively intact.28,164 These results indicate that the preoptic area is not as crucial for behavioral thermoregulatory processes as it is for autonomic processes.27,163 Alternatively, lesions of the lateral hypothalamus, which is involved in various reward systems, result in the loss of behavioral thermoregulation.165 Recent studies involving the use of positron emission tomography and functional magnetic resonance imaging have demonstrated that temperature signals from the body surface reach the insular cortex.38,79,138 However, insular activation correlates with the discrimination between hot and cold rather than with thermal pleasure, so this system is likely minimally involved with behavioral thermoregulatory processes. Alternatively, thermal pleasantness is clearly important for behavioral thermoregulation. In studies involving functional magnetic resonance imaging, it has been shown that activation of the amygdala, mid-orbitofrontal and pregenual cingulate cortices, and striatum is correlated with thermally related pleasant and unpleasant feelings.91,156 Because behavioral processes are usually activated before body core temperature changes via the feed-forward system, signals from the skin are important. However, severe deviations in core temperature disrupt this system. When this occurs, the person no longer feels too hot or too cold, and the desire to take corrective action is lost. Regional differences in the contribution of the body surface to thermal comfort are present.132 Facial cooling produces the most pleasant experiences during mild heat exposure, whereas during cold exposure, local warming of the chest and abdomen leads to the most pleasant sensations. This would induce us to preferentially cool the head in the heat and to huddle or add clothing to warm the torso in the cold.

LOCAL MODULATION As with shivering, most problems that involve behavioral temperature regulation probably emanate from disruption of centrally generated output. The muscles used to move the body are fairly resistant to thermal incapacitation, as described previously; however, if this occurs, a major disruption of the body’s thermal defense ensues.

Important Modifications of Thermoregulatory Responses In addition to establishing the status of the body temperature when the regulatory system is functioning normally, monitoring body temperature provides a significant diagnostic indicator for many pathologic conditions. Whether the goal is to stabilize or monitor the body temperature, it is necessary to understand the

NORMAL VARIATIONS IN THE REGULATED TEMPERATURE AND IN THE ABILITY TO MAINTAIN BODY TEMPERATURE The same body temperature can represent a different state of affairs even under regularly encountered circumstances. Some of these conditions are noted here. Level of Activity Activity normally leads to increases in body temperature. However, the level of activity does not appear to provide direct input to the regulator of body temperature, unlike the feedforward input that is received from the peripheral temperature. Thus, the magnitude of the error signal for increased heat dissipation is determined simply by the increase in body temperature.180 Someone who is exercising heavily (or who has just exercised) in a neutral environment will have an unusually high body temperature, whereas someone who is sleeping or resting quietly will have a relatively low body temperature. At a given level of exercise, core temperature will plateau 30 to 40 minutes after the exercise is initiated; higher levels of exercise result in higher plateau levels of the core temperature. For someone who is working at 50% of their maximal aerobic capacity, the increase in core temperature is about 1° C (1.8° F).135 Circadian Changes Body temperature shows cyclic changes throughout the day. Some of this variation is the result of the daily cycle of activity, as described previously. However, there also exists a circadian rhythm for the regulated body temperature. This sinusoidal rhythm accounts for much of the observed variations in body temperature. In a study that involved 700 observations of 148 healthy individuals, the daily mean oral reading was 36.8° C (98.2° F). However, this was only a midpoint; the mean earlymorning low was 36.4° C (97.6° F), and the mean late-afternoon high was 36.9° C (98.4° F).135 These diurnal changes definitely reflect alterations in the controller, because the body temperature thresholds for eliciting sweating and peripheral vasodilation are significantly lower in the early morning than in the afternoon or evening, whereas the sensitivities and maximal response levels remain unchanged.2,3 The body’s biologic clock may directly modulate the body temperature rhythm. The suprachiasmatic nucleus in the hypothalamus is the main pacemaker for the circadian system of the body. The core molecular mechanisms of the circadian clock, which consist of autoregulatory transcription and translation loops by the clock genes, show a periodicity of approximately 24 hours. Removing the circadian clock abolishes the body temperature rhythm as well as the circadian influences on thermoregulatory responses.130,188 Thermoregulatory responses to exercise are affected by the circadian time. At the daily low (5:00 AM), the perceived exertion for a standardized task is the greatest, and thermoregulation is less effective than at the time of maximum temperature (5:00 PM). At the time when the body temperature is rising at the fastest rate (11:00 AM), heat loss mechanisms are less responsive; alternatively, at 11:00 PM, when the body temperature is falling at the fastest rate, heat loss mechanisms are much more responsive.190 An excellent overview of body temperature cycles is available.154 Interindividual Differences Most oral temperature measurements are between 36.0° C (96.9° F) and 37.1° C (98.9° F) in the early morning. Corresponding values for the late afternoon are 36.3° C (97.4° F) and 37.4° C (99.4° F). On the basis of interindividual differences and diurnal changes, it has been suggested that the upper limit for a normal oral temperature should be 37.2° C (98.9° F) in early morning, which then increases gradually to 37.8° C (99.9° F) by early afternoon and remains at that level until early evening.110 These values delineate the 99th percentile for body temperature observed during the respective time periods.

Alternatively, it is important to be aware that the normal body temperature of some individuals falls outside of population norms. The authors encountered one person whose core temperature was consistently 35.5° to 36° C (95.9° to 96.8° F). This person mentioned that on one occasion he had felt chills and malaise, but he was told by his physician that his temperature of 37° C (98.6° F) was normal. However, for this person, it was not; his core temperature of 37° C (98.6° F) in fact represented a febrile state. Many individuals with atypical body temperatures are aware of their condition, and it is prudent to ask about this possibility. Age The circadian rhythm of body temperature develops soon after birth. Although newborns display small-amplitude rhythms, the patterns are not circadian. Circadian rhythmicity begins to develop during the second and third weeks of life, and, after a progressive increase in amplitude, the typical adult temperature rhythms are reached by the age of 2 years.154 Under thermoneutral conditions, rectal temperatures of older adults are similar to those of younger people, whereas oral and axillary temperatures are slightly lower.88 Of the major regulatory systems, temperature regulation is unique in the extent to which the effector organs are “borrowed” from other systems. This makes developmental assessments difficult, because functional changes may be secondary to changes in primary systems such as the skeletal muscles or the blood vessels. Other difficulties, which have been detailed by Cooper,36 include inconsistencies between chronologic age and physiologic viability and the increased incidence of interfering disease states and cerebral microinfarcts as aging progresses. Thermoregulatory capacities of the young show a progressive increase, but they are not fully developed until after puberty. Effectors that are more important to infants than to adults include certain behavioral responses (e.g., calling for help) and the ability to activate thermogenic brown adipose tissue. Shivering is not present in infants; it develops fully only after several years of nervous system maturation. Metabolism in infants is increased to some degree by the increase in motor activity that accompanies cold stress.97 Sweating is present and effective in children, but the typical high capacity for evaporative heat loss that is present in adults is attained only during the changes that occur with puberty.50 Factors that affect loss of body heat during cold stress throughout the adult years have been investigated with a multiple regression analysis to evaluate fitness, fatness, and age from the 20s to the early 50s. Fitness has no effect, but fatness retards heat loss. Aging during this period is correlated with progressive weakening of the vasoconstrictor response to cold.21 Individuals in their late 60s and beyond have a definite decrease in thermoregulatory capacity. Sweating is lessened in response to passive heating,82 vascular responses to heating and cooling are significantly reduced,94,97 and a distinct shivering tremor is rarely observed.97 In older adults, thermoregulatory sympathetic nerve impulses to the skin are reduced by 60%,62 and there is lower resting metabolic rate.192 Young children and older adults are, without a doubt, particularly vulnerable to thermal extremes and should be given treatment priority when possible. Both groups are susceptible to climatic heat injury, and, when their core temperatures exceed 40° C (104° F) and are accompanied by altered mental status, treatment should be immediate, even at the risk of misdiagnosing a febrile condition. As for all such cases, most clothing should be removed; ice, if it is available, should be placed around the groin, in the axillae, and around the neck. Cool water should be sprayed on the skin, and then the individual should be fanned. Blood gas and electrolyte status should be determined and any appropriate treatment measures taken.25,30 Gender Women have a number of physiologic and morphologic characteristics that produce subtle differences in the regulation of body temperature. Such attributes include smaller blood volume, lower hemoglobin concentration, smaller heart, smaller lean body mass, greater percentage of subcutaneous and total body fat, greater surface area–to–mass ratio, higher threshold core temperature for 113

CHAPTER 4  Thermoregulation

many conditions that affect both the regulated temperature and the effectiveness of the thermoregulatory system. In the following sections, these circumstances are elucidated.

PART 2  COLD AND HEAT

cutaneous vasodilation and sweating, greater resting vasoconstriction in the hands and feet, geometrically thinner extremities, and cyclic changes in sex hormone levels.120 Some reports have shown that when age, thermal accli­ mation, body size, maximal aerobic capacity, cardiovascular responses during exercise, and relative workload are matched, thermoregulatory gender differences are relatively negligible.58 Nevertheless, in situations such as those encountered in the U.S. Navy, men and women do not tend to be matched for such nonthermoregulatory factors, and different thermal exposure standards may be required for different genders.65 The menstrual cycle, menopause, and pregnancy are all associated with important effects on the thermoregulatory system. Relative to the early follicular phase of the menstrual cycle, core temperature is typically 0.3° C (0.5° F) higher during the late follicular phase and 0.7° C (1.3° F) higher during the luteal phase.102 Postmenopausal hot flashes are experienced by most women and involve increases in sweating, vasodilation, and heart rate. Heat and exercise may be particularly stressful during and after these episodes. The proximate mechanism appears to involve estrogen activating the central noradrenergic system53 as well as circulating serotonin levels.116 In addition, hot flashes may be associated with activation of the insular cortex.54 Some information about hormonal effects has been gained by studying postmenopausal women who are undergoing hormone replacement therapy. Administered estrogen acts to lower the core temperature at which heat loss effector mechanisms are activated and results in lowered core temperature. The addition of exogenous progestins blocks these effects.18 By contrast, animal studies have shown that estrogen acts to augment heat production78 and to maintain core temperature in the cold.189 Epidemiologic studies have indicated that lower testosterone concentration may be associated with the sensation of cold.60 Pregnancy is of special concern to the physician in the wilderness. This concern does not apply to well-hydrated women who are exercising at submaximal levels, because the thermoregulatory system makes adaptive adjustments as pregnancy proceeds. In the course of a pregnancy, basal body temperature shows a continuous decline, and heat-loss responses are elicited at progressively lower levels so that, near term, the steady-state temperature during exercise is about 1° C (1.8° F) lower than it was before conception. This reduces thermal stress on the fetus, which is typically 0.5° C (0.9° F) warmer than the mother.35,177 However, concern is warranted if hyperthermia develops in pregnant women. Animal experiments and epidemiologic analysis both indicate that, during pregnancy, it is dangerous for body temperature to exceed 39° C (102.2° F). During the first half of pregnancy, excessive body temperature is likely to produce birth defects; during the latter half, birth weight is more likely to be affected. The fifth week after conception, which is the period of neural tube closure, is a particularly vulnerable time for the fetus.108 Because women in the early stages of pregnancy may be unaware of their condition, it is critical that heat stress be promptly treated in women of childbearing age. When exercising, it is important that pregnant or potentially pregnant women acclimatize gradually to extreme thermal environments, remain well hydrated, wear loose-fitting clothing, exercise at a comfortable pace, and avoid swimming in warm water or immersing themselves in hot tubs.177 A program of water aerobics for pregnant women was reported to decrease requests for analgesia when these women gave birth, and was not found to be detrimental to the health of the mother or the child.4

Induced Alterations of the Regulated Temperature The optimal body temperature is not always the same. In certain conditions of stress or vulnerability, the regulated temperature of the body may be altered; this is often an adaptive response to a particular physiologic crisis. Some of these situations are delineated in the following sections of this chapter. In such circumstances, altered body temperature may be beneficial and should not necessarily be manipulated until the underlying condition is improved. 114

FEVER Increased body temperatures have been associated with illnesses for thousands of years. On the basis of the population data presented previously, febrile body temperatures for resting young adults include morning temperatures that are equal to or that exceed 37.3° C (99.2° F), which increase gradually to 37.8° C (100.0° F) for early afternoon and evening. Such elevated temperature needs to reflect a regulated increase to be considered a true fever. Pathogens and cancers are the usual causes of such increases in the regulated temperature, but they are not directly responsible for the increased body temperature; rather they interact with components of the immune system such as macrophages, T cells, monocytes, and Kupffer cells as well as with glial, epithelial, and many other types of cells. This interaction stimulates the cells to produce pyrogenic cyotokines,113 including interleukin-1, interleukin-6, and macrophage inflammatory protein-1. Cytokines act on cells in the vicinity of the anterior hypothalamus and induce them to release prostaglandin E2, which leads to an increase in the regulated temperature.100 Important avenues by which cytokine-mediated pyrogenic signals reach the brain include peripheral inputs from the abdominal vagus nerve160 and central inputs via the subfornical organs.182 Aspirin and related drugs block fever by inhibiting prostaglandin synthesis.100 Interleukin-1 and other cytokines have many effects in addition to causing fever; these include decreased appetite, hypoferremia, activation of B and T lymphocytes, and increased slow-wave sleep.99 The increase in body temperature during fever helps with many immune functions; neutrophil migration, release of reactive oxygen intermediates and nitric oxide by neutrophils, and interferon production are all augmented. It has been suggested that the most important aspect of fever is to greatly increase the temperatures of the peripheral tissues via selection of a warmer microclimate, addition of insulation, and postural changes. As peripheral temperatures increase from typical levels (i.e., 29° to 33° C [84.2° to 91.4° F]) to those that approximate core temperature, activation, proliferation, and effector production in peripheral cells involved in cell-mediated and humoral immunity are greatly increased and show temperature coefficients (Q10) of 100 to 1000. By contrast, the Q10 for the effectiveness of the newly created effectors themselves, as well as for antigen-nonspecific defense systems, are much lower at about 1.5 to 5.36.100,101,161 The presence and beneficial effects of fever have been documented in a variety of cold- and warm-blooded vertebrates and even in some invertebrates. Under most conditions, it is probably not advisable to alleviate a fever. Exceptions include malignant hyperthermia and particularly high fevers during pregnancy.100,101 In addition, for patients with limited fluid, oxygen transport, or cardiopulmonary reserves, a febrile response should be treated with antipyretics.94 Consequences of the decreased immune response can be treated after the emergency.

ALCOHOL, ANESTHETICS, AND TOXINS Increases in the blood concentrations of ethanol, anesthetics, and a number of toxic substances lead to substantial decreases in body temperature.42,172 In many cases, this fall is caused by a decrease in the regulated temperature. In the case of high concentrations of alcohol and certain toxins, the reduction appears to be an adaptive adjustment that promotes survival. These chemicals disrupt protein structures within the cell membrane, and this effect is counteracted by a lower temperature.42 Indeed, mouse studies have shown that lowered body temperature counteracts ethanol toxicity.114 In humans as well, decrease in the regulated temperature is caused by increases in blood ethanol concentration. After ingestion of ethanol (3.0  mL/kg body weight) at 33° C (91.4° F), sweat rate increased and body temperature fell. Although skin temperature did not increase, subjects reported a warm sensation that paralleled the increase in sweat rate.199 At 18° C (64.4° F), body temperature decreased continuously before and after the drinking of alcohol, with no facilitation of metabolic heat production. During this period, the thermal discomfort sensation became more intense, although the discrimination of cold per se was impaired after the

SEVERE HYPOXIA AND ENDOTOXIN SHOCK When inspired oxygen concentration falls to 10% to 12%, a substantial decrease in the regulated temperature occurs. This reaction has been documented with the use of behavioral responses in fish, amphibians, reptiles, and mammals.59,193 For humans who are exercising in 28° C (82.4° F) water under eucapnic conditions, decreasing inspired oxygen to 12% lowers the core temperature thresholds for vasoconstriction and shivering and increases the rate of core cooling by 33%.87 The value of the resultant lowered body temperature is clear: the affinity of hemoglobin for oxygen is increased, and overall metabolic rate is decreased. The mechanism underlying the change in the regulated temperature may involve differential sensitivities of central neurons; hypoxia specifically increases activity of warm-sensitive neurons in the POAH.184 A somewhat similar regulated hypothermic response occurs when an animal is exposed to very high levels of pyrogens; the same response occurs under less extreme conditions in weak or malnourished animals. The lowered body temperature may serve to decrease the energy costs of maintaining a high body temperature for a severely compromised animal.159

ALTERED SYSTEM RESPONSIVENESS AND CAPACITIES A number of situations alter responsiveness of the thermoregulatory system. Awareness of these conditions is important when assessing the thermoregulatory capabilities of a particular person and when determining possible causes for hyperthermia or hypothermia.

THERMAL ACCLIMATION Thermoregulation is affected by chronic exposure to very cold or hot environments as well as by chronic exercise in cool or warm ambient temperatures. Such exercise in a cool environment greatly increases responsiveness of the sweat glands; if exercise is in the heat, the central temperature at which sweating is initiated is also lowered. The net consequence of these adjustments is that a heat- and exercise-acclimated individual can workout at a given level with far less increase in core temperature.129 Exercise in humid heat appears to decrease resting core temperature in acclimated individuals.145 Increases in both core and skin temperatures contribute to various changes involved in heat acclimation.152 Physical training also increases skin blood flow at any given increase in core temperature.85 Although acclimation to

warm conditions produces many changes in the cardiovascular system, the basic baroreflex responses are not altered.195 Heat acclimation may result in protective cellular adaptations. Intracellular heat shock protein 72 is likely involved in the maintenance of cellular protein conformation and homeostasis during hyperthermia, inflammation, and injury.123 A 10-day heat- and exercise-acclimation test increased heat shock protein 72 levels in peripheral blood mononuclear cells.194 Chronic cold exposure alters many thermoregulatory systems and involves long-term evolutionary changes and thermal acclimation. In many cases, resting metabolic rate is increased after repeated cold exposure;20,204 however, repeated exposure to very cold environments may produce the opposite effect. For example, eighty 30-minute sessions at 5° C (41° F) decreased the metabolic response to a standard cold-air test and often led to lower internal temperatures in these cold-acclimated individuals.74 When the extremities are initially exposed to cold, strong vasoconstriction is seen. At some point, however, cold-induced removal of the superficial α-receptor inhibition leads to vasodilation of the fingers, which warms the extremities and protects against frostbite. This response has a genetic component; for individuals who are not cold acclimated, this response is very strong among Inuit Eskimos, moderate among whites, and minimal among Chinese from Hong Kong. Individual differences in the vasodilation response to cold determine the relative likelihood of the development of frostbite. An environmental influence in this response is also likely; fishermen in northeastern Canada did not exhibit vasoconstriction of the fingers when exposed to cold.63

COMPETITION WITH OTHER HOMEOSTATIC SYSTEMS In addition to a constant core temperature, the body has many other requirements. When fluid balance or energy requirements are not met, thermoregulatory responses can be compromised. For heat production and heat conservation, an adequate energy supply, patent nervous system, and functional effector organs are critical. Thus, hypoglycemia decreases the core temperature at which shivering is initiated while leaving the thresholds for sweating and vasodilation unaffected.143 During exercise, heat is generated by activity of the muscles. About 80% of the energy consumption is converted into heat, with only about 20% going to the actual work produced by contraction of the muscles. High muscle temperature increases efficiency of muscle contraction.7,8 However, an excessive rise in body temperature impairs endurance performance. It is well appreciated that 40° C (104° F) is very near the upper limit of core body temperature when trying to maintain prolonged exercise. The time to exhaustion during heavy exercise is affected by the initial body temperature.61,134,136 In a heat-acclimation study,  2 subjects exercised until exhaustion at 60% of their maximum VO for 9 to 12 consecutive days at 40° C (104° F).136 The time to exhaustion became progressively longer with acclimation, but core temperature at the time of exhaustion remained at about 40° C (104° F). When body temperature was altered by water immersion before bicycle ergometer exercise at 40° C (104° F), time to exhaustion became progressively longer as initial body temperature was progressively lowered. Again, body temperature at exhaustion remained at about 40° C (104° F).61 For the maintenance of exercise performance and body temperature in a warm environment, body water status is critical.121,167 It is common for a person who is working in the heat to lose 1 L of water per hour. Even when fluids are readily available, maintaining a euhydrated state may be difficult. For hypohydration during continued activity, each percent decrease in body weight leads to a core temperature increase of about 0.15° C (0.27° F). This decreased heat dissipation is mediated by two mechanisms. At a given core temperature, hypertonicity decreases the sweating response, and hypovolemia reduces skin blood flow.167 Hyperhydration has no effect on thermoregulation during compensable exercise heat stress.104 During uncom­ pensable exercise heat stress, hyperhydration slightly increases the time to exhaustion but only by delaying hypohydration; 115

CHAPTER 4  Thermoregulation

ingestion of ethanol.197,198 However, lower blood ethanol levels associated with moderate consumption in humans have minimal and inconsistent effects on thermal balance of the whole body.46,86 Excellent overviews of the effects of general anesthetics on perioperative thermoregulation are available.171,173 Many of these substances (e.g., halothane, fentanyl and nitrous oxide, enflurane, isoflurane) in anesthetic doses act in a similar manner. Heat-loss thresholds are increased by about 1° C (1.8° F), and heat-maintenance thresholds are lowered by approximately 2.5° C (4.5° F). Interestingly, in the typical clinical dose range, the gain (sensitivity) of the effector responses is nearly normal. In the conditions under which general anesthetics are normally administered, body temperature decreases significantly. An initial rapid drop is caused by redistribution of heat; cool blood from the periphery lowers central core temperature. A second and slower decrease results from a fall in body heat content. Finally, a plateau is reached, either because heat production and heat loss are passively balanced or because heat maintenance thresholds are reached. During postanesthetic recovery, there is vigorous shivering. Anesthetic-induced hypothermia is reduced in patients with higher preoperative systolic blood pressures. This difference is associated with higher preoperative plasma norepinephrine levels, which may intensify the vasoconstriction response.92 Cutaneous warming before and during anesthesia prevents the development of hypothermia and decreases the incidence of infectious complications.103,171

thermoregulation is not affected.105 It is important to be alert to the possibility of dehydration in many atypical situations. For example, swimmers training in an outdoor pool with a water temperature of 26° C (78.8° F) lost sufficient fluid (i.e., 2.5% of their body weight) in 3 hours to compromise thermoregulatory responses.176 Hypoxia can undermine thermoregulatory vascular responses because of demands that compete or operate at cross-purposes. Thus, in a hot environment, hypoxia reduces skin blood flow at a given sweat rate. In the cold, hypoxia enhances core cooling by delaying the onset of vasoconstriction and cooling.119

doses of these substances impair or abolish both autonomic and behavioral aspects of thermoregulation. Body temperature then changes passively, depending on the thermal environment. This can be particularly dangerous when elevated levels of alcohol or similar substances are combined with heat stress. Impaired ability to dissipate heat is then combined with the enhanced toxicity of increased tissue temperature. Drugs that increase metabolic heat production (e.g., amphetamines, ecstasy [3,4-methylenedioxymethamphetamine], cocaine) are also particularly dangerous to use in the heat. In addition, cocaine interferes with heat dissipation mechanisms and with the perception of warmth.19,39

ALCOHOL, DRUGS, ANESTHETICS, AND TOXINS

REFERENCES

Although moderate doses of anesthetics and toxins may elicit adaptive changes in a regulated body temperature, elevated

Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 5 

Accidental Hypothermia DANIEL F. DANZL

Although used for medical purposes for millennia, cold modalities were not scientifically evaluated until the 18th century. The hemostatic, analgesic, and therapeutic effects of cold on various conditions were well known. Biblical references cite truncal rewarming of King David by a damsel; various remedies were mentioned by Hippocrates, Aristotle, and Galen.270 Folklore from Maine still recounts the buggy ride of “Frozen Charlotte.” The effects of cold on human performance are perhaps best documented in military history.62,247 Frosty conditions have decided many battles.137 Numerous casualties occur even in training, such as four students of the U.S. Army Ranger School in 1995. Most cold injuries encountered today affect the urban destitute and wilderness and sports enthusiasts, such as skiers, hunters, sailors, climbers, and swimmers.6,164,298 The popularity of Arctic and mountain expeditions has increased the number of persons at risk.2,156 Among those challenging the environment are climbers of Mt Everest, Mt Hood, and Mt McKinley.127,233,257

Epidemiology In most countries, primary hypothermia deaths are considered violent and are classified as accidental, homicidal, or suicidal.39 Deaths from secondary hypothermia are usually considered natural complications of systemic disorders, including trauma, carcinoma, and sepsis. The true incidence of secondary hypothermia throughout the world is unknown because hypothermic persons found indoors usually have other serious and diverting medical illnesses. In addition, delays are common between hospital admission and death, so secondary hypothermia is significantly underreported. In contrast, death certificate data more accurately quantify primary hypothermia.80 Hypothermia occurs in various locations and in all seasons.244,315,363 In a multicenter North American survey of 428 cases of civilian accidental hypothermia, 69 occurred in Florida.59,342 Urban settings account for the majority of cases in most industrialized countries.59,168,331 There is an annual average of over 600 deaths attributed to primary hypothermia in the United States. Around one-half of these fatalities are in patients over age 65 years.40,151,152 The reason for any year-to-year decline in fatalities is unknown. Of note, the incidence of secondary hypothermia fatalities is far greater, but there are no reliable histologic criteria to confirm that hypothermia is the cause of death.279 116

CLASSIFICATIONS Accidental hypothermia is best defined as the unintentional decrease of around 2° C (3.6° F) in the “normal” core temperature of 37.2° to 37.7° C (99.0° to 99.9° F) without disease in the preoptic and anterior hypothalamic nuclei (Table 5-1). Classically, hypothermia is defined as a core temperature below 35° C (95° F). Hypothermia is both a symptom and a clinical disease entity. When sufficient heat cannot be generated to maintain homeostasis and core temperature drops below 30° C (86° F), the patient becomes poikilothermic and cools to the ambient temperature.204,306 Among clinical classifications, the most practical division includes healthy patients with simple environmental exposure (primary), those with specific diseases that produce hypothermia (secondary), and those with predisposing conditions. Other divisions that reflect the etiology of hypothermia include immersion versus nonimmersion, and acute versus chronic heat loss.225,249 Various physiologic stressors and other factors can impair thermoregulation.307 Age extremes, state of health and nutrition, type of exposure, and a multitude of intoxicants or medications can jeopardize thermostability by decreasing heat production or increasing heat loss. Physiologic stressors also include dehydration, sleep deprivation, and fatigue. These challenges increase heat loss via evaporation, radiation, conduction, and convection, and compensatory responses often fail.225 The resulting mortality rates range to well over 50% in many clinical series, depending largely on the severity of risk factors and on patient selection criteria.59,244,289,363 For safety, experimental investigations of induced hypothermia in human volunteers usually terminate cooling at about 35° C (95° F). Naturally, this precludes analysis of some of the more significant pathophysiologic features of moderate or severe hypothermia. Design limitations also occur in studies of anesthetized animals, because the results of these experiments require varying degrees of extrapolation to humans. For example, large differences exist both in the cardiovascular responses to interventions and in the amounts of peripheral musculature that are present, particularly in nonporcine animal models. As a result, clinical treatment recommendations must be predicated on the degree and duration of hypothermia and on the predisposing factors that are subsequently identified.125

For online-only figures, please go to www.expertconsult.com

Fahrenheit†

Celsius*

Fahrenheit†

Celsius*

95 94 93 92 91 90 89 88 87 86 85 84 83 82 81 80 79 78 77 76 75 74 73 72 71 70 69 68 67 66 65 64

35.00 34.44 33.89 33.33 32.78 32.22 31.67 31.11 30.56 30.00 29.44 28.89 28.33 27.78 27.22 26.67 26.11 25.56 25.00 24.44 23.89 23.33 22.78 22.22 21.67 21.11 20.56 20.00 19.44 18.89 18.33 17.78

63 62 61 60 59 58 57 56 55 54 53 52 51 50 49 48 47 46 45 44 43 42 41 40 39 38 37 36 35 34 33 32

17.22 16.67 16.11 15.56 15.00 14.44 13.89 13.33 12.78 12.22 11.67 11.11 10.56 10.00 9.44 8.89 8.33 7.78 7.22 6.67 6.11 5.56 5.00 4.44 3.89 3.33 2.78 2.22 1.67 1.11 0.56 0.00

Pathophysiology NERVOUS SYSTEM

*C = (F − 32) × 5/9 † F = 9/5 C + 32

Normal Physiology of Temperature Regulation Warm-blooded animals maintain a precariously dynamic equilibrium between heat production and heat loss.166,167 The normal diurnal variation in humans is only 1° C (1.8° F). Because physiologic changes occurring in humans are modified by predisposing or contributory factors, the normal responses to severe temperature depression require significant extrapolation.229,258

Numbing cold depresses the central nervous system, producing impaired memory and judgment, slurred speech, and decreased consciousness. During cold-weather expeditions, leaders are prone to risk-taking behavior and its attendant trauma. Temperature-dependent enzyme systems in the brain do not function properly at cold temperatures that are well tolerated by the kidneys. As a result, most patients are comatose below 30° C (86° F), although some remain amazingly alert.147 Neurons are initially stimulated by a 1° C (1.8° F) drop in temperature, but the brain does not always cool uniformly during accidental hypothermia. After the initial increase, there is a linear decrease in cerebral metabolism by 6% to 10% per degree Celsius from 35° C (95° F) to 25° C (77° F). Hypothermia can afford cerebral protection because of the diminished cerebral metabolic requirements for oxygen.108 The electroencephalogram is abnormal below 33.5° C (92.3° F) and becomes silent at 19° to 20° C (66.2° to 68° F). The triphasic waves commonly noted in hypothermia are also observed in various metabolic, toxic, and diffuse encephalopathies. Visual evoked potentials, another objective measure of cerebral function, become smaller as the mercury drops. After cerebral cortical function becomes impaired, lower brainstem functions are also deranged. Cerebrovascular autoregulation is protectively intact until the temperature drops below 25° C (77° F). Although vascular resistance is increased, blood flow is disproportionately redistributed to the brain. In canine studies, blood flow in the brain, muscle, kidneys, and myocardium recovers quickly to control levels after rewarming. Flow deficits persist in the pulmonary, digestive, and endocrine systems for up to 2 hours after rewarming. Chilling the peripheral nervous system increases muscle tension and preshivering tone, eventually leading to shivering. Shivering, which is also centrally controlled, is a much more efficient heat producer than are voluntary muscle contractions of the extremities.

Cold exposure

Thermosensitive end-organs (cutaneous and others)

Blood temperature

Lateral spinothalamic tract

Direct reflex vasoconstriction

Relevant hypothalamic nuclei (preoptic and anterior)

Involuntary muscle contraction (shivering)

Endocrinologic

Autonomic nervous system

Extrapyramidal stimulation of voluntary skeletal muscles

Adaptive behavioral responses

FIGURE 5-1  Physiology of cold exposure.

117

CHAPTER 5  Accidental Hypothermia

Basal heat production usually averages 40 to 60 kcal/m2 of body surface area per hour, which approximates the heat from a 100-watt incandescent bulb. This increases with shivering thermogenesis,243 food ingestion, fever, activity, and cold stress. Normal thermoregulation in vertebrates involves transmitting cold sensation to hypothalamic neurons via the lateral spinothalamic tracts and the thalamus (Figure 5-1). The physiologic characteristics of the four zones of hypothermia appear in Table 5-2. A complete discussion of the physiology of thermoregulation and cold exposure is presented in Chapters 4 and 6.

TABLE 5-1  Fahrenheit-to-Celsius Conversion Scale

PART 2  COLD AND HEAT

TABLE 5-2  Characteristics of the Four Zones of Hypothermia Core Temperature Stage Mild

Moderate

Severe

Profound

°C

°F

37.6 37.0 36.0 35.0 34.0

99.7 ± 1 98.6 ± 1 96.8 95.0 93.2

33.30

91.4

32.0 31.0 30.0

89.6 87.8 86.0

29.0 28.0 27.0 26.0 25.0

84.2 82.4 80.6 78.8 77.0

24.0 23.0 22.0 20.0 19.0 18.0 13.7 15.0 10.0 9.0

75.2 73.4 71.6 68.0 66.2 64.4 56.7 59.0 50.0 48.2

Characteristics Normal rectal temperature Normal oral temperature Increases in metabolic rate, blood pressure, and preshivering muscle tone Urine temperature 34.8° C (94.6° F); maximal shivering thermogenesis Development of amnesia, dysarthria, and poor judgment; maladaptive behavior; normal blood pressure; maximal respiratory stimulation; tachycardia, then progressive bradycardia Development of ataxia and apathy; linear depression of cerebral metabolism; tachypnea, then progressive decrease in respiratory minute volume; cold diuresis Stupor; 25% decrease in oxygen consumption Extinguished shivering thermogenesis Development of atrial fibrillation and other arrhythmias; poikilothermia; pupils and cardiac output two-thirds of normal; insulin ineffective Progressive decrease in level of consciousness, pulse, and respiration; pupils dilated; paradoxical undressing Decreased ventricular fibrillation threshold; 50% decrease in oxygen consumption and pulse; hypoventilation Loss of reflexes and voluntary motion Major acid–base disturbances; no reflexes or response to pain Cerebral blood flow one-third of normal; loss of cerebrovascular autoregulation; cardiac output 45% of normal; pulmonary edema may develop Significant hypotension and bradycardia No corneal or oculocephalic reflexes; areflexia Maximal risk of ventricular fibrillation; 75% decrease in oxygen consumption Lowest resumption of cardiac electromechanical activity; pulse 20% of normal Electroencephalographic silencing Asystole Lowest adult accidental hypothermia survival106 Lowest infant accidental hypothermia survival264 92% decrease in oxygen consumption Lowest therapeutic hypothermia survival258

CARDIOVASCULAR SYSTEM Many cardiovascular responses caused by or associated with hypothermia are well described.206,207 Cold stress increases consumption of myocardial oxygen. Autonomic nervous system stimulation causes tachycardia and peripheral vasoconstriction, both of which increase systemic blood pressure and cardiac afterload. As core temperature drops, there is a fairly linear decrease in pulse rate. After premonitory tachycardia, decremental bradycardia produces a 50% decrease in heart rate at 28° C (82.4° F). Because this bradycardia is caused by decreased spontaneous depolarization of pacemaker cells, it is refractory to atropinization. If there is a “relative” tachycardia not consistent with the degree of hypothermia, the clinician should be concerned. Associated conditions include occult trauma with hypovolemia, drug ingestion, and hypoglycemia. During hypothermic bradycardia, unlike normothermia, systole is prolonged longer than diastole. In addition, the conduction system is much more sensitive to cold than is the myocardium, so the cardiac cycle is lengthened. Cold-induced changes in pH, oxygen, electrolytes, and nutrients also alter electrical conduction.224 Hypothermia progressively decreases mean arterial pressure and cardiac index. Cardiac output drops to about 45% of normal at 25° C (77° F). Systemic arterial resistance, determined by invasive hemodynamic monitoring, is increased. Even after rewarming, cardiovascular function may remain temporarily depressed, with impaired myocardial contractility, metabolism, and peripheral vascular function.341 Mild, steady hypothermia in patients with poikilothermic thermoregulatory disorders causes electrocardiographic (ECG) alterations and conduction abnormalities.68 First the PR, then the QRS, and most characteristically the QTc intervals are prolonged. Clinically invisible increased preshivering muscle tone can obscure the P waves; ST-segment and T-wave abnormalities are inconsistent.9,347 Of note, ordinary surface ECG electrodes, when attached to dry skin, will accurately reflect cardiac electrical activity. Needle electrodes are not necessary to detect weak ECG signals.187 118

The J wave (Osborn wave or hypothermic hump; (Figure 5-2), first described by Tomaszewski in 1938, occurs at the junction of the QRS complex and the ST segment. It is not prognostic but is potentially diagnostic.112,197 J waves occur at any temperature below 32.2° C (90° F) and are most frequently seen in leads II and V6. When core temperature falls below 25° C (77° F), J waves are found in the precordial leads (especially V3 or V4). The size of the J waves also increases with temperature depression, but is unrelated to arterial pH.373 J waves are usually upright in aVL, aVF, and the left precordial leads.3,175,262 J waves may represent hypothermia-induced ion fluxes, resulting in delayed depolarization or early repolarization of the left ventricle, or there may be an unidentified hypothalamic or neurogenic factor. J waves are not pathognomonic of hypothermia but occur also with central nervous system lesions, focal cardiac ischemia, and sepsis. They may also be present in young, healthy persons. When pronounced, J waveform abnormalities can simulate myocardial infarction. Computer software is not widely available that can successfully recognize and suggest the diagnosis of hypothermia.202,235,255 The prehospital capability to differentiate between J waves and injury current is important in rural and wilderness settings.57 Thrombolysis is unstudied in hypothermia but would be expected to exacerbate coagulopathies.110 Below 32.2° C (90° F), all types of atrial and ventricular arrhythmias are encountered.75 The His-Purkinje system is more sensitive to cold than is the myocardium. As a result, conduction velocity decreases and electrical signals can disperse. Because conduction time is prolonged more than the absolute refractory period, reentry currents can produce circus rhythms that initiate ventricular fibrillation (VF). In addition to causing bradycardia, widening the QRS complex, and prolonging the QT interval, hypothermia increases the duration of action potentials (Figure 5-3, online).21,22 During rewarming, nonuniform myocardial temperatures can disperse conduction and further increase the action potential duration, another mechanism to develop the unidirectional blocks that facilitate reentrant arrhythmias. At temperatures between 25° and 20° C (77° and 68° F), myocardial conduction time is prolonged further than the

CHAPTER 5  Accidental Hypothermia

FIGURE 5-2  The J or Osborn wave of hypothermia. Note that the obvious J waves were not properly interpreted by the computer.

absolute refractory period. Another arrhythmogenic mechanism is development of independent electrical foci that precipitate arrhythmias. Various electrolyte abnormalities can further complicate the situation during hypothermic conditions, because they exacerbate the effects of prolonged action potentials. Most conspicuously, hypothermia-induced cellular calcium loading mimics digitalis toxicity and may predispose to a forme fruste of torsades de pointes. Hypothermia-induced VF and asystole often occur spontaneously below 25° C (77° F). The VF threshold and transmembrane resting potential are decreased. Because the heart is cold, the conduction delay is facilitated by the large dispersion of repolarization, and the action potential is prolonged. The increased temporal dispersion of the recovery of excitability is linked to VF. Nature’s model of resistance to VF is the heart of hibernating animals during rewarming.163 Animals with this capacity seem to be protected by a shortened QT duration and a calcium channel handling system that prevents intracellular calcium overload. Asystole and VF may both result from hypovolemia, tissue hypoxia, therapeutic manipulations, acid–base fluxes, autonomic dysfunction, and coronary vasoconstriction coupled with increased blood viscosity. Other causes may include rough handling or jostling, sudden vertical positioning, and acute metabolic stress from exertion or very rapid rewarming.

CORE TEMPERATURE AFTERDROP Core temperature afterdrop refers to the continued decline in a hypothermic patient’s temperature after removal from the cold (see also Chapter 6). Contributing to afterdrop is the simple temperature equilibration between the warmer core and cooler periphery. Circulatory changes account for another set of observations. The countercurrent cooling of blood that perfuses cold extremities results in core temperature decline until the existing

temperature gradient is eliminated. In cold-water immersion, post-rescue collapse may also result from abrupt hypotension after loss of hydrostatic squeeze contributed by the water. The incidence and magnitude of core temperature afterdrop vary widely in clinical experiments and in surgically induced hypothermia.103,104,125 Hayward128 measured his own esophageal, rectal, tympanic, and cardiac temperatures (via flotation tip catheter) during rewarming after being cooled in 10° C (50° F) water. On three different days, rewarming was achieved via shivering thermogenesis, heated humidified inhalation, and warm bath immersion. Coincident with a 0.3° C (0.5° F) afterdrop during warm bath immersion, his mean arterial pressure fell 30% and his peripheral vascular resistance fell 50%. Therefore the circulatory mechanism is another major contributor to afterdrop. A human study of peripheral blood flow during rewarming from mild hypothermia suggests that minimal skin blood flow changes can also lead to afterdrop (Figure 5-4). The largest core temperature afterdrops occur when subjects are rewarmed with plumbed garments and heating pads. In summary, core temperature afterdrop appears to become most clinically relevant when a large temperature gradient exists between the periphery and the core, particularly in dehydrated, chronically cold patients. Both conductive and convective mechanisms are responsible for afterdrop.104 Stimulating peripheral blood flow can increase afterdrop. Major afterdrops are also observed when frostbitten extremities are thawed before crystalloid volume resuscitation and thermal stabilization of the core temperature.

RESPIRATORY SYSTEM Any exposure to a big chill initially stimulates respiratory drive, which is followed by progressive depression of respiratory minute volume as cellular metabolism is depressed. The respiratory rate often falls to 5 to 10 breaths/min below 30° C (86° F), and ultimately brainstem neurocontrol of ventilation fails. An 119

PART 2  COLD AND HEAT

The etiology of the cold diuresis is multifactorial.114,115 Some of the suggested mechanisms include inhibition of antidiuretic hormone (ADH) release and decreased renal tubular function. Neither hydration nor ADH infusions seem to influence the diuretic response, which appears to be an attempt to compensate for initial relative central hypervolemia caused by vasoconstrictive overload of capacitance vessels. The diuresis may also be pressure related, caused by impaired autoregulation in the kidneys. Cold diuresis has circadian rhythmicity and correlates with periods of shivering. Cold water immersion increases urinary output 3.5 times, and the presence of ethanol impressively doubles that diuresis.

A

B

FIGURE 5-4  Infrared scan of the palmar hand surface. Blue, 43° C (109.4° F); red, 68° C (154.4° F). A, At room temperature. B, After 5 minutes in a cold room, with evidence of vasoconstriction. (Courtesy Naval Health Research Center, San Diego, Calif.)

important physiologic observation is that carbon dioxide production drops 50% for each 8° C (14° F) fall in temperature. In severe hypothermia, carbon dioxide retention and respiratory acidosis reflect the aberrant responses to normothermic respiratory stimuli.99 Other pathophysiologic factors contributing to ventilation– perfusion mismatch include decreased ciliary motility, increased quantity and viscosity of secretions, hypothermic acute respiratory distress syndrome, and noncardiogenic pulmonary edema.332 The thorax loses elasticity, and pulmonary compliance drops. The respiratory “bellows” stiffen and fail because contractile efficiency of the intercostal muscles and diaphragm declines. Pertinent potentially protective or detrimental factors that affect tissue oxygenation in endothermic humans are listed in Box 5-1.

RENAL SYSTEM The kidneys respond briskly to hypothermia-induced changes in the vascular tree’s capacitance. Peripheral vasoconstriction can result initially in a relative central hypervolemia, producing diuresis, even with mild dehydration. In addition, renal blood flow is depressed by 50% at 27° to 30° C (80.6° to 86° F), which decreases glomerular filtration rate. Nevertheless, there is an initial large diuresis of this dilute glomerular filtrate, which does not efficiently clear nitrogenous wastes.

BOX 5-1  Oxygenation Considerations

During Hypothermia

Detrimental Factors • Oxygen consumption increases with rise in temperature; use caution if rewarming is rapid; shivering also increases demand • Decreased temperature shifts oxyhemoglobin dissociation curve to the left • Ventilation–perfusion mismatch; atelectasis; decreased respiratory minute volume; bronchorrhea; decreased protective airway reflexes • Decreased tissue perfusion from vasoconstriction; increased viscosity • “Functional hemoglobin” concept: capability of hemoglobin to unload oxygen is lowered • Decreased thoracic elasticity and pulmonary compliance Protective Factors • Reduction of oxygen consumption by 50% at 28° C (82.4° F), 75% at 22° C (71.6° F), and 92% at 10° C (50° F) • Increased oxygen solubility in plasma • Decreased pH and increased PaCO2 shift oxyhemoglobin dissociation curve to right

120

COAGULATION Coagulopathies often develop in hypothermic patients because the enzymatic nature of the activated clotting factors is depressed by cold.88 In vivo, prolonged clotting is proportional to the number of steps in the cascade. For example, at 29° C (84.2° F), a 50% to 60% increase in the partial thromboplastin time (PTT) would be expected. Kinetic tests of coagulation, however, are performed in the laboratory at 37° C (98.6° F). As the blood warms in the machine, the enzymes between the factors in the cascade are activated. The sample of warmed in vitro blood then clots normally.77 The reversible hemostatic defect created by hypothermia may not be reflected by the “normal” prothrombin time (PT), PTT,292 or international normalized ratio (INR). This coagulopathy is basically independent of clotting factor levels and cannot be confirmed by laboratory studies performed at 37° C (98.6° F). Treatment is rewarming and not simply administration of clotting factors.288 When rapid rewarming is difficult, concentrations of 0.01 to 1 nM of desmopressin may partially reverse hypothermiainduced coagulopathy in vitro.376 Thrombocytopenia as a cause of bleeding becomes progressively significant in severe hypothermia. Proposed mechanisms include direct bone marrow suppression and splenic or hepatic sequestration. Thromboxane B2 production by platelets is also temperature dependent, so cooling skin temperature produces reversible platelet dysfunction. Thrombocytopenia is a common but poorly recognized corollary of hypothermia in older adults and neonates. Coagulopathy in trauma patients is attributed to enzyme inhibition, platelet alteration, and fibrinolysis.320 The critical temperature at which enzyme activity slows significantly is 34° C (93.2° F).358 In addition, clot strength weakens as a result of platelet malfunction. Fibrinolysis is not significantly affected at any temperature in the range measured (33° to 37° C [91.4° to 98.6° F]) (see Trauma, later). Physiologic hypercoagulability also develops during hypothermia, with a sequence similar to that seen in disseminated intravascular coagulation (DIC). This produces a higher incidence of thromboembolism during hypothermia. Causes include thromboplastin release from cold tissue, simple circulatory collapse, and release of catecholamines and steroids. Because fibrin splitproduct levels can be normal, bleeding is not always considered a hematologic manifestation of DIC.282 Whole blood viscosity increases with the hemoconcentration seen after diuresis and the shift of fluid out of vascular compartments. Red blood cells (RBCs) simply stiffen and have diminished cellular deformity when chilled.276 The elevated viscosity of hypothermia is also exacerbated by cryoglobulinemia. Cryofibrinogen is a cold-precipitated fibrinogen occasionally seen with carcinoma, sepsis, and collagen vascular diseases. Blood viscosity is also increased by the transient increases in platelet and RBC counts seen with mild surface cooling. This could explain the increased mortality from coronary and cerebral thromboses that occur in winter.225

Predisposing Factors The factors that predispose to hypothermia can be separated into those that decrease heat production, those that increase heat loss, and those that impair thermoregulation.225 There is significant overlap between these groups (Box 5-2).

Decreased Heat Production Endocrinologic Failure • Hypopituitarism • Hypoadrenalism • Hypothyroidism • Lactic acidosis • Diabetic and alcoholic ketoacidosis Insufficient Fuel • Hypoglycemia • Malnutrition • Marasmus • Kwashiorkor • Extreme physical exertion Neuromuscular Physical Exertion • Age extremes • Impaired shivering • Inactivity • Lack of adaptation Impaired Thermoregulation Peripheral Failure • Neuropathies • Acute spinal cord transection • Diabetes Central or Neurologic Failure • Cardiovascular accident

• Central nervous system trauma • Toxicologic effects • Metabolic failure • Subarachnoid hemorrhage • Pharmacologic effects • Hypothalamic dysfunction • Parkinson disease • Anorexia nervosa • Cerebellar lesion • Neoplasm • Congenital intracranial anomalies • Multiple sclerosis • Hyperkalemic periodic paralysis Increased Heat Loss Environmental • Immersion • Nonimmersion Induced Vasodilation • Pharmacologic effects • Toxicologic effects Erythrodermas • Burns • Psoriasis • Ichthyosis • Exfoliative dermatitis

DECREASED HEAT PRODUCTION Thermogenesis is decreased at both extremes of age. In older adults, neuromuscular inefficiency and decreased physical activity impair shivering. Aging progressively diminishes homeostatic and cold adaptive capabilities. Although most older adults have normal thermoregulation, they tend to develop conditions that impair heat conservation.283,286 Older adults are physiologically less adept at increasing heat production and the respiratory quotient (the ratio of the volume of carbon dioxide produced to the volume of oxygen consumed per unit of time). Impaired thermal perception, possibly caused by decreased resting peripheral blood flow, leads to poor adaptive behavior. Metabolic studies also demonstrate that in severely hypothermic older adults, lipolysis occurs in preference to glucose consumption.256,271 Neonates have a large surface area–to–mass ratio, relatively deficient subcutaneous tissue layer, and virtually no behavioral defense mechanisms. Newborn “unadapted” infants attempt to thermoregulate with initial vasoconstriction and acceleration of metabolic rate. In contrast, “adapted” infants who are older than 5 days can increase lipolysis immediately and burn oxidative brown adipose tissue. No cause-and-effect relationship has been found between hypothermia and the mortality rate of premature infants.129,301 Although the smaller infants in a neonatal intensive care unit are at the greatest risk for hypothermia, mortality is related to hypothermia only in larger neonates. Emergency deliveries and resuscitations are responsible for most acute neonatal hypothermia. Other common risk factors are prematurity, low birth weight, inexperienced mother, perinatal morbidity, and low socioeconomic status. In babies with more chronically induced subacute hypothermia, lethargy, a weak cry, and failure to thrive are common.335 Many cold infants have “paradoxical rosy cheeks,” looking surprisingly healthy. After the first few days of life, hypothermia frequently indicates septicemia and carries a high mortality rate. Low weight and malnutrition are common. Hypothermia in a low-birth-weight neonate should suggest the possibility of

CHAPTER 5  Accidental Hypothermia

BOX 5-2  Factors Predisposing to Hypothermia Iatrogenic • Emergency childbirth • Cold infusions • Heatstroke treatment Miscellaneous Associated Clinical States • Multisystem trauma • Recurrent hypothermia • Episodic hypothermia • Shapiro syndrome • Infections: bacterial, viral, parasitic • Pancreatitis • Carcinomatosis • Cardiopulmonary disease • Vascular insufficiency • Uremia • Paget disease • Giant cell arteritis • Sarcoidosis • Shaken baby syndrome • Systemic lupus erythematosus • Wernicke-Korsakoff syndrome • Hodgkin’s disease • Shock • Sickle cell anemia • Sudden infant death syndrome

intracranial hemorrhage; hypothermia is also observed in shaken baby syndrome. Endocrinologic failure, including hypopituitarism, hypoadrenalism, and myxedema, commonly decreases heat production. Interestingly, congenital adrenal hyperplasia with mineralocorticoid insufficiency is more common in cold climates, possibly an adaptive response to prolonged exposure to cold temperatures, because “normal” cold diuresis is reduced in these patients. Hypothyroidism is often occult, with no history of cold intolerance, dry skin, lassitude, or arthralgias. The physician should check for a thyroid scar or any history of thyroid hormone replacement. The degree of temperature depression correlates fairly directly with mortality. Eighty percent of patients in myxedema coma, which is several times more common in female patients, are hypothermic. The effects of insufficient nutrition extend from hypoglycemia to marasmus to kwashiorkor. Kwashiorkor is less often associated with hypothermia than is marasmus, because of the insulating effect of hypoproteinemic edema. Central neuroglycopenia distorts hypothalamic function. Many alcoholic patients with hypothermia are hypoglycemic. Malnutrition decreases insulative subcutaneous fat and directly alters thermoregulation. Poor nutrition predisposes to hypothermia and its attendant clumsiness in older adult women with femoral neck fractures. Partly because of fuel depletion, hypothermia is as great a threat as hyperthermia in marathon races run in cool climates. Runners slowing from fatigue or injury late in a race are at serious risk of hypothermia.170

INCREASED HEAT LOSS Poorly acclimated and insulated individuals often have high diaphoretic, convective, and evaporative heat losses during exposure to cold. Because the skin functions as a radiator, any dermatologic malfunction increases heat loss. Such erythrodermas include psoriasis, exfoliative dermatitis, and toxic epidermal necrolysis. Hypothermia with hypernatremic dehydration is also seen in congenital lamellar ichthyosis. 121

PART 2  COLD AND HEAT

Burns and inappropriate burn treatment cause excessive heat loss, as do other iatrogenic factors, including massive cold intravenous (IV) infusions and overcooling heatstroke victims.188 When carbon dioxide is used for abdominal insufflation before laparoscopy, warming the gas before administration helps prevent hypothermia. Environmental immersion exposure is discussed in detail in Chapter 6.102 Many pharmacologic and toxicologic agents both increase heat loss and impair thermoregulation.165-167,343 The most common is ethanol, which interacts with every putative thermoregulatory neurotransmitter. Although ingestion of ethanol produces a feeling of warmth and perhaps visible flushing, it is the major cause of urban hypothermia.59,244 In fatal cases of accidental hypothermia, many victims are under the influence of ethanol. In children with ethanol intoxication, hypothermia is common. Ethanol is also a poikilothermia-producing agent that directly impairs thermoregulation at high or low temperatures.165 Body temperature is lowered both from cutaneous vasodilation with radiative heat loss and from impaired shivering thermogenesis. Chronic ethanol ingestion damages the mamillary bodies and posterior hypothalamus, which modulates shivering thermogenesis.277 Ethanol also increases the risk for being exposed to the environment, by modifying protective adaptive behavior. The ultimate example is paradoxical undressing, or removal of clothing in response to a cold stress. As an organic solvent, ethanol confers a few theoretically redeeming qualities in freezing cold injuries by lowering the cellular freezing point.114,115 The neurophysiologic effects of ethanol are modified by duration and intensity of exercise, food consumption, and applied cold stress.94 Aging increases sensitivity to the hypothermic actions of ethanol in some primate experiments. Chronic ingestion yields tolerance to its hypothermic effects, and rebound hyperthermia may be seen during withdrawal. Conditions associated with ethanol ingestion that adversely affect heat balance include immobility and hypoglycemia.368 Inhibited hepatic gluconeogenesis coexists with malnutrition. Hypothermic alcoholic ketoacidosis is reported.363 Intravenous thiamine is diagnostic and therapeutic for Wernicke’s encephalopathy, another cause of reversible hypothermia. The acute triad of global confusion, ophthalmoplegia, and truncal ataxia is often masked by hypothermia, and temperature depression may persist for weeks.

IMPAIRED THERMOREGULATION Various conditions that impair thermoregulation can be considered as having central, peripheral, metabolic, and pharmacologic or toxicologic effects. Central Central conditions may directly affect hypothalamic function and mediate vasodilation. Traumatic lesions include skull fractures, especially basilar, and intracerebral hemorrhages, most commonly chronic subdural hematomas. Pathologic lesions include neoplasms, congenital anomalies, and Parkinson disease. Patients with Parkinson disease or Alzheimer’s disease, because of global neurologic impairment, are particularly at behavioral risk. Finally, cerebellar lesions also impede heat production because of inefficient choreiform shivering. Hypothermia can occur with Reye’s syndrome. In Hodgkin’s disease, hypothermia is seen only in previously febrile patients with advanced disease, independent of cell type. This seems to be a disease-associated functional disorder of thermoregulation, similar to that seen in anorexia nervosa. Centrally induced hypothermia is completely antagonized with thyrotropin-releasing hormone. Peripheral Peripheral thermoregulation fails after acute spinal cord transection. Victims are functionally poikilothermic as soon as peripheral vasoconstriction is extinguished.242 Other peripheral impediments to thermostability include neuropathies and diabetes mellitus. Hypothermia is more common in older adult diabetics than in the general population, even after excluding patients with diabetic metabolic emergencies. The common denominator in 122

metabolic derangements may be abnormal plasma osmolality that interferes with hypothalamic function. Similar causes of hypothermia include hypoglycemia, diabetic ketoacidosis, and uremia. Remarkably, the pH was 6.67 in one hypothermic survivor with lactic acidosis, and 6.41 in another.253 Pharmacologic or Toxicologic Numerous medications and toxins in therapeutic or toxic doses impair centrally mediated thermoregulation and vasoconstriction.172,272,377 The usual offenders are barbiturates, benzodiazepines, phenothiazines, and the cyclic antidepressants. Reduced core temperature may be a prodrome of lithium poisoning. Organophosphates, narcotics, glutethimide, bromocriptine, erythromycin, clonidine, fluphenazine, bethanechol, atropine, acetaminophen, and carbon monoxide all cause hypothermia. In experimental studies, hypothermia after acute carbon monoxide poisoning is associated with increased mortality.

RECURRENT HYPOTHERMIA Recurrent and episodic hypothermias are widely reported. The recurrent variety is more common and is usually secondary to ethanol abuse, with one person having survived 12 episodes.56 Severe, recurrent presentations are also caused by self-poisoning and anorexia nervosa. Persons with episodic hypothermia can be divided into two groups, albeit with significant overlap, as follows: Group 1: Diaphoretic episodes precede the temperature decline, which lasts several hours. This group includes those with hypothalamic lesions and agenesis of the corpus callosum (Shapiro syndrome) and persons with spontaneous periodic hyperthermia. Resultant hyperhidrosis and hypothermia are successfully treated with clonidine, a centrally acting α-adrenergic agonist. The hypothermia of corpus callosum agenesis is also seen with hypercalcemia and status epilepticus. Because no hypothermia results from experimental sectioning of the corpus callosum, associated lesions, including lipomas, probably cause thermoinstability. Spontaneous periodic hypothermia may reflect a diencephalic autonomic seizure disorder and can accompany paroxysmal hypertension. Vasomotor and thermoregulatory mechanisms are successfully treated with anticonvulsants. Florid psychiatric symptoms often mask these intermittent hypothermic episodes. Group 2: The second group consists of persons who remain cold for days to weeks, rather than hours. These people have more seizure disorders, and the central hypothalamic thermostat is set abnormally low. Patients with intermittent hypothermia usually show some characteristics of both groups.225 Circadian rhythm disturbances are also seen in persons with neurologic disorders who have chronic hypothermia.

PREDISPOSING INFECTIONS OR CONDITIONS Among the infestations and infections that may elevate or depress core temperature are septicemia, pneumonia, peritonitis, meningitis, encephalitis, bacterial endocarditis, typhoid, miliary tuberculosis, syphilis, brucellosis, and trypanosomiasis.214 Other diseases, in addition to cerebrovascular and cardiopulmonary disorders, that produce secondary hypothermia include systemic lupus erythematosus, carcinomatosis, pancreatitis, and multiple sclerosis. Hypothalamic demyelination may explain episodic hypothermia observed in some patients with multiple sclerosis. Hypothermia can also result from low cardiac output after a major myocardial infarction, which can be reversed by intra-aortic balloon counterpulsation. Finally, causes include vascular insufficiency, giant cell arteritis, uremia, sickle cell anemia, Paget disease, sarcoidosis, and sudden infant death syndrome. Magnesium sulfate infusion during preterm labor can produce hypothermia with fetal and maternal bradycardia, and hypothyroidism can be manifested as hypothermia after preeclampsia (see Box 5-2).

TRAUMA Hypothermia protects the brain from ischemia but can result in arrhythmias, acidosis, and coagulopathies, and it can extract a

Presentation The patient’s history may suggest hypothermia.33 Diagnosis becomes fairly simple when exposure is obvious, as with avalanche victims. Subtle presentations, however, predominate in urban settings. Victims often complain only of vague symptoms, including hunger, nausea, fatigue, and dizziness. Predisposing underlying illness or ethanol ingestion is also common, as are major trauma, immersion, overdose, cerebrovascular accidents, and psychiatric emergencies (Box 5-3).

During the head, eye, ear, nose, and throat examination, abnormal findings can include decreased corneal reflexes, mydriasis, strabismus, flushing, erythropsia, facial edema, rhinorrhea, and epistaxis. Mild hypothermia usually does not depress pupillary light reflexes. Cardiovascular findings after initial tachycardia include bradyarrhythmias and hypotension. Heart sounds may be muffled and distant. Tachypnea, an early respiratory finding, is usually followed by progressive hypoventilation with bronchorrhea and adventitious sounds. Because the gastrointestinal tract is depressed, abdominal distention or rigidity, ileus, obstipation, and poor rectal tone are often present. Gastric dilation is common in neonates and myxedematous adults. Urinary output ranges from initial polyuria resulting from cold diuresis to anuria. The incidence of testicular torsion increases because of cremasteric contractions. Diffuse neurologic abnormalities vary widely. Some persons can still converse at 32° C (89.6° F) and are normoreflexic. The level of consciousness generally declines proportionate to the degree of hypothermia. The presence of ataxia and dysarthria may mimic a cerebrovascular accident. Speed of reasoning and memory registration are also impaired. Amnesia, antinociception, anesthesia, or hypesthesia can develop. Cranial nerve abnormalities are present after bulbar damage from central pontine myelinolysis. These extraocular muscle movement abnormalities, like extensor plantar responses, do not directly correlate with the degree of hypothermia. Hyperreflexia predominates from 35° to 32.2° C (95° to 90° F) and is followed by hyporeflexia. The plantar response remains flexor until 26° C (78.8° F), when areflexia develops. The knee jerk is usually the last reflex to disappear and the first to reappear during rewarming. From 30° to 26° C (86° to 78.8° F), both contraction and relaxation phases of reflexes are prolonged equally. In myxedema, however, the relaxation phase of the ankle reflex is more prolonged than the contraction phase.225 Spinal cord and other central nervous system lesions may be obscured by depressive neurologic changes that normally accompany hypothermia. Psychiatric presentations and suicide attempts associated with hypothermia are commonly misdiagnosed initially. Preexisting psychiatric disorders can blossom in the cold, even if they were stabilized in temperate climates.30 Mental status alterations include anxiety, impaired judgment, perseveration, neurosis, and psychosis.156 Leaders of expeditions can become moody, apathetic, uncooperative, and risk taking. Older adult patients often withdraw in confusion, become silent, and display lassitude and poor judgment. A peculiar flat affect is common, and psychomotor impairment can resemble organic brain syndrome. Early in hypothermia, simply losing effective use of the hands can be devastating. Appropriate behavior adapted to the cold, such as seeking a heat source, is often lacking. An extreme example is paradoxical undressing.183 The clothing is removed in a preterminal effort to address impending thermoregulatory collapse, and many persons are mistakenly identified as sexual assault victims. This phenomenon is also seen in hypothermic children. Undressing may also occur as a result of Alzheimer’s disease before wandering in the cold.182 Musculoskeletal posturing can extend to pseudo–rigor mortis. Preshivering muscle tone is increased before core temperature drops to 35° C (95° F), and muscular rigidity, paravertebral spasm, and even opisthotonos may occur. Extremity compartment syndromes often develop because of associated conditions causing prolonged compression and immobility, in addition to compartment hypertension seen during reperfusion of frostbitten extremities. Dermatologic presentations of hypothermia include erythema, pallor, edema, and scleral edema. Cold urticaria, frostnip, frostbite, and gangrene should also cause the clinician to consider this diagnosis. Pernio is also observed with chronic myelomonocytic leukemia.

Laboratory Evaluation ACID–BASE BALANCE The strategy for achieving and maintaining acid–base balance in hypothermia differs from that of normothermia.65,126,153,180 After 123

CHAPTER 5  Accidental Hypothermia

high metabolic cost during rewarming.97 Hypothermia hinders protective physiologic responses to acute trauma and affects pharmacologic and therapeutic maneuvers necessary to treat injuries.18,27 An inverse relationship usually exists between the Injury Severity Score (ISS) and core temperature of traumatized patients on arrival in the emergency department (ED). This observation does not settle whether hypothermia is just another risk factor for increased mortality or reflects the fact that the most severely injured patients are in hemorrhagic shock.132 One study assessed the impact of hypothermia as an independent variable during resuscitation from major trauma.97 Patients not aggressively rewarmed with continuous arteriovenous rewarming (CAVR) had increased fluid requirements, increased lactate levels, and increased acute mortality. Of the clinical entities associated with hypothermia, traumatic conditions causing hypotension and hypovolemia most dramatically jeopardize thermostability. Hypothermia is often obscured by obvious hemorrhaging and injuries. Liberalized indications for Focused Assessment With Sonography for Trauma (FAST) ultrasound examinations can minimize unnecessary computed tomography (CT) imaging. On the other hand, traumatic neurologic deficits, including paresis and areflexia, can be misattributed to hypothermia. In trauma patients requiring surgery, the mean temperature loss was greater in the ED than in the operating room.117 Thermal insults are often added during a trauma resuscitation. The patient is completely exposed for examination, and resuscitative procedures cause further heat loss.308 In a study stratifying subjects with the anatomic ISS, hypothermic patients had a higher mortality rate than did similarly injured patients who remained normothermic.171 Another study did not corroborate this finding,322 but those investigators stratified using trauma revised injury severity score (TRISS) methodology, which is probably less valid during hypothermia because its physiologic components overestimate injury severity. To illustrate this point, some component of hypotension is normal for a given degree of hypothermia. Various adverse physiologic events accompany hypothermia with trauma. Decreased skin and core temperatures without compensatory shivering thermogenesis are reported in patients with major trauma as defined by the ISS. Hypothermia directly causes coagulopathies in trauma patients through at least three avenues (see Coagulation, earlier).33 The cascade of enzymatic reactions is impaired, and plasma fibrinolytic activity is enhanced, producing a clinical presentation similar to that of DIC. Also, platelets are poorly functional and become sequestered. Hypothermia is protective only when induced before shock occurs. This reduces adenosine triphosphate (ATP) utilization while ATP stores are still normal, as during elective surgery. ATP stores in traumatized patients are already depleted. Hypothermia worsens the effects of endotoxins on clotting time in vitro and may synergistically exacerbate the coagulopathy seen in trauma.88 The average temperature of 123 initially normothermic trauma patients in whom lethal coagulopathies developed was 31.2° C (88.2° F). In another study, postinjury life-threatening coagulop­ athy in the seriously injured who require massive transfusion was predicted by persistent hypothermia and progressive metabolic acidosis.50,89 The appropriate target core temperature for a hypothermic patient with an isolated severe head injury may be 32° to 33° C (89.6° to 91.4° F). This target temperature balances neuroprotection against the adverse hematologic and physiologic consequences of hypothermia19,231,232 (see Cerebral Resuscitation, later.)

Head, Eye, Ear, Nose, Throat • Mydriasis • Decreased corneal reflexes • Extraocular muscle abnormalities • Erythropsia • Flushing • Facial edema • Epistaxis • Rhinorrhea • Strabismus Cardiovascular • Initial tachycardia • Subsequent tachycardia • Arrhythmias • Decreased heart tones • Hepatojugular reflux • Jugular venous distention • Hypotension • Peripheral vasoconstriction Respiratory • Initial tachypnea • Adventitious sounds • Bronchorrhea • Progressive hypoventilation • Apnea Gastrointestinal • Ileus • Constipation • Abdominal distention or rigidity • Poor rectal tone

• Gastric dilation in neonates or in adults with myxedema • Vomiting Genitourinary • Anuria • Polyuria • Oliguria • Testicular torsion

124

Dermatologic • Erythema • Pallor • Cyanosis • Icterus • Scleral edema • Ecchymosis • Edema • Pernio • Frostnip • Frostbite • Panniculitis • Cold urticaria • Necrosis • Gangrene

Psychiatric • Impaired judgment • Perseveration • Mood changes • Peculiar “flat” affect • Altered mental status • Paradoxical undressing • Neuroses • Psychoses

initial respiratory alkalosis from hyperventilation when a person first becomes chilled, a common underlying disturbance is mixed acidosis. The respiratory component of the acidosis is caused mainly by direct respiratory depression. In addition, as body temperature decreases, solubility of carbon dioxide in blood increases. Further contributors to the metabolic component of this acidosis include impaired hepatic metabolism and acid excretion, lactate generation from shivering, and decreased tissue perfusion.134 Nevertheless, reliable clinical prediction of the acid– base status in accidental hypothermia is not possible. In one series of 135 cases, 30% were acidotic and 25% alkalotic.244 Circulatory changes also prevent adequate mobilization and delivery of organic acids to buffer systems. As in normothermia, mixed venous blood may best reflect acid–base status during resuscitation.328 Despite flow changes in a canine model of moderate hypothermia, a significant correlation persists between arterial and mixed venous pH. The arteriovenous change in pH is 0.03 to 0.04 pH unit. The buffering capacity of cold blood is also markedly impaired. In normothermia, when the arterial partial pressure of carbon dioxide (PaCO2) increases 10 mm Hg, a decrease in pH of 0.08 unit occurs. At 28° C (82.4° F), the decrease in pH doubles to 0.16 unit. The accepted earlier assumption was that 7.42 was the ideal “corrected” patient pH at all temperatures and that therapy should be directed at maintenance of the corrected arterial pH at 7.42.362 A better intracellular pH reference is electrochemical neutrality, at which pH equals pOH. Because the neutral point of water at 37° C (98.6° F) is pH 6.8, Rahn281 hypothesizes that this normal 0.6 unit pH offset in body fluids should be maintained at all temperatures. Because the neutral pH rises with cooling, so should blood pH (Figure 5-5).287 Relative alkalinity of tissues makes physiologic sense. Intracellular electrochemical neutrality ensures optimal function of enzyme systems and transport proteins at all temperatures

• Suicide • Organic brain syndrome • Anorexia nervosa • Depression • Apathy • Irritability Musculoskeletal • Increased muscle tone • Shivering • Rigidity or pseudo–rigor mortis • Paravertebral spasm • Opisthotonos • Compartment syndrome

Neurologic • Depressed level of consciousness • Ataxia • Dysarthria • Amnesia • Anesthesia • Areflexia • Poor suck reflex • Hypoesthesia • Antinociception • Initial hyperreflexia • Hyporeflexia • Central pontine myelinolysis

and allows excretion of the neutral intracellular waste product urea.13 Depressed metabolism and carbon dioxide generation are physiologic responses to temperature depression, because each temperature has its associated metabolic rate. Ventilation is intrinsically adjusted to maintain a net charge on the defended parameter, the peptide-linked histidine imidazole buffering system.

8.0

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7.7

pH

PART 2  COLD AND HEAT

BOX 5-3  Signs of Hypothermia

7.4 7.1

ter

l wa

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6.8 0 40 37

30

20

10

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Temperature (° C) FIGURE 5-5  Neutrality is the pH of water at any given temperature. At 25° C (77° F), the neutral pH of water is 7.0; at 37° C (98.6° F), it is 6.8. An ectotherm’s physiologic 0.6 pH offset from neutral water progressively diminishes if the arterial blood gases are temperature corrected. After the in vitro sample is warmed in the analyzer to 37° C (98.6° F), do not mathematically correct the reported values to reflect the in vivo temperature.

HEMATOLOGIC EVALUATION Severity of blood loss is easily underestimated. Hematocrit value increases because of a decline in plasma volume that leads to a 2% increase per 1° C (1.8° F) fall in temperature. In addition, total RBC mass might already be low because of preexisting anemia, malnutrition, leukemia, uremia, or neoplasm. The white blood cell count is frequently normal or low, even if sepsis is present. As a result, systemic leukopenia does not imply absence of infection, especially if the patient is at either age extreme, is debilitated, intoxicated, myxedematous, or has secondary hypothermia.214 The leukocyte count also drops during hypothermia because of direct bone marrow depression and hepatic, splenic, and splanchnic sequestration. Serum electrolyte levels must be continuously monitored and rechecked during warming. There are no safe predictors of electrolyte values.125 Serum electrolytes fluctuate with temperature, duration of exposure, and rewarming technique selected. Both membrane permeability and sodium–potassium pump efficiency also change with temperature. Isolated temperature depression per se has no consistent effect on sodium and chloride levels until well below 25° C (77° F). Plasma electrolyte levels are also affected by ongoing fluid shifts, prehydration, rehydration, and endocrine or gastrointestinal dysfunction. The plasma potassium level is independent of temperature. Empirical potassium supplementation during hypothermia often results in normothermic toxicity. From a clinical perspective, hypokalemia occurs as potassium moves into the musculature and not simply out of the body through kaliuresis. The physiologically illogical discrepancy of decreasing potassium level with decreasing pH results from greater intracellular than extracellular pH changes. Hypokalemia is much more common in prolonged or chronically induced hypothermia. Systemic potassium deficiencies can also be exacerbated by prior diuretic therapy, alcoholism, diabetic ketoacidosis, hypopituitarism, and inappropriate antidiuretic hormone secretion. Hypokalemic digitalis sensitivity can be masked by hypothermia, and gradual correction of persistent and severe hypokalemia during rewarming is necessary for optimal cardiac and gastrointestinal function. When hyperkalemia is identified, the physician should search for other causes of metabolic acidosis, crush injury or rhabdomyolysis, renal failure, postsubmersion hemolysis, or hypoaldosteronism. Temperature depression can increase hyperkalemic cardiac toxicity. An important caveat is that the well-known diagnostic ECG changes are often obscured by hypothermia, and VF can occur with serum potassium levels of less than 7 mEq/L. *References 16, 66, 180, 200, 287, 328.

Hypothermia has no consistent effect on magnesium or calcium levels. Severe hypophosphatemia can occur during treatment of profound hypothermia. Although increases in serum enzyme levels are not seen in mild experimental hypothermia, numerous serum enzymes are elevated when diffuse intracellular structural damage occurs in severe accidental hypothermia. Creatine kinase (CK) levels over 200,000 international units are observed, and rhabdomyolysis is often present.56 Inhibition of cellular membrane transport decreases glucose utilization. In addition, insulin release and activity are markedly reduced below 30° C (86° F). Because target cells are insulin resistant, hyperglycemia is commonly seen initially. Markedly elevated glucose levels often correlate with hyperamylasemia and increased cortisol secretion.363 Acute hypothermia initially elevates the serum glucose level through catecholamine-induced glycogenolysis. Chronic exposure after exhaustion and glycogen depletion leads to hypoglycemia. The symptoms often resemble those of hypothermia. Cold-induced renal glycosuria is common and does not imply normoglycemia or hyperglycemia. When hypoglycemia and central neuroglycopenia are present, correction improves the level of consciousness only to that expected for the current core temperature. Cholesterol and triglyceride levels are also often below normal. Hyperglycemia that persists during and after rewarming should suggest diabetic ketoacidosis or hemorrhagic pancreatitis. Insulin is ineffective until the core temperature is well above 30° to 32° C (86° to 89.6° F) and therefore should be withheld to avoid iatrogenic hypoglycemia after rewarming. Although prior renal disease should be a consideration, blood urea nitrogen (BUN) and creatinine concentrations are often elevated because of decreased nitrogenous waste clearance by the cold diuresis. Because of ongoing fluid shifts, BUN poorly reflects circulatory volume status.100 The relationship between primary accidental hypothermia and hyperamylasemia appears to correlate with the severity of temperature depression, but preexisting or hypothermia-induced pancreatitis is present in up to 50% of patients in some urban series. Because the abdominal examination is frequently unreliable, amylase and lipase levels should be measured, except in minor cases.47 Ischemic pancreatitis is attributable to microcirculatory collapse in hypothermia. Decreased pancreatic blood flow activates many proteolytic enzymes. The extent of hyperamylasemia can correlate with mortality rates. Hypothermia with hypothalamic astrocytoma and pancreatitis also occurs.

Treatment Four decisive factors should be considered when assessing nonperfusing, severely hypothermic victims at the site. Rescuers should reconsider the decision to resuscitate if there is evidence of asphyxia or lethal injuries. A rigid thorax precludes closedchest cardiopulmonary resuscitation (CPR), and a probable field core temperature below 10° to 12° C (50° to 53.6° F) is ominous. Pulses are difficult to palpate in vasoconstricted and extremely bradycardic patients. If possible, check for an organized rhythm on a cardiac monitor. Doppler ultrasound is an ideal tool to assess cardiac activity.29,250 The combination of cold and exhaustion is a common cause of hypothermia in the field.154,245 The individual’s cold tolerance depends on temperature, wind, clothing worn, and wetness. It does not take an extremely cold temperature to produce hypothermia after energy depletion. As mental function decreases, the victim cannot respond to the rising threat. Judgment is impaired, and the victim seldom takes necessary precautions to prevent further disaster.25 Field presentation of victims who are awake covers a wide spectrum. Some persons are obtunded but conscious. Victims may or may not be shivering and often have a distant gaze and slurred speech.101 The type of power available in the transport vehicle determines the options for active rewarming. These include forced-air warming devices, heated IV fluids, and resistive and combustive heat.103,104,111 125

CHAPTER 5  Accidental Hypothermia

One homeostatic approach to maintain a steady pH is to keep the bicarbonate content constant. This is achievable only if total blood carbon dioxide content does not change. Because carbon dioxide solubility increases with temperature depression, alveolar ventilation must increase to compensate by lowering the PaCO2. Active ectotherms exhibit this respiratory adaptation and do not depress their respiratory minute volume when cold. This response, termed the ectothermic, or alpha-stat, strategy, allows them to maintain total bicarbonate and carbon dioxide content while increasing pH.269 Hibernating mammals are far more acidic because of respiratory acidosis and use an acid–base strategy that suppresses metabolism, termed the endothermic, or pH-stat, strategy. The ideal acid–base strategy continues to be debated.138,180,293 Some of the surgical literature about induced hypothermia, which clearly differs from accidental hypothermia, suggests that the alpha-stat approach improves neurologic outcome and also cellular and myocardial function.* On the other hand, various animal models suggest that the pH-stat strategy may be better.74 In summary, it seems that accidental hypothermia in a human should not be considered a protective form of hibernation. The ectothermic (alpha-stat) approach appears to ensure adequate alveolar ventilation and acid–base balance at any temperature when the uncorrected pH is 7.42 and the uncorrected PaCO2 is 40 mm Hg.

PART 2  COLD AND HEAT

FIGURE 5-6  In this patient, ventricular fibrillation developed during a code 3 transport by emergency medical services to the emergency department. Note the pronounced J waves after the QRS complexes.

Comatose victims require careful handling because they are extremely likely to develop VF and asystole with rough handling (Figure 5-6). Gurneys should be carried or rolled slowly to avoid jostling, and “code 3, full lights and sirens” transport should be avoided if victims are perfusing adequately. It is often impossible for rescuers to separate primary from secondary hypothermia when an unwitnessed cardiac arrest victim is found in a frigid environment. Because patients with cold, stiff, and cyanotic primary hypothermia and fixed and dilated pupils have been “reanimated,” the treatment dictum for prehospital personnel remains, “No one is dead until warm and dead.”10 A succinct summary of prehospital care of the hypothermic patient is rescue, examine, insulate, and transport. The initial rescuer and first responder often encounter obstacles to preventing further heat loss.246,357 In certain imposing geographic settings, treatment protocols are helpful to standardize treatment while tacitly acknowledging that available health care facilities may offer limited expertise and equipment. All treatment recommendations must be adapted to local rescue systems and facilities.76,295 Aeromedical transport is often ideal in these circumstances.370 In difficult environments, proper protocols with rehearsal and critique of mass casualty plans in the cold are far more important than similar adjuncts in flat and consistently sunny terrain. The history obtained at the scene helps determine optimal treatment. The pertinent past medical history regarding prior cardiopulmonary, endocrinologic, and neurologic conditions is particularly helpful. The circumstances of discovery, duration of exposure, associated injuries or frostbite, and obvious predisposing conditions should be recorded, as should the Glasgow Coma Scale score, although none of these is predictive. No prognostic neurologic scale during hypothermia is valid, but trends are often useful. Accurate field measurement of core temperature is difficult. The International Commission for Mountain Emergency Medicine recommends tympanic or esophageal field measurements, although they have significant limitations. Never insert an esophageal probe unless the patient is already tracheally intubated.295 Prolonged field treatment should be avoided whenever possible, although the rescuer must attempt to prevent further heat loss (Box 5-4). The rescuer should anticipate the presence of an irritable myocardium, hypovolemia, and a large temperature gradient between the periphery and the core. The crux of the prehospital quandary surrounds the safety of providing prehospital heat. On the one hand, the original “metabolic icebox” concept245,246 implies that the risk of inducing a nonperfusing rhythm in a hostile environment justifies simple stabilization of the core temperature. On the other hand, the warmer the heart, the better. Core temperature can decrease beyond reversal. Operant factors impacting the decision whether or not to provide prehospital heat include core temperature, fluid status, predisposing factors, extent of frostbite, length and type of exposure, available expertise and position of transport, and type of active rewarming available. The rescuer should stabilize injuries, protect the spine, splint fractures, and cover open wounds. Rescuer safety factors commonly include unstable snow or ice and falling rocks. Passive external rewarming with dry insulating materials minimizes conductive, convective, evaporative, and radiant heat losses. Remove any wet clothing from awake victims, and insulate them with sleeping bags, insulated pads, bubble wrap, metallized or regular blankets, or even newspaper. One device, the 126

Hypothermic Stabilizer Bag, has a nylon shell and a polyester-pile liner to wick moisture. In a survey of common field rewarming methods used by mountain rescue teams, the most common techniques include chemical pads, sleeping bags, body-to-body contact, and hot water bottles.123 If extrication will be delayed, give mildly hypothermic patients warm, sweet drinks, warm gelatin (Jell-O), Tang, juice, tea, or cocoa, because carbohydrates fuel shivering. Avoid heavily caffeinated drinks. Because a significant diuresis is usually associated with the cooling process, the victim’s fluid balance must be assessed. Once mildly hypothermic victims are well hydrated, they can be walked out to safety. Handle severely hypothermic victims gently, immobilizing them to prevent exertion. Although exercise can rewarm a person more rapidly than can shivering, it also markedly increases afterdrop.100,104 Because of autonomic dysfunction, victims should be kept in a horizontal position whenever possible to minimize orthostatic hypotension. Vigorously massaging cold extremities is also contraindicated, because skin rubbing, like ethanol, suppresses shivering thermogenesis and increases cutaneous vasodilation. Field management of the comatose victim first involves ventilation to raise oxygen saturation. Rescue breathing may be difficult because of chest stiffness and significant resistance to diaphragmatic motion. Forced ventilation increases oxygenation, which helps stabilize the heart electrically. The single greatest factor in maintaining perfusion is oxygenation provided during severe hypothermia.101 During a storm, prolonged field rewarming may be the only viable option until meteorologic conditions become more favorable for land or, preferably, aeromedical evacuation.370 Many prehospital medications freeze in solution. If this occurs, their pharmacologic activity after thawing is indeterminate (see Appendix at the end of this book).

BOX 5-4  Preparing Hypothermic Patients for Transport 1. The patient must be dry. Gently remove or cut off wet clothing, and replace it with dry clothing or a dry insulation system. Keep the patient horizontal, and do not allow exertion or massage of the extremities. 2. Stabilize injuries (i.e., the spine; place fractures in the correct anatomic position). Open wounds should be covered before packaging. 3. Initiate heated intravenous infusions (IVs) if feasible; bags can be placed under the patient’s buttocks or in a compressor system. Administer a fluid challenge. 4. Active rewarming should be limited to heated inhalation and truncal heat. Insulate hot water bottles in stockings or mittens, and then place them in the patient’s axillae and groin. 5. The patient should be wrapped. Begin building the wrap by placing a large plastic sheet on the available surface (floor, ground), and on it place an insulated sleeping pad. A layer of blankets, a sleeping bag, or bubble wrap insulating material is laid over the sleeping pad. The patient is then placed on the insulation. Heating bottles are put in place along with IVs, and the entire package is wrapped layer over layer, with the plastic as the final closure. The patient’s face should be partially covered, but a tunnel should be created to allow access for breathing and monitoring.

inhalation rewarming devices in volunteers, however, which suggests the importance of proper instruction for the rescuer.324 Under certain conditions, the impact of inhalation therapy on the rate of rewarming may not be significant.111 In shivering, mildly cold patients, the thermal advantage is minimal.71,72,241 One rewarming device weighs 3 kg, including oxygen tank, and consists of an oxygen cylinder, demand valve, 2-L reservoir bag, soda lime, and pediatric water canister. An in-line thermometer measures mean air temperature at the face mask. In the field, heat and moisture exchangers are practical, light, and inexpensive. They are, however, less efficient than are active humidifiers.217,219 The Res-Q-Air model HT1000 is a lightweight, portable, noninvasive core-rewarming system that delivers heated humidified air or oxygen at 42° to 44° C (107.6° to 111.2° F). It operates from any 12-volt DC power source. This system consists of a heating chamber connected via a corrugated hose to a one-way flow valve and an oronasal mask. The temperature is controlled by a transducer in the one-way flow valve that provides feedback to the electronic control circuits. Although surface rewarming suppresses shivering, it may be the only option when the victim is isolated from medical care. Active external rewarming options include radiant heat, warmed objects placed on the patient, and body-to-body contact. Care must be exercised not to burn victims with hot objects, including commercially produced hot packs. Total body contact rewarming may carry some risk,125 but logistical impediments limit the use of this method unless extrication will be significantly delayed. In a prospective prehospital rewarming study, hot pack rewarming was the only technique that increased body temperature during transport.357 A hydraulic sarong or vest, in which heated water is circulated via a hand pump, is also used occasionally.123 Immersion rewarming is dangerous in the field because monitoring and resuscitation capabilities are limited. The Norwegian HeatPac Personal Heater can deliver 100 watts for 8 hours. The charcoal “vest” burns a briquette and has a favorable heat-to-weight ratio, unlike most rewarming devices.48 Battery polarity is critical to prevent carbon monoxide exposure.324 This device uses a single D battery that must be inserted correctly to avoid a CO exhaust hazard. It is durable, lightweight (1 kg), efficient, and effective. It circulates hot air within a blanket or sleeping bag and provides a comfortable, warm, and dry environment for transporting victims. Allow the unit to heat up for 5 minutes before use. Another option under development is a modified forced-air warming system for field use.71,100,105 The Portable Rigid ForcedAir Cover is heated with a Bair Hugger 505 Heater/Blower. It covers the patient’s trunk and thighs and can adapt to various transport vehicle power sources. Experimentally, convective warming is more efficient than is resistive heating.158

PREHOSPITAL LIFE SUPPORT A patent airway and the presence of respirations must be established (Figure 5-7). The victim may appear apneic if respiratory minute ventilation is significantly depressed. A common error in tracheally intubated patients is overzealous assistance of ventilation, which can induce hypocapnic ventricular irritability. The indications for prehospital endotracheal intubation are identical to those under normothermic conditions. Appropriate ventilation with 100% oxygen may protect the heart during extrication and transport. Avoid overinflation of the tracheal cuff with frigid ambient air. As the victim warms, air in the cuff can expand and kink the tube. Careful protection and fixation of the tubing of the cuff port during extremely cold conditions are necessary to prevent breakage and cuff leak. Palpation of peripheral pulses is often difficult in vasoconstricted and bradycardic patients. Apparent cardiovascular collapse may actually reflect cardiac output that is depressed just enough to meet minimal metabolic demands. The rescuer should auscultate and palpate for at least 1 minute to find pulses if a cardiac monitor or ultrasound is unavailable. Iatrogenic VF can easily result from chest compressions that were not indicated. If a cardiac monitor is available, use maximal amplification to search for QRS complexes. If the victim is in VF, the rescuer 127

CHAPTER 5  Accidental Hypothermia

The rescuer should administer an IV fluid challenge with 250 to 500 mL heated (37° to 41° C [98.6° to 105.8° F]) 5% dextrose in normal saline solution. Empiric 50% dextrose is indicated only in select cases. The safety of several reversal agents, such as naloxone or flumazenil, used in the field is unknown. Concerns regarding these agents before warming include precipitation of acute withdrawal, seizures, and markedly increased oxygen utilization. Most patients are volume depleted. Nevertheless, iatrogenic volume overload should be avoided, because myocardial contractility is impaired. Improvisation during transport is often helpful. For example, a plastic IV container can be placed under the patient’s back, shoulders, or buttocks to add warmth and infusion pressure. Taping heat-producing packets to IV bags is another option. These heating agents may be chemical packets or phase-change crystals, which produce heat for up to several hours. A variety of “hot pack” hypothermia devices are commercially available, including the Wilderness IV Warmer and the Ultimate Hot Pack. Another commercially available device is the Wilderness Oxygen Warmer. IV fluid compressors are bulb-inflating cuffs that surround IV pouches to maintain flow. The Israeli army has a spring steel compressor system for IV bags. Portable IV fluid heaters are commercially available. The devices fit in-line and are DC powered. Commercial heaters are available that are powered by a PhysioControl battery or from a DC converter plugged into an AC outlet. The Hot Sack IV Warmer runs on 12 volts from any vehicle or portable battery. The current drain is 4 amperes, and the insulation case loses only 0.5° C (0.9° F) over 10 minutes. In a study comparing IV warming techniques, meals ready to eat (MRE) heat packs or a camp stove outperformed standard chemical heat packs.275 Another option is an in-line battery-powered, disposable, lightweight fluid-warming device (Thermal AngelTex). Peripheral vessels may be difficult to locate, and IV lines are hard to maintain during transport. Ideally, IV fluids should be warmed to body temperature or slightly higher, but total body warming is not accomplished with IV fluids in the field. Using intraosseous infusions may provide a reasonable pathway for fluid replacement in the field when peripheral vessels have collapsed and cannot be entered. The methods selected to stabilize core temperature should be tailored to the severity of hypothermia and the field circumstances. Gently removing or cutting off wet clothing while the patient remains prone may be the best option to limit heat loss and prevent orthostasis. Passive external rewarming with waterproof insulation suffices for mild chronic hypothermia. In their series of patients requiring cardiopulmonary bypass (CPB), Walpoth and colleagues354,355 “maintained” hypothermia during transport. Whether supplemental active field rewarming should be initiated en route to the ED, and in which subsets of patients, is not definitively established. Intentionally maintaining hypothermia during transport seems wise only for patients with an isolated closed-head injury. For long helicopter or ambulance transports, the ideal ambient temperature in the vehicle is unclear. Rescue personnel comfort is important to maximize performance, and it is unlikely that heating the interior above 25° C will accelerate the rate of rewarming or induce vasodilation. “Field rewarming” is a misnomer, because adding much heat to a hypothermic patient in the field is difficult.81 Warmed IV solutions, heated sarongs, or heated humidified oxygen can provide only a small amount of heat input. Hot water bottles or heat packs can be placed in the axillae, in the groin, and around the neck. Casualty evacuation bags are available in many models and designs. Some have more insulation than others, and some have specialized zippers and openings that allow access to the victim during transport. Most bags are windproof and waterproof. Experimentally, convective air warming is more effective than resistive heating158 and might be a viable option in some transport situations. Inhalation therapy is safe for active rewarming of victims with profound hypothermia in the field.125 It helps prevent respiratory heat loss, which represents an important percentage of heat production when the core temperature is below 32° C (89.6° F). Technical difficulties have been experienced while using

PART 2  COLD AND HEAT

Rescue/examine Responsive

Yes

No Respirations No

Yes

Heated humidified ventilation

Assume cardiac output

Insulate IV D5 NS

Cardiac monitor

Electrical complexes

Cardiac monitor

Nonperfusing rhythm

Heated humidified oxygen

Gentle evacuation

Central pulse

No (PEA)

Chest compression

Yes Hospital assessment

FIGURE 5-7  Prehospital life support. PEA, Pulseless electrical activity.

should attempt defibrillation initially with 2 watt sec/kg up to 200 watt sec. The energy requirement for defibrillation does not increase in hypothermia. If the patient does not respond, defer further attempts, and assume that the victim must be rewarmed at least past 30° C (86° F) before further attempts.7 Do not perform defibrillation if organized narrow electrical complexes are seen on the monitor. Most monitors and defibrillators have not been tested for operation at temperatures below 15.5° C (59.9° F). Standard monitor leads do not always stick well to cold skin, so benzoin may be useful. If this fails, needle electrodes may be necessary. Another option is to puncture the Gelfoam conventional monitor pad with a small-gauge injection needle.359 Unresponsive victims should be carefully assessed for a central pulse before assuming they have pulseless electrical activity (PEA). The lowest temperature at which mechanical reestablishment of cardiac activity has been successful is 20° C (68° F),61 and defibrillation attempts rarely succeed below 30° C (86° F). If resuscitation in the field is unsuccessful, rewarming and CPR should be continued during transport to the ED.268

MANAGEMENT IN THE EMERGENCY DEPARTMENT The history obtained from a hypothermic patient is often unreliable, so it is prudent to confirm hypothermia and monitor with continuous core temperature measurements. Diagnostic errors in the ED usually result from incomplete monitoring of vital signs. Doppler ultrasound may be necessary to locate a pulse and should be supported by continuous ECG monitoring. The physician should also address the requirements for resuscitation and initiate advanced life support when necessary (Box 5-5). Temperature Measurement Most hospitals have adequate equipment for accurate core temperature measurement.259 Rectal measurements are most practical clinically for mild cases but may not reflect cardiac or brain temperatures.133 An indwelling thermistor probe placed to a depth of 15 cm (6 inches) is fairly reliable unless adjacent to cold feces. Rectal temperature lags behind core temperature fluctuations and is also affected by lower-extremity temperatures (Table 5-3).364 Esophageal temperature measurements are far preferable in severe cases and when airway protection is provided with endotracheal intubation. Esophageal temperature approximates cardiac temperature. Because the upper one-third of the esophagus is near the trachea, the probe may read falsely high during heated 128

inhalation therapy if the probe is positioned too proximally. The probe should be placed 24 cm (9.5 inches) below the larynx. The greatest discordance between rectal and esophageal temperatures is noted during the transition phase between cooling and rewarming. Tympanic temperature theoretically approximates hypothalamic temperature and can be accurately measured with thermometers that are in contact with the tympanic membrane. Because these are impractical except in anesthetized patients, external auditory canal thermometers that measure infrared emission from the tympanic membrane are available. These are not actually “tympanic” thermometers, but this term is used extensively.379 Unfortunately, the external auditory canal thermometers are not very sensitive. Tympanic thermometers are inaccurate when compared with a true core temperature measured with a pulmonary artery catheter.85 Although bladder temperature measurement devices can be incorporated into the urinary drainage catheter, the readings are frequently unreliable. They are falsely elevated with heated peritoneal lavage and, more commonly, low as a result of coldinduced diuresis and crystalloid resuscitation. Initial Stabilization After core temperature measurement, all clothing should be gently removed or cut off with minimal patient manipulation.268 BOX 5-5  Resuscitation Requirements Thermal Stabilization • Conduction • Convection • Radiation • Evaporation • Respiration Maintenance of Tissue Oxygenation • Adequate circulation • Adequate ventilation Identification of Primary Versus Secondary Hypothermia Rewarming Options • Passive external rewarming • Active external rewarming • Active core rewarming

Type

Advantages

Considerations

Rectal

Convenient Continuous monitoring

Esophageal

Convenient Continuous monitoring

Tympanic

Approximates hypothalamic temperature via internal carotid artery Convenient Continuous monitoring

Insert 15 cm (6 inches) Lags during transition from cooling to rewarming Falsely elevated with peritoneal lavage Falsely low if probe is in cold feces or when lower extremities are frozen Insert 24 cm (9.5 inches) below larynx Tracheal misplacement Aspiration Falsely elevated with heated inhalation Probe: tympanic membrane perforation; canal hemorrhage Infrared: unreliable; cerumen effect

Bladder

Unreliable Falsely elevated with peritoneal lavage Falsely low with cold diuresis

Immediately insulate the patient with dry blankets. Apply a cardiac monitor, and insert intravenous catheters as needed. Arterial catheter insertion may help in managing selected profoundly hypothermic patients. Pulmonary artery catheters can precipitate cardiac arrhythmias and should be reserved for complex cases. Insertion of pulmonary artery catheters into cold vessels may perforate the pulmonary artery.46 Central venous catheters should not be inserted into the right atrium, because this could precipitate arrhythmias.312 A better option is temporary catheterization of the femoral vein. The accuracy of pulse oximetry during conditions of poor perfusion is unclear, because there are no studies in accidental hypothermia.190 In one study of hypothermic patients on CPB, the finger probes were inaccurate.43 The probe may be made more reliable if a vasodilating cream is applied first. In addition, there is a lag time in pulse oximetry with hypoxic desaturation in anesthetized hypothermic subjects. There is decreased failure of forehead pulse oximetry in comparison to fingertip readings.226 In theory, combining pulse oximetry with near-infrared spectroscopy could provide tissue perfusion information during hypothermic vasoconstriction. More practically, an accurate core and peripheral muscle temperature would prove just as useful. The value of end-tidal carbon dioxide measurements to assess adequacy of tissue perfusion and tracheal tube placement is established at normal temperatures. Most of these devices, however, measure only the carbon dioxide content of dehumidified air and thus cannot be used during airway rewarming. Laboratory evaluations to be considered, except in some cases of mild hypothermia, include blood glucose, arterial blood gases, complete blood cell count, electrolytes, BUN, creatinine, serum calcium, serum magnesium, serum amylase and lipase, PT, PTT, INR, platelet count, and fibrinogen level. A toxicologic screen should be considered if the level of consciousness does not correlate with the degree of hypothermia. Selective studies of thyroid function, cardiac markers, and serum cortisol levels are indicated.58 The indications for radiography should be liberalized from normothermia. Radiologic evaluation of poorly responsive patients must include cervical and other spine images to detect occult trauma. Chest radiographs may predict lung collapse during rewarming when cardiomegaly and redistribution of vascularity are already present. Abdominal imaging should be obtained when the physical examination is unreliable. Bowel sounds are usually diminished or absent in severe hypothermia, and rectus muscle rigidity is frequently present. Pneumoperitoneum, pancreatic calcifications, or hemoperitoneum may be

noted. Small bowel dilation is associated with cold-induced mesenteric vascular occlusion, and colonic dilation is often present in conjunction with myxedema coma. The use of focused abdominal sonography may be helpful.54 Nasogastric tube insertion should be performed after endotracheal intubation in moderate or severe hypothermia, because gastric dilation and poor gastrointestinal motility are common. Indwelling bladder catheters with urine meters are needed to monitor urine output and the cold diuresis.

Fluid Resuscitation Most fluid shifts are reversed by rewarming, and mild hypothermia usually requires only modest amounts of crystalloids. In more severe cases, volume shifts and elevated blood viscosity from hemoconcentration, lowered temperature, increased vascular permeability, and low flow state mandate aggressive fluid resuscitation. The viscosity of blood increases 2% per degree Celsius drop in temperature; therefore hematocrit values over 50% are commonly seen. Low circulatory plasma volume is often coupled with elevated total plasma volume during rewarming. Hemodilution is usually not a problem and is seen only during massive crystalloid resuscitation of actively hemorrhaging patients.32,56 Most patients are significantly dehydrated, with free water depletion elevating serum sodium concentration and osmolality. During the descent into a hypothermic state, normal physiologic cues for thirst become inactive and access to water is often difficult. Because hypothermia results in natriuresis, saline depletion may be present. Further causes of sodium losses include prior diuretic therapy and gastrointestinal losses. Preexisting total body sodium excess is seen with congestive heart failure, cirrhosis, and nephrosis. In these cases, serum sodium and osmolality values are often normal. Rarely, serum sodium level is low because of free water excess. Other causes include myxedema, panhypopituitarism, and inappropriate antidiuretic hormone secretion. Most adult patients with a core temperature below 32.2° C (90° F) should receive an initial fluid challenge with 250 to 500 mL of warmed 5% dextrose in normal saline solution. Theoretically, Ringer’s lactate solution should be avoided because a cold liver cannot metabolize lactate. In severe cases, some clinicians favor a mixture of crystalloids and colloids. The victim should be monitored for standard clinical signs of fluid overload, including rales, jugular venous distention, hepatojugular reflux, and S3 cardiac gallop. Persistent cardiovascular instability often reflects inadequate intravascular volume. As mentioned, a properly placed central venous pressure catheter, such as a femoral line that does not enter and irritate the right atrium, has a role. Pulmonary wedge pressure measurements are rarely indicated. The need for RBC transfusions is determined by the corrected hematocrit; blood dilution with warmed infusate does not cause significant hemolysis. In many cases, rapid volume expansion is critical. Circulatory volume is decreased and peripheral vascular resistance is increased. In neonates, adequate fluid resuscitation markedly decreases mortality. Adults receiving hemodynamic monitoring show improvement of cardiovascular efficiency during crystalloid administration. VF immediately after rescue is attributed to both core temperature afterdrop and vascular imbalance in patients who are moved suddenly from a horizontal supine position.218 The fluxing relationship between active vascular capacity and circulating fluid volume depends not only on the mechanism of cooling but also on the method of rewarming. Hypothermic patients, particularly those with frostbite, are at high risk for extremity compartment syndromes and rhabdomyolysis. Pelvic fracture belt slings should be considered only to temporarily stabilize coexistent exsanguinating major pelvic fractures.

Rewarming Options PASSIVE EXTERNAL REWARMING Because hypothermia is an extremely heterogeneous condition and evidence-based treatment guidelines do not exist, rigid treatment protocols are ill advised.295,299,380 A versatile approach to 129

CHAPTER 5  Accidental Hypothermia

TABLE 5-3  Core Temperature Measurements

PART 2  COLD AND HEAT

BOX 5-6  Rewarming Techniques Passive External • Thermal stabilization Active External • Radiant heat • Hot water bottles • Plumbed garments • Electric heating pads and blankets • Forced circulated hot air • Immersion in warm water • Negative-pressure rewarming Core • Inhalation rewarming • Heated infusions • Gastric and colonic lavage • Mediastinal lavage • Thoracic lavage • Peritoneal lavage • Diathermy • Hemodialysis • Venovenous extracorporeal blood rewarming • Arteriovenous extracorporeal blood rewarming • Cardiopulmonary bypass

rewarming can be developed after careful consideration of the observations from animal experiments, human experiments on mild hypothermia, and various clinical reports (Box 5-6).118,119,278 Treatment should be predicated on the presenting pathophysiology and the available resources and expertise. The initial key treatment decision is whether to use passive or active rewarming (Box 5-7). Noninvasive passive external rewarming (PER) is ideal for most previously healthy patients with mild hypothermia. The patient is covered with dry insulating materials in a warm environment to minimize the normal mechanisms of heat loss. When the wind is blocked, less heat escapes via radiation, convection, and conduction. Conditions with higher ambient humidity slightly limit respiratory heat loss. Aluminized body covers also reduce heat loss.82,143 Nevertheless, endogenous thermogenesis must generate an acceptable rate of rewarming for PER to be effective.260 Humans are functionally poikilothermic below 30° C (86° F), and metabolic heat production is less than 50% of normal below 28° C (82.4° F). Shivering thermogenesis is also extinguished below 32° C (89.6° F). This thermoregulatory neuromuscular response to cold normally increases heat production from 250 to 1000 kcal/hr unless glycogen is depleted before or during cooling. Older adult patients in whom mild hypothermia develops gradually are less acceptable candidates for PER. When rewarming times are markedly prolonged (over 12 hours), complications tend to increase. Patients who are centrally hypovolemic, glycogen depleted, and without normal cardiovascular responses should be stabilized and rewarmed at a conservative rate. In a multicenter survey, the rewarming rates for older adults in the first (0.75° C [1.35° F]), second (1.17° C [2.11° F]), and third (1.26° C [2.27° F]) BOX 5-7  Indications for Active Rewarming • Cardiovascular instability • Moderate or severe hypothermia (<32.2° C [90° F]) (poikilothermia) • Inadequate rate or failure to rewarm • Endocrinologic insufficiency • Traumatic or toxicologic peripheral vasodilation • Secondary hypothermia impairing thermoregulation • Identification of predisposing factors (see Box 5-2)

130

hours far exceeded 0.5° C (0.9° F) per hour, with no increase in mortality rate (Figure 5-8, online).59

ACTIVE REWARMING Active rewarming, which is the direct transfer of exogenous heat to a patient, is usually required with temperatures below 32° C (89.6° F).208 Rapid identification of any impediment to normal thermoregulation, such as cardiovascular instability or endocrinologic insufficiency, is essential.209 Intrinsic thermogenesis may also be insufficient after traumatic spinal cord transection or pharmacologically induced peripheral vasodilation. Some patient populations generally require active rewarming.63,195 For example, aggressive rewarming of infants minimizes energy expenditure and decreases mortality. In these circumstances, vigorous monitoring for respiratory, hematologic, metabolic, and infectious complications is essential.350 When active rewarming is needed, heat can be delivered externally or to the core. Active external rewarming (AER) techniques deliver heat directly to the skin. Examples include forcedair rewarming, immersion, arteriovenous anastomosis rewarming, plumbed garments, hot water bottles, heating pads and blankets, and radiant heat sources.349 During rewarming of hypothermic patients, there are metabolic pH and inflammatory interleukin fluxes.238,344 Cytokine production may be activated by accidental hypothermia.1

ACTIVE EXTERNAL REWARMING The interpretation of survival rates with AER is affected by various risk factors and patient selection criteria.63,317 Some experimental and clinical reports link AER with peripheral vasodilation, hypotension, and core temperature afterdrop, but previously healthy, young, and acutely hypothermic victims are usually safe candidates for AER.32 Heat application confined to the thorax may mitigate many of the physiologic concerns pertaining to the depressed cardiovascular and metabolic systems, which are unable to meet accelerated peripheral demands.340 Combining truncal AER with active core rewarming may further avert many potential side effects.73 Forced-Air Surface Rewarming Forced-air surface warming systems efficiently transfer heat.11,103,160,195,196 The Bair Hugger uses hot forced air circulated through a blanket. The air exits apertures on the patient side of the cover, permitting the convective transfer of heat.237,306 In one study that rewarmed accidental hypothermia victims in the ED, rewarming shock and core temperature afterdrop were not noted321 with the use of heated inhalation and warmed IV fluids. A group also treated with a convective cover inflated at 43° C (109.4° F) rewarmed 1° C (1.8° F) per hour faster than a group covered with a cotton blanket (1.4° C [2.5° F] per hour). Experimentally, resistive external heating is more effective than passive metallic-foil insulation.120 A study of full-body forced-air warming compared a commercially available convective blanket with simple air delivery beneath bedsheets.181 Directed 38° C (100.4° F) warm air under the sheets warmed standardized thermal bodies containing water very efficiently. Commercially available convective air rewarming devices (WarmTouch, whole-body blanket) are also effective. Another option is conductive warming with a warm water–filled heat exchange blanket (Blanketrol). The use of forced-air surface warming systems is most practical in the ED.193,211 Although these devices decrease shivering thermogenesis, afterdrop is minimized and heat transfer can be significant. Thermal injury to poorly perfused, vasoconstricted skin using some of the other external heat application techniques is a hazard in both adults and children.123,188 In particular, avoid resistanceheat electric blankets on which a patient lies, because vasoconstricted capillaries are compressed and burns occur easily. Another active external rewarming option is a thermoregulatory system that circulates warm water through energy transfer pads placed on the chest and lower limbs (Arctic Sun). The core temperature measured via probe is fed back to the control module.

Arteriovenous Anastomosis Rewarming The original description of this noninvasive AER technique was by Vangaard and colleagues345 in 1979. Exogenous heat is provided by immersion of the lower parts of the extremities (hands, forearms, feet, calves) in 44° to 45° C (111.2° to 113° F) water. The heat opens arteriovenous anastomoses (AVAs). These organs are 1 mm (0.4 inch) below the epidermal surface in the digits.17,71,243 Countercurrent heat loss is minimized because the superficial veins are not close to the arterial tree. To be efficacious, the cutaneous heat exchange area must include the lower legs and forearms, and the water must be 44° to 45° C (111.2° to 113° F). Advantages with AVA rewarming include patient comfort and decreased afterdrop after cooling.317 A permutation of AVA rewarming is negative-pressure rewarming. Under hypothermic conditions, the AVAs remain closed during peripheral vasoconstriction. In combination with localized heat application, application of subatmospheric pressure theoretically distends the venous rete and increases flow through the AVAs. To initiate negative-pressure rewarming, the forearm is inserted through an acrylic tubing sleeve device fitted with a neoprene collar. This allows an airtight seal to form around the forearm. After a vacuum pressure of −40 mm Hg is created, heat is applied over the dilated AVAs. The thermal load can be provided via an exothermic chemical reaction or a heated perfusion blanket. The clinical efficacy of AVA rewarming in accidental hypothermia is unclear. Studies concluding that heat exchange is ineffectual used cooler water applied only on the hands and feet.37,52 The potential for superficial burns of anesthetic, vasoconstricted skin is a consideration. Another caveat is hypotension precipitated in hypovolemic patients who remain semiupright with this technique. In one study, the rate of core rewarming increased dramatically,113 but another study comparing negativepressure rewarming with forced-air warming failed to replicate these results.329 Active Core Rewarming Various techniques that can effectively deliver heat to the core290,303,345 include heated inhalation, heated infusion, diathermy, lavage (gastric, colonic, mediastinal, thoracic, peritoneal), and extracorporeal rewarming. Average first-hour rewarming rates reported with some of these techniques in one multicenter study are listed in Figure 5-8, online. Although hemodynamic instability impacts the rewarming strategy, noninvasive techniques often succeed unless there are significant comorbidities.288 Airway Rewarming The effectiveness of the respiratory tract as a heat exchanger varies with technique and ambient conditions.241 Because dry air has low thermal conductivity, complete humidification coupled with an inhalant temperature of 40° to 45° C (104° to 113° F) is required.286 The main benefit of airway rewarming is prevention of respiratory heat loss. Heat yield can represent 10% to 30% of the hypothermic patient’s heat production when respiratory minute volume is adequate.28 The rate of rewarming is greater using an endotracheal tube (ETT) than by mask. In one series, the reported rewarming rate with a 40° C (104° F) aerosol was 0.74° C (1.33° F) per hour via mask and 1.22° C (2.2° F) per hour via ETT.244 In a multicenter survey,59 the average first- and second-hour rewarming rates in severe cases were 1.5° to 2° C (2.7° to 3.6° F) per hour. Because

100

O2 (% saturation)

Immersion in a 40° C (104° F) circulating bath presents difficulties in monitoring, resuscitation, treatment of injuries, and maintenance of extremity vasoconstriction to prevent core temperature afterdrop. In normothermic men with coronary artery disease, the cardiovascular stress and arrhythmogenic response to immersion in a hot tub are mild, less than those induced by exercise.4 In contrast, placing the hands and feet in warm water theoretically opens arteriovenous shunts and accelerates rewarming in acute hypothermia. The attraction to Scandinavian palmar heat packs may reflect this physiology.

of the decremental efficiency at higher temperatures, the rate is slower (10 kcal/hr) in mild cases.59 Thermal countercurrent exchange in the cerebrovascular bed of humans64 affects the efficiency and influence of heated-mask ventilation during hypothermia. Known as the rete mirabile, this system could preferentially rewarm the brainstem. Heated inhalation via face mask continuous positive airway pressure (CPAP) may correct the ventilation–perfusion mismatch.38 Heated humidified oxygen via face mask is not feasible in some patients with coexistent midface trauma. Heat liberated during airway rewarming is produced mainly from condensation of water vapor. The latent heat of vaporization of water in the lungs is slightly lower than 540 kcal/g H2O. This is multiplied by the liters per minute ventilation to calculate the quantity of heat transfer. When core temperature is 28° C (82.4° F), the rate of rewarming with heated ventilation at 42° C (107.6° F) equals endogenous heat production. Although the effect on overall thermal balance can be minimal, there may be preferential rewarming of thermoregulatory control centers.56 Heated humidified inhalation ensures adequate oxygenation, stimulates pulmonary cilia, and reduces the amount and viscosity of cold-induced bronchorrhea. Although preexisting premature ventricular contractions (PVCs) may reappear during rewarming, there is no evidence that inhalation rewarming precipitates new, clinically significant ventricular arrhythmias. Vapor absorption does not increase pulmonary congestion or wash out surfactant. When the pulmonary vasculature is heated, warmed oxygenated blood that returns to the myocardium could attenuate intermittent temperature gradients. The amplitude of shivering is also lowered, an advantage in more severe cases. This suppression could decrease heat production in mild hypothermia, although experimentally the core temperature continues to rise.52 There are numerous oxygenation considerations in hypothermia (see Box 5-1). The “functional” value of hemoglobin at 28° C (82.4° F) is 4.2 g/10 g in patients on CPB.93 The oxyhemoglobin dissociation curve also shifts to the left (Figure 5-9). This impairs release of oxygen from hemoglobin into the tissues. Although some patients can self-adjust their respiratory minute volume (RMV) for current carbon dioxide production, this may not be possible if there are additional toxins or metabolic depressants.56 Most humidifiers are manufactured in accordance with International Standards Organization (ISO) regulations. The humidifier will not exceed 41° C (105.8° F) close to the patient outlet with a 6-foot tubing length.353 If the decision is made to alter equipment, carefully monitor the temperature and do not exceed 45° C (113° F). The only report of thermal airway injury was in a patient ventilated via endotracheal tube for 11 hours with 80° C (176° F) inhalant. Strategies to circumvent the 41° C ceiling include reduction of tubing length, adding additional heat sources, disabling the humidifier safety system, and placing the temperature probe

NORMAL

50

T 37° C pH 7.40

0 0

50

100

PO2 (mm Hg) FIGURE 5-9  Oxyhemoglobin dissociation curve at 37° C (98.6° F). At colder temperatures, the curve shifts to the left.

131

CHAPTER 5  Accidental Hypothermia

Immersion

PART 2  COLD AND HEAT

outside the patient circuit.353 Label all modified equipment to avoid routine use. A volume ventilator with a heated cascade humidifier can also deliver CPAP or positive end-expiratory pressure (PEEP) if needed during rewarming. The airway rewarming rates clinically range from 1° to 2.5° C (1.8° to 4.5° F) per hour.59 In stable patients, circumventing the 41° C ceiling may not be worth the effort because the clinical benefit is modest.180 Heat and moisture exchangers function like artificial nares by trapping exhaled moisture and then returning it. They provide inadequate humidification to treat accidental hypothermia. With prolonged use, ETT occlusion and atelectasis are both problems.45 Airway rewarming is indicated in the ED when core temperature is lower than 32.2° C (90° F) on arrival. Although airway rewarming provides less heat than do other forms of active core warming, it prevents normal respiratory heat and moisture loss and is safe, fairly noninvasive, and practical in all settings. Heated Infusions Cold fluid resuscitation of hypovolemic patients can induce hypothermia. In one series of previously normothermic patients with major abdominal vascular trauma, the average postresuscitation temperature was 31.2° C (88.2° F) in those with refractory coagulopathies. IV fluids are heated to 40° to 42° C (104° to 107.6° F), although higher temperatures may be safe. The amount of heat provided by solutions becomes significant during massive volume resuscitations.27,313 One liter of fluid at 42° C (107.6° F) provides 14 kcal to a 70-kg patient at 28° C (82.4° F), elevating the core temperature almost 0.33° C (0.6° F). Significant conductive heat loss occurs through IV tubing, so long lengths of IV tubing increase heat loss, especially at slow flow rates.84 IV tubing insulators are available. There are various methods to achieve and maintain ideal delivery temperature of IV and lavage fluids in hypothermia, but there is no standardized approach.124,297 Blood preheated to 38° C (100.4° F) in a standard warmer is useful, but clotting and shortened RBC life are hazards with blood-warming packs. Local microwave overheating hemolyzes blood. An alternative is to dilute packed RBCs with warm calciumfree crystalloid. The Level 1 fluid warmer (Level 1 H-1200 Fast Flow Fluid Warmer with integrated air detector/clamp) warms cold crystalloid and blood via a heat exchanger at flow rates of up to 500 mL/min. A more portable and compact option is the Ranger. Unlike the Level 1, however, this unit must remain above the level of the patient, and the infusion capability is much lower. The Thermal Angel is a portable, lightweight, battery-powered infusion warmer that has the advantage of portability to the initial point of rescue or trauma. Microwave heating of IV fluids in flexible plastic bags is another option when more standardized heaters are unavailable. The plasticizer in the polyvinyl chloride containers is stable to microwave heating. Heating times should average 2 minutes at high power for a 1-L bag of crystalloid. The fluid should be thoroughly mixed before administration, to eliminate hot spots. Rapid administration of fluid into the right atrium at a temperature significantly different from that of circulating blood may produce myocardial thermal gradients.320 In one study, heated IV fluid, up to 550 mL/min, was administered through the internal jugular vein without complication. In an experimental canine model with adequate cardiac output, central infusion of extremely hot (65° C [149° F]) IV fluids accelerates rewarming without hemolysis.90,309 Using amino acid infusions may accelerate energy metabolism.305 Fever is common in patients receiving hyperalimentation. In patients recovering from elective surgery, however, amino acids have no significant thermogenic effect.139 The results might differ in energy-depleted patients with chronically induced accidental hypothermia. In summary, intravenous solutions and blood should be routinely heated during hypothermia resuscitations. Various blood warmers are available commercially, but countercurrent in-line warmers are the most efficient techniques.157 A mathematic model indicates that infusion heating devices are essential in trauma patients with high fluid requirements.27 132

HEATED IRRIGATION Gastrointestinal Irrigation Heat transfer from irrigation fluids is usually limited by the available surface area, so do not use irrigation as the sole rewarming technique. The irrigant should not exceed 45° C (113° F). Direct gastrointestinal irrigation is less desirable than irrigation via intragastric or intracolonic balloons because of induced fluid and electrolyte fluxes. Exceeding 200- to 300-mL aliquots may force fluid into the duodenum; therefore frequent fluid removal via gravity drainage minimizes “lost” fluid. A log of input and output is essential. This facilitates estimation of fluid balance during resuscitation and helps determine if irrigation should be abandoned in anticipation of dilutional electrolyte disturbances. To avoid these limitations, a double-lumen esophageal tube is available, as are other modified Sengstaken tubes.199 Patients should be tracheally intubated before gastric lavage. Because of the proximity of an irritable heart, overly vigorous placement of a large gastric tube is ill advised. In a multicenter survey, gastric, bladder, and colon lavage rewarmed severely hypothermic patients at 1° to 1.5° C (1.8° to 2.7° F) for the first hour and 1.5° to 2° C (2.7° to 3.6° F) for the second hour.59 Commercially available kits designed for gastric decontamination are convenient (Figure 5-10). The use of a Y connector and clamp simplifies the exchanges. Ideal dwell times for thermal exchange depend on flow rates and may average several minutes. In direct gastric lavage, warmed electrolyte solutions, such as normal saline or Ringer’s lactate, are administered via nasogastric tube.213 After 15 minutes, the solution is aspirated and replaced with warm fluids. Disadvantages include the small surface area available for heat exchange and the large amount of fluid escaping into the duodenum.36 Regurgitation is common, and the technique must be terminated during CPR. Esophageal and bladder heat exchange are also very limited.201,285,359,360 Aesthetic obstacles aside, heat transfer through colonic irrigation is negligible. Mediastinal Irrigation Mediastinal irrigation and direct myocardial lavage are alternatives in patients lacking spontaneous perfusion. A standard left thoracotomy is performed while CPR is continued. Opening the

Warm saline

15 min

Drainage

FIGURE 5-10  Gastric lavage.

Thoracic Lavage Irrigation of the hemithoraces is a valuable rewarming adjunct.14,34,35,189,356 An important semantic issue is that closed thoracic lavage via two thoracostomy tubes differs from open mediastinal and direct myocardial lavage. With the latter, closedchest CPR is not possible. Two large-bore thoracostomy tubes (36F to 40F in adults; 14F to 24F, ages 1 to 3; 20F to 32F, ages 4 to 7) are inserted in one or both of the hemithoraces. One is placed anteriorly in the second to third intercostal space at the midclavicular line, and the other in the posterior axillary line at the fourth to fifth intercostal space. Normal saline heated to 40° to 42° C (104° to 107.6° F) is then infused via a nonrecycled sterile system (Figure 5-11, A).185 A high-flow countercurrent fluid infuser heats to 40° C (104° F) and delivers normal saline in 1-L or preferably 3-L bags into the afferent chest tube.83,278 This author prefers connecting into the tubing with standard 0.19-inch internal-diameter suction connection tubing and a sterilized plastic graduated two-way connector, because this facilitates adaptation to any size chest tube (see Figure 5-11, A). The effluent is then collected in a thoracostomy drainage set. The reservoir must be emptied frequently. Alternatively, when a single chest tube is used, 200- to 300-mL aliquots are used for

irrigation, and suctioning is achieved through a Y connector. The Y connector is also useful for irrigating both hemithoraces with a single fluid warmer (Figure 5-11, B). Fluid can be infused into the anterior higher chest tube (afferent limb) and suctioned or gravity drained out the lower posterior tube (efferent limb) into a water-seal chest drain.122 Infusion inferoposteriorly with suction anteriorly can increase dwell times.159 The efficiency of thermal transfer varies with flow rates and dwell times. Once the patient is successfully rewarmed, the upper tube should be removed and the lower one left in place to allow residual drainage. Closed sterile thoracic lavage is a natural choice in the ED during potentially salvageable cardiac arrest resuscitations.369 Thoracic lavage is an option either as a bridge to CPB or when CPB is initially unavailable. In patients who are perfusing, this technique should be considered hazardous unless extracorporeal rewarming capability is immediately available. Many hypothermic trauma patients are irrigated successfully during surgery. The clinically reported infusion rates range from 180 to 550 mL/min. The overall rate of rewarming should easily equal or exceed that achievable with peritoneal lavage and is often 3° to 6° C (5.4° to 10.8° F) per hour. The surface area of the pleural space is well perfused. An added benefit is preferential mediastinal rewarming. In addition, closed-chest compressions during cardiac arrest can maintain perfusion. Open cardiac massage of a rigid, contracted heart may not be possible in severe cases before bypass, which is a problem with mediastinal irrigation.5,53,58 Various complications should be considered. Left-sided thoracostomy tube insertion into patients who are perfusing could easily induce VF. Patients with pleural adhesions or a history of pleurodesis have poor infusion rates, and subcutaneous edema may develop. If the fluids are infused under pressure without adequate drainage, intrathoracic hypertension or even a tension hydrothorax can develop and cause expected adverse cardiovascular effects.174,274 Peritoneal Lavage Heated peritoneal lavage is a technique available in most facilities (Figure 5-12). Heat is conducted intraperitoneally via isotonic dialysate delivered at 40° to 45° C (104° to 113° F).348 Before lavage is initiated, chest and abdominal radiographs should be obtained because subsequent films may reveal Warmed saline

Saline

Rib 2

AA

Heat exchanger

3

S V C

Lung

RB

4

Fluid warmer

T6

Air eliminator

Midclavicular line Postaxillary line

5 6

Saline out

B

Autotransfusion bag

A

Water seal chest drain FIGURE 5-11  Thoracic lavage. A, Cycle. B, Cross section.

133

CHAPTER 5  Accidental Hypothermia

pericardium is unnecessary unless an effusion or tamponade is present. The physician bathes the heart for several minutes in 1 to 2 L of an isotonic electrolyte solution heated to 40° C (104° F), then suctions and replaces warm fluids.34 The physician may attempt internal defibrillation after myocardial temperature reaches 26° to 28° C (78.8° to 82.4° F). Unless a perfusing rhythm is achieved, lavage is continued until myocardial temperature exceeds 32° to 33° C (89.6° to 91.4° F). A standard post-thoracotomy tube in the left side of the chest could provide an avenue for continued rewarming via thoracic irrigation. A median sternotomy also allows ventricular decompression and direct defibrillation.212 One potential disadvantage of both these techniques is that open cardiac massage of a cold, rigid, and contracted heart may not generate flow.5,53 Unless immediate CPB is an option, mediastinal irrigation and direct myocardial lavage are indicated only if cardiac arrest has occurred. In this circumstance, personnel skilled in the technique should also initiate all other available rewarming modalities.

PART 2  COLD AND HEAT

14F catheter

Peritoneum Fascia of linea alba

A Wire FIGURE 5-13  Peritoneal lavage. A 14F catheter is of a caliber that can infuse fluids rapidly. Catheter

Umbilicus

B

8F catheter

C FIGURE 5-12  Peritoneal lavage. A, Mini-laparotomy for peritoneal lavage. B, The catheter in place with the needle removed and the wire introduced. C, An 8F catheter is introduced over the wire, and the wire is then removed.

134

subdiaphragmatic air introduced during the procedure. The bladder and stomach must be emptied before insertion of the catheter. The two common techniques for introducing fluid into the peritoneal cavity are the mini-laparotomy and the percutaneous puncture. The “minilap” requires an infraumbilical incision through the linea alba. A supraumbilical approach is necessary if previous surgical scars, a gravid uterus, or pelvic trauma is identified. The peritoneum is punctured under direct visualization and dialysis catheter(s) inserted. A much simpler and more rapid technique is the guidewire, or Seldinger, variation of the percutaneous puncture. The site is infiltrated if necessary with lidocaine, and a small stab incision is made. An 18- to 20-gauge needle penetrates the peritoneum, and a guidewire is introduced. Entry into the peritoneum is usually recognizable by a distinct “pop.” A disposable kit is available (Arrow Peritoneal Lavage Kit [AK09000]). The 8F lavage catheter is inserted over the wire and advanced into one of the pelvic gutters. Double-catheter systems with outflow suction speed rewarming. Normal saline, lactated Ringer’s solution, or standard 1.5% dextrose dialysate solution with optional potassium supplementation can be used.82 Isotonic dialysate is heated to 40° to 45°C (104° to 113° F). Up to 2 L is then infused (10 to 20 mL/kg), retained for 20 to 30 minutes, and aspirated. The usual clinical exchange rate is 6 L/hr, which yields rewarming rates of 1° to 3° C (1.8° to 5.4° F) per hour. An alternative for severe cases is a larger catheter, as found in cavity drainage kits (Arrow 14F [AK-01601]) (Figure 5-13). The catheter can be placed with the Seldinger technique. The higher drainage capability markedly increases exchange rates and minimizes the dwell times necessary for maximal thermal transfer. The flow rate via gravity through regular tubing is approximately 500 mL/min, which can be tripled under infusion pressure. A unique advantage of peritoneal dialysis is drug overdose and rhabdomyolysis detoxification when hemodialysis is unavailable. In addition, direct hepatic rewarming reactivates detoxi­ fication and conversion enzymes. Peritoneal dialysis worsens preexisting hypokalemia. Vigilant electrolyte monitoring is essential before empirical modification of the dialysate. The presence of adhesions from previous abdominal surgery increases the complication rate and minimizes heat exchange. Peritoneal dialysis during standard mechanical CPR is as effective as partial cardiac bypass in resuscitating severely hypothermic dogs.364 In contrast to AER, peritoneal lavage rewarming did not require significantly greater quantities of crystalloids and bicarbonate. This exchange rate is rarely possible in humans. Bowel infarction may be a concern when using prolonged warm peritoneal dialysis in patients with severe hypothermia with inadequate visceral perfusion during CPR. Peritoneal lavage is invasive and should not be routinely used in treating stable, mildly hypothermic patients. This technique is

ENDOVASCULAR WARMING Another active rewarming option that is emerging is endovascular warming with commercially available temperature control devices. They are used in EDs for therapeutic cooling of resuscitated comatose cardiac arrest patients.367 Less invasive and technically easier than extracorporeal rewarming, endovascular systems that involve femoral vein catheterization may prove to be a promising alternative. The closedloop catheter has a temperature control element at the tip. Available models have a fail-safe feature on the console that must be circumvented to allow rewarming if the core temperature is below 30° C (86° F).203

EXTRACORPOREAL BLOOD REWARMING Table 5-4 summarizes the techniques for extracorporeal blood rewarming. Hemodialysis Standard hemodialysis is widely available, practical, portable, and efficient, and should be strongly considered in perfusing patients with electrolyte abnormalities, renal failure, or intoxication with a dialyzable substance.149,254,267 Two-way flow catheters allow the option of cannulation of a single vessel.205,327 A Drake-Willock single-needle dialysis catheter can be used with a portable hemodialysis machine and an external warmer. After central venous cannulation, exchange cycle volumes of 200 to 250 mL/min are possible. Although heat exchange is less than with standard two-vessel hemodialysis, the ease of percutaneous subclavian vein placement is a major advantage. Hemodialysis via two separate singlelumen catheters placed in the femoral vein can achieve continuous blood flow at 450 to 500 mL/min.135,136 In-line hemodialysis also TABLE 5-4  Techniques for Extracorporeal Blood

Rewarming

Technique

Comments

Cardiopulmonary bypass

Full circulatory support Perfusate temperature gradient: consider 5°-10° C (9°-18° F) Flow rates of 2-7 L /min (average, 3-5 L /min) Rate of rewarming, up to 9.5° C (17.1° F) per hour Consider if K <10 mmol/L, pH >6.5, at least 10°-12° C (50°-53.6° F) Percutaneous Seldinger technique to insert catheters Requires blood pressure of ≥60 mm Hg No need for perfusionist/pump/ anticoagulation Average flow rates of 225-375 mL/min Rate of rewarming, 3°-4° C (5.4°-7.2° F) per hour Consider for trauma Circuit not complex Efficient nonbypass modality Volume infusion to augment cardiac output Flow rates of 150-400 mL /min Rate of rewarming, 2°-3° C (3.6°-5.4° F) per hour Widely available Portable and efficient Single or dual catheter Exchange cycle volumes, 200-500 mL /min Rate of rewarming, 2°-3° C (3.6°-5.4° F) per hour Consider if there are electrolyte/toxicologic derangements

Continuous arteriovenous warming

Venovenous rewarming

Hemodialysis

Modified from Danzl DF: Hypothermia, Semin Resp Crit Care Med 23:57, 2002.

Water outlet

Cold blood inflow

CHAPTER 5  Accidental Hypothermia

indicated in combination with all available rewarming techniques in cardiac arrest patients.

Femoral artery Femoral vein

Warm blood outflow

Water inlet (40° C) Filter

FIGURE 5-14  Schematic of continuous arteriovenous rewarming.

simplifies correction of electrolyte abnormalities. Local vascular complications, including thrombosis of vessels and hemorrhage secondary to anticoagulation, may occur. Continuous Venovenous Rewarming In extracorporeal venovenous rewarming, blood is removed, usually from a central venous catheter, heated to 40° C (104° F), and returned via a second central or large peripheral venous catheter. Flow rates average 150 to 400 mL/min.116,131,319,336 The circuit is not complex and is more efficient than many other non-bypass modalities. There is no oxygenator, and because the method does not provide full circulatory support, volume infusion is the only option to augment inadequate cardiac output. Although the use of CAVR is limited by profound hypotension, high-flow venovenous rewarming may prove to be an alternative.162 In another variation of the extracorporeal venovenous circuit, blood is removed from the femoral vein, heparinized, and sent through a blood rewarmer via an infusion pump accelerator. It is neutralized with protamine before reinjection into the subclavian or internal jugular vein, which would preferentially rewarm the heart. Another option is to insert a femoral vein dual-lumen dialysis catheter. Continuous Arteriovenous Rewarming CAVR involves the use of percutaneously inserted femoral arterial and contralateral femoral venous catheters.95,96,98 This technique requires a blood pressure of at least 60  mm  Hg. The Seldinger technique is used to insert 8.5F catheters. Heparinbonded tubing circuits obviate the need for systemic anticoagulation. CAVR has principally been performed on traumatized patients (Figure 5-14). The blood pressure of spontaneously perfusing traumatized hypothermic patients creates a functional arteriovenous fistula by diverting part of the cardiac output out of the femoral artery through a countercurrent heat exchanger (e.g., Level 1; FloTem IIe). The heated blood is then returned with admixed heated crystalloids via the femoral vein. The additional fluids are titrated and infused by piggyback until hypotension is corrected.251 The rate of rewarming exceeds that of hemodialysis. CAVR does not require the specialized equipment and perfusionist necessary for CPB. The average flow rates are 225 to 375 mL/ min, resulting in a rate of rewarming of 3° to 4° C (5.4° to 7.2° F) per hour. Because the catheters are 8.5F, the patient must weigh at least 40 kg. Coagulation begins to appear in the heparinized circuits at around 3 hours. Cardiopulmonary Bypass Partial or complete CPB should be considered in unstable, severely hypothermic patients.15,117,186,289,372 Favorable considerations include absence of severe head injury or asphyxia.314 Some 135

PART 2  COLD AND HEAT

centers initiate CPB only if the presenting arterial pH is above 6.5, serum potassium is below 10 mmol/L, and core temperature is above 10° to 12° C (50° to 54° F).142,337,355 Fischer’s considerations for CPB include a potassium level under 10 mmol/L in adults or under 12 mmol/L in children, coupled with a core temperature below 30° C (86° F). Patients are not resuscitated if extreme hyperkalemia is identified in a patient with a temperature over 30° C (86° F).92 A major advantage of CPB is preservation of oxygenated flow if mechanical cardiac activity is lost during rewarming.70,150,155,234 CPB is three to four times faster at rewarming than other active core rewarming (ACR) techniques, and it reduces the high blood viscosity associated with severe cases. CPB should also be considered when severe cases do not respond to less invasive rewarming techniques, in patients with completely frozen extremities, and when extensive rhabdomyolysis is accompanied by major electrolyte disturbances.169 Various extracorporeal rewarming techniques can be lifesaving in select profound cases of hypothermia.127 Althaus and colleagues describe complete recovery in three severely hypothermic tourists after prolonged periods of cardiac arrest and CPR.5 In another review of 17 cases, there were 13 survivors.318 Walpoth and co-workers354,355 report rewarming 32 patients with CPB, of which 15 are long-term survivors. The average age was 25.2 years. Their mean presenting esophageal temperature was 21.8° C (71.2° F), and the mean interval between discovery and CPB was 141 minutes. The standard femoral–femoral circuit includes arterial and venous catheters, a mechanical pump, a membrane or bubble oxygenator, and a heat exchanger (Figure 5-15). A 16F- to 30F venous cannula is inserted via the femoral vein to the junction of the right atrium and the inferior vena cava. The tip of the shorter 16F to 20F arterial cannula is inserted 5 cm (2 inches) or proximal to the aortic bifurcation. Antretter and colleagues8 use 32F venous and 28F arterial cannulas with the open surgical technique, and 21F venous and 19F arterial cannulas if inserted percutaneously. Closed-chest compressions can be maintained during percutaneous or open surgical technique insertion and may help decompress the dilated nonbeating heart. Transesophageal echocardiography can help evaluate ventricular load and valve function. Heated, oxygenated blood is returned via the femoral artery.20 Femoral flow rates of 2 to 3 L/min can elevate core temperature 1° to 2° C (1.8° to 3.6° F) every 3 to 5 minutes. In a review by Splittgerber and co-workers,318 the mean CPB temperature increase was 9.5° C (17.1° F) per hour. Most pumps can generate full flow rates up to 7 L/min. Long222 recommends considering

Oxygenator and vortex pump Portable bypass machine

Heat exchanger

the use of vasodilator therapy with IV nitroglycerin to facilitate perfusion. He initiates bypass flow rates at about 2 L/min and gradually increases to 4 to 5 L/min. Vasoactive agents may be needed to maintain the cardiac index at 30 L/min/m2 or more and a (low) systemic vascular resistance of 1000 dynes/sec × cm−5 or less.228 The optimal temperature gradient and bypass rewarming rates are unknown. One study of rewarming via CPB in a swine model cooled to 23° C (73.4° F) addresses this concern. An excessive temperature gradient between brain tissue and circulant adversely affected electroencephalographic (EEG) regeneration. The other theoretical concern is the possibility of increased bubbling if high perfusate temperature gradients are used. Most investigators use 5° C (9° F) gradients23 or 10° C (18° F) gradients.24 Eventually, neuromonitoring during rewarming will provide some answers. In severe cases, evoked cerebral responses before EEG regeneration could help assess the recovering brain.304 A variety of techniques decrease the need for IV anticoagulation with heparin, which previously limited clinical applicabil184 ity. Heparin-coated perfusion equipment was used successfully without systemic heparinization in a patient with hypothermic cardiac arrest (23.3° C [73.9° F]) and intracranial trauma.351 The use of nonthrombogenic pumps, coupled with enhanced physiologic fibrinolysis seen in the first hour of CPB, also succeeds experimentally. Complications with the standard technique include vessel damage, air embolism, hemolysis, DIC, and pulmonary edema (Box 5-8). Endothelial leakage increases compartment pressures and exacerbates frostbite. If adequate flow rates of 3 to 4 L/min (50 to 60 mL/kg/min) cannot be maintained, thoracotomy or a venous catheter with side holes, augmenting intravascular volume, should be considered. With all four of these techniques, there is no proof that rapid acceleration of the rate of rewarming improves survival rates in patients being perfused. The value of the maintenance of some degree of mild hypothermia after hypothermic cardiac arrest and extracorporeal rewarming is speculative. With accidental hypothermia, patients may have had neuroprotection before cardiac arrest from hypothermia. Potential complications of uncontrolled rapid rewarming in severe hypothermia include DIC, pulmonary edema, hemolysis, and acute tubular necrosis. As an alternative, a conservative core-rewarming approach can be highly effective for patients with severe hypothermia, despite hemodynamic instability.291 In hypothermic cardiac arrest, rewarming should be attempted via CPB and hemodialysis when CPR is not contraindicated (Box 5-9), unless frozen intravascular contents prevent flow.

Arterial line 16-20F

Venous line 16-30F

FIGURE 5-15  Femoral–femoral bypass.

136

BOX 5-9  Contraindications to Initiating

Complications • Vascular injury • Air embolism • Pulmonary edema • Coagulopathies (hemolysis, disseminated intravascular coagulation) • Frostbite tissue damage • Extremity compartment syndromes

• Do-not-resuscitate status is documented and verified. • Obviously lethal injuries are present. • Chest wall depression is impossible. • Any sign of life is present. • Rescuers are endangered by evacuation delays or altered triage conditions.

Cardiopulmonary Resuscitation   in Accidental Hypothermia

Contraindications • Futile resuscitations • Lack of venous return • Intravascular clots or slush • Complete heparinization would be hazardous* • Cardiopulmonary resuscitation is contraindicated (see Box 5-9)

From Danzl DF, Pozos RS, Auerbach PS, et al: Multicenter hypothermia survey. Ann Emerg Med 16:1042, 1987. Developed in conjunction with the Wilderness Medical Society.

irradiation “until they squealed and suckled.” Subsequently, 20 of 28 human infants rewarmed with microwave irradiation at 90 to 100 watts survived. The temperature rose an average 1° C (1.8° F) after 6 to 7 minutes, and the average infant required 45 minutes to achieve a rectal temperature of 36° C (96.8° F). In an experimental study of men cooled to 35° C (95 ° F), warm water immersion rewarming is more rapid than radio-wave rewarming with 2.5 watts/kg.178 Both ultrasonic and low-frequency microwave diathermy can deliver large quantities of heat below the skin. As dosimetry guidelines develop, potential complications and ideal application sites for this experimental technique deserve further study in the hospital. In the field setting, potential problems with power supply and electronic and navigational interference compound the physiologic problems.

*Unless with athrombogenic tubing or adequate physiologic fibrinolysis.

Clotted atrial blood or failure to obtain venous return indicates that these techniques will be futile. If experienced personnel and necessary equipment are unavailable, all other rewarming techniques should be used in combination.23,350,370 Diathermy Diathermy, the transmission of heat by conversion of energy, is a potential rewarming adjunct in accidental hypothermia.140,220 Large amounts of heat can be delivered to deep tissues with ultrasonic (0.8 to 1 MHz) and low-frequency (915 to 2450 MHz) microwave radiation. Short-wave (13.56 to 40.68 MHz) modalities are high frequency and do not penetrate deeply. Contraindications include frostbite, burns, significant edema, and all types of metallic implants and pacemakers. Under ideal conditions in a laboratory study, radio-wave frequency (13.56 MHz) electromagnetic regional heating of hypothermic dogs after immersion does not damage tissue at 4 to 6 watts/kg and rapidly elevates core temperature.365 Zhong and colleagues381 successfully rewarmed 16 piglets with microwave FIGURE 5-16  Emergency department algorithm. ACR, Active core rewarming; AER, active external rewarming; CPB, cardiopulmonary bypass; PEA, pulseless electrical activity; PER, passive external rewarming.

Cardiopulmonary Resuscitation Basic and advanced life support recommendations in hypothermia continue to evolve (Figure 5-16).* Cardiac output generated with closed-chest compressions maintains viability in select patients with hypothermia.325 The optimal rate and technique are unknown. Definitive prehospital determination of cardiac *References 7, 67, 91, 180, 316, 323, 334.

Yes

Responsive No Respirations Yes

No Tracheal intubation and heated humidified oxygen

Cardiac monitor

Cardiac monitor Electrical complexes

Core temperature

Central pulse

Below 32.2° C (90° F) Above 32.2° C (90° F) PER

Yes

Arrest rhythm Attempt defibrillation

No (PEA)

ACR and truncal AER

All ACR and CPB

137

CHAPTER 5  Accidental Hypothermia

BOX 5-8  Extracorporeal Rewarming

PART 2  COLD AND HEAT

activity requires a cardiac monitor, because misdiagnosis of cardiac arrest is a hazard. Peripheral pulses are difficult to palpate when extreme bradycardia is present with peripheral vasoconstriction.130,366 Asystole may be as common a presenting rhythm as VF. In the field, differentiating VF from asystole may be impossible. Possible causes of VF include acid–base fluxes, hypoxia, and coronary vasoconstriction with increased blood viscosity. Chest compressions and various therapeutic interventions are also implicated, but not proven causes.121,265 The role of acid–base fluxes is not clear. Mild alkalosis appears somewhat protective against VF during controlled, induced hypothermia.200

RESPIRATORY CONSIDERATIONS When cardiopulmonary arrest develops during resuscitation, noncardiac causes are often pulmonary emboli or progressive respiratory insufficiency. Provision of adequate oxygen supply is essential during rapid rewarming. For each 1° C (1.8° F) rise in temperature, oxygen consumption increases up to three times (see Box 5-1).93 Endotracheal intubation and ventilation decrease atelectasis and ventilation–perfusion mismatch. Complete airway protection averts aspiration, which is otherwise common with depressed airway reflexes, bronchorrhea, and ileus. Carbon dioxide production also drops by one-half with an 8° C (14.4° F) fall in the temperature. During induced hypothermia, carbogen (1% to 5% carbon dioxide added to oxygen) facilitates acid–base management by allowing adjustment of the fractional inspired carbon dioxide concentration (FICO2) while adjusting the ventilation. Past controversy regarding the hazards of endotracheal intubation reflected coincidental episodes and a mis-citation by Fell and colleagues87 regarding a series of hypothermic overdoses reported by Lee and Ames.210 Fell and colleagues stated that “endotracheal intubation was followed by cardiac arrest in a large proportion of cases,” whereas Lee and Ames merely cautioned of that possibility. In a multicenter survey, endotracheal intubation was performed on 117 patients by multiple operators in various settings.59 No induced arrhythmias were recognized, which is consistent with several reports.209,244 Potential arrhythmogenic factors include hypoxia, mechanical jostling, and acid–base or electrolyte fluctuations. The indications for endotracheal intubation in hypothermia are identical to those in normothermia.54,107 It is required unless the patient possesses intact protective airway reflexes. Ciliary activity is depressed in hypothermia, frothy sputum produces chest congestion, and bronchorrhea resembles pulmonary edema. Fiberoptic or blind nasotracheal intubation may be preferable to cricothyroidotomy when cold-induced trismus or potential cervical spine trauma is present. Oral rather than nasal intubation is advisable in patients with coagulopathy, to avoid causing major epistaxis. Rapid-sequence intubation may be impossible when severe cold-induced trismus is present and the mandible will not move. In the milder cases, hypothermia prolongs the duration of neuromuscular blockade. Drug metabolism is also prolonged with vecuronium and atracurium. As a result, avoid using neuromuscular blockers.180 Efficacy, metabolism, and clearance are very unpredictable, and assessment of sedation adequacy is difficult.

BLOOD FLOW DURING CHEST COMPRESSIONS During normothermic conditions, blood flow partially results from phasic alterations in intrathoracic pressure and not just from direct cardiac compression. Niemann and co-workers261 demonstrated that antegrade flow occurs without left ventricular compression in a normothermic canine model. Closed-chest compressions increase intrathoracic pressure.227 When thoracic inlet venous valves are competent, the resultant pressure gradient between arterial and venous compartments generates supradiaphragmatic antegrade flow. Clinical observations challenge the “cardiac pump” model. This model is predicated on closure of the mitral valve and opening of the aortic valve during chest compression. This allows a forward stroke volume. During release of compression, transmitral flow 138

can fill the left ventricle. Optimal cardiac output is thus generated by achieving the maximal compression rate that allows maximal left ventricular end-diastolic filling. Interestingly, transesophageal echocardiography in a canine model demonstrates mitral valve closure during chest compression except during low-impulse (downstroke momentum) compressions. Compression of a cold, stiff chest wall may be equivalent to low impulse.53 In hypothermia, the role of a “thoracic pump” with the heart as a passive conduit is an attractive hypothesis. The phasic alterations in intrathoracic pressure generated by compressions are equally applied to all of the cardiac chambers and thoracic vessels. The mitral valve remains open during compression, and blood continues to circulate through the left side of the heart. Myocardial compliance can be severely reduced in hypothermia. Althaus and colleagues5 noted at thoracotomy in one of three survivors of hypothermia that “the heart was found to be hard as stone and it is hardly conceivable how effective external cardiac massage could have been.” Open cardiac massage can be combined with mediastinal irrigation when immediate cardiopulmonary bypass is an option.34-36 Chest wall elasticity is also decreased with cold, as is pulmonary compliance. If the abdominal muscles are not kneadable, anticipate that the stiff chest wall will prevent adequate ventilation. Lastly, more force is needed to depress the chest wall sufficiently to generate intrathoracic vascular compartment pressure gradients. Despite these potential physiologic explanations, a large number of neurologically intact survivors are reported after prolonged closed-chest compressions. The explanation lies in measuring intrathoracic pressures during hypothermic closedchest compressions. Perfusion enhancement maneuvers remain largely unstudied in hypothermia. Ancillary abdominal binding might favorably inhibit paradoxical diaphragmatic motion.53,261 Simultaneous compression and ventilation can increase flow in the heart’s left side. Ventilation with the proper carbogen concentration also allows high ventilatory rates while maintaining uncorrected PaCO2 at 40 mm Hg. Placement of a counterpulsation intra-aortic balloon is another option. Mechanical thoracic compression devices could be useful during prolonged resuscitations with limited availability of personnel. In addition, an automatic mechanical chest compression device may serve as a bridge while establishing the capability for CPB.366 During hypothermic cardiac arrest in swine, cardiac output, cerebral blood flow, and myocardial blood flow averaged 50%, 55%, and 31%, respectively, of those achieved during normothermic closed-chest compressions.230 Blood flow to these areas did not decrease with time, unlike in the normothermic group. No significant difference in flow generated appeared between normothermic and hypothermic swine at 20 minutes. Hypothermic rheologic changes, including increased viscosity, also affect flow. Peripheral vascular resistance is expected to increase during vasoconstriction, but in the swine there was no difference in systemic and organ vascular resistance between normothermic and hypothermic CPR.230 In a multicenter survey of 428 cases, 9 of the 27 patients receiving CPR initiated in the field survived, as did 6 of 14 patients with ED-initiated CPR.59 Based on these cases and a literature review, CPR standards in hypothermia are proposed (see Box 5-9). Because cardiac output is the product of heart rate and stroke volume, the optimal closed-chest compression rate should be the fastest rate allowing optimal ventricular filling. Many patients have recovered neurologically after slow compression rates. One recovered after 220 minutes at half the normal compression rate.263 The optimal rate probably has a direct linear relationship with the degree of hypothermia. Tissue decomposition, apparent rigor mortis, dependent lividity, and fixed, dilated pupils are not reliable criteria for withholding CPR. In addition, intermittent flow may provide adequate support during evacuation. Although one position paper implies otherwise, in the opinion of this author CPR should not be withheld only because continuous chest compressions cannot be ensured.42,76 Intermittent flow may be preferable to no flow. The lowest temperature documented in an infant survivor of

Cerebral Resuscitation The ability to reestablish cerebral blow flow with CPR and improve neurologic outcome is inversely proportional to the duration of cardiac arrest. Significant delay can markedly elevate the cerebral perfusion pressure (CPP) required to establish cerebral blood flow (CBF).19 It appears that thermal stabilization rather than aggressive field rewarming should be the focus, except for severely hypothermic victims or those in cardiac arrest. Mild hypothermia may be therapeutic and improve neurologic outcome after global cerebral ischemia. Hypothermia decreases glutamate release, metabolic demand, free radical formation, and release of inflammatory cytokines.109,294 In the prehospital setting, addressing disproportionate hypotension, hypoperfusion, and hypoxia is paramount. Once the airway is secured, elevating the head 5 to 10 degrees can attenuate intracerebral hypertension induced by global cerebral ischemia. Normally, CBF is independent of CPP over a range of pressures. After cerebral autoregulation is extinguished, CBF passively depends on the arterial blood pressure. When venous access is difficult, medications may be administered intratracheally or via the intraosseous route. Of interest, large internal jugular catheters may partially obstruct cerebral venous outflow.232 Because hypoxemia is the rule, supplemental oxygen should be initiated when available. The goal is normoxia. The prolonged use of 100% oxygen after the return of spontaneous circulation may increase oxidative brain injury by generating reactive oxygen species, including superoxide and hydrogen peroxide. The rescuer should avoid positive end-expiratory pressure unless it is essential to maintain normoxia, because it decreases cerebral venous outflow. Cerebral vasculature autoregulation may be lost after global brain ischemia, and yet hypocarbia-induced vasoconstrictive mechanisms remain intact. Therefore avoid protracted hyperventilation except in the rare case of a cranially traumatized hypothermic victim with impending uncal herniation. In the field, attempt to ventilate the patient at a rate that would maintain the uncorrected partial pressure of carbon dioxide (PCO2) between 35 and 40 mm Hg.231 Postischemic hyperglycemia is potentially detrimental, because glucose levels over 250 mg/dL are associated with lactate generation and exacerbation of metabolic acidosis. Cerebral resuscitation strategies in hypothermia reflect complex neurophysiology.294 The brain, although making up only 2% of total body weight, requires 15% of the cardiac output and consumes 20% of the available oxygen at 37° C. Cerebral blood flow depends on the CPP, which equals the mean arterial pressure minus the intracranial pressure. When the CPP drops below 50 to 60 mm Hg, CBF drops. Once CBF is below 20%, a cascade is initiated that includes the failure to maintain ionic gradients in neurons, cellular depolarization, and acidosis. Even when cold, neurons are more susceptible to hypoxic insult than are glial or endothelial cells.148,173 When reperfusion is reestablished, the initial transient hyperemic period is characterized by increased CBF with low oxygen consumption. This lasts for minutes and is followed by the “no reflow” phase, which lasts for hours. Reperfusion is also characterized by both cytotoxic edema during ischemia, and vasogenic edema caused by blood–brain barrier injury. Intraluminal vascular damage is caused by nitric oxide (NO) and reactive oxygen species (ROS), and proteases inflict abluminal injury.44 The decrease in CBF decreases mitochondrial ATP generation. Ionic gradients collapse across the neuronal membrane, as a result of failure of the Na–K pump. Sodium influx results in

depolarization, which causes axonal release of the excitatory neurotransmitter glutamate. Glutamate is the ultimate trigger of neuronal injury caused by N-methyl-D-aspartate receptor activation, because it allows cellular calcium influx.192 Second messengers in the cascade are signals during ischemia from trigger events that activate other second messengers or perpetrators of damage. Intracellular overload of calcium inhibits mitochondrial respiration. In addition, nitric oxide synthase generates NO and ROS, both of which damage DNA and increase cytokine levels. In the field, emphasis should be placed on avoidance of factors known to exacerbate adverse neuronal responses to cerebral ischemia: disproportionate hypotension, hypoperfusion, hyperglycemia, hypoxia, and hyperoxia.239

Resuscitation Pharmacology The pharmacologic effects of medications are temperature dependent. The lower the temperature, the greater is the degree of protein binding. Enterohepatic circulation and renal excretion are also altered, so abnormal physiologic drug responses should be anticipated. The usual clinical scenario consists of substandard therapeutic activity while the patient is severely hypothermic, progressing to toxicity after rewarming.204 Medications are not given orally because of decreased gastrointestinal function, and intramuscular medications are avoided because they may be erratically absorbed from vasoconstricted sites. The pharmacologic manipulation of respiratory drive, pulse, and blood pressure is generally not indicated except in profound cases. When a relative tachycardia is not consistent with temperature depression, the possibility of hypovolemia, hypoglycemia, or a toxic ingestion should be considered. Vasopressors are potentially arrhythmogenic, might lower VF threshold, and cannot increase peripheral vascular resistance if the vasculature is already maximally constricted.209 If intra-arterial pressure is not consistent with the degree of hypothermia, judicious use of inotropic agents may be necessary.266 Dopamine can be a successful adjunctive treatment.300 Dopamine reverses cardiovascular depression under hypothermic conditions, equivalent to up to 5° C (9° F) rewarming. Dopamine decreases systemic vascular resistance at low infusion doses and increases it at high infusion rates.266 Shock requiring vasoactive drugs is a risk factor for mortality.36 In severe cases, the target mean arterial pressure is around 60 mm Hg. Epinephrine and vasoconstrictors should probably be avoided.194,198 Balancing the need for flow versus pressure, Zandstra recommends labetalol and IV nitroglycerin. This therapy can be coupled with 2 to 4 mcg/kg of dopamine, which is less arrhythmogenic than are exogenous catecholamines.378 Epinephrine is not recommended by the American Heart Association for hypothermic cardiac arrest below 30° C (86° F). In porcine models, there is no evidence that repeated or highdose epinephrine during hypothermic CPR improves outcome.194,198 In the same model, a single 0.4 unit/kg dose of vasopressin below 30° C (86° F) improved defibrillation success.302 There is conflicting evidence regarding cardiovascular function after rewarming. In some studies, there is complete reversal of cold-induced changes, whereas in another, the physiologic response to norepinephrine is paradoxical.361 Patients with profound hypothermia after ethanol ingestion have been resuscitated with low-dose dopamine support. In frostbite victims, however, the use of catecholamines may jeopardize the extremities.222,223 Catecholamines also exacerbate preexisting occult hypokalemia. The effect of temperature depression on the autonomic nervous system is complex. In primates, cooling produces a biphasic response in plasma catecholamine concentrations. After an initial increase, the autonomic nervous system switches off at 29° C (84.2° F),41 suggesting that catecholamine support might be useful below that temperature. The initial rise in catecholamine levels could also be caused by acute respiratory acidosis, which stimulates the sympathetic nervous system.31 Low-dose dopamine (1 to 5  mcg/kg/min) or other catecholamine infusions are generally reserved for disproportionately severe hypotensive patients who do not respond to crystalloid resuscitation and rewarming. 139

CHAPTER 5  Accidental Hypothermia

accidental hypothermia is 15.2° C (59.4° F); in an adult, 13.7° C (56.7° F); and in induced hypothermia, 9° C (48.2° F).51,59,106,258,264 One patient recovered after 6.5 hours of closed-chest compressions.215 In Saskatchewan 1994, a 2-year-old child reportedly recovered from a core temperature of 13.9 ° C (57° F). Remarkably, a physician who authored the report was successfully resuscitated from 13.7° C (57° F) after she received 165 minutes of CPR and then CPB.106

PART 2  COLD AND HEAT

THYROID The most dramatic Rip Van Winkle–type of rude awakening from hypothermic myxedema coma was Dr. Richard Asher’s patient in the 1950s. He was successfully metabolically aroused from a 7-year, 30° C (86° F) slumber. Ironically, so was a quiescent oat cell carcinoma. Cold induces stimulation of the hypothalamic-pituitary-thyroid axis. Unless myxedema is suspected, empirical therapy is not recommended. A history of neck irradiation, radioactive iodine, Hashimoto’s thyroiditis, or surgical treatment of hyperthyroidism should heighten the clinician’s suspicion of myxedema. Failure to rewarm despite an appropriate course of therapy is a further clue.225 Myxedema coma is usually precipitated in older adult patients with chronic hypothyroidism who are stressed by trauma, infection, anesthesia, or medication ingestion. Typical nonspecific laboratory abnormalities include hyponatremia, anemia, and liver enzyme and lipid elevations. If myxedema coma is suspected, thyroid function studies, including serum thyroxine (T4) by radioimmunoassay, triiodothyronine (T3) resin uptake, and thyroidstimulating hormone level, should be obtained and serum cortisol level measured. Given the appropriate index of suspicion, the physician should administer 250 to 500 mcg levothyroxine (T4) intravenously over several minutes without waiting for confirmatory laboratory results. Daily injections of 100 mcg are required for 5 to 7 days. The clinician should consider adding at least 100 to 250 mg of hydrocortisone to the first 3 L of intravenous fluid. Absorption of T4 is erratic if the drug is given orally or intramuscularly. The onset of action of T3 is more rapid, which jeopardizes cardiovascular stability; therefore T3 is avoided in acute replacement therapy. The onset of action of T4 is 6 to 12 hours, evidenced by continuous improvement of the vital signs during rewarming. Up to one-half of the T4 is eventually converted by the peripheral tissues into T3.

spontaneously during rewarming, and digitalization or other pharmacologic intervention is not warranted. Electrophysiologic studies show that the interval prolongation present on His bundle electrocardiography is unresponsive to atropine. Mesenteric embolization is a potential hazard when the rhythm converts back to sinus rhythm. Hypothermia renders the negative inotropic effects of calcium channel blockers redundant.56 In summary, all new atrial arrhythmias usually convert spontaneously during rewarming and should be considered innocent. Attention is directed toward correcting acid–base, fluid, and electrolyte imbalances and avoiding administration of atrial antiarrhythmics.

VENTRICULAR ARRHYTHMIAS Because preexisting chronic ventricular ectopy may be suppressed in a cold heart, the physician noting ectopy during rewarming is placed in a quandary. The history from the hypothermic patient may be unproductive, and the past cardiac history is often unavailable. Transient ventricular arrhythmias should generally be left untreated. In one study of 22 continuously monitored patients with hypothermia, supraventricular arrhythmias were common (9 cases) and benign.284 Ventricular extrasystoles developed in 10 patients, but none experienced ventricular tachycardia or VF during rewarming. The terminal rhythm in the 8 who died while being monitored was asystole and not VF. The energetics of the fibrillating hypothermic ventricle suggest that asystole may consume less energy and be more protective. Pharmacologic options are limited, because hypothermia induces complex physiologic changes that result in abnormal responses.374 Drug metabolism and excretion are both progressively decreased. In normothermia, class IA ventricular antiarrhythmics have negative inotropic and indirect anticholinergic effects, and they moderately decrease conduction velocity (Box 5-10). Procainamide increases the incidence of VF during hypothermia. Quinidine has been useful during induced profound

CORTICOSTEROIDS Acute cold stress and many coexisting disease processes stimulate cortisol secretion. The free active fraction of cortisol decreases as the temperature drops because of increased protein binding, and cortisol utilization is similarly decreased. The increase in adrenocorticotropic hormone (ACTH) and adrenal steroid secretion may also be a neurogenic or an emotional response in the conscious subject to an unpleasant environment. Experimentally, inhibition of ACTH secretion during hypo­ thermia is mediated by decreased hypothalamic secretion of arginine vasopressin. This decreases pituitary responsiveness to corticotropin-releasing factor, inhibiting corticotropin release. Thus exogenous arginine vasopressin could prove helpful during rewarming. Cold exposure also induces adrenal unresponsiveness to ACTH. As a result, false diagnosis of decreased adrenal reserve is possible and does not represent functional adrenal insufficiency, because ACTH levels return to normal after rewarming. Serum cortisol levels are commonly elevated. Secondary adrenal insufficiency resulting from panhypopituitarism may also coexist with myxedema. Empirical administration of corticosteroids is indicated if hypoadrenocorticism is suspected on the basis of a previous history of corticosteroid dependence, suggestive physical findings, or an inexplicable failure to rewarm. The use of narcotic antagonists in hypothermia is reported. Naloxone may reduce the severity of hypothermia in drug overdoses and in spinal shock and appears to have activity at the µ-opioid receptor sites.56

Resuscitation Complications ATRIAL ARRHYTHMIAS All atrial arrhythmias, including atrial fibrillation, should have a slow ventricular response with the temperature depression. Atrial fibrillation is commonly noted below 32° C (89.6° F) in accidental hypothermia victims. Atrial fibrillation usually converts 140

BOX 5-10  Antiarrhythmic Agents Class I. Sodium Channel Blockers IA. Conduction and depolarization moderately slowed, and action potential duration (APD) and repolarization prolonged • Disopyramide • Procainamide • Quinidine IB. Conduction and depolarization minimally slowed, and APD and repolarization shortened • Lidocaine • Mexiletine • Moricizine • Phenytoin • Tocainide IC. Conduction and depolarization markedly slowed, and APD and repolarization prolonged • Encainide • Flecainide Class II. β-Adrenergic Blockers Class III. Antifibrillatory Properties (APD Prolonged) • Amiodarone • Bretylium • D-sotalol Class IV. Calcium Channel Blockers • Diltiazem • Verapamil Unclassified • Adenosine • Magnesium sulfate

The ideal ventricular antiarrhythmic would do the following: • Cause no further decrease in conduction velocity • Shorten the action potential duration (APD) • Lengthen the APD only in warmer regions of the myocardium to reduce dispersion • Possess direct antifibrillatory properties

hypothermia, preventing VF during cardiac manipulation at 25° to 30° C (77° to 86° F). No reports detail the effects of disopyramide. The role of the class IB agent lidocaine for prophylaxis or treatment is unresolved. In animal studies, lidocaine and propranolol have minimal hemodynamic effects in hypothermia. If normothermic effects persisted during hypothermia, the class IB agents would appear attractive because they minimally slow conduction while shortening the action-potential duration (APD). The class III agent bretylium tosylate, a unique bromobenzyl quaternary ammonium compound, has been effective in several animal studies and ineffective in others.78,326 It is not commercially available. This class of agents seems most ideal pharmacologically because it possesses direct antifibrillatory properties. The ability to prolong the APD is temperature dependent. Ideally, a drug would lengthen the APD only in warmer regions of the myocardium to reduce dispersion (Box 5-11). Two cases of chemical ventricular defibrillation after infusion of bretylium (10 mg/kg) in accidental hypothermia are reported.54,191 In the first study to evaluate the effects of bretylium administered after induction of hypothermia, Murphy and co-workers252 noted that only 1 of 11 dogs given bretylium (mean, 40.5 mg/kg) before five invasive maneuvers developed VF. No dog, including control subjects, showed fibrillation during endotracheal intubation. Of note in discussions regarding prophylaxis, 3 of the 11 dogs converted to VF during the drug infusion. The effect of bretylium on plasma catecholamines and electrically induced arrhythmias has also been studied. Because catecholamine levels increase during cooling, the demonstrated protection appears to result from alteration of electrophysiologic properties of the cardiac tissues. Amiodarone is another class III drug that possesses direct antifibrillatory activity. In a canine model of severe hypothermic VF, neither bretylium nor amiodarone improved resuscitation.326 The safety of the class III antiarrhythmic agent D-sotalol is problematic.22 It has temperature-dependent effectiveness and lengthens prolonged action potentials more efficiently at long pacing cycle lengths. Also of note, magnesium sulfate at a dose of 100 mg/kg IV can spontaneously defibrillate most patients on CPB at 30° C (86° F) with induced hypothermia. Emergency transvenous intracardiac pacing of bradyarrhythmias is extremely risky with cold hearts because it commonly precipitates VF. New arrhythmias that develop after rewarming may, on rare occasions, require pacing. Transcutaneous pacing (TCP) with low-resistance electrodes seems far preferable before stabilization.144 In a canine model, TCP restored and maintained hemodynamic stability and rewarmed hypothermic animals twice as rapidly as it did the controls.69 In summary, there are no commercially available ventricular antiarrhythmics proved safe and effective in accidental hypothermia.

SEPSIS In hypothermia, the classic signs of infection, including erythema and fever, are absent.229 Rigors and shakes resemble shivering. The initial history, physical, and laboratory data are often unreliable, so repeated evaluations and comprehensive culturing are mandatory in the ED. The 10% subset of patients with sepsis syndrome who present with a hypothermic response have a significantly increased frequency of shock and death, and this secondary hypothermia does not appear to be protective. Hypothermia compromises host defenses and results in serious bacterial infections. These significant infections can be

accompanied by minimal inflammatory response. Some common causative organisms include gram-negative bacteria, grampositive cocci, oral anaerobes, and Enterobacteriaceae.214 The core endotoxin components of gram-negative bacteria normally signal macrophages. At a normal or elevated temperature, active cytokine triggers include tumor necrosis factor, interleukin-1, and interleukin-6. The potential role of antiendotoxin monoclonal antibodies in patients with accidental but not cytokine-induced hypothermia is unresolved. Bone marrow release and circulation of neutrophils are compromised for up to 12 hours. In addition, human and porcine neutrophils are susceptible to hypothermia. In vitro, neutrophil migration and bacterial phagocytosis are reduced at 29° C (84.2° F). Neutrophilic extermination of various bacteria, including Staphylococcus aureus and Streptococcus faecalis, is also impaired. Acquired neutrophil dysfunction occurs. In addition, hypothermia is associated with decreased neutrophil levels in neardrowned children. As a clinical demonstration of the importance of these factors, therapeutic maintenance of hypothermia to control cerebral edema in near drowning is abandoned because of the substantial incidence of infectious complications. The incidence of infection varies dramatically with the victim’s age and the clinical series reported.214,363 In one large group of infants, over one-half were septic. Although there were no reliable indicators of infection, some suggestive clues emerged. Serum glucose and leukocyte abnormalities, anemia, uremia, and bradycardia were often identified. In addition to Staphylococcus and Streptococcus, the predominant organisms were Haemophilus and Enterobacteriaceae. Lung infections, usually in the right upper lobe, were reported in many hypothermic infants by El-Radhi and colleagues.79 Evaluation of the gastric aspirate was another diagnostic predictor of sepsis in the majority of infected infants. In several studies, sepsis was found in a large percentage of hypothermic infants. In this age-group, empirical broad-spectrum antibiotics are warranted. In adults, the incidence of infection ranges from less than 1% to over 40%, depending on patient selection criteria.58 In the urban series of Lewin and co-workers,214 serious soft tissue or pulmonary infections were present in one-half the patients. Occult bacteremia was present in less than 1% of White’s series363 of 102 patients, and results were negative in all of the 46 lumbar punctures. In other studies of hypothermic older adult patients admitted to hospitals, most have had evidence of probable or definite infections.60 In summary, unlike children and older adults, most previously healthy young adults do not need empirical antibiotic prophylaxis. Nevertheless, treatment indications should be liberalized from normothermia. They should include failure to rewarm, and any suspicion or evidence of aspiration, myositis, chest film infiltrate, bacteriuria, or persistent altered mental status. In choosing broad-spectrum coverage, the physician should consider altered drug interactions, volumes of distribution, protein binding, hepatic metabolism, and renal excretion.

Forensic Pathology Macromorphologic and micromorphologic lesions are variable and nonspecific in hypothermia, and there is no single pathognomonic finding at autopsy.216,280,339 Establishing hypothermia as the primary cause of death requires an adequate history of exposure and the absence of other lethal findings at necropsy.5,161 Unnatural deaths in nursing home patients, for example, may be significantly underreported for these reasons.49 Macroscopic skin changes can suggest the diagnosis. Hyperemia of the dorsa of the hands and knees is commonly found. Nonpathognomonic findings have been identified in the pancreas, lungs, and heart. Pancreatic findings include fat necrosis, aseptic pancreatitis, and hemorrhage. Pulmonary changes consist of intra-alveolar, interstitial, and intrabronchial hemorrhages. An eye that has been directly exposed to the environment could be a chemical indicator of both the environmental and victims temperatures at the time of death. Vitreous humor chemistry profiles at autopsy can reveal that glucose concentration and total carbon dioxide content vary inversely with temperature, with 141

CHAPTER 5  Accidental Hypothermia

BOX 5-11  Antiarrhythmic Characteristics

PART 2  COLD AND HEAT

To function optimally “as the water stiffens” requires an understanding of the principles of heat conservation and loss.176 Welltrained and educated urban adults can participate in prolonged Arctic maneuvers safely.310,311,333 To maintain core temperature in the narrow band necessary for peak functioning in cold environments, appropriate adaptive behavioral responses are essential.145 Autonomic and endocrinologic mechanisms are only supplemental. Studies of human cold adaptation reach highly variable conclusions. Explanations for these discrepancies include changes in core and shell temperatures and in metabolic rates before and after cold adaptation. Hypothermic, insulative, isometabolic cold adaptation may be associated with local cold adaptation of the extremities.375 Excellent physical conditioning with adequate rest and nutrition is paramount.26 Hikers and skiers must be accompanied by a partner and should wear effective thermal insulation. Wet inner garments must be changed promptly. Persons who exert themselves, including long-distance skiers, should switch garments depending on current exertional heat production.146,148 Because dehydration must be avoided, drinking from a cold stream is preferable to snow ingestion. Significant energy is needed to convert ice at 0° C (32° F) into water. All areas with a large surface area–to–volume ratio should be well insulated.331 Excellent synthetic insulating materials include Gore-Tex, Flectalon, Thinsulate, and taslanized nylon. Under certain circumstances, insidious hypothermia may develop during exposure to cold water because of the effects of increased insulation on compensatory physiologic events.12,177 The army mnemonic COLD, in reference to insulation with clothing, means clean, open during exercise to avoid sweating, loose layers to retain heat, and dry to limit conductive heat losses. For a complete discussion of preventive measures, see Chapters 8 and 9. Prevention of urban accidental hypothermia requires continuous public education. For example, the optimal safe indoor temperature recommendation for older adults has risen to 21.1° C (70° F). Energy assistance and temporary sheltering are effective measures, and selective heating of sleeping quarters and use of electric blankets are economic suggestions. Prewarming the bed and bedroom at night may be the best overall advice to older adults.

are warm and dead.”248 Clearly, some victims are indeed “cold and dead,” and it would be useful to safely identify them.10 Survival is difficult to predict because human physiologic responses to temperature depression vary so widely.236,240,273 The type and severity of the underlying or precipitating disease process are two determinants.346 Age extremes, although not statistically correlated with survival, are commonly associated with severe illnesses. In a multicenter survey, however, there were no significant age differences in mortality.59 Gender, trauma, infection, and toxin ingestions affected survival differently in multiple, uncontrolled clinical studies.141 There were no clinically significant differences in male versus female profiles in the multicenter survey.59 From a large hypothermia database, a hypothermia outcome score could enable multiple observers at different sites to assess treatment modalities and outcome predictors.291 Prehospital cardiac arrest, low or absent blood pressure reading, elevated BUN, and the need for either endotracheal or nasogastric intubation in the ED were significant predictors of outcome after multivariate analysis.55,179 In a multiple regression analysis of 234 cases in Swiss clinics,221 the biggest negative survival factors were asphyxia, slow rate of cooling, invasive rewarming, asystole, and development of pulmonary edema or adult respiratory distress syndrome. The largest single-hospital series of adult hypothermic cardiac arrest patients rewarmed with CPB is reported from Finland. Patients with cold exposure or immersion without suffocation or asphyxia tolerated prolonged CPR before CPB.314 Positive predictors of survival include rapid cooling rate, presence of VF during cardiac arrest, and narcotic or ethanol intoxication. In a study of 29 patients below 30° C (86° F), mode of cooling was the only independent risk factor.273 In a study of CPB survivors, 15 of the 32 patients are longterm survivors.355 Their neuropsychological functioning after prolonged prehospital circulatory arrest is very encouraging. These patients were not asphyxiated before becoming hypothermic. Vretenar and colleagues352 reviewed the literature regarding the outcomes of 68 other patients resuscitated with CPB. The survival rate was 60%, and the coldest survivor had been 15° C (59° F). In a series of 26 patients given extracorporeal rewarming, those with nonasphyxiated deep accidental hypothermia had a reasonable prognosis.86 There is a need for a valid triage marker of death, because vital organ damage is difficult to predict. In one retrospective analysis of primarily avalanche burial victims, extreme hyperkalemia was noted on initial examination, and resuscitation proved fruitless.296 In the Mt Hood tragedy, the nonsurvivors were also hyperkalemic (serum potassium level greater than 10 mmol/L).127 Although a serum potassium level of 10 mmol/L appears to be a reasonable ceiling for viability, a child at 14.2° C (57.6° F) with a potassium level of 11.8 mmol/L did well.70 In both of these reports, asphyxia and compression injury may have been contributory. Other indicators of a grave prognosis include a core temperature below 12° C (53.6° F), arterial pH below 6.5, or evidence of intravascular thrombosis (direct visualization; fibrinogen below 50 mg/dL).

Outcomes

REFERENCES

Partially in reaction to the dramatic reports of reanimations, the historic standard of care has been that “no one is dead until they

Complete references used in this text are available online at www.expertconsult.com.

values significantly higher in the winter. An elevated vitreous glucose in a nondiabetic victim should suggest hypothermia. The total urinary catecholamine, particularly epinephrine, content was high in one group of casualties known to be hypothermic. Erosions of the gastric mucosa, termed Wischnewsky spots, are also frequently found.330,338,371 In addition, exposure to extreme cold should be suspected when unusual intravascular hemolysis, which is seen after freezing of blood, is observed in a corpse. Fatty degeneration in renal tubule epithelia may help confirm the diagnosis.279

PREVENTION

142

CHAPTER 6 



Immersion Into Cold Water GORDON G. GIESBRECHT AND ALAN M. STEINMAN

The authors of this chapter hail from two different countries that view and measure temperature differently. The United States uses ° F (Fahrenheit), whereas the country up north uses ° C. (Some people think that the letter C stands for “Celsius,” but it actually means “Canadian.”) The author from up north has provided a conversion chart to allow neighbors from either side of the border to get on the same thermal wavelength (Box 6-1). Immersion in cold water is a hazard for anyone who participates in recreational, commercial, or military activities in the oceans, lakes, and streams of all but the tropical regions of the world. Recreational aquatic activities include swimming, fishing, sailing, power boating, ocean kayaking, white-water rafting, canoeing, ocean surfing, windsurfing, waterskiing, diving, hunting, and using personal watercraft. In addition, winter activities like driving on icy roads and snowmobiling can involve cold-water exposure as a result of accidental entry into lakes and streams.1 Commercial activities that involve water include fishing, shipping, offshore oil drilling, and diving. Military operations over cold water include Coast Guard (Figure 6-1), Navy, and Marine Corps missions. Army, Air Force, and Marine Corps forces may encounter cold-water exposure during winter operations on land. The definition of cold water is variable. The temperature of thermally neutral water, at which heat loss balances the heat production of a nude subject at rest (i.e., not shivering), is approximately 33° to 35° C (91.4° to 95° F).16,18 Hypothermia eventually results from immersion in water at less than this temperature. For practical purposes, significant risk for immersion hypothermia usually begins in water colder than 25° C (77° F),114,162,163 and it is quite significant in water colder than 15° C BOX 6-1  The Official Canadian Temperature

Conversion Chart

10° C (50° F) Americans shiver uncontrollably. Canadians plant gardens. 0° C (32° F) American water freezes. Canadian water gets thicker. −18° C (0° F) New York City landlords finally turn on the heat. Canadians have the last cookout of the season. −51° C (−60° F) Mt St. Helens freezes. Canadian Girl Guides sell cookies door to door. −114° C (−173° F) Ethyl alcohol freezes. Canadians get frustrated when they can’t thaw the keg. −273° C (−460° F) Absolute zero; all American atomic motion stops. Canadians start saying, “Cold, eh?” −295° C (−500° F) Hell freezes over. A U.S. hockey team beats Canada in the Olympic gold medal game.

(59° F). Table 6-1 shows the variation in water temperature throughout the year at various sites in North America.180 Figure 6-2 shows typical worldwide sea-surface temperatures for April, with data from 2005.126 With the use of 25° C (77° F) as the defining point for cold water, the risk of immersion hypothermia in North America is nearly universal during most of the year. Cold-water immersion is associated with two significant medical challenges: near drowning and hypothermia. This chapter discusses the physiologic responses to and treatment of immersion hypothermia, the risk of near drowning with respect to the physiologic consequences of sudden immersion in cold water, and the problems of survival in rough seas. Controversies are also identified and discussed. Chapter 5 discusses land-based hypothermia; Chapter 75 provides a more complete discussion of drowning; and Chapter 77 discusses diving injuries. Since the previous edition of this textbook was published, many audiovisual resources have been produced; several are listed in the Video Resources section at the end of this chapter.

History and Epidemiology The history of human association with the sea and with inland waters provides abundant examples of the effects of accidental cold-water immersion. Case studies demonstrate the scope of the problem. Perhaps the most famous occurrence was the sinking of the Titanic in 1912. After striking an iceberg at approximately 11:40 PM on April 14, the ship sank in calm seas, but the water temperature was near 0° C (32° F). Of the 2201 people on board, only 712 were rescued, all from the ship’s lifeboats. The remaining 1489 people died in the water, despite the arrival of a rescue vessel within 2 hours. Nearly all of these people were wearing “life preservers,” yet their causes of death were officially listed as drowning.119 However, it is more likely that their deaths were caused by immersion hypothermia. Survivors reported hearing victims’ screams for periods long enough (i.e., more than 1 hour) to indicate that the individuals in the water survived for a period of time sufficient to result in severe hypothermia.102,110

FIGURE 6-1  Canadian Coast Guard rescue boat in rough seas. (Courtesy Canadian Coast Guard.)

For online-only figures and videos, please go to www.expertconsult.com

143

PART 2  COLD AND HEAT

RECREATIONAL ACTIVITIES AND COLD WATER

Case 6-3  “SKATING” ON THIN ICE

A Canadian Red Cross Report stated that, from 1991 to 2000, there were 5900 water-related deaths in Canada. Two hundred and eighty-three (21%) of recreational boating drownings occurred in “extremely cold” water, which means that it was colder than 10° C (50° F). Of the 14% of all boating drownings in which the victims were wearing personal flotation devices (PFDs), most of these occurred in cold water, and death resulted from hypothermia. Of note is that 232 snowmobilers drowned after breaking through the ice, and 218 individuals died after falling through the ice during other activities. Cases 6-1 to 6-4 illustrate potential problems that might occur with immersion hypothermia during recreational boating, hiking, snowmobiling and other activities.

In the winter of 1997-1998, four people died when their snowmobile broke through the thin ice of Lake Scugog, which is near Toronto, Ontario, Canada. The deaths occurred, ironically, during Snowmobile Safety Week in North America. The Canadian Safety Council reported that, in 1997, 101 people were killed in snowmobile mishaps, the majority of them by drowning and hypothermia after crashing through ice on frozen rivers and lakes.1

Case 6-1  LONGTERM IMMERSION IN MODERATELY COLD WATER On February 28, 2009, four friends who were all former or current football players in their mid-twenties set out on a fishing trip in a 21-foot boat into the Gulf of Mexico west of Tampa Bay, Florida. According to the survivor’s account,148 their boat capsized in a storm before they could return to shore, and the four men were thrown into the 18° C (65° F) water. Weather conditions were 4.3-m (14-foot) seas and 15 to 18 m/sec (30 to 35 knot) winds. None of the men were wearing PFDs at the time of the capsizing. One of the survivors dove under the boat to retrieve three keyhole PFDs and one seat cushion. Despite their large size (≈190 cm [74.8 inches] tall and ranging from 98 to 120 kg [216 to 265 lb] in weight) and high level of muscle mass and physical fitness, the men all developed hypothermia as a result of the combination of a low level of body-fat insulation, the cold water temperature, the effect of the wind on their wet clothing, and the strenuous work to remain on the boat or to get out of the water. Two victims died after about 13 hours, a third died after 25.5 hours, and the lone survivor was rescued after 43 hours by the U.S. Coast Guard. The first casualty was the lightest (≈98 kg [216 lb]) and wore only swimming trunks and a keyhole PFD; he had discarded his t-shirt, wind pants, and jacket to try to dive under the boat for supplies. The second casualty, who died at about the same time, was the heaviest (≈120 kg [265 lb]), but he had spent far more time immersed in the water than the others had. The third casualty survived another 12 hours, but he perished nearly 18 hours before the lone survivor was rescued. That casualty had also taken off his wind jacket and pants, which were later lost, so that he could dive under the boat. During the first 13 hours, he struggled to help the other victims while he was in the water, and he had little insulation from the seat cushion, which he wore on his back; he later switched to the keyhole PFD that had been worn by the first casualty. These early conditions likely put him behind the survival curve of his remaining companion. The survivor (≈109 kg [240 lb]) had the double advantage of less direct water exposure (he spent more time positioned on top of the boat, often holding onto the motor) and more insulation (i.e., sweatpants, sweatshirt, water-resistant and fleece-lined hooded coat, skullcap, and gloves). He had a core temperature (Tco) of 31.9° C (89.5° F) after 43 hours at sea (Figure 6-3, online). This case will be referenced throughout this chapter. Case 6-2  PANIC IN ICE WATER In February 1990, four teenage boys broke through the ice on Convict Lake in California. After one boy escaped and summoned help, a series of adults—including two lay and three professional rescuers—approached and also broke through the ice. It was not until a properly equipped rescue team arrived “that a safe rescue attempt could be made … on one lone adult. In just fifteen minutes, three boys and four of their five adult rescuers were dead.”48 Despite the common belief at the time, the victims did not perish as a result of hypothermia but rather from cold- and panic-induced incapacitation and drowning. 144

Case 6-4  PROBLEMS WITH COLD-WATER RESCUE In the winter of 1988, two men died of hypothermia when their nine-man rowing scull sank during a winter storm on a small lake in western Canada. The nine rowers were immersed in 4° C (39.2° F) water. They struggled to hang on to their overturned vessel in 0.6 to 1.0 m (1.97- to 3.28-foot) waves and 30 km/hr (18.7 mph) winds for more than 50 minutes before rescuers could reach them. One man drowned just before rescue; the others were all conscious when they were pulled from the water. However, during the 13-minute boat transport to shore, three of the thinnest victims lost consciousness, and one of these men suffered cardiopulmonary arrest. His Tco in the hospital 44 minutes after rescue was 23.4° C (74.1° F); subsequent resuscitation efforts were unsuccessful. The remaining seven survivors were resuscitated from Tcos of as low as 25° C (77° F). This case illustrates the rapidity of onset of immersion hypothermia in lean subjects and the potentially serious consequences of cardiovascular instability, circumrescue collapse, and post-rescue Tco afterdrop in individuals with immersion hypothermia (see Physiologic Responses to Cold-Water Immersion with the Head Above Water, later).58 Case 6-5  DANGERS OF FISHING IN COLD WATER In December 2004, the fishing vessel Northern Edge capsized near Nantucket, Massachusetts, in 4° C (39.2° F) water and 3- to 4-m (9.84- to 13.12-foot) seas. Five of the six crewmembers lost their lives.184 In several similar cases in the same region, seven fishermen on three different vessels lost their lives during a 30-day period in the winter of 2004-2005.181 In June 2003, the charter fishing vessel Taki Tooo, which was carrying 17 passengers and crew, capsized in the turbulent waters of the Tillamook River bar on the Oregon coast, with the loss of 11 lives. The water temperature was 10° C (50° F).183 In April 2001, the fishing vessel Arctic Rose sank in the Bering Sea of Alaska, with a loss of 15 crewmembers.184 The vessel sank so quickly that there was no time for either a distress call to be made or for the crewmen to don survival suits. Case 6-6  COLD-WATER FISHING FATALITIES A 1999 U.S. Coast Guard Fishing Vessel Casualty Task Force Report181 found that, in just 2 months (December 1998 and January 1999), 20 commercial fishing vessels were lost at sea. During these mishaps, 21 persons on board died, mainly from exposure to cold water as a result of the vessel sinking or capsizing or from persons falling overboard. From 1994 to January 1999, U.S. Coast Guard statistics show that 396 fishermen lost their lives while fishing. Of these, 298 died from cold-water immersion as a result of falling overboard or of the vessel sinking, capsizing, or flooding. In 1998, the death rate for fishermen was 179 per 100,000 workers; this is 16 times higher than the rates for firefighters and police officers.

COMMERCIAL ACTIVITIES ON COLD WATER Numerous examples of maritime occupational accidents exist. In 1982, the offshore mobile oil-drilling platform Ocean Ranger collapsed in mountainous seas near Newfoundland, Canada; the water temperature was −1° C (30.2° F). Eighty-four workers were plunged into the water, and, despite the presence of a rescue vessel, all of them died. Immersion hypothermia was a significant factor in these deaths, although the inabilities of the workers to

0 7 4 11 14 10 21 17 3 2 26 24

Kodiak, Alaska Victoria, British Columbia Astoria, Oregon San Francisco, California San Diego, California Mobile, Alabama Miami, Florida Norfolk, Virginia Cape May, New Jersey Traverse City, Michigan Puerto Rico Honolulu, Hawaii

0 7 5 11 14 10 21 16 3 1 26 24

(32) (44.6) (41) (51.8) (57.2) (50) (69.8) (60.8) (37.4) (33.8) (78.8) (75.2)

February 2 (35.6) 7 (44.6) 7 (44.6) 12 (53.6) 15 (59) 14 (57.2) 23 (73.4) 15 (59) 5 (41) 1 (33.8) 26 (78.8) 24 (75.2)

March 4 (39.2) 9 (48.2) 10 (50) 12 (53.6) 16 (60.8) 21 (69.8) 25 (77) 18 (64.4) 10 (50) 1 (33.8) 26 (78.8) 24 (75.2)

April 7 (44.6) 10 (50) 13 (55.4) 12 (53.6) 17 (62.6) 23 (73.4) 27 (80.6) 20 (68) 14 (57.2) 1 (33.8) 26 (78.8) 25 (77)

May 9 (48.2) 11 (51.8) 16 (60.8) 12 (53.6) 18 (64.4) 28 (82.4) 29 (84.2) 24 (75.2) 19 (66.2) 3 (37.4) 27 (80.6) 25 (77)

June 12 11 19 13 20 29 30 26 23 5 27 26

(53.6) (51.8) (66.2) (55.4) (68) (84.2) (86) (78.8) (73.4) (41) (80.6) (78.8)

July 12 11 21 13 20 29 30 26 23 10 27 26

(53.6) (51.8) (69.8) (55.4) (68) (84.2) (86) (78.8) (73.4) (50) (80.6) (78.8)

August 10 11 17 12 20 27 29 25 21 10 28 27

(50) (51.8) (62.6) (53.6) (68) (80.6) (84.2) (77) (69.8) (50) (82.4) (80.6)

September 7 10 13 12 18 23 27 25 17 6 27 26

(44.6) (50) (55.4) (53.6) (64.4) (73.4) (80.6) (77) (62.6) (42.8) (80.6) (78.8)

October 4 9 9 11 16 19 25 21 11 5 27 25

(39.2) (48.2) (48.2) (51.8) (60.8) (66.2) (77) (69.8) (51.8) (41) (80.6) (77)

November

2 8 5 11 15 14 23 21 6 4 26 25

(35.6) (46.4) (41) (51.8) (59) (57.2) (73.4) (69.8) (42.8) (39.2) (78.8) (77)

December

FIGURE 6-2  Worldwide sea surface temperatures for April 2005. (From the National Center for Environmental Prediction, Space Science and Engineering Center, University of Wisconsin–Madison. http://www.ssec.wisc.edu/data/sst/latest_sst.gif.)

Temperatures of <25° C (77° F) are noted in red.

(32) (44.6) (39.2) (51.8) (57.2) (50) (69.8) (62.6) (37.4) (35.6) (78.8) (75.2)

January

Site

TABLE 6-1  Mean Water Temperatures in ° C (° F)

CHAPTER 6  Immersion Into Cold Water

145

PART 2  COLD AND HEAT

suits, inflatable life rafts) is primarily a response to the needs of people who work in cold-water environments. The value of various types of protective clothing is examined later in this chapter.

VEHICULAR ACTIVITIES ON ICE

FIGURE 6-4  Sinking fishing vessel. (Courtesy U.S. Coast Guard.)

combat rough seas and to maintain airway freeboard (i.e., the distance between the water surface and the mouth) were also major problems.127 Fishing vessel mishaps are a common cause of immersion hypothermia. Cases 6-5 to 6-6 illustrate the problems that face the commercial fishing industry (Figure 6-4).

MILITARY ACTIVITIES AND COLD WATER The extensive use of combat ships and aircraft in World War II, particularly in the north Pacific and north Atlantic oceans, provided many examples of accidental immersion in cold water. Molnar reviewed several hundred of these cases.124 Among them was the following: “A ship was rammed, and it sank in 3 minutes. Thirty survivors were picked up from rafts after exposure of 1.5 to 4 hours. Some drowned and others died of exposure because the water was 4° C (7.2° F) with high seas and a wind velocity of scale 7. Some of the survivors who held on to ropes couldn’t let go and rescuers had to cut frozen rope to release them. It appears miraculous how the survivors could have endured such cold water. Most of those who were rescued were in an unconscious state and, when they became conscious, complained of numbness of extremities and hands.” The Falklands War in 1982 provided further examples of immersion hypothermia related to naval combat. The Argentinian cruiser General Belgrano sank in approximately 5° C (9° F) water, which resulted in the deaths of many sailors. Some of the deaths from cold occurred even after the sailors had managed to emerge from the water into life rafts. Maritime military operations are not the only source of hypothermia casualties in the armed forces; land operations, either during combat or training, also have immersion hypothermia risks. In March 1995, four U.S. Army Rangers died and four others were hospitalized during a training mission in a Florida swamp. The water at the exercise site was deeper and colder than was customary for this exercise. Consequently, the Rangers were forced to spend more than 6 hours in cold and wet conditions, much of the time partially immersed in the 15° C (59° F) water. Night conditions and difficulties encountered during the medical evacuation of the accident victims contributed to the hypothermia deaths.17,186 In March 2001, two U.S. Coast Guard crewmen drowned after immersion in cold water, when their four-man vessel capsized in the waves of the Niagara River bar in Lake Ontario. The water temperature was 2° C (3.6° F). All of the crewmen were wearing dry suits with insulation as well as PFDs, but they were without insulated headgear. They left the boat to swim towards a buoy. Vigorous swimming caused water intrusion into two of the dry suits, as did the coxswain’s use of a neck ring device before capsizing. This leakage resulted in severe immersion hypothermia and subsequent drowning.182 The relatively high fatality rate from accidental immersion in cold water in various military, commercial, and recreational settings has stimulated technologic advances in protective clothing and rescue devices. The current availability of commonplace items of survival equipment (e.g., wet suits, dry suits, survival 146

Motor vehicle submersions account for approximately 10% of all drownings, including approximately 400 fatalities in North America each year.177,201 Although most of these deaths occur in open water during spring, summer, or fall, many also occur during the winter, when vehicles break through the ice while traversing either makeshift (e.g., ice fishing) or official (e.g., winter roads) transport routes. In 2005, a heavy machine operator was maintaining an icy road when his snowplow broke through the ice, and he drowned.91 The ice-cold water temperature was cited as a contributing factor to his death. In summary, numerous case histories and statistical evidence document the significance of cold-water immersion as a cause of the environmental emergencies of drowning and hypothermia. Although drowning is relatively easy to prevent (e.g., with the use of PFDs, water safety training, and the restriction of alcohol use), hypothermia is not easy to prevent. Hypothermia is now more widely recognized than in the past, but the prevention of immersion hypothermia is still a difficult and often expensive proposition. Therefore, in regions with cold water (which includes most of the North American continent), cold-water safety, knowledge of cold-water risks, and the use of appropriate flotation and protective clothing are essential.

Physiologic Responses to Cold-Water Immersion With the Head Above Water The effect of sudden cold-water immersion on humans is poorly understood by the general public as well as by medical and rescue personnel. Many individuals believe that an individual who falls into ice water will die of hypothermia within minutes, even if that person is dressed in winter clothing. In a series of surveys of continuing medical education attendees,47 75% of respondents felt that, under these conditions, a victim would experience life-threatening hypothermia in less than 30 minutes. As discussed later in this chapter, most adults can survive for an hour or more if they take appropriate action. The improper assumption of rapid and impending death only serves to induce panic, poor decisions, and exhaustion as a result of thrashing about, thereby causing problems for both primary victims and for the persons trying to rescue them. The primary pathophysiologic effects of hypothermia are a decrease in tissue metabolism and the gradual inhibition of neural transmission and control. However, during the initial stages of cooling of an intact and conscious victim, secondary responses to skin-temperature cooling predominate. Sudden immersion in cold water results in an immediate decline in skin temperature, which, in turn, initiates shivering thermogenesis with increases in metabolism, ventilation, heart rate, cardiac output, and mean arterial pressure. As body temperature declines and shivering ceases, metabolism, heart rate, mean arterial pressure, and cardiac output decrease proportionally with the fall in Tco, whereas hematocrit and total peripheral resistance increase. Renal diuresis and extravascular fluid shifts can lead to a considerable loss of intravascular volume, thus decreasing systemic perfusion. A more detailed description of the pathophysiologic effects of systemic hypothermia is provided in Chapter 5: Accidental Hypothermia. The following section pragmatically describes the effects of the pathophysiologic changes that accompany cold-water immersion and the impact of these changes on survival. The body’s responses and mechanisms of death during coldwater immersion can be divided into four phases: (1) initial immersion and the cold shock response; (2) short-term immersion and the loss of performance; (3) long-term immersion and the onset of hypothermia; and (4) circum-rescue collapse just before, during, or after rescue. Each phase is accompanied by specific survival hazards for the immersion victim that originate

PHASE 1: THE COLD SHOCK RESPONSE (0 TO 2 MINUTES) The cold shock response occurs within the first few minutes of cold-water immersion and depends on the extent and rate of skin cooling. The responses are generally those that affect the respiratory system, heart, and the body’s metabolism (Figure 6-5).36,175 Rapid skin cooling initiates an immediate gasp response, an inability to hold one’s breath, and hyperventilation. The gasp response may cause drowning if the head is submersed during the initial entry into cold water. The subsequent inability to hold one’s breath may further potentiate drowning in high seas. Subsequent hyperventilation will normally diminish within seconds to minutes, but it could be increased and exaggerated indefinitely as a result of emotional stress and panic. Uncontrolled hyperventilation can cause numbness, muscle weakness, or fainting, which may lead to drowning. Any of these respiratory responses can

lead to pulmonary aspiration of water. Panic may ensue, with subsequent drowning. These responses may be viewed on several video links listed in the Video Resources section at the end of this chapter. Skin cooling initiates peripheral vasoconstriction as well as increased cardiac output, heart rate, and arterial blood pressure. Increased workload on the heart may lead to myocardial is­ chemia and arrhythmias, including ventricular fibrillation. Sudden death can occur either immediately or within a matter of minutes after immersion as a result of syncope or convulsions, which can lead to drowning, vagal cardiac arrest, or ventricular fibrillation in susceptible individuals.* Cold shock can occur in water colder than 20° C (68° F), with symptoms increasing as water temperature decreases to freezing. Staged entry into cold water attenuates respiratory responses because of a gradual increase in thermal stimulation. The best advice to combat this phenomenon is, when possible, to control entry into cold water by entering slowly and most importantly by *References 23, 44, 103, 118, 167.

FIGURE 6-5  Possible cold shock responses. ↑, Increase; ↓ decrease. (From Edmonds C, Lowry C, Pennefather J: Cold and hypothermia. In Diving and subaquatic medicine, Oxford, UK, 1992, Butterworth-Heinemann.)

RAPID SKIN COOLING STIMULATION OF PERIPHERAL RECEPTORS

GASP REFLEX AND HYPERVENTILATION

HYPOCAPNIA

PERIPHERAL VASOCONSTRICTION

↑ HYPERTENSION (arterial and venous pressure)

INABILITY TO HOLD BREATH

Respiratory alkalosis

↑ Filling pressure

↑ Cardiac output

Inspiratory shift

Ventricular fibrillation

↓ Cerebral blood flow

TACHYCARDIA

↑ WORK OF HEART

Vessel rupture

↓ Coronary blood flow

↓ Serum and body fluid Ca2+

Dyspnea

Cerebrovascular accident

Tetanic spasms Convulsions

↑ Ventricular irritability

Panic Cerebral hypoxia

Arrhythmias/ ventricular fibrillation

Swim failure Disorientation Loss of consciousness

Myocardial ischemia

INHALATION OF WATER

Stimulation of nasal and glottal receptors

Drowning

Vagal arrest

147

CHAPTER 6  Immersion Into Cold Water

from or are influenced by a variety of pathophysiologic mechanisms. Deaths have occurred during all four phases of immersion.

Ventilation volume (liters • min–1)

execute a plan of action: (1) try to enter the water without submersing the head; (2) escape (i.e., pull oneself out of the water, inflate, and board a life raft); (3) minimize exposure (i.e., get as much of one’s body as possible out of the water and onto a floating object); (4) ensure flotation if one must remain in the water (i.e., don or inflate a PFD); and (5) call for assistance (i.e., activate signaling devices). It may be difficult to execute these actions when cold shock responses predominate. However, after respiratory effects are under control, immediate action should be taken. If self-rescue is not possible, actions to minimize heat loss should be initiated by remaining as still as possible in the heat escape lessening position (HELP), in which the arms are pressed against the chest while the legs are pressed together, or by huddling with other survivors (Figure 6-8, online).86 Drawstrings should be tightened in clothing to decrease the flow of cold water within clothing layers. Many of these responses can be viewed on several video links in the Video Resources section at the end of this chapter.

Non-staged

60 50 40 30 20

Staged

10 0

Respiratory frequency (breaths • min–1)

PART 2  COLD AND HEAT

70

50

PHASE 3: ONSET OF HYPOTHERMIA (IMMERSION OF MORE THAN 30 MINUTES)

Non-staged

45 40 35 30 25 20

Staged

15 –20

0

30

60

90

120

150

180

Immersion time (s) FIGURE 6-6  Respiratory responses (minute ventilation and respiratory rates) to sudden and graded immersion into cold water. (From Hayward JS, French CD: Hyperventilation response to cold water immersion: Reduction by staged entry, Aviat Space Environ Med 60:1163, 1989.)

keeping the head from being submersed. One should never dive into cold water! After cold-water immersion, it is important to focus on surviving the first minute by not panicking and by consciously getting one’s breathing under control. Figure 6-6 shows that minute ventilation and breathing frequency increase dramatically with rapid immersion in cold water. These responses are blunted by more than 50% with graded immersion.

PHASE 2: COLD INCAPACITATION (5 TO 15 MINUTES) For those who survive the cold shock response, significant cooling of peripheral tissues—especially in the extremities— continues, with most of the effect occurring during the first 15 minutes of immersion. This cooling has a direct deleterious effect on neuromuscular activity.186 This effect is especially significant in the hands, where blood circulation is negligible,34 which leads to finger stiffness, poor coordination of gross and fine motor activity, loss of power,* and swim failure (Figure 6-7, online). It has been shown that this effect is primarily the result of peripheral rather than central cooling.63 The loss of motor control makes it difficult if not impossible to execute survival procedures, such as grasping a rescue line or hoist. The ultimate cause of death is drowning, either through the failure to initiate or maintain survival performance (i.e., keeping afloat, swimming, or grasping onto a life raft) or excessive inhalation of water under turbulent conditions. These phenomena have obvious survival implications. It is of course advisable to avoid cold-water exposure completely. If cold-water immersion occurs, it is best to quickly determine and *References 40, 51, 133, 134, 191.

148

Most cold-water deaths likely result from drowning during the first two phases of cold-water immersion, as discussed previously. In general, true hypothermia usually only becomes a significant contributor to death if immersion lasts more than 30 to 60 minutes. A recent survey indicates that even medical practitioners greatly underestimate the time required for a person to become hypothermic in cold water.47 In fact, 75% of respondents felt that a properly clothed adult would become hypothermic after less than 15 minutes in ice water (0° C [32° F]) (Figure 6-9, online). An individual who survives the immediate and shortterm phases of cold-water immersion faces the possible onset of hypothermia, because continuous heat loss from the body eventually decreases Tco. Many predictive models to determine the Tco response to cooling are based on the relationships between body composition, thermoregulatory response (i.e., shivering thermogenesis), clothing and insulation, water temperature, and sea conditions (see Cold-Water Survival, later).* Even in ice water, a victim may not drown when he or she becomes unconscious as a result of hypothermia (≈30° C [86° F]) if a PFD is worn or if some other factor prevents the need for vigorous exercise to prevent drowning. If the head is kept above water, the victim could still survive for up to 1 hour before the heart stops as long as the sea is relatively calm and waves do not wash over the mouth. It is important for members of the public to be educated about the fact that they are not necessarily going to die if they are suddenly immersed in cold water (Box 6-2). The relative contributions of the first three phases to death in cold water of varying temperatures are estimated schematically in Figure 6-10. In colder water, if no flotation is worn (top panel), death occurs as a result of cold shock or cold incapacitation. Only if flotation is worn (bottom panel) will a victim survive long enough to die as a result of hypothermia (Box 6-3). BOX 6-2  The 1-10-1 Principle If you fall into ice-cold water, remember that you have   1 minute—10 minutes—1 hour.* • You have 1 minute to get your breathing under control, so don’t panic. • You have 10 minutes of meaningful movement to get out of the water or to attain a stable situation. • You have up to 1 hour until you become unconscious from hypothermia if you don’t panic or struggle unnecessarily. If you are wearing a PFD, you may have another hour until your heart stops beating as a result of hypothermia. *Times are subject to individual variability and factors such as body size, water temperature, and amount of the body immersed.

*References 90, 163, 197, 202, 207.

Relative contribution to death (%)

100.0 90.0 80.0 70.0 Cold incapacitation Cold shock Hypothermia

60.0 50.0 40.0 30.0 20.0 10.0 0.0 0

5

A

10

15

20

Water temperature (° C) CAUSE OF DEATH (WITH FLOTATION)

Relative contribution to death (%)

100.0 90.0 80.0 70.0 60.0

Cold incapacitation Cold shock Hypothermia

50.0 40.0 30.0 20.0 10.0 0.0 0

B

5

10

15

20

Water temperature (° C)

FIGURE 6-10  Estimation of the relative contributions of cold shock, cold incapacitation, and hypothermia to death in water at different temperatures. A, Estimation if no flotation is available. B, Estimation if flotation is available.

PHASE 4: CIRCUM-RESCUE COLLAPSE Anecdotal cases of fatalities among immersion hypothermia victims have been noted during the immediate pre- and postrescue periods, despite the survivor being recovered in an apparently stable and conscious condition. The hypothermic victim may experience symptoms that range from fainting to cardiac arrest. These events are often referred to as cases of “rewarming shock” or “post-rescue collapse.” Golden and colleagues73 noted that deaths can occur either shortly before rescue, during rescue, or after rescue, and they have used the term circum-rescue collapse to describe these events. Deaths have occurred within minutes before rescue, while climbing out of the water, while BOX 6-3  Controversy Box: Time to Hypothermia Most people greatly underestimate the amount of time required to become hypothermic in very cold water. This is important, because if a victim thinks that hypothermia will set in very quickly, panic is more likely. A proper understanding of the fact that cold shock is initially the greatest threat will help the victim to focus more on controlling the gasp reflex and to get control of his or her breathing.

being hoisted onto a helicopter, within a few minutes of entering a warm compartment of a rescue vessel, 20 to 90 minutes after rescue, in a hospital after transport, and during the 24-hour period after rescue.71,73,100,116 Three causes of circum-rescue collapse have been proposed: (1) afterdrop, which is a continued drop in Tco after recovery; (2) collapse of arterial pressure (Figure 6-11, online); and (3) factors that potentiate the risk of ventricular fibrillation (e.g., hypoxia, acidosis, rapid changes in pH). These causes are discussed further later in this chapter. When rescue is imminent, mental relaxation and the decreased output of stress hormones may result in a drop in blood pressure, which may cause fainting and drowning. The act of rescue itself may also cause sudden collapse. Pulling a victim out of the water in a vertical position removes hydrostatic squeeze around the lower limbs and may cause blood pooling in these extremities, with subsequent decreased blood pressure. Extra cardiac work or rough handling may induce reflex cardiac arrest of the cold heart. Afterdrop is a well-known phenomenon that occurs after the removal of a victim from cold-water immersion. Tco continues to decline (i.e., afterdrop) in both animate and inanimate objects, although cold-water immersion has ended.* Afterdrop of as much as 5° to 6° C (9° to 10.8° F) has been observed in humans (Figure 6-12, online).6,43,161 This afterdrop was long proposed to be the major cause of post-rescue death, because further cooling of the heart might result in a temperature at which ventricular fibrillation or cardiac arrest could occur.13 Golden and colleagues73 discount the importance of this phenomenon and propose the collapse of arterial pressure as the cause of death during rescue. They correctly point out that after­ drop that occurs in victims who were hypothermic yet warm enough to climb on board a ship without assistance would be unlikely to cause enough myocardial cooling to result in cardiac arrest or ventricular fibrillation. Those clinicians also propose that removal from cold water results in a precipitous fall in blood pressure, inadequate coronary blood flow, and myocardial is­ chemia, which possibly precipitate ventricular fibrillation. This mechanism is likely the main factor in both pre-rescue collapse and collapse that occurs during rescue. A fall in blood pressure before removal from the water may be the result of reduced sympathetic tone or catecholamine secretion when rescue is imminent. Hypotension during and shortly after rescue may be caused by a sudden decrease in hydrostatic pressure on the body (i.e., removal of the hydrostatic squeeze of water pressure that exists during immersion), hypovolemia, or impaired baroreceptor reflexes. However, this mechanism cannot fully account for all of the other post-rescue deaths that occur 20 minutes to 24 hours after rescue. The importance of continued myocardial cooling cannot be discounted. Fibrillation of a cold heart can be initiated by mechanical stimuli, hypoxia, acidosis,131 and rapid changes in pH.101 In dogs, myocardial cooling from 30° to 22° C (86° to 71.6° F) has been shown to cause a five-fold decrease in the electrical threshold for ventricular fibrillation.25 It is also likely that an increase in the rate of myocardial cooling may stimulate fibrillation. On the basis of the large afterdrop values described previously, it is plausible that continued Tco cooling in significantly hypothermic victims could result in ventricular fibrillation, caused primarily by spontaneous fibrillation of the cold myocardium or secondary to a cold-induced increase in sensitivity to other fibrillation stimuli. Finally, death may occur within minutes to hours after rescue. A rescued victim may be severely compromised with cold alkaline or acidic blood in the extremities, a heart that is extremely prone to failure, a decrease in or a loss of consciousness, or low blood volume (hypovolemia). Sudden redistribution of blood to the extremities (especially the lower extremities) may cause collapse as a result of decreased blood pressure and cardiovascular instability, sudden return of metabolic by-products to the irritable heart, or continued decrease in temperature (afterdrop) of an irritable heart. The Tco will continue to drop, and the heart will *References 2, 13, 20, 57, 75, 141, 147, 194.

149

CHAPTER 6  Immersion Into Cold Water

CAUSE OF DEATH IN COLD (NO FLOTATION)

PART 2  COLD AND HEAT

react with profound tachycardia or fibrillation. Up to 20% of persons who are recovered alive die as a result of circum-rescue complications, either before or during rescue, or within hours after rescue.

Factors That Affect Cooling of the Body’s Core Normal body Tco fluctuates around 37° C (98.6° F). The clinical definition of hypothermia is a Tco of 35° C (95° F) or lower; however, any exposure to cold that lowers the Tco to less than a normal level results in the body becoming hypothermic. Although various temperatures and terms have been used to classify different levels of hypothermia, the following classifications (Figure 6-13) will be used here. With mild hypothermia (Tco = 32° to 35° C [89.6° to 95° F]), thermoregulatory mechanisms continue to operate fully, but ataxia, dysarthria, apathy, and even amnesia are likely. With moderate hypothermia (Tco = 28° to 32° C [82.4° to 89.6° F]), effectiveness of the thermoregulatory system (i.e., shivering thermogenesis) diminishes until it fails; there is a continued decrease in the level of consciousness, and cardiac dysrhythmias may occur. With severe hypothermia (Tco <28° C [82.4° F]) consciousness is lost, shivering is absent, acid–base disturbances develop, and the heart is susceptible to ventricular fibrillation or asystole. Death from hypothermia is generally a result of cardiorespiratory failure. If a victim of cold-water immersion can avoid drowning during the initial few minutes after water entry, the prevention of hypothermia becomes an important problem. Survival time in cold water, which is based on the pathophysiologic effects of decreasing Tco, is not a precise calculation. Large individual variations among survivors with regard to body morphology and state of health and fitness, in combination with many exogenous variables that affect cooling rate (e.g., clothing, water temperature, sea state, flotation, behavior), preclude exact predictions of survival time. However, sufficient experimental data and case history findings exist to allow for generalizations. At a Tco of 34° C (93.2° F), there is a significant deleterious effect on manual dexterity and “useful function” in cold water.24,132 If a survivor is trying to combat rough seas, this level of dysfunction may potentiate drowning. At a Tco of 30° C (86° F), unconsciousness is probable. Even if a survivor is wearing a self-righting PFD that has been designed to maintain airway freeboard in an

Classifications

Core temperature

unconscious person, drowning is probable at this Tco in all but the calmest seas. At a Tco of less than 25° C (77° F), ventricular fibrillation or asystole often occur spontaneously.29 Of these three Tcos, 30° C (86° F) is the most practical for defining the limits of survival in cold water.* The rate of body Tco cooling during cold-water immersion depends on the following variables: water temperature and sea state; thermal protection; body morphology; amount and surface area of the body immersed in water; behavior (e.g., excessive movement) and posture (e.g., HELP, huddle) of the body in the water; shivering thermogenesis; and other nonthermal factors.

WATER TEMPERATURE AND SEA STATE These variables are critically important to the intensity of the cold shock response, the onset of physical and mental impairment, and the rate of Tco cooling. Figure 6-14 graphically illustrates the inverse linear relationship between water temperature and Tco cooling rate.82 Water conducts heat away from the body approximately 25 times as fast as does air at the same temperature.125

THERMAL PROTECTION A large number of studies over the past few decades have evaluated the relationships of different types of protective clothing with heat loss and cooling rates.† Nearly all of these studies have been conducted in calm water or in laboratory settings. As illustrated by the cooling rate data in Tables 6-2 and 6-3, such studies have generally shown that, in calm water, intact “dry” and insulated garments provide better protection than do “wet” insulated garments and that well-insulated garments provide significantly better protection than do poorly insulated garments. Figure 6-15, online shows various types of cold-water protective garments. Although calm-water studies have value in that they compare the relative degree of protection afforded by different types of protective clothing, many immersion accidents occur in rough water.143,168,169 In this environment, a survivor’s cooling rate may be affected by swimming to maintain airway freeboard, passive *References 18, 29, 158, 159, 163. † References 5, 35, 83, 89, 98, 99, 109, 132, 150, 158, 159, 166, 170, 172, 173, 175, 198, 203.

Patient’s ability to rewarm without external heat source

Clinical presentation

Normal

Above 35° C (95° F)

Cold sensation; shivering

Mild

35-32° C (95–90° F)

Good

Moderate

32-28° C (90–82° F)

Limited

Below 30° C (86° F) shivering stops; loss of consciousness

Severe

Below 28° C (82° F)

Unable

Rigidity Vital signs reduced or absent Severe risk of mechanically stimulated (rough handling) ventricular fibrillation (VF)

Below 25° C (77° F)

Unable

Spontaneous ventricular fibrillation (VF); cardiac arrest

Physical impairment • Fine motor • Gross motor

Mental impairment • Complex • Simple

Bold text shows the major thresholds between stages of hypothermia.

FIGURE 6-13  Classification of levels of hypothermia on the basis of core temperature and clinical presentation.

150

Flight suit Float coat

0.06

Shorty wet suit Aviation coveralls

Cooling rate (° C min–1)

0.05

Boatcrew coveralls Wet suit

0.04

Calm Rough

Dry suit Survival suit

0.03

0

1

2

3

4

Cooling rate (° C/hr)

0.02

FIGURE 6-16  A comparison of mean rectal temperature cooling rates in lean male subjects in calm versus rough seas at 10.7° C (51.3° F). The flight suit, when used as a control garment, is equivalent to lightweight clothing. (From Steinman AM, Hayward JS, Nemiroff MJ, et al: Immersion hypothermia: Comparative protection of anti-exposure garments in calm vs rough seas, Aviat Space Environ Med 58:550, 1987.)

0.01

0

5

10

15

20

25

Water temperature (° C) FIGURE 6-14  Relationship between water temperature and mean rectal temperature cooling rate in lightly clothed nonexercising males and females during immersion in seawater. (From Hayward JS: The physiology of immersion hypothermia. In Pozos RS, Wittmers LE, editors: The nature and treatment of hypothermia, Minneapolis, 1983, University of Minnesota Press.)

body movements caused by waves, flushing of cold water through “wet” suits, and leakage of cold water into “dry” suits. For example, subjects in a wave tank demonstrate higher energy expenditure and faster cooling rates than do subjects in calm water.81 Several experimental studies have demonstrated

TABLE 6-2  Mean Linear Cooling Rates for Lean Men

Dressed in Various Types of Garments in Calm Water at 10° C (50° F)

Type of Protective Clothing Control (equivalent to ordinary street clothes) “Wet” Design Thermal float coat (loose-fitted, 5.4-mm [0.21-inch] closed-cell, foam-insulated jacket) Short wet suit (custom-fitted, 3.2-mm [0.13-inch] closed-cell, foam that covers the arms, the trunk, and the upper thighs) Insulated coveralls (loose-fitted, 3.2-mm [0.13-inch] closed-cell foam that covers the extremities and the trunk) Full wet suit (custom-fitted, 4.8-mm [0.19-inch] closed-cell foam that covers the extremities and the trunk) “Dry” Design Immersion suit (loose-fitted, 4.8-mm [0.19-inch] closed-cell foam with sealed openings)

Cooling Rate Given as ° C/hr ± Standard Deviation (° F/hr ± Standard Deviation) 3.2 ± 1.1 (5.8 ± 2.0) 1.6 ± 0.6 (2.9 ± 1.1)

significantly faster cooling rates for human volunteers wearing “wet” protective garments in rough or turbulent water142,158,203 as compared with persons in calm water. Even “dry” suits have shown degradation of protection in rough water. In a study of dry immersion suits in 16° C (60.8° F) water, Ducharme and Brooks found that wave heights of up to 70 cm (28 inches) resulted in a 14% decrease in total suit insulation and an average 45% decrease in thermal resistance at the head and trunk regions of the suits.31 Figure 6-16 shows a comparison of cooling rates for lean males dressed in the various types of protective clothing shown in Figure 6-15 in both calm and rough waters at approximately 10° C (50° F).158 The most dramatic differences occurred in the loose-fitted “wet” protective clothing (e.g., float coat, insulated coveralls), where cooling rates nearly doubled in rough seas as compared with those seen in calm seas. This was primarily caused by the flushing of cold water through the garments. However, even the tight-fitted full “wet” suit allowed for a 30% faster cooling rate in rough water as compared with that seen in calm water. The “dry” suit, which did not leak, showed no significant difference between calm and rough seas.

TABLE 6-3  Comparison of Mean Cooling Rates

for Thin Men (Mean Body Fat = 9.1%) Wearing Various Types of Protective Clothing in Calm Water at 11.8° C (53° F)

1.2 ± 0.4 (2.2 ± 0.7) Clothing Type 1 ± 0.4 (1.8 ± 0.7) 0.7 ± 0.3 (1.3 ± 0.5)

0.5 ± 0.3 (0.9 ± 0.5)

From Steinman AM, Hayward JS, Nemiroff MJ, et al: Immersion hypothermia: Comparative protection of anti-exposure garments in calm versus rough seas, Aviat Space Environ Med 58:550, 1987.

Dry, closed-cell foam insulation (4.8-mm [0.19-inch] thick) Wet, closed-cell foam insulation (4.8-mm [0.19-inch] thick) Dry and uninsulated (watertight shell over lightweight clothing) Control (lightweight clothing alone)

Ratios as Compared With Control

Mean Cooling Rate Given as ° C/hr (° F/hr)

Direct

Inverse

0.31 (0.56)

0.14

7.35

0.54 (0.97)

0.23

4.26

1.07 (1.93)

0.47

2.15

2.3 (4.14)

1

1

From Hayward JS: Design concepts of survival suits for cold-water immersion and their thermal protection performance. In 17th symposium of the SAFE (Survival and Flight Equipment) Association. Van Nuys, Calif. 1979.

151

CHAPTER 6  Immersion Into Cold Water

0.07

of Protective Clothing in Rough Seas

Estimated Survival Time (hr) (95% Confidence Interval)

Clothing Type

Time to Incapacity (hr) (Temperature = 34° C [93.2° F])

Time to Unconsciousness (hr) (Temperature = 30° C [86° F])

Time to Cardiac Arrest (hr) (Temperature = 25° C [77° F])

0.4-1.3 0.9-2.7

0.8-2.6 1.6-5.2

1.3-4.3 2.5-8.4

Control (lightweight clothing) Torn, non–foam-insulated, dry coveralls (50.8 mm [2-inch] tear in left shoulder) Closed-cell foam-insulated, wet coveralls (3.2-mm [0.13-inch] thick insulation in loose-fitted coveralls) Closed-cell foam-insulated, custom-fitted wet suit (4.8-mm [0.19-inch] thick insulation; tight-fitted) Intact, non-foam–insulated, dry coveralls (watertight shell over thick, fiberfill, insulated underwear)

1-2.9

1.9-6

3-9.9

1.6-4.7

3.1-9.9

4.9-16.2

2.9-8.8

5.7-18.2

9.1-30

From Steinman AM, Kubilis P: Survival at sea, report no. CG-D-26-86, United States Coast Guard. 1986, National Technical Information Service.

Estimated survival times in rough seas, on the basis of experimental data, were published for thin males wearing different types of protective clothing in 6° C (42.8° F) water.159 Table 6-4 shows these times for three different levels of survival. Underlying these estimations are the following assumptions: 1. Cooling rates are linear.89,158,159,163 2. Initial Tco is 37.5° C (99.5° F). 3. Survivors are able to maintain airway freeboard until unconsciousness occurs at a rectal temperature of 30° C (86° F). 4. Self-righting flotation maintains airway freeboard when survivors are unconscious. By comparing these estimated survival times with those of Figure 6-17 (i.e., calm-water survival times), the reader must recall that Figure 6-17 concerns only survival to a Tco of 30° C (86° F). Furthermore, the zone in the graph must be adjusted downward for rough seas and for survivors wearing only lightweight clothing, and it should be adjusted upward for survivors wearing insulated clothing. For 6° C (42.8° F) water, the survival times (to a Tco of 30° C [86° F]) correlate well between Figure 6-17 and Table 6-4. We must emphasize that the estimates in Table 6-4 pertain to lean individuals with a mean body fat level of only 11.1%. Because many populations of adults (e.g., offshore oil workers) in the 30- to 50-year-old age range average 25% to 30% body fat, the estimates of “time to unconsciousness” and “time to cardiac arrest” must be considered conservative for a broader spectrum of adults. A recent video production called Cold Water Boot Camp (see Video References section at the end of this chapter) tested various flotation ensembles, including closed-cell and inflatable PFDs, heavy dry suits, and lighter extended-wear (paddling) dry suits. Figure 6-18 schematically shows that Tco and survival time decrease as the amount of thermoprotection and flotation decreases (Box 6-4).

BOX 6-4  Controversy Box: Flotation Clothing Impedes

Escape from Submersed Vehicles

In many winter road jurisdictions, workers are mandated to wear thermoprotective flotation jackets or overalls. Some workers resist wearing this clothing because of fears that clothing buoyancy may impede exit by forcing the occupant upward against the roof of the vehicle and that increased bulk may impede passage through a window or hatch. Flotation jackets or overalls do not pose an exit threat and should be considered safe for ice road use. Inflatable PFDs have been considered as an option, but, because they may be inflated prematurely before exit, they might impede exit and are not recommended for vehicle use in any situation.59

152

BODY MORPHOLOGY (SIZE AND COMPOSITION) Children cool faster than adults because children have a greater surface area–to–mass ratio. Cooling rate is generally proportional to surface area, whereas the amount of heat that can be lost is proportional to mass. Thus, a large surface area–to–mass ratio favors cooling. Similarly, smaller adults generally cool faster than do larger adults, and tall, lanky individuals cool faster than do short, stout individuals. Body composition is also important. 12 11 10

Death from hypothermia highly probable

9 Survival time (hr)

PART 2  COLD AND HEAT

TABLE 6-4  Estimated Survival Times for Lean Subjects (Mean Body Fat = 11.1%) Wearing Various Types

8 7 6

rs

ole

5

ow

4

Sl

3

e Av

2

co

rag

t Fas

1 0 0

5

10

rs

ole

o ec

lers

coo

Death from hypothermia highly improbable 15

20

25

Water temperature (° C) FIGURE 6-17  Predicted calm-water survival time (defined as the time required to cool to 30° C [86° F]) in lightly clothed, nonexercising humans in cold water. The graph shows a line for the average expectancy and a broad zone that indicates the large amount of individual variability associated with different body sizes, builds, fatness levels, physical fitness levels, and states of health. The zone would include approximately 95% of the variations expected for adult and teenage humans under the conditions specified. The zone would be shifted downward by physical activity (e.g., swimming) and upward slightly for heavy clothing or protective behaviors (e.g., huddling with other survivors, adopting a fetal position in the water). Specialized insulated protective clothing (e.g., a survival suit or wet suit) is capable of increasing survival time from 2 to 10 times (or more) the basic duration shown here. For the zone in which death from hypothermia is highly improbable, cold shock on initial immersion can potentiate death from drowning, particularly for those who are not wearing flotation devices. (From the U.S. Coast Guard: Addendum to the National Search and Rescue (SAR) Manual, COMDTINST M16120.5 and COMDTINST M16120.6. 1995.)

Core temperature

Flotation Moderate thermal protection

Flotation No thermal protection No flotation No thermal protection Time

FIGURE 6-18  Schematic estimation of core temperature and survival times with varying flotation devices and thermal protective clothing.

Subcutaneous fat is a very efficient insulator against heat loss, and cooling rate is inversely related to skinfold thickness. For example, subjects in the tenth percentile for skinfold thickness wearing light clothing in 5° C (41° F) water have nine times the cooling rate of subjects in the ninetieth percentile for skinfold thickness.132 Figure 6-19 shows the linear relationship between change in Tco and mean skinfold thickness.101 Shivering, which is a primary defense against Tco cooling, also varies with skinfold thickness. At a given skin temperature, the shivering response is less in humans with greater amounts of subcutaneous fat.108 In moderately cold water temperatures (18° to 26° C [64.4° to 78.8° F]), Tco cooling has been shown to proceed at the same rate in high- and low-fat individuals because of greater shivering thermogenesis in the low-fat subjects. However, at colder water temperatures (8° C [46.4° F]), Tco cooling is attenuated by greater amounts of subcutaneous fat and body mass as a result of increased insulation.53 In general, for a survivor who is immersed in cold water, the Tco cooling rate is fairly linear after Tco begins to decline. This has been shown to be true for mildly hypothermic experimental subjects. The only data that exist for severely hypothermic

Fall in Tre ° C

2.0

humans are those from the infamous Dachau concentration camp atrocities, in which conscious victims were inhumanely cooled to death in ice water.2 Because these unfortunate victims were emaciated and ill, these data do not apply to healthy cold-water immersion subjects and should be considered atrocious. The advantage of body fat as an insulator against cold has been discussed previously in the section about pathophysiology and cooling rates. With the use of an extrapolation of a linear cooling rate to 30° C (86° F), Figure 6-17 shows predicted calmwater survival times of lightly clothed, nonexercising humans in cold water. The graph shows a line for the average survival expectancy. A broad zone indicates the large amount of individual variability associated with different body sizes, builds, and degrees of fatness. The zone would include approximately 95% of the variation expected for adult and teenage humans under the conditions specified. For the zone in which death from hypothermia is highly improbable, cold water still potentiates death from drowning as a result of cold shock (as discussed previously) during the first few minutes of immersion, especially for those who are not wearing PFDs. It is important to note that Figure 6-17 discusses only calm-water survival times. Because roughwater conditions decrease survival times, as will be discussed later in this chapter, Figure 6-17 may be useful for estimating maximum survival times for an individual who is immersed in cold water. Search and rescue organizations might find such a maximum survival time helpful, because they often use the longest possible survival time to decide when to terminate a search effort.

AMOUNT OF BODY IMMERSED Because of the difference in thermal conductivity between air and water (as discussed previously), heat loss from body surfaces immersed in cold water is far greater than from body surfaces exposed to cold air, even considering the effect of windchill. Thus, immersed victims should attempt to get as much of their bodies out of the water as possible (Figure 6-20). This issue is discussed in greater detail in Cold-Water Survival, later in this chapter.

HEAD IMMERSION Exposure of the dorsal head to cold water may increase a survivor’s rate of cooling and adversely affect mental performance. Survival may depend on the ability to conduct multiple tasks to avoid drowning and hypothermia. The ability to carry out these tasks involves both physical components, which are affected by local muscle and nerve temperature,63 and mental components, which are affected by brain temperature;50 both may be adversely affected by hypothermia. Head immersion has traditionally been of concern in survival situations.69 In the absence of water in the airways, heat is lost

1.5

1.0

0.5

0.05

0.10

0.15

0.20

0.25

Reciprocal of mean skinfold thickness mm–1

FIGURE 6-19  The relationship between subcutaneous fat thickness in 10 men and the decline in rectal temperature during 30-minute immersions in stirred water at 15° C (59° F). Skinfold thickness is given as a mean of readings at the biceps, the abdomen, and subscapular and subcostal sites. Tre, Rectal temperature. (From Keatinge WR: Survival in cold water, ed 2, Oxford, 1969, Blackwell Scientific Publications.)

FIGURE 6-20  Nick Schuyler sitting atop an overturned boat, awaiting rescue. He survived for 43 hours in 18° C (64° F) water, whereas his three companions perished after 13 to 25 hours. His position on top of the boat decreased his heat loss, and his bright-colored jacket and keyhole personal flotation device resulted in him being seen by U.S. Coast Guard personnel. (Courtesy U.S. Coast Guard.)

153

CHAPTER 6  Immersion Into Cold Water

Flotation High thermal protection

Esophageal temperature (° C)

PART 2  COLD AND HEAT

through the head either via convection (heat loss from the blood that perfuses the scalp) or conduction (direct heat loss through bone and soft tissue).206 One hypothesis predicts substantial heat loss through the head because of abundant scalp vascularity and because the scalp vasculature does not vasoconstrict in response to cold as do superficial blood vessels in other body areas.45 Alternatively, heat loss from the back of the head might be minimal, because dorsal head and neck immersion would only involve an additional 3% to 5% of the body surface area.107 In addition, conductive heat loss directly through the scalp and skull is likely to be minimal.206 A few studies have addressed the head cooling of animals in water22 or of humans in cold air,45,139 but only one human study has included cold-water exposure of the head. Alexander reported the data regarding head cooling from studies carried out on prisoners of war in Dachau during World War II.2 These studies were horrific, reprehensible, and grossly unethical, and the results are considered invalid and unusable because of the emaciated condition of the prisoners as well as questions regarding the protocol and accuracy of the results. Few experimental data are available to evaluate the effects of mild hypothermia on mental performance. A few medical studies have evaluated the impairment of memory among divers during cold-water dives.9,190,193 Two other studies involved cognitive testing during hypothermia without direct head cooling.19,50 Lockhart and colleagues111 recently evaluated the effects of dorsal head and neck immersion among human subjects immersed in 10° C (50° F) water on Tco cooling rates and mental performance. Dorsal head and neck immersion (with the body insulated) resulted in a cooling rate of 0.4° ± 0.2° C/hr (0.7° ± 0.4° F/ hr). Body immersion with the head, neck, and upper thorax out of the water resulted in a cooling rate of 1.5° ± 0.7° C/hr (2.7° ± 1.3° F/hr). Immersion of both the whole body and the dorsal head and neck nearly doubled the cooling rate to 2.8° ± 1.6° C/ hr (5.0° ± 2.9° F/hr) (p <0.0002). In addition, there were significant correlations between diminished cognitive performance and decreasing Tco. The time required to correctly complete the Stroop Color-Word Test increased as Tco decreased (p <0.001). The number of correct responses decreased with Tco for digit symbol coding (p <0.02), backward digit span (p <0.05), and paced auditory serial addition testing (p <0.05). Figure 6-21 demonstrates the effects of different PFDs on the position of the head in water. Giesbrecht and co-workers46 repeated the head-cooling study with the use of subjects immersed in 12° C (53.6° F) whose

38.0 37.5

†

37.0 36.5

†

*

36.0

*

35.5 35.0

**

34.5 34.0 33.5 –20

–10

0

10

20

30

Time (min) Body insulated, head out Body insulated, dorsal head in Body exposed, head out Body exposed, dorsal head in FIGURE 6-22  Core-temperature response to immersion in 12° C (54° F) water with the head out or the dorsum immersed in body-insulated and body-exposed conditions; shivering was inhibited with meperidine to mimic a severely nonshivering victim. (From Giesbrecht G, Lockhart T, Bristow G, et al: Thermal effects of dorsal head immersion in cold water on nonshivering humans, J Appl Physiol 99:1958, 2005.)

shivering thermogenesis had been inhibited with intravenous meperidine to model severe hypothermia.67 When the body was insulated, there was no Tco cooling with the head out of the water, and immersing the dorsum of the head had no further effect. However, when the body was not insulated but instead exposed to the cold water, Tco decreased at 3.6° C/hr (6.5° F/hr). In this condition, also immersing the dorsum of the head significantly increased the rate of Tco cooling to 5.0° C/hr (9° F/hr) (Figure 6-22). These results did not confirm the supposition of proportionately greater heat loss from the head. The measured heat loss from the head in both head-immersed conditions was only about 60 kJ as compared with 18 kJ to 33 kJ in the two head-out conditions. By contrast, total body heat loss in the body-exposed configurations was about 1100 kJ and 1260 kJ, respectively, for head-out and back-of-the-head-in conditions. Thus the head accounted for only about 3% and 5% of the total body heat loss, respectively, in the body-exposed conditions. The majority of the difference in heat loss in the body-immersed conditions came from immersion of the anterior thorax rather than from the dorsal head and neck. Nevertheless, it is important to recognize that, although there was not a significant increase in heat loss through the head, there was a disproportionate increase in Tco cooling. Although the mechanisms for this disparity have not yet been determined, the implications are clear for manufacturers and survivors. During long-term cold-water immersion, it is advantageous to keep the head out of the water. If this is not possible (i.e., most survival suits place the victim in a supine position), the survival ensemble should include a hood with as much insulation as is practical (Box 6-5).

BEHAVIOR AND POSTURE OF THE BODY IN COLD WATER

FIGURE 6-21  Effectiveness of various types of personal flotation devices for keeping the head and the upper chest out of the water. Top left, Type I jacket; top right, Type 3 jacket; bottom left, typical keyhole inflatable jacket; bottom right, waist-mounted inflatable device. (Courtesy Gordon G. Giesbrecht.)

154

Behavioral variables also affect Tco cooling rate. Hayward and colleagues used infrared thermography to demonstrate that, despite marked peripheral vasoconstriction, heat losses are high in the groin, the lateral and central thorax, and the neck.85 In the groin and neck, which are regions with relatively thin layers of peripheral soft tissue, blood flow through the large and relatively superficial femoral vessels, carotid arteries, and jugular veins potentiates heat flow to the cold water. In the lateral and central thorax, the relative absence of tissue (muscle and subcutaneous fat) insulation in combination with the high thermal conductivity

Heat Through Your Head

This common belief has caused many incorrect and even dangerous actions, such as going to extreme lengths to retrieve hats or to removing clothing when immersed to place it on the head for thermal protection. In a cold-water immersion scenario, 90% to 95% of heat loss occurs through the cold-exposed body. It has been demonstrated that, under similar thermal stresses, relative heat loss from the head (per unit of surface area) is not that much higher than that from other areas of the body. However, under certain conditions, increased heat loss from the head can cause a disproportionate decrease in body Tco. Thus head contact with cold water should be minimized whenever possible by changes in posture and maximum practical insulation.

of rib bone potentiates heat loss from the relatively warm lungs to the cold environment. Furthermore, exercise or excessive movement in the water greatly increases heat loss from active muscles. The effect of activity on total heat balance depends on the balance among the many factors illustrated in Figure 6-23. In normothermic circumstances, heat produced locally in peripheral muscles is transferred to the core via venous return. By contrast, during cold-water immersion, physical activity may actually increase heat loss through increased blood flow to the periphery. This is especially true when immersed victims engage in excessive movement in the water (e.g., swimming, performing the vigorous extremity movements that are necessary to maintain airway freeboard in rough seas). Hayward and colleagues86 demonstrated that minimizing both voluntary activity and exposure of major heat loss areas of the skin to cold water are the most effective ways to minimize a decline in Tco. They showed that treading water and drownproofing significantly increased the cooling rate. Despite increased metabolic heat production during exercise, the increased surface heat loss resulted in faster Tco cooling during exercise in cold water. They also developed two well-known cold-water survival techniques: HELP and the group huddle (Figure 6-8). These adaptive behaviors reduce Tco cooling by 69% and 66% of that of control conditions, respectively.82 When the sea is not calm, it may be difficult to perform the group huddle with complete thermal efficiency. However, other advantages of this position include the maintenance of group contact and morale. Sagawa and colleagues concluded that the lowest water temperature in

which humans could maintain normal Tco by generating body heat through muscular activity is 25° C (77° F), although there may be individual variations.145

EXERCISE Normally the advice is to not exercise while awaiting rescue in cold water. This is because of the understanding that, although metabolic heat production will increase, exercise increases blood flow to muscles and causes increased heat loss to the water, with a net result of increased Tco cooling. A recent study by Færevik and colleagues39 was conducted in subjects wearing neoprene survival dry suits in a wave tank with water temperature of 0° C (32° F) and air temperature of 5° C (23° F). When subjects remained still, Tco dropped more during 3 hours of immersion than it did during 6 hours of immersion during which they performed leg exercises for 5 minutes every 20 minutes (Figure 6-24). Thus, if enough insulation is worn, the heat of exercise can be contained within the insulation, which attenuates the drop in Tco.

SHIVERING Shivering is a thermoregulatory function during which involuntary muscle contraction increases heat production in an effort to prevent or minimize Tco cooling. Shivering intensity increases as Tco and skin temperatures decrease. Generally shivering intensity is maximal at a Tco of 32° to 33° C (89.6° to 91.4° F) and a skin temperature of approximately 20° C (68° C). However, shivering heat production is lower at any given skin temperature among individuals with higher levels of subcutaneous fat.108,199 Thermal balance during shivering depends on the same factors as it does during voluntary activity (see Figure 6-23). Figure 6-25, online illustrates how shivering heat production can maintain Tco in cold air and how it can arrest the fall in Tco in both warm and cool water. In colder water, the combination of shivering thermogenesis and body insulation (as a result of peripheral vasoconstriction) may result in maintenance of a steady-state Tco, albeit below normothermic levels. At even lower water temperatures, Tco will continue to decrease. This decrease accelerates when shivering thermogenesis eventually stops as a result of hypothermia-induced thermoregulatory impairment (this occurs when Tco <≈30° C [86° F]). The power of shivering is especially important during consideration of the clinical

37.8

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FIGURE 6-23  Factors that influence total thermal balance during increases in metabolic heat production (i.e., voluntary exercise and involuntary shivering).

A, Non exercise B, Intermittent leg exercise

FIGURE 6-24  Rectal temperature for six subjects during immersion in 0° C (32° F) water and −5° C (−23° F) air. A, No exercise, and B, intermittent leg exercise for 5 minutes every 20 minutes (mean ± standard deviation). *, There is a significantly higher rectal temperature in condition B as compared with condition A from 40 to 180 minutes. (From Faierevik H, Reinertsen RE, Giesbrecht GG: Leg exercise and core cooling in an insulated immersionsuit under severe environmental conditions, Aviat Space Environ Med 81:1, 2010.)

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CHAPTER 6  Immersion Into Cold Water

BOX 6-5  Controversy Box: You Lose Most of Your

PART 2  COLD AND HEAT

classification of hypothermia and rewarming therapies, because this valuable heat source is an efficient mechanism for rewarming the core during postimmersion recovery and resuscitation. This is discussed in more detail in Rescue and Management, later in this chapter.

NONTHERMAL FACTORS Underwater divers often experience “symptomless” or “undetected” hypothermia. Several factors contribute to increased cooling. Heat is lost through direct conduction to cold water and through the breathing of compressed air. Breathing compressed air at depth alters human thermoregulation. Mekjavic and colleagues studied the effects of hyperbaric nitrogen at 6 atm;117 these researchers also simulated inert gas or “nitrogen” narcosis with the inhalation of 30% nitrous oxide.136 They demonstrated a decrease in the Tco threshold for shivering and an increase in the rate of Tco cooling of up to twofold under these conditions. In a separate study, this group demonstrated qualitatively similar effects of insulin-induced hypoglycemia.137 Hypercapnia and hypoxia may also be present in various underwater scenarios. Hypercapnia has been shown to lower the shivering threshold94 and to transiently inhibit shivering. Both hypercapnia94 and hypoxia95 have also been shown to accelerate Tco cooling. Alcohol consumption is frequently associated with immersion hypothermia, because ethanol impairment of mental and motor performance is often the cause of accidental immersion. Social drinking can result in carelessness. Intoxicated mariners or others near water often fall from a boat, ship, gangway, wharf, or bridge into the water. Drunken drivers capsize or collide. On the basis of the frequency of occurrence alone, the consequences of alcohol ingestion warrant special considerations. Studies of the effects of moderate doses of ethanol (i.e., blood alcohol levels of 50-100 mg/dL, which is the range associated with legal impairment) on cold stress have established the following: 1. The rate of heat loss is not significantly increased. Alcohol has a primary vasodilatory effect under normothermic conditions.38,83,100 Under hypothermic conditions, where vasoconstriction predominates, alcohol lowers the vasoconstriction threshold during the moderate cold stress of 28° C (82.4° F) water immersion, but does not affect the shivering threshold or the rate of Tco cooling.93 2. The rate of heat production is slightly decreased. For immersion in water colder than 28° C (82.4° F), a moderate ethanol dose inhibits the metabolic response to cold.42,115 Shivering thermogenesis is reduced in cold water by approximately 10% to 20%. 3. The cooling rate is not significantly increased.42,93,115 Because the body’s cooling rate in cold water is influenced more by the rate of heat loss than by the rate of heat production, the slight reduction in shivering thermogenesis induced by moderate ethanol ingestion is outweighed by factors that affect heat loss (e.g., peripheral vasoconstriction, body fat). Because these do not vary with alcohol use when the person is cold stressed, the cooling rate does not change. 4. Fatigue potentiates thermoregulatory impairment by alcohol. Exhaustive exercise leading to fatigue (which is characterized by hypoglycemia and the depletion of glycogen reserves) in combination with a moderate dose of ethanol significantly reduces resistance to cold.78,96 Alcohol inhibits gluconeogenesis,76,96 so the ability to provide glucose to maintain shivering is reduced. If a person enters cold water in this condition, his or her cooling rate is likely to be greater than in the absence of ethanol. 5. The perception of cold is diminished. Experimental studies of humans in cold water show that moderate alcohol dose to some extent relieves feelings of intense cold.42,101 This cognitive alteration may be functionally related to the reduced shivering response. 6. Cold-induced diuresis is increased. Alcohol inhibition of antidiuretic hormone augments immersion diuresis.26 During the first hour of cold-water immersion, the urine flow rate can be more than six times normal (i.e., up to 156

approximately 8 mL/min). For longer immersions (i.e., >1 hour), alcohol potentiates the development of dehydration and hypovolemia. For most humans, high doses of alcohol (i.e., blood levels of >200 mg/dL) have an anesthetic effect. The major impairment of mental, motor, and involuntary function (including thermoregulation) occurs. Alcoholics who “pass out” in cold locations (i.e., “urban hypothermia”) rapidly and passively become hypothermic.28,121 When highly intoxicated persons enter cold water (usually by falling in), hypothermia is seldom a problem, because such persons usually drown quickly.

Cold-Water Survival Cold-water survival depends on avoidance of drowning and hypothermia and on the many factors related to these risks, including the following: ability to control the cold shock response; ability to swim and maintain airway freeboard; the availability and type of a PFD; availability of a life raft or other floating object to increase buoyancy; behavior of the survivor in water; decision to swim for shore or to wait for rescue; availability of signaling devices (e.g., whistles, flares, strobe lights, radios, mirrors) and the ability to use them; and proximity of rescue personnel.154,155,159

ABILITY TO CONTROL THE COLD SHOCK RESPONSE As previously discussed, sudden immersion in cold water initiates a cardiorespiratory cold shock response that significantly potentiates the risk of drowning. This response and the resulting incapacitation that can accompany it have been suspected as the primary causes of drowning after short-term (i.e., <10 minutes) immersion in cold water.165 Abrupt tachycardia and hypertension induced by sudden immersion in cold water can produce incapacitating cardiac dysrhythmias in susceptible individuals and myocardial infarction or cerebrovascular accident in persons with arterial disease or hypertension.165 In addition, reflex gasping and hyperventilation165,174 significantly shorten the duration of breath holding.84,88,165 Figure 6-26 illustrates this phenomenon. Loss of breath-holding capacity can have severe consequences for survivors attempting underwater egress from a submerged vehicle or from a capsized vessel or aircraft or for survivors who are simply trying to maintain airway freeboard in a rough sea or a white-water river.88,144,169 Respiratory difficulties induced by the cold shock reflexes make breathing while swimming extremely difficult. Golden and Hardcastle have demonstrated a “swim stroke/respiration asynchrony” that leads to water inhalation and swimming failure.70 Golden and colleagues have shown that even persons who are considered good swimmers (at least in warm water) can only swim for a few minutes in cold water. Swimming ability and survival time in cold water are further diminished by the subjective perception of shortness of breath and panic reactions from unexpected cold-water immersion.165 The work that is required to swim in cold water is greater than that in warm water because of the former’s higher viscosity (e.g., water at 4.7° C [40.5° F] has a viscosity that is 67% higher than that of water at 23.7° C [74.7° F]).104 The increased work of swimming in cold water potentiates the onset of fatigue. The combination of all of these factors may incapacitate even physically fit and capable swimmers. Keating and colleagues observed sudden incapacitation in two experimental subjects (who were good swimmers) who were immersed in 4.7° C (40.5° F) water.104 One subject inhaled water because of respiratory difficulty and fatigue after swimming for 7.5 min and had to be pulled from the water. The second subject lasted only 1.5 min before he “floundered and sank without managing to reach the side of the pool, which was about one meter from his head, and had to be pulled” out of the water. The observed frequency of such swimming failures and unexpected submersions has led the U.S. Coast Guard to coin the term “sudden disappearance syndrome” to describe the phenomenon.178 The magnitude of the cold shock response can be attenuated through increased insulation, graded immersion (see Figure 6-6),

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Drowning is the most immediate survival problem after water entry. To maintain airway freeboard and to avoid drowning, a survivor must possess the physical skills and psychological aptitude to combat the effects of wave action.155,169 Although a PFD assists with maintenance of airway freeboard, waves can still submerge a survivor’s head, even in moderately calm seas.65,154,178 To reduce risk of drowning in rough seas, a survivor can increase effective airway freeboard by partially exiting the water (e.g., clinging to an overturned vessel or other debris floating in the water) or by climbing totally out of the water onto a life raft or a capsized vessel. In both of these environments, the survivor may still have to cope with the effects of cold wind, spray, and waves (Figure 6-27; see also Figure 6-20).

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Water temperature (° C) FIGURE 6-26  Effect of water temperature on maximum breath-hold duration in young, physically fit human subjects (80 men and 80 women). The first submersion was sudden after sitting comfortably in air at a mean temperature of 11.3° C (52.3° F). The second submersion followed 2 minutes of acclimatization to the water. The last 10 seconds of the acclimatization was accompanied by 10 seconds of hyperventilation. (From Hayward JS, Matthews BR, Overweel CH, et al: Temperature effect on the human dive response in relation to cold-water near-drowning, J Appl Physiol 56:202, 1984.)

and habituation to cold immersion. Tipton and colleagues demonstrated that habituating subjects to 10° C (50° F) water resulted in a 16% reduction in respiratory rate during the first 30 seconds of immersion in 10° C (50° F) water and a 26% reduction in respiratory rate during the 30 sec to 180 sec interval after immersion in 10° C (50° F) water. Tidal volume and heart-rate response demonstrated similar declines in habituated subjects.171 Habituation through cold-water survival training may thus be an important safety measure for workers in cold-water environments. Protective clothing also diminishes the cold shock response that occurs as a result of the initial immersion in cold water. Clothing (e.g., well-fitted wet suits, dry suits with adequate seals) that limits the amount and ingress velocity of water that reaches a subject’s skin significantly decreases cardiorespiratory reflex responses to sudden immersion.118,172,173,175 Tipton and Golden demonstrated that subjects who were wearing wet suits that protected the torso but that left the limbs exposed had significantly reduced respiratory reflex responses but not reduced heart-rate responses as compared with control subjects with neither torsos nor limbs protected. They concluded that the limbs may be more important than the torso with regard to the cardiac response to sudden cold-water immersion.172 Tipton and colleagues also demonstrated that even loose-fitting and poorly insulated clothing can attenuate the magnitude of the cold shock response as compared with immersion in swimming trunks only.173 When volunteers were immersed in 10° C (50° F) water wearing either conventional clothing or conventional clothing plus windproof/showerproof foul-weather clothing,

Survivor location has a significant effect on Tco cooling rate and survival time. The U.S. Coast Guard and other rescue organizations recommend that a survivor of a maritime accident in cold seas get as much of his or her body out of the water as possible to minimize the cooling rate and maximize survival time.159,178 This recommendation derives from the higher thermal conductivity of water as compared with air at the same temperature. However, survivors who are exposed to cold air are still at risk from hypothermia as a result of convective, evaporative, and radiant heat losses. In a rough sea environment, wind increases the magnitude of convective heat loss, and spray and periodic wetting from breaking waves result in conductive heat loss.162,164 Steinman and colleagues confirmed these observations.159 The cooling rates of thin male subjects wearing different types of protective clothing were compared for three survival situations: 1. Immersion in 6° C (42.8° F) water with 1.5 m (4.9 ft) breaking waves. 2. Exposure to 7.7° C (45.9° F) air, continuous water spray at 6° C (42.8° F), continuous 28 to 33 km/h (17.40 to 20.50 mph) wind, and occasional breaking waves while sitting atop an overturned boat (see Figure 6-27). 3. Exposure to 7.7° C (45.9° F) air and occasional breaking waves while sitting in an open one-man life raft. The results of the study are shown in Figure 6-28. For each type of garment worn, cooling rates were considerably faster in the water than atop the boat (despite the effects of wind, spray, and breaking waves) or within the raft. These experimental conditions were tragically reproduced in real life for the four football players whose boat capsized in the Gulf of Mexico, as described previously. Only one of the men

FIGURE 6-27  Testing protective clothing atop an overturned boat with exposure to wind, spray, and breaking waves. (Courtesy Allen M. Steinman.)

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CHAPTER 6  Immersion Into Cold Water

cardiopulmonary and thermal responses were significantly less than those found with swimming trunks alone. Mental preparation should be used to avoid panic, to decrease emotional response, and to make a conscious effort to control breathing.

PART 2  COLD AND HEAT

Environment Water 5.82

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FIGURE 6-28  Mean linear cooling rates (° C/hr) for lean males in three survival environments: (1) water = immersion in 6.1° C (43.0° F) breaking waves; (2) boat = 5-min immersion in 6.1° C (43.0° F) water followed by exposure to 7.7° C (45.9° F) air atop an overturned boat with continuous 28 to 33 km/hr (17.4 to 20.5 m/hr) wind, water spray, and occasional breaking waves; and (3) raft = exposure to 7.7° C (45.9° F) air in an open, one-man life raft preceded by 5-min immersion in 6.1° C (43.0° F) water. AC, Air-crew coveralls; BC, boat-crew coveralls; FS, flight suit (lightweight clothing); NI, intact, non–foam-insulated “dry” coveralls; NX, NI with a 5-cm tear in the left shoulder, thus permitting water to leak into the suit and degrade its insulation; WS, wet suit. Blank squares indicate combinations of garments and environments that were not tested. (From Steinman AM, Kubilis P: Survival at sea: The effects of protective clothing and survivor location on core and skin temperature, USCG Rep No. CG-D26-86, Springfield, Va., 1986, National Technical Information Service.)

survived the heavy seas, high winds, and 18° C (65° F) water. He survived for 43 hours, primarily by getting out of the water and sitting atop the capsized boat (see Figure 6-20). The other three men spent a lot more time immersed and wore less insulation; thus they cooled faster and perished (see Survival Modeling, later, for further discussion). Survivors should attempt to get as much of their bodies out of the water as possible, even if it means exposure to cold wind and spray. Even rescue and medical personnel who frequently work in wilderness environments poorly understand this recommendation. A widespread misunderstanding of the concept of windchill128 causes many to conclude that survivors have higher heat losses if they are exposed to wind, especially if they are wet, than if they are immersed in water.159 The term windchill, which was originally used by Siple and Passel151 to describe the increase in heat loss from unprotected skin exposed to wind, is frequently used in the communication media without regard to the difference between exposed and unexposed skin. This leads many to erroneously believe that windchill temperature applies to both clothed and unclothed areas of the body. Furthermore, common experiences during recreational activities at the beach, lake, or swimming pool, where people subjectively feel colder after leaving the water (because of evaporative heat loss from the skin) than they do while swimming, reinforce this misunderstanding. This has occasionally led survivors to abandon a position of relative safety atop a capsized vessel and to reenter the water, usually with tragic results. The sensation of coldness, which is skin dependent, does not reliably convey information about rate of heat loss when two radically different environments (e.g., air and water) are compared.

DECISION TO SWIM FOR SHORE OR TO WAIT FOR RESCUE During cold-water immersion, physical activity increases heat loss through increased blood flow to the periphery. This is especially pertinent when immersed victims engage in excessive movement in the water (e.g., swimming, performing the vigorous extremity movements necessary to maintain airway freeboard in rough seas). The decision to swim for shore or to wait for rescue is crucial for a survivor of cold-water immersion. The increased cooling rate associated with swimming might lead one to conclude that holding still is preferable to an attempt to swim for safety. However, if the survivor can make it to shore or even to shallow water, survival is likely to be prolonged, despite the risk of lower 158

Tco. Lonsbury and co-workers specifically evaluated this issue by comparing the cooling rates and swimming distances for both novice and expert swimmers in a swimming plume.32 Experimental subjects, who were wearing average clothing (i.e., no specific insulation against cold-water immersion) and PFDs, were immersed in 10° C (50° F) water and either remained still in a HELP position or swam against a current that was matched with their swimming ability. Swimming resulted in a 17% faster rate of Tco cooling as compared with holding still. The novice swimmers traversed about 800 m (2625 ft) and the expert swimmers about 1400 m (4593 ft) during their swims. Thus, swimming may well have allowed the subjects to achieve safety ashore, despite the faster cooling rate. The researchers also found that the probability of a successful survival outcome depended on the decision to swim for safety early during a survival event. If the subjects had cooled for 30 minutes before attempting to swim, the likelihood of success was significantly reduced. The decision to swim or to remain still ultimately depends on the immersed individual’s understanding of the many variables that affect a successful outcome, including the following: body morphology and cooling rate; water temperature; wave conditions and currents; proximity of shore; proximity of rescue personnel; swimming ability; and availability of signaling devices, flotation devices, and protective clothing. There is no uniformly correct answer to the question, “Should I swim for it?” Each survival situation must be evaluated individually; a suggested algorithm appears in Figure 6-29 (also see Box 6-6).

SURVIVAL MODELING When a rescue organization is tasked with searching for victims in cold water, it is important to have an accurate estimate of how

BOX 6-6  Controversy Box: Always Stay with Your Boat For many scenarios in which warmer water temperature allows for longer survival and in which rescue is likely to occur, this is good advice. However, in colder water in secluded areas, the decision is not as clear, especially if rescue is unlikely. First, the decision to swim to safety should be made only if the victim is wearing a PFD, if the likelihood of rescue is low, and if the victim can reach shore within 45 minutes. With a PFD, if swim failure occurs, the victim will still remain afloat. Without a PFD, swim failure will result in drowning (see Figure 6-29).

CHAPTER 6  Immersion Into Cold Water

Accidental cold-water immersion

Don’t panic, breathing under control

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Decide early Commit to decision FIGURE 6-29  Algorithm for making the decision to stay or swim when immersed in cold water. PFD, Personal flotation device.

long the victims might survive and thus continue to warrant search resources. Various prediction models have been devised to assist with these difficult estimates. The Cold Exposure Survival Model was devised by Tikuisis to provide a sophisticated set of survival-time estimates for individuals who are immersed in cold, rough seas and for survivors who are partially immersed or exposed to cold wind under wet conditions.162,163 The model was developed on the basis of experimental data about cooling with different types of flotation devices and thermal protective clothing (Figure 6-30),158,159 shivering control and capacity,38 body composition (Figure 6-31), and other factors. The Cold Exposure Survival Model has been used for many years by both the Canadian and U.S. Coast Guards. Recently, the U.S. Coast Guard started using a new decision tool: the Probability of Survival Decision Aid (PSDA), which was developed by Xu and colleagues.205 Although the Cold Exposure Survival Model is based on a one-cylinder model, which assumes that most heat loss comes from the torso in cold victims, the PSDA includes six cylinders that represent the head, torso, arms, hands, legs, and feet. For example, Figure 6-32 shows predicted survival times for victims in varying water temperatures. Presently the PSDA predicts the time required for Tco to drop to 34° C (93.2° F) (i.e., functional time) and to 30° C (86° F) (i.e., survival time). When the PSDA was applied to the four football players whose boat capsized (as described previously in Recreational Activities and Cold Water), the survival time predictions for the first and third fatalities (13.5 and 25.7 hours, respectively) were very close to the actual survival times of approximately 13.0 and 25.5 hours. The heaviest victim (the second fatality) died much sooner (13.5 hours) than was predicted (37.3 hours). However, his symptoms were much different and indicated that more than hypothermia was involved. Instead of the expected hypothermia-induced gradual loss of physical abilities and the expected level of mental abilities and responsiveness, he was very agitated and aggressive, and he vigorously and continuously tried to get away from the boat. He eventually took off his lifejacket and forcefully dove under the surface and drowned. Therefore, it is likely that some other factors also contributed significantly to his death.

Because this victim spent so much more time immersed in the water than did the others, he may have ingested significant amounts of seawater; this was described and would be consistent with some of his actions and symptoms. Finally, the lone survivor lasted longer than predicted with a Tco of approximately 32° C (89.6° F) after 43 hours; the PSDA predicted he would cool to 28° C (82.4° F) after 41 hours. Interestingly, at this point, he was still shivering vigorously, likely as a result of his excellent physical condition; normally he would have been expected to stop shivering many hours before rescue. This long-lasting and high-intensity shivering heat production would have a significant affect in attenuating the drop in Tco. Predictive modeling has many inherent complications, but the PSDA results indicate the value of modeling as well as of providing some insight into the thermophysiology and pathophysiology present during this epic struggle.

SIGNALS Effective signals can greatly increase the chance of survival by bringing rescue and shortening the duration required to survive. Figures 6-33 and 6-34 show various types of signals, including dye, smoke, group formations, streamers, and flares. One inherent signal can be the clothing that is worn. It is a great advantage to wear colorful PFDs or other colorful clothing. For example, the U.S. Coast Guard rescue personnel found Nick Schuyler after 43 hours of immersion in the Gulf of Mexico because of his bright orange jacket (see Figure 6-20).

Physiologic Responses to Cold Water Submersion With the Head Under Water Drowning is covered in detail in Chapter 75: Submersion Injuries and Drowning. However, a brief discussion is included here to provide a more complete discussion of cold-water immersion. There have been several recent advances in our understanding of why individuals can survive cold-water submersion for as long as 66 minutes8 with full or partial neurologic recovery (i.e., coldwater near drowning). The most important factors in these unusual cases are low water temperature and subsequent brain 159

MECHANISMS FOR BRAIN AND BODY COOLING Children have an advantage in cold-water submersion incidents, because their greater surface area–to–mass ratio allows for faster conductive cooling, which provides cerebral protection on the

basis of decreased cerebral metabolic requirements of oxygen (CMRO2). The mammalian dive reflex, which initiates intense bradycardia and shunts blood flow to important core organs such as the heart and brain, has also been implicated. A third factor that has recently been explored is the possibility that cold-water ventilation may result in rapid and extensive cooling during submersion. The effectiveness of the human dive reflex, especially the breath-hold response, is controversial. Nemiroff, who reported one of the largest series of successful resuscitations of submersion victims, feels the dive reflex plays an important role, particularly in children and infants and especially in neonates.129,130 Hayward and colleagues88,138 feel that the enhanced success of resuscitation associated with cold-water submersion is more a result of hypothermia than of the dive reflex.

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PART 2  COLD AND HEAT

cooling. This principle has been used in clinical practice for years. For example, cardiopulmonary bypass used to cool neurosurgical patients to a Tco of approximately 9° C (48.2° F) made it possible to arrest brain blood flow for at least 55 minutes, with full neurologic recovery.135 The full explanation for these recoveries relates to both (1) the mechanisms for and amounts of brain and body cooling and (2) the mechanisms for the protective effect of this cooling.

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FIGURE 6-30  Prediction of survival time (ST) for an average individual under varying degrees of clothing protection (see Figure 6-15). A, For immersion in rough seas versus water temperature, low = nude, flight suit, float coat, aviation coveralls, boat-crew coverall, or torn coverall); medium = short wet suit or full wet suit; and high = dry coverall or dry suit. B, For exposure to air at 20 km/hr (12.4 m/hr) under wet conditions versus air temperature, low = nude, flight suit, or aviation coverall; medium = float coat, boat-crew coverall, short wet suit, full wet suit, dry coverall, or torn coverall; and high = dry suit. (From Tikuisis P: Predicting survival time at sea based on observed body cooling rates, Aviat Space Environ Med 68:441, 1997.)

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FIGURE 6-31  Predicted survival time (ST) for individuals wearing boatcrew coveralls (see Figure 6-15) for A, immersion in rough seas versus water temperature; and B, exposure to air at 20 km/hr (12.4 miles/hr) under wet conditions (i.e., clothing wetness of 1550 g/m2) versus air temperature. The lower and upper boundaries of the shaded regions represent predictions for lean and fat individuals, respectively. (From Tikuisis P: Predicting survival time at sea based on observed body cooling rates, Aviat Space Environ Med 68:441, 1997.)

CHAPTER 6  Immersion Into Cold Water

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30

35

Immersion time (hr) FIGURE 6-32  Effect of water temperature on predicted number of survivors using the Probability of Survival Decision Aid. (From Xu X, Amin M, Santee WR: Probability of Survival Decision Aid (PSDA), USARIEM Technical Report T08-05. Natick, Mass., 2008, U.S. Army Research Institute of Environmental Medicine.)

It is important to note that the protective effect of cooling depends on the Tco at cessation of oxygen delivery and the subsequent rate and extent of the decrease of Tco. Because Tco is likely to be near normal at the onset of an accidental submersion, rapid cooling after the onset of ischemia is important for survival. Conduction alone probably cannot account for the rapid decrease in Tco that occurs during cold-water submersion incidents. Conn and colleagues studied cold-water (4° C [7.2° F]) drowning in shaved and anesthetized dogs, and found that submersed dogs continued to breathe the cold water for an extended period of time.22 Tco decreased by 11° C (19.8° F) after 4 minutes in the completely submersed dogs as compared with only 3° C (5.4° F) in the control dogs, which were immersed with their heads out and did not breathe cold water. It is likely that the rapid cooling was the result of convective heat exchange in the lungs as

FIGURE 6-34  Differences in visibility in water based on suit color (top) and whether a group is stationary in a star formation (middle) or kicking the legs (bottom). (Courtesy Gordon G. Giesbrecht.)

compared with only surface conduction in the control dogs. The general conclusion that brain cooling is accelerated considerably by respiration of cold water has been proposed by others54,68,74 and mathematically predicted by Xu and colleagues.206 Although breath holding may occur during submersion, a physiologic break point occurs, at which time involuntary breathing movements predominate.4 This factor, when coupled with unconsciousness, could reasonably be expected to result in the respiration of water, at least under certain circumstances. Experimental and anecdotal evidence in humans is rare. However, one helicopter crash survivor reported that, after being trapped underwater for some time, he recalled feeling that he was about to die and that he was breathing water in and out just before escaping the cockpit.12 Whether or not this occurred has not been confirmed.

MECHANISMS FOR THE PROTECTIVE EFFECT OF BRAIN COOLING

FIGURE 6-33  Dye marker (top) and smoke flare (bottom) signals. (Courtesy Gordon G. Giesbrecht.)

Hypothermia provides an advantage during anoxic periods, such as cold-water submersion, because of what is known as the “metabolic icebox.” Whole-body or focal hypothermia has long been used to extend biologic survival time during surgery under ischemic conditions. Cerebral protection under hypothermic conditions has commonly been attributed to decreased cerebral metabolic requirements for oxygen, according to the temperature coefficient (Q10) principle. Although the Q10 of the whole body is about 2, the Q10 of the brain increases from approximately 3 between 27° and 37° C (80.6° and 98.6° F) to 4.8 between 17° and 27° C (62.6° and 80.6° F).120 On the basis of these values, if the brain could survive an ischemic insult for 5 minutes at 37° C (98.6° F), cooling to 27° C (80.6° F) or to 17° C (62.6° F) would provide 15 and 72 minutes of protection, respectively, based 161

140 Survival time (min)

PART 2  COLD AND HEAT

160

120 100 80 60 40 20 0 7

17

27

37

Core temperature (° C) FIGURE 6-35  Schematic presentation of survival time at different core and brain temperatures. A, Prediction based on a temperature coefficient (Q10) of 2. B, Prediction based on a Q10 of 3. C, Prediction based on the Q10 effect plus other factors, such as changes in neurotransmitter release (i.e., glutamate and dopamine). Actual survival times are from both neurosurgical and accidental hypothermia cases. Most of these cases fall outside of the range predicted based on Q10 alone; thus some other factors must also contribute to survival.

solely on the decreased CMRO2 (Figure 6-35). Although long survival times at brain temperatures of less than 20° C (68° F) may be predicted on the basis of increasing Q10 and diminishing CMRO2, some additional mechanisms may be required to explain intact survival after prolonged submersion, when reported Tcos are often above 30° C (86° F). These factors are schematically shown in Figure 6-36, online. Since the early 1990s, several studies that have been directed mainly toward the protection of the brain during or after cerebral ischemic events have demonstrated that even moderate brain cooling of 3° to 5° C (5.4° to 9° F) provides substantial cerebral protection from ischemic insult.* Submersion likely promotes cerebral death as tissue ischemia depletes high-energy phosphates and leads to membrane depolarization. This stimulates release into the extracellular space of excitatory neurotransmitters such as glutamate and dopamine, which mediate postsynaptic depolarization and cause calcium entry into the cell. Calcium influx mediates production of oxygen and hydroxyl free radicals (which may be involved in reperfusion injury) and release of free fatty acids, which results in eicosanoid synthesis.176 Various animal studies have shown that cooling the brain by only 3° to 5° C (5.4° to 9° F) before ischemia delays terminal depolarization and does the following: reduces the initial rate of rise of extracellular potassium;97 results in complete suppression of glutamate release and 60% reduction in the peak release of dopamine;15 attenuates ischemia-induced damage to endothelial cells;29,30 reduces hydroxyl radical production;66 and improves postischemia glucose use.64 These results relate to mechanisms other than decreased CMRO2, which may explain cerebral protection during cold-water near drowning. In summary, these findings indicate the following: (1) if the brain cools even by only 3° to 5° C (5.4° to 9° F), it is protected in excess of what would be predicted from decreased CMRO2 alone; (2) protection results from additional protective mechanisms of cooling related to neurotransmitter release, calcium flux, eicosanoid synthesis, and perhaps other phenomena; (3) the mammalian dive reflex may result in cold-induced circulatory adjustments that favor conservation of oxygen for the heart and the brain; and (4) cold-water ventilation may accelerate brain cooling and provide further protection.

IMPLICATIONS FOR SURVIVAL The paradox of whether Tco cooling is an advantage or a disadvantage depends on whether there is cessation of oxygen delivery, *References 14, 15, 64, 123, 146, 204.

162

and, if so, what Tco is when anoxia occurs and how much the Tco subsequently declines. These factors are schematically illustrated in Figure 6-36, online. If oxygen delivery is not compromised (i.e., during immersion hypothermia), then Tco cooling will eventually lead to death from cardiac arrest. However, if oxygen delivery is compromised (i.e., during submersion hypothermia and coldwater near drowning), Tco and brain cooling will prolong survival as compared with a condition in which Tco cooling does not occur (i.e., myocardial infarction). These factors are important to understanding whether children have a survival advantage over adults during cold stress. Because children cool faster, their body size would be an advantage when oxygen supply is compromised during cold-water submersion. However, when the oxygen supply is uninterrupted during head-out immersion or in cold air, the small body size becomes a disadvantage, because the onset of severe hypothermia is not as fast.

Rescue (Self-Initiated or Assisted) SELF-RESCUE FROM OPEN WATER OR AN ICE HOLE Most people have a poor understanding of how their bodies will react during cold-water immersion. Although there is individual variability, the following general principles apply. First, get breathing under control, because gasping and hyperventilation may result in gulping water or even drowning. One should be able to control breathing within 30 seconds to 2 minutes. In icecold water, loss of arm control and of the ability to grasp is progressive and begins to occur within the first 3 to 15 minutes. In open water, self-rescue may involve pulling oneself onto a floating object and out of the water as much as possible. If a person has fallen through the ice, it is usually best to turn and face the direction from which he or she came. The ice traveled over has already been proved capable of holding one’s weight. Swim to the ice ledge on the entry side of the hole. The self-rescue exit is illustrated in Figure 6-37 and can be seen in Cold Water Boating, listed in the Video References

Hold on

Kick your feet to get horizontal

Kick and pull

Slide along: DO NOT STAND

FIGURE 6-37  Self-rescue technique after falling through ice. Place the arms on the ice and kick the feet (i.e., flutter kick) until the body is horizontal with the water surface, then kick vigorously with the legs and pull the body along the ice surface. Slide or roll away from the hole, and do not stand up until it is certain that the ice is thick enough to hold body weight. (Courtesy Wilderness Medicine Newsletter. Available at http://www.wildernessmedicinenewsletter.com.)

Assess the Situation 1. Assess the victim’s physical and emotional condition. 2. Assess the ice and water conditions (e.g., ice thickness, water current). 3. Assess the equipment that you have that might be useful in a rescue. 4. Assess the rescue skills that are possessed by you and by those who are with you. Follow the Rescue Sequence The rescue sequence progresses from lowest-risk actions to highest-risk actions. Low-risk actions should be taken first. Progression to higher-risk actions is dictated by training level and available equipment. 1. Shore-assisted rescues involve talking, throwing, and reaching; untrained bystanders should limit themselves to these techniques. 2. Platform-assisted rescues involve working from or with a flotation platform (e.g., an inflatable boat or other buoyant device). 3. Finally, in a “go” rescue, the rescuer approaches and contacts the victim. This should only be done by trained personnel wearing PFDs and thermally protective dry suits (Figure 6-38). Rescuers should always perform the lowest-risk rescue first and then contact professional authorities, if possible.

UNTRAINED BYSTANDER RESCUE Every year, newspaper articles describe the death of well-meaning bystanders who rush to help victims who have fallen through the ice. It is extremely important that the untrained bystander apply the acronym STOP to his or her actions: stop, think, observe, and plan. Stop the urge to rush up to help the victim,

A

B

ASSISTED RESCUE OF A VICTIM WHO HAS FALLEN THROUGH THE ICE Self-rescue and assisted rescue both have three guidelines: (1) acknowledge the danger of the situation; (2) assess the situation; and (3) follow the rescue sequence. Recognize the Danger 1. Recognize that ice conditions are unsafe and that no one else should approach the area. 2. Recognize that the victim is in an urgent situation that is potentially life threatening but that, if proper action is taken, there is more time than might be expected to make safe and effective decisions. 3. Recognize your own limitations in terms of training and equipment.

C FIGURE 6-38  The professional rescue of a volunteer from ice water. A rescue sling is placed around the victim’s chest (A), and the rescuer then enters the water to help the victim out of the water (B). Both individuals are then pulled along the ice to safety (C). (Courtesy Gordon G. Giesbrecht.)

163

CHAPTER 6  Immersion Into Cold Water

section at the end of this chapter. It is initiated by putting the arms up on the ice and getting as much of the upper body out of the water as possible. Kick the legs vigorously to bring the body into a horizontal position. Next, kick and pull yourself forward and get on top of the ice. Once up on the ice edge, it is best to crawl or roll away from the hole until the ice is thick enough to stand on. Use ice picks, car keys, a knife, or any other available object to get a better grip on the ice. Once on solid ice, remember that hypothermia and frostbite pose threats to survival. The first thing to do is to wring the water out of clothing. It might seem that this would make one colder, but wringing out the clothing increases its insulation value, which is best in the long run. Next, decide whether to stay and try to get warm and dry by a fire or to seek shelter. If shelter is reasonably close (i.e., <30 min of exposure to the cold air), it may be beneficial to walk to safety. If it is more than 30 minutes away, it may be better to stay and build an emergency fire and campsite. It is extremely important to protect the hands from becoming frostbitten. Wring water from gloves or mittens. If the fingers are still very cold, place each hand in the opposite armpit. If necessary, pull the arms inside the jacket to place the hands directly against the skin of the armpit. When the hands have recovered, it is imperative to start a fire to warm up and dry the clothing. Although a person who cannot get out of the cold water unaided might not yet be very hypothermic, physical incapacitation will get worse within 10 to 15 minutes. Consciousness will remain for an hour or so, until Tco decreases from 37° C to about 30° C (99° F to about 86° F), so one should work to extend survival time to widen the window of opportunity for rescue. Recall the 1-10-1 principle for responses during cold-water immersion (but remember that time estimates are subject to individual variability): you have 1 minute to get your breathing under control, 10 minutes of meaningful movement, and 1 hour until you become unconscious as a result of hypothermia. Swimming should be minimized, because it causes the body to lose heat much faster than does remaining as still as possible, and it also causes exhaustion. Clothes should be kept on in the water, because they help to conserve body heat. Although the air initially trapped in clothing will eventually be forced out, it helps with flotation while it remains. Wet clothing does not cause a person to sink. The main effect of water in clothing is that its inertia makes movement difficult. The weight of water in clothing becomes a problem only when trying to exit the water. In all cases (even if wearing a thermal protection suit or a PFD), use the ice edge for support. Extend the arms over the ice and press the legs together to help to conserve body heat. Keep the head and upper body as far out of the water as possible to conserve as much body heat as possible. Remain as still as possible. This will decrease heat loss, but it may also result in the arms freezing to the ice. After about 1 hour, when consciousness is lost from severe hypothermia, drowning occurs unless the head is prevented from slipping beneath the water. If one is frozen to the ice, drowning will be prevented, and a victim might survive yet another hour before the heart stops beating (generally at a Tco <25° to 28° C [77° to 82° F]). Thus, this could double the survival time and perhaps allow rescue.

PART 2  COLD AND HEAT

because you are likely to fall through the ice and become another victim. Think and observe the victim and the surrounding conditions, including any material that might be used in a rescue attempt. Finally, plan how to assist the victim out of the water. Untrained bystanders should limit themselves to techniques that progress from talking to throwing to reaching. Talk Encourage the victim to calm down and not panic. Direct the victim to an area of strong ice, and instruct the victim to execute a self-rescue by placing the arms on the ice, kicking until the body is horizontal on the water surface, and then kicking and pulling up onto the ice. Direct the victim to crawl and roll away from the hole until stronger ice is reached. Throw Any buoyant item can be thrown to the victim to assist him or her with remaining buoyant, especially if the ice is continually breaking and not providing a secure base of support. If possible, tie a rope or cord to the object; this could allow you to pull the victim out of the water. If only a cord or rope is available, tie a large loop at the end to make it easier for the victim to hold on to it. After the rope has been grabbed, instruct the victim to put the loop over his or her body and under the arms, to put an arm through the loop and bend the elbow around the rope, or to simply hold onto the loop. Reach It may be possible to reach a victim with some implement, such as a tree branch, a ladder, or anything else that can be pushed out on the ice. Care must be taken to not get too close to the hole when trying to reach the victim with any implement. Any rescue that requires the rescuer to approach the hole in the ice should be left to trained personnel. An untrained bystander who cannot perform a rescue with the use of these techniques should help the victim to widen the window of opportunity for trained rescuers to arrive. Instruct the victim to stop struggling and to hold his or her arms still on the ice. The objective is to let the arms freeze to the ice. Make sure that someone contacts emergency personnel. Wait with the victim, and provide continuous encouragement that he or she can survive; let him or her know that help is on the way.

RESCUE BY TRAINED PERSONNEL These paragraphs are not meant to provide in-depth training for professional rescue workers but rather to describe some of the basics of high-risk rescues. The techniques used by any professional rescuer should follow the policies and procedures of their local jurisdictions.

Trained personnel should first use the lower-risk techniques that were described earlier. If these do not work, personnel should implement the higher-risk techniques described by many ice-rescue training institutions.48 Briefly, trained rescuers must not go on the ice unless they are wearing a thermal protective dry suit and a PFD. The rescuers should also be secured by a safety rope that is operated by a trained colleague. Platform-assisted rescues involve working from or with a flotation platform, such as an inflatable boat or another buoyant device. These techniques involve pushing or being transported on the buoyant platform. The first choice is to push the platform toward the victim and to use it as a reaching device. Alternatively, the rescuer can make contact with the victim directly from the platform. Finally, during a “go” rescue, the rescuer approaches and contacts the victim directly. Standard lifesaving techniques should be used to ensure that a panicking victim does not pose a threat to the rescuer. After the victim is securely contacted, the victim and the rescuer can be pulled toward shore by the attendants on shore (see Figure 6-38).

RESCUE FROM OPEN WATER Retrieval of a victim from cold-water immersion must be performed with caution. Sudden reduction of the “hydrostatic squeeze” applied to tissues below the water’s surface may potentiate hypotension, especially orthostatic hypotension.73 Because a hypothermic patient’s normal cardiovascular defenses are impaired, the cold myocardium may be incapable of increasing cardiac output in response to a hypotensive stimulus. A victim’s vertical posture may also potentiate hypotension. Hypovolemia as a result of combined cold- and immersion-induced diuresis as well as increased blood viscosity potentiate these effects.27 Peripheral vascular resistance may be incapable of increasing, because vasoconstriction is already maximal as a result of cold stress. The net result of the sudden removal of a hypothermic patient from the water is similar to sudden deflation of antishock trousers on a patient in hypovolemic shock: abrupt hypotension. This has been demonstrated experimentally in mildly hypothermic human volunteers,72 and it has been suspected as a cause of post-rescue death in many immersion hypothermia victims.73,157 Accordingly, rescuers should attempt to maintain hypothermic patients in a horizontal position during retrieval from the water and aboard the rescue vehicle (Figure 6-39).3,73,157 If rescuers cannot recover the patient horizontally, they should place the victim in a supine posture as soon as possible after removal from cold water (Box 6-7).157 Helicopter hoist extractions can be performed directly by a rescue swimmer (Figure 6-40) or with a rigid litter from a boat (Figure 6-41, online). FIGURE 6-39  Single (A) and double (B and C) sling techniques affect how vertical the victim is during extraction from the water. The rescue slings provide a leverage advantage, especially when there is high freeboard (A and B). A wet victim is wrapped in a makeshift vapor barrier to minimize evaporative and convective heat loss during boat transport (D). (Courtesy Gordon G. Giesbrecht.)

A

B

C

D

164

BOX 6-8  Controversy Box: Prehospital Warming is

Although severe hypothermia is a critical condition, rescue and treatment do not necessitate rapid and reckless actions. Rescuers and medical providers should take the time required to safely remove the victim from the cold stress and then do as much as possible to be gentle and to keep the patient horizontal. The patient’s core has been cooling gradually for a long time (i.e., hours or even days), and a delay of a few minutes to get organized for treatment will not make the patient’s condition worse. However, rushing may result in patient jostling that induces ventricular fibrillation and cardiac arrest.

For many decades, it was believed that warming would cause massive vasodilation and result in cardiac arrest as a result of a precipitous drop in blood pressure or Tco or the return of noxious metabolites from the periphery. Many studies have demonstrated that a very cold patient will display intense vasoconstriction such that only massive heating from warm-water immersion could override this thermoregulatory response. Any heat source (other than a warm water bath) that is available in a prehospital setting will likely be safe. Thus it is now widely accepted that gradual core rewarming through the application of heat to the chest and axillae is valuable as long as cardiovascular stability is maintained.

Presents an Emergency That Must be Dealt With Quickly

The patient’s Tco may continue to decline—depending on the quality of insulation provided, the patient’s endogenous heat production, active or passive manipulation of extremities, and the site of Tco measurement—even after he or she has been rescued as a result of the physiologic processes described earlier as “afterdrop.” To diminish this effect, the patient’s physical activity must be minimized. Conscious patients should not be required to assist with their own rescue (e.g., by climbing up a scramble net or a ship’s ladder) or to ambulate when they are out of the water (e.g., by walking to a waiting ambulance or helicopter).49,122,157 Physical activity increases afterdrop, presumably by increasing perfusion of cold muscle tissue with relatively warm blood.11,52,53,55 As this blood is cooled, venous return (the circulatory component of afterdrop) contributes to a decline in myocardial temperature, thereby increasing the risk for ventricular fibrillation.87 Experiments on moderately hypothermic volunteers with esophageal temperatures of 33° C (91.4° F) demonstrated a threefold greater afterdrop during treadmill walking than while lying still.10,56 Such an exercise-induced enhancement of afterdrop could precipitate post-rescue collapse. Throughout the rescue procedures and during subsequent management, hypothermic patients must be handled gently.3,77,122 Excessive mechanical stimulation of the cold myocardium is another suspected cause of death after rescue.110,192 Several extraction techniques are presented in Figure 6-39 and can be seen on the videos in the Video References section at the end of this chapter. The technique depends on the number of rescuers, the design of the boat platform and the resultant freeboard, and the equipment on hand. Victims can be pulled by their clothing or PFDs; placed into single or double rescue slings, rescue nets, or even hoists; and extracted either head first or horizontally. It is easier to be gentle and to keep the victim horizontal if there are low gunnels or if the boat has a rescue port on the side. If possible, the method that will be used to package the patient (see Packaging, later) should be prepared ahead of

Dangerous and Should Be Avoided

time. Regardless of the technique used, care should be taken to be as gentle as possible and to lift the patient directly into the packaging system.

Medical Management This section describes prehospital management of hypothermia with specific reference to immersion pathophysiology. The hospital management of both accidental immersion and land-based hypothermia is described in Chapter 5: Accidental Hypothermia. Prehospital management of hypothermia patients, both in the field and during transportation to a site of definitive medical care, varies with the patient’s level of hypothermia, the rescuer’s level of training, the resuscitative equipment available, type of transportation, and time required for delivery to definitive care. Medical personnel must exercise good clinical judgment to balance all of these factors to select appropriate therapeutic modalities (Box 6-8). The primary goals of prehospital management of victims of accidental immersion hypothermia are prevention of cardiopulmonary arrest; prevention of continued Tco decline; moderate safe core rewarming, if practicable; and transportation to a site of definitive medical care.* Aggressive rewarming in the field has been contraindicated in the past, because the means to either diagnose or manage the many potential complications of severe hypothermia are unavailable in this setting.122 However, in the prehospital scenario of cold-water immersion, there is no source of heat that could be considered aggressive. Figure 6-42 indicates the levels of aggressiveness and effectiveness of various sources of heat for hypothermia and frostbite treatment. When transportation to a site of definitive care will take more than 30 minutes or is impossible, rewarming in the field with the use of the principles and techniques of management described in the following paragraphs may be appropriate (Box 6-9).

EXAMINATION, TRIAGE, AND LIFE SUPPORT Because hypothermia affects virtually every physiologic process, rescuers should manage a severely hypothermic patient as they would a victim of multiple trauma.156,157 Rescuers should not focus solely on Tco to the exclusion of other potentially life-threatening problems. Conversely, when the incident includes cold exposure, care must be taken to not focus solely on trauma injuries. Several *References 33, 79, 105, 112, 152, 157. BOX 6-9  Controversy Box: Afterdrop Is an Artifact

and Is Unimportant

FIGURE 6-40  A U.S. Coast Guard helicopter hoist rescue with a rescue swimmer and a victim. (Courtesy Gordon G. Giesbrecht.)

Rescuers and emergency medical personnel should be aware that Tco will continue to drop after an individual has been removed from the cold stress (see Figure 6-12). Although some decrease is inevitable, the understanding is that anything that increases blood flow to cold tissue (e.g., the legs) will increase afterdrop. Thus, patients should be kept from walking and remain horizontal, and the arms and legs should not be rubbed or massaged in an effort to warm the patient.

165

CHAPTER 6  Immersion Into Cold Water

BOX 6-7  Controversy Box: A Hypothermic Patient

PART 2  COLD AND HEAT

Power source

Heat level/ aggressive

Heat source Prehospital

Treatment effectiveness

Hospital

Hypothermia

Frostbite

XX

XXX

Fire Nonelectric

Chemical pack

–

√

IV fluid

√

–

√ –

–

√

√

√

√

Low-to-moderate heat

Warm sweet drink Inhalation warming

Non-aggressive

Warm water bottles Warm body Charcoal HeatPac

–

√√

√

Electric blanket

Electric blanket

√

√

Water blanket

Water blanket

√

√

Forced air warming

√√

√

XX

– – – –

Electric Forced air 120 VAC warming Warm shower Warm bath

Warm bath Lavage CAVR Fem-fem

XXX

High heat

√√√ √√√

Aggressive

√, Effectiveness

–

√√√ √√√√

Bypass –, Not effective or applicable

–

X, Harmful

FIGURE 6-42  Heat sources that could be used for hypothermia rewarming classified by location, heat level or aggressiveness, and treatment effectiveness for hypothermia and frostbite.

patients have died of hypothermia when treatment focused only on non–life-threatening physical injuries. It is rarely possible to measure Tco in the field. However, a diagnosis can be made on the basis of the patient’s history (to confirm that the main insult is cold exposure) and his or her signs and symptoms (see Figure 6-13). Generally, if a patient is mentally alert and shivering vigorously, he or she can be considered mildly hypothermic. If shivering is waxing and waning or absent or if consciousness is diminished or absent, he or she can be considered moderately to severely hypothermic. In accordance with standard emergency medical procedures, the ABCs of first aid—airway, breathing, and circulation—are essential.3,157 Rescuers should ensure an open airway and confirm the presence of adequate ventilation and circulation. If the patient is severely hypothermic, respirations and pulse may be slow, shallow, and difficult to detect3,156; therefore, rescuers should take 30 to 45 seconds to assess these vital signs.3 If neither the pulse nor breathing is detectable, rescuers should commence cardiopulmonary resuscitation (CPR) in accordance with normal basic life support protocols.3,156 Figures 6-43 and 6-44 are treatment algorithms for field treatment and medically equipped emergency personnel.152 Cardiac rhythm should be carefully monitored. Percutaneous electrodes may be required to overcome interference from muscle fasciculations or shivering.3 Endotracheal intubation and administration of heated and humidified air or oxygen are useful for management of apnea or hypoventilation and for reduction of further respiratory heat loss.3 Mouth-to-mouth or mouth-to-mask ventilation also provides heated and humidified air. If oxygen is available, it may supplement mouth-to-mouth or mouth-to-mask ventilation. Mouth-to-mouth or mouth-to-mask ventilation has the added advantage of providing a small amount of carbon dioxide for the patient’s inspired gases. This may be useful for prevention of hypocapnea as a result of relative hyperventilation in a severely hypothermic victim whose metabolic production of carbon dioxide is diminished.28 This is important because hypocapnea may decrease the threshold for ventricular fibrillation. Hypothermic patients with any detectable pulse or respiration do not require the chest compressions of CPR, although severe bradycardia and bradypnea may be present.3,156 This differs from 166

HYPOTHERMIA: FIRST-AID PREHOSPITAL CARE Rescue/examine

Responsive?

Yes

No

Respiration?

Yes Assume cardiac output

Shivering?

Yes

No

Pulse? (Check for 60 sec)

Spontaneous rewarming (insulate, vapor barrier, provide fuel)

Heat optional

No Ventilate 3 minutes

Heat desirable

Yes

No

Continue ventilation if still apneic

CPR

Heat if possible Hospital FIGURE 6-43  Algorithm for field treatment of a hypothermic victim.

BOX 6-10  Controversy Box: CPR Should be Started

Rapidly if a Pulse Cannot be Found Quickly

Rescue/examine

A hypothermic patient has been cooling for a long time, and it will likely not affect the outcome if a few minutes are taken to ensure that the heart is not functioning before commencing CPR. Premature chest compressions can cause an irritable heart to fibrillate. An initial pulse check should be done for 60 seconds. If no pulse is found, 3 minutes of rescue breathing might oxygenate the heart enough to strengthen contractions. If a pulse still cannot be found after another 60-second check, it can be assumed that the heart is not functioning, and chest compressions can be started in accordance with local jurisdiction protocols (see Figure 6-43).152

Responsive?

Yes

No

Respiration?

Yes Assume cardiac output

Shivering?

Yes

No

Spontaneous rewarming (insulate/ vapor barrier)

Heat if possible

No Ventilate 1–2 minutes

Cardiac monitor

Non-arrest rhythm

Arrest rhythm

Ventilate if apneic

Cardiac monitor

Central pulse

PEA

CPR

Yes

Heat if possible Hospital FIGURE 6-44  Algorithm for emergency medical treatment of a hypothermic victim.

normothermic CPR protocols, with which chest compressions may be indicated if bradycardia fails to provide sufficient cardiac output or systolic blood pressure.3 Because the metabolic requirements of hypothermic patients are reduced, bradycardia and bradypnea may still meet tissue oxygen requirements.29,49 Inappropriate administration of chest compressions in an attempt to augment cardiac output may precipitate ventricular fibrillation from mechanical stimulation of the irritable myocardium29 (Box 6-10). If a victim of cold-water immersion is found floating face down, drowning should be suspected and managed accordingly (see Chapter 75: Submersion Injuries and Drowning). In this case, correction of anoxia is paramount, and consideration of hypothermia is of secondary importance.3,130 Normal advanced cardiac life support protocols should not be routinely applied to severely hypothermic patients in cardiac arrest, because management beyond basic life support differs from that used for normothermic patients.3,29 Defibrillation and pharmacologic interventions are usually ineffective for myocardial temperatures of less than 30° C (86° F).3,7,29 Furthermore, repeated defibrillatory shocks may damage the myocardium.3,156 Defibrillation should be limited to three shocks at 200, 300, and 360 joules, consecutively, for patients who are colder than 30° C (86° F).3 Administered medications are ineffective, and they may accumulate to toxic levels,

because drug metabolism by the hypothermic liver and kidneys is reduced.29,196 For hypothermic patients with a Tco of more than 30° C (86° F), normal advanced cardiac life support protocols may be used.3 All intravenous fluids should be warmed before administration. However, it may be necessary to extend the recommended interval for intravenous medications because of the patient’s reduced metabolic rate. For the unconscious hypothermic patient who is not in cardiopulmonary arrest, endotracheal or nasotracheal intubation should be performed gently. The insertion of pacemaker wires and central venous catheters has been suspected of precipitating ventricular fibrillation, but prior ventilation with 100% oxygen has been associated with a decreased risk for this complication.27,28 Rescuers should not withhold endotracheal intubation, if indicated, for fear of precipitating ventricular fibrillation.3 If the patient does not require immediate life support intervention, a thorough and systematic examination must be performed as quickly as possible before the initiation of treatment for hypothermia. Because severely hypothermic patients may have a markedly depressed mental status, they may not respond normally to painful stimuli. Victims of immersion hypothermia may have suffered trauma before entering or while in the water. Central nervous system, skeletal, and soft-tissue injuries may be overlooked unless a careful examination occurs. Attention should be paid to the patient’s mental status and other central nervous system signs. Rescuers should evaluate the level of consciousness, presence or absence of shivering, and pupillary size and light reflex. Pupils may appear fixed and dilated in an unconscious and severely hypothermic patient, thus simulating the appearance of death. The diagnosis of death should not be made in a hypothermic patient, particularly in a field setting, unless resuscitation efforts fail after adequate rewarming efforts. The vital signs should be carefully measured, with particular attention paid to the Tco. A low-reading thermometer that is capable of recording down to 20° C (68° F) is required. Esophageal temperature at the level of the atria is the most clinically useful Tco obtainable, because this site most closely parallels cardiac temperature.56,87 However, most rescue personnel are almost never equipped to measure esophageal temperature. Rectal temperature is the most easily obtained Tco, yet rescuers often show reluctance to obtain a recording from this site in the field, and incorrect thermometer placement may cause an erroneous reading. If neither esophageal nor rectal temperature is taken, oral or axillary temperature is of limited value. Neither of these will accurately reflect Tco in a victim of immersion hypothermia. Facial cooling affects oral temperature, and cold skin temperature affects axillary recordings. However, the patient’s Tco will not be lower than that indicated by an oral or axillary recording. Thus, rescuers can use even superficial temperatures in a limited way to monitor the patient’s status, although this is not ideal. Hemorrhage should be controlled in the usual manner. Antishock trousers are normally contraindicated, because they are likely to be ineffective in the face of the maximal vasoconstriction already present in a severely hypothermic patient.29 Because hypothermia itself can cause hypotension without massive fluid losses, antishock trousers should be used only if they are required for temporary stabilization of a suspected pelvic fracture.29 167

CHAPTER 6  Immersion Into Cold Water

HYPOTHERMIA: EMS PREHOSPITAL CARE

PART 2  COLD AND HEAT

INSULATION, STABILIZATION, AND REWARMING After recovery of the patient from the water and management of immediate life-threatening emergencies, the next objectives are prevention of further heat loss and efforts at moderate rewarming (i.e., 1° to 2° C/hr [1.8° to 3.6° F/hr]). Strategies for moderate rewarming in the field vary with the equipment available, training of rescue personnel, environmental conditions, and length of time required for transport to a site of definitive care. Maximum insulation of the whole body from any further environmental cooling is an obvious first requirement. The main goals for rescue personnel are to maintain or improve cardiorespiratory stability and to minimize Tco afterdrop, which can depress cardiac temperature and potentiate ventricular fibrillation. Packaging The purpose of packaging a patient in the field or during prehospital transport is to minimize all sources of heat loss (i.e., evaporation, conduction, convection, and radiation). Rescuers should maintain the patient in a horizontal position to prevent hypotension, and movement of the patient must be kept to a minimum. Clothing should be cut away if it is wet and if the patient is in a sheltered area. The patient’s skin should be dried with gentle blotting motions (no rubbing), and the patient should be protected by dry and insulating clothing and blankets, a sleeping bag, or a specialized rescue bag (Figure 6-45). This protection must include the head and neck. Incorporation of a windproof and waterproof layer or vapor barrier is of value for prevention of convective and evaporative heat loss. This is particularly important for patients who require helicopter evacuation, because downwash from helicopter rotor blades can reach wind speeds in excess of 160 km/hour (100 mph), thereby potentiating significant heat loss from windchill. It is important to note that the vapor barrier should also protect the insulation from becoming wet. Therefore, if the patient is dry, the vapor barrier can be wrapped around the outside of the insulation. However, if the patient is wet and his or her clothing cannot be changed (i.e., a survivor picked up by a small rescue boat), the vapor barrier should be placed around the patient inside the insulation layers. Spontaneous Rewarming Patients who are only mildly hypothermic (i.e., exposed to cold water for a relatively short time, fully conscious, and vigorously shivering with a Tco of >32° to 33° C [89.6° to 91.4° F]) are usually capable of rewarming themselves without difficulty. Heat production from shivering can reach levels that are five to six times that of the resting metabolic rate.38 Shivering is thus a highly effective means of rewarming, particularly if rescuers insulate the patient’s

BOX 6-11  Controversy Box: Airway Warming

Effectively Warms the Core

It is important for an emergency medical provider to know that airway warming does not significantly warm the body core (see Figure 6-12). However, the method does have some advantages. Most of the heat transfer occurs in the upper airways and may warm certain areas in the brainstem. Moisture loss is eliminated. It is important to know that some additional warming techniques—preferably application of heat to the chest and axillae—are necessary to actually raise the temperature of the heart.

head and body with vapor-barrier garments to minimize evaporative heat loss.56 Vigorous shivering has been shown to be capable of producing rewarming rates of as high as 3° to 4° C/hr (5.4° to 7.2° F/hr).49,56,62 Patients who are conscious and vigorously shivering are generally not a medical emergency and usually do not require immediate transportation for definitive care. However, rescuers should be aware that prolonged periods of shivering consume the patient’s endogenous energy reserves. Thus rescuers should administer oral glucose-containing fluids to conscious patients who have adequate cough and gag reflexes. Attention to energy reserves in unconscious and severely hypothermic patients is also important. Warmed intravenous glucose solutions are useful for these patients as part of definitive resuscitative and rewarming protocols, which are described later in this chapter.3,29 Alcoholic beverages are contraindicated in all cases. Inhalation Warming Rescuers should attempt to minimize respiratory heat losses. Hypothermic patients lose up to 11 to 13 kcal/hr through inhalation of relatively cold and dry air and through exhalation of water-saturated air at near Tco.65,200 Administration of heated and humidified air or oxygen at approximately 42° to 46° C (108° to 115° F) can result in net positive gain of 17.1 kcal/hr. Although this is a relatively small amount of heat compared with the total kilocalories required to completely rewarm the hypothermic patient, heated and humidified ventilation is of value for insulating the airway from further evaporative heat loss. However, some studies have shown that inhalation rewarming reduces metabolic heat production provided by shivering.54 In experimental subjects whose shivering was pharmacologically inhibited, inhalation warming did not appear to provide any advantage over spontaneous rewarming.67 Other suggested benefits of inhalation warming include rehydration, stimulation of mucociliary activity in the respiratory tract, and direct heat transfer from the upper airways to the hypothalamus, brainstem, and other brain structures. Any warming of the respiratory, cardiovascular, or thermoregulatory centers could be of benefit. Although research continues regarding efficacy of airway rewarming, most hypothermia treatment protocols continue to recommend inhalation warming as an adjunct to overall rewarming strategies.* Warmed Intravenous Fluids Administration of warmed intravenous fluids is beneficial for reversing hypothermia-induced dehydration and hypovolemia.29,156 Replacement of fluids before rewarming has been shown in dogs to augment cardiac output.140 Dextrose 5% in water or normal saline and normal saline alone are preferable to lactated Ringer’s solution, because a hypothermic liver may be unable to metabolize lactate normally.157 Administration of 300 to 500 mL should occur fairly rapidly, with the remainder of the liter administered over the next hour.5 In no case should cold intravenous fluids be administered. Plastic intravenous fluid bags can be easily carried inside of a rescuer’s clothing (preferably next to the skin) to keep the fluids warm and to supply some perfusion pressure (Box 6-11).

FIGURE 6-45  Packaging of a cold-stressed volunteer. Clothing was removed, the skin was dried with blotting motions, and the volunteer was then placed in an insulated bag and wrapped with a vapor barrier. (Courtesy Gordon G. Giesbrecht.)

168

Body-to-Body Rewarming Body-to-body warming of the hypothermic patient has long been advocated as an acceptable field treatment. Sir John Franklin, in *References 3, 27, 29, 33, 49, 157, 195.

FIGURE 6-46  Placement of a charcoal heater on the chest. Warming ducts are wrapped over the shoulders and touching the neck, under the axillae, and over the chest. This configuration provides heat to two of the three main areas for heat transfer to a cold patient.

his 1823 text Narrative of a Journey to the Shores of the Polar Sea in the Years 1819, 20, 21, describes this technique for resuscitation of an expedition member who was recovered from ice water.41 When wrapped together in a blanket or sleeping bag, a rescuer can donate body heat to a hypothermic patient. However, experimental studies on human volunteers have failed to demonstrate a rewarming advantage with this technique for shivering individuals. When subjects were cooled to an average Tco of 34.6° C (94.3° F), body-to-body rewarming proved no better than did shivering alone.62 In this study, the heat donated by the rescuers was only sufficient to offset the heat lost by the inhibition of shivering. Several theoretic arguments mediate against the routine use of body-to-body rewarming for shivering patients in the field: (1) the large heat loss of an immersion hypothermic victim (e.g., 300 kcal in cooling an average normothermic adult to a Tco of 33° C [91.4° F]) is unlikely to be reversed by the relatively small amount of heat provided by the donor (i.e., a resting, nonshivering adult produces only about 100 kcal/hr);62 (2) rescuers provide a relatively small surface area that is in direct contact with the hypothermic victim through which to donate heat; (3) peripheral vasoconstriction in the victim will limit heat flow to the core;37 and (4) external heat from body-to-body contact will inhibit the hypothermic victim’s endogenous heat production through shivering.56 However, for severely hypothermic and nonshivering victims or for victims whose shivering thermogenesis is inhibited by alcohol, medications, age, or anything else, body-to-body rewarming may be used. Furthermore, body-to-body rewarming may provide important psychological support to the patient. For these reasons, rescuers should weigh the likelihood of effective rewarming against the advantages and disadvantages of body-to-body rewarming when devising a field rewarming strategy for any particular hypothermic patient. Heating Pads The application of external moderate heat sources to hypothermic patients has been a traditional method of field rewarming. Particularly when they are applied to the patient’s thorax, neck, and groin (i.e., areas with high potential for conductive heat transfer),85 hot water bottles, chemical and charcoal heat packs (Figure 6-46), heating pads, and other warmed objects have been used to attempt to stabilize the patient’s Tco. If a patient is shivering vigorously, the Tco will warm at a similar rate as with external heat.* For more severely hypothermic patients who are not shivering, these types of external heat sources would help to stabilize and even increase the patient’s Tco, which would likely remain low if no heat were added. A recent study demonstrated that charcoal heating provides a significant rewarming advantage for hypothermic subjects when shivering was pharmacologically inhibited.92 *References 21, 56, 80, 113, 160.

Arteriovenous Anastomoses Rewarming The arteriovenous anastomoses (AVA) rewarming technique relies on the physiologic AVAs that exist in human digits and on the superficial venous rete in the forearms and the lower legs. Warming these areas opens the AVA and increases superficial venous return via the rete. Warmed venous blood thus reaches the core without excessive countercurrent heat loss to cold arteries (i.e., superficial veins are not in close contact with arteries). As a result of the pioneering work of Vanggaard and Gjerloff,189 who proposed AVA rewarming, the Royal Danish Navy has been using this technique since 1970.187 Recent experimental studies have confirmed the efficacy of this technique.188 Mildly hypothermic subjects with an esophageal temperature of 34.2° C (93.6° F) whose hands, forearms, feet, and lower legs were immersed in either 42° C (108° F) or 45° C (113° F) water had a smaller postcooling afterdrop as compared with shivering alone (0.4° C [0.7° F] as compared with 0.6° C [1.1° F]) and a significantly faster rate of rewarming (6.6° C/hr [11.9° F/hr] and 9.9° C/hr [18° F/hr]) as compared with shivering alone (3.4° C/hr [6.1° F/hr]). Although this technique may be difficult to implement in some field settings, it may be practical for mildly hypothermic victims on rescue vessels or other vehicles where a source of warm water is available. As with heating pads and other sources of external heat, however, rescuers should be concerned about the possibility of thermal burns. In the previously described study, no burns were observed in the experimental subjects, even when their extremities were immersed in 45° C (113° F) water, although some subjects complained of initial discomfort at this temperature. Rescuers opting to use AVA rewarming should perhaps start with a water temperature of 42° C (108° F) and gradually raise the temperature to 44° C (111° F).188 Another concern with AVA rewarming concerns potential cardiovascular instability. Hypotension may occur as a result of an increase in peripheral blood flow in a hypovolemic patient. If the patient is required to be in a semi-upright position to receive AVA rewarming, orthostatic hypotension could potentially add to cardiovascular instability. No experimental data support these potential cardiovascular problems, but studies of AVA rewarming have only been performed on mildly hypothermic subjects.188 Further research is required to evaluate the efficacy and safety of AVA warming on severely hypothermic patients. Forced Air Warming Forced air warming (FAW) is a technique that was derived from a treatment modality used to prevent or reverse hypothermia in surgical patients.106,149 Convective heat transfer is provided by warm air blown into warming covers over the patient’s body. Both experimental and clinical data support the efficacy of this technique on mild, moderately, and severely hypothermic patients. In mildly hypothermic experimental subjects, FAW was associated with a 30% smaller afterdrop as compared with shivering alone. Furthermore, during the initial 35 minutes of rewarming, shivering patients experienced net heat loss of 30 to 50 W as compared with net heat gain from FAW of 163 to 237 W.61 In moderately to severely hypothermic patients with a mean rectal temperature of 28.5° C (83.3° F) who were treated in an emergency department, FAW (when used in conjunction with warmed intravenous fluids and inhalation warming) achieved a rewarming rate of 2.4° C/hr (4.3° F/hr), which was nearly twice that of patients treated only with warmed intravenous fluids and inhalation warming (1.4° C/hr [2.5° F/hr]).153 In another series of experiments involving human subjects, a FAW device designed for field use was associated with significantly higher Tco rewarming rate (5.8° C/hr [10.4° F/hr]) as compared with shivering alone (3.4° C/hr [6.1° F/hr]), but it showed 169

CHAPTER 6  Immersion Into Cold Water

Rescuers should be aware of several potential hazards with this rewarming technique. Hypothermic skin is very sensitive to heat and easily injured. All sources of external heat must be separated from direct contact with the patient’s skin to prevent severe thermal burns.156 Third-degree burns have resulted from the application of a lukewarm hot-water bottle directly to a hypothermic child’s skin.129 Furthermore, heat packs that make use of burning charcoal as a heat source can create a carbonmonoxide hazard within an enclosed space.160

Core temperature (° C)

PART 2  COLD AND HEAT

REWARMING

40 35 30

Start cooling

High heat

Shivering

Shivering or moderate heat Invasive heat

End cooling

High heat

Moderate heat

Nonshivering 25

End cooling

No heat

20 Time

FIGURE 6-47  Schematic illustration of the effectiveness of various rewarming techniques under shivering and nonshivering hypothermic conditions. The dashed line indicates the approximate core temperature at which shivering is spontaneously abolished.

no advantage over shivering with regard to decreasing afterdrop.35 When shivering was inhibited with meperidine in human volunteers,57 FAW was associated with 50% decrease in afterdrop and 600% increase in rewarming rate as compared with spontaneous rewarming alone.67 A different prototype FAW device that made use of a collapsible rigid patient cover and that was evaluated experimentally on nonshivering human volunteers was associated with smaller afterdrop and faster rewarming rate as compared with spontaneous rewarming alone.60 In summary, FAW has shown significant promise as both a field and hospital treatment modality. It is a safe and noninvasive technique that can both decrease afterdrop and increase the Tco warming rate of immersion hypothermic patients. Figure 6-47 schematically illustrates Tco responses to various rewarming methodologies under mild (i.e., shivering intact) and severe (i.e., shivering absent) hypothermic conditions.

TRANSPORTATION Stabilization, insulation, and rewarming of the hypothermic patient should be started during transport of the patient to an appropriate medical center for definitive rewarming. If possible, the receiving facility should be selected on the basis of its knowledge of and experience with management of hypothermic patients. In the same manner that victims of multiple trauma are most appropriately managed in trauma centers, severely hypothermic patients are best managed in hospitals equipped to handle potential complications and to provide core rewarming therapies. For example, a hospital with cardiac bypass rewarming capabilities may be a better choice for management of a severely hypothermic patient than a hospital without such qualifications, even if the former may require a longer transport time.

170

FIGURE 6-48  Norwegian ice breaker.

During transport to a site for definitive medical care, emergency medical personnel should frequently monitor the patient’s Tco and other vital signs. In addition, they should attach an electrocardiography monitor and continue administration of warmed intravenous fluids, heated and humidified air or oxygen, and other rewarming efforts discussed previously. Rescuers should maintain the hypothermic patient in a supine posture, and they should restrict the voluntary movements of conscious individuals. At the receiving facility, rescuers should ensure that the patient is carried (rather than allowed to walk) to the treatment location. In summary, prehospital rescue and management of immersion hypothermia victims requires understanding the physiologic events that occur during cooling and recovery. With such understanding, medical personnel can better prepare for and manage this potentially difficult environmental emergency. When prehospital care is performed safely and effectively, definitive hospital care is more likely to have a successful outcome. Finally, it should be noted that, if you are from a Nordic country, you are oblivious to cold, and this chapter is likely irrelevant to you (Figure 6-48).

VIDEO RESOURCES 1. Cold Water Boot Camp. Available at www.coldwaterbootcamp.com 2. Cold Water Boating (©2008—State of Alaska, Department of Natural Resources, Division of Parks and Outdoor Recreation, Office of Boating Safety). Available at www.expertconsult.com. 3. The Cold, Hard Facts of Winter Roads Safety (©2007—Manitoba Infrastructure and Transportation/University of Manitoba). Available at www.expertconsult.com.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

36

CHAPTER 7 

Nonfreezing Cold-Induced Injuries

20

CHRISTOPHER H.E. IMRAY AND JOHN W. CASTELLANI

Nonfreezing cold-induced injury (NFCI) is a clinical syndrome that results from damage caused to tissues exposed to cold temperatures at or above the freezing point of water (0° to 15° C [32° to 59° F]). NFCI does not involve tissue freezing, which distinguishes it both clinically and pathologically from frostbite.36 The earliest descriptions of this syndrome had their origins in the military. Baron Dominique Jean Larrey, Napoleon’s chief surgeon, used the word congelation to describe the nonfreezing injuries together with frostbite casualties that occurred during the 1812 assault on Russia.92 Historically, infantry regiments have been decimated by cold and wet conditions, and many medical advances in understanding the pathophysiology and clinical course of NFCI have occurred after wars.2,35 However, it has been observed that the continuity of research tends to lag during the periods between major military campaigns.98 Developments in prevention of cold injury have flourished as new clothing and footwear have been designed, but little progress has been made in the treatment of NFCI. There is a rise in the number of people pursuing recreational activities in harsh environments, and as a consequence, civilian NFCI is becoming more prevalent. However, because many physicians are unfamiliar with NFCI, it may go undiagnosed during assessment of the cold-exposed victim.98 This results in unnecessary hospital admissions and potentially harmful and expensive therapy.41 Proper education and awareness of the hazards innate to the cold environment should mean that NFCI is preventable in most circumstances. This chapter explores the history, epidemiology, pathophysiology, and current prevention and treatments of NFCI, as well as pernio (chilblains), cryoglobulinemia, and cold urticaria.

Epidemiology Individuals suffering cold and wet extremities for extended periods are at risk for NCFI. During the 1800s, NFCI was observed more frequently when the temperature hovered around the freezing point—when the ground was muddy rather than frozen.43,91 Standing or sitting for long periods, wearing constrictive footwear, malnutrition, fatigue, or the blunt trauma of marching on cold, wet feet all added to the severity of injury.92 Original animal studies that modeled NFCI demonstrated that cold temperatures near the freezing point were more likely to cause injury when the extremities were wet than when they were dry.10,91 Ambient temperature and wind speed can both influence cooling.32,114 With “shelter limb” (dependency without cold) and “paddy foot” (wet but not cold), one observes an injury that has no apparent distinguishing differential feature from NFCI. This suggests that neither cold nor wet is a prerequisite to developing the injury. It appears that NFCI is a reperfusion injury that develops after a sustained period of peripheral vasoconstriction.98

MILITARY In combat settings, there is rarely the time, equipment, or opportunity to apply appropriate remedies to NFCI. In the 1854 Crimean War, cold injury was documented more often among “the men in the trenches [who] were so restricted in their movements.… Frequently this position happened to be the bottom of a trench knee-deep in mud and water or half-filled with snow.”91 In November 1944, during World War II, American forces sustained

11,000 cases of trench foot.110 Evaluation of possible risk factors for cold injury during the 1982 war in the Falkland Islands has been published. A year after exposure, there were no cases of cryoglobulinemia or hematologic evidence to suggest that any of the men who developed cold injury had abnormal circulating proteins, plasma hyperviscosity, or indicators of alcohol abuse.20 In the 1990s, both the U.S. Army and the Israel Defense Forces recorded that the majority of nonfreezing cold injuries occurred during routine training exercises, rather than during combat operations.26,68,73

ETHNICITY Historically, the first reports of increased susceptibility in certain ethnic groups (blacks) to cold-weather injury came from the American Civil War.87 It was also noted that there was an increased incidence of cold injuries among blacks in the cold winter conflict in the Ardennes in 1944 during World War II.110 A major retrospective study looking at 2143 U.S. Army cold-weather injury hospital admissions between 1980 and 1999 found that the injury rates for men and women were 13.9 and 13.3 per 100,000 soldiers, respectively.26 Increased rank and experience were associated with a decrease in cold-weather injuries. There were 3.3 times more blacks hospitalized than whites, (95% confidence interval [CI], 3.1-3.7), and infantry and gun crews appeared to be at greater risk. There was a marked reduction in the number of soldiers admitted to the hospital between 1980 and 1999, from greater than 30 cases per 100,000 soldier years to almost zero. Young male African Caribbeans in the British Army have been found to have a 30 times greater chance of developing peripheral cold injury and are more severely affected than are their white counterparts following similar climatic exposure, using similar clothing and equipment. Pacific Islanders carry a 2.6 times increased risk, whereas being a Gurkha appears to be protective.15 Peripheral vascular responses to a local cold stress were studied in four groups of Indians: South Indians, North Indians, Gurkhas, and high-altitude natives of 3,500 meters (11,483 feet). The heat output and cold-induced vasodilation (CIVD) were highest in high-altitude natives, with the lowest observed in South Indians.67

PREVALENCE In most North Atlantic Treaty Organization (NATO) countries, prevalence of NFCI injuries appears to be static or decreasing among military personnel. However, in the British military, there appears to be a marked increase in the incidence of reported cold-weather injury. Over a 4-year period, the reported rate increased from 9 per 1000 to 30 per 1000 recruits, with the majority of cases (90%) originating during field-based training. Independent factor analysis demonstrated that African Caribbeans were 13.2 (95% CI, 9.5-18.4, probability [p] <0.01) times more likely to report cold injury and 27.3 (95% CI, 16.3-45.9, p <0.01) times more likely to be medically discharged than were whites.113 The rise in NFCI in the military of the United Kingdom (UK) may be caused by increased exposure, lower threshold to diagnose the condition, increased awareness, or recruiting of a different and more sensitive population. Alternatively, the rise may be caused by a type I statistical error (poor specificity of the tests used to diagnose NFCI or excessive credulity) or a type II error

For online-only figures, please go to www.expertconsult.com

171

PART 2  COLD AND HEAT

(poor sensitivity of the tests used to diagnose NFCI). Perhaps other countries are failing to diagnose and report the condition.52

CIVILIAN The environmental conditions that can produce NFCI in military settings are also found in the context of wilderness medicine. Outdoor recreation may lead to cold, dehydrated, exhausted, and wet hikers exposed to the elements for an extended period. These individuals may be unwilling or unable to take the time and effort to care for their wet boots and socks, and they may be unaware of the risks inherent in the situation. Other civilian populations at risk for NFCI include the homeless,116 older adults,83 and alcoholics.98 Personal Administration Proper protective equipment and appropriate use are important factors reducing the incidence of NFCI. Factors affecting the incidence of frostbite are closely related to those affecting NFCI. A surprisingly high incidence of frostbite has been reported in mountaineers. In one study, the mean incidence was 366 per 1000 population per year. Mild (grade 1) injury (83.0%) and hand (26.4%) and foot (24.1%) involvement were most common. There was a significant relation between lack of proper equipment (odds ratio 14.3) or guide (p <0.001) and the injury. Inappropriate clothing, lack or incorrect use of equipment, and lack of knowledge of how to deal with cold and severe weather were claimed to be the main reasons for the injury.47 Cold injury is uncommon in Antarctica. Despite this, it warrants a continued high profile, because under most circumstances, it may be regarded as an entirely preventable occurrence.16 It has been suggested that prolonged heavy load carriage during a 109-day Arctic expedition may have impaired blood flow or nerve conduction in the hands and inhibited cold acclimatization. However, a different response was observed in the feet, where there was improvement in cold acclimatization despite development of moderate trench foot.77 Civilian Case Reports Laden and colleagues64 reported cold injury to a diver’s hand after a 90-minute dive in 6° C (42.8° F) water. With the advent of “technical diving,” characterized by going deeper for longer (often in cold water), and adventure tourism, it was suggested that this extremely painful condition was likely to increase in prevalence. Older adult patients commonly present to the hospital following their collapse and a period of distressing immobilization on the floor. A case of bilateral trench foot in an older adult immobile patient has been reported.112

Skin—A Thermoregulatory Organ Thermoregulation is a major function of skin in humans, and it is achieved by large fluxes in cutaneous blood flow.65 The metabolic requirements of skin are fixed and relatively modest; the observed large fluctuations in cutaneous blood flow are primarily determined by the individual’s thermoregulatory needs. Arteriovenous anastomoses (AVAs) abound in the extremities. The AVAs are coiled muscular-walled vessels approximately 35 µm in diameter and have little basal tone. They are under dual control. First, there is central hypothalamic control via the sympathetic nervous system. Second, there is direct local control allowing dilation under warm conditions and constriction with a cold stimulus. The two effects may be additive. Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. When core temperature exceeds 37.5° C (99.5° F), the hypothalamus reduces vasoconstrictor drive to the AVAs and vasodilation occurs. As a result, a lowresistance shunt in the dermal venous plexus opens, which in turn increases local heat loss. Under cold conditions there is an increase in sympathetic tone, resulting in local arteriovenous vasoconstriction and reduction in cutaneous blood flow. Under basal conditions, a 70-kg (154.3-lb) person has a total cutaneous blood flow of 200 to 500 mL/min. With external 172

heating to maintain skin temperature at 41° C (105.8° F), this may increase to 7000 to 8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may diminish it to 20 to 50 mL/min. Heat is dissipated by four processes: radiation, conduction, convection, and evaporation. Cutaneous vascular tone is inversely related to ambient temperature. Cold-induced vasoconstriction is attenuated by α2-receptor blockers and by sympathetic inhibition. Reduction in ambient temperature results in insertion of more α2-receptors from the myocyte Golgi apparatus into the plasma membrane, raising affinity for the sympathetic neurotransmitter norepinephrine. At the same time, endothelial nitric oxide synthase (eNOS) activity declines, resulting in vasoconstriction of AVAs. Core temperatures have a strong influence over cutaneous sympathetic vasomotor activity. Vascular endothelium regulates local vascular tone by secreting vasoactive agents, including the vasoconstrictor endothelin and the vasodilators nitric acid and prostacyclin. Endothelin causes long-lasting vasoconstriction and is elevated in hypoxia, preeclampsia, and hemorrhagic stroke.

ORTHOSTASIS Orthostasis causes immediate reduction in local blood flow. Indeed, cutaneous perfusion is reduced by approximately twothirds as a result of the poorly understood arteriolar-venous response. It is believed that this response helps maintain central arterial pressure during standing and also reduces dependent edema formation. Long periods of sitting or standing tend to exacerbate this response.

COLD-INDUCED VASODILATION When the hand or foot is cooled to 15° C (59° F), maximal vasoconstriction and minimal blood flow occur. If cooling continues to 10° C (50° F), vasoconstriction is interrupted by periods of vasodilation and an associated increase in blood and heat flow. This CIVD, or “hunting response,” occurs in 5- to 10-minute cycles to provide some protection from the cold. Prolonged repeated exposure to cold increases CIVD and offers some degree of acclimatization. Inuit, Sami, and Nordic fishermen have a very strong CIVD response and very short intervals between dilations, which may contribute to maintenance of hand function in the cold environment.44 CIVD responses are more pronounced when the body core and skin temperatures are warm (hyperthermic state) and suppressed when they are cold (hypothermic state), when compared with normothermia.22,23,78 Cheung and Mekjavic17 investigated whether CIVD responses of one finger can predict the responses of other fingers and also whether the CIVD of fingers could predict CIVD responses of the feet and toes. They found that CIVD is highly variable across the fingers and is not a generalizable response across either digits or limbs. Paradoxical CIVD will normally prevent tissue damage, but in conditions such as Raynaud’s disease, the vessels of the toes and fingers exhibit an exaggerated and sustained vasoconstriction response, resulting in blanching, numbness, and paresthesias and in severe cases tissue loss. Subjects with a weak CIVD to experimental cold-water immersion of the fingers in a laboratory setting have been shown to have a higher risk for local cold injuries when exposed to cold in real life.24 There is a strong relationship between the mean temperature of the fingers during cold-water immersion and toes during cold-air exposure (correlation coefficient for bivariate analysis [r ] = 0.83, p <0.01), showing that a weak CIVD response in the hand correlates with a weak response in the foot.105 Felicijan and colleagues33 found evidence for significant enhancement of the CIVD response after brief high-altitude acclimatization and that these changes were especially prominent in the feet of Alpinists when compared with controls. Temperatures of the extremities can drop surprisingly quickly in the field. Toe temperatures of 10 subjects were monitored in the field in Arctic Norway (minimum air temperature −27° C [−16.6° F]). The lowest skin temperature recorded was 1.9° C (35.4° F). The mean estimated time for toe temperature to cool from 25° C (77° F) to 5° C (41° F) was 109 minutes (standard

Trench Foot (Immersion Foot) PATHOPHYSIOLOGY Continuous exposure to a cold, wet environment causes skin breakdown, directly cools nerves in the area of exposure, and causes prolonged vasoconstriction. NFCI is primarily caused by prolonged vasoconstriction, which in turn causes direct injury to the vessels (and endothelium) that supply blood to nerves, fat, and muscle cells.49,72,98 Pain, fear, constrictive footwear, and immobility interact in maintaining vasoconstriction through a heightened sympathetic nervous system response or by mechanically limiting blood flow (Figure 7-1). Nerve cooling has been suggested as a contributing factor in the development of NFCI. Large myelinated fibers (C fibers) are most susceptible to prolonged cold exposure.53,61,62,88 In severe nonfreezing cold injury, there is characteristic peripheral nerve damage and tissue necrosis.54 Clinical sensory tests indicate damage to both large- and small-diameter nerves. The prolonged cold injury affects blood vessels serving these large myelinated fibers, with subsequent ischemia causing decreased oxygen to the nerve, resulting in the appearance of a primary nervous system injury58,59 (Figures 7-2 to 7-5). Vasoconstriction is mediated by presynaptic vesicle release of norepinephrine and neuropeptide Y from sympathetic nerve fibers that interact postsynaptically on smooth muscle at α2C6,18 and Y195 receptors. Recent work100 demonstrated that coldinduced vasoconstriction is mediated by Rho kinase. The prolonged decrease in blood flow caused by vasoconstriction causes

Local nerve cooling

Cold-wet exposure

Swelling and breakdown of skin

Vasoconstriction

Pain and fear

↓ Local blood flow

Local nerve damage

Constrictive footwear Immobility

Ischemia

Endothelial damage

Sensory impairment

Loss of vasodilation

Cold sensitization

FIGURE 7-1  Schematic of factors and mechanisms that contribute to nonfreezing cold injuries.

Percent of NBF baseline

120 100 80

Control Experimental

60 40 20 0

100 min

200 min

250 12h D1 D2 D3 D5 min

Time (min, hr and day) FIGURE 7-2  Laser Doppler mean nerve blood flow (NBF) in control and experimental animals at 10-minute intervals during nerve cooling and rewarming (up to 250 minutes) and at follow-up examination immediately before sacrifice (at various times up to 5 days). Note that the nerve blood flow falls steeply over 20 minutes and reaches its nadir (25% of baseline) 180 minutes after the onset of cooling. Nerve blood flow remains significantly reduced up to 5 days after cold injury. (Modified from Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)

direct injury to capillary endothelium. Studies indicate that the endothelial lining separates from underlying cells, leaving “gaps.”31 Leukocytes and platelets fill in these gaps and accumulate to further decrease capillary blood flow, leading to ischemia and eventual tissue hypoxia (Figure 7-6, online). The degree and duration of cold exposure determine severity of the injury. Animal models have been developed to understand the underlying pathophysiology of NFCI. Thomas and co-workers99 developed a rat model of NFCI by immersing the tail in 1° C (33.8° F) water for 6 to 9 hours and characterized the loss of CIVD and a prolonged decrease in tail blood flow followed by an increase in blood flow above baseline. This pattern is similar to that clinically observed in humans during the prehyperemic phase followed by the hyperemic phase. In rats, absence of CIVD with prolonged cold exposure is similar to this prominent and consistent finding of NFCI in humans. Stephens and associates95 used the rat tail model in an attempt to elucidate possible mechanisms that cause vascular endothelial damage. Their preliminary data suggest that acute cold-water exposure causes loss of nitric oxide–dependent endothelial function and possibly a change in smooth muscle contractility. Using a rabbit hind limb model, Irwin53 demonstrated that cold-water immersion damaged large myelinated fibers while sparing small myelinated and unmyelinated fibers. Nonfreezing cold injuries affect many different types of tissue. Pathologic examination of specimens displays a variety of lesions in skin, muscle, nerves, and bone.8,9,38 Muscles exhibit separation of cells and damage to muscle fibers, described as acidophilic and hyalinized (Zenker’s hyaline degeneration). The myoplasm within muscle loses its cross striation, and the healing muscle appears to undergo fibrous tissue replacement. One of the major pathologic processes in cold injury is progressive microvascular thrombosis following reperfusion of the ischemic limb, with cold-damaged endothelial cells playing a central role in the outcome of these cold-injured tissues.71 Reperfusion of previously ischemic tissues causes free radical formation, leading to further endothelial damage and subsequent edema. With restoration of blood flow, there is reintroduction of oxygen species within cells that further damages cellular proteins, DNA, and the plasma membrane. Free radical species may also act indirectly in redox signaling to initiate apoptosis. Leukocytes may accumulate in small capillaries, obstructing them and leading to more ischemia.59 In an in vivo rabbit hind limb model subjected to 16 hours of cold immersion (1° to 2° C [33.8° to 35.6° F]), there was 173

CHAPTER 7  Nonfreezing Cold-Induced Injuries

deviation [SD], 10.2) at an ambient temperature of −21° C (−5.8° F). One subject experienced a toe temperature below 5° C (41° F) for 2.9 hours during a 27-hour period. Surprisingly, none of the subjects demonstrated clinical signs of cold injury, but this does not mean that this exposure was without risk.101 The cutaneous microcirculation of skin was assessed in patients with sequelae from local cold injuries. All patients reported cold intolerance 3 to 4 years after the primary cold injury (sustained during military service).4 The transcutaneous oxygen tension was decreased, but oxygen reappearance time, oxygen recovery index, postocclusive reactive hyperemia, and venoarterial reflex were normal. No capillary nailfold abnormalities were found. Local cold injuries appear to cause disturbances in the CIVD, impaired cold tolerance, and increase the risk for future cold injuries. There is evidence to suggest disturbances of reflex mechanisms mediated by the central nervous system. Neurophysiologic factors seem more important than ischemic mechanisms in the pathophysiology of late sequelae with peripheral cold-weather injuries.

PART 2  COLD AND HEAT

V A M

A

B

C

D

E

FIGURE 7-3  Sciatic nerve epineurial microvessels before, during, and following nerve cooling (1° to 5° C [33.8° to 41° F]). A, Normothermia. Arteriole (A), venule (V), and metarterioles (M) have a normal appearance. B, One hour after the commencement of nerve cooling the diameter of both the arteriole and venule are reduced by approximately 40%. Under a dissecting microscope, erythrocytes present a granular appearance in both vessels (arrows). Note occlusive aggregations (open arrow) in metarteriole and the suggestion of leukocyte clumping in the venule (arrow head). C, Two hours after nerve cooling, segmental occlusive aggregates are seen in the venule (arrows). The arterioles contain prominent rouleaux (open arrows). D, Three hours after nerve cooling, there is stasis of flow in both vessels. An occlusive aggregate (arrow) is now seen in the arteriole, and those in the venule have extended (open arrows). E, After 1 hour of nerve rewarming (37.5° C [99.5° F]), the venule still exhibits multiple segmental occlusions (arrows). Erythrocyte granulations (open arrows) in the arteriole indicate poor reperfusion. Bars represent 100 mm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)

A

B

C

D

FIGURE 7-4  Electron micrographs of endoneurial vessels in cooled sciatic nerve. A, An empty capillary with a degenerating pericyte 1 hour after nerve rewarming. Bar represents 2 µm. B, Aggregating platelets (arrows) 24 hours after cooling. Bar represents 2 µm. C, Platelets, adherent to the endothelium of a venule, show varying degrees of degranulation without pseudopod formation, 48 hours after nerve cooling. Two red blood cells are trapped within this platelet thrombus. Bar represents 1 µm. D, A thrombus formed of platelets, red blood cells, and fibrin 5 days after nerve cooling. The blood vessel wall is necrotic. Bar represents 2 µm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)

174

B

FIGURE 7-5  Electron micrographs of cooled sciatic nerve fibers. A, A rat sciatic nerve fiber, 12 hours after nerve cooling, illustrating myelin unraveling and intramyelinic edema (arrow). B, A rat sciatic nerve fiber 2 days after cooling, exhibiting a shrunken axon and marked periaxonal edema. Bars represent 1 µm. (From Jia J, Pollock M: The pathogenesis of non-freezing cold nerve injury: Observations in the rat, Brain 120:631, 1997.)

reduction in the number of myelinated nerve fibers of all sizes, most marked in large-diameter fibers, a feature consistent with is­chemic neuropathy and reperfusion injury.54 Unmyelinated fibers showed only minor damage. The resulting evidence has suggested that both of these mechanisms may contribute to the nerve injury. There is further extensive supporting evidence that established NFCI is associated with histologic and/or clinical evidence of nerve damage.27,30,59,76 Das and colleagues25 demonstrated that quinacrine, an antioxidant, decreased damage to cell membrane phospholipids upon rewarming and reperfusion, although more recent studies97 have shown no benefit from antioxidant use. Most importantly, both these studies used models that assumed that cold-induced nerve injury, rather than capillary or endothelial damage, is the primary cause of NFCI.

CLINICAL PRESENTATION Trench foot and immersion foot are clinically and pathologically indistinguishable but have different etiologies. The term trench foot originated during the trench warfare of World War I,110 when soldiers wore wet boots and socks for prolonged periods.5 Immersion foot was first medically documented during World War II among shipwreck survivors whose feet had been continuously immersed in cold water.21 Both injuries occur when tissue is exposed to cold and wet conditions at temperatures ranging from 0° to 15° C (32° to 59° F). Colder temperatures decrease the time required to induce NFCI.10,92 Severe nerve damage from immersion foot has been seen after exposure periods of 14 to 22 hours.103,104 Immersion foot injury may extend proximally and involve the knees, thighs, and buttocks, depending on the depth of immersion.111 Clinically, NFCI is insidious in onset, with progression from initial exposure through three distinctive phases (prehyperemic, hyperemic, posthyperemic). These phases have variable time courses and may overlap. Prehyperemic Phase During the prehyperemic phase, the affected limb, both during and immediately after cold exposure, appears blanched, yellowish white, or mottled but seldom blistered (Figure 7-7).104 Whayne and DeBakey110 state that the degree of edema during this prehyperemic stage is less severe if the feet are intermittently rewarmed during the course of exposure. Whereas muscle cramps are common, pain is rare.43,92 The single most important diagnostic criterion is loss of a sensory modality, most typically complete local anesthesia, which is distinct from premonitory feelings of extreme cold in the affected periphery, almost invariably in the feet although hands can also be affected. With further exposure, the cold sensation leads to complete anesthesia with loss of proprioception, resulting in numbness and gait disturbances. This sensation has been described as “walking on air” or “walking on

cotton wool.”104 Capillary refill is sluggish, and pedal arterial pulses are usually absent, except through Doppler examination.70 Intense vasoconstriction is the predominant feature of this stage.46 Hyperemic Phase Within several hours after rewarming, the extremities become hot, erythematous, painful, and swollen (Figures 7-8 to 7-11; Figure 7-9, online), with full bounding pulses.109 Impairment of the microcirculation is evident through delayed capillary refill98 (Figure 7-12, online) and petechial hemorrhages.45 Sensation returns first to proximal regions and then extends distally, rapidly progressing to a severe, burning, or throbbing pain and reaching maximal intensity in 24 to 36 hours.103,104 Affected areas have marked hyperalgesia to light touch. This pain is aggravated by heat and dependent positioning and often worsens at night, when even the pressure of sheets may become unbearable.46 After 7 to 10 days, the nature of the pain changes to “shooting or stabbing.”103 The sensory deficits usually diminish, but paresthesias continue, and anesthesia may be extensive on the toes and plantar foot surfaces.111 Vibratory sensation is reduced or lost, whereas proprioception is usually retained. Anhidrosis coincides with the extent of sensory loss.98 Vascular injury is evident in vessel reactivity. Skin temperature gradients are absent, with digits often as warm or warmer than the groin or axillae. When the affected limbs are lowered, blood pools, turning the extremity a deep purple-red color, whereas

FIGURE 7-7  Prehyperemic phase of immersion foot. These feet are still mostly numb and very cold to the touch. (British Crown Copyright/ MOD.)

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CHAPTER 7  Nonfreezing Cold-Induced Injuries

A

PART 2  COLD AND HEAT

blanching occurs when the limb is raised. Tense edema becomes marked during this stage. Blisters containing serous or hemorrhagic fluid may form, indicating more severe injury.98 The superficial epidermis becomes thick, indurated, and desquamated. Eschars form (Figures 7-13 and 7-14) and eventually

FIGURE 7-8  Hyperemic phase of nonfreezing cold injury. This person spent 18 hours during the winter bailing out a boat that threatened to capsize in Prince William Sound, Alaska. (Courtesy James O’Malley, MD.)

slough, leaving a pink dermis (Figure 7-15). In more severe cases, the skin may become gangrenous (Figure 7-16). This is rare, and with appropriate care, gangrene is usually minimal.1,109,110 Muscles may show weakness with impaired electrical responses, slowing of plantar deep tendon reflexes, and intrinsic muscle atrophy.103,104 In milder cases, this stage peaks at 24 hours; in more severe cases, the hyperemic phase may take 6 to 10 weeks to resolve.98 Posthyperemic Phase The posthyperemic phase lacks obvious physical signs. In mild cases, this phase may be absent104; in other cases, it may last weeks, months, or years after the hyperemic phase has subsided.70,103 The extremities transition from a consistent warmth to noted coolness, with affected areas becoming cold sensitive, remaining so for hours after exposure despite normal warming processes. After 6 to 10 weeks, patients often complain of spontaneous hyperhidrosis, and sweat rashes are common in areas with heavy perspiration.103 On a warm day, socks are quickly soaked; extremities may sweat excessively, even when cold. Hyperhidrosis predisposes to chronic paronychial infections. Sweating may be more pronounced at the margins of anhidrotic and analgesic areas.104 During the posthyperemic phase, the paresthesias and extreme pains typical of the hyperemic phase have usually resolved, replaced by dull aches and anesthesia that may persist for months to years.110 Recurrent edema of the feet, return of paresthesia,

FIGURE 7-13  Severe nonfreezing cold injury. This Argentinian soldier had been unable to care for his feet for many weeks. (British Crown Copyright/MOD.)

FIGURE 7-10  Hyperemic phase of immersion foot. The characteristic redness of the stage is absent because of the pigmented skin, but the feet are swollen and painful. (British Crown Copyright/MOD.)

FIGURE 7-11  Hyperemic phase in moderately severe nonfreezing cold injury. Swollen, red, and persistent pain in the feet of an infantry soldier from the Falklands War. (British Crown Copyright/MOD.)

176

FIGURE 7-14  Severe nonfreezing cold injury in an Argentinian mine layer who wore his boots for 47 straight days during the Falklands War. (Courtesy M.P. Hamlet.)

FIGURE 7-15  Severe nonfreezing cold injury in a British sailor during World War II. (Courtesy M.P. Hamlet.)

and further blistering are common, especially after long walks. Intrinsic muscle and ligament atrophy tend to resolve,104 but in severe cases, fibrous scarring may lead to rigidity and permanent contracture of the toes.111 Decalcification of bones similar to that seen with osteoporosis is frequently observed.102 Immobility and pain in severe cases may lead to prolonged convalescence of 6 or more months.111 In the most severe cases, gangrene can develop, and ablative surgery in the form of amputations of digits or even major lower limb amputation becomes necessary. Neuropathic tissue is susceptible to local trauma, ulceration, and eventually local osteomyelitis and sinus development (Figures 7-17 to 7-19). Appearance and behavior of the neuropathic foot have many similarities to those of the diabetic foot. In the diabetic foot, infections tend to be polymicrobial with Staphylococcus aureus, Staphylococcus epidermidis, and Enterococcus and Streptococcus species being most commonly isolated from bone culture. However, aerobic gram-negative rods (such as Pseudomonas aeruginosa) and obligate anaerobic species may be found.52 Partial foot amputations may result in significant alterations in functional biomechanics of the foot. Because this is often associated with alterations in the sensory nerve supply to the feet, ongoing disabling problems can persist (Figure 7-20).52 More Severe Injuries NFCI can vary in severity from mild to severe. In severe cases, cold sensitization is so serious that individuals are unable to work outside. There is often persisting edema and hyperhidrosis, making the individual susceptible to fungal infections. Chronic pain may resemble causalgia or reflex sympathetic dystrophy. The profound sensory neuropathic foot can develop ulcerations

FIGURE 7-16  The Argentinian mine layer seen in Figure 7-14, several weeks later. (Courtesy M.P. Hamlet.)

FIGURE 7-18  Same patient as in Figure 7-17, 24 months after nonfreezing cold injury with chronic discharging sinuses from osteomyelitis of the first metatarsal. (Courtesy Christopher H.E. Imray, MD.)

and tissue loss, ultimately resulting in either minor or major lower limb amputation. Ongoing care with a foot specialist who can arrange for custom-made shoes and insoles appears to improve functional outcome. Multidisciplinary team approaches to coordinating care leading to healing of the ulcerated neuropathic foot using patella weight-bearing orthoses has been described.63 NFCI pain is often so severe as to require tricyclic antidepressants, which may need to be instituted at an early stage.51,98 Failure to do so increases the risk for developing severe chronic pain resistant to all subsequent treatment modalities. Early involvement of

FIGURE 7-19  Magnetic resonance imaging scan of the patient in Figures 7-17 and 7-18, 24 months after nonfreezing cold injury with chronic discharging sinuses from osteomyelitis of the first metatarsal head. (Courtesy Christopher H.E. Imray, MD.)

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CHAPTER 7  Nonfreezing Cold-Induced Injuries

FIGURE 7-17  Patient 24 months after nonfreezing cold injury. Amputation of third, fourth, and fifth toes on the left foot. (Courtesy Christopher H.E. Imray, MD.)

PART 2  COLD AND HEAT

Sympathectomy Recovery during the posthyperemic phase may be hastened with physiotherapy and exercise to rehabilitate atrophied intrinsic muscles.110,111 Lumbar sympathectomy has been theorized to reduce disabling contracture by decreasing vascular tone, increasing circulation, and hastening collagen and fibrous tissue absorption. In severe cases of NFCI exhibiting atrophic rigid feet, small case studies have shown symptomatic improvement after sympathectomy,111 but other clinicians feel that there is little therapeutic advantage to the procedure.109 Tissue-Freezing Complications Frostbite and NFCI injuries do not necessarily occur in isolation, so when assessing an individual, both diagnoses need to be entertained. Following exposure to severe cold, careful appraisal of the injury allows selection of optimal treatment.

A

B FIGURE 7-20  A guillotine transmetatarsal amputation of the left foot was undertaken 6 months after severe nonfreezing cold injury. The patient was treated with delayed primary split-skin grafting. This  photograph was taken 12 months after the original injury and shows that the split-skin graft has taken, but is now ulcerated as a result  of the shear forces generated by walking on the insensate tissue.  A, Transverse view from the bottom of the foot. B, Lateral view. (Courtesy Christopher H.E. Imray, MD.)

pain specialists is important. It is essential to control pain following NFCI at the earliest opportunity.

TREATMENT Hypothermia The treatment required for the general effects of cold is different from that needed for localized NFCI. Core temperature must be raised while the extremities are kept cool.109-111 Injured feet should be elevated and exposed to steady cool air from a fan.109,111 Extremity cooling lowers metabolic requirements to a point where vascular oxygen supply can sustain tissue demand. Continuous cooling brings rapid improvement in pain, edema, and vesiculation.109,111 Local cooling should be continued until pain is relieved, circulation has recovered, and hyperemia subsides.111 The affected extremities should never be rubbed, which may compound the injury.2 Rewarming Treatment is limited to symptomatic relief and reversing ischemia while minimizing progression of disease. Rewarming injured tissues increases metabolic demand of damaged cutaneous cells to a greater extent than can be provided by the supply capability of the injured subcutaneous blood vessels.111 Tissue anoxia and endothelial cell injury, coupled with reflex vasodilation, lead to fluid transudation, increasing edema, skin necrosis, and worsening pain.109,111 178

Drugs Diagnosis of NFCI is often difficult or delayed. In view of involvement of the α-receptors in the control of peripheral circulation and the apparent noradrenergic sensitization,36 it was believed that vasodilators or α-blocking drugs might be beneficial. However, there is no evidence to support this approach. Because painful rewarming and persistent pain are features of NFCI, it is important to attempt to alleviate pain at an early stage. Although simple analgesics may be of benefit, Thomas and Oakley98 observed that quinine sulfate (200 to 400 mg, given at night) appeared more successful than regular analgesics, although others have since commented that they are not useful. Since 1982, the standard treatment in the armed forces of the United Kingdom, first proposed by Riddell,85 has been amitriptyline hydrochloride, in doses of 50 to 100 mg given at night. Incremental increases in dosage may be required with both drugs if pain breaks through after initial relief.37

ASSESSING THE SEVERITY OF NONFREEZING COLD-INDUCED INJURY Following the initial injury, there develops increased sensitivity to cold. There are often few objective clinical signs of a nonfreezing cold injury. A careful history of cold exposure, clear history of the typical rewarming symptoms and signs, detailed examination, and special investigations combine to build a case consistent with NFCI. Corroborative evidence of an appropriate cold exposure and symptoms consistent with NFCI from medical records is vital. Special Investigations Infrared thermography can be used to assess the individual’s response to a standardized cold stress and may be helpful in confirming the diagnosis, assessing the severity of injury, and monitoring recovery from NFCI (Figure 7-21). Although the infrared thermography test is used extensively by the UK military, it is not widely used elsewhere.50,57 There appears to be significant intraindividual variability in the responses of some individuals to the current infrared thermography test. As a result, interest is shown in the use of gentle exercise before the infrared thermography cold sensitivity test and also in the use of laser Doppler flowmetry to try to improve the assessment used to classify nonfreezing cold injury.29 Careful experimental design to validate any potential new tests against suitable controls, both preexposure and postexposure, will be required.

PREVENTION The simplest way to prevent NFCI is to avoid prolonged exposure to cold, wet environments. This can be difficult to achieve. During military conflict, completing the assigned mission may require performing in a cold, wet environment for sustained periods of time in cramped, immobile positions. During mountain rescues, individuals may be so focused on helping to save others that they do not take adequate care to prevent NFCI. Prevention can be achieved by encouraging activities that promote blood flow to the feet, rotating personnel out of cold,

34 32 30 28 26 24 20.9° C FIGURE 7-21  Infrared thermography in the assessment of the consequences of nonfreezing cold injury. The upper sequence of three images was taken from an uninjured, asymptomatic control; the lower sequence from a patient who had sustained nonfreezing cold injury and subsequently complained of sensitivity. In both the control and patient, the first (left) image was taken after resting in ambient air temperature of 30° C (86° F). The second (center) image was taken immediately after the foot had been immersed in water at 15° C (59° F) for 2 minutes. The final (right) image was taken 5 minutes after removal from the water, again in 30° C (86° F) air. The upper series shows feet that were warm at rest, which rewarmed briskly after mild cold stress, and recovered almost completely within 5 minutes after removal from the water. The lower series shows a severe degree of cold sensitization; the feet were much colder than the surrounding air at rest, and once cooled, took a long time to rewarm, remaining much cooler than the control foot at 5 minutes after immersion. The scale at far right indicates the color– temperature relationship. (Copyright British Crown Copyright/MOD. Reproduced with the permission of Her Britannic Majesty’s Stationery Office. From Thomas JR, Oakley HN: Nonfreezing cold injury. In Pandolf KB, Burr RE, editors: Textbook of military medicine: Medical aspects of harsh environments, vol 1, Washington, DC, 2002, Office of the Surgeon General, Borden Institute, pp 467-490.)

wet environments on a regular basis, keeping feet dry by early changing of wet socks, maintaining core body temperature by limiting sweat accumulation into clothing and dressing in layers, and by educating people about the early signs and symptoms of nonfreezing cold injuries. Changing socks two to three times during the day is mandatory in cold, wet environments. The military suggests that optimal care entails air drying feet for at least 8 hours out of every 24.14,116 Vapor-barrier boots do not allow sweat to evaporate, and in some situations, this increases maceration.3 These boots should be taken off each day, wiped to remove moisture and debris, and allowed to dry. Footwear should not constrict blood flow; sizing is important as is educating the user not to tie his or her shoelaces too tightly. Prophylactic treatment with topical skin silicone preparations (antiperspirants) has proved effective.40 The effect is believed to be caused by prevention of hyperhydration of the stratum corneum.14,28 However, stickiness, adherence of sand and grit to the foot, and product bulkiness make this technique marginally acceptable to infantry soldiers in combat situations.40 In small clinical trials, silicone ointment applied only to the sole of the foot instead of to the entire foot (thus reducing surface area exposed to dirt retention, amount of material transported by the soldier, and expense) was sufficient to prevent NFCI.28 As a consequence of the apparent increasing incidence of NFCI in the British military, preventive steps are being taken. These include improved education of recruits and existing personnel about prevention measures and equipment and early recognition. Well-designed equipment, supplied to appropriate personnel, and used in a timely and appropriate way should reduce the incidence of injury. The severity of current UK military NFCI events appears to be relatively mild in comparison with civilian NFCI injuries (see Figures 7-17 to 7-19) and military historical controls (see Figures 7-13 to 7-16). This raises the question of whether (1) there is a

continuous spectrum of disease, (2) there is a bimodal distribution of the disease with milder and more severe forms of NFCI, or (3) the commonly presenting form is the same disease process that has been investigated in the past. Perhaps the lack of clarity lies in the UK military’s decision to use infrared thermography as one of the bases for diagnosis, severity, and progression of NFCI. There appears to be a lack of published control data on subjects’ prior response to cold exposure, so that the test cannot be compared with the normal variability in the population. One approach would be to screen potential recruits. This requires a test with high sensitivity and specificity. However, individual variation in the control of peripheral blood flow is so great that no assessment currently available meets these requirements.12,22,24,98 Reducing the incidence of cold injury in military training requires striking a delicate balance between training, realism, and safety. Training in demanding environments runs real risks of injuring personnel, but the benefits to soldiers in their necessary field skills are vital if they are to avoid future NFCI.98

Pernio (Chilblains) Pernio (perniones), or chilblains, are localized, inflammatory, bluish red lesions caused by an abnormal reaction to a cold, damp environment. This mild form of cold injury is prevalent in the temperate climates of northwestern Europe,66 and it is found worldwide throughout temperate and northern zones.41,69,70,79 Pernio is less common in very cold climates where well-heated houses and adequate warm clothing are common.80 In a study of 111 patients, 67 (60.4%) were males and 44 (39.6%) were females. Eighty-nine (80.2%), 90 (81.1%), and 90 (81.1%) patients had onset in relation to lower temperature (<10° C [50° F]), relatively low atmospheric pressure (<1500 kPa), and higher relative humidity (>60%), respectively. Susceptibility to chilblains appeared to increase when ambient temperature was less than 10° C (50° F) and relative humidity more than 60%.84 Acute pernio has a seasonal incidence, with reversible symptoms more common in cold weather. The acute form is seen primarily in schoolchildren and young adults under the age of 20 years, with the highest incidence in adolescent females.66 It can occur in mildly cold settings such as logging, kayaking, snowmaking,46 winter horseback riding, and hiking.82 Pernio can be caused by brief (30 minutes) cold exposure, often appearing several hours after exposure, with the skin lesions fully developed within 12 to 24 hours.79 Characteristic locations for these lesions are the feet, hands, legs, and thighs. Single or multiple, erythematous, purplish, edematous lesions form, with vesicles in severe cases. Symptoms include intense pruritus, burning, or pain, often worsened by subsequent warmth. The lesions of acute pernio are self-limited and usually resolve within a few days to 3 weeks,80 occasionally leaving residual hyperpigmentation.19 Although the healing process appears to occur as the plaques resolve, pain often persists. Subsequent mild cold exposure may trigger paresthesias, edema, and skin scaling.46 Chronic perniosis usually progresses over several winters after repeated episodes of acute pernio, rarely progressing from the initial injury to chronic irreversible skin changes within a single season.66 Repeated episodic seasonal lesions may become edematous, with permanent discoloration and subcutaneous nodule formation. The nodules are firm and painful, ultimately rupturing, which provides pain relief and leaves a shallow ulcer with pigmented atrophic skin. These ulcers may grow larger and coalesce, remaining open, which leads to permanently swollen extremities, scaly pigmented skin, and unremitting pain aggravated by light pressure. Pernio is believed to be caused by prolonged cold-induced vasoconstriction with subsequent hypoxemia and vessel wall inflammation.41,55 Subcutaneous arterial vasoconstriction is documented by both pathologic66 and arteriographic studies.93 Histologic examinations show a lymphocytic vasculitis and papillary dermal edema with pervasive inflammatory changes.41,55,66 The differential diagnosis includes lupus erythematosus, Raynaud’s disease, polycythemia vera, atheromatous embolization, erythema nodosum, and livedo vasculitis with ulcerations. 179

CHAPTER 7  Nonfreezing Cold-Induced Injuries

36.0° C 36

PART 2  COLD AND HEAT

Treatment of pernio is accomplished by drying and gently massaging the affected skin. Active warming above 30° C (86° F) significantly worsens the pain and should be avoided.46 Although therapeutic regimens in the literature include nicotinic acid,42 ultraviolet irradiation,48 thymoxamine,56 intravenous calcium combined with intramuscular vitamin K,34 corticosteroids,39 and sympathectomy in severe cases,66 few have proved to be either effective or universally accepted. Recently, nifedipine (20 mg, 3 times daily) has been shown to be effective for treatment of severe perniosis. Patients treated had a significantly reduced time for clearance of lesions, decreased pain and irritation of existing lesions, and less development of new pernio.41,86 Preventing pernio is relatively simple. Recommended prophylactic measures include minimizing cold exposure with suitable clothing when outdoors and maintaining adequate warm temperatures indoors.

Cryoglobulinemia Cryoglobulins are cold-precipitable serum immunoglobulins.96 These cryoimmunoglobulins were first reported in a patient with multiple myeloma115 and were subsequently recognized to occur in a diverse group of hematologic malignancies, acute and chronic infections, and collagen vascular diseases.94,106 Cryoglobulins are classified as three types. Type I cryoglobulins (10% to 15% of total) are composed of a monoclonal immunoglobulin, primarily IgG. Type II cryoglobulins (50% to 60% of total) are polyclonal, most frequently IgG and IgM. The IgM fraction usually has rheumatoid factor activity. Type III cryoglobulins (25% to 30% of total) are also composed of polyclonal IgG and IgM fractions. In general, the higher the protein concentration, the higher the temperature at which precipitation begins. Of clinical relevance is the composition of the cryoprecipitate. For example, IgM is intrinsically more viscous than is IgG, and patients with monoclonal IgM cryoglobulin have an amplified hyperviscosity. Because extremity temperatures can reach 30° C (86° F), in vivo cryoprecipitation may directly contribute to impaired capillary blood flow.46 There are many clinical conditions that are associated with cryoglobulinemia.96 Infections (viral, bacterial, fungal, parasitic), hematologic diseases (chronic lymphocytic leukemia, multiple myeloma), and autoimmune diseases (rheumatoid arthritis, pulmonary fibrosis, inflammatory bowel disease) are all associated with cryoglobulinemia. Hepatitis C is considered a principal trigger of cryoglobulinemia. Serum cryoglobulin values do not usually correlate with clinical severity or disease prognosis96 but may serve as a marker of the disease. Cryoglobulinemia is characterized by a clinical triad of purpura, weakness, and arthralgias. A large clinical trial showed that two-thirds of patients diagnosed with cryoglobulinemia initially presented with symptoms of skin lesions or Raynaud’s disease–like vasomotor attacks. Mucosal bleeding, visual disturbances, and abdominal pain were less common. Cold sensitivity was apparent in less than one-half of these patients.13 Symptoms associated with cryoglobulins include typical Raynaud’s phenomenon, dependent purpura, cutaneous vasculitis with ulceration, retinal hemorrhages, coagulopathies, glomerulonephritis, renal failure, and cerebral thrombosis. Treatment of cryoglobulinemia should be directed at the severity of the symptoms and to the disease causing the cryoglobulinemia. Because hepatitis C virus (HCV) is implicated in many cases of types II and III cryoglobulinemia, targeting HCV is the treatment of choice to eliminate cryoglobulinemia. Interferon, prednisone, and ribavirin have all been used to treat HCV and associated cryoglobulinemia. For non–HCV-associated cryoglobulinemia with mild to moderate symptoms (purpura, arthralgia, sensory neuropathy), immunosuppression with corticosteroids and analgesics is the treatment of choice.96 A low-antigencontent diet (rice, fresh vegetables, fruit, tea) has been shown to improve purpura.81 With severe manifestations of disease such as renal failure, neurologic impairment, disabling paresthesias or myalgias, plasmapheresis may be helpful in reducing the cryoimmunoglobulin concentration below a critical point to alleviate symptoms.13 Plasmapheresis is used in conjunction with corticosteroids or other drugs, because discontinuing 180

FIGURE 7-22  Cold urticaria. The hives occurred within minutes of holding an ice cube against the skin. (From Habif TP: Clinical dermatology, ed 4, Philadelphia, 2004, Mosby, with permission.)

plasmapheresis treatment usually causes reappearance of the cryoglobulinemia.96

Cold Urticaria Cold urticaria is a physical urticaria characterized by development of either localized or generalized wheals and itching after skin exposure (air, liquid, object) to cold89 (Figure 7-22). It most frequently affects young adults with a duration of 4 to 5 years, although primary cold urticaria can occur at any age. Women are twice as likely to be affected.90 The incidence rate is approximately 0.05% of the population. Symptoms are usually limited to cold-exposed skin areas.89 Local symptoms include redness, itching, wheals, or edema of the exposed skin. The wheals last approximately 30 minutes. Systemic reactions can also occur, and symptoms of this include fatigue, headache, dyspnea, and hypotension. Swimming in cold water is the most common trigger of severe reactions. This may lead to hypotension, fainting, shock, and possibly death.7,45 Suffocation may also occur after consuming cold drinks as a result of pharyngeal angioedema.89 Secondary urticaria occurs in 5% of patients with cold urticaria.45 The wheals are more persistent and may be associated with purpura and vasculitis on skin biopsy. This disorder is associated with an underlying disorder such as cryoglobulinemia, cold agglutinins, paroxysmal hemoglobinuria, or connective tissue disease.107 In addition, there is a rare autosomal dominant familial form that has its onset in infancy and is associated with arthralgias and leukocytosis.108 The cause of cold urticaria is unknown. Cold urticaria has been associated with viral or bacterial infections,89,90 as well as infections of the upper respiratory tract, teeth, and urogenital tract. It has been reported to involve the release of histamine,60 leukotrienes, and other mast-cell mediators,90 possibly mediated by IgE and IgM. Support for an IgE-mediated mechanism comes from successful treatment11 using an anti-IgE (omalizumab). The diagnosis of cold urticaria is made through the ice cube test in the majority of patients,74 in which a hive is induced by holding an ice cube to skin for 3 to 5 minutes. If the results are equivocal, a cold-water immersion test of submerging a forearm for 5 to 15 minutes in water at 0° to 8° C (32° to 46.4° F) establishes the diagnosis. Treating cold urticaria with antihistamines is the most effective option. However, to sufficiently reduce symptoms may require dosing up to four times the recommended dose.75,89,90 In addition, other therapies include leukotriene antagonists, cyclosporine, corticosteroids, and anti-IgE.90 Individuals with severe reactions should have an emergency kit containing corticosteroids, antihistamines, and epinephrine. Based on the finding that infectious disease may be a trigger for cold urticaria, earlier treatment with antibiotics for infectious diseases may also be warranted.90

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 8 



Frostbite LUANNE FREER AND CHRISTOPHER H.E. IMRAY

Frostbite is a true freezing injury, and depending on the severity, ice crystals will tend to form in deep and/or superficial tissues. The degree of injury is a complex interaction of many factors, including environmental (e.g., temperature, windchill, length of exposure, altitude) and individual (e.g., genetics, comorbidities, medications and drugs, clothing, skin products, previous frostbite injury, among other factors). This chapter reviews current understanding of the history, epidemiology, physiology, pathophysiology, classification, risk factors, clinical presentation, field and hospital evaluation and treatment, prevention, and consultation strategies for the management of frostbite. Although the principles of prevention and treatment of frostbite transfer from urban to wilderness settings, the time to definitive treatment is often prolonged and resources are almost always limited in the wilderness setting; therefore, wherever possible, we incorporate special considerations for wilderness management of frostbite injuries. Hypothermia and nonfreezing cold-induced injuries are discussed in Chapters 5 and 7.

History of Frostbite A 5000-year-old pre-Columbian mummy discovered in the Chilean mountains is widely recognized as the earliest documented evidence of frostbite.138 In 218  BC, Hannibal lost nearly one-half of his army of 46,000 to cold injuries in only 15 days when they crossed the Pyrenean Alps. Dr. James Thatcher wrote in 1778 that 10% of George Washington’s army had been left to perish in the winter cold during his campaign against the British soldiers.151 Despite the fact that frostbite was a known consequence of military campaigns in the cold for thousands of years, the first authoritative report of mass casualties was by Baron Larrey,93 surgeon-in-chief of Napoleon’s army during the invasion of Russia in the winter of 1812-1813. Larrey introduced the concept of friction massage with ice or snow, avoidance of heat in thawing, and the idea that cold injuries were similar to burn injuries. These concepts are better understood against the background as viewed by Larrey;93 soldiers with cold injuries rapidly rewarmed their extremities over roaring fires (65° to 75° C [149° to 167° F]) after long marches, only to renew the trek and refreeze their extremities the next day. Larrey recognized that warming was good, but he cautioned against the use of excessive heat and ultimately recognized the freeze–thaw–freeze cycle. Napoleon left France with 250,000 men and returned 6 months later with only 350 effective soldiers. The remainder were casualties to cold or starvation.93 During both world wars and the Korean conflict, at least 1 million cases of frostbite occurred.129,130,167,184 High-altitude frostbite, first described in 1943, was recognized from the treatment of aviators in World War II, when gunners of aircraft flying between 7620 and 10,668 m (25,000 and 35,000 feet) fired machine guns through open waist pots, removing their bulky mittens and jackets to improve the dexterity that they felt was crucial to saving their lives.184 Until the 1950s, treatment of cold injuries basically followed Larrey’s guidelines. In 1956, experimental laboratory work encouraged Merryman, the Public Health Service district medical officer in Tanana, Alaska, to try rapid rewarming at 37.8°C (100° F) on a patient with frostbite and hypothermia.20,117 This was the genesis and has become the cornerstone of the method currently used in Alaska and popularized by Mills.117,119

Epidemiology No comprehensive statistical data are available on the incidence of frostbite, but it is much more prevalent during military campaigns and is a known hazard for mountain climbers and polar explorers. The typical frostbite victim is working or recreating in cold and/or high-altitude environments, is homeless, or is accidentally trapped outdoors in the winter;86,89,133 is 30 to 49 years old;136,181 and in more than half of urban cases, is intoxicated.115,177

CIVILIAN In the nonadventurer U.S. civilian population, Mills had collected 500 cases in Alaska by 1963, Cook County Hospital in Chicago recorded 843 cases from 1962 to 1972, and Detroit Receiving Hospital reported on 154 patients treated between 1982 and 1985.12,64,90,117 The incidence of frostbite in Finland, calculated in a 9-year retrospective query of hospital admissions, was 2.5 cases per 100,000 inhabitants.76

MILITARY AND OCCUPATIONAL The mean annual incidence of frostbite in the Finnish military was reported as 1.8 per 1000, with the head, hands, and feet most commonly affected.95 In a more recent study of almost 6000 Finnish military recruits, 44% reported at least one episode of frostbite during their lifetime, and the annual incidence was 2.2%; the head, hands, and feet were the sites most commonly afflicted.38 Among refugees navigating a high-altitude military line of control during December 1988 to March 2003, 2564 cases of frostbite were treated at local hospitals in Muzaffarabad, Azad Kashmir.81

MOUNTAINEERING A 10-year retrospective survey of medical records of the British Antarctic Survey revealed that the incidence of frostbite was approximately 65.6 per 1000 per year.23 During a 10-year period in the Karakorum mountains, 1500 cases of frostbite were treated at tertiary care medical facilities; all victims were males ages 17 to 43 years. The incidence is unknown because the total number of potential exposures was unrecorded.61 In a questionnaire-based study of 637 mountaineers, the mean incidence of frostbite was 366 per 1000 population per year,60 and out of 2219 south-side Mt Everest climbers in 7 years (2001 to 2007), the base camp medical clinic at Mt Everest saw 35 cases of frostbite (and estimates at least a comparable number did not seek treatment at the facility).47

Anatomy and Physiology Physiologically, humans are tropical beings, better suited to losing heat than retaining it. When naked and at rest, a person’s neutral environmental temperature is 28° C (82.4° F); with an environmental drop of only 8° C (14.4° F), metabolic rate must double to avoid lowering of body temperature. The rate at which heat is lost by radiation is a function of the temperature of the cutaneous surface, which in turn is primarily a function of the rate of blood flow through the skin. Heat is poorly conducted from warmer internal tissue to the cutaneous surface because adipose tissue is a good heat insulator. As a result, the cutaneous circulation is key to the development of frostbite. Because of its role in thermoregulation, normal

For online-only figures, please go to www.expertconsult.com

181

PART 2  COLD AND HEAT

blood flow of skin far exceeds its nutritional obligation. The skin holds a complex system of capillary loops that empty into a large subcapillary venous plexus containing the majority of the cutaneous blood volume. Under normothermic conditions, 80% of an extremity’s blood volume is in the veins of skin and muscle. Skin blood volume depends in part on tone in resistance and capacitance vessels, and tone in turn depends largely on ambient and body temperature. Under basal conditions, a 70-kg (154.3-lb) person has a total cutaneous blood flow of 200 to 500 mL/min. With external heating to maintain skin temperature at 41° C (105.8° F), this may increase to 7000 to 8000 mL/min, whereas cooling the skin to 14° C (57.2° F) may diminish it to 20 to 50 mL/min. Blood flow through apical structures such as the nose, ears, hands, and feet varies most markedly because of the richly innervated arteriovenous connections. Blood flow to hand skin can be increased from a basal rate of 3 to 10 mL/min/100 g of tissue to a maximum of 180 mL/min/100 g of tissue. This cutaneous vascular tone is controlled by both direct local and reflex effects. Indirect heating (warming a distant part of the body) results in reflex-mediated cutaneous vasodilation, whereas direct warming results in vasodilation dominated by local effects. When both types (central and peripheral) of heating or cooling are present, their effects are additive. Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. Vasodilation in the hands and feet is passive, so maximal reflex vasodilation occurs after sympathectomy. When the hand or foot is cooled to 15° C (59° F), maximal vasoconstriction and minimal blood flow occur. If cooling continues to 10° C (50° F), vasoconstriction is interrupted by periods of vasodilation and an associated increase in blood and heat flow. This cold-induced vasodilation (CIVD), or “hunting response,” recurs in 5- to 10-minute cycles to provide some protection from the cold. There is considerable individual variation in the amount of CIVD, and it is believed this might explain some of the variation in susceptibility to frostbite. Prolonged repeated exposure to cold increases CIVD and offers some degree of acclimatization. Inuit, Sami, and Nordic fishermen have a strong CIVD response and very short intervals between dilations, which may contribute to maintenance of hand function in the cold environment.57 Normal skin maturation and tissue function rely on main­ tenance of permeability and integrity of all tissue membranes. A steady-state relationship of prostaglandins (PGs), particularly PGE2 (vasodilator) and PGF2α (vasoconstrictor), is crucial for normal skin function. An imbalance may disrupt cell membrane equilibrium. This relationship is controlled through PGE2-9-ketoreductase and nicotinamide adenine dinucleotide phosphate (NADPH). Low concentrations of PGE2-9-ketoreductase found in normal skin emphasize an active biologic presence. It is not difficult to imagine why frostbite tends to affect tissues that are acral and receive diminished blood supply as a result of vasoconstriction (e.g., fingers, toes, ears, nose), thereby conserving heat for the core. The nose and corneas may be difficult to protect from cold wind and are particularly vulnerable; face coverings such as a balaclava and goggles should be considered in extreme conditions. In addition, men who jog, ski, or otherwise exercise in the cold may be prone to penile frostbite, especially if fast speeds create a headwind. Clothing then becomes moist with sweat in the groin, and the tip of the penis is vulnerable, especially if unprotected by a wind-resistant or windproof outer layer.47,66

Pathophysiology of Frostbite The pathophysiology of frostbite has been categorized in several different ways, illustrating the numbers of variables that affect the extent and depth of tissue damage. Frostbite may be divided into four pathologic phases: prefreeze, freeze–thaw, vascular stasis, and late ischemic. Overlap occurs among these phases. The changes during each phase vary with rapidity of freezing and duration and extent of injury. Some feel that it is conceptually clearer to divide pathologic changes occurring in frostbite into two categories: those resulting 182

from direct cellular injury and those from indirect cellular effects, or progressive dermal ischemia,125 a similar pathophysiology seen in thermal burn patients.109,110,150

DIRECT CELLULAR INJURY Regardless of the classification scheme, researchers agree that the changes caused by direct injury include the following:196,197 • Extracellular ice formation • Intracellular ice formation • Cell dehydration and shrinkage • Abnormal intracellular electrolyte concentrations • Thermal shock • Denaturation of lipid–protein complexes Cells subjected to a slow rate of cooling (hours) develop ice crystals extracellularly in the cellular interspaces. Rapid cooling (seconds to minutes) produces intracellular ice crystals, which are more lethal to the cell and less favorable for cell survival. In a clinical cold injury, the slower rate of freezing does not produce intracellular crystals;112,113 however, the extracellular ice formed is not innocuous. It draws water across the cell membrane, contributing to intracellular dehydration. The theory of cellular dehydration was originally proposed by Moran124 in 1929 and subsequently supported by Merryman’s study of “ice-crystal nucleation.”112,113,115 Cellular dehydration produces modification of protein structure by high electrolyte concentration, alteration of membrane lipids, alteration of cellular pH, and imbalance of chemical activity.106,107,116 This phenomenon subsequently permits a marked and toxic increase of electrolytes within the cell, leading to partial shrinkage and collapse of its vital cell membrane. These events are incompatible with cell survival. Not all the water within a cell is freezable. A small amount of unfrozen water, “bound water,” constitutes up to 10% of the total water content and is held tightly in the protein complex within the cell. No matter how rapid or marked the cold injury, this bound water remains liquid. At temperatures below −20° C (−4° F), approximately 90% of available water is frozen.194 Although the theory of ice crystal disruption of cell structure is attractive, it has yet to be conclusively proved. Thermal shock defines the phenomenon of sudden and profound temperature change in a biologic system. Precipitous chilling has been theorized to be incompatible with life, but the severity of this phenomenon is debatable. Another poorly understood concept is the manner in which subzero temperatures produce denaturation of lipid–protein complexes. One proposed theory hypothesizes the detachment of lipids and lipid protein from cell membranes as a consequence of the solvent action of a toxic electrolyte concentration within a cell.99,100 There is no direct evidence supporting an alteration of enzyme activity during freezing, but DNA synthesis is inhibited.74 On the other hand, there is indirect evidence of ox liver catalase inactivation caused by denaturation and structural alteration of lactic acid dehydrogenase after freezing and thawing.102,166

INDIRECT CELLULAR DAMAGE/PROGRESSIVE DERMAL ISCHEMIA Indirect cellular damage secondary to progressive microvascular insults is more severe than is the direct cellular effect. This is supported by the observation that skin tissue subjected to a standard freeze–thaw injury, which consistently produced necrosis in vivo, survived as a full-thickness skin graft when transplanted to an uninjured recipient site.190 Conversely, uninjured full-thickness skin did not survive when transferred to a recipient area pretreated with the same freezing injury. Thus, direct skin injury is reversible. The progressive nature of injury is probably secondary to microvascular changes. Approximately 60% of skin capillary circulation ceases in the temperature range of 3° to 11° C (37.4° to 51.8° F), whereas 35% and 40% of blood flow ceases in arterioles and venules, respectively.148 Capillary patency is initially restored in thawed tissue, but blood flow declines 3 to 5 minutes later. Three nearly simultaneous phenomena occur after thawing: momentary and initial vasoconstriction of arterioles and venules, resumption of capillary circulation and blood flow, and showers of emboli coursing

Reports in the 1940s documenting the histopathology of frostbite injury to the skin were not comprehensive. Historically, studies by several investigators have been limited to skin biopsies without documentation of location, exposure time, temperature, or time elapsed since the injury.159 More recently, experimental studies have been able to document the histopathology of skin changes under controlled conditions. In 1988, Schoning and Hamlet161,162 used a Hanford miniature swine model for frostbite injury (−75° C [−103° F] exposure for up to 20 minutes) to note progressive epithelial damage. Early changes included vacuolization of keratinocytes, and there was loss of intercellular attachments and pyknosis over a period of 1 week or more. This subsequently progressed to advanced cellular degeneration and formation of microabscesses at the dermoepidermal junction. Later changes included epithelial necrosis and regeneration, either separately or together within the same tissue. Such histopathologic data favor the current standard of conservative delayed-surgical management of frostbite injury. However, Marzella and associates104 used a New Zealand white rabbit ear model of frostbite injury and proposed that the skin necrosis induced by frostbite injury was merely a reflection of damage to the target cell—the endothelial cell. After sub­ mersion of a shaved rabbit ear in 60% ethyl alcohol at −21° C (−5.8° F) for 60 seconds, the entire microvasculature demonstrated endothelial damage within 1 hour; erythrocyte extravasation occurred within 6 hours. These early vascular changes in the rabbit ear model are in contradistinction to the timing of vascular changes in the Hanford miniature swine model reported by Schoning and Hamlet.162 These clinicians performed biopsies on animals exposed to frostbite injury (−75° C [−103° F] for up to 20 minutes) and evaluated the specimens for vascular inflammation, medial degeneration, and thrombosis. The earliest change documented both grossly and microscopically was hyperemia. Within 6 to 24 hours, leukocyte migration and vasculitis were noted. However, the most severe vascular changes of thrombosis and medial degeneration were not observed for 1 to 2 weeks after the injury. Whether or not changes in the epidermis are primary or secondary to damage of underlying endothelial cells, it is clear that these tissues have potential, although limited, capacity for regeneration. Human experience clearly suggests that robust local tissue inflammation and coagulation stimulate microvascular thrombosis and progressive cell death.125 A perfect representative animal model for frostbite has yet to be found. A wide range of animal models is used to create and assess the condition. Developing a consistent reproducible and appropriate model would facilitate frostbite research.171 As early as 1991, Manson and co-workers101 proposed that frostbite is characterized by acute tissue injury induced by freezing and thawing. Initial complete ischemia is followed by reperfusion and later, tissue necrosis. They suggested that the vascular events supported the hypothesis that free radical–mediated reperfusion injury at thawing might contribute to tissue necrosis after frostbite in a manner similar to that seen after normothermic ischemia. Supporting evidence included electron micrographs showing the appearance of severe endothelial cell injury beginning during freezing and extending through early reperfusion. Later, neutrophil adhesion, erythrocyte aggregation, and microvascular stasis were seen.

Definitions and Classifications Classically, frostbite has been described by its clinical presentation, but this can be difficult to predict in the field and before rewarming.85,117 Mills124,126 favors the use of two simple classifications: mild (without tissue loss) and severe (with tissue loss.) Historically, and following the classification of thermal burn injury, frostbite has been divided into “degrees” of injury based on acute physical findings after freezing and rewarming. Frostnip (Figure 8-1, online ; also see Figure 9-8) is superficial and associated with intense vasoconstriction. It is characterized by discomfort in the involved parts. Symptoms usually resolve spontaneously within 30 minutes, and no tissue is lost. There is some question whether this qualifies as cold-induced injury, because neither frozen extracellular water nor progressive tissue loss is routinely demonstrated. 183

CHAPTER 8  Frostbite

through microvessels.197 Ultimately, there is progressive tissue loss caused by progressive thrombosis and hypoxia. This is similar to the tissue loss seen in the distal dying random flap and the no-reflow phenomenon. For both of these, in addition to the effect of arachidonic acid metabolites, oxygen free radicals have been shown to be detrimental and to contribute to tissue loss. It has been proposed that this may be the case with frostbite injury.19 Emerging concepts, perhaps including the deleterious role of protein kinase C in reperfusion injury, will no doubt be incorporated into our understanding of frostbite injury as scientific understanding evolves. Considerable evidence points to the primary alteration of the cold injury being injury to vascular endothelium.196 Seventy-two hours after a freeze–thaw injury, there is loss of vascular endothelium in the capillary walls, accompanied by significant fibrin deposition. The endothelium may be totally destroyed, and fibrin may saturate the arteriole walls.122,196,197 Ultrastructural derangement of endothelial cells after the thaw period has been observed by electron microscopy in capillaries of the hamster cheek pouch following subzero temperatures.144 The endothelial injury was confirmed by demonstrating fluid extravasation from vessels almost immediately after thawing.197 As in other forms of trauma, vascular endothelial cells swell and protrude inward into the lumen until they lyse. Venules appear more sensitive to cold injury than do other vascular structures, partly because of lower flow rates. Arterioles, with a rate of flow almost twice that of venules, are less damaged by freezing and develop stasis later than do venules. Capillaries manifest the fewest direct effects of cold injury, but their flow is quickly arrested as a result of their position between arterioles and venules. Generalized stasis and cessation of flow are noted at the point of injury within 20 minutes after freeze and thaw. “White thrombi” (blood cells and fibrin) follow platelet thrombi as blood flow progressively slows. Sludging and stasis result in ultimate thrombosis. Microangiography after cold injury shows that although spasm of the arterioles and venules exists, it is not marked enough to completely account for the decreased flow of progressive microvascular collapse.9 In the 1950s, Kulka87,88 observed that vascular thrombosis after cold injury advanced from the capillary level to that of the large vessels and ultimately resulted in ischemic death of progressively larger areas. Viable dermal cells may be observed histologically in cold-injured tissues for up to 8 days or until there occurs occlusion of local vessels. This emphasizes that a major role is played by vascular insufficiency and that direct injury to cellular structures and mechanisms may be reversible. Because Cohnheim had shown changes in cold injury to be similar to changes seen in other inflammatory states, Robson and Heggers150 postulated that the progressive ischemia seen in frostbite might be caused by the same inflammatory mediators responsible for progressive dermal ischemia in the burn wound. They evaluated blister fluid from patients with hand frostbite, measuring levels of PGE2, PGF2α, and thromboxane B2 (TXB2). Levels of the vasoconstricting, platelet-aggregating, and leukocytesticking prostanoids (PGF2α and thromboxane A2 [TXA2]) were markedly elevated. The investigators postulated that massive edema after cold injury was due either to leakage of proteins caused by release of these prostanoids or to leukocyte sludging in the capillaries and increased hydrostatic pressure. Studies have confirmed the similarity between cold injury and the burn wound.19 Severe endothelial damage was observed by researchers studying a minimal cold-injury model in the hairless mouse.13 In addition, the sequence of endothelial damage, vascular dilation, vascular incompetence, and erythrocyte extravasation was confirmed. This led to speculation that arachidonic acid metabolites, which may originate from severely damaged endothelial cells, are important in progressive tissue loss. Significantly absent from in vivo and microscopic observations were vascular spasm, thrombosis, and fibrin deposition, all of which have previously been implicated as pathophysiologic mechanisms. A rabbit ear model demonstrated increased tissue survival after blockade of the arachidonic acid cascade at all levels.145 The most marked tissue salvage resulted when specific TXA2 inhibitors were used. This has now been shown to be effective in clinical situations.64

PART 2  COLD AND HEAT FIGURE 8-2  A Nordic skier with first-degree frostbite (central pallor having cleared after rewarming) of the abdominal skin. This skier reported having skied for 90 minutes in −23.3° C (−10° F) temperature, unaware that his shirt, underneath a parka, had come untucked from his trousers. (Courtesy Luanne Freer, MD.)

First-degree injury shows numbness and erythema. There may initially be a white or yellowish, firm plaque in the area of injury. There is no tissue loss, although edema is common (Figure 8-2). Second-degree injury results in superficial skin vesiculation (Figure 8-3). Clear or milky fluid is present in the blisters, surrounded by erythema and edema. Third-degree injury shows deeper blisters, characterized by purple, blood-containing fluid (Figure 8-4). This indicates that the injury has extended into the reticular dermis and beneath the dermal vascular plexus. Fourthdegree injury is completely through the dermis, and involves relatively avascular subcuticular tissues (Figure 8-5). This tends to cause mummification, with muscle and bone involvement (Figure 8-6). Less severe bone injury in children may affect the growth plate and result in developmental digital deformities.16,22 Cauchy and colleagues26 proposed a different classification of frostbite injury for the hand and foot that is based on the risk for

FIGURE 8-3  A climber with second-degree frostbite of the fifth finger sustained after only several seconds’ exposure to −45.6° C (−50° F) windchill when gloves were briefly removed to handle placement of a carabiner to the fixed rope. Clear bullae developed after rewarming. (Courtesy Luanne Freer, MD.)

FIGURE 8-5  A climber with fourth-degree or severe frostbite injury just hours after rewarming. Note absence of any blistering. Fingers are insensate, and capillary refill is absent. (Courtesy Luanne Freer, MD.)

amputation of the affected part. An early prognosis for frostbite patients may be delayed by the lack of useful clinical guidelines; this new classification scheme (Tables 8-1 to 8-3) is intended to help resolve such issues. The four severity levels proposed provide earlier prediction of the final outcome of frostbite injury by using a technetium-99m (99mTc) bone scan in conjunction with the clinical findings on presentation. It was noted that the probability of bone amputation for the hand and foot could also be correlated to the extent of frostbite injury seen at the time of initial presentation and early 99mTc bone scanning. In a review of 70 cases of severe frostbite injury, the probability of bone amputation was 1% for the distal phalanx, 31% for involvement of the middle phalanx, 67% for the proximal phalanx, and 98% and 100%, respectively, for involvement of the metacarpal/metatarsal and carpal/tarsal bones (see Table 8-3). Grade 1 lesions do not require hospitalization or bone scans. Grade 2 lesions may require brief hospita­ lization and bone scans. Rapid rewarming and treatment with antibiotics and oral vasodilators appear to be sufficient for healing. Grade 3 lesions are connected with a significant risk for amputation and require rapid rewarming, antibiotics, aspirin, and intravenous (IV) vasodilators. Grade 4 lesions have high risk for amputation and complications such as thrombosis, sepsis, and other systemic problems (see Table 8-3). Cauchy’s clinical/99mTcbased classification scheme appears particularly useful in its ability to predict at a very early stage subsequent outcome from a frostbite injury.

Contributing Factors TEMPERATURE AND WINDCHILL Air alone is a poor thermal conductor, and cold air alone is not nearly as dangerous a freezing factor as is a combination of wind and cold.194 Wind velocity in combination with temperature establishes the windchill index. For example, an ambient

FIGURE 8-4  A climber with second-, third-, and fourth-degree frostbite of the hand. Note fingers 1 to 4 with hemorrhagic bullae over the areas of third-degree injury, clear bullae over the dorsum of the hand with second-degree injury, and deeply violaceous and unblistered fourth-degree injury of the distal phalanx of the fifth finger. (Courtesy Luanne Freer, MD.)

184

FIGURE 8-6  Photographs of 8-week follow-up of hand pictured in Figure 8-5, showing complete mummification and autoamputation of remaining digits. (Courtesy Luanne Freer, MD.)

Grade 1

Grade 2

Grade 3

Grade 4

Extent of initial lesion at day 0 after rapid rewarming Bone scanning at day 2

Absence of initial lesion

Initial lesion on distal phalanx

Initial lesion on carpal/tarsal

Useless

Blisters at day 2

Absence of blisters

Hypofixation of radiotracer uptake area Clear blisters

Initial lesion on intermediary (and) proximal phalanx Absence of radiotracer

Prognosis at day 2

No amputation

Tissue amputation

Sequelae

No sequelae

Fingernail sequelae

Hemorrhagic blisters on the digit Bone amputation of the digit Functional sequelae

Absence of radiotracer uptake area on the carpal/tarsal Hemorrhagic blisters over carpal/ tarsal Bone amputation of the limb± systemic involvement± sepsis Functional sequelae

From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001.

TABLE 8-2  Management of Frostbite Injuries of the Extremities On day 0, treatment consists of rapid rewarming for 2 hours in 38° C (100.4° F) water bath, with intravenous infusion of 400 mg chlorohydrate of vasodilator (buflomedil) and 250 mg aspirin. Subsequent treatment depends on the extent of the initial lesion, as follows: Grade 1* Absence of Initial Lesion

Grade 2 Initial Lesion Over Distal Phalanx

Grade 3 Initial Lesion Over Intermediary (and) Proximal Phalanx

Grade 4 Initial Lesion Over Carpal/Tarsal

No hospitalization Oral treatment for 1 week (aspirin, vasodilator) —

Hospitalization 2 days Possibly a bone scan at day 2

Hospitalization 8 days Bone scan at day 2

Hospitalization intensive care unit Bone scan at day 2

Oral treatment for 3 weeks (aspirin, vasodilators), dressing — —

IV administration for 8 days (aspirin, vasodilators), dressing Bone scan near day 8 Bone amputation near day 30

Recovery with moderate sequelae

Bone amputation of the digit with functional sequelae

IV administration for 8 days (aspirin, vasodilators), dressing Possibly antibiotics Early bone amputation near day 3 if sepsis Bone amputation of the limbs with systemic involvement

— — Recovery

From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001. IV, Intravenous. *See Figure 8-2.

temperature of −6.7° C (−19.9° F) with a 45-mph wind has the same cooling effect as does a temperature of −40° C (−40° F) with a 2-mph breeze184,186,189 (Figure 8-7, online). Thus, it is important to think in terms of heat loss, not cold gain. Frostbite occurs when the body is unable to conserve heat or protect against heat loss.

TABLE 8-3  Probability of Amputation Based

on the Extent of the Initial Lesion Extent (Level of Involvement)

Probability of Bone Amputation (95% CI)

Hand

5 4 3 2 1

(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)

100— 100— 83 (66;100) 39 (25;52) 1 (00;03)

Foot

5 4 3 2 1

(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)

100— 98 (93;100) 60 (45;74) 23 (10;35) 0—

Hand and foot

5 4 3 2 1

(carpal/tarsal) (metacarpal/metatarsal) (proximal phalanx) (intermediary phalanx) (distal phalanx)

100— 98 (95;100) 67 (55;79) 31 (22;41) 1 (00;02)

From Cauchy E, Chetaille E, Marchand V, et al: Retrospective study of 70 cases of severe frostbite lesions: A proposed new classification scheme, Wilderness Environ Med 12:248, 2001. CI, Confidence interval.

CONDUCTION The type and duration of cold contact are the two most important factors in determining the extent of frostbite injury.184,186,189 Touching cold wood or fabric is not nearly as dangerous as is direct contact with metal, particularly by wet or even damp hands.51 This is a result of differences in thermal conductivity between the materials. Deep, loose snow, which traditionally has been thought to insulate from the cold, may actually contribute to frostbite. Temperature measured beneath deep snow is frequently much lower than that on the surface. Washburn189 recounts one expedition to Mt McKinley, Alaska, when members of his party found it extremely difficult to keep their feet warm, despite a clear, sunny, −16° C (3.2° F) day with little wind. One member inadvertently dropped a thermometer in the snow and noted that it registered −25.6° C (−14.1° F). Feet must be dressed for the temperature at their level, not for surface temperature protection.189

ALTITUDE Ambient temperature drops by approximately 1.0° C (1.8° F) for every 150 m (492 feet) of height gain. Many serious cases of frostbite originate at high altitude, but it is difficult to sort out the independent risk for hypobaria/hypoxia versus cold exposure. Hashmi and colleagues61 reported 1500 cases of highaltitude frostbite and observed a “very steep upward curve” beyond a height of 5182 m (17,000 feet) above sea level. CIVD has been shown to be diminished in non-native visitors to high altitude.52 Some important sequelae of high-altitude acclimatization, namely erythrocytosis (an increase in red blood cells to maintain oxygen transport in the hypobaric environment) and high-altitude dehydration, result in hyperviscosity that may make frostbite more likely. Garvey and associates50 demonstrated that 185

CHAPTER 8  Frostbite

TABLE 8-1  Proposed Classification for Severity of Frostbite Injuries of the Extremities

PART 2  COLD AND HEAT

erythremia in the setting of a hypobaric environment provoked procoagulability in a rhesus monkey model. Recent evidence using a real-time video-imaging technique compared the sublingual microcirculation at sea level and at altitude.103 The study showed significant reduction in microcirculatory flow index (MFI) at high altitude (4900 m [16,076 feet]) when compared with sea level in small (<25 µm) and medium (26 to 50 µm) blood vessels (Figure 8-8). Larger vessels were not studied because of the relative paucity of their representation in the vascular bed studied. The results also showed further reduction in MFI within small and medium vessels at extreme altitude (6400 m [20,997 feet]). The very marked slowing of blood flow in the microcirculation at high altitude is easily appreciated (clips can be seen online at http://www.sdfimaging. net/dsmsealevelmicrocirc.wmv and http://www.sdfimaging.net/ dsm6400metermicrocirc.wmv). Stagnant hypoxia may occur in tissues as a result of reduced microcirculatory blood flow and consequent failure of oxygen mass transfer. Furthermore, disparity of oxygen supply and demand at a microvascular level could lead to heterogeneous tissue oxygenation and cellular hypoxia.73 These preliminary data are the first evidence demonstrating clear reduction in microcirculatory blood flow at altitude and may in part explain the apparent increased incidence of frostbite at extreme altitude, because a reduction in flow will be associated with reduction in heat transfer. Further studies to assess the potential reversibility with supplemental oxygen are indicated. Hypoxic neurologic dysfunction is a feature among nonsurvivors at extreme altitude; failure to adequately protect extremities may contribute to the high incidence of frostbite at extreme altitude.42 Inadequate fluid intake and poor nutrition are also possible risk factors.121,142

FIGURE 8-9  Sherpa climber on day 4 of treatment for second-degree frostbite from propane leak in backpack on Mt Everest. (Courtesy Luanne Freer, MD.)

COOLANTS Not all victims of frostbite are exposed to cold environments. Case reports cite toxic dermatologic effects of propane, butane, chloroethane, and liquid oxygen47,91,164,179,183 application to the skin, either intentionally, but exceeding time exposure for cryotherapy, or accidentally (Figure 8-9), as in the case of severe frostbite requiring skin grafting in a child improperly using a toilet air freshener containing propane and butane.91 Careless use of ice to cool a soft tissue injury can result in frostbite,55 and patients should be instructed to place a towel or other fabric between ice packs and bare skin to prevent this complication.

Clothing

A

The degree of inadequacy of protective clothing varies with conditions and may contribute to insufficient conservation of body heat.33 Tight-fitting clothing may produce constriction, which hinders blood circulation and lessens the benefit of heat-retaining air insulation. Wet clothing transmits heat from the body into the environment, because water is a thermal conductor superior to air by a factor of about 25.85 Clothing that transmits moisture away from the body may be protective if an outer wind-resistant layer decreases heat loss. However, this wind-resistant layer must retain the same transmission capabilities; otherwise, clothing will still become moist. Clothes that decrease the amount of surface area may decrease frostbite risk. Mittens are more protective than gloves, because gloves have a greater surface area and prevent air from circulating between fingers. Poorly fitted boots notoriously generate frostbite injuries, even when worn with excess socks (Figures 8-10 and 8-11; Figure 8-10, online). Although up to 40% of total body heat loss can occur through exposed head and neck areas,178 a more recent study has refuted the widely held belief that the head loses proportionally more heat than does the rest of the body. In fact, any uncovered part of the body loses heat in proportion to the body surface area exposed; appropriate protection is important for all exposed skin.140

SKIN WETNESS/UNWASHED SKIN

B FIGURE 8-8  Sublingual microcirculatory flow at sea level (A) and 4900 m (16,076 feet) (B). There is a significant reduction in microcirculatory flow index at high altitude (4900 m) when compared with baseline in small (<25 µm) and medium (26 to 50 µm) blood vessels, Caudwell Xtreme Everest Expedition. (From Martin DS, Ince C, Goedhart P, et al: Abnormal blood flow in the sublingual microcirculation at high altitude. Eur J Appl Physiol 106:473, 2009.)

186

Development of frostbite does not depend simply on ambient temperature and duration of exposure. Along with windchill, humidity and wetness also predispose to frostbite. Skin wetting adds an increment of heat transfer through evaporation and causes wet skin to cool faster than dry skin.123 More important, water in the stratum corneum can terminate supercooling by triggering water crystallization not only in this layer but also in the underlying tissue. Skin wetness is therefore conducive to frostbite because it allows crystallization to terminate supercooling after approximately one-half of the exposure time required by dry skin. This substantiates the following clinical observation: “It has been found that supercooling displays itself in greater degree in skin that remains unwashed. Washing the skin

Impaired local circulation is a primary contributor to frostbite. Cigarette smoking causes vasoconstriction, decreased cutaneous blood flow, and tissue loss in random skin flaps.94 Reus and colleagues147 documented that smoking induced arteriolar vasoconstriction and decreased blood flow in a nude subject. Although red blood cell velocity increased, the net effect was a decrease in blood flow in the cutaneous microcirculation during and immediately after smoking. Curiously, habitual heavy smokers show higher scores on the Resistance Index of Frostbite (RIF), which correlates with lower risk for frostbite.29 Empirically, one could conclude that smoking, which induces vasoconstriction, should place one at increased risk for frostbite, and research supports this.30,38,61

COMORBIDITIES Drugs known to have vasoactive properties may predispose to or compound frostbite injury. Disease states that alter tissue perfusion, such as diabetes, atherosclerosis, arteritis, and Raynaud’s disease, predispose to frostbite (Figure 8-12).34,88

PREVIOUS FROSTBITE INJURY

FIGURE 8-11  Subject on South Col, Mt Everest (7950 m [26,083 feet]) with excess socks in hand, about to descend, Caudwell Xtreme Everest Expedition. (Courtesy Christopher H.E. Imray, MD.)

encourages freezing, whereas rubbing the skin with spirit and anointing it with oil discourages it. The capacity to supercool greatly would seem to be connected with relative dryness of the horny layers of the skin. It is well known that Arctic explorers leave their skin unwashed.”96

ALTERED MENTAL STATUS (ALCOHOL, DRUGS, MENTAL ILLNESS) Putting on clothes in response to cold is not a reflex but requires a conscious decision. When the ability to decide or to act is impaired, there is a risk for cold-induced injury; not surprisingly, alcohol has been implicated in up to 53% of nonmilitary frostbite cases.177 Once the injury had occurred, alcohol intake probably did not significantly alter the course of events. Barillo and associates7 experimentally demonstrated increased mortality and a detrimental effect of ethanol on tissue perfusion associated with severe murine frostbite. Alcohol consumption promotes peripheral vascular dilation and increases heat loss, making an exposed part more susceptible to frostbite.149 In one series of 20 urban frostbite patients, all had overt or covert psychiatric disease.135 This prompted a retrospective review that suggested that between 61% and 65% of victims of urban frostbite suffer from psychiatric disease, and some centers now advocate psychiatric screening in all cases of urban frostbite injury.

On the basis of clinical observations, an individual who has experienced prior cold injury is placed in a high-risk category during subsequent cold exposure.118,193 For undefined reasons, cold injury sensitizes an individual, so that subsequent cold exposure, even of a lesser degree, produces more rapid tissue damage.84 Cold-induced neuropathy may play an important role in the long-term sequelae of cold sensitivity after local cold injury. An alteration in somatosensory function was found, and this was more pronounced in lower limb injuries.4

IMMOBILITY Military studies emphasize that long periods of immobility contribute to the extent of cold injury.84,85 Motion produces body heat and improves circulation, especially in endangered limbs.

GENETIC PREDISPOSITION The deletion genotype (DD) for the angiotensin I–converting enzyme (ACE) has been associated with increased vascular reactivity in vivo and in vitro.18,65 Kamikomaki77 proposed that a case of frostbite in a climber with ACE DD allele was caused by genetic propensity for vasoconstriction.

FATIGUE During World War II and the Korean conflict, clinical studies indicated that cold injuries occurred with higher frequency among soldiers in retreat.129,130,193 Fatigue and apathy also increase the incidence of cold injury. When warfare is proceeding toward defeat, or in conditions of starvation, soldiers often become indifferent to personal hygiene and clothing, and the frequency of frostbite increases.83 Overexertion increases heat loss. A large amount of body heat can be expanded by panting, and perspiration further compounds the problem of chilling. Both panting and sweating consume energy, which compounds the fatigue factor.

FIGURE 8-12  A 54-year-old man had an acute primary episode of Raynaud’s disease after surfing for 80 minutes in water that was 21° C (69.8° F). The distinctive asymmetric pallor of the terminal phalanges of the fourth digit on the right hand persisted for 40 minutes. A sharp demarcation between the second and third phalangeal joints was evident, but no other symptoms were apparent. The pallor spontaneously resolved without cyanosis or redness of the affected area. Medical evaluation subsequently revealed no disorder known to cause secondary Raynaud’s phenomenon. (From Bluto MJ, Norman DA: Acute episode of Raynaud’s disease, N Engl J Med 347:992, 2002.)

187

CHAPTER 8  Frostbite

SMOKING

PART 2  COLD AND HEAT

Civilian clinical studies are inadequate for statistical evaluation of factors such as race and previous climatic environmental exposure.84,109,111 In a recent study, blacks were found to have difficulty generating increased metabolic rate (measured by  2 ] and rectal temperature) after acute oxygen consumption [ VO cold exposure, and researchers suggest this group may be at greater risk for cold injury.40 Military studies suggest that women30 and blacks30,52 may be more susceptible to cold injury. One author postulates that blacks are three to six times more susceptible to frostbite than are whites because blacks tend to initiate shivering at lower core temperatures and tend to have long, thin fingers and toes, as well as thin arms and legs, which do not conserve heat as efficiently as do their white counterparts. In testing, black fingers cool faster when immersed in cold water and reach a lower temperature before hunting reaction ensues.52 Individuals with type O blood52 and from warmer climatic regions in the United States tend to be more susceptible.193 An increased incidence of frostbite was reported in nearly 6000 military recruits with cold-provoked white finger syndrome and in those with hand/arm vibration in both exposure classes analyzed.38,128 A low RIF, determined in a simple laboratory test, may be indicative of increased risk for cold injuries during operations in the field.29

Clinical Presentation In most patients, the initial clinical observation is coldness of the injured part, and more than 75% complain of numbness. The involved extremity feels clumsy or “absent” because of ischemia following intense vasoconstriction. When numbness is present initially, it is frequently followed by extreme pain (76% of patients) during rewarming. Throbbing pain begins 2 to 3 days after rewarming and continues for a variable period, even after dead tissue becomes demarcated (22 to 45 days). After about a week, the victim usually notices a residual tingling sensation, a result of ischemic neuritis, which explains why this sensation tends to persist longer than other symptoms. Severity of the injury usually defines the extent of neuropathologic damage. Because different injuries are influenced by so many environmental and individual factors, there may be a great deal of variation in symptoms. In patients without tissue loss, symptoms usually subside within 1 month, whereas in those with tissue loss, disablement may exceed 6 months. In all cases, symptoms are intensified by a warm environment. Other sensory deficits include spontaneous burning and electric current–like sensations. The burning sensation, which is frequently early in presentation, subsides within 2 to 3 weeks and is usually not present in victims with tissue loss. In victims without tissue loss, the burning sensation may resume on wearing shoes or increasing activity. The electric current–like shock is almost universal (97%) in patients with tissue loss. It usually begins 2 days after injury, lasts for about 6 weeks, and is particularly unpleasant at night. All frostbite victims experience some degree of sensory loss for at least 4 years after injury and perhaps indefinitely. The clinical appearance of frostbite depends on how quickly the injured patient presents to care, and it is important to note that this appearance may initially be deceiving.12,129 Patients in the Alps who arrive by helicopter within minutes of their injury may present quite differently than do Himalayan climbers, who have nearly all rewarmed during self-descent and may be fortunate to arrive at definitive care even several days after injury. Regardless of venue, only a few patients arrive with tissue still frozen. At first, the extremity appears yellowish white or mottled blue. It may be insensate and may appear frozen solid, regardless of the depth of the injury. With rapid rewarming there is almost immediate hyperemia, even in some of the most severe injuries. Sensation returns after thawing and persists until blebs appear. At this point, some effort may be made to assess the severity of the injury. After the extremity is rewarmed, edema appears within 3 hours and lasts 5 days or longer, depending on the severity of the case.129 Vesicles or bullae appear 6 to 24 hours after rapid rewarming.112,130 Clear bullae confer a better prognosis than hemorrhagic bullae, which indicate deeper injury. During the first 9 to 15 days, severely frostbitten skin forms a black, hard, and 188

A

B FIGURE 8-13  Photo of climber 24 hours (A) and approximately 2 weeks after (B) deep frostbite injury to fingers, showing eschar formation. (Courtesy Luanne Freer, MD.)

usually dry eschar, whether or not vesicles are present (Figure 8-13).130 Mummification forms an apparent line of demarcation in 22 to 45 days.129

Field Treatment In 1957, Hurley68 stated, “Tissue cells can be affected by freezing in three different ways: (1) a certain number of cells are killed; (2) a certain number remain unaffected; and (3) a large number are injured but may recover and survive under the right circumstances.” Clearly, the major treatment effort must be to salvage as many cells in the third group as possible. Frostbite treatment is directed separately at the pre-thaw and post-thaw intervals.

SELF-RESCUE IN THE FREEZING ENVIRONMENT The International Commission for Alpine Rescue (ICAR) gives specific recommendations for self-rescue to those working, recreating, or otherwise exposed to a cold environment (Box 8-1). These guidelines advise seeking shelter from cold and wind, drinking warm fluids, removing wet clothing, taking ibuprofen, and attempting self-rewarming for 10 minutes. If at high altitude, supplemental oxygen is advised, and if sensation does not return, the victim is advised to discontinue any further exposure and seek treatment.172 Although these guidelines may seem common sense to most, climbers appreciate these guidelines for safety and self-rescue when in an exposed, potentially dangerous, and remote setting.

IN THE PREHOSPITAL FREEZING ENVIRONMENT The Alaska State guidelines for field treatment and transport of patients with frostbite recommend the following: If transport time will be short (1 to 2 hours at most), the risks posed by improper rewarming or refreezing outweigh the risks of delaying treatment for deep frostbite. If transport will be prolonged (more than 1 to 2 hours), frostbite will often thaw spontaneously. It is more important to prevent hypothermia than to rewarm frostbite rapidly in warm

BOX 8-2  Alaska State Guidelines for Prehospital

Emergency Treatment In the Open With Possible Onset of Frostbite • Move out of the wind/consider turning back/drink fluids (warm if possible) • Remove boots—but consider possible problems with replacement if swelling occurs • Remove socks/gloves if wet. Exchange for dry clothing • Warm by placing foot/hand in companion’s armpit/groin for 10 minutes only • Replace boots • Give one dose of aspirin or ibuprofen to improve circulation (if available and not contraindicated) • Don’t rub the affected part because this may cause tissue damage • Don’t apply direct heat If there is sensation, the victim can continue to walk If there is no sensation, the victim should go to the nearest warm shelter (hut/base camp) and seek medical treatment At high altitude, give oxygen if available

First Responder/Emergency Medical Technician— I, II, III/Paramedic/Small Bush Clinic Evaluation and Treatment A. Anticipate, assess, and treat the patient for hypothermia, if present. B. Assess the frostbitten area carefully because the loss of sensation may cause the patient to be unaware of soft tissue injuries in that area. C. Obtain a complete set of vital signs and the patient’s temperature. D. Remove jewelry and clothing, if present, from the affected area. E. Obtain a patient history, including the date of the patient’s last tetanus immunization. F. If there is frostbite distal to a fracture, attempt to align the limb unless there is resistance. Splint the fracture in a manner that does not compromise distal circulation. G. Determine whether rewarming the frostbitten tissue can be accomplished in a medical facility. If it can, transport the patient while protecting the tissue from further injury from cold or impacts. H. If the decision is made to rewarm frostbitten tissue in the field, you should prepare a warm water bath in a container large enough to accommodate the frostbitten tissues without them touching the sides or bottom of the container. The temperature of the water bath should be 99° to 102° F   (37° to 39° C). • Generally, patients with frostbite do not require opiates for pain relief; they occasionally need non-opiate pain medication or anxiolytics. If possible, consult a physician regarding the administration of oral analgesics, such as acetaminophen, ibuprofen or aspirin. Aspirin or ibuprofen may help improve outcomes by blocking the arachidonic acid pathway. • Immersion injury or frostbite with other associated injuries may produce significant edema and high pain levels. These patients may need opiate pain medications for initial treatment. In this case, advanced life support personnel should administer morphine or other analgesics in accordance with physician-signed standing orders or online medical control. I. A source of additional warm water must be available. J. Water should be maintained at approximately at 99° to   102° F (37° to 39° C) and gently circulated around the frostbitten tissue until the distal tip of the frostbitten part becomes flushed. K. Pain after rewarming usually indicates that viable tissue has been successfully rewarmed. L. After rewarming, let the frostbitten tissues dry in the warm air. Do not towel dry. M. After thawing, tissues that were deeply frostbitten may develop blisters or appear cyanotic. Blisters should not be broken and must be protected from injury. N. Pad between affected digits and bandage affected tissues loosely with a soft, sterile dressing. Avoid putting undue pressure on the affected parts. O. Rewarmed extremities should be kept at a level above the heart, if possible. P. Protect the rewarmed area from refreezing and other trauma during transport. A frame around the frostbitten area should be constructed to prevent blankets from pressing directly on the injured area. Q. Do not allow an individual who has frostbitten feet to walk except when the life of the patient or rescuer is in danger. Once frostbitten feet are rewarmed, the patient becomes nonambulatory.

of Potential Frostbite

Adapted from Syme D (for ICAR Medical Commission): Position paper: On-site treatment of frostbite for mountaineers. High Alt Med Biol 3:297, 2002. ICAR, International Commission on Alpine Rescue.

water. This does not mean that a frostbitten extremity should be kept in the cold to prevent spontaneous rewarming. Anticipate that frostbitten areas will rewarm as a consequence of keeping the patient warm and protect them from refreezing at all costs.31 The Joint Commission of Health and Human Services, emergency medical services, and public health departments for Alaska have published further guidelines for prehospital and bush clinic care of frostbite. These guidelines are widely regarded as stateof-the-art recommendations and appear in Box 8-2. If a patient is referred from a nearby location, no attempt at field rewarming is indicated. Vigorous rubbing is ineffective and potentially harmful. The extremity should not be intentionally rewarmed during transport and should be protected against slow partial rewarming by keeping the patient away from intense campfires and car heaters. All constrictive and wet clothing should be replaced by dry, loose wraps or garments. The extremity is padded and splinted for protection, and ibuprofen 400 mg twice daily (which may be more beneficial than aspirin because aspirin may block more of the inflammatory cascade than is helpful) may be initiated. Although there is a correlation between the length of time tissue is frozen and the amount of time required to thaw that tissue, there is no direct correlation between the length of time tissue is frozen and subsequent tissue damage. Still, “rapid” transport of frostbite patients (within 2 hours) is appropriate. Otherwise, rapid rewarming should be instituted (goal to see blush of rewarming and/or 15 minutes immersed in rewarming fluid) and the victim transported with protective, dry, nonadherent dressings to prevent refreezing. Appropriate and adequate analgesia should be administered (opiates either IV or intramuscularly [IM]) may be required). Blisters should be left intact. Patients with long transport times are at greater risk for (refreezing) recurrent injury. All efforts should be made to prevent subsequent refreezing, because this creates an infinitely worse result than does delayed thawing (Figures 8-14 to 8-16; Figure 8-16, online). A victim who must walk through snow should do so before thawing frostbitten feet (see Figure 8-10). During transport, the extremities should be elevated and tobacco smoking prohibited.119 Alcohol ingestion is contraindicated. The Wilderness Medical Society convened a panel of experts to review recent literature and ICAR and Alaska State guidelines in order to apply evidence grades based on the quality of supporting evidence, and balance between the benefits and risks for each modality according to methodology stipulated by the American College of Chest Physicians. A document of these graded guidelines is projected to be published in 2011.

Treatment of Frostbite

From Department of Health and Social Services, Division of Public Health Section of Community Health and EMS: State of Alaska cold injuries guidelines, 2003 version rev 2005. http://www.chems.alaska.gov.

189

CHAPTER 8  Frostbite

BOX 8-1  Guidelines From ICAR for Self-Treatment

PART 2  COLD AND HEAT

Definitive Treatment IMMEDIATE TREATMENT

A

B FIGURE 8-14  A, Day 2 after exposure: field rewarming of frostbite injury to Mt Everest summiteer at 6400 m (20,997 feet); B, day 3: field treatment of frostbite injury at 5300 m (17,388 feet). (Courtesy Christopher H.E. Imray, MD.)

A

B FIGURE 8-15  A, Six weeks after injury: third toe is showing signs of recovery; B, 10 weeks after injury: primary closure was achieved with full-thickness skin cover, to optimize the functional result. (Courtesy Christopher H.E. Imray, MD.)

190

Once in the emergency department, if tissues are still frozen, rapid rewarming should be started immediately. Any associated traumatic injuries or medical conditions should be identified. Systemic hypothermia should be corrected to a core temperature of at least 34° C (93.2° F) before frostbite management is attempted. Fluid resuscitation is usually not a problem with isolated frostbite injuries, although one case of rhabdomyolysis and acute renal failure has been reported.152 Treatment is directed at the specific pathophysiologic effects of the frostbite injury, either blocking direct cellular damage or preventing progressive microvascular thrombosis and tissue loss. Direct cellular damage is treated by rapid thawing of all degrees of frostbite with immersion in gently circulating water warmed to between 40° and 42° C (104° and 107.6° F).84 Adherence to this narrow temperature range (as long as it is easy to monitor in the hospital) is important, because rewarming at lower temperatures is less beneficial for tissue survival48,64 and rewarming at higher temperatures may compound the injury by producing a burn wound.120 Frozen extremities should be rewarmed until the involved skin becomes pliable and erythematous at the most distal parts of the frostbite injury. This usually takes less than 30 minutes. Active motion during rewarming is helpful, but massage may compound the injury. Extreme pain may be experienced during thawing, and unless otherwise contraindicated, parenteral analgesics are administered. Rapid return of skin warmth and sensation with the presence of an erythematous color is a favorable sign, whereas the persistence of cold, anesthetic, and pale skin is unfavorable. Rapid rewarming reverses the direct injury of ice crystal formation in the tissue. However, it does not prevent the progressive phase of the injury. McCauley and associates109,110 have designed a protocol based on the pathophysiology of progressive dermal ischemia that has been quite successful in minimizing production of local and systemic thromboxane by injured tissues. All but the most minor frostbite cases should be admitted to the hospital. Victims with minor injuries should be admitted if, after rapid rewarming, a warm environment cannot be ensured for the patient. No patient should ever be discharged into subfreezing weather. Even with a warm car waiting, the patient should be allowed to leave only with proper clothing (such as stocking cap, wool mittens, and wool socks). Because the majority of frostbite injuries necessitate admission to the hospital, a discussion of the protocol is warranted. White or clear blisters, which represent more superficial injury, are debrided to prevent further contact of PGF2α or TXA2 with the damaged underlying tissues. Unlike the clear blisters, hemorrhagic blisters reflect structural damage to the subdermal plexus. It may be worthwhile to aspirate the thromboxane-containing fluid out of these blisters, but debridement may promote desiccation of the deep dermis and allow conversion of the injury to a full-thickness injury. Therefore hemorrhagic blisters are left intact. A specific thromboxane inhibitor, like Aloe vera gel, is placed on the wounds to prevent further formation of this vasoconstricting mediator,63 and dressings should accommodate for expected increasing edema. Aspirin was originally given systemically to block production of PGF2α and TXA2. The correct dose of aspirin to block PGF2α is difficult to determine, so it has been replaced with ibuprofen by many clinicians. Aspirin may, however, still have a useful antiplatelet action if ibuprofen is not available. Ibuprofen not only inhibits the arachidonic acid cascade but has the additional benefit of fibrinolysis. Oxygen should be used to achieve normoxia in a hypoxic patient and is used for frostbite injuries occurring at extreme altitude.

Evaluation and Treatment in the Hospital OVERALL STRATEGY Frostbite is a thermal injury affecting the vasculature, microvasculature, and tissues of the extremities and as such shares many

INITIAL ASSESSMENT OF FROSTBITE AND OTHER INJURIES A rapid and detailed clinical assessment of the patient on arrival in the emergency department is mandatory. The standard approach of assessing the airway, breathing, and circulation clearly takes precedence over assessment of the frostbite injury. History and examination may reveal coexisting problems, and although the frostbite injuries may be visually distressing and severe, it is possible that there are more serious injuries or medical conditions that need to be treated first. Particular attention needs to be paid to hypothermia, limb fractures, the peripheral circulation, and any coexisting trauma. Coexisting medical conditions such as poor glycemic control and alcohol/drug use need to be considered. Principles Hurley68 stated in 1957 that frostbite will result in three zones of tissue injury: dead tissue, normal living tissue, and an interface zone. If we develop this concept further, immediately after the index frostbite injury the size of the interface zone will be maximal and is potentially salvageable. Weeks after injury, the interface zone will be negligible; as a result, the interface zone has a “dynamic” component.47,68 The aim of early evaluation of the frostbite injury is to try to determine the exact extent of the three zones so that a subsequent multifaceted management plan may be directed to optimize tissue salvage in the dynamic interface zone. The initial injury, individual’s response, ambient temperature, and time from initial cold injury at the presentation at the hospital all contribute to how extensive the intermediate potentially salvageable interface zone will be. The patient who is transferred from the mountainside directly to the emergency department by helicopter will have a relatively large potentially salvageable interface zone when compared with a patient who has undergone a much more lengthy evacuation from a remote climbing region of the Himalayas.

PATIENT CARE Specialist Nursing Care Almost all urban patients with significant frostbite should be admitted to the hospital, given that alcohol intoxication, psychiatric illness, and homelessness are common features of the urban frostbite patient; immediate discharge is rarely prudent. Overall goals of hospital treatment include keeping the patient quiet, well nourished, suitably hydrated, and pain-free. Wound care must be meticulous to avoid further trauma. Injured extremities should be elevated above heart level to attempt to minimize edema. Physiotherapy is important, and the patient should be encouraged to mobilize as soon as possible.192 Extremities should be treated with clean dressings and twice-daily whirlpool baths with antiseptics such as chlorhexidine or povidone-iodine. Topical Aloe vera gel should be applied every 6 to 8 hours through resolution of blisters. This encourages the eschars created by the blisters to separate from underlying healthy tissue. Although patients may be nursed anywhere that these objectives can be achieved, vascular surgery or plastic surgery/burns wards (with multidisciplinary input) tend to be most appropriate for the more severe injuries. Frostbite blisters have been shown to contain high concentrations of the vasoconstricting metabolites of arachidonic acid, PGF2α and TXB2 which are known to mediate dermal ischemia in burns and pedicle flaps. It is suggested that they may play a role in the pathogenesis of frostbite, and so early debridement, either with needle aspiration or surgical debridement, is indicated.150

TECHNIQUES TO EVALUATE TISSUE PERFUSION Over the years, several diagnostic tests have been used to attempt to predict severity and prognosis of frostbite injury. These include plain radiographs, infrared thermography, angiography,56 triplephase bone scanning,27 laser Doppler, digital plethysmography,146 and magnetic resonance imaging/magnetic resonance angiography (MRI/MRA). It appears that the most promising approaches are triple-phase bone scanning10,27 and MRI/MRA.8 Early diagnostic angiography (before tissue plasminogen activator [t-PA]) may become the most appropriate first-line investigation for the patient presenting acutely with severe frostbite injury without significant comorbidities.165 Duplex Ultrasonography Duplex ultrasonography uses B-mode, pulsed wave Doppler ultrasonography to visualize the blood flow within a vessel and color flow Doppler imaging to visualize the structure and hemodynamics within a vessel. In a modern vascular unit, there is a move toward using duplex ultrasound examination as the firstline investigative examination, reserving angiograms for situations in which a therapeutic intervention is required. Ease of access, portability, and the ability to make repeat examinations give the technique certain advantages over other imaging modalities. Many remote research stations and even large expeditions may have portable ultrasound machines. Duplex imaging has been used in the field at altitudes as high as 7950 m (26,083 feet) (Figure 8-17, online). Ultrasound has been used to determine the need for sympathetic blockade after frostbite.146 Magnetic Resonance Angiography MRI/MRA investigation has a theoretical advantage over 99mTc bone scanning because it allows direct visualization of vessels (both patent and occluded), as well as imaging of surrounding tissues. It has been suggested that it shows a more clear-cut line of demarcation of ischemic tissue.8 The other advantage of MRA over angiography is that it is noninvasive. However, there are relatively few accounts of its use in frostbite evaluation in the literature. Technetium-99m Scanning The first description of 99mTc scanning for assessment of bone viability in patients with frostbite injuries was in 1976.98 The degree of accretion of the 99mTc was found to depend on integrity of the vascular supply. It was successfully used to distinguish viable from nonviable bone. However, Miller and Chasmar114 found that very early 99mTc bone scanning in frostbitten patients was not as accurate an indicator of the ultimate extent of tissue loss as was scanning at 5 days after injury. They also noted that lesions appeared to fluctuate in extent over a 3-week period. Cauchy and colleagues25,26 recognized that existing frostbite classifications were based on retrospective diagnoses and were not useful for predicting the extent of final tissue loss and prognosis for frostbite patients. The 3- to 6-week waiting period often necessary to determine severity of the lesion and resultant need for amputation often caused considerable distress for patients. They suggested a new classification system that begins at day 0 (just after rewarming) and is based mainly on the topography of the lesion and on early bone scan results. This appears to be a very useful classification for the physician and patient, in that it allows accurate determination at a very early stage of the likely extent of subsequent tissue loss (see Tables 8-1 to 8-3). An interesting insight into some of the possible mechanisms involved in certain frostbite injuries was described by Salimi and co-workers,156 who designed an experimental model to study the pathogenesis and treatment of frostbite. Using 99mTc radionuclide imaging, they monitored the evolution and extent of tissue damage relative to temperature, rate of freezing, and controlled rewarming. Characteristic serial changes were demonstrated on sequential scans. Initial nonperfusion was followed by perfusion and finally again by nonperfusion; this occurred in all areas in which necrosis subsequently developed. The reappearance of nonperfusion corresponded to vascular injury. Vessel thrombosis 191

CHAPTER 8  Frostbite

clinical features with both vascular injuries and burn wounds. This section discusses the aspects of definitive patient care, including complete patient assessment, specific evaluation of the frostbite injury regarding perfusion and tissue viability, and optimal medical management, including proper selection of candidates for endoluminal treatments such as catheter-directed thrombolysis. Early and late reconstructive surgery, ablative surgery, rehabilitation, and frostbite prevention strategies are discussed.

PART 2  COLD AND HEAT

was found on pathology examination and may be related to reperfusion injury. These clinically relevant observations gave evidence to support the concept of temporal “perfusion flux” in blood flow to a frostbitten extremity. The initial reduction is often followed by a temporary hyperperfusion phase before the final infarction phase (probably secondary to endothelial dysfunction and thrombin accumulation). Consequently, measurement of tissue perfusion at a single time point may not be as accurate in predicting outcome as originally believed. Additional supporting evidence for perfusion flux in frostbite comes from Cauchy and associates,25,27 who performed a more detailed analysis of two-phase 99mTc bone scans. Sensitivity of the technique was enhanced by performing a second scan more than 5 days after rewarming. Comparative analysis of the two scans demonstrated that some of the lesions continued to evolve between day 2 and day 8. Based on this finding, they suggested that the outcome of lesions could still be modified during this period. However, in the case of severe sepsis, the results of the first bone scan can be used as an indication for emergency amputation.26 Although the large retrospective study of Cauchy and colleagues using two-phase bone scintigraphy suggested that nonuptake (or low uptake) in frostbite lesions had a strong correlation with the subsequent need for amputation, another prospective study has questioned some aspects of the technique.10 This study compared 22 controls with 20 patients with frostbite. Serial scintigraphy using 99mTc was performed in some patients. In line with the perfusion flux concept, the study suggests that scintigraphy results are somewhat more variable than previously suggested and that moderate to severe frostbite lesions can be classified as having infarcted, ischemic, or hibernating (viable) tissue, similar to the classification employed when using myocardial scintigraphy. Absence of uptake of 99mTc, even after the initial 10 days in this study, did not necessarily indicate infarction and the need for amputation, because many such lesions retain potential for vasodilation and recovery. Triple-phase bone scanning (using 99mTc) has now become more widely used in specialty units, often within the first few days of presentation. This technique assesses tissue viability in an effort to allow early debridement of soft tissue and early coverage of ischemic bony structures.58 There are few prospective data on the efficacy of 99mTc scanning in predicting the outcome of frostbite injuries. However, it remains a very useful way of assessing potential tissue loss69 (Figures 8-18 to 8-21).

MEDICAL MANAGEMENT Drugs used in the management of frostbite are summarized in Table 8-4. Tetanus Prophylaxis Frostbite should be considered to be a high-risk injury. Tetanus prophylaxis status should be completed in all patients according to currently accepted guidelines.32 Heparin Heparin is a naturally occurring anticoagulant that prevents formation of clots and extension of existing clots within blood vessels. Although true thrombi are not present in dilated, erythrocyte-filled vessels immediately after thawing, they form over the next few days. Heparin has been suggested as a possible treatment for frostbite.163 Lange and Loewe92 demonstrated its usefulness in experimental frostbite. Subsequent investigations have been unable to substantiate these findings, and there is no evidence that heparin alters the natural history of frostbite.16 However, most experts would agree that deep vein thrombosis (DVT) prophylaxis is indicated in any relatively immobile frostbite patient. Indications and Recommendations for Antibiotics There has long been awareness of the potential for infectious complications in frostbite patients.134 The metabolic requirements of infected and healing tissue are increased over those of normal 192

A

B FIGURE 8-18  Frostbitten left hand of a climber (A) taken 36 hours after injury, while climbing in Antarctica (B) Note the discoloration and blister formation, iodine warming towels, and aseptic techniques used in tented field hospital. The digital image was reviewed within 6 hours by Christopher H.E. Imray, MD, in the United Kingdom, and management advice was given over the Internet. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)

tissue. Consequently, should the marginally perfused interface zone become infected, the resulting tissue loss is likely to be increased. Although there is little published evidence with regard to the use of antibiotics in the frostbite patient, antibiotics are widely used. When the skin is edematous, penicillin is administered prophylactically because edema inhibits the skin’s inherent streptococcal properties.125 If there are clinical signs of infection, antibiotic use is absolutely indicated. Wound cultures should be taken from infected tissue to guide therapy, but while awaiting identification of species and sensitivities, practitioners should be aware that the common causative organisms include Staphylococcus aureus, β-hemolytic streptococci, gram-negative rods, and anaerobes. Empiric use of antibiotics to cover these likely organisms should be considered pending culture results. In a 12-year retrospective study, factors found to correlate significantly with amputation were duration of exposure, lack of proper attire, remote geographic location, presence of wound infection, and delay in seeking treatment. Prophylactic systemic antibiotics did not decrease the incidence of wound infection.181 This paper supports the approach of deferring the use of anti­ biotics until a clinically relevant infection develops. Topical: Aloe vera Experimental evidence from the frostbite rabbit ear model has suggested a clearly defined role for thromboxane as a mediator of progressive dermal ischemia in frostbite injuries. Rapid rewarming helps to preserve tissue by limiting the amount of direct

CHAPTER 8  Frostbite

A

FIGURE 8-21  Hands of patient in Figures 8-18 to 8-20 after 5 days of intravenous iloprost. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)

B FIGURE 8-19  Condition of hands of patient in Figure 8-18 on patient’s arrival in the United Kingdom, 5 days after initial injury. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and non-freezing cold injuries, Postgrad Med J 85:481, 2009.)

cellular injury. Selective management of blisters helps protect the subdermal plexus, and application of Aloe vera cream (e.g., Dermaide Aloe cream or gel) combats the local vasoconstrictive effects of thromboxane (Figure 8-22). Animal studies suggest thromboxane appears to be a mediator of progressive dermal ischemia in frostbite. In a rabbit ear frostbite model, Heggers and associates64,109 compared the effect of (1) the antiprostanoids (methylprednisolone), (2) aspirin combined with Aloe vera, (3) methimazole, and (4) a control group that received no therapy. Methimazole treatment gave 34.3% tissue survival; Aloe vera, 28.2% survival; aspirin, 22.5% survival; and methylprednisolone, 17.5% survival. In a human study of 154 patients with frostbite, there was significant improvement in outcome and reduction in amputation rates of treated patients compared with controls (p < 0.001). It was concluded that morbidity of progressive dermal ischemia in frostbite may be decreased by therapeutic use of inhibitors of the arachidonic acid cascade.

ANTIPROSTAGLANDIN AGENTS

L

L

Nonsteroidal antiinflammatory drugs, such as ibuprofen, act as a necessary adjuvant to rewarming, because they inhibit inflammatory reactions and pain by decreasing prostaglandin synthesis.64 Oral administration of ibuprofen decreases systemic levels of thromboxane. Ibuprofen 400 mg may be given by mouth and should be continued at a dose of 12 mg/kg of body weight per day. McCauley and co-workers111 treated 38 patients with frostbite in a protocol designed to decrease production of thromboxane locally and prostaglandins systemically. All patients recovered

R

Marker

R

FIGURE 8-20  Technetium-99m bone scans performed on arrival of patient in Figures 8-18 and 8-19 in the United Kingdom. The scans show minimal perfusion to the terminal phalanges in the left hand, suggesting that amputation of the distal phalanges is likely to be necessary. (Courtesy Christopher H.E. Imray, MD. From Imray C, Grieve A, Dhillon S, et al: Cold damage to the extremities: Frostbite and nonfreezing cold injuries, Postgrad Med J 85:481, 2009.)

FIGURE 8-22  Aloe vera cream being applied at the Everest Base Camp Medical Clinic. Note the care being taken to apply nonconcentric dressings to allow for edema formation. (Courtesy Suzanne Boyle, MD.)

193

PART 2  COLD AND HEAT

TABLE 8-4  Frostbite Management: Drugs, Doses, and Modes of Action and Rationale* Intervention

Dose

Action

Aspirin Ibuprofen Aloe vera gel or cream Oxygen Hyperbaric oxygen therapy Iloprost Nitroglycerin Papaverine Reserpine Buflomedil Pentoxifylline 10% Dextran 40 t-PA LMW heparin

75-250 mg orally once daily 400 mg bid or tid orally With dressing changes every 6 hr 2 L/min above 4000 m (13,123 ft) or when SpO2 is below 90% 2-2.5 atm 1-2 hr daily

Antiplatelet agent, improve rheology Antiprostaglandin effect Topical antiprostaglandin effect Improve tissue oxygenation Improve tissue oxygenation, improve rheology

2-10 mg/hr IV titrated against side effects 100 mcg IA single dose 300 mg over 1hr IA 0.1 to 0.25 mg once daily 400 mg IV or 300 mg bid orally 400 mg tid orally for 2-6 weeks 20 mL bolus, 20 mL/hr IV 1 mg/hr IA or IV Prophylactic dosage subcutaneously Therapeutic dosage subcutaneously

Vasodilator, improve rheology Vasodilator Vasodilator Vasodilator Vasodilator, improve rheology Vasodilator, improve rheology Improve rheology Thrombolytic agent DVT prevention, anticoagulant Maintain patency of recently thrombolysed vessels

Tetanus prophylaxis

bid, Twice a day; DVT, deep vein thrombosis; IA, intra-arterially; IV, intravenously; LMW, low molecular weight; SpO2, oxygen saturation as measured by pulse oximetry; tid, 3 times a day; t-PA, tissue plasminogen activator. *This table is intended to be used as a potential frostbite formulary reference, not as a protocol for treatment. See text for further discussion.

without significant tissue loss. Increased tissue survival was demonstrated experimentally with preservation of the dermal microcirculation by using antiprostaglandin agents and thromboxane inhibitors.

VASODILATORS The equation determining fluid flow within a tube was first described by the French physician and physiologist Jean Poiseuille in the 1840s. He demonstrated that flow was related to perfusion pressure, radius,4 length, and viscosity. In a frostbite patient, each of these parameters (other than length) can be optimized using appropriate medical interventions. Iloprost Prostaglandin E1 (PGE1) is a vasoactive drug that dilates arterioles and venules, reduces capillary permeability, suppresses platelet aggregation, and activates fibrinolysis. Its intra-arterial use has been effective in treating ischemic peripheral vascular disease. The potentially beneficial effect in treating frostbite injuries with intra-arterial PGE1 was first assessed in an animal model.195 PGE1 reduced the magnitude of frostbite injury when the injured limb was slowly rewarmed. The data suggested a possible role for the use of PGE1 in frostbite patients who have not undergone rapid rewarming. Since the first description of its use in patients,59 PGE1 has been used with some success in frostbite injuries.69,192 Further experimental evidence implicates an inflammatory process in the underlying mechanism of tissue injury. It has been postulated that progressive ischemic necrosis is secondary to excessive TXA2 production, which upsets the normal balance between prostacyclin (prostaglandin I2) and TXA2.132 A recent study24 printed as a research letter showed a pro­ mising decrease in the digit amputation rate with the use of intravenous iloprost in severe frostbite injuries. The clinicians compared results of a trial of 47 frostbite patients who were rapidly rewarmed, received 250 mg of aspirin and 400 mg IV buflomedil, and who were then randomized to receive 250 mg aspirin per day, plus either buflomedil, iloprost, or r-TPA with iloprost. The iloprost group had the lowest overall amputation rate, and though the ideal dose is undetermined, this encouraging data will most likely lead to more clinical research and hope for future frostbite victims. Iloprost is best given as an IV infusion either through a peripheral or central line in a specialist vascular or highdependency unit. The diluted iloprost should be delivered by an accurate rate delivery system such as a syringe driver. The infusion is started at a rate 2 mg/hr and incrementally increased up to 10 mg/hr; titrated against the side effects of facial flushing, 194

headache, nausea, and flulike symptoms; and infusion is usually run for 5 days.69,70 Reserpine Reserpine is a powerful vasodilator that acts by inhibiting uptake of norepinephrine into storage vesicles.137 For frostbite, it is used intra-arterially. The first description in the treatment of frostbite was by Snider and colleagues.169 An animal study suggested that a regional “medical sympathectomy” may be beneficial in reducing tissue loss following frostbite, especially when rapid rewarming cannot be performed.168 Pentoxifylline Pentoxifylline, a methylxanthine-derived phosphodiesterase inhi­ bitor, has been widely used to treat intermittent claudication, arterial disease, and peripheral vascular disease and has yielded some promising results in human frostbite trials.62 It increases blood flow to the affected extremity, increases red cell deformability, decreases platelet hyperactivity, helps normalize the prostacyclin–to–TXA2 ratio, and has been shown to enhance tissue survival. Pentoxifylline is also presumed to lower pathologically increased levels of fibrinogen and so may protect against vascular endothelial damage. The drug’s efficacy has been demonstrated in animal studies and approaches the effectiveness of Aloe vera. The combination of pentoxifylline and Aloe vera appears to be synergistic.116 A similar synergy of aspirin and pentoxifylline was demonstrated in an animal study.143 Hayes and co-workers62 have proposed a treatment using pentoxifylline in conjunction with the traditional therapy of rewarming, soaks, pain management, and vesicle debridement. They recommend pentoxifylline in the controlled-release form of one 400-mg tablet 3 times a day with meals, continued for 2 to 6 weeks. Controlled studies of pentoxifylline in the management of frostbite have yet to be performed. Buflomedil Buflomedil hydrochloride is a vasoactive drug that may have a number of effects, including inhibition of α-receptors, inhibition of platelet aggregation, improved erythrocyte deformability, nonspecific and weak calcium antagonistic effects, and oxygensparing activity.28,105,108 A case series of 20 patients reported that early administration of IV buflomedil appeared to reduce the risk for subsequent amputation.45 However, buflomedil has not been shown to reduce microcirculatory damage from acute experimentally induced freeze injury.37 Although buflomedil does not have U.S. Food and Drug Administration (FDA) approval, it has been used extensively in France to treat frostbite, with considerable beneficial effect.26

Low-Molecular-Weight Dextran It has been observed that shortly after thawing, cold-injured vessels become dilated and filled with clumps of erythrocytes. These clumps can be easily dislodged by gentle manipulation and do not represent true thrombosis. Although the mechanism that leads to erythrocyte clumping is not completely understood, it may reflect cold-induced increase in blood viscosity. This suggests that use of low-molecular-weight (LMW) dextran may be beneficial for early treatment of frostbite. Although no controlled clinical trial of LMW dextran has been reported, there has been experimental evidence to support its use. Weatherly-White and colleagues190 demonstrated that use of LMW dextran, 1g/kg/day, protected against tissue loss in the rabbit ear model. This led to the suggestion that the use of 1 L of 6% dextran IV on the day of injury, followed by 500 mL on each of 5 successive days, might be of benefit.151 The extent of tissue necrosis was also found to be significantly less than in controls when hemodilution with dextran was combined with water bath rewarming with our present understanding of the etiology of frostbite and introduction of newer techniques such as t-PA, there appear to be fewer instances when LMW dextran may be used and have a demonstrable benefit.

ENDOVASCULAR INTERVENTIONS Thrombolysis With Tissue Plasminogen Activator Treatment of embolic and thrombotic peripheral vascular disease has changed radically over the last 10 years. In 1963, Fogarty and co-workers43 reported treating acute occlusion of a peripheral vessel by a remote embolectomy catheter technique. The artery is surgically opened distant to the site of the embolus. A deflated catheter balloon is passed from the proximal artery beyond the embolus, the balloon is then inflated, and the catheter withdrawn, removing the embolus. More recently, catheterdirected thrombolysis has been used to clear distal arteries and the microvasculature using a thrombolytic agent such as t-PA. Found in vascular endothelial cells, t-PA has fibrinolytic action and plays an important role in the dynamic balance between clot formation and lysis. Plasminogen and t-PA bind to the fibrin surface of the thrombus, resulting in production of plasmin and subsequent dissolution of the thrombus. t-PA has been used extensively in coronary, cerebrovascular, and peripheral arterial disease.131 A small retrospective study reported successful use of catheterdirected intra-arterial t-PA to reduce amputation rates in frostbite.17 Among the six patients who received t-PA within 24 hours of injury, 6 of 59 (10%) affected fingers or toes were amputated, compared with 97 of 234 (41%) among those who did not receive t-PA. It was postulated that rapid clearance of the microvasculature improves tissue salvage. The protocol in this study employed a 2- to 4-mg bolus of t-PA after the catheter was secured and total maximum dose of 1 mg/hr run continuously while simultaneous heparin was given at 500 units/hr through the access sheath and continued for 72 to 96 hours. When there was evidence of digital flow by angiography, t-PA was discontinued. The clinicians noted that there was limited benefit for administration of t-PA when treatment was started more than 24 hours after the initial injury. Twomey and associates176 reported another series using 0.15 mg/kg IV t-PA bolus, followed by 0.15 mg/kg/hr infusion over the next 6 hours to a total dose of 100 mg. Heparin was started after completion of the t-PA infusion, and the partial thromboplastin time was adjusted to two times that of normal control. Coumarin was initiated 3 to 5 days after t-PA and continued for 4 weeks in this study, which found decreased amputation rates similar to those in the study by Bruen and colleagues.17 Successful use of the combination of intra-arterial t-PA and vasodilators infused coaxially has recently been described.36 After proper rewarming, the patient undergoes an arteriogram to assess perfusion and document vascular flow cutoff if present. Clinicians describe a response rate of approximately 80% if treatment can be started early.

Current Strategy for Imaging and Thrombolysis in the Acute Phase of Frostbite It is important to realize that the role of thrombolytic therapy in the treatment of frostbite is evolving rapidly. The aim of t-PA treatment is to attempt to clear the microvascular thrombosis. However, there are both risks and benefits to t-PA therapy, and an appropriate balance needs to be struck. The Patient t-PA should be considered for patients with a “significant” deep frostbite injury presenting to an appropriately equipped unit within 24 hours of the injury. A significant frostbite injury will vary from individual to individual, dominant versus nondominant hand, occupation, hands versus feet, and existing comorbidities. The injury will usually extend proximal to the proximal interphalangeal joints. Experienced clinicians familiar with the techniques need to evaluate each injury to determine whether intervention with t-PA is justified. Tissue Plasminogen Activator in the Field If a frostbite patient is being cared for in a remote area, transfer to a facility with t-PA administration and monitoring capabilities should be considered if the injury has occurred recently and the patient will arrive in the specialist unit within the first 24 hours of the injury. Use of t-PA in the field setting is currently not recommended because it may not be possible to detect and treat bleeding complications. The Hospital Unit The hospital unit needs intensive care monitoring capabilities and the hospital should be familiar with intra-arterial angiography and t-PA. A review of absolute and relative contraindications of t-PA should be undertaken. The Massachusetts General Hospital group has proposed a screening and treatment tool for thrombolytic management of frostbite, including a protocol165 (Table 8-5). Choice of Imaging in the Patient Presenting Within 24 Hours of Injury Angiography or 99mTc scanning should be used to evaluate the initial injury and monitor progress after t-PA per local protocol and resources. Angiography is an invasive procedure but allows both diagnostic and therapeutic measures to be carried out, unlike 99mTc scanning, which is only diagnostic. Logical practice TABLE 8-5  A Proposed Screening and Treatment

Tool for the Use of Thrombolysis in Cases of Frostbite

Treatment Screen (Four “Yes” Answers Required to Proceed to Angiography) Are the patient’s gas exchange and hemodynamics stable? Is flow absent after rewarming (no capillary refill or Doppler signals)? Was the cold-exposure time less than 24 hr? Is the warm-ischemia time less than 24 hr? Treatment Protocol Perform angiography with intra-arterial vasodilators If there is still no flow after angiography with vasodilators, infuse tissue plasminogen activator (t-PA) with systemic heparinization, with priority to the hands—other sites receive a systemic dose Repeat angiography every 24 hr Indications for Stopping the Infusion of t-PA When restored flow has been confirmed by angiography or clinical examination If a major bleeding complication occurs After 72 hr of treatment Postlysis Anticoagulation One month of subcutaneous low-molecular-weight heparin at a prophylactic dose From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.

195

CHAPTER 8  Frostbite

BLOOD VISCOSITY

PART 2  COLD AND HEAT

dictates that angiography be used to monitor intra-arterial t-PA and 99mTc scanning used to monitor IV administration of t-PA. There is no evidence to demonstrate superiority of one imaging modality over the other.

A series of case reports suggests significant beneficial effects from HBO.5,44,127,185,187 The role of HBO in frostbite therapy warrants further investigation because it is a relatively safe and inexpensive treatment.188

Choice of Imaging in the Patient Presenting After 24 Hours of Injury In patients with delayed presentation (greater than 24 hours from the time of injury), 99mTc25-27 or MRA8 can be used to predict at an ultraearly stage the likely levels of tissue viability/amputation where t-PA is not being considered.

Epidural Spinal Cord Stimulation An anecdotal case series that described epidural spinal cord stimulation versus conventional treatment reported good therapeutic effects in four young patients with frostbite of the lower limbs. The authors state the mechanism of action is unknown but the treatment is reported to have resulted in rapid recovery, reduced pain, and more peripheral level of amputation.3

Papaverine Papaverine is a powerful topical and intravascular vasodilator that is used clinically as a smooth muscle relaxant in microvascular surgery and has been used to treat cerebral vasospasm.78 The exact mechanism of action remains to be determined, but it appears that inhibition of the enzyme phosphodiesterase, thus causing elevation of intracellular cyclic adenosine monophosphate levels, may be key. This might improve outcomes in early frostbite. When used in conjunction with intra-arterial t-PA in older patients, papaverine appears to cause a less pronounced drop in systemic blood pressure than does intra-arterial nitroglycerin in older adults.35

ADJUNCTIVE TREATMENTS Sympathectomy Cutaneous vessels are controlled by sympathetic adrenergic vasoconstrictor fibers, and vascular smooth muscles have both α- and β-receptors. Because vasodilation of the extremities is passive, maximal reflex vasodilation occurs after sympathectomy. The role of sympathectomy, either surgical (open or minimally invasive) or chemical, has yielded mixed results. Early sympathectomy, performed within the first few hours of injury, increases edema formation and leads to increased tissue destruction. However, if performed 24 to 48 hours after thawing, it is believed to hasten resolution of edema and decrease tissue loss.173 Sympathectomy may have a role in preventing some long-term sequelae of frostbite, such as pain (often caused by vasospasm), paresthesias, and hyperhidrosis.173 In a study of 66 persons with frostbite, 15 patients with acute, bilaterally equal severe injuries were treated with immediate intra-arterial reserpine in one limb and ipsilateral surgical sympathectomy. Efficacy of therapy was assessed by comparison of the sympathectomized limb with the contralateral untreated limb. There was no conservation of tissue, resolution of edema, pain reduction, or improved function in sympathectomized limbs compared with those treated with intra-arterial reserpine. One patient demarcated more rapidly, and one other patient appeared to be protected from recurrent injury. Sympathectomy was not effective therapy for acute frostbite, even when achieved early with intraarterial reserpine. Late protection against subsequent cold injury appears to be the only benefit of surgical sympathectomy for frostbite.14 Because surgical sympathectomy is irreversible, great caution should be exercised when considering its use, particularly with the advent of alternative IV vasodilators. Many would argue there is now no role for its use in the early management of frostbite. Hyperbaric Oxygen Evaluating the effectiveness of use of hyperbaric oxygen (HBO) in the management of frostbite is difficult. Several animal studies have demonstrated it to be of no benefit,125 yet two recent studies in humans have yielded excellent results.41,185 Although the proposed mechanisms of action are multiple, the major changes are postulated to occur in the microcirculation. HBO reportedly increases erythrocyte flexibility and decreases edema formation in postischemic tissues, and it is bacteriostatic. Such actions may counteract the vascular congestion, platelet aggregation, and infiltration of leukocytes seen in the microcirculation of frostbite patients. Finderle and Canker41 report successful HBO treatment of a patient at 2.5 atm for 90 minutes daily for 28 sessions in a multiplace chamber, without significant tissue loss; this treatment started 12 days after injury. HBO may also act as an antioxidant. 196

Surgical Treatment The conventional teaching is that early surgical intervention has no role in the acute care of frostbite. However, early surgical intervention in the form of fasciotomy is required for compartment syndrome in the immediate post-thaw scenario (secondary to a reperfusion injury) or for ischemia from a constricting eschar or subeschar infection.53 Decompressing escharotomy incisions are rarely necessary to increase distal circulation. If such escharotomies are necessary to decompress digits and facilitate joint motion, incisions along the transaxial line have been suggested as being the most appropriate.111 However, many plastic and vascular surgeons would consider using transaxial with axial incisions on the trunk and axial fasciotomy type of incisions in the limbs (Figure 8-23). It is important that incisions avoid injury to the underlying structures. Occasionally, early amputation is indicated if liquefaction, moist gangrene, or overwhelming infection and sepsis develop.1 There is rarely any urgency to intervene, and so amputation should be undertaken by a surgeon with appropriate experience, usually 4 to 8 weeks after the injury. In the vast majority of cases, it is a failure to delay surgery that is the major source of avoidable morbidity. The functional end result of any surgery needs to be considered. Ideally, when major limb loss is foreseen, early involvement of a multidisciplinary rehabilitation team will result in better long-term function.72 A conservative approach was reported as being successful in what must be one of the largest number of cases (847) of frostbite dealt with simultaneously (2-week period) during the IndoPakistan conflict in 1971.6 A combination of LMW dextran, an antiinflammatory agent (oxyphenbutazone), and a vasodilator (isoxsuprine hydrochloride) was used for the third- and fourthdegree injuries, improving limb salvage in comparison with historical controls. Surgical intervention is normally reserved for late treatment of frostbite. This is most often necessary if frostbite is very severe or if treatment has been delayed. Aggressive therapeutic measures can often prevent or reduce progressive injury and

FIGURE 8-23  Axial fasciotomies on the dorsum of the left hand. (Courtesy Christopher H.E. Imray, MD.)

TELEMEDICINE

FIGURE 8-24  Bilateral below-knee amputation for frostbite in a homeless patient. (Courtesy Christopher H.E. Imray, MD.)

gangrene. If gangrene ensues, amputation or debridement with resurfacing may be necessary (Figure 8-24). Surgery should be accomplished only after the area is well demarcated, which generally requires 4 to 8 weeks. Historically, aggressive early debridement and attempted salvage have been thought to jeopardize recovering tissue and add to tissue loss. Gottlieb and associates54 and Greenwald and colleagues58 have taken a much more aggressive approach to coverage of severe frostbite injury. Using 99mTc phosphate bone scans, they identify nonperfused tissue by 10 days after injury and surgically remove necrotic tissue. The remaining nonvascularized and nonviable, yet non-necrotic and noninfected, tissue is salvaged by early coverage with well-vascularized tissue. Theoretically, if nonvascularized tissue has not undergone autolysis and is not infected, it should behave like a composite graft. Preliminary reports are promising, because with better imaging, more accurate prediction of viable tissue is possible. Anecdotal reports suggest that there may be increased risk for infection when complex reconstructions are undertaken at an early stage.70

AMPUTATION Surgery should usually be delayed unless there is evidence of overwhelming sepsis.1 Because there is rarely a rush, a suitably experienced multidisciplinary surgical team familiar with performing a range of amputations should undertake the procedure(s). Careful preoperative planning involving the relevant medical, surgical, physiotherapy, and occupational therapy teams should take place.69,72 The level and type of tissue excised during the amputation will be determined by the specific injury or injuries. Vascular surgeons are usually the most experienced in lower limb minor and major amputations, resulting from their experience with diabetic feet. Plastic or hand surgeons usually have the most upper limb experience; however, these skill bases vary from hospital to hospital.

Recently, increased use of the Internet to access expert advice has been driven by patients and clinicians with more limited experience in treatment of frostbite, permitting a virtual opinion from anywhere in the world.71 The United Kingdom–based service can be accessed via the Diploma in Mountain Medicine or the British Mountaineering Council website: http://www. thebmc.co.uk/Category.aspx?category=19. The service is run by diploma faculty members and being increasingly used by climbers and physicians worldwide, often to obtain a second opinion or to seek specialized advice. It is also possible to follow up patients in a “virtual clinic,” reviewing recent digital images and discussing management options by phone or via e-mail69 (see Figures 8-18 to 8-21). Digital images have been used to assess wound healing in conjunction with HBO therapy.44

Long-Term Sequelae of Frostbite Until 1957, little was recorded about the long-term sequelae of frostbite injuries. Blair and colleagues11 studied 100 veterans of the Korean conflict 4 years after their injuries. In order of decreasing frequency, the victims reported excessive sweating, pain, coldness, numbness, abnormal skin color, and joint stiffness. The investigators noted frequent asymptomatic abnormalities of the nails, including ridges and inward curving of the edges. In general, the degree of long-term disability was related to the severity of the original injury. Symptoms were worse in cold than in warm weather. This is attributed to the fact that vessels do not react as well to stress.163 Previously injured blood vessels do not constrict when exposed to cold as effectively as do normal vessels, and they do not dilate as effectively when vasoconstriction is blocked. Hyperhidrosis is probably both a cause and result of frostbite. Hyperhidrosis suggests the presence of an abnormal sympathetic nervous response induced by cold injury and is abolished by sympathetic denervation. Sensitivity to cold and predisposition to recurrent cold injury should suggest hyperhidrosis. Blanching and pain on subsequent cold exposure may be a nuisance or may be dramatic enough to suggest a diagnosis of Raynaud’s phenomenon (see Figure 8-12). Almost without exception, after sympathetic interruption, a painful, shiny, cyanotic, and sweaty limb becomes warm, dry, and useful.161,162 Schoning160 examined the changes in the sweat glands of Hanford miniature swine after experimental frostbite injury to determine the etiology of hyperhidrosis. She noted that severe sweat gland changes were of two types: degeneration with necrosis and squamous metaplasia. Clearly, if hypohidrosis was a sequel to frostbite injury, morphologically normal and active sweat glands would be an expected 197

CHAPTER 8  Frostbite

Following amputation, primary skin cover is usually preferred. The temptation to preserve bone length by accepting closure by secondary intention or skin grafting needs to be balanced against the problems associated with a dysfunctional neuropathic weight-bearing stump. Split grafts grafted directly onto bone tend to ulcerate as a result of shear forces on insensate grafted skin as soon as the patient mobilizes and becomes weight bearing, and a delayed revision then becomes necessary. Inappropriate attempts at preserving long bone length also restricts use of modern “intelligent” prosthetic limbs; preoperative consultation with the rehabilitation/prosthetic team is strongly advised. The patellar tendon–bearing orthosis technique was originally designed to support body weight for treatment of the below-knee segment that is structurally inadequate or causes severe pain.154,174 The technique allows unloading of the leg at the below-knee level while retaining full knee movement. It is beneficial in treatment of plantar neuropathic ulcers of the feet, allowing the patient to mobilize while minimizing further damage from vertical and horizontal shear forces. Using this approach, with early bedside interventions as part of an integrated approach (including aggressive vascular/endovascular surgery), the major lower limb amputation rate and length of stay have both been significantly reduced.79

PART 2  COLD AND HEAT

finding. One can conclude that hyperhidrosis lacks histologic documentation. A beneficial effect of open cervicothoracic sympathectomy for postfrostbite sequelae in 48 patients has been described.80 The minimally invasive endoscopic transthoracic sympathectomy approach reduces surgical trauma, allows more rapid recovery (Figure 8-25), and may have a limited role in late persisting palmar hyperhidrosis. Iontophoresis may be of benefit in plantar hyperhidrosis. The late abnormalities of change in skin color, including depigmentation of dark skin and an appearance resembling erythrocyanosis in light skin, are most likely the result of ischemia.11 Similarly, the nail abnormality is comparable with that seen with ischemia. Usually, neither of these sequelae requires treatment. Late symptoms of joint stiffness and pain on motion are relatively common and are undoubtedly related to the underlying scars and mechanical problems occasioned by the variety of amputations. “Punched-out” defects in subchondral bone of involved limbs have been noted. These localized areas of bone resorption generally appear within 5 to 10 months after injury and may heal spontaneously. Vascular occlusion is the probable cause of these lesions. Such bone involvement in close proximity to joint surfaces may help to explain joint symptoms. The effects of frostbite on premature closure of epiphyses in the growing hand have recently been reemphasized.191 Extent of premature closure has been correlated with severity of frostbite and noted in partial-thickness injuries. In the digits, premature closure is more frequent from a distal to proximal direction (distal interphalangeal greater than proximal interphalangeal greater than metacarpophalangeal). The thumb has been less often involved. In only 2% of cases does partial epiphyseal closure cause angular deformity. Cold-induced neuropathy may play an important role in the long-term sequelae of cold sensitivity after local cold injury. An alteration in somatosensory function was found that was more pronounced in lower limb injuries.4 Changes in nerve conduction

velocity measurements may provide objective findings in coldinjured patients and in those with few or no conspicuous clinical signs. Tissue that has recovered from frostbite is more susceptible to further injury. This needs to be recognized when advising individuals about a return to environments where they may be at risk. Preventive measures remain the mainstay of primary and secondary treatment.69 Malignant transformation of old frostbite scars is a rare but well-recognized condition with reports dating back to 1930.175 They are sometimes described as Marjolin’s ulcer,180 but more usually as squamous carcinomas.39 One of the largest series of patients found that the tumors tended to be low grade and unlikely to metastasize; the physicians advocated surgical excision.153

Prediction of Individuals at Risk Recent experimental techniques have been studied to predict which individuals are susceptible to frostbite injury. Predicting those at risk would be helpful to assess risk for people planning to work or travel to high altitude or into extreme cold and may be particularly valuable to military recruiting and planning. It would also be particularly helpful when trying to advise those who have sustained a previous cold injury. RIF finger skin temperature response, determined in a simple laboratory test, may be related to the risk for cold injuries during operations in the field.29 The reproducibility of the time course of CIVD suggests this methodology may be of value for further studies examining the mechanism of the response.126 Kamikomaki77 proposed that a case of frostbite in a climber with ACE DD allele was caused by genetic propensity for vasoconstriction. Perhaps we will see the evolution of testing for genetic predisposition to frostbite as a screening tool in the future. Thermography is an easy, noninvasive method for monitoring thermal changes after experimental frostbite, but its clinical value is as yet unresolved.37,75,158 Laser Doppler techniques have been used to assess efficacy of HBO treatment of frostbite. The number of visible nutritive capillaries in frostbitten areas was shown to increase.41

Prevention

A

In 1950, Herzog67 and Lachenal made a successful lightweight bid without oxygen for the summit of Annapurna, the first 8000-m (26,247-foot) peak to be climbed. Herzog lost his gloves near the summit, and the summit team spent a night out in a crevasse. Both climbers suffered severe frostbite to their hands and feet. In a heroic retreat, Dr. Jacques Oudot first gave intra-arterial vasodilators and then performed field amputations without anesthetic. Eleven of the 210 deaths on Mt Everest between 1921 and 2006 were attributable to hypothermia,42 and a significant proportion of climbers attempting to climb to extreme altitude develop frostbite,47 suggesting that climbing above 8000 m (26,247 feet) carries significant risk for permanent cold injury (see Figure 8-7, online).

STRATEGY TO PREVENT FROSTBITE

B FIGURE 8-25  A, One of the two 3-mm thoracoscopic port insertions into the axilla for a right endoscopic transthoracic sympathectomy (ETS) performed under general anesthesia; B, view of right sympathetic chain during ETS. (Courtesy Christopher H.E. Imray, MD.)

198

Prevention of frostbite is the key to safe and successful travel and work in cold environments. General prevention strategies are summarized in Box 8-3. Sound preparticipation education, selection of proper clothing, optimal nutrition, and hydration are all keys to a good outcome. Washburn’s recommendations,189 originally published in 1962, remain as relevant as ever: • Dress to maintain general body warmth. In cold, windy weather, the face, head, and neck must be protected, because enormous amounts of body heat can be lost through these parts. • Eat plenty of appetizing food to produce maximal output of body heat. Diet in cold weather at low altitude should tend toward fats, with carbohydrates intermediate and proteins least important. As altitude increases above 3048 m (10,000 feet), carbohydrates become most important and proteins remain least. • Do not climb under extreme weather conditions, particularly at high altitudes on exposed terrain, or get too early

Good experience is the base of core survival skills • Wear protective clothing—layers, loose, heat insulating • Avoid constriction of body parts with clothing • Stay dry • Wear wind protection • Hands: • Wear mittens instead of gloves • Use chemical hand warmers • Feet: • Avoid tight-fitting boots • Wear suitably warm boots such as triple-layer extremealtitude boots • Use electric-heated insoles • Ensure adequate nutrition • Maintain hydration • Take aspirin (if not contraindicated) • Use supplemental oxygen at extreme altitude

a start in cold weather. The configuration of a mountain can help the climber find maximal shelter and solar warmth. • Avoid tight, snug-fitting clothing, particularly on the hands and feet. Socks and boots should fit closely, with no points of tightness or pressure. In putting on socks and boots, a person should carefully eliminate all wrinkles in socks. Old matted insoles are to be avoided. • Avoid perspiration under conditions of extreme cold; wear adequately ventilated clothing. If perspiring, remove some clothing or slow down. • Keep the feet and hands dry. Even with vapor-barrier boots, socks must not become too wet. All types of boots must be worn with great care during periods of inactivity, especially after exercise has resulted in damp socks or insoles. Wet socks in any type of boot soften the feet and make the skin more tender, greatly lowering resistance to cold and simultaneously increasing the danger of other foot injuries, such as blistering. Extra socks and insoles should always be carried. Light, smooth, dry, and clean socks should be worn next to the skin, followed by one or two heavier outer pairs. • Wear mittens instead of gloves in extreme cold, although gloves can be worn for short intervals when great manual dexterity is required for specialized work such as photography or surveying. In these situations, a mitten should be worn on one hand and a glove temporarily on the other. If bare-finger dexterity is required, silk or rayon gloves should be worn, or metal parts that must be touched frequently should be covered with adhesive tape. Occasionally, the thumbs should be pulled into the fists and held in the palms of the mittens to regain the warmth of the entire hand. • Be careful while loading cameras, taking pictures, or handling stoves and fuel. The freezing point of gasoline (−57° C [−70.6° F]) and its rapid rate of evaporation make it very dangerous. Metal objects should never be touched with bare hands in extreme cold, or in moderate cold if the hands are moist. • Mitten shells and gloves worn in extreme cold should be made of soft, flexible, dry-tanned deerskin, or moose, elk, or caribou hide. Horsehide is less favorable because it dries stiffly after wetting. Removable mitten inserts or glove linings should be of soft wool. • Mittens should be tied together on a string hung around the neck or tied to the ends of parka sleeves. Oiled or greased leather gloves, boots, or clothing should never be used in cold weather operations. • Keep toenails and fingernails trimmed. • Hands, face, and feet should not be washed too thoroughly or too frequently under rough weather conditions. Tough, weather-beaten face and hands resist frostbite most effectively.

• Wind and high altitude should always be approached with respect. They can produce dramatic results when combined with cold. Exercise should not be too strenuous in extreme cold, particularly at high altitude, where undue exertion results in panting or very deep breathing. Cold inspired air will chill the whole body and under extreme conditions may damage lung tissue and cause internal hemorrhage. • When a person becomes thoroughly chilled, it takes several hours of warmth and rest to return to normal, regardless of superficial feelings of comfort. A person recovering from an emergency cold situation should not venture out into extreme cold too soon. • Avoid tobacco or alcohol at high altitudes and under conditions of frostbite danger. • A person who is frostbitten or otherwise injured in the field must remain calm. Panic or fear results in perspiration, which evaporates and causes further chilling. • Tetanus immunity should be current.

CHEMICAL OR OTHER WARMERS The well-equipped sojourner at extreme altitude or in cold environs should have a wide selection of gloves and mittens, including spares (Figure 8-26, online). In addition to protective clothing and insulation, external heat sources are advisable. A recent paper by Sands and co-workers157 assessed the efficacy of commercially available disposable chemical hand and foot warmers. They found that there were variations between the devices, but a strong relationship between the mass of the devices and the duration of their heat production. Although concern has been expressed as to whether the chemical hand warmers (Figure 8-27, online) function at the low levels of oxygen found at extreme altitude, anecdotally they function well.70 Electric foot warmers are probably more useful in extreme cold and high altitude (Figure 8-28) than are chemical foot warmers, where removing boots to insert warmers may be not only impractical, but unwise. New lithium batteries opened for summit day are probably superior to rechargeable units. Chemical warmers also occupy a significant volume, resulting in pressure points that can either overheat and burn or lead to blistering.70

Potential Future Developments PREVENTIVE STRATEGIES Over the past decade, there has been substantial improvement in available equipment; in part this is caused by increased numbers of climbers attempting 8000-m (26,247-foot) peaks. Consequently there is considerable financial incentive for developing state-of-the-art equipment. Current 8000-m boots are rated down to −50° to −60°C (−58° to −76° F) (see Figure 8-28). As new technologies, such as “intelligent fabrics” or temperatureresponsive fibers, are developed, numerous outdoor applications are likely to occur. Newer insulating materials have already given rise to significantly better boots, gloves, and mittens (see Figures 8-26 to 8-28). Climbing equipment has also improved. For example, newer step-in crampons greatly reduce the time involved in fitting the crampons and the likelihood of having to adjust them while climbing, both of which substantially reduce the risk for cold exposure.

Possible Future Treatments TRANSCATHETER ARTERIAL THROMBOLYSIS A recent case report study describes successful use of a combination of endoluminal approaches in a patient with frostbite affecting both hands. Upper extremity and hand angiography performed within 16 hours of the frostbite injury demonstrated thrombotic occlusive disease and vasospasm. Bilateral brachial artery catheters were placed and a papaverine infusion initiated, followed by intra-arterial t-PA thrombolysis.155 In a second case report, a 16-year-old boy was treated for hypothermia and concomitant 199

CHAPTER 8  Frostbite

BOX 8-3  Strategies for Prevention of Frostbite

PART 2  COLD AND HEAT

A

B

FIGURE 8-28  Triple-layer, 8000-m mountaineering boots (A) rated to −55° C (−67° F) and electric boot warmers (B) used on a frostbite-free summit day on Mt Everest. (Courtesy Christopher H.E. Imray, MD.)

frostbite of the right foot and both hands.165 The patient was rewarmed and then treated with selective angiography and an intra-arterial vasodilator (nitroglycerin), followed by intra-arterial t-PA thrombolysis, which resulted in salvage of the limbs, but loss of the right great toe (Figures 8-29 to 8-32). “A Proposed Screening and Treatment Tool for the Use of Thrombolysis in Cases of Frostbite” was included in the case report (see Table 8-5).

TIMING OF INTRA-ARTERIAL THROMBOLYSIS FOR FROSTBITE Current opinion suggests that t-PA for acute frostbite may be beneficial if it can be started within 24 hours of the initial injury. However, there is considerable evidence from both the treatment of acute coronary syndrome21 and treatment of acute stroke82 that there is a variable window of opportunity for successful t-PA treatment. The timing of intervention for frostbite is yet to be

determined, but longer delays are likely to be associated with poor outcomes36 and are more likely to require secondary interventions such as fasciotomies for reperfusion injuries, or subsequent amputations.70

ULTRASOUND-ACCELERATED THROMBOLYSIS In vitro work has shown ultrasound accelerates transport of recombinant t-PA into clots.46 Ultrasound is believed to reversibly loosen fibrin strands and reduce their diameter, exposing more individual strands, increasing thrombus permeability, and exposing more plasminogen receptor sites for binding.15 More rapid and complete thrombolysis has been reported with the use of this technique than with standard catheter-directed thrombolysis. A study has suggested percutaneous ultrasound-accelerated thrombolysis is more effective at clearing clots than is catheterdirected thrombolysis in patients with acute massive pulmonary embolism.97

A A

B

B FIGURE 8-29  Early appearance of hands. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)

200

FIGURE 8-30  Initial angiographic images of the hands of the patient in Figure 8-29. After the infusion of vasodilators, diagnostic angiographic images of the hands show relatively preserved perfusion of the thumbs and ring fingers, but abrupt termination of the proper digital arteries of each of the remaining fingers at the midphalangeal level. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)

A FIGURE 8-32  Appearance of right hand of the patient in Figures 8-29 to 8-31 at approximately 30 days. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)

VACUUM-ASSISTED CLOSURE THERAPY

B FIGURE 8-31  Repeat images of the hands of the patient in Figures 8-29 and 8-30 after 24 hours of intra-arterial catheter-directed thrombolytic therapy with tissue plasminogen activator show markedly improved perfusion at all levels. (From Sheridan RL, Goldstein MA, Stoddard FJ, et al: Case 41-2009: A 16-year-old boy with hypothermia and frostbite, N Engl J Med 361:2654, 2009.)

ANTIPLATELET AGENTS There have been significant advances in the understanding, management, and outcomes of patients with acute coronary syndrome via introduction of IV antiplatelet agents, such as glycoprotein IIb/IIIa inhibitors. Inhibiting platelet aggregation is a vital link in optimizing outcome.141 In a pilot study, outcomes in unstable symptomatic carotid patients appeared to be improved using a glycoprotein IIb/IIIa inhibitor.182 There is likely to be a role in frostbite treatment for use of combination oral (aspirin and clopidogrel) and/or IV antiplatelet agents to improve vessel patency after t-PA clearance of thrombus.

TUMOR NECROSIS FACTOR-α There is evidence for the role of tumor necrosis factor-α–induced reactive oxygen species in endothelial dysfunction during reperfusion injury.49 Investigation into the effects of inhibition of phosphodiesterase type 4 and tumor necrosis factor-α on local and remote injuries following ischemia and reperfusion injury has suggested it may be possible to modify the processes.170 This particular approach might offer improved outcome in early frostbite.

Vacuum-assisted closure therapy has been shown to be beneficial in accelerating wound healing in partial diabetic foot amputations.2 This therapy can be used in community and specialty hospitals, and in many tertiary care hospitals it is being administered through specialist tissue viability nurses. There has been a recent anecdotal report of a good outcome with frostbite.139

FROSTBITE THROMBOLYSIS REGISTRY AND THE INTERNET One of the persisting characteristics of frostbite research is the lack of good evidence to support newer treatments. An international frostbite thrombolysis registry would allow pooling of data, accelerating the learning process.

Conclusion Although still potentially a disastrous injury associated with a high morbidity rate, frostbite can now be treated more effectively to ensure tissue loss is minimized and functional outcome maximized. With adequate preventative measures, the risk for frostbite injury can be reduced. Research progress is likely to be slow because injuries tend to be variable and unpredictable and presentation is often significantly delayed, making subjects difficult to standardize for comparison in treatment groups. A good animal model for basic research is lacking, and apart from the military, there is little likelihood of achieving significant funding for research programs.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 9 



Polar Medicine BETTY CARLISLE, LESLEY J. OGDEN, IAN DAVIS, AND KENNETH V. ISERSON

Like much of wilderness medicine, polar medicine’s identity derives to a large extent from its setting. Polar, however, can be defined in several different ways. Geographically, the Arctic and Antarctic circles, at latitudes 66 degrees, 33 minutes north and south, delimit areas in which the sun does not rise or set on at least 1 day of the year. A more functional definition is the 10°

isotherm, which joins those areas in which the average temperature in the warmest month of the year is 10° C (50° F); this correlates roughly with the tree line. For medical purposes, the definition of polar is more complex. Although climate and geography are clearly important, the salient features of polar medicine are logistic and experiential. Unlike

For online-only figures, please go to www.expertconsult.com

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high-altitude medicine or hyperbaric medicine, for example, polar medicine is not unified by an underlying pathophysiology. High-altitude medicine is a medical field because of the environment’s effect on the human organism, but polar medicine is largely medical practice within this setting. Medical practice in isolated settings is paradigmatic of wilderness medicine: the patient population is essentially, if not literally, a small demographic island. A provisional definition of polar medicine, then, could be “the practice of medicine in isolated settings within an extreme cold environment.” It is the cold, remoteness, hostility, and unforgiving nature of the environment in which humans struggle to survive, let alone work, that make medicine in polar areas, and in particular Antarctica, so challenging.66

The Distinction Between Arctic and Antarctic Medicine Although the polar regions share the predominant attributes of cold, dark, isolation, and severe weather, they display many important contrasts. The Arctic has been described as a frozen sea nearly surrounded by land, whereas Antarctica is a land and ice mass circumscribed by ocean. The moderating effect of the North Polar waters compared with the elevation (2835 m [9301 feet]) of the South Polar plateau accounts for the roughly 40° C (72° F) differences in wintertime low temperatures. On a plot of temperature versus humidity, the polar plateau is more similar to Mars than to the rest of the earth. The flora and fauna are unique to each area. The Arctic has an abundance of land- and sea-based animals as well as migratory birds and plant life. On the other hand, the Antarctic has no permanent land-based animals, although there are migratory birds, as well as a rich marine life and limited plant life. The differences in population patterns mark an important north–south disjunction in polar studies in general and in polar medicine in particular. The northern polar or frigid areas above 66° latitude comprise a frozen sea that is surrounded by eight countries, each with its unique set of populations and medical care services. The countries of the Arctic are Canada, Finland, Greenland (Denmark), Iceland, Norway, Russia, Sweden, and the United States. Together, they make up approximately 8% of the earth’s surface. Human population is scattered throughout the Arctic, with several relatively large urban areas, but for the most part the Arctic is sparsely populated, totaling less than 1% of the world’s population.124 The overall estimated population of the Arctic as defined by the Antarctic Monitoring and Assessment Programme (AMAP) is approximately 4 million; indigenous peoples make up 10% of that population, and constitute the majority of the total population in Greenland and in sparsely settled areas of northern Alaska and Canada.62,123 Within the Arctic, there are 8 major indigenous peoples and more than 30 minority groups. Some of these peoples have separate governments, languages, and socioeconomic possibilities. There are no indigenous peoples in Antarctica, which is regulated by the Antarctic Treaty, with 12 original and currently a total of 47 signatory countries.4 This complex treaty helps delineate the relationships of the countries that are active in Antarctica and how the continent is to be best preserved and used for peaceful purposes. Seven countries claim territorial rights.4 Of the 79 stations in Antarctica, 39 are operated year-round.22 The total population living in Antarctica, all seasonal, now exceeds 4400 persons in the summer and well over 1100 in the winter.18 In the Arctic, there are two overlapping but distinct spectra of medical problems—those of indigenous Arctic people and those of visitors and immigrants to the polar region. Many of the medical problems among the Inuit, Sami, Chukchi, Nenet, and other northern groups are those of populations making the often Faustian demographic and cultural transition to a Western industrialized society. Thus medical practice among these groups is similar to that among many other displaced indigenous populations. In a sense, the current illnesses and health risks of the indigenous Arctic populations are the results of contamination from distant sources and too much contact with other cultures.14 In contrast, medical problems in Antarctica among the usually 202

young and fit scientific, commercial, tourist, and expedition support personnel are often related to trauma and the environment and thus fall more appropriately under the purview of travel or expedition medicine. Furthermore, tourist cruise ships often bring older adults, whose complex medical problems can create logistic dilemmas. It makes sense to focus not only on the health of elite visitors to these remote areas but also on the health of the local population and the effects caused by visitors.

Importance of Polar Medicine INCREASES IN TOURISM AND EXPEDITIONS The combined geographic polar regions cover about one-sixth of the earth’s surface, and their territory in the imagination has been enlarged by several remarkable expeditions and recent popular magazine articles and books on polar tourism. In the past decade, there has been a veritable explosion of tourist activities in both the Arctic and the Antarctic. Despite or because of the forbidding environment, tourism of various sorts is increasing.77 The Arctic is a trendy destination. An estimated 1.5 million tourists visit the Arctic each year, up from 1 million in the prior decade.122 In 1980, it was estimated that a total of 31,000 paying tourists, adventurers, or guests of national scientific expeditions had ever visited Antarctica, but its increasing lure has led to explosive growth. According to International Association of Antarctica Tour Operators (IAATO) statistics, more than 62,000 tourist, staff, and crew visited Antarctica by air or ship in 2009. Since 1989, tourists have visited approximately 200 sites, including 20 research stations in the Antarctic Peninsula region, the most common site for tourists. About 50 of these sites have received more than 100 visitors in any one season, and about the same number have been visited only once. Most visits are to one of 35 sites. Fewer than 10 sites receive around 10,000 visitors each season. The British Antarctic Survey (BAS) monitors Port Lockroy and maintains an ongoing program on the effects the 10,000 visitors per year have on wildlife and ecology of the area.49 Although the bulk of tourists visit aboard cruise ships, there is an increasing number of overland participants who engage in camping, kayaking, diving, skydiving, mountaineering, Arctic or Antarctic traverses, polar challenges, and adventure tourism.50,77 Concerns about the dramatic increase in tourism and its effect on the ecosystem have led to a movement to limit the total number of tourist visits per year. The World Wildlife Fund and the United Nations have proposed guidelines to developing ecofriendly tourism in the Arctic. The guidelines cover its impact on the environment as well as on local populations. In April 2009 the consultative countries of the Antarctic Treaty endorsed a proposal to limit the size of cruise ships and the number of tourists who can go ashore at any one time and to eventually make it binding to all parties.122 This increasing number of visitors and expeditioners has created interest in polar medicine, in particular as it relates to land-based and extreme expeditions. Wilderness medicine courses specific to polar medicine are now offered. Tourist vessels generally carry a physician and sometimes a nurse. Although facilities vary in level of care, all have preparations for the most frequently encountered medical problems. Most illnesses are upper respiratory infections, gastrointestinal (GI) problems, motion sickness, and mild bruises or strains. As might be expected given the ages of many visitors, an occasional cardiac event or serious fracture occurs. The occasional expeditioner who needs rescue or assistance from a scientific station uses scarce resources.23,77 One peculiar phenomenon is that when patients and medical/rescue/evacuation resources are from different countries, a complex flurry of high-level diplomatic interchange must often occur before help can be rendered. Perhaps the most notable tourist fatalities were associated with the ill-fated skydiving venture at the South Pole, which resulted in the death of three of the four participants,45 and the Air New Zealand flight that crashed into Mt Erebus with the death of all 257 people aboard.83 Hazards are inherent in any expedition and may well be the attraction for some participants. To be allowed to participate in risky activities, some tourists may fail to declare serious medical

GEOPOLITICAL CONCERNS The interests of governments in polar regions have not lagged behind those of tourists. Political and territorial concerns have been important in both polar regions. With increasing exploration of mineral and oil reserves and fishing potential, migrating humans will continue to bring medical problems with them. Although the Antarctic Treaty of 1959 prohibits territorial or commercial claims, seven nations have made sectoral claims on the continent. Some of these claims overlap and in the future may lead to a less-thanpeaceful resolution. Yet in early 2010, Australia failed to legally pursue Japan for ramming and sinking an antiwhaling boat in Antarctic waters supposedly governed by Australia. The most common reason given was that Australia feared that the International Court of Justice would nullify all territorial claims to and national governance over parts of the continent. Concern about the environmental impact of increasing human activity in polar regions seems to be tempering the pace of development, but as national resources diminish, the Antarctic may come under increasing pressure to open up to extraction, similar to the situation in the Arctic.

INCREASES IN RESEARCH ACTIVITIES Scientific research has been a part of polar exploration throughout this century. There are scientific and medical journals devoted to the polar regions, and thousands of articles are indexed each year in the Antarctic Bibliography (http://www.coldregions.org/ antinfo.htm). The International Journal of Circumpolar Health (http://ijch.fi/Issues.htm) is a richer source for health issues in polar regions. Antarctic research continues to expand. All the continent’s permanent stations are primarily there to support research. The biggest study is the IceCube project at the South Pole station, which uses a series of downward-looking detectors spread over a square kilometer to look for traces of the notoriously elusive neutrinos, invisible particles churned out by nuclear reactions. The detectors seek particles that have already passed through the earth. The South Pole also hosts two large telescopes. Another huge project involving multiple countries is ice core drilling, designed to catalog climate changes of tens of thousands of years. Other scientific endeavors include marine biology and ocean dynamics research; atmospheric and climatologic research, including air cleanliness monitoring and ice sheet movements; medical research (primarily at Japanese and Chinese stations)80; biologic research (ecosystems, penguins, seals, bacteria, lichen); seismic monitoring; aerial and sea floor mapping with unmanned vehicles in the harsh environment; paleontology; meteorite searches; and demonstrations of alternative power in extreme circumstances (e.g., wind generators at New Zealand’s Scott Base). Some observers have discerned a north–south split, perceiving research in Antarctica as having more of a political motivation and that in the Arctic as being more practical. For both scientific and political reasons, an important part of scientific research in polar regions concerns environmental issues. The remoteness of these regions enhances their value as benchmarks for studies of pollution. Indeed, several worrisome facts have been revealed about the contamination of formerly pristine wilderness, such as

widespread radioactive contamination, the prolonged effective half-life of radioactive fallout deposits,115,125 and increased chemical contamination, particularly in animals high on the food chain, with persistent organic compounds, heavy metals, and other contaminants affecting the environment and food supply.68,125 Widening of the ozone hole carries implications of increased ultraviolet (UV) radiation. As occupational and environmental health issues draw more attention, this aspect of polar medicine assumes greater importance.27,28

Brief History of Human Habitation in Polar Regions A perspective on the contrasts between Arctic and Antarctic medicine may be sharpened by a brief summary of human habitation in polar areas. Humans are known to have inhabited Arctic regions for at least 4500 years. Anthropologists have uncovered evidence for several waves of population migration from Siberia through northern Canada to Greenland. Each of these migrations was probably linked to climatic conditions, and each resulted in a distinct set of cultures. The general pattern was of a nomadic life with population densities of approximately one person per 400 km2 (154.4 square miles).52,118 In more recent times, this longestablished and remarkable adaptation to a hostile environment has been disturbed. The pace of cultural change increased dramatically during the second half of the 19th century, when the whaling industry moved into Hudson Bay, leading to sustained contact between Europeans and the Inuit. In the early part of the 20th century, religious missions, trading company posts, government stations, church missions, and eventually medical clinics and schools began to encourage permanent settlements, roughly quadrupling the population density.52 In some areas, such as Eurasia, large industrial and mining cities arose. This change in population distribution has at times led to conflict between indigenous and European cultures, and it has had significant environmental and medical consequences.126 The known history of human exploration of Antarctica, unlike that of the Arctic, is quite recent. Recorded sightings of the continent date only to around 1800, and “winter-over” sojourns did not occur for another century. Waves of settlement can also be observed to have occurred in Antarctica; there was sealing in the early 19th century and whaling in the early 20th, and there has been scientific exploration since the mid-20th century.118 The heroic era of Antarctic exploration occupied the early years of the 20th century, with exploits such as the highly publicized race for the South Pole between Roald Amundsen and Robert Scott in 1911, the extraordinary survival of the crew of the 1914 Endurance expedition, led by Ernest Shackleton,61 and the heroic survival of Douglas Mawson, an Australian geologist who wintered alone after his other expedition members perished.72 Perhaps because of these and other dramatic events, and perhaps because of the absence of an indigenous population and a scarcity of easily exploited resources, human activities in the Antarctic have retained a somewhat more expeditionary flavor than in the Arctic. This has helped shape the contrasts in medical practice between the northern and southern polar regions.

Arctic Medical Problems EFFECTS OF CULTURAL AND DEMOGRAPHIC TRANSITION The Arctic is not a homogeneous region. Although the population is only approximately 4 million, it is very diverse, with few features in common except the latitude of residence and hours of daylight. Medical problems among indigenous populations in the Arctic, approximately 10% of the total population, are characteristic of displaced aboriginal people elsewhere in the world. There is a wide range of interrelated factors, including demographics; the social, economic, and physical environments; personal health practices; and availability of good-quality and culturally appropriate health care services.12,53 Although increased contact with industrialized cultures has brought benefits, it has also brought many problems. Some of the benefits include 203

CHAPTER 9  Polar Medicine

problems that later precipitate emergency medical evacuation. Thus one real concern is increased risk taking and the consequences thereof, or the dilemma between what is reasonable and what is foolhardy. From a medical perspective, making a risk assessment is multifactorial and differs for people, places, and goals. Hazards of an evacuation need to be assessed for both the patient and rescuers. Setting guidelines and anticipating needs in pre-event preparation are the keys to successful evacuation.46 Because of the occasional tourist in need of expeditious medical evacuation, IAATO and other governmental groups have suggested requiring insurance to defray the costs associated with these evacuations. There is also discussion of the ethical versus medicolegal implications of whether to render aid. The overriding issue should be care of the patient. Polar Challenges and expeditions are discussed later (see Medical Aspects of Arctic Racing).

PART 2  COLD AND HEAT

greatly improved life expectancy, largely due to a decrease in morbidity and mortality from infectious diseases and diseases of childhood (prevented by vaccines). Nevertheless, in indigenous Arctic peoples of the United States, Canada, and Greenland, infant mortality is higher and life expectancy is lower when compared with Arctic dwellers in Nordic countries.98 For many years, health care has lagged behind national norms in the Canadian Arctic, with infant mortality 2 to 3.5 times the national average.113 Age-adjusted death rates are also telling, with 8.4 per 1000 Northern Canadian people, compared with 5.8 per 1000 for the Canadian national average; 14.3 per 1000 in Greenland and up to 29.2 per 1000 in parts of Russia. Other striking statistics reveal a suicide rate in Nunavik six times that of the southern provinces of Canada,60,119 and an unintentional accidental death rate three to four times higher than the national average. Tuberculosis has decreased but is still unacceptably prevalent at 47 versus 7.1 per 100,000 persons. Diabetes mellitus has increased to 5% of the population of 30- to 39-year-olds, compared with 1% in the general Canadian population. In a population in which dental caries were previously almost unknown, the need for restorative dental work is up to 60%. Widely prevalent alcoholism and tobacco use greatly contribute to these problems.10,42,113 As the Arctic environment and indigenous Arctic populations make the cultural and demographic transitions to a Western industrialized way of life, the spectrum of medical problems has shifted. Changing social patterns have resulted in disturbing trends: increasing numbers of young adolescent mothers, rising prevalence of gonorrhea and syphilis among Greenlanders, and concerns about other transmissible diseases, such as viral hepatitis and acquired immunodeficiency syndrome (AIDS).76,130 Changes from the traditional diet and lifestyle have led to increased obesity, diabetes, cardiovascular disease, and mental health problems, including depression, binge drinking, alcoholism, and higher suicide rate.12,113,119

ENVIRONMENTAL AND OCCUPATIONAL HEALTH PROBLEMS Transboundary pollutants, primarily from Eurasia and the North American continent, have made deep and lasting changes.10 The Arctic, once viewed as pristine, is now considered a pollutant sink. Even so, promising new data reflect that strict environ­ mental control (e.g., bans/restrictions on uses and emissions of persistent organic pollutants [POPs]) is working.123 The nuclear accident at Chernobyl in April 1986 led to cesium-134 and cesium-137 levels in reindeer meat 50 to 100 times those considered safe, forcing destruction of the Sami reindeer herds. During that same time, lake fishing and berry picking were curtailed because of contamination.37,126 Fortunately, research 20 years since this accident demonstrates thriving flora and fauna even in the most contaminated areas, demonstrating a rebounding environment. Nevertheless, the young people exposed to the nuclear accident have shown an impressive increase in thyroid cancers, and those exposed to the highest doses of radiation show an increase in leukemias, solid cancers, and circulatory system diseases.114 Industrial emissions from neighboring regions, including an estimated 100 million tons of sulfur dioxide, have led to the “Arctic haze” phenomenon, a gradual whitening of the historically deep-blue Arctic sky.37 Environmental impacts have had direct health consequences.10,42 During the last 500 years, industrial pollution has led to a sevenfold increase in lead levels in human tissues in the Arctic.37 Another survey found blood mercury levels above the normative limit in over 10% of Sami reindeer herders in northern Finland. In North Greenland, a study revealed that in 84% of human mothers, blood mercury levels were above the World Health Organization provisional limit.39 Oceans, rivers, and lakes reveal contamination and concentration of heavy metals in fish.126 Further contamination of the food chain with long-lasting POPs, including polychlorinated biphenyls (PCBs) and many organic pesticides, is increasingly identified.28,126 Long-term consequences of environmental pollutants on the health of the Arctic dwellers continue to be studied.27,28 Recent work suggests that the endocrine-disrupting effects of PCBs may have changed the normal ratio of male-to-female births from 1.05 to 1.02 in the past 30 204

years.12 It has been documented that the concentrations of PCBs in breast milk are seven times higher in the Arctic than in Quebec.113 As previously noted, fallout from radioactive testing has caused river pollution, and other environmental degradations have affected the food chain, such that it is estimated that an increase in certain cancers has been noted in both animals and humans.132 Fear of the effect of pollutants has caused many to abandon or significantly limit their consumption of traditional foods (e.g., marine mammals, fish, terrestrial mammals, and birds). Unfortunately, this can have negative nutritional effects, such as obesity, diabetes, and increased cardiovascular disease, and in some instances relative malnutrition.38 Tragically, POPs, even in low concentrations, have been shown to cause increased risk for diabetes, so both consumption of traditional foods and changes in diet to processed foods have contributed to the increased rate of diabetes in these regions.123 In some areas, consumption of traditional marine foods has led to blood levels of mercury exceeding current recommendations. Local health departments have to weigh overall nutritional benefits of traditional land and marine food sources against the potential longterm risks of neuropsychological and other potential health problems, particularly in newborns and infants.68 Fortunately, new trends show human exposure to pollutants in the Arctic is decreasing. For example, the number of Arctic childbearing-age women with excessive levels of PCBs, mercury, and lead is decreasing. This is believed to be due to dietary changes and increased awareness of the problem. However, new research is demonstrating many additional chemicals, some newly developed, that have the potential to collect in the Arctic food chain, so ongoing research, identification of these chemicals, and regulation of them are essential to continue improving the health of indigenous peoples.123 Nontoxicologic factors also make important contributions to Arctic morbidity and mortality. Accidents are more prevalent in the Arctic. In younger (up to age 35) Inuit groups, injuries account for approximately one-third of all deaths.15 It is striking that Alaska’s occupational death rate is three to four times that of the U.S. national average deaths per 100,000 workers, but this is markedly improved from five times the national average in the 1990s.85 With establishment of the Alaska surveillance system in 1991, there has been a 50% reduction in work-related deaths, including a significant reduction in commercial fishing deaths and very sharp decline in helicopter logging–related deaths.21 These data reflect in part the inherently hazardous working conditions and occupations and possible demographic biases of a young population. Other factors, however, may play a role. Because aircraft are a predominant mode of transportation in polar regions, it is not surprising that Alaska accounted for greater than one-third of all air crashes in the United States and 20% of the fatalities from 1990 to 2008.84 Nonscheduled or commuter plane (less than 30 seats) flights, commonly used in isolated areas, pose a risk for fatal crash six times that of scheduled airline flights, a figure not surprising given the often extremely challenging flying conditions (terrain, weather, and isolated landing sites with limited navigational aids and operator error). In recent years, the pilot occupational fatality rate has fallen from 298 to 148 per 100,000 (less than twice the rate for all U.S. pilots), felt to be due largely to increased awareness and proactive intervention in the industry.84 Overall, the mortality rate for Alaska natives is 939 per 100,000 per year as compared with the overall U.S. rate of 698.9 per 100,000 per year.123

PSYCHOSOCIAL HEALTH PROBLEMS With social disruption and increased environmental and occupational health risks, psychological problems in the Arctic have achieved greater visibility in recent years. For a variety of reasons, stress seems to be higher in winter. One survey of over 7000 adults living north of the Arctic Circle found a prevalence of midwinter mental distress of 14% in men and 19% in women.40 Most other studies suggest that this figure may be low. One study among Inuit found that 22%, or one in five, experience depression during the winter months, and 7% appeared to have seasonal affective disorder (SAD).36 Cultural stress, erosion of traditional lifestyles, and substance abuse are all contributory

CURRENT AND FUTURE TRENDS In summary, indigenous populations of the Arctic show lower life expectancy, higher rates of infectious diseases, higher infant mortality, and higher rates of injuries and suicides when compared with norms in their respective countries.123 Fortunately, there are encouraging signs related to Arctic health care. The incidence of low birth weight, 5.5% in the central Canadian Arctic, has decreased, although it is still higher than that among non-Arctic dwellers.12 Tuberculosis, which incapacitated up to 20% of the Canadian Inuit by 1950, has largely been brought under control, although the rate of occurrence is still as much as 10 times the national average.15 Trends in environmental and occupational health problems show increased monitoring, intervention, and improvement. Unfortunately, the age-adjusted incidence of diabetes mellitus is dramatically rising among First Nations populations.25 An important development in recent years has been the institution of trauma registries to track and target significant causes of morbidity and mortality. Recent research emphasizes that injury prevention is not solely a function of safer design of equipment but is a complex interplay of environment, activity, and people, notably including personal risk-taking behavior. If current trends continue toward greater economic independence and education of Arctic peoples, such potentially modifiable adverse health behaviors may recede in importance in coming years.58,59

Antarctic Medical Practice Medical practice, problems, and their study in the Antarctic are somewhat different from those in the Arctic. Extreme isolation makes Antarctic medicine unique. Because of the remoteness, it may not be possible to medically evacuate (medevac) a patient for weeks or even months. It might be easier to medevac from the international space station than from some of the more remote Antarctic stations.35 In general, the population is adult and is physically and mentally healthy, although at least the U.S. Antarctic Program grants health waivers to some individuals with certain chronic diseases so that they can visit or work for a limited time. Winter-over personnel, including those spending a year or more at a time in Antarctica, are required to pass medical screening that varies in intensity with the various national programs. Most stations only house adults. There are two exceptions: Chile and Argentina have families living at their principal bases and have even had children born on them. All stations have some form of medical care, usually a station physician. The more temporary camps have varied medical support, ranging from firstaid wilderness responders to paramedics or midlevel providers with limited medical supplies. In general, the permanent yearround bases have more sophisticated facilities, with radiograph, laboratory, surgical, and dental provisions and a reasonably

well-stocked pharmacy for expected emergencies. There is at least one physician and sometimes nurses and ancillary medical personnel.

MEDICAL STATIONS IN ANTARCTICA Medical facilities in the Antarctic polar regions can be conveniently divided into permanent and expeditionary facilities. As a result of community expectations and long-term commitment to research in Antarctica, a notable shift from an expeditionary to an operational attitude has occurred in many of the Antarctic programs. What type of physician is needed? To paraphrase Grant, the physician cannot be too specialized in approach; broad knowledge and a wide range of practical skills are necessary to provide good Antarctic medical care.35 Specialization in emergency medicine or the equivalent seems to be a suitable choice, especially to deal with emergencies. In nearly all bases, there is no room for the luxury of anesthetists and surgeons, dermatologists, and psychiatrists. These roles reside within the same person. However, modern communication, including video teleconferencing (VTC), help the polar physician be less isolated from advice, counsel, and guidance. For a significant proportion of the Antarctic population, it is still extremely difficult and costly to evacuate patients.35 The following is a description of the personnel and facilities in the U.S. Antarctic Program; other nations maintain similar facilities. McMurdo Station (MCM) has the largest population— around 200 in the winter and 1200 in the summer. Whereas the winter MCM and South Pole populations are isolated, their summer populations constantly have an influx of rotating personnel that bring new diseases. In the summer season, the medical component is staffed with two physicians, a physician’s assistant or nurse practitioner, an Air Force flight surgeon, a dentist, a radiograph technician, a laboratory technician, and a physical therapist. In the winter, the staff is composed of one physician, a physician’s assistant, and a physical therapist. All are cross trained on site. (Other large national stations provide necessary additional training in advance.) In addition, MCM has a full fire department with paramedics who respond to emergencies on station. The South Pole population peaks at 250-plus in summers and reaches a nadir of around 50 in the winter. There is one physician, a physician’s assistant or nurse practitioner, and a volunteer trauma team trained on station. Palmer Station is the smallest, with a population of 45 in the summer and a low of 10 to 20 persons in the winter. There is one physician, and volunteers are trained on site to provide assistance. How well these volunteers can function was demonstrated in 2009 when the station’s physician developed a peritonsillar abscess. She had one of the station emergency medical technicians needle drain and then incise it under topical and local anesthesia. She then used VTC and an intraoral camera to consult with an otolaryngologist based in the United States. She improved within a few days.26 The Australian stations have one physician. Before deployment, there is a 2-week training course for two of the crew in operating-theater nursing skills and for two persons in anesthesia assisting. The predeployment training has proved very valuable, as was clearly demonstrated in the case of a scientist who fell into a crevasse and suffered serious injuries, including internal bleeding, that required on-site surgery (Figure 9-1).102 All permanent U.S. medical facilities have digital radiograph and ultrasound capabilities, laboratory equipment for blood chemistries and cardiac enzymes, and the capability to perform immunologic testing for β-hemolytic Streptococcus, infectious mononucleosis, and influenza A, as well as common resuscitative equipment, including Life Pak 12 and Zoll monitor/defibrillators, portable ventilators, and crash carts similar to those in most emergency departments. The pharmacies are well stocked and cover a broad range of potential medical problems. There is no blood storage, but in the event of significant bleeding, a “walking blood bank” (walkin donor system) is activated. To facilitate this process, all winterover and most summer personnel are blood typed and screened for hepatitis B, C, and human immunodeficiency virus (HIV). After a series of acute cholelithiasis cases, South Pole winter-over personnel are now screened with ultrasound for gallbladder 205

CHAPTER 9  Polar Medicine

factors.12 Studies investigating scientific staff at Arctic research stations are relatively uncommon, but they show patterns of sleep disturbances, depression, and alcohol use reminiscent of those in Antarctic stations. The double apparent risk factors of high latitude and displaced indigenous populations have made alcohol abuse and concomitant violence a serious problem in the Arctic. In Greenland, one in three Inuit dies a violent death, and roughly 25,000 adults consume 28 million cans of beer a year, one of the highest per capita consumptions of alcohol in the world. Prevalence of “binge drinking” among Arctic peoples ranges from 12% to 39%, with male rates being greater than female rates. Fetal alcohol syndrome is 13% higher in Alaska than in the continental United States.12 One study compared alcohol consumption by the Greenland Inuit with nonindigenous local inhabitants and found that alcohol consumption was less among the Inuit. However, other studies found the reverse.60 Accidents are the leading cause of death in the Arctic, and one-third of these are estimated to be alcohol related. In the Canadian Arctic, alcohol consumption is one and a half times the national average, and Inuit and Indians between 15 and 24 years of age have a suicide rate up to 11 times the national average. In some communities, for boys and men ages 15 to 29, suicides are the most common form of injury leading to death.60,82

PART 2  COLD AND HEAT

FIGURE 9-2  Historic midwinter rescue at the South Pole. Twin Otter aircraft flown by pilots from Canadian Kenn Borek Air Service.

FIGURE 9-1  Trauma and rescue teams are frequently composed of volunteers and at least one experienced, trained individual. This rescuer is practicing for possible extrication of a victim from a crevasse. (Courtesy Betty Carlisle.)

disease. The Australian physician undergoes prophylactic appendectomy. Otherwise, the experience has been that early antibiotic therapy can abort an acute appendicitis attack, allowing the appendix to be removed electively at a later time. The South Pole does not have 24-hour satellite coverage, but year-round stations have facilities for telemedicine, including live camera, still photos, fax, and digital radiography for transmission and consultation via satellite and the Internet. VTC, used for many years in Antarctica by multiple programs,35 came of age at the South Pole in 2002 with a midwinter repair of a patellar tendon rupture. The tendon was surgically reattached by the base physician under the direction of consultants at major medical centers via live video and voice connection. Various physicians at Antarctic stations are also able to consult with colleagues via VTC, such as with the South Pole medical staff’s successful management of a severely hypotensive tourist in 2009 with VTC input from MCM clinicians. In addition, telemedicine has been used for diagnosis and consultation in the treatment of a wide variety of ailments, including acute cholecystitis, ophthalmologic lesions, pancreatitis, pericarditis, fracture treatment, psychological consultations, radiologic reports, and many other situations. Telemedicine has improved the quality and availability of sophisticated care in these and other remote, hostile environments. Medevacs are frequently dangerous and costly. Summer is the only season during which some stations can be reached for an evacuation. Winter evacuations are infrequent, very dangerous, and costly. Logistically it may be 2 or more weeks before a rescue can take place, and for some stations it may not even be possible. A historic medical evacuation from the South Pole was undertaken in the winter of 2001 with the first successful landing of a twin Otter aircraft in full darkness at a temperature of −68.9° C (−92° F) (Figure 9-2). This event, while fraught with danger, has opened new possibilities and has been repeated.16,19 To further increase the ability to provide medical assistance, even during the winter months, the U.S. Air Force recently proved their capability of landing C-17 aircraft at MCM using night-vision goggles and made successful air drops of critical equipment at the South Pole. Certainly, though, prevention through careful screening of candidates and increased use of telemedicine as a way to avoid medevacs still remains the ultimate goal. To reduce the number of medical crises and need for urgent medical evacuations, all participants must pass a “physical qualification test.” Medical clearance criteria are used as a screening tool. To establish appropriate guidelines, evidence-based criteria from the medical literature, historical data of the Antarctic 206

Program, and guidelines from other programs, such as the National Aeronautics and Space Administration (NASA), the Peace Corps, and the Navy, that have activities in remote areas were used. What appears to be lacking is screening for body mass index and alcoholism. However, up to 30% of all medical evacuations (both emergent and urgent) have been for trauma— that is, they were not related to the evaluation criteria. Of emergent and urgent evacuations, 10% were for GI and 8% for cardiovascular reasons (Figure 9-3). Considering only truly emergent medical evacuations, 28% were for cardiovascular and 28% were for GI reasons (Table 9-1). Figure 9-4, online is a chart showing the number of medevacs from MCM and the South Pole station.

SOMATIC HEALTH PROBLEMS Many of the primarily somatic health problems in Antarctica have to do with cold, altitude, and trauma and are thoroughly covered in the chapters on those topics. In a midwinter setting where a tossed mug of coffee freezes before the liquid hits the ground, the dangers of frostbite are clear. Anyone gasping for breath after climbing the six flights of stairs with 92 steps from the tunnel to the living area of the South Pole’s elevated station, or who has lost 5 kg (11 lb) in the first 2 weeks merely from resting Pregnancy Ophthalmic 1% 0% Vascular Diabetes 3% Pulmonary 1% 4% Neurological 2% Genitourinary 4% Infections 2% Dental 7% Anxiety/ depression 5%

Injuries 42%

Tissue mass/ tumor 6% Cardiovascular 8%

Gastrointestinal 10%

Altitude related 5%

FIGURE 9-3  Evacuations for medical reasons, with percentages of 5-year totals (1998-2003). (From Mahar H [Safety and Health Officer, OPP/NSF]: Medical clearance criteria: Revalidation study. Personal communication, 2003.)

Reason for Evacuation Injury Tissue mass/tumor Cardiovascular Genitourinary Gastrointestinal Altitude related Pulmonary Vascular TOTALS

1998-1999

1999-2000

2000-2001

2001-2002

2002-2003

5 Year Total

Percent of 5-Year Total

1 — — — 1 — — 1 3

1 1 1 — — — — — 3

— — — 1 — — — — 1

— — 1 — 3 — — — 4

1 — 3 — 1 1 1 — 7

3 1 5 1 5 1 1 1 18

17 6 28 6 28 6 6 6 —

From Mahar H (Safety and Health Officer, OPP/NSF): Medical clearance criteria: Revalidation study. Personal communication, 2003.

tachycardia and tachypnea, can appreciate the physiologic stresses of rapid ascent to an equivalent of 3200 m (10,499 feet). Likewise, the dangers of UV exposure at altitude with an ozone hole and snow surface reflectance of 80% to 90% can become painfully evident to the unwary visitor.20,112 Cold-Related Problems Cold is a dominant factor in polar medicine. It can be a source of humor, such as the infamous “300 Degree Club” at the South Pole. Membership requires sprinting, while somewhat less than completely clothed, from a 93.3° C (200° F) sauna to the Pole outside at an ambient temperature of −73.3° C (−100° F) or lower. Similarly, the quintessential polar first-aid story involves creative solutions to the problem of finding warm fluids,2 but it would be reckless to forget the ever-present danger of such a hostile environment. Windchill commonly drops the effective temperature far below −73° C (−100° F). It has been estimated that under the most severe winter conditions, an inactive person in full polar clothing could undergo a life-threatening drop in core temperature in only 20 minutes. Airplane refueling crews and others working with liquids at polar ambient temperatures are constantly reminded that even a small splash can mean instant frostbite.31 Rescue and treatment are complicated by the additional need for both victim and rescuer to avoid hypothermia and frostbite.52,54 Disorientation and confusion from hypothermia, clumsiness from bulky clothing, and degraded performance characteristics of equipment and intravenous (IV) fluids can complicate otherwise straightforward procedures. A recent case report describes almost immediate freezing of fluid in IV lines and shattering of the plastic IV tubing despite vigorous attempts to warm them.54 Simple devices commonly used in warmer settings, such as air splints and pneumatic antishock garments, would be similarly unusable. In more sophisticated equipment, batteries rapidly fail, unwinterized mechanical moving parts seize up, and metal objects become dangerous sources of frostbite. Clothing, not normally considered a medical topic, assumes special importance in the polar environment (Figure 9-5).73,100 Although the clothing used for many polar research programs in the summer seems adequate, a strong argument can be made for specialized winter gear, possibly adapted from the space program, that would allow relatively delicate manipulation of scientific equipment while offering protection from the cold. In fact, at temperatures below those of most military specifications, material properties of equipment, including plastic electrical insulation, create unexpected hazards, such as splitting of insulation and other plastics, and extreme rigidity of cables and hoses such that they cannot be used. Fortunately, the importance of ergonomic issues in the design of machinery and clothing for polar conditions is receiving increased attention.44,128 There is new research on use of personal heaters, which are particularly effective for extreme cold and for sedentary work in the cold.106 Phase-change material can store latent heat and then release it during periods of low activity.100 These newer materials will allow thinner gloves with high thermal protection to be worn for work in the cold that requires dexterity, and they will be particularly effective for persons whose efforts alternate between heavy work that can produce sweating and light work with associated cooling (Figure 9-6, online). In addition, as phase-change material clothing becomes readily available, clothing will be lighter and less bulky,

particularly advantageous when doing intricate work in the cold as well as alternating active with sedentary work in the cold. Altitude Illnesses Altitude illness can be a major issue at many Antarctic stations, camps, and research locations, including the South Pole, Vostok, and Mt Erebus. A literature-based approach to preventing altitude illness with the least possible adverse outcomes over the season was to administer acetazolamide (Diamox) 250 mg twice per day starting 24 hours before altitude exposure. Participants voluntarily took this medication for an additional 3 days of exposure. If the individual still had symptoms, such as observed periodic breathing or headache, the dose would be increased to 3 times a day. Dexamethasone (Decadron) 4 mg twice a day beginning the day of ascent was used as a alternative for persons who had experienced serious side effects or allergic reactions, who had an allergy to sulfa-containing medications, or who had no notice before having to ascend to high altitude. This was also continued for 3 days at altitude. After 3 days at altitude, the body’s own compensatory mechanisms have had time to adjust to the new environment, and the medication is no longer needed. Because medication use was voluntary, complications seen from not taking it included high-altitude pulmonary edema requiring use of a Gamow bag before urgent evacuation, relative hypoxemia, and decreased work tolerance. Complications from taking acetazolamide included dehydration and electrolyte abnormalities in patients who were already ill or had severe underlying

FIGURE 9-5  Clothing is an important topic in polar medicine. A researcher prepares to leave the station for an extended time at −56.7° C (−70° F). The total weight of his clothes is 11.5 kg (25.4 lb). Notice the multiple layers for each area of the body. (Courtesy Stephen Warren.)

207

CHAPTER 9  Polar Medicine

TABLE 9-1  Emergent Evacuations

PART 2  COLD AND HEAT

diseases.51 Please see Chapter 1 for current recommendations for prophylaxis and treatment of high-altitude related illnesses. Nutritional Studies Nutrition occupies a key niche throughout the history of polar expeditions. Early expeditions in both polar regions provided several examples of nutritional illnesses, including scurvy and possible hypervitaminosis A and lead poisoning. More sophisticated nutritional analyses have been possible during recent expeditions,112,116 and advances continue to be made in development of lightweight but nutritionally dense rations. When participants in endurance events are well trained, it is possible to compete without loss of lean body mass.70 Although many prolonged unsupported expeditions include an element of malnutrition or even starvation, protein synthesis is still active.116,117 During a Canadian-Soviet transpolar ski trek, participants skiing approximately 20 km/day (12.4 miles/day) at a speed of about 3.5 km/hr (2.2 miles/hr) while carrying 37- to 45-kg (81.6to 99.2-lb) packs showed increased strength, decreased body fat, and increased high-density lipoprotein cholesterol. A paradoxical drop in aerobic power was noticed, perhaps because of intensive pretraining and conditioning, as well as increased efficiency of skiing as the trip progressed. More recently in a nonsupported, two-man, 86-day trans-Greenland trip, well-trained and experienced skiers eating an adequate caloric diet had little if any significant impairment. Their average energy intake in rugged terrain was 28 to 34 kJ/day (6688 to 8121 cal/day) and in level terrain 14 to 16 kJ/day (3344 to 3822 cal/day).31 Although applicability of these figures to more sedentary polar sojourners is probably limited, work is being done to alter the diets of more sedentary expeditions to improve the lipid profile of participants.71 Better availability of common foods and fresh fruits and vegetables during the summer, and frozen foods in the winter at the permanent stations allow participants to choose a healthier diet. However, frequent fried and high-fat food intake leads to elevation of lipid profiles and the associated increase in cardiovascular risks. Some studies have demonstrated that it is possible to make simple and acceptable changes in food preparation that have a significant impact on lowering cardiovascular risk factors of winter-over personnel.6,71 An area that has received increased attention involves the possibility that the prolonged low dose of sunlight may have longterm effects on bone metabolism and immune and cardiovascular systems. One study showed a decrease in the 25-hydroxy metabolite of vitamin D (25OHD) as UV radiation ceased. However, the active metabolite 1,25-dihydroxyvitamin D (1,25[OH]2D) did not show such variation.101 A few studies have demonstrated significant decreases in serum vitamin D as measured by 1,25(OH)2D and associated increases in serum osteocalcin during the dark period, possibly indicating bone remodeling.133 Another study in which low doses of vitamin D were given showed increased bone mass in lumbar vertebrae and leg bones, but no bone mass increase in the pelvis or upper extremities. This was felt to be the result of vigorous activity over the winter. The study also showed a decrease in serum calcium and 25OHD levels during the winter.86 A study was undertaken in the 2003-2004 Antarctic summer and followed 53 Australian expeditioners for 2 years. It showed that they became vitamin D deficient after just a few months; after 12 months, this began to result in loss of bone density. Further study is planned to identify the minimal dose of supplementation needed to prevent deficiency and whether these expeditioners have greater risk for developing osteoporosis in later life.55 Because many participants return for successive winters, further studies are needed to delineate possible long-term effects of bone mass after redeployment. Infection and Epidemiology With particular reference to the space station analogy, a number of studies have taken advantage of the physical isolation of Antarctic stations as a natural laboratory for infectious disease epidemiology. Because microorganisms are believed not to survive the extreme cold long enough to be carried in by winds, midwinter respiratory tract infection outbreaks in the absence of outside contacts have suggested that such organisms could persist in clothing or other fomites.97 208

Despite a widely reported leukopenia, decrease in cell-mediated immunity, and decreases in salivary IgA and IgM during the isolation of wintering over, it is not clear whether persons emerging from Antarctic stations are more susceptible to infection,30 or whether the changes in immunity are related to the stress associated with a winter over. Circadian Rhythms, Endocrine Studies, and Sleep Research Pioneering studies of Natani and colleagues79 and Shurley and co-workers on sleep electroencephalograms at the old South Pole station demonstrated clear patterns of sleep disturbances and “free cycling” of the sleep–activity cycle. Some of these findings have been extended in more recent studies. For example, among four subjects at a small winter-over camp, summer sleep cycles synchronized within the group and with clock time. During 126 days of sunless winter, rhythms free cycled in all four people and then resynchronized with reappearance of the sun.57 The degree of synchrony versus free cycling appears to depend on a number of factors, notably zeitgeber strength (an environmental agent or event that provides the cue for setting or resetting a biologic clock—that is, activities, social contacts, and the most important zeitgeber in nature, light).32 Studies in Indian stations also confirm continuing sleep pattern changes.13 A number of studies have examined the effect of prolonged polar residence on diurnal variations in the level of melatonin. Its important role in free radical scavenging and sleep regulation is beginning to be elucidated.56 Melatonin has been studied as a chronobiotic and is used as a supplement to treat circadian rhythm disorders.5,109 Of the various studies using melatonin to treat sleep disorders, including delayed sleep phase and for night-shift workers, most have only small numbers of participants. Although the initial studies are promising, more research needs to be done. It appears that exogenous melatonin can be used effectively for most persons. The short-term side effects (headache, nausea, and drowsiness) are few. There are no longterm studies. Use of blue-enriched white light in the workplace improved alertness, performance, and sleep quality, as well as daily resetting of the melatonin cycle.29,75,109 Other endocrine fluctuations also appear to be correlated with the length of the day.122 Some endocrine studies have examined the effects of prolonged residence in polar regions with a longer than diurnal time constant. Twenty-four-hour urinary excretion of catecholamines increases in the cold, but social stresses appear to overwhelm climatic determinants of catecholamine metabolism, correlating with increases in diastolic blood pressure and pulse during the year.41 A more consistent pattern of elevated thyroid-stimulating hormone (TSH), decreased free thyroid hormones, and increased triiodothyronine (T3) clearance after several months has been demonstrated. It has been suggested that rapid clearance of T3 is caused by the cold. A pattern of increased pituitary release of TSH in response to IV thyrotropin-releasing hormone and increased serum clearance of orally administered T3 has been identified and dubbed the “polar T3 syndrome.”24 The full clinical significance of these findings remains unclear, but it appears that the T3 may well be related to the winter-over syndrome (see later).87,95 Several studies that used thyroxine supplementation noted improvement in midwinter cognitive function, mood, and vigor.102,105,127 Environmental Health Issues Because of Antarctica’s isolation, it seems a particularly disturbing site for litter and pollution. As in the Arctic, events such as the early problems with a nuclear reactor at MCM (since removed) and the 1989 oil spill from the Bahia Paraiso near Palmer Station, and studies by groups such as Greenpeace, have focused attention on environmental health risks in the Antarctic.78,125 Environmental inspections at a broad range of Antarctic stations have raised concern about toxic effluents and heavy-metal residues, as well as about radioisotopes used for research. To address these issues, a number of countries have begun to implement more responsible waste-management and water-monitoring policies and are taking corrective actions. Most have active recycling programs in place, and many cleanups are in progress or have been completed. Currently, most stations, including all U.S.

Occupational Health and Injury Prevention Rigorous studies of risk are important for injury prevention. Unfortunately, they are complex and often bedeviled by challenges, including controversial data, multiple variables, and biases. For example, for purposes of occupational epidemiology, it may ultimately prove useful to stratify the Antarctic sojourner population into groups such as sport expeditions, military, commercial, and scientific, but the health behaviors of these groups overlap, and few studies have gone beyond aggregate descriptive statistics. There is no current system for archiving these data, except by individual programs or organizations; therefore much of the data is not available for review. There were plans to address this issue at the Council of Managers of National Antarctic Programs (COMNAP) at the planning meeting for the International Polar Year of 2007-2008.9 Unfortunately, because of funding issues, this has not been done.33 Even from these broad statistics, some figures emerge that may be useful cognitive anchors. There were 16 fatalities from 1947 to 1999 in the Australian Antarctic Program, but only 1 fatality in the past decade. Among 3500 scientists and support personnel (2000 person-years), there were 4 medical deaths, 2 myocardial infarctions, 1 case of appendicitis, 1 perforated gastric ulcer, and 1 cerebral hemorrhage. The remainder of the events were accidents involving falls, head injuries, hypothermia, drowning, crush injury, and burns.65,67 There have been 60 deaths in the U.S. Antarctic Program since 1946.1,69 These can be ranked by cause: aviation, 61%; vehicles, 11%; ships, 7%; recreational, 7%; station/industrial, 5%; field activities, 5%; and other, 4%.69 Although it is difficult to adhere to standard occupational safety practices when in a remote location, new guidelines and serious efforts in some of the programs have led to improved worker and participant safety. A review of data for the Australian National Antarctic Research Expedition (ANARE) 2002-2003 season listed the following reasons for medical consultation: medical (e.g., upper respiratory, GI), 39%; injuries (sprains, strains, dermatologic, lacerations, fractures), 27%; follow-up visits, 24%; and preventive (immunizations, midyear examinations, wellness programs), 10%.17 For the 2004-2005 season, Antarctica New Zealand (ANZ) reported the following: musculoskeletal, 42%; medical (e.g., upper respiratory infections, GI), 22%; other injuries, 20%; dermatologic, 15%; and preventive, dental, and other, 8%.99 Usually, most visits are related to injuries, and the next most frequent medical clinic visits are attributable to upper respiratory infections. Environmental problems include dry skin and fissures, particularly on fingertips as a result of cold and very dry conditions. Cyanoacrylate glue hastens healing of disabling fingertip and heel fissures.7 Coldinduced urticaria, frostnip, and frostbite are frequently underreported, except for moderate to severe cases. Small nasal bleeds occur frequently, but they rarely require treatment beyond instruction to use petrolatum or antibiotic/antiseptic ointment once or twice a day to protect the delicate nasal epithelium, which easily becomes dehydrated or can suffer frostnip. Although the bulk of care is limited to routine visits, the pathologic conditions encountered even among this carefully screened population have included myocardial infarctions, massive GI bleeds, unreported Crohn’s disease, bowel obstructions, acute cholelithiasis with pancreatitis, pulmonary emboli, massive head injuries, fractures, crush injuries, newly diagnosed schizophrenia, and cancer. Fire Safety In light of the extreme cold, it is somewhat counterintuitive that fire is a major concern and significant danger at all Antarctic stations. This surprising assessment rests on a number of factors. Cold temperatures severely limit the utility of water for fire suppression. Firefighting equipment may become inoperative in extreme cold, and frequent high winds can fan fires. The extremely low absolute humidity in many polar regions results in an even lower relative

humidity when outside air is warmed in station dwellings. This in turn leads to increased static electricity and dryness of combustibles, already at risk from frequent use of space heaters. Finally, alternative food, shelter, and fuel are limited. Elaborate predeployment training, frequent on-site drills, and keen awareness of potential fire hazards have correlated with a satisfactory fire safety record to date, but this good fortune cannot be taken for granted. One of the most life-threatening events was the explosion and fire at Vostok in 1982, leaving the station basically without power or adequate heat. Only one person died, however there were several injuries, and the winter crew had to endure 8 months without a power plant to supply heat.103 In 2001, the BAS Rothera Station lost its new Bonner Lab building when an electrical short started a fire. No one was injured, but with 50- to 70-knot winds, little could be done to save the station.11 Although fire-suppression systems are built into the newer buildings, a historic A-frame building at New Zealand’s Scott Base burned down in May 2009 and, much more seriously, a two-story building at Russia’s Progress Station burned down in October 2008, killing one person and seriously injuring two others. Because the building contained their radio equipment, they could not contact the outside world for 4 days after the event. In Antarctica, fire is an ever-present threat. Tourist Safety Polar regions are imbued with a sense of the exotic, conjuring up “images of hardship, personal valor, danger, adventure, and of course, the hero.”111 As transportation increasingly opens up previously inaccessible areas, this image attracts growing tourist traffic and, with it, hot debate from both legal and environmental viewpoints. The essential medicolegal issue is the extent of governmental organizations’ responsibility for medical care of participants in nongovernmental activities, whether scientific, political, or commercial. Although this discussion started much earlier, it is still ongoing.77 When a tourist group requires aid beyond its own capabilities, whose responsibility is it? To what extent should a research station with limited medical supplies be required to divert some of those supplies to an individual who presumably bears responsibility for planning his or her own medical coverage? By default, stations provide what assistance they can, although they often try to bill tourist companies and their insurance agencies for costs involved in patient treatment or transport. The Antarctic Treaty Consultative Meeting XXXI provided attendees with a list of guidelines recommended before trips to Antarctica, including travel insurance, contingency plans and other necessary equipment.3 Air Safety As in the Arctic, reliance on aircraft for transportation has highlighted the critical importance of air safety. The worst Antarctic air accident was the crash of an Air New Zealand tourist “flightseeing” DC-10 on Mt Erebus in November 1979.83 This accident killed all 257 people aboard and temporarily ended such flights, although IAATO records indicate that overflights are now happening with new guidelines in place. There have been 35 airrelated fatalities in the U.S. Antarctic Program since 1946 from crashes related to either fixed-wing or rotor aircraft.69,111 A skiequipped LC-130 Hercules crashed at the remote D-59 camp in 1971 (Figure 9-7). Fortunately, none of the 10 crew members aboard was injured, but during a salvage operation in 1987, another LC-130 bringing supplies to D-59 crashed nearby, killing two and injuring nine. More recently, a helicopter crash occurred in the dry valleys; both the pilot and passenger were seriously injured. After a weather delay, they were extricated and evacuated to New Zealand for definitive care.17,81 The review of literature for air crashes in Antarctica is exhaustive. With better weather prediction and increased safety standards, the accident profile is improving.

PSYCHOSOCIAL HEALTH PROBLEMS As the U.S. Polar Manual explained in 1965, “No psychiatric case ever got better in the cold.”43 For many, polar living arrangements and psychosocial issues may be more important than the strictly medical or environmental factors. Psychiatric problems are 209

CHAPTER 9  Polar Medicine

stations, discharge raw sewage. Proposals are in place to find a way to ameliorate the contamination from raw sewage that is discharged into the sea, and/or into large bubble holes in the ice for the inland stations. The BAS Rothera Station installed a sewage treatment plant with significant improvement in the nearshore marine environment.47,48,74

PART 2  COLD AND HEAT

Judicious use of monitoring can help identify persons who may need intervention before an accident happens.

FIGURE 9-7  LC-130 Hercules partially stuck in a hidden crevasse, demonstrating the inherent hazards of working in Antarctica. (Courtesy National Science Foundation photo archive.)

mentioned even in reports of early expeditions, and almost any participant in expeditions will recognize Thor Heyerdahl’s observation: “The most insidious danger on any expedition where men have to rub shoulders for weeks is a mental sickness that might be called ‘expedition fever’—a psychological condition that makes even the most peaceful person irritable, angry, furious, absolutely desperate because his perceptive capacity gradually shrinks until he sees only his companions’ faults while their good qualities are no longer recorded by his grey matter.”121 Most psychological problems, primarily sleep disturbances, are minor and temporary. Many disturbances are more related to the social environment than to the physical environment.89,108 Appropriate lighting or changes in photo periodicity (the duration of daylight and darkness in a 24-hour period) help improve mood and sleep.91,129 In addition to appropriate exercise facilities, opportunities for quality mental stimulation and frequent contact with friends and family via the Internet and telephone can help maintain stability. Except for insomnia, which is perhaps endemic, the incidence of psychiatric problems is lower than expected in the overall population. Many nations use formal and informal psychological screening, especially for participants planning to winter over in Antarctica. How well the screens function is debatable. A British study showed that an extensive psychological screening examination weeded out many participants with problems with “defensivehostility” and “emotion-focused coping.” Simple interviews did not identify these problems.34 Alcohol Abuse Adjustment to psychosocial stresses in polar communities depends on a complex array of sociocultural factors. One coping mechanism is alcohol use. As in many isolated communities at high latitudes, alcohol use can disrupt or lubricate social interactions. In the U.S. Antarctic Program, summer support-staff members are not infrequently terminated for alcohol abuse, and both summer and winter-over staff are occasionally prohibited from purchasing alcohol. In some instances, interventions with group support are found to be very effective. At many Antarctic stations, alcohol is easily available and may be subsidized. In some stations, rations can be excessive or nonexistent. Observations are that at least 50% of recreational injuries are alcohol related. Recommendations have called for routine monitoring of alcohol levels of anyone involved in an accident111 or even prohibition of alcohol at Antarctic stations. However, as with prohibition in other countries, this might create more problems than it might solve. 210

Psychoneuroimmunology Psychological stress at research stations may arise from several sources. One is the environment itself; environmental severity has been found to be an independent predictor of hostility and anxiety after wintering over.90 Perhaps more important is the perception of the environment. Newcomers to the South Pole station are usually observed wearing a full 12-kg (26.5-lb) polar outfit at −20° C (−4° F) for several weeks after arrival. By midwinter, the same individuals think little of walking short distances in only workout shorts and a T-shirt at −60° (−76° F). Stress can also result from disjunction between a person’s original motivation for joining the program and the realities of life in the station—that is, the sociocultural environment. This may be the greatest determinant of difficulties.90 Studies suggest that people who go to Antarctic stations to seek thrills or to challenge themselves often have more difficulty sustaining their motivation and performance than those who go to accomplish a scientific mission or even those primarily motivated to earn money. In general, older individuals who are somewhat introverted are able to set work goals and work toward them, and persons who have broadly defined hobby interests seem to cope better with the social isolation and dynamics of wintering over. One study found that members with low social coherence reported significantly more depression, anxiety, and anger than did individuals belonging to expeditions with high social cohesion.88,130 Small-Group Dynamics In addition to external climate and internal motivational factors, stress can arise from interpersonal interactions. Although there are many exceptions, participants in the Antarctic program often speak of a tendency for personnel to form cliques or microcultures. People may cluster according to ordinary personal chemistry, along lines of OAE (Old Antarctic Explorer) versus novice, winter-over versus summer status, or according to scientific, civilian, or military affiliation. With time, such social clusters can be a source of support or of friction. In an attempt to unify the core group, winter-overs participate in a mini–Outward Bound type of group bonding experience before deployment. Social isolation is an important factor in polar communities, although this isolation has been lessened by modern communications and transportation. A number of studies have drawn parallels between group processes in polar stations and those in other isolated and confined environments, such as submarines or in space. As space travel becomes a reality, studies on group selection, leadership style, and interaction between the isolated group and headquarters take on urgency.35,63,93,131 Collaborative efforts are being made between many stations and space agencies, in particular the European Space Agency (ESA) and the NASA program.108 Cross-cultural and cross-gender issues by research groups are currently being studied at the international station, Concordia, particularly as an analog for long-distance space missions. Whereas in some areas cross-gender differences increase difficulties, in others they are beneficial. Further studies on rigorous selection criteria and training before deployment will avoid the problems that have occurred with sexual harassment. It is felt that the positive effect of better communication, less rude behavior, and increased supportive environment outweigh the negative effect. Other stations have already gone through this process.63,108 Winter-Over Syndrome Stressors such as those mentioned previously can result in what has been termed the winter-over syndrome. The historically oftmentioned “Big Eye” or “20-foot stare in a 10-foot room” seems to be less common now, perhaps because the stations are increasingly comfortable and have stimulating environments. But the constellation of depression, hostility, sleep disturbances, and impaired cognition still seems to be both common and underreported.94,95,105 The winter-over syndrome is not a static condition but a time- and individual-dependent process. At the South Pole research station, for example, winter-over staff characteristically

Seasonal Affective Disorder A probable contributor to and confounder of the winter-over syndrome is the apparently fairly consistent exacerbation of stress and depression under conditions of winter or night, leading to seasonal affective disorder (SAD). Subsyndromal SAD (S-SAD) is perhaps a better definition of what is experienced by many who winter over in the dark latitudes.92 Further studies indicate that S-SAD may be part of the T3 syndrome.95 Correlations with melatonin levels have been shown to be associated with the frequent sleep disturbances at higher latitudes, both with advanced or delayed phases, and with increased latency.5,129 In some studies, melatonin’s chronobiotic properties are used to resynchronize the individual’s sleep.5 Other studies have demonstrated the effectiveness of light therapy in helping resynchronize the body.129 SAD may be no more prevalent in Antarctica than at lower latitudes; some of the depressive symptoms may well be the result of social isolation or related to seasonal changes.96 Beneficial Effects of Isolation An interesting point is that isolation may have positive as well as negative effects.96 Isolation is not synonymous with loneliness and depression, as Amundsen reported from his sojourn at Framheim. In fact, a subset of “professional isolates” may actually prefer polar stations to “normal” society.120 In some cases, reentry and adaptation to the rest of the world can take up to 6 months. The positive effect of isolation may be reflected in a study of somatic complaints, published in 1992, that compared Navy volunteers who qualified for winter duty in Antarctica and wintered over, with those who were physically qualified but were assigned elsewhere because of the limited number of winter assignments. Those who spent the winter in Antarctica had fewer illnesses and hospitalizations after the winter-over period. These volunteers were followed an average of 5.4 years after the winter period. It was also noted that the complex psychophysiologic symptoms experienced during the winter-over period were probably adaptive coping mechanisms. Coping led to a process of negotiation leading to compromise, which frequently led to finding new strategies or resources that could be used for subsequent stressful experiences. Newer studies confirm the salutogenic effect of completing a long-term contract in an isolated environment.88,96 Screening and Selection Based on the preceding findings, several attempts have been made to refine the selection and screening processes for successful polar and space sojourners. It is not surprising that previous successful polar experience seems to be among the best predictors of subsequent high performance. Biographic data, peer ratings, psychometric testing, and interviews all seem helpful in selection, although each has weaknesses and inconsistencies. Recent studies have suggested that team climate significantly related to the perception of good leadership.110 More research needs to be done to explore the characteristics and behaviors that constitute effective leadership, in order to guide selection of crew and leader.14,110 Early studies led to the tripartite “ability, stability, compatibility” criteria for successful participation in the Antarctic programs.34 This simple but useful scheme recognizes that technical skill, emotional equilibrium, and interpersonal skills all play important roles in an individual’s performance and internal satisfaction. It would be desirable to improve measurement and predictive usefulness of these factors; such studies remain at the active frontier of Antarctic research.34

Overview and Future Developments A point made early in this chapter was the challenge inherent in meaningfully synthesizing Arctic and Antarctic medicine. Reflection on some of the issues raised previously suggests several common areas of linkage and directions for future work.

ISSUES OF METHODOLOGY AND MEDICAL EPISTEMOLOGY The state of knowledge about the human factors involved in living in the Antarctic is still rudimentary, although renewed interest by NASA and the ESA in Antarctica as a space analog has led to increased research funding and should lead to better information. Studies in polar settings are often handicapped by extremely difficult research conditions and may never achieve the statistical power and validity expected of counterparts in more forgiving climes. Commonly encountered methodologic problems include, most notably, small sample sizes, unknown effect sizes, measurement of proxy variables, and multiple confounders.

FOURTH WORLD MEDICAL DECISION MAKING Polar medical lore is replete with stories like that of the physician of the sixth Soviet Antarctic Expedition at Novolazarevskaya Station, who performed an appendectomy on himself in April 1961 with assistance from the station mechanic.107 Although the basic principles of emergency medicine, epidemiology, occupational health, psychology, and other disciplines still apply in polar settings, the spectrum of health problems and some important aspects of their management are undoubtedly skewed. However, with newer and improved technical communication modalities and transportation, delivery of advanced care in the polar latitudes has improved, and many lessons learned in Antarctica are applicable to space exploration and settlement. Fourth World medicine requires distillation of medical practice into a compact yet comprehensive package that is sufficiently robust to travel well. Novel constraints and the inherently unpredictable nature of a hostile environment further stretch the usual, already-tentative rules and thresholds of medical decision making. Perhaps to a greater extent than in most settings, prevention and preparation are paramount in polar medicine. As might be imagined, cold and its effects on both humans and equipment exacerbate the risks from even minor mishaps, altitude impairs tissue oxygenation and wound healing, and bulky clothing restricts dexterity and vision. Isolation from medical facilities exerts a multiplier effect on these risks. Victim extrication and resuscitation that would be routine in most urban or suburban settings present overwhelming challenges in polar settings.102 With lives at stake, arguments have been made for planning for worst-case scenarios rather than only for likely situations.111 On the other hand, a realistic balance point on the cost-versusutility curve, based on estimated risks, must be set for each situation. Given existing fiscal and logistic constraints, preventive measures should take priority over higher-cost options.8 A recurrent medical issue in polar stations involves contingency planning and the optimal level of inventory. This question applies equally to drugs, equipment, training, and personnel and is faced immediately by any incoming physician. “Just in time” principles of inventory management are not likely to be appropriate.8,111 Combined improvements in communications systems, the Internet, and the powerful tool of telemedicine with its many modalities have transformed what was once an extremely isolated practice of medicine. The advantages of rapid access to organized databases and remote consultations for radiology and other specialties via video are realities. Telemedicine is in place and functioning in many northern Arctic regions. The Australian, British, Italian, and United States Antarctic Programs and many others have been using it successfully for a number of years.35,56,64,104 Physiologic, psychological, and occupational health data can be monitored or retrieved, ultimately linking geography and information flow and allowing nearly real-time consultation and guidance from multiple specialists. These promising tools 211

CHAPTER 9  Polar Medicine

report a recognizable pattern of fluctuating activity and mood. There is often a mixture of relief, pride, and fearful anticipation as the last LC-130 flight departs in mid-February, followed by a period of frenetic activity to beat inventory deadlines, file resupply orders, launch projects, and prepare the station for winter. As work and recreation routines develop, mood generally drops with the setting sun. A rise in mood occurs toward sunrise but is followed with anticipation, increase in anxiety, and stress as the time of the arrival of the first return flight draws near. Studies at the Australian stations of Mawson and Macquarie Island suggest that the influx of new staff at station opening may actually be associated with increased depression.

PART 2  COLD AND HEAT

are real solutions to the problems of isolation faced by earlier physicians.

Medical Aspects of Arctic Racing In the spring of 2003, the first-ever Polar Challenge race, from Resolute Bay in northern Canada to the Magnetic North Pole (1996 position), took place, with Dr. Ian Davis as senior medical officer. The Polar Challenge is run annually as an ultra-extreme endurance race covering 580 km (360 miles) in temperatures down to −48° C (−54.4° F) with windchill −54.4° (−65.9° F). Teams of two or three persons race the distance on foot and skis, pulling pulks, which are small sleds weighing up to 80 kg (176 lb) attached to the skier. Teams pass through two manned checkpoints during the race. The medical needs of the competitors and support staff are unique in such a challenging and harsh environment. Provision of medical care has been perfected and refined over the preceding 7 years.

THE MEDICAL TEAM Before the start of the race, and after consultation with local hospitals, an emergency evacuation plan is written for extrication of racers to the most appropriate trauma/emergency medical facility, depending on the type of injury. At each checkpoint, a physician is available to provide treatment and consultation to the racers. A more experienced polar physician forms part of the mobile medical team (contacted via satellite pager), which also includes a navigator and a local Inuit guide/mechanic. This team is placed strategically on the ice for the duration of the race. It responds to any medical event either by snowmobile or on foot, with full air evacuation support on standby at all times. The race physicians carry an extensive range of equipment and drugs (Box 9-1) designed to handle any eventuality in this environment. This kit is refined annually after each postrace injury debriefing.

PRERACE SELECTION AND TRAINING Competitors for the race range in ability from experienced and very well trained Arctic travelers to complete novices. Ages so far have ranged from 20 to 65 years with a mix of two-thirds men and one-third women, totaling 80 racers in 7 years. All are offered the same training program (Box 9-2). If required, experts are available for extra tutoring specifically tailored to individual needs. When they join the race, competitors are sent a standard medical questionnaire that is used as a tool for excluding

BOX 9-2  Training Program for Polar Challenge

Competitors

In the 6 months before the race, training is carried out in three locations: the United Kingdom (UK), Austria, and northern Canada. UK Training • Fitness training • Navigation • Firearms • Polar bear training • Medical training for cold-weather injury avoidance and treatment Austrian Training • Polar clothing and equipment • Pulk packing (small sleds for gear, attached to skier by a flexible harness) • Arctic food • Stove use • GPS navigation • Medical training for cold-weather injuries • Firearms • Ski technique and tent craft • Cold-water immersion exercise Northern Canada Training • Cold-weather injuries • Communications • Safety • Evacuation • Firearms • Polar bears • Navigation • Mini 3-day expedition (fully guided) to start line of race

medically unsuitable applicants. Conditions such as cardiac disease and insulin-dependent diabetes would prove very difficult to treat in such a remote and hostile environment. The practicalities of racing with such conditions are discussed in detail with applicants, and then a decision is made as to whether they will take part in the event. Through a process of reflective practice, the training program has been refined, with the result that the current program achieved a 98% competitor completion rate.

BOX 9-1  Physician’s Medical Bag Drugs Multiples of the drugs found in the competitors’ medical bags, plus the following physician-use-only drugs: • Ketamine, 100 mg/mL, 10-mL vials • Morphine, 10 mg/mL, 1-mL vials • Midazolam, 5 mg/mL, 2-mL vials • Flumazenil, 0.1 mcg/mL, 5-mL vials • Adrenaline, 1 in 1000 (1 mg/mL), 1-mL vials • Hydrocortisone, 100 mg/mL, 1-mL vials • Prednisolone, 5-mg tablets • Salbutamol, 90 mcg per metered inhalation • Metoclopramide, 10 mg/mL, 1-mL vials • Lidocaine 1%, 10 mg/mL, 10-mL vials • Oxybuprocaine hydrochloride eye drops, 0.4% • Norethisterone, 5-mg tablets • Dexamethasone drops for ears Medical Equipment • Trauma kit, including chest tube • Suture kit • Urinary catheter kit • Airway kit, including bag valve mask

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TEAM MEDICAL TRAINING Each team is required to carry a prepacked medical bag. The bags and their contents are identical for all teams. Constructed of lightweight yet tough material, they have two outer pockets and internal color-coded pouches, whose contents are listed in Box 9-3. Each bag contains a color-coded contents list with instructions for use. This makes giving advice over the sate­ llite telephone much easier, reducing the likelihood of error. Each race physician knows which drugs are in which color-coded pouch and so can instruct racers accordingly. The external pouches contain emergency dressings and wound and blister treatments. Before the race, competitors are given both group and individual instructions on the contents of the medical pack and their use. They receive lectures on cold-weather injuries and how to avoid them, as well as instructions on what to do in a crisis. The medical packs can be individualized if racers have specific medical needs.

ARCTIC RACING INJURIES ENCOUNTERED TO DATE Frostnip in varying degrees has been seen in most competitors during the race, regardless of their previous cold-weather experience. It has affected mainly the extremities, such as the nose,

CHAPTER 9  Polar Medicine

BOX 9-3  Polar Challenge Medical Advice Sheet 2005 Suspected fractures or serious trauma or illness—tent up and call for help Painkillers • Begin with regular simple pain relief. Use acetaminophen (paracetamol), 500 mg, 1 to 2 tablets, maximum of 8/day. • If needed, add acetaminophen with codeine (paracetamol [325 mg] plus codeine [30 mg]), maximum of 4/day. • For increased pain relief, take an antinflammatory (do not take if have stomach ulcers or asthma). Try either (but not together in the same 24 hours) diclofenac (50-mg tablets, 3/day), or piroxicam (20-mg tablets, 1 per day). Take with food. • For headache, try the above. If this does not work, take 2 aspirin (325 mg) plus 1 metoclopramide tablet (10 mg) repeated twice a day. If headache is increasingly severe, contact the physician.

FIGURE 9-8  Frostnip ear. (Courtesy Ian Davis.)

Antibiotics • If worried about infection, call physician, giving the site of the infection and symptoms. We will then advise. • If your communications break down, take Augmentin (500 mg) for any suspected infection. Take 1 tablet, 3/day for 1 week. Do not take Augmentin if allergic to penicillin. If you have an allergy to penicillin, take azithromycin (500 mg, 1 tablet per day for 5 days). Eyes • Any problems with eyes, please try contacting physician first. Otherwise, chloramphenicol eye drops is a good general antibiotic for eyes. If your eyes generally become very sore/red and watery, you may have snowblindness, so call for advice. Gut • Diarrhea—Take Imodium (2 mg, 1 tablet after each explosion!!). • Heartburn—Try Gaviscon. If this doesn’t work, take 1 lansoprazole (Zoton), 30 mg, fast-tab per day. • Constipation—Drink lots of fluids and take senna, 25 mg, 2 tablets at night. • Abdominal pain—Contact physician.

A

Allergy • Piriton (chlorpheniramine maleate 4 mg) 1 tablet 3/day. Nausea and Vomiting • Metoclopramide tablets (10 mg, 1 tablet 3/day). Skin • Any general rashes (groin, etc.)—Apply clobetasone 0.05% cream (Trimovate, green tube) twice a day. • Injuries to finger tips and burns—Use silver sulfadiazine 1.0% (Flamazine) cream twice a day. Cold Sores • Acyclovir 5.0% cream, apply 5 times a day over affected area. Blisters • Try using DuoDerm (hydrocolloid dressing), which can be cut to size. Leave at least a 2-cm margin of the dressing around the blister. Leave on for 3 days before changing it. It is normal while the DuoDerm is on the skin to accumulate a blob of fluid buildup over the affected area. General Wound Care • Lacerations—Depending on size, use either MedLogic skin protectant (similar to Steri-Strips) with glue, or just glue on its own (octyl cyanoacrylate [Dermabond, LiquiBand]). • Larger wounds—Apply direct pressure with a dressing, and call for advice.

ears, and fingertips (Figure 9-8). All cases were treated by rewarming and diligent future protection. The number of frostnip injuries decreased after a team buddy system was instituted, which led to rapid prediction of impending injury and timely avoidance.

B FIGURE 9-10  A, Frostbitten fingers. B, After recovery from frostbite. (Courtesy Ian Davis.)

Frostbite was seen in six competitors, five of whom had finger injuries (Figure 9-9, online). All the fingers made a complete recovery largely as a result of early detection and rapid evacuation of affected competitors from the race to a rewarming and treatment facility. One case of fingertip frostbite was caused by a fuel spill onto the fingertips, which caused rapid freezing and subsequent injury. This competitor was a highly experienced Arctic traveler and was therefore allowed to continue, subsequently making a full recovery during the race (Figure 9-10). The final case of frostbite was more unusual, affecting a competitor’s penis (Figure 9-11). After urinating, he forgot to close the zipper correctly on his wind suit. After walking into a headwind with a windchill factor of −80° C (−112° F) for an hour, he discovered his foreskin to be frozen. Rapid evacuation prevented further damage and, after a circumcision on his return to the United Kingdom, he made a complete recovery both in sensation and function. During the event, this competitor could easily have gone into urinary retention and would have been catheterized accordingly, making it essential to carry such equipment in the physician’s medical kit. Musculoskeletal injuries, most commonly of the lower back, shoulders, knees, and wrists (related to cross-country skiing and pulk pulling), were seen in most of the competitors. They were 213

PART 2  COLD AND HEAT

FIGURE 9-11  Frostbitten foreskin. (Courtesy Ian Davis.)

all treated with appropriate analgesia and advice from both the mobile and static medical teams. This enabled most competitors to finish, with only 5% of the total having to withdraw for this reason. The most serious musculoskeletal injury was a dislocated shoulder, which was relocated by a teammate using a slow Kocher’s method. The race physician talked him through this maneuver over the satellite telephone. This competitor went on to finish the race. Snowblindness was seen in 4% of racers (Figure 9-12, A). Diagnosis in the field was achieved with the aid of fluorescein stain, and the eyes were treated with topical local anesthetics, antibiotics, oral analgesia, rest, and eye patches (Figure 9-12, B). All affected racers went on to complete the race. Dermatologic problems, including sweat rashes, were seen mainly in the groins of male racers. All were treated successfully using appropriate topical creams. All the female racers (and none of the male racers) developed a cold-induced urticarial rash isolated to the anterior surfaces of the thighs (Figure 9-13). This was treated with oral antihistamines

A

FIGURE 9-13  Cold-induced rash. (Courtesy Ian Davis.)

and topical corticosteroids but was difficult to cure, taking days to weeks to resolve in a warmer environment after the race. Steps are being taken to design clothing for female competitors to prevent this from happening in the future. Blisters were seen in 30% of competitors. All were treated effectively using DuoDerm hydrocolloid dressings. This type of dressing is extremely adherent and can be cut to any shape and applied for up to 5 days. Extra adherence at the edges of these dressings on high-friction areas like the heels can be obtained by using zinc oxide tape. Trench foot was reported in two competitors at a late stage in the race (Figure 9-14). Both were treated after completion of the race. Diligent foot care during the race would have helped prevent this injury. Respiratory disease was seen once in a hypothermic competitor who collapsed during a storm with a severe case of asthma. The victim was unable to speak in complete sentences and was so cold that he had stopped shivering. He was rewarmed in a prewarmed tent and treated with inhaled salbutamol and IV corticosteroids, followed by oral corticosteroids and oral antibiotics, with air evacuation as soon as there was a weather window. The competitor made a full recovery. Fatigue and hypothermia affected all racers to varying degrees. Despite consuming 7000 cal and drinking 4 L per day, most competitors are likely to lose 10% of their body weight. Training is given to all the teams on how to treat a teammate with severe fatigue and hypothermia. Only two competitors have withdrawn for such reasons (Figure 9-15, online). GI problems were mainly diarrhea, which was treated with loperamide and adequate hydration. Constipation, anticipated in the medical packs with senna tablets, has not yet been a problem. Psychological problems, such as fear of polar bear attack or of becoming lost or injured, have led to at least one person pulling out of the race. Lacerations and split skin were seen in some competitors; the lacerations were minor. All victims were treated very successfully

B FIGURE 9-12  A, Snowblindness. B, Eye patches. (Courtesy Ian Davis.)

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FIGURE 9-14  Trench foot. (Courtesy Ian Davis.)

using tissue glues (octyl cyanoacrylate tissue adhesive). This proved much more effective than did teaching competitors suturing techniques. Other potential injuries that are anticipated include major trauma from polar bear attack or firearms injury; burns, both minor (from stoves) and major (from tent fires); carbon monoxide poisoning; long-bone fractures; medical emergencies (e.g., anaphylaxis, cardiac problems, infection, and pneumothorax); surgical emergencies (e.g., abdominal sepsis from appendicitis); dental problems; and problems unique to female racers, including vaginal candidiasis, menstrual problems, and urinary tract infections.

THE USE OF FROZEN MEDICATIONS The medical literature is relatively sparse on this topic.31 One of the authors has rewarmed frozen fluorescein stain, oxybuprocaine hydrochloride 0.4%, ophthalmic local anesthetic, corticosteroid creams, antifungal creams, inhaled salbutamol, and IV

hydrocortisone, all of which worked normally after rewarming. All forms of tablet medications warmed from frozen have also been fine after rewarming. A study from the BAS found that most medications remained stable, even after multiple freeze-thaw cycles. The exception was hydrocortisone cream, although the investigator also recommended against subjecting eye medications to temperature extremes. Medical devices, such as IV cannulas, worked normally after rewarming, as did all forms of tape and dressings. Frozen IV fluids expanded when frozen, perforated the bags, and thus leaked when rewarmed. Acknowledgments. Special thanks to Kenneth H Willer, MLS, Manager—Library Services, Samaritan Health Services, Corvallis, Ore, [email protected].

REFERENCES Complete references used in this text are available online at www. expertconsult.com.

CHAPTER 10 

Pathophysiology of Heat-Related Illnesses LISA R. LEON AND ROBERT W. KENEFICK*

Heat illnesses are best viewed as existing along a continuum, transitioning from the mild conditions of heat cramps and heat exhaustion to the life-threatening condition of heatstroke. Environmental heat exposure is one of the most deadly natural hazards in the United States, with approximately 200 heatstroke deaths per year. Although the majority of heatstroke deaths are observed in vulnerable populations during annual heat waves, young fit individuals may also succumb to heatstroke while engaging in strenuous activities such as athletic competitions, military operations, or occupational tasks. Multiorgan system failure is the ultimate cause of heatstroke death, and there is a complex interplay among the physiologic and environmental factors that compromise an individuals’ ability to adequately respond to heat stress. The pathophysiology of heatstroke is thought to be caused by a systemic inflammatory response that occurs in response to endotoxin leakage from the gut, but there remains limited understanding of the mechanisms that mediate morbidity and mortality. This chapter provides an overview of the pathophysiologic responses that are observed in patients and experimental animal models at the time of heatstroke collapse and during long-term recovery. A brief discussion is provided on current clinical heatstroke treatments and promising avenues of research that may aid in the development of more effective interventions and/or treatments to prevent this debilitating illness.

Heat Stress and Thermoregulation FOUR AVENUES OF HEAT EXCHANGE Mammals and other homeotherms are capable of maintaining body temperature within a fairly narrow range (approximately *Approved for public release: Distribution is unlimited. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Army or the Department of Defense. Any citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement of approval of the products or services of these organizations.

35° to 41° C [95° to 105.8° F]) despite large fluctuations in environmental temperature. Environmental variables that have the largest impact on heat exchange are temperature; humidity; radiation from the air, water, or land; and air or water motion.88 To maintain stable body temperature, organisms rely on four avenues of heat exchange: conduction, convection, radiation, and evaporation. Dry heat exchange is achieved by conduction, convection, and radiation. The effectiveness of these mechanisms depends on differences between the skin and environmental temperatures. That is, dry heat loss occurs when skin temperature exceeds that of the environment, and dry heat gain occurs when environmental temperature exceeds that of the body. Conduction occurs when the body surface is in direct contact with a solid object and depends on the thermal conductivity of the object and the amount of surface area in contact with the object. Conduction is typically an ineffective mechanism of heat exchange because of behavioral adjustments that minimize contact with an object. For example, the wearing of shoes is an effective behavioral adjustment that minimizes conduction of heat from a hot surface (e.g., desert sand to the foot). Within the body, conductive heat transfer occurs between tissues that are in direct contact with one another, but is limited by poor conductivity of the tissues. For example, subcutaneous fat has approximately 60% lower conductivity than does the dermis and impedes conductive heat loss.332 Convection is a mechanism of dry heat transfer that occurs as air or water moves over the skin surface. The windchill index is an example of the convective cooling effect of wind velocity. The rate of convective heat transfer depends on the temperature gradient between the body and environment, thermal currents, bodily movements, and areas of the body surface that are exposed to the environment, which can vary dramatically with different clothing ensembles. Within the body, convective heat transfer occurs between blood vessels and tissues and is most efficient at the capillary beds, which are thin-walled and provide a large surface area for heat exchange. Radiative heat transfer is electromagnetic energy that is exchanged between the body and surrounding environmental objects and is independent of air velocity or temperature. It is effective even

For online-only figures, please go to www.expertconsult.com

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PART 2  COLD AND HEAT

when air temperature is below that of the body. All objects within our environment absorb and emit thermal radiation, but clothing can reduce radiant heat that impinges on the skin from various environmental sources. Evaporation represents a major avenue of heat loss when environmental temperatures are equal to or above skin temperature or when body temperature is increased by vigorous physical activity. In humans, evaporative cooling is achieved as sweat is vaporized and removes heat from the skin surface, with approximately 580 kcal of heat lost per each liter of evaporated sweat.94 The most important environmental variables affecting evaporative cooling are ambient humidity and wind velocity. Sweat is converted to water vapor and readily evaporates from the skin in dry air with wind, whereas the conversion of sweat to water vapor is limited in still or moist air. If sweat accumulates and fails to evaporate, sweat secretion is inhibited and the cooling benefit is negated. Small mammals, such as rodents, do not possess sweat glands but achieve evaporative cooling by grooming nonfurred and highly vascularized skin surfaces, such as the ears, paw pads, and tail, with saliva that evaporates in a manner similar to that of sweat in humans.104,294

BODY TEMPERATURE CONTROL Regulation of a relatively constant internal temperature is critical for normal physiologic functioning of tissues and cells because membrane fluidity, electrical conductance, and enzyme functions are most efficient within a narrow temperature range. By convention, thermal physiologists describe body temperature control with a two-compartment model that consists of an internal core (i.e., viscera and brain) and an outer shell (i.e., subcutaneous fat and skin) (Figure 10-1).70 The skin is the final barrier between the body and the environment and functions as a conductive pathway for heat transfer to the environment, while also serving as the primary site to sense changes in environmental temperature. Skin temperature

37° C

36° C

37° C

Core

32° C

Core

Shell 28° C

34° C

31° C

Cold

Warm

FIGURE 10-1  Distribution of temperatures within the human body into core and shell during exposure to cold and warm environments. The temperatures of the surface and thickness of the shell depend on the environmental temperature: the shell is thicker in the cold and thinner in the heat. (From Elizondo RS: Human adaptation to hot environments. In Rhoades RA, Pflanger RG, editors: Human physiology, ed 3, Philadelphia, 1996, Saunders. Reprinted with permission of Brooks/Cole, a division of Thomson Learning. http://www.thomsonrights.com.)

216

may fluctuate because of changes in environmental temperature, relative humidity, wind velocity, and radiation. Heat-transfer mechanisms are evoked in response to changes in body heat storage (S), which depends on metabolic rate, work, and the four avenues of heat exchange, as follows: S = M − (W) − (E) − (C) − (K) − (R) where M is metabolic rate, W is work, and E, C, K, and R are evaporative, convective, conductive, and radiant heat transfer, respectively.132 The impact of the four avenues of heat exchange on total body storage depends on a variety of organismal (e.g., age, gender, adiposity), environmental (e.g., humidity, wind velocity), and occupational (e.g., protective clothing, work intensity) variables. Under conditions in which heat production and/ or heat gain exceeds heat loss, such as during exercise or heat exposure, positive heat storage occurs and body temperature increases. When heat loss exceeds heat production and/or heat gain, such as during prolonged cold exposure, negative heat storage occurs and body temperature decreases.88 Endothermic animals use both autonomic and behavioral thermoeffector mechanisms to regulate body temperature. Autonomic thermoeffector responses are often referred to as “involuntary” and include sweating, vasodilation, vasoconstriction, piloerection (furred mammals), and shivering and nonshivering thermogenesis (brown fat heat production). Behavioral thermoeffector mechanisms are considered “voluntary” and include clothing changes, use of heat or air conditioning systems, huddling or use of blankets, fan cooling, and seeking of shade or shelter. Rather than working independently of one another, autonomic and behavioral thermoeffector mechanisms typically function in concert to maintain temperature control. For example, evaporative cooling in rodents requires autonomic stimulation of salivation and behavioral spreading of saliva onto nonfurred surfaces.104,294 Many large species in the wild use natural water sources to facilitate cooling. Elephants spray water onto their skin surface, and hippopotamuses and other species are often observed near or in watering holes. Water is a more effective medium to facilitate convective heat transfer than air, because of its high heat-transfer coefficient (approximately 25 times greater than air),305 even if the water temperature is tepid. However, voluntary suppression of behavioral mechanisms of cooling in humans can increase the risk for thermal injury. This is illustrated by older adults who refuse to use air conditioning systems or leave their residences during heat waves, or highly motivated athletes and military personnel who voluntarily dehydrate and/ or sustain a high rate of work in hot weather. Regulation of body temperature is best conceptualized as a negative-feedback system consisting of sensors, integrators, and effectors. In vertebrates, neurons in the skin, spinal cord, and abdomen sense thermal stimuli and convert those signals to action potentials that are transmitted by afferent sensory neurons to the preoptic area of the anterior hypothalamus (POAH). The POAH is considered the main central nervous system (CNS) site for thermoregulatory control because it receives and integrates synaptic afferent inputs and evokes corrective autonomic and behavioral thermoeffector responses for body temperature regulation.28 A diagrammatic representation of this negative-feedback loop is shown in Figure 10-2. The concept of a temperature set point was developed as a theoretical framework to examine regulated and unregulated changes in body temperature.19 The temperature set point is analogous to a thermostat that controls a mechanical heating device; under homeostatic conditions, body temperature is approximately equal and oscillates around the temperature set point. Environmental perturbations, such as heat and exercise, cause body temperature to deviate from the set-point temperature as heat gain and/or production exceeds heat loss and the organism becomes hyperthermic (body temperature is greater than the set-point temperature). During prolonged cold exposure, heat loss exceeds heat gain and/or production and the organism becomes hypothermic (body temperature is less than the set-point temperature) (Figure 10-3). Regulated increases and decreases in the temperature set point are referred to as fever and regulated hypothermia (also called anapyrexia), respectively, and are protective immune

Exercise

↑ Temperature Heat gain/production > heat loss ∆S>0 Thermal receptors (skin, spinal cord, abdomen) Sensory afferent signals Preoptic anterior hypothalamus (POAH) Thermoregulatory Integration Center Motor efferent signals Behavioral and autonomic thermoeffectors Heat loss > heat gain/production

thought to protect against injury and inflammation by reducing production of harmful enzymatic end products that compromise tissue function under conditions of low oxygen supply. In bumblebees, infected worker bees spend significantly more time in cooler temperatures outside of the nest than healthy worker bees; this cold-seeking behavior is associated with increased survival from parasitic infection.118,213 Mice inoculated with influenza virus also show cold-seeking behavior and develop regulated hypothermia, which is associated with improved infection outcome.153 Other environmental insults that induce regulated hypothermia in small rodents include hypoglycemia,34,98 hypoxia,194,252 hemorrhage,119 dehydration,129 infection,153,176,264 and heatstroke.173,174 Mechanisms of Heat Dissipation During Thermal Stress Cardiovascular mechanisms have evolved to shunt warm blood from the body core to the skin surface and increase heat loss during thermal stress. Arteriovenous anastomoses (AVAs) are collateral connections between adjacent blood vessels that increase the volume of blood that is delivered to a particular tissue. Mean skin blood flow can vary approximately 10-fold in humans depending on the thermal environment. The hands and feet are concentrated with AVAs that serve as effective areas for dry heat loss. The nonfurred surfaces of small rodents, such as the ears, tail, and paw pads, also have an abundance of AVAs and a large surface area to facilitate convective heat transfer.92,99 During exercise heat

↓ Total body heat storage FIGURE 10-2  Diagrammatic representation of the negative feedback pathway regulating core temperature in homeotherms. Climatic heat stress and exercise (metabolic work) cause heat gain/heat production to exceed heat loss (ΔS > 0) and increase body temperature above baseline. The increase in total body heat storage is sensed by thermal receptors in the skin, spinal cord, and abdomen, which transmit action potentials via sensory afferent nerves to the preoptic area of the anterior hypothalamus (POAH). The POAH receives and integrates synaptic afferent inputs and evokes corrective behavioral (e.g., fanning, removal of clothing) and autonomic (e.g., vasodilation, sweating) thermoeffector responses to decrease total body heat storage and return body temperature to baseline. Solid line indicates stimulatory pathway; dashed line indicates inhibitory pathway.

responses to infection, inflammation, or trauma. Fever is defined as a regulated increase in the temperature set point and is actively established and defended by heat-producing (e.g., shivering and nonshivering thermogenesis) and heat-conserving (e.g., peripheral vasoconstriction, huddling to reduce exposed body surface area) thermoeffectors (see Figure 10-3).132 An individual is considered normothermic once fever is established and body temperature oscillates around the new elevated temperature set point (see Figure 10-3). The highly regulated nature of fever was first suggested by Liebermeister in the 1800s when it was observed that individuals actively reestablished an elevation in body temperature following experimental warming or cooling.180,286 Fever is a protective immune response used by invertebrates, fish, amphibians, reptiles, and mammals to survive infection or injury.* The protective effects of fever are mediated by increased mobility and activity of white blood cells,218,313 increased production of interferon (IFN; antiviral and antibacterial agent) antibodies,64 and reduced plasma iron concentrations, the effects of all of which inhibit the growth of pathogens.89,156 In mammals, inhibition of fever using antipyretic drugs (e.g., aspirin) increases mortality from bacterial and viral infections, which speaks to the importance of fever as an immune response.126,315 Many species also develop regulated hypothermia to survive severe environmental insults. Regulated hypothermia is elicited in response to a decrease in the temperature set point and is actively established and defended by behavioral and autonomic heat-loss mechanisms.132 The Q10 effect states that each 10° C (18° F) change in body temperature is associated with a twofold to threefold change in enzymatic reaction rates. Based on this relationship, a regulated decrease in body temperature is *References 32, 54, 154, 216, 256, 316.

HYPERTHERMIA

HP = HL

HG/HP >HL

HL >HG/HP

HP = H L

Tset Tc

Heat stress, exercise FEVER

HP = HL HC/HP >HL

HP = HL

HL >HC/HP

Tset Tc

Infection, inflammation

FIGURE 10-3  The theoretic concept of core temperature (Tc) changes mediated by a change in the temperature set point (Tset). Hyperthermia represents an increase in Tc in the absence of a change in Tset. In response to climatic heat stress, exercise, or the combination of these factors, heat gain (HG) and/or heat production (HP) exceed heat loss (HL) and Tc rises above Tset as the organism becomes hyperthermic. In response to removal from the heat, cooling, or cessation of exercise, HL exceeds HG/HP and Tc returns to baseline. Fever is defined as a regulated increase in body temperature that is actively established and defended by behavioral and autonomic thermoeffector responses that increase heat conservation (HC) and/or HG and decrease HL to increase Tc to a new elevated level. The rising phase of fever is associated with shivering (increases HP) and the donning of blankets (increases HC). The individual feels “cold” until a new elevated level of Tc is attained. Note that while fever is maintained, Tc oscillates around Tset and the individual is considered normothermic with HP = HL. Once fever breaks, HL exceeds HC/HP as the individual sweats, removes clothing, and so forth, to return Tc to the baseline level.

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CHAPTER 10  Pathophysiology of Heat-Related Illnesses

Heat stress

PART 2  COLD AND HEAT

stress, increased blood flow to the skin surface is accompanied by sweat secretion. The density, secretion rate, and activation threshold of regional sweat glands determine the volume of sweat loss at a body site. In humans, the back and chest have the highest sweat rates for a given body temperature change, whereas only approximately 25% of total sweat is produced by the lower limbs.217 Additional factors affecting sweat rate include clothing characteristics, environmental conditions, and rate of metabolic heat production. Panting is an effective method of evaporative heat dissipation in large animals, such as birds, dogs, sheep, and rabbits, and occurs at a resonant ventilation frequency that requires minimal energy expenditure.107,257,329 Humans and rodents do not pant per se, but breathing frequency and minute volume increase during severe heat exposure to facilitate evaporative cooling from the respiratory surfaces. In humans, the contribution of respiratory evaporative cooling is small compared with that of skin evaporative cooling (Figure 10-4).

DEHYDRATION AND ELECTROLYTE IMBALANCE Water requirements during heat exposure are primarily determined by a person’s sweat losses. Water depletion dehydration develops when the rate of water replacement is not adequate, which can be a result of a mismatch between fluid intake and sweat loss, lack of water availability, or use of diuretic medications. Sweat rates may range from 0.3 to approximately 3 L/hr during athletic or occupational activities, depending on the environmental conditions and type, duration, and intensity of work.47,143 If high sweat rates are maintained without adequate replenishment of lost water, this can cause electrolyte imbalances that impede the efficiency of autonomic mechanisms of thermoregulatory control. For example, hyperosmolarity alters heat responsiveness of warm-sensitive neurons in the POAH and limits the effectiveness of evaporative heat loss.121,219,276 Severe hypernatremic dehydration is associated with brain edema, intracranial hemorrhage, hemorrhagic infarcts, and permanent brain damage (Figure 10-5, online).214 Severe reductions in electrolytes can have a profound impact on heatstroke outcome. Symptomatic hyponatremia (decreased serum sodium concentration) is a relatively rare condition, but it has been observed in marathon runners and military recruits during training exercises as a consequence of overconsumption of hypotonic fluids with inadequate replacement of sodium losses.210,230 Intracellular swelling is a severe consequence of hyponatremia that may cause CNS dysfunction. Hypokalemia (decreased serum potassium concentration) may be caused by overproduction of aldosterone, excessive sweating, or respiratory alkalosis. Any cause of overproduction of urine (polyuria) potentially causes urinary potassium loss.323 Potassium is a potent vasodilator of blood vessels to the skeletal and cardiac muscles, so excessive loss of this electrolyte can have detrimental effects, such as decreased sweat volume, cardiovascular instability, and reductions in muscle blood flow that predispose to skeletal muscle injury (i.e., rhabdomyolysis).158,279

Heat Illnesses Heat illnesses are best viewed as existing along a continuum that transitions from the mild conditions of heat cramps and heat exhaustion to more serious conditions of heat injury and heatstroke (Table 10-1). Heat cramps are typically brief but can cause agonizing pain in the skeletal muscles of the limbs and trunk. Cramps may be recurrent but are typically confined to the skeletal muscles that are involved in vigorous exercise in the heat. Skeletal muscle spasms in the extremities may be sporadic, but they are painful and develop most frequently in persons who are not acclimatized to physical exertion. However, heat cramps may also occur in fit athletes who are salt depleted. Heat cramps do not predispose to more serious heat illness and are not associated with com­ plications beyond muscle soreness. The cause of heat cramps is not fully understood, but cramps are thought to occur in response to increased intracellular calcium release that stimulates actin– myosin filaments and muscle contraction. Current treatments 218

A

B

C FIGURE 10-4  Infrared images of various surface regions. The brighter the color, the warmer the surface temperature. A, Female runner after 45 minutes of exercise in a 23° C (73.4° F) environment. Note that the palms of the hands and the face are substantially warmer than the rest of the body surface. B, Two polar bears. Note that only the snout, eyes, ears, and footpads are noticeably different from the surroundings. C, Sled dog relaxing shortly after completing the 17.7-km (11mile) ceremonial starting leg of the 2005 Iditarod Trail Sled Dog Race. The course of the Iditarod is greater than 1850.7 km (1150 miles) from Anchorage to Nome, Alaska. Ambient conditions were 0° C (32° F) with a lightly overcast sky and no wind. The infrared shot shows that the dog’s entire snout is white, meaning it is the hottest part of the body surface. The armpits and ears also are warmer. Maybe that is why dogs love to roll around in the snow, face first, on a warm day. (A and B from Grahn D, Heller HC: The physiology of mammalian temperature homeostasis, TraumaCare 14:52, 2004, with permission; C courtesy D. Grahn, photo by Matthew Grahn.)

Condition

Symptoms

Management

Heat cramps Heat rash (miliaria rubra) Heat exhaustion

Brief, painful skeletal muscle spasms Blocked eccrine sweat glands

Rest; replacement of electrolytes; avoid salt tablets Cool, dry affected skin area; topical corticosteroids, aspirin Move supine individual to cool, shaded environment, and elevate legs; loosen or remove clothing, and actively cool skin; administer oral fluids Ensure an open airway, and move to a cool environment. Immediately cool to <39° C (102.2° F) using ice packs, water bath, wetting with water and continuous fanning; IV fluid administration; reestablish normal CNS function; avoid antipyretics or drugs with liver toxicity

Heatstroke

Mild to moderate illness with inability to sustain cardiac output; moderate (>38.5° C [101.3° F]) to high (>40° C [104° F]) body temperature; often accompanied by dehydration Profound CNS abnormalities (agitation, delirium, stupor, coma) with severe hyperthermia (>40° C [104° F])

Data from Bouchama A, Knochel JP: Heat stroke. N Engl J Med 346:1978, 2002; and Winkenwerder W, Sawka MN: Disorders due to heat and cold. In Goldman L, Ausiello DA, Arend W, et al, editors: Cecil textbook of medicine, ed 23, Philadelphia, 2007, Saunders, pp 763-767. CNS, Central nervous system; IV, intravenous.

include rest and replacement of electrolytes with fluids or salted food. Salt tablets should be avoided because they can cause gastrointestinal irritation and may stimulate excess potassium loss in the distal tubules of the kidneys. Heat exhaustion (also referred to as heat prostration or heat collapse) is a mild to moderate form of heat illness that is associated with moderate (>38.5° C [101.3° F]) to high (>40° C [104° F]) elevations in core temperature and an inability to sustain cardiac output.335 The signs and symptoms of heat exhaustion include fatigue, dizziness, headache, nausea, vomiting, malaise, hypotension, and tachycardia with potential for collapse. Heat exhaustion can occur with or without exercise in hot environments and may progress to a moderately severe condition without associated organ damage. Heat exhaustion is often observed in older adults as a result of medications (e.g., diuretics), inadequate water intake that leads to dehydration, or preexisting cardiovascular insufficiency that predisposes to collapse. Treatment should consist of placing the individual in a recumbent position in a cool environment to normalize blood pressure. Oral fluid ingestion with electrolytes is often adequate for recovery; intravenous (IV) fluid administration may be warranted in severely dehydrated individuals. Heat injury is a moderate to severe condition characterized by tissue (e.g., skeletal muscle) or organ (e.g., gut, kidney, spleen, liver) damage and hyperthermia (core temperature usually, but not always >40° C [104° F]).335 Heat injury may progress to heatstroke if the patient is not rapidly cooled. Heatstroke is life threatening, with the patient presenting with profound CNS abnormalities, such as delirium, agitation, stupor, seizures, or coma and severe hyperthermia (core temperature typically, but not always >40° C [104° F]).335 Reliance on a specific core temperature value for clinical diagnosis of heatstroke is ill advised, because there is wide interindividual variability in documented cases. One of the main reasons for a lack of clinical treatments for heatstroke is the complicated nature of the syndrome, because there are different classifications based on etiology and pathophysiologic mechanisms of injury. Classic (also known as passive) heatstroke occurs at rest in vulnerable individuals, such as infants and older adults. Several intrinsic factors may predispose infants to heatstroke death. These include increased surface area–to–body mass ratio (accelerates heat gain), limited effective mechanisms of thermoregulation (e.g., suppressed behavioral adjustments), increased risk for dehydration (e.g., lack of water availability), and preexisting respiratory infections. Many older individuals have preexisting conditions, such as mental illness, prescription drug use (e.g., diuretics, anticholinergics), or infections that predispose to passive heatstroke (Box 10-1).6,56,312 Exertional heatstroke (EHS) has a different etiology than classic heatstroke and affects young healthy populations that perform strenuous physical activity or work in temperate or hot weather. During exercise, approximately 80% of expended energy is released as heat that must be dissipated from the body to avoid hyperthermia. Military and athletic populations are composed of young, healthy individuals who are highly motivated to perform strenuous physical activity in hot weather, which increases the risk for EHS. A recent epidemiologic study identified a variety of factors

that predispose to EHS, including gender (women greater than men), geographic region of origin (northern greater than southern states), preexisting illness, and race or ethnicity (whites greater than blacks).40 Unfortunately, exercise induces physiologic responses similar to those of heat stress, such that teasing apart the influence of these two factors in EHS is difficult.

Heatstroke Epidemiology and Risk Factors The ability to perform strenuous work in a hot environment is inversely related to the heat stress level, which can be assessed BOX 10-1  Predisposing Risk Factors for Serious Heat

Illness

Environmental Factors High ambient temperature High humidity Lack of air movement Trees and shrubbery Access to air conditioning Lack of shelter Heat wave (3 or more days of temperatures >32.2° C [90° F]) Individual Factors Age (small children, older adults) Obesity Poor physical fitness level Lack of acclimatization Dehydration Drug Use Diuretics Anticholinergics (e.g., atropine) β-blockers (e.g., propranolol) Antihistamines Amphetamines (e.g., Ecstasy) Ergogenic aids (e.g., ephedra) Antidepressants Alcohol consumption Compromised Health Status Viral infection (e.g., pneumonia, mononucleosis) Inflammation (e.g., fever) Skin disorders (e.g., miliaria rubra, burns) Cardiovascular disease Diabetes mellitus Malignant hyperthermia Sickle cell trait Data from references 6, 58, 196, 318, and 340.

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CHAPTER 10  Pathophysiology of Heat-Related Illnesses

TABLE 10-1  Heat Illness Symptoms and Management

PART 2  COLD AND HEAT

using the wet bulb globe temperature (WBGT) index. The WBGT for indoor or outdoor environments is determined in the following manner: Indoor WBGT = 0.7 Tw + 0.3 Tamb Outdoor WBGT = 0.7 Tw + 0.2 Tbg + 0.1 Tamb where Tw is the natural wet bulb temperature, Tbg is the black globe temperature, and Tamb is the dry bulb temperature. Tbg determines the radiant heat load with a specialized thermometer that is surrounded by a 6-inch–diameter blackened sphere. The WBGT is the most widely used index to determine safe limits of physical activity and establish strategies to minimize the incidence of heat illness during military, athletic, or occupational tasks. The WBGT index does not take into consideration different clothing ensembles or exercise intensities, so the most practical and safe application of this measurement requires adjustment for these factors. Heat waves are defined as three or more consecutive days during which the environmental temperature exceeds 32.2° C (90° F).41 In the summer of 2003, Europe experienced 22,000 to 45,000 heat-related deaths during a 2-week period in which the average temperature was 3.5° C (6.3° F) above normal.189,273 The European continent has experienced an increase in minimum daily temperatures over the last 30 years, and this trend will likely increase if average global temperatures continue to rise. A 1.4° to 5.8° C (2.5° to 10.4° F) increase in minimum daily temperatures in Europe is predicted over the next century.131,337 Most prediction models suggest that heat waves in the future will be more severe and longer in duration. Predictions based on climate variability data from the 1995 Chicago and 2003 Europe heat waves suggest that by 2090, heat waves in these cities will be 25% to 31% more frequent and last 3 to 4 days longer.203 Another prediction model suggests a 253% increase in annual heatstroke deaths in the United Kingdom by 2050.61 The impact of climate change is not equally distributed across the globe because of regional variability in thermal tolerance that influences the incidence of heatstroke mortality. A study of 11 U.S. cities showed that threshold temperatures for heatstroke mortality are higher in warmer southern cities than in cooler northern cities.53 A comparison of temperature–mortality relationships in southern Finland, southeastern New England, and North Carolina indicated that lower temperature thresholds in cooler climates are coupled with steeper temperature–mortality relationships.62 Similarly, the upper safety limits of environmental temperatures in the Netherlands, London, and Taiwan are 16.5°, 19°, and 29° C (61.7°, 66.2°, 84.2° F), respectively.192 A case study of 15 Marine recruits who collapsed from heatstroke during training exercises in South Carolina showed that 73% previously resided in northern states and that 60% of cases occurred during the second week of training during the hottest summer months.232 From 1980 to 2002, the highest EHS incidence in military recruits was in nonacclimatized individuals from northern, cold-climate states who were enlisted for less than 12 months.40 During July, many regions of the world have a WBGT index that is greater than 29° C (84.2° F), and military training often occurs in environments with a WBGT index that is greater than 35° C (95° F). During peacetime exercises, approximately 25% of fatal military EHS cases occur during the hottest summer months in recruits who have been in training camp less than approximately 2 weeks.192 Individuals from northern states are expected to be less acclimatized to hot, humid summer conditions than are those from southern states. Heat acclimatization improves thermotolerance but requires several days to weeks of exposure to similar heat stress and exercise conditions to be fully effective. This likely accounts for hot days early in the summer showing a greater impact on heatstroke morbidity and mortality than those cases occurring later in the training process, after the protective effects of heat acclimatization have been realized.105 Humanity’s impact on the landscape in conjunction with increased production of greenhouse gases may be creating the largest climate change. Urban heat islands are created in cities when vegetation is removed and blacktop roads and concrete buildings are erected. Temperatures may be 30° to 40° C (54° to 72° F) higher on asphalt roads and roof tops compared with 220

those of the surrounding air.85 Since 1978 urban sprawl has accounted for an increase in city temperatures in southeastern Asia of approximately 0.05° C (0.09° F) per decade.343 Across the entire land mass of the United States, the surface temperature has increased approximately 0.27° C (0.49° F) per century because of changes in the land cover arising from agricultural and urban development.139 Concrete and asphalt surfaces cool slowly during the nighttime when air temperature decreases, and this increase in urban heat storage magnifies the intensity of heat exposure experienced by individuals living in concrete urban structures.49,165 Several social factors predispose older adults to heatstroke mortality, including living alone, inability or unwillingness to leave one’s home, residing on the top floor of buildings (heat rises), and annual income of less than $10,000.221 Most heat wave early warning systems emphasize use of air-conditioning systems, but availability and use of the units are limited by socioeconomic status because they are expensive to operate.56,221 A working air conditioner was the strongest protective factor against mortality during the 1999 heat wave in Chicago; fan cooling did not afford protection.221 High mortality rates were recorded in Chicago despite extensive programs to educate high-risk populations, such as advising older adults to seek cool shelters or use air-conditioning systems. Approximately 10,000 elders died during the France heat wave of 2003 primarily because of lack of air-conditioning units in residences and hospitals.63,312 In 2005, Hurricane Katrina ravaged the U.S. Gulf Coast, and electrical failures caused high heatstroke mortality of older adults confined to residences, retirement homes, and hospitals because local temperatures exceeded 43° C (109.4° F). Increases in the average human lifespan, global climate change, and use of medications that compromise cardiovascular adjustments to heat stress will necessitate increased reliance on artificial cooling systems and educational programs to prevent heatstroke deaths in vulnerable populations, such as older adults. The high death toll of older adults because of excessive heat per se may be small compared with that caused by aggravation of a preexisting illness. Heat stress refers to environmental and metabolic conditions that increase body temperature; heat strain refers to the physiologic consequences of heat stress. Heat strain imposes large cardiovascular demands on the body. Blood flow is shunted from the viscera to the skin surface to dissipate excess heat to the environment, making cardiovascular fitness a more important factor than age in determining an individual’s susceptibility to heatstroke. Austin and Berry10 examined 100 cases of heatstroke during three summer heat waves in St. Louis and found cardiovascular illness in 84% of patients. Levine181 found heatstroke deaths to be associated with arteriosclerotic heart disease (72%) and hypertension (12%). Cardiac deficiency impedes heat loss and compromises the ability to maintain cardiac output during prolonged heat exposure, leading to circulatory collapse and death. Older individuals may have impaired baroreceptor reflex modulation, lower sweat rates, longer time to onset of sweating, and diminished sympathetic nerve discharge, all of which increase the risk for heatstroke morbidity and mortality.130,144,291 Minson and colleagues210 demonstrated that during heat exposure, older men relied on a higher percentage of their cardiac chronotropic reserve compared with younger men. Preexisting infection or inflammation may compromise an individual’s ability to appropriately respond to heat stress and can be a complicating factor, regardless of age. Fifty-seven percent of heatstroke patients more than 65 years old had evidence of infection upon clinical admission during a Chicago heat wave in 1995.56,157 In Singapore, a young EHS victim had been ill for 3 days before heatstroke collapse.43 It has been proposed that acute illness or inflammation can cause transient susceptibility to heatstroke in young, fit individuals who exercise in the heat. For example, idiosyncratic episodes of hyperthermia were associated with acute cellulitis and gastroenteritis in soldiers exercising in the heat.39,146 Four male Marine recruits presented with viral illness (mononucleosis, pneumonia) before collapse from exertional heat illness (EHI) during training exercises associated with “the Crucible” at Parris Island, South Carolina.289 Peripheral blood mononuclear cells (PBMCs) from these recruits expressed higher levels of IFN-inducible genes than did those

SKIN DISORDERS The skin is the largest organ of the body and an important area for effective heat exchange with the environment. A number of skin disorders can adversely affect temperature control and increase susceptibility to heat illness. Miliaria rubra (also known as prickly heat, sweat rash, or heat rash) occurs when sweat gland ducts become blocked with dead skin cells or bacteria (e.g., Staphylococcus epidermidis). The obstruction causes eccrine secretions of the sweat glands to accumulate in the ducts or leak into the deeper layers of the epidermis, causing a local inflammatory reaction associated with redness and blisterlike lesions. Individuals with miliaria rubra are at increased risk for heat illness when a large area of the skin is affected. If heat illness is expected, the affected area of the skin should be cooled and dried to control infection, and topical corticosteroids or aspirin may be effective in reducing swelling and irritation. Sunburn can impair sweating and cause fever, which increase the risk for heat illness. If the sunburn covers more than 5% of the body, heat exposure should be avoided until the skin has healed. Sunburn is a preventable disorder with the use of sun-blocking lotions, protective clothing, and shelter from sun exposure.

Pathophysiology of Heatstroke The pathophysiologic responses to heatstroke range from those conditions that are experienced immediately following collapse to long-term changes that persist for several weeks, months, or years following hospital treatment and release. Currently more is known about the immediate heatstroke responses because clinical records document symptoms during hospital treatment. However, clinical and experimental research has seen a shift within the past decade toward a focus on understanding the pathophysiologic responses that mediate long-term injury. It is now believed that the long-term pathophysiologic responses to heatstroke are caused by a systemic inflammatory response syndrome (SIRS) that ensues following heat-induced damage to the gut and other organs.24 Following damage to the epithelial membrane of the gut, endotoxin that is normally confined to the lumen of this organ is able to leak into the systemic circulation and elicit immune responses that cause tissue injury. The thermoregulatory, immune, coagulation, and tissue injury responses that ensue during the long-term progression of heatstroke closely resemble those observed during clinical sepsis and are likely mediated by similar cellular mechanisms. Clinical records have provided an extensive database of the immediate consequences of heatstroke, whereas the majority of knowledge regarding the pathophysiologic mechanisms of heat-induced SIRS has been obtained from experimental animal studies. Although there are several gaps in our knowledge of the specific factors that predispose to multiorgan system failure, this is an exciting area of research that is expected to progress at a rapid rate because of continued advancements in experimental and genetic technologies. Figure 10-6 provides an overview of the current understanding of the pathophysiologic responses that are thought to initiate and mediate heat-induced SIRS, which will be discussed in detail here.

BODY TEMPERATURE RESPONSES At the time of heatstroke collapse, the severity of hyperthermia varies widely between individuals, with reported core temperature values ranging from approximately 41° C (105.8° F) to 47° C (116.6° F).* During a summer heat wave in St. Louis in the 1950s, the core temperature of 100 heatstroke patients ranged from 38.5° to 44° C (101.3° to 111.2° F), with 10% of mortalities occurring below 41.1° C (106° F).10 In some instances, individuals may tolerate hyperthermia without adverse side effects. During a competitive marathon race in California, a 26-year-old man maintained a rectal temperature of 41.9° C (107.4° F) for approximately 45 minutes without clinical signs of heat illness.197 However, there are several reports of athletic, military, and occupational workers with core temperatures below 41.9° C (107.4° F) who were hospitalized, experienced permanent CNS impairment, or died from EHS (Table 10-2). Hypothermia and fever are core temperature responses that are often observed in patients and experimental animal models during heatstroke recovery. Hypothermia is not a universal heatstroke recovery response in humans but has been anecdotally observed following aggressive cooling treatment. Hypothermia manifests as a rapid undershoot of body temperature below 37° C (98.6° F) and is thought to represent a loss of thermoregulatory control following heat-induced damage to the POAH. However, evidence in support of this hypothesis is lacking because autopsy reports and experimental animal studies have failed to detect histologic damage to the POAH despite extensive damage in other organs.174,192 Because hypothermia is not observed in all heatstroke patients, it continues to be regarded as a pathologic recovery response. In experimental animals, hypothermia is a natural heatstroke recovery response that is associated with behavioral and autonomic thermoeffector responses that support a decrease in core temperature. Mud puppies are ectothermic species that rely on behavioral adjustments, such as the selection of different microclimates, to control body temperature. Mud puppies heat shocked to approximately 34° C (93.2° F) *References 26, 42, 109, 112, 188, 289.

221

CHAPTER 10  Pathophysiology of Heat-Related Illnesses

from controls who participated in the training event but did not collapse.289 High plasma levels of IFN-α and IFN–γ mediate flulike symptoms during viral infection and are often associated with EHI/EHS.24,289 In rats, exposure to lipopolysaccharide (LPS), a cell wall component of gram-negative bacteria, exacerbated inflammation, coagulation, and multiorgan system dysfunction from heat exposure.182 Taken together, these findings suggest that a preexisting inflammatory state compromises an individual’s ability to respond to heat stress with appropriate thermoregulatory or immune responses to prevent collapse or multiorgan system failure and death. The annual Muslim pilgrimage to Mecca (i.e., the Hajj) is associated with high heatstroke incidence each year and provides many lessons regarding etiologic factors that increase susceptibility. The Hajj takes place in the hot desert environment of Saudi Arabia during the extreme weather months of May to September, when temperatures range from 38° to 50° C (100.4° to 122° F).151 Hot weather combined with physical exertion (first day consists of a 3.5-km [2.2-mile] jog), heavy clothing that is traditional to the region (limits heat dissipation), and an older population (approximately 50 years is an advanced age for this region) predispose many individuals to heatstroke. Clothing has a significant impact on Muslim women because they are required to wear darker clothing that covers a larger surface area of the body than does clothing worn by men.114 Medical conditions, such as diabetes, cardiovascular abnormalities, or parasitic diseases, are common.151 Heatstroke is a major concern, but heat exhaustion with water or salt depletion is also prevalent. Overcrowding and congestion impose large demands on sanitation services, as exemplified in the 1980s, when approximately 2 million people participated in the Hajj. Advances in modern technologies, such as more rapid transport to the area, will likely introduce additional factors (e.g., lack of acclimatization, increased greenhouse gas production, increased congestion) to this already complex situation. Protective clothing is a significant predisposing factor to EHS during athletic (heavy uniforms), military (chemical protective clothing), or occupational activities (e.g., pesticide application, firefighting, and race car driving). Protective clothing often consists of multiple layers that insulate anatomic sites from heat exchange, including the skin and head.251 The wearing of protective clothing during strenuous work can quickly result in a dangerous elevation in body temperature. Fifty-one cases of EHI were observed in military trainees in San Antonio, Texas, during participation in a 9.3-km (5.8-mile) march in full battle dress uniform and boots.285 Lack of acclimatization to athletic uniforms and high environmental temperatures results in the majority of cases of EHS in athletes occurring on the second or third day of exposure to hot weather before these individuals are acclimatized to the uniforms and environmental temperatures.97,260

PART 2  COLD AND HEAT

Climatic heat stress and exercise

Heat strain

Cardiovascular responses Gut constricts

Skin dilates

Heat cytotoxicity (Intestine, kidney, spleen, endothelium) HSPs

Ischemia ↑ Gut epithelial membrane permeability Increased tight junction permeability

Systemic inflammatory response syndrome (fever, DIC, rhabdomyolysis, tissue injury) Anergy (Th1 > Th2 response)

Endotoxin

Innate immune system TLR4

Multi-organ system failure

Cytokines

Adaptive immune system FIGURE 10-6  Summary of heatstroke pathophysiologic responses that culminate in multiorgan system failure. An increase in heat strain stimulates a reflexive increase in cutaneous blood flow and decrease in splanchnic blood flow to facilitate heat dissipation to the environment. Gut ischemia causes increased epithelial membrane permeability and leakage of endotoxin into the systemic and portal circulation. Toll-like receptors (e.g., TLR4) detect pattern-associated molecular patterns on the cell membrane of endotoxin and stimulate proinflammatory and antiinflammatory cytokine production. Heat is toxic to several organs and stimulates secretion of heat shock proteins (HSPs) that interact with cytokines and other proteins to mediate the systemic inflammatory response syndrome (SIRS) of the host. Peripheral and central nervous system actions of cytokines and other mediators of SIRS are thought to mediate many of the adverse consequences of the heatstroke syndrome that lead to multiorgan system failure and death. DIC, Disseminated intravascular coagulation.

behaviorally selected a cooler microclimate and maintained a significantly lower body temperature than did nonheated controls during 3 days of recovery.130 This study did not determine the impact of hypothermia on survival, but the association of decreased body temperature with the selection of cool microclimates indicated that this was a regulated response to a decrease in the temperature set point. Small rodents, such as mice, rats, and guinea pigs, showed reductions greater than 1.0° C (1.8° F) in body temperature that were associated with improved survival following passive heatstroke. In mice, hypothermia was associated with an approximately 35% decrease in metabolic heat production and the behavioral selection of microclimates that precisely regulated the depth and duration of this response.174 Exposure of mice to warm ambient temperatures that prevented heat-induced hypothermia caused increased intestinal damage and mortality.173,333 Hypothermia likely provides protection against heat-induced tissue injury in a manner similar to that shown for protection against other extreme environmental insults based on the temperature coefficient (Q10) effect. A common heatstroke recovery response observed in patients and animal models is recurrent fever during the days and weeks of recovery.9,10,173,192,204 In mice, fever was observed within a day after passive heatstroke collapse and associated with an approximately 20% increase in metabolic heat production and increased plasma levels of the proinflammatory cytokine interleukin (IL)6.154,172,174 IL-6 is an important regulator of fever during infection and inflammation and may regulate fever during heatstroke recovery.172 In patients, fever is reestablished following clinical cooling.192 This is reminiscent of Liebermeister’s experimental observations of the recurrence of fever following experimental cooling of the POAH of rats.180,192 In experimental animal models, the inability to recover from hypothermia and develop fever is associated with increased mortality, suggesting that fever may be important for the resolution of infection.173 However, in a case report of human heatstroke, fever was associated with poor outcome. An amateur long-distance runner was hospitalized for 10 days after collapsing from EHS during a 9.7-km (6-mile) footrace.204 Moderate fever (>38° C [100.4° F]) was evident during the first 4 days of hospitalization, but on the tenth day the patient experienced convulsions and a rapid increase of body temperature to 41° C (105.8° F). Rapid cooling and aspirin were ineffective in reducing body temperature, and the patient died.204 The inability of aspirin to inhibit the rapid rise in body temperature suggests that this was not a true fever response, but rather a pathologic response to increased metabolic heat production induced by the convulsions. It is important to recognize that there is an optimal temperature range above which the protective

TABLE 10-2  Clinical Characteristics of Exertional Heat Illness Cases Activity Military Training Army (aviation) Army (basic) Army (basic) Army (Singapore) Marine Corps Marine Corps Marine Corps NBC Athletic Events 6-Mile run Marathon run Marathon run Hajj rituals Migrant farming Firefighter training

Body Temperature ° C (° F)

Age (Years)

Length of Hospitalization

>39.0 (102.2) 40-41.1 (104-106) 41.1 (106) 40-42 (104-107.6)† <38.9-40.0 (102-104) 39-42.5 (102.2-108.5)†‡ 41.1 (106) 41.3 (106.3)

18-59 18-41 20 18-29 17-30 17-19 NR 25

10 min 24 hr to 12 d 5d 45 min to 99 hr None >1 d ≤12 hr 12 d

CNS dysfunction207,* Death192 Recovery233 Death43 Recovery106 Recovery289 Hospitalization106 Recovery51

39.2 (102.6)§ 40.7 (105.3)‡ 41.9 (107.4) <42 (107.6) ≥42 (107.6) 43.9 (111) 42.2 (108) 42.6 (108.7)

29 Late 30s 26 32-80 NR NR 44 22

10 d 5d None NR NR NR None 9d

Death204 Recovery261 Recovery197 Ataxia, infarction, death341 Death341 Recovery341 Death220 Death219

CNS, Central nervous system; NR, not reported; NBC, nuclear, biological, and chemical protective clothing. *CNS dysfunction includes agitation, confusion, disorientation, delirium, poor memory, convulsions, and/or coma. † Indicates patient cohorts with documented prodromal illness before heatstroke collapse. ‡ Body temperature measured several minutes after collapse or cooling. § Patient temperature increased to 41° C (105.8° F) on day 10 of hospitalization before death.

222

Outcome

TABLE 10-3  Toll-Like Receptors of the Innate

IMMUNE RESPONSES

Toll-Like Receptor

Ligand

Cell/Tissue Types

TLR1

Triacyl lipopeptide

TLR2

Lipopolysaccharide Peptidoglycan Lipoteichoic acid Measles virus Human cytomegalovirus Hepatitis C virus Zymosan Necrotic cells Viral double-stranded RNA

Monocytes, macrophages, DCs, polymorphonuclear leukocytes, B and T cells, NK cells Monocytes, granulocytes Brain, heart, lung, spleen

During heat stress, blood flow to the skin is increased to facilitate heat loss to the environment and reduce the rate of total body heat storage. Increased skin blood flow is accompanied by a fall in splanchnic (i.e., visceral organ) blood flow as a compensatory mechanism to sustain blood pressure. Endotoxin is normally confined to the gut lumen by tight junctions of the epithelial membrane, but these junctions can become “leaky” following prolonged reductions in blood flow that cause ischemic stress.108,164 There are several lines of evidence that support the hypothesis that endotoxin leakage from the gut lumen into the systemic circulation is the initiating stimulus for heat-induced SIRS. First, systemic injection of LPS into experimental animals induces symptoms similar to those observed in heatstroke, including hyperthermia, hypothermia, fever, hypotension, cytokine production, coagulation, and tissue injury.175,268 Second, increased portal or systemic endotoxin levels are observed in heatstroke patients and animal models. In primates, circulating endotoxin was detected at rectal temperatures above 41.5° C (106.7° F) with a precipitous increase at approximately 43.0° C (109.4° F).90 Splanchnic blood flow shows an initial decrease at 40° C (104° F); the liver, which is an important clearance organ for endotoxin, shows damage at body temperatures of approximately 42° to 43° C (107.6° to 109.4° F).* In a young athlete with a body temperature of 40.6° C (105.1° F) on the second day of football practice, high circulating levels of endotoxin were associated with hemorrhagic necrosis of the liver.97 In heatstroke patients, endotoxin was detected at approximately 42.1° C (107.8° F) and remained elevated despite cooling.26 Third, rats rendered endotoxin tolerant following the systemic injection of LPS are protected from heatstroke mortality.66,67 The protective effect of endotoxin tolerance is related to enhanced stimulation of the liver reticuloendothelial system (RES), which is composed of monocytes, macrophages, and Kupffer cells that are important for endotoxin clearance.66,67 RES stimulation reduced and RES blockade increased mortality of heat-stressed rats.67 Fourth, antibiotic therapy protects against heatstroke in several species. In dogs, antibiotics reduced gut flora levels and improved 18-hour survival rates by more than threefold when provided before heat exposure.37 In rabbits with heatstroke, hyperthermia and endotoxemia were reduced following oral antibiotics.36 Anti-LPS hyperimmune serum reversed the heatstroke mortality rates of primates and returned plasma LPS levels to baseline, but it was ineffective at the highest body temperature of 43.8° C (110.8° F), indicating that hyperthermia can cause irreversible organ damage and death.91 Heat-induced SIRS is initiated by the innate and adaptive immune systems, which interact to sense the presence of endotoxin and orchestrate an immunologic response. The innate immune system comprises monocytes, macrophages, and neutrophils that use pattern recognition receptors (PRRs) on their cell surfaces to recognize pattern-associated molecular patterns (PAMPs) on the cell surface of endotoxin and other invading pathogens.137 Toll-like receptors (TLRs) are a class of PRRs that have been widely studied in the immune response to infection.208,314 Ten mammalian TLRs have been identified, and the specific pathogenic ligands that activate these PRRs are known (Table 10-3). TLR4 is the principal receptor for LPS that stimulates gene transcription factors, such as NF-κB, to increase the synthesis of a variety of immune modulators in response to endotoxin. Endotoxin infection (i.e., sepsis) is associated with increased expression of TLR4 on circulating human PBMCs, as well as on mouse liver and spleen macrophages.307,308 In the 1960s, a spontaneous mutation in the TLR4 gene was discovered in C3H/HeJ mice, which has been an important animal model to determine the role of TLR4 in endotoxin responsiveness. C3H/HeJ mice show a diminished response to bacterial infection, but increased mortality from SIRS, because of an inability to respond appropriately *References 29, 30, 43, 108, 147, 225.

Immune System

TLR3

TLR4

TLR5

Lipopolysaccharide Fibrinogen Heat shock proteins High mobility group box 1 Flagellated bacteria

TLR6

Diacyl lipopeptide

TLR7

Single-stranded RNA

TLR8

Single-stranded RNA

TLR9

CpG DNA

TLR10

Unknown

DCs, T cells, NK cells, monocytes, granulocytes Placenta, pancreas B cells, DCs, monocytes, macrophages, granulocytes, T cells Spleen Monocytes Ovary, prostate B cells, monocytes Thymus, spleen, lung Monocytes, B cells, DCs Lung, placenta, spleen, lymph node, tonsil Monocytes Lung, placenta, spleen, lymph node, bone marrow, PBLs B cells, DCs Spleen, lymph node, bone marrow, PBLs B cells Spleen, lymph node, thymus, tonsil

Data from Medvedev AE, Sabroe I, Hasday JD, et al: Tolerance to microbial TLR ligands: Molecular mechanisms and relevance to disease, J Endotoxin Res 12:133, 2006; and Tsujimoto H, Ono S, Efron PA, et al: Role of Toll-like receptors in the development of sepsis, Shock 29:315, 2008. CpG, Deoxycytidylate-phosphate-deoxyguanylate; DC, dendritic cell; DNA, deoxyribonucleic acid; NK, natural killer; PBL, peripheral blood leukocyte; RNA, ribonucleic acid.

to endotoxin and induce the full complement of immune responses.103 Inability to respond to antigens is known as anergy and is a proposed mechanism that predisposes to increased risk and mortality from bacterial infection.117 Given that TLR4 mutations exist in humans, this may be one (of several) genetic factors that predispose to mortality associated with heat-induced SIRS, although the association of mortality with TLR4 polymorphisms remains controversial.5,75 C3H/HeJ mice have not been tested for their resistance to heatstroke morbidity/mortality but are a useful experimental model to determine the roles of TLR4 and anergy in this syndrome. Specificity of immune responses is provided by B and T cells of the adaptive immune system. These cells respond to antigens by secreting cytokines, which are intercellular immune signals that elicit proinflammatory (Th1 type) and antiinflammatory (Th2 type) actions during the progression of SIRS. The actions of cytokines depend on the nature of the danger signal, the target cells with which they interact, and the cytokine “milieu” in which they function. Th1 and Th2 cytokines function in a negative feedback pathway to regulate each other’s production and maintain a delicate balance of inflammatory reactions. Anergy is thought to be a consequence of inadequate Th2 cytokine production late in SIRS. For example, increased patient mortality from peritonitis is associated with the inability to mount a Th2 cytokine response.117 223

CHAPTER 10  Pathophysiology of Heat-Related Illnesses

effects of fever are no longer realized because of the toxic effect of high body temperature on cell function.155

PART 2  COLD AND HEAT

Alarmins are endogenous PAMPs that are released from stressed or injured tissues and initiate restoration of homeostasis following an infectious or inflammatory insult.17 High mobility group box 1 (HMGB1) is a highly conserved nuclear protein that functions as an alarmin following release from necrotic (but not apoptotic) cells.272 Necrosis is the premature death of cells in a tissue or organ in response to external factors, such as pathogens and toxins. Because necrosis is detrimental to the host, it is associated with an inflammatory response. Apoptosis refers to genetically programmed cell death that does not elicit an inflammatory response, because apoptosis is beneficial to the host. Release of HMGB1 from necrotic cells stimulates Th1 cytokine production late in the sepsis syndrome and is a purported mediator of lethality; this shift in the balance of cytokines from a Th2 to Th1 phenotype is a potential mechanism of sepsis lethality. In human PBMCs, HMGB1 interacts with TLR2 and TLR4 to enhance Th1 cytokine production in synergy with LPS.124 Elevated serum HMGB1 levels are observed 8 to 32 hours following LPS injection in mice. Anti-HMGB1 antibodies did not protect against LPSinduced mortality unless the antibodies were provided 12 and 36 hours after LPS exposure.324 The delayed kinetics of HMGB1 and the association of elevated serum levels of this protein with poor outcome in sepsis patients suggest that HMGB1 detection late in SIRS may be a sensitive clinical marker of disease severity.115,297,324

Extrinsic pathway TISSUE INJURY

Intrinsic pathway CONTACT ACTIVATION

Tissue Factor (TF)

Factor VII

Factor VIIa

Factor XIIa Factor XIa Factor IXa

Factor XII Factor XI

Factor IX

VIIIa

Factor V

Factor Xa Factor Va

Anticoagulation Protein C

Factor X

Protein S

Activated protein C (APC) Prothrombin

Thrombin

Factor VIIIa

Fibrinogen

Fibrin

Factor VIII

Clot

COAGULATION Disseminated intravascular coagulation (DIC) is a common clinical symptom of heatstroke and manifests in two different forms (Figure 10-7). Microvascular thrombosis is a form of DIC characterized by fibrin deposition and/or platelet aggregation that occludes arterioles and capillaries and predisposes to multiorgan system dysfunction.177 Microvascular thrombosis is commonly observed in response to sepsis or trauma. DIC associated with consumptive coagulation is characterized by excessive blood loss when platelets and coagulation proteins are consumed faster than they are produced.8,12 Hemorrhagic complications in heatstroke victims include prolonged bleeding from venipuncture sites or other areas (e.g., gums), which can have a fatal outcome.148 The primary event that initiates coagulation in heatstroke patients is thermal injury to the vascular endothelium.21,24,215 In vitro studies have shown the ability of heat (43° to 44° C [109.4° to 111.2° F]) to directly activate platelet aggregation and cause irreversible hyperaggregation despite cooling.87,333 Cancer patients treated with whole-body hyperthermia (41.8° C [107.2° F] for 2 hours) showed decreased fibrinogen and plasminogen at body temperatures as low as 39° C (102.2° F), alterations in factor VII activity at 41.8° C (107.2° F), and decreased platelet concentrations from the time of maximum body temperature through 18 hours of recovery.295 Several proteins, including HMGB1, IL-1, tumor necrosis factor (TNF), and activated protein C (APC), affect the coagulation, anticoagulation, and fibrinolytic pathways. In rats, HMGB1 in combination with thrombin caused excess fibrin deposition in glomeruli, prolonged clotting times, and increased sepsis mortality compared with thrombin alone.133 The effect of HMGB1 protein was demonstrated in vitro to be caused by inhibition of the APC pathway and stimulation of tissue factor expression on monocytes.133 Cytokines stimulate microvascular thrombosis by interacting with neutrophils, macrophages, platelets, and endothelium to increase expression of intracellular adhesion molecules. Increased expression of cell adhesion molecules, neutrophil adhesion, and release of reactive oxygen species caused endothelial activation and injury.201,330 APC is an important component of the anticoagulation pathway that inactivates factors Va and VIIIa to inhibit fibrin clot formation. In septic patients, reduced APC production was associated with increased risk of mortality from systemic inflammation and DIC.78,179 In addition to its anticoagulation properties, APC possessed antiinflammatory and antiapoptotic properties that protected against experimental sepsis and heatstroke.44,302 Typical clinical measures of coagulation include prothrombin time (PT), activated partial thromboplastin time (aPTT), and 224

Plasminogen activator Inhibitor 1

Fibrinolysis Plasminogen tPA

Plasmin

Fibrin degradation products

FIGURE 10-7  Pathways of disseminated intravascular coagulation (DIC). The coagulation cascade is stimulated by the extrinsic pathway (also known as the tissue factor [TF] pathway) and the intrinsic pathway (also known as the contact activation pathway). Both pathways represent a series of enzymatic reactions that result in formation of a fibrin clot. Fibrinolysis represents the pathway by which the fibrin clot is resorbed through the actions of plasmin. The major physiologic anticoagulant is protein C, which is activated by protein S and inactivates factors Va and VIIIa to inhibit clot formation. Lipopolysaccharide, interleukin-1, and tumor necrosis factor affect DIC by stimulating TF formation and inhibiting the inactivation of factors Va and VIIIa, which prolong clot formation.

fibrinogen. PT in combination with aPTT assesses the time for plasma clot formation to occur in response to exogenous tissue factor and is a sensitive measure of responsiveness of the coagulation pathway. The reference range for PT is approximately 12 to 15 seconds and may be prolonged severalfold in heatstroke patients. The aPTT normally ranges from approximately 30 to 40 seconds and is used clinically to monitor treatment effects of anticoagulants, such as heparin. Fibrinogen is an acute phase protein synthesized by the liver that is normally in the range of 2 to 4 g/L. Low fibrinogen levels indicate liver damage or DIC, whereas elevated levels are a clinical sign of systemic inflammation. DIC can be difficult to diagnose, but low fibrinogen levels with prolonged PT or aPTT are strong clinical indicators in critically ill patients.

TISSUE INJURY Multiorgan system failure is the ultimate cause of heatstroke mortality and is a consequence of SIRS, which ensues following heat-induced damage to the gut and other tissues.24 A variety of noninfectious and infectious clinical conditions are associated with SIRS, and similar physiologic mechanisms are thought to mediate the pathogenesis of these conditions (Box 10-2). The term sepsis refers to SIRS associated with the presence of infection. Much of the understanding of pathophysiologic mechanisms mediating heat-induced SIRS has been obtained from sepsis studies. Provided here is an overview of the responses that constitute heat-induced SIRS and current understanding of

Illness

Clinical Neurologic symptoms (fatigue, weakness, confusion, stupor, coma, dizziness, delirium) Tachycardia Nausea, vomiting, diarrhea Headache Hypotension Oliguria, multiorgan system failure Hyperventilation Shock Laboratory Metabolic acidosis Elevated hematocrit Elevated blood urea nitrogen (BUN), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) Elevated lactate Disseminated intravascular coagulation Elevated cytokines Circulating endotoxin

the pathophysiologic mechanisms that mediate the adverse events of this syndrome. The severity of heatstroke is primarily related to the extent of damage to the brain, liver, and kidneys and is clinically identified by elevations in serum biomarkers, such as creatine kinase (CK), blood urea nitrogen (BUN), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). CK is released from muscle and is a marker of skeletal muscle injury (also known as rhabdomyolysis), myocardial infarction, muscular dystrophy, and acute renal failure.1,274,322 BUN is a measure of the amount of nitrogen in the blood in the form of urea, which is secreted by the liver and removed from the blood by the kidneys. A high BUN concentration is typically regarded as an indication of impaired renal function, although BUN levels may be altered by conditions unrelated to heat illness, including malnutrition, highprotein diets, burns, fever, and pregnancy.1,267 AST is released by the liver and skeletal muscle and may be a clinical sign of congestive heart failure, viral hepatitis, mononucleosis, or muscle injury. ALT is released by the liver, red blood cells, cardiac muscle, skeletal muscle, kidneys, and brain tissue. AST and ALT are common clinical markers of liver function in heatstroke patients despite multiple tissue sources of these enzymes and occasional false-negative results that complicate interpretation. Unfortunately, all of these biomarkers are released by a variety of tissues and altered by heat-exhaustive exercise, so they do not always provide a precise measure of the extent of tissue injury.95,102,283 The extent and time course of organ injury vary widely between individuals. Tissue injury manifests as primary and/or secondary multiorgan dysfunction, depending on whether heat toxicity alone or in combination with SIRS causes cellular damage.4,192 Gut epithelial barrier disruption is an example of primary organ dysfunction that is evident at the time of heatstroke collapse. Hyperthermia degrades epithelial membrane integrity and causes microhemorrhages, dilation of the central lacteals of the microvilli, and blood clots within the stomach and small intestine (Figure 10-8).27,108,172 It is often difficult to determine if organ injury is caused by primary or secondary factors.* For example, protein clumping in kidney tubular epithelial cells may be a consequence of heat toxicity, elevated myoglobin levels, or DIC.† A conscious mouse model has shown that kidney damage is present within approximately 2 hours following heatstroke collapse and remains elevated through approximately 24 hours of recovery.172 In heatstroke patients, acute renal failure is a nearly universal finding that is accompanied *References 21, 56, 97, 171, 172, 192. † Reference 27, 43, 97, 147, 172, 188, 249, 323.

by decrements in function within 24 hours of admission to the intensive care unit.244 In patients that survive more than 24 hours, severe hypotension, dehydration, BUN, and oliguria are associated with tubular necrosis or intertubular edema.192 Primary changes in the spleen are even less well understood, but cytoplasmic protein clumping is thought to be a consequence of this organ being “simply cooked and coagulated.”43,172 CNS dysfunction is a hallmark of heatstroke that is dominant early in the disorder. Patients are often confused, delirious, combatant, or comatose at the time of clinical presentation. Hyperthermia with exercise is also associated with reduced cerebral blood flow, which may account for these CNS abnormalities.228 Despite rapid treatment, approximately 30% of heatstroke survivors experience permanent decrements in neurologic function.6,24,56 CNS dysfunction is often associated with cerebral edema and microhemorrhages at autopsy in heatstroke patients.* The blood–brain barrier (BBB) is a semipermeable membrane that allows selective entry of substances (e.g., glucose) into the brain while blocking the entry of other substances (e.g., bacteria). Hyperthermia increases BBB permeability in experimental animal models, which permits leakage of proteins and pathogens from the systemic circulation into the brain. Computed tomography (CT) scans have been used to examine CNS changes in heatstroke patients. In the 1995 Chicago heat wave, atrophy, infarcts of the cerebellum, and edema were evident in older adult victims. CT scans also revealed severe loss of gray-white matter discrimination (GWMD), which was associated with headache, coma, absence of normal reflexive responses, and multiorgan dysfunction.299 Loss of GWMD is a consequence of increased brain water content, which is in line with occurrence of edema in heatstroke victims. If GWMD provides an early, sensitive measure of brain injury, it will be a powerful prognostic indicator of outcome for heatstroke patients. EHS is often associated with rhabdomyolysis, which is a form of skeletal muscle injury caused by the leakage of muscle cell contents into the circulation or extracellular fluid. Myoglobin released from damaged muscle cells is filtered and metabolized by the kidneys. When severe muscle damage occurs, the renal *References 48, 140, 192, 281, 282, 284, 299.

15 min

30 min

45 min

60 min

FIGURE 10-8  Effect of heating on villus structure. Representative light micrographs of rat small intestinal tissue over a 60-minute course  at 41.5° to 42° C (106.7° to 107.6° F). Note the generally normalappearing villi at 15 minutes (slight subepithelial space at the villous tips), compared with initial sloughing of epithelia from villous tips at 30 minutes, massive lifting of epithelial lining at top and sides of villi at 45 minutes, and completely denuded villi at 60 minutes. Bars represent 100 µm. (From Lambert GP, Gisolfi CV, Berg DJ, et al: Selected contribution: Hyperthermia-induced intestinal permeability and the role of oxidative and nitrosative stress, J Appl Physiol 92:1750, 2002, with permission.)

225

CHAPTER 10  Pathophysiology of Heat-Related Illnesses

BOX 10-2  Predisposing Risk Factors for Serious Heat

PART 2  COLD AND HEAT

threshold for filtration of myoglobin is exceeded, and this protein appears in the urine in a reddish brown color.86 Myoglobin is toxic to nephrons and causes overproduction of uric acid, which precipitates in the kidney tubules to cause acute renal failure, coagulopathy, and death if not rapidly detected and treated.11,86,185,242,323 Not all cases of rhabdomyolysis are associated with myoglobinuria; many patients can be asymptomatic. Clinical markers of rhabdomyolysis include elevated myoglobin, CK, aldolase, lactate dehydrogenase, ALT, and AST, which are influenced by a variety of factors (type, intensity, and duration of exercise; gender; temperature; altitude) and released by more than one organ or tissue.50,205,263 If a clinical diagnosis of rhabdomyolysis is confirmed, immediate medical attention is imperative because approximately 50% mortality rates from acute renal failure have been documented for this condition. Liver failure is one of the most common causes of morbidity and mortality in patients during the later stages of recovery. The time course of liver damage differs from that of the other organs and often does not peak until approximately 24 to 48 hours after heat exposure. For example, liver damage consisting of centrilobular degeneration and necrosis with parenchymal damage was only evident in EHS patients that survived more than 30 hours.192 In addition, enhanced breakdown of fat or an inability of the mitochondria to use fat results in heatstroke-associated fatty liver changes.43 Disturbances in plasma glucose homeostasis are a sign of liver damage that may cause hyperglycemia or hypoglycemia as a result of dysfunction of phosphoenolpyruvate carboxykinase, which is a regulatory enzyme of the liver’s gluconeogenic pathway.21,171,172 Liver dysfunction may also contribute to increased circulating endotoxin levels because of the important bacterialclearance function of this organ.30,225 Unfortunately, many heatstroke patients require liver transplantation. Use of antipyretic drugs, such as acetaminophen (Tylenol), has been associated with hepatic failure.93,113,114,269,319 Many patients are released from the hospital following several days or weeks of treatment and continue to experience organ dysfunction during the ensuing years of recovery. Following the 2003 heat wave in France, mortality rates increased from 58% at day 28 of hospitalization (mean hospital stay was 24 days) to 71% mortality by the second year of recovery.6 An epidemiologic study of military EHS patients showed an approximately twofold increased risk for death from cardiovascular, kidney, and liver disease within 30 years of hospitalization.321 Several of the clinical responses (hyperthermia, dehydration, kidney and liver damage) occurring during progression or shortly after heatstroke collapse are clinically recognized and treated. However, those occurring during the months and years following hospitalization are underreported. The mechanisms responsible for long-term decrements in organ function remain poorly understood.

of cytokine neutralization in altering heatstroke mortality in animal models. Peripheral injection of IL-1β, IL-2, IL-6, IL-10, TNF-α, and platelet-activating factor into experimental animals replicates the pathophysiologic responses observed in heatstroke, including hyperthermia, hypothermia, fever, increased vascular permeability, DIC, and death.* Simultaneous injection of multiple cytokines (e.g., IL-1 and TNF) is most effective in mimicking heatstroke symptoms and has shed light on cytokine interactions in vivo that orchestrate SIRS. Increased circulating levels of IL-1α, IL-1β, IL-1 receptor antagonist (IL-1ra, a naturally occurring antagonist of IL-1), IL-6, soluble IL-6 receptor (sIL-6R), IL-8, IL-10, IL-12, IFN-γ, TNF-α, and soluble TNF receptor (sTNFR) concentrations are commonly observed at the time of heatstroke collapse or shortly after cooling.† Sustained high IL-6 levels during cooling correlate with heatstroke severity, tissue injury, and death, whereas high circulating IL-8 levels are implicated in leukocyte activation and coagulation in EHS patients.23,125 The reciprocal regulation of IL-12 and IL-10 production suggests complex interactions in heat-induced SIRS, but the function of these cytokines has not been clearly delineated. As previously mentioned, high IFN-inducible gene expression and IFN-γ levels are clinical measures of viral or intracellular bacterial infection and are evident in EHS patients with preexisting infections.289 The failure of clinical and animal studies to correlate cytokine production with specific heatstroke responses is probably caused by the short half-lives of these proteins, local tissue concentrations exceeding those in the circulation, or the presence of soluble cytokine receptors that mask detection or alter cytokine action(s).‡ For example, the sTNFR inhibits the actions of TNF and is often higher in heatstroke survivors than nonsurvivors, suggesting that TNF may mediate lethality.109 On the other hand, the sIL-6R may potentiate endogenous IL-6 effects by increasing the concentration of available IL-6 signaling receptors on cell membranes (known as a trans-signaling effect) or reduce IL-6 signaling through competitive binding with IL-6 receptors that are already present on the cell membrane (Figure 10-9). Although cytokines are known to interact with one another, their soluble receptors, and other endogenous stress hormones (e.g., glucocorticoids) during SIRS, it remains unknown how these interactions in vivo affect heatstroke outcome. Taken together, results from the few antagonism/neutralization studies that have been conducted to date indicate that high levels of cytokines may be detrimental for heatstroke recovery, but baseline (permissive) actions of some cytokines (e.g., IL-6, TNF, or proteins affected by their actions) appear to be essential for survival.170 Clearly, more research is required in this area to determine the multitude of cytokine actions in heat-induced SIRS and determine the protective versus detrimental effects of the proteins on multiorgan system function.

CYTOKINES

HEAT SHOCK PROTEINS

Cytokines are a class of intercellular protein messengers released from macrophages, T and B cells, endothelial cells, astrocytes, and other cell types that mediate inflammatory reactions to disease and injury.46,141,195,280,309 Cytokine-inducing stimuli include bacterial and viral infection,65,243 psychological stress,191,234 heat stress,* wholebody hyperthermia,222 and exercise.38,209,224,298 The defining characteristics of cytokines include a lack of constitutive production, the ability to regulate each other’s production, and overlapping actions that depend on the target cell type and cytokine milieu in which they function. Cytokines act over short distances and time spans (half-life is generally less than 60 minutes) and are usually present at low concentrations in the circulation. Cytokines bind reversibly to high-affinity cell-surface receptors and stimulate intracellular signaling pathways (e.g., NF-κB) that alter the transcription of genes involved in immune responses. There are several lines of evidence that link cytokines with symptoms of heat-induced SIRS. These include induction of heatstroke symptoms by cytokine injection in experimental animal models, association of increased circulating cytokine levels with heatstroke morbidity/mortality, and effectiveness

Heat shock proteins (HSPs) are molecular chaperones that prevent misfolding and aggregation of cellular proteins during exposure to stressful stimuli.76,111,134,184 HSPs are found in organisms ranging from bacteria to humans. Their chaperoning activities protect against environmental (heavy metals, heat stress), physiologic (cell differentiation, protein translation), and pathologic (infections, ischemia/reperfusion) stimuli that cause cellular damage.134,160,184 HSPs were originally discovered in Drosophila melanogaster, when puffs associated with novel protein synthesis appeared on the giant chromosomes of the salivary glands in response to heat stress.259,303 It was later discovered that heat denaturation of mature proteins inside the cell was the cellular signal that increased protein synthesis in response to heat stress in Drosophila.120 HSPs are grouped into families according to their molecular mass, cellular localization, and function (Table 10-4). HSP 27 (also referred to as sHSP) is a constitutively expressed cytosolic and nuclear protein with cytoskeletal stabilization and

*References 20, 27, 36, 116, 172, 181.

226

*References 154, 162, 168, 169, 235, 237, 277, 306. † References 20, 26, 27, 109, 112, 172. ‡ References 2, 20, 23, 26, 109, 112, 159, 275.

IL-6

sIL-6R IL-6 IL-6R

IL-6 gp130

gp130

sIL-6R

Signal

Classic signaling

antiapoptotic functions.7,167,241 HSP 60 exists in the mitochondria and cytosol, is released from PBMCs on LPS stimulation, and functions as a “danger” signal for the innate immune system. HSPs interact with PAMPs, such as TLRs, to stimulate monocytes, macrophages, and dendritic cells to produce cytokines.35,226 The HSP 70 family has been extensively studied for protective function(s) against thermal stress,142,340 ischemia/ reperfusion,196,248,293 tissue injury,33 glucose deprivation,334 and sepsis.166,317 HSP 70s function in concert with other molecular chaperones, such as HSP 90 and HSP 110, to facilitate LPS and antitumor responses.127 HSP gene expression is mediated primarily at the level of gene transcription by a family of heat shock transcription factors (HSFs) that interact with the heat shock regulatory element (HSE) in the promoter region of genes. HSF-1 is the major stress responsive element in mammalian cells that is activated by febrile-range temperatures.318,338 HSF-1 interacts with HSEs on cytokine genes to alter transcription and confer protection against endotoxin and TABLE 10-4  Heat Shock Protein Structure and

Function

Family

Function

Attributes

HSP 27 (sHSP)

Antiapoptotic

Constitutively expressed Cytosolic and nuclear Mitochondria and cytosol

HSP 60

Cytoskeletal stabilization Protein refolding Prevents aggregation of denatured proteins Immune responses

HSP 70 family   HSP 72   HSP 73 (HSC 70)

Thermotolerance Molecular chaperone

  HSP 75   HSP 78 (GRP 79, Bip)

Molecular chaperone Cytoprotection

HSP 90 family: HSP 90   GRP 96

HSP 110/104

Glucocorticoid receptor functioning Glucose regulation Molecular chaperone Tumor antigen presentation

Highly inducible Constitutively expressed Mitochondrial Endoplasmic reticulum Cytosolic and nuclear Endoplasmic reticulum Cytosolic

Data from Hartl FU, Hayer-Hartl M: Molecular chaperones in the cytosol: From nascent chain to folded protein, Science 295:1852, 2002; and Kregel KC: Heat shock proteins: Modifying factors in physiological stress responses and acquired thermotolerance, J Appl Physiol 92:2177, 2002. Bip, Binding protein; GRP, glucose regulated protein-78; HSC, heat shock cognate; HSP, heat shock protein.

gp130

Signal

Trans-signaling

other infectious/inflammatory stimuli. In gene-transfected human PBMCs, inhibition of TNF-α, IL-1β, IL-10, and IL-12 in response to LPS was specific to HSPs 70 overexpression.59 A lack of effect of HSP 70 on IL-6 gene transcription may be an indirect mechanism of protection, because IL-6 functions in a regulatory feedback loop to inhibit IL-1 and TNF production, which are Th1 cytokines with potent proinflammatory activities.59,71,73,325 In murine macrophages, HSP 70 inhibited IL-12 (Th1) and stimulated IL-10 (Th2) production in response to LPS.325 The shift from Th1 to Th2 cytokine production may be a mechanism by which HSP 70 protects against bacterial infection. Heat strain is a consequence of the time and intensity of heat exposure. These factors interact in vivo to influence the magnitude and kinetics of HSP expression. In human PBMCs, maximal expression of intracellular HSPs 70 was observed between 4 and 6 hours after a brief heat shock (43° C [109.4° F] for 20 minutes).288 Increased expression of HSPs 10, 20, 40, 60, 70, 90, and 110 was observed in PBMCs from EHS patients or following exposure to hypoxia in vitro.287,289 Anatomic differences in the magnitude and kinetics of in vivo expression have also been observed, with HSP 70 expression occurring within 1 hour in the brain, lungs, and skin and delayed until 6 hours after heat exposure in the liver of rats.18 In mice, liver expression of HSP 70 showed a progressive increase from approximately 6 to 24 hours following collapse from passive heatstroke.171 In rats, a high rate of passive heating (0.175° C [0.315° F]/min) induced greater HSP 70 expression in the liver, small intestine, and kidneys than did a lower rate of heating (0.05° C [0.09° F]/min), despite attaining the same maximum body temperature (42° C [107.6° F]).80 Differences in tissue blood flow and metabolic activity likely account for regional differences in HSP expression during passive and exertional heat exposure. Thermotolerance is the term used to describe the noninheritable, transient resistance to a lethal heat stress that is acquired following previous exposure to a nonlethal level of heat stress. Increased HSP 70 expression is a mechanism of thermotolerance that protects against heat-induced increases in epithelial permeability. A unique in vitro model system consisting of highresistance Madin-Darby canine kidney (MDCK) epithelial cell monolayers was developed to examine the relationship between HSP 70 expression and changes in epithelial integrity with heat exposure. Following heat stress to 38.3° C (100.9° F), MDCK monolayers showed an increase in permeability that was reversible with cooling.212 If the monolayers were preexposed to a conditioning heat stress of 42° C (107.6° F) for 90 minutes, subsequent exposure to a higher temperature of 39.4° C (102.9° F) was required to increase monolayer permeability.21 The association of a thermotolerant state with increased HSP 70 expression suggests that HSPs shift the temperature threshold upward to prevent heat-induced disruptions in epithelial permeability.212 Follow-up studies showed that HSPs interact with proteins in the tight junctions of the epithelium to regulate permeability. Occludin is a plasma-membrane protein located at tight junctions that was increased, along with HSPs 27, 40, 70, and 90, in intestinal 227

CHAPTER 10  Pathophysiology of Heat-Related Illnesses

FIGURE 10-9  IL-6 receptor signaling pathways. Classic signaling involves binding of IL-6 to the membrane bound IL-6 receptor (IL-6R), which stimulates an interaction between the IL-6:IL-6R complex and the membrane-bound glycoprotein 130 (gp130) to initiate intracellular signaling. Trans-signaling occurs when the extracellular domain of the membrane-bound IL-6R is proteolytically cleaved, leading to generation of the soluble IL-6R (sIL-6R) that binds IL-6. The IL-6:sIL-6R complex can stimulate cells that only express gp130 (i.e., do not normally possess the transmembrane IL-6R) to transmit an intracellular signal. Cells that express gp130 only would not be able to respond to IL-6 in the absence of sIL-6R.

PART 2  COLD AND HEAT

epithelial monolayer (Caco-2) cells exposed to 39° or 41° C (102.2° or 105.8° F).60 Treatment of Caco-2 cells with quercetin (an inhibitor of HSF-1) inhibited HSPs and occludin expression and reversed the thermotolerant state of these cells.60 These studies demonstrate a complex interaction between HSPs and tight-junction proteins for modulation of epithelial barrier function during thermal stress. It is interesting to speculate that differences in HSP expression profiles may be a sensitive marker of heat stress susceptibility among different populations. During the life of an organism, there is an accumulation of protein damage caused by continual oxidant and free radical activity within cells. The lifespan of Drosophila was extended by heat shock treatment or the addition of HSP 70 gene copies, suggesting that increased protein chaperonin activity may protect against aging.148,301 In rats, aging was associated with a significant reduction in liver HSP expression following passive heat exposure, which was associated with greater liver damage compared with that observed in young rats.161,342 Older animals do not appear to have a global inability to express HSP, because exertional heat stress can induce expression profiles similar to those of mature rats.161 Rather, aging is associated with a reduction in the threshold for HSP stimulation.161 Similarly, Fargnoli and co-workers74 showed that global reduction in protein synthesis was not responsible for decreased HSP induction in aged lung fibroblasts. Alzheimer’s disease is thought to be a consequence of decreased HSP function that results in increased deposition of abnormally folded proteins.211 It is anticipated that screening for altered HSP titers will help to identify individuals with reduced thermotolerance caused by aging, infection, or other conditions that may predispose to heatstroke.150

Heatstroke Treatments (See Chapter 11) Current heatstroke therapies fall into two categories: supportive therapies directed at the immediate clinical symptoms and therapies directed at the causative mechanisms of injury. The primary objectives of clinical heatstroke treatments are to reduce body temperature as rapidly as possible, reestablish normal CNS function, and stabilize peripheral multiorgan system function. Supportive therapies consist of rapid cooling and IV fluid administration for restoration of normal blood pressure and tissue perfusion, whereas advanced therapies are directed at the coagulation and inflammatory disturbances that cause organ failure. Despite these efforts, heatstroke morbidity and mortality rates remain quite high, and multiorgan system dysfunction continues to claim the lives of heatstroke victims during ensuing years of recovery.6,321 This section discusses conventional clinical treatments of heatstroke, as well as innovative treatment strategies targeted at SIRS to mitigate injury and death.

possibility of peripheral vasoconstriction with cooling, the skin may be massaged to stimulate increases in cutaneous blood flow. Regardless of the treatment strategy, current medical doctrine dictates that heatstroke patients are cooled as rapidly as possible until normal CNS function is reestablished. Dantrolene and nonsteroidal antiinflammatory drugs (NSAIDs) have been tested for their effects on body cooling, but neither class of drugs has shown efficacy for protection against heatstroke. Dantrolene is a calcium-lowering agent that protects against hyperthermia by lowering intracellular calcium concentrations in skeletal muscle to decrease muscle tone. Dantrolene is effective for the treatment of malignant hyperthermia (MH), which is a genetic mutation that predisposes to involuntary muscle contractions and rigidity following exposure to general anesthetics or muscle-depolarizing agents. Dantrolene has been considered as a treatment for heatstroke, but animal and human heatstroke studies have failed to validate its use for this condition. In a study of heatstroke patients, dantrolene decreased the required cooling time by approximately 20 minutes but had no effect on recovery. Similarly, a randomized, double-blind, placebo-controlled trial of Hajj heatstroke patients failed to show a cooling advantage of dantrolene over traditional cooling methods.22,43 MH is distinct from exertional or passive heatstroke, so it is not surprising that this drug does not protect equally against these diverse conditions. (MH is discussed in detail later in this chapter.) NSAIDs have been considered as therapeutics based on their potent antiinflammatory and antipyretic effects. The action(s) of classic NSAIDs, such as, aspirin, ibuprofen, and acetaminophen, are attributed primarily to blockade of the cyclooxygenase (COX) pathway of eicosanoid metabolism (Figure 10-10). Prostaglandins are synthesized by the COX pathway in response to a variety of stimuli (e.g., bacterial infection, heat shock) and regulate a multitude of physiologic responses, including fever, inflammation, and cytokine production. During fever, prostaglandins are released in response to proinflammatory cytokines (e.g., IL-1, IL-6) and stimulate an increase in the temperature set point to induce fever.292 Inhibition of prostaglandin production by NSAIDs is the primary mechanism for the antipyretic (i.e., fever-reducing) actions of these drugs. However, hyperthermia in response to heat exposure is not caused by an increase in the temperature set point but by an unregulated increase in body temperature that occurs when heat gain exceeds heat loss in an absence of a change in the temperature set point. Rather than providing a beneficial effect, NSAIDs are contraindicated as a treatment for heatstroke because of the potential toxic effects of these drugs on liver function and a lack of clinical and/or experimental data to support their use. For example, pretreatment with sodium salicylate was without effect on skin

COOLING Rapid cooling is considered the single most important treatment for protection against permanent CNS damage and death from heatstroke. To facilitate cooling, the individual should be placed into a supine position and as many clothes as possible removed to expose a large surface area of the body to facilitate heat transfer. If the individual is comatose, he or she should be placed onto his or her side to ensure an open airway. Conventional methods of cooling include cold or ice water immersion, packing ice around the body, sponging with (or without) fanning, or use of a hypothermia blanket. The goal of all cooling methods is to rapidly decrease and maintain body temperature below 39° C (102.2° F) and to prevent rebound hyperthermia. The use of an ice bath or ice packs on the skin surface has met with some resistance because it is thought that cooling of the skin will elicit peripheral vasoconstriction and shivering, which can increase heat production and counteract the cooling effect. This was shown in an experimental study in which young, fit test subjects were heat stressed to 40° C (104° F) and experienced shivering and cold sensations during immersion in cold water.339 Because the threshold for activation of shivering is increased in heatstroke patients, the risk for cold or ice water immersion eliciting such a response and compromising the benefits of cooling is unlikely. However, to minimize the 228

Cell membrane NSAIDs Acetaminophen Salicylic acid Ibuprofen

Liver toxicity

Phospholipids PLA2

Arachidonic acid (AA)

COX Prostaglandins Thromboxanes Fever Platelet aggregation Vasomotor changes Inhibit IL-1, IL-2

LOX Leukotrienes Leukocyte aggregation Vascular permeability Induce IFNγ, IL-1, IL-2

FIGURE 10-10  Eicosanoid metabolism is initiated when cell membrane phospholipids are converted to arachidonic acid (AA) by the enzymatic actions of phospholipase A2 (PLA2). Cyclooxygenase (COX) converts AA to prostaglandins and thromboxanes, whereas the lipooxygenase (LOX) pathway is responsible for the production of leukotrienes. Nonsteroidal antiinflammatory drugs (NSAIDs) block the action of COX enzymes with potential toxic effects on the liver. IFNγ, Interferon-γ; IL-1, interleukin-1; IL-2, interleukin-2.

FLUID RESUSCITATION (See Chapter 70) One of the first lines of defense against permanent tissue damage is treatment with resuscitation fluids. The objective of IV fluid administration is to restore intravascular volume and rehydrate the interstitium to stabilize cardiovascular functioning, improve tissue perfusion, and maintain immune function. The resuscitation fluid needs to be safe, efficacious, inexpensive, easy to transport for use in military or athletic settings, and have the capability to restore tissue oxygen perfusion and minimize cellular/tissue injury. Blood provides oxygen-carrying capacity and volume, but supply is limited and there is a risk for allergic or infectious reactions, difficulties with crossmatching, and potential for high hemoglobin levels to increase blood viscosity and reduce nutrient flow to the tissues.255,258 Balanced salt solutions, such as saline and lactated Ringer’s, have a long shelf life and are inexpensive and in unlimited supply with a minimal risk for disease transmission. However, they are able to freely cross semipermeable capillary membranes, which increases the risk for tissue edema and makes frequent transfusions necessary to maintain adequate plasma volume.110,145,304 Tissue edema increases the distance from blood vessels to tissue mitochondria and limits oxygen delivery to the tissues. There is a greater risk for edema in heatstroke patients because of increases in capillary permeability and lack of muscle movement that limits the flow of lymph following collapse. To minimize the adverse consequences of balanced salt solutions, these fluids may be replaced with colloid solutions. Natural colloids, such as albumin, possess antioxidant properties that reduce tissue injury during times of oxidant stress but carry a risk for infection.84,328 Dextran is an artificial colloid that was in use after World War II until adverse hemostatic effects restricted its use to specific clinical conditions, such as deep vein thrombosis and pulmonary embolism.15,55 Hydroxyethyl starch (HES) is a blood plasma substitute that exerts high colloidal pressure to stimulate movement of fluid from the interstitial space into the blood vessel lumen for plasma volume expansion.239,336,344 Smallvolume treatment with HES protected against heatstroke mortality in rats, but use of HES in other heatstroke animal models and humans has not been validated.187 Because of severe dehydration and acute renal failure with heatstroke, fluid shifts from the interstitial fluid into the vessel lumen may mean HES will not be well tolerated in severe heatstroke patients.

ANTICOAGULANTS Anticoagulants (e.g., heparin, aspirin) have been examined for heatstroke protection, with mixed results. Heparin therapy has been associated with positive heatstroke outcome in patients, although it is difficult to dissociate the direct effects of this therapy from other clinical treatments.245,290 The mechanisms of heat-induced DIC may include prostaglandin synthesis, because aspirin has shown protection against platelet hyperaggregation in vitro and in animal models. In human volunteers, ingestion of aspirin 12 to15 hours before blood sampling or heat exposure of cells was effective in inhibiting platelet hyperaggregation.87 However, aspirin was ineffective if provided after heat exposure, even though complete inhibition of the arachidonic acid pathway was achieved.87 The ability of aspirin to protect guinea pigs from DIC induced by Staphylococcus aureus suggests that similar activities function in vivo to control platelet reactivity.227 However,

there is currently insufficient evidence to support the use of aspirin as a preventive measure in heatstroke patients. Given the hormonal and metabolic alterations that accompany heatstroke, including dehydration, increased catecholamine levels, hypoxia, and others, the mechanisms responsible for DIC extend beyond those mediated by prostaglandins alone. Furthermore, aspirin and other antiinflammatory drugs can cause liver damage if consumed in large quantities, as previously mentioned. Recombinant APC is an effective antiinflammatory drug for the treatment of sepsis and may also hold promise as a treatment for heatstroke patients. APC efficacy appears to depend on a variety of patient conditions, including age (most effective in patients over 50 years of age), extent of organ dysfunction (benefit not apparent if failure of only one organ), and the presence of shock at the time of infusion, which improves its efficacy.327 In rat heatstroke models, the efficacy of APC depends on the time of treatment. A single dose of recombinant human APC provided at the onset of heatstroke inhibited inflammation and coagulopathy, prevented organ failure, and improved survival; however, if treatment was delayed for 40 minutes following the onset of heatstroke, there was no beneficial effect on survival time.45 The efficacy of APC was less obvious in a baboon heatstroke model. Infusion for 12 hours following heatstroke onset attenuated plasma IL-6, thrombomodulin, and procoagulant components but had no effect on mortality.25 APC is the first biologic agent approved in the United States for the treatment of severe sepsis on account of two decades of research in this area,327 but there is insufficient evidence to justify the use of this treatment in heatstroke patients.

ANTICYTOKINE THERAPIES As previously described, attenuations in splanchnic blood flow during heatstroke contribute to increased gut permeability and a rise in circulating endotoxin. This series of events is hypothesized to stimulate elevations in plasma cytokine levels that have been implicated in the adverse consequences of SIRS. Based on these findings, the question arises: Do anticytokine therapies represent an efficacious treatment strategy for heatstroke? There have been no controlled studies examining the efficacy of anticytokine therapies on patient outcome with heatstroke. However, clinical sepsis trials indicate that potential protective effects of anticytokine therapies need to be viewed with cautious optimism. Sepsis patients display high circulating IL-1 levels that correlate with morbidity and mortality, but IL-1ra treatment has been unsuccessful in reducing mortality.236,253 A comparison of 12 randomized, double-blind multicenter trials of more than 6200 sepsis patients showed no significant benefit of antiendotoxin antibodies, ibuprofen, plasminogen-activating factor receptor antagonist, anti-TNF monoclonal antibody, or IL-1ra on all-cause mortality.57 There are several explanations for negative results from anticytokine therapies, including the possibility that the mediator has no pathophysiologic role in the response, the agent failed to neutralize the protein (because of a lack of biologic activity, competition by other mediators, inadequate anatomic distribution), compensatory increase of other mediator(s) with similar activities, administration too early or late in the course of disease, too-short therapy duration, or the need for combination therapy.198 Kinetic studies have shown the half-life of IL-1ra to be approx­ imately 20 minutes, and phase III clinical trials showed that circulating IL-1β levels at the time of clinical treatment were undetectable in 95% of the patient population.77,246 Exposure to anticytokine therapies before sepsis onset is thought to be desirable (but practically infeasible), although this may suppress shifts in Th1/Th2 immune responses that are important for the resolution of infection. On the other hand, anticytokine therapies given too late in sepsis progression may shift the Th1/Th2 milieu in an unpredictable manner or have no effect because of the overwhelming nature of the septic event.100 The transient nature of cytokine production and/or clearance and lack of correlation between serum levels and disease severity further complicate treatment scenarios. Given the short half-life of TNF-α (approximately 6 to 7 minutes)16 and biphasic clearance patterns of IL-1β and IL-6 (rapid disappearance in the first 3 minutes followed by an attenuated clearance over the next 1 to 4 hours),152 the narrow 229

CHAPTER 10  Pathophysiology of Heat-Related Illnesses

temperature and pulse rate but significantly increased the rate of body temperature rise and potentiated hyperthermia in men walking in a hot environment.135 As previously mentioned, the use of antipyretic drugs, such as acetaminophen, has been anecdotally associated with the need for liver transplantation.93,113,114,269,319 Recurrent hyperthermia is a common heatstroke recovery response that is thought to be a true fever and a prostaglandinmediated response to endotoxin leakage and cytokine stimulation. Whether the effects of NSAIDs on cytokine expression or body temperature will protect or exacerbate heatstroke sequelae in vivo is unknown but is an important area of investigation, given the high use of NSAIDs as over-the-counter medications for pain and/or fever relief in our society.

PART 2  COLD AND HEAT

protective window in which anticytokine therapies may be effective is a difficult obstacle to overcome. Interleukin-10 is a potent antiinflammatory cytokine that suppresses production of several proinflammatory cytokines, including IL-1β, IL-6, and TNF-α, and is an important negative feedback loop during infection/disease.101,311 Few, if any, studies have investigated the efficacy of IL-10 treatment for heatstroke recovery, although the cytokine has been commonly used in the treatment of multiple autoimmune diseases, including rheumatoid arthritis, Crohn’s disease, multiple sclerosis, and sepsis.31,229 As with other cytokines, the timing of IL-10 administration must be carefully considered. IL-10 decreases IFN-γ production by natural killer and Th1 cells, which may suppress the clearance of infectious organisms (via IFN-γ).254,320 Consistent with anticytokine therapies, beneficial effects of exogenous IL-10 administration depend on multiple factors, including time of administration, route, and the site to which the cytokine is targeted.229,265 These considerations, along with the immune suppressive and unpredictable nature of IL-10–based therapies, have resulted in diminished enthusiasm for anticytokine therapies for sepsis.

Heatstroke Prevention Heatstroke is currently a more preventable than treatable disease. The most effective preventive measures include acclimatization to the heat, reductions in the duration and extent of physical activity, rescheduling of activities to cooler times of the day, increased consumption of nonalcoholic fluids, and removing vulnerable populations, such as those with preexisting viral or bacterial infections, from the heat stress environment. Fan cooling has not shown protection against heatstroke and is associated with increased thermal discomfort at temperatures higher than 38° C (100.4° F).149

HEAT ACCLIMATIZATION Climatic heat stress and exercise interact synergistically to increase body temperature (core and skin) and cardiovascular strain and to decrease performance in the heat. Heat acclimatization is the within-lifetime changes in an organism (as opposed to evolutionary changes) that protect against these negative effects of heat strain. Heat acclimatization occurs following exposure to the natural environment, whereas heat acclimation develops following exposure to artificial conditions. However, these terms are used interchangeably because they induce similar physiologic adaptations.331 Heat acclimation occurs following repeated bouts of heat exposure that are of sufficient intensity, frequency, duration, and number to elevate core and skin temperature and induce profuse sweating. Heat acclimation may be achieved following exercise or rest in the heat, although the former method is more effective. It is important to note that heat acclimatization is specific to the climate and activity level; therefore, if individuals will be working in a hot, humid climate, heat acclimatization should be conducted under similar conditions (Box 10-3). Although heat acclimation does not require daily exposure to heat and exercise, the rapidity with which biological adaptations are achieved is slower with less frequent exposures. This was shown experimentally in human volunteers in whom heat acclimation was achieved following 10 days of daily heat exposure but required 27 days when the frequency of exposure was reduced to every third day of experimentation (conditions 47° C [116.6° F], 17% relative humidity).74 Continual 24-hour exposures are also not required, because daily 100-minute periods of exposure were adequate to produce heat acclimation in subjects exposed to dry heat.183 However, because of the transient nature of the biologic adaptations, continued heat exposures are required to maintain the acclimated state. Aerobically trained athletes retain heat acclimation benefits longer than do unfit individuals, because they are exposed to high body temperatures during training exercises.240 Improvements in thermal comfort and exercise performance are achieved in heat-acclimated individuals through a variety of physiologic mechanisms, including a lower threshold and higher rate of skin blood flow, reduction in metabolic rate, earlier onset 230

BOX 10-3  Heat Acclimation Strategies Must Mimic Climate of Athletic Event or Occupational Setting and Include Adequate Heat Stress • Heat must be sufficient to cause heavy sweating • Use exercise/rest cycles to intensify or diminish the effect of the heat stress on bodily functions • Include at least 6 to 14 days of adequate heat stress. • Exercise daily for at least 90 minutes Start With Acclimation and Exercise Training • Be flexible in scheduling training • Build confidence • Performance benefits may take longer to achieve than physiologic benefits Methods of Heat Acclimation • Use a climate-controlled room (sauna or heat chamber) or hot weather • Incorporate training by including additional acclimation sessions Days Leading to Athletic Performance or Event • Start slowly, and decrease training duration and intensity; limit heat exposure • Acclimatize in heat of the day • Train in coolest part of the day • Use appropriate work/rest cycles • Be vigilant of salt and fluid needs, especially during the first week of acclimation

and rate of sweating, and improvements in cardiovascular function and fluid balance.271 Figure 10-11, online illustrates the effect of 10 days of heat acclimation on heart rate, core temperature, and mean skin temperature responses of subjects walking on a treadmill in a desert type of environment.70 On the 10th day of acclimation, heart rate was lower by approximately 40 beats/min, and rectal and skin temperatures were reduced approximately 1° C (1.8° F) and 1.5° C (2.7° F), respectively (see Figure 10-11, online).69 Once heat acclimation is achieved, skin vasodilation and sweating are initiated at a lower core temperature threshold, and higher sweat rates can be sustained without the sweat glands becoming “fatigued.”52,81 Whereas an unacclimated individual will secrete sweat with a sodium concentration of approximately 60 mEq/L (or higher), the concentration of secreted sodium from the sweat glands of an acclimated individual is significantly lower at approximately 5 mEq/L.262 This effect of heat acclimation on salt conservation is thought to be caused by increased aldosterone secretion or responsiveness of the sweat glands to this steroid hormone, which is released by the adrenal cortex and increases the resorption of ions and water in the distal tubules and collecting ducts of the kidneys.82,151 Overall improvements in fluid balance with heat acclimation include reduced sweat sodium losses, a better matching of thirst to body water needs, and increased total body water and blood volume.190,270 Provided that fluids are not restricted during physical activities, heat-acclimated individuals will be better able to maintain hydration during exercise and showed a marked reduction in “voluntary” dehydration.13,69,271 Although there is controversy regarding the ability of heat acclimation to alter the maximum temperature that can be tolerated during exercise in the heat,223 individuals who live or train in hot environments may experience reduced incidence of syncope (Figure 10-12).13,96,247 An essential cellular adaptation of heat acclimation is altered expression or reprogramming of genes that encode constitutive and stress-inducible proteins.122 Heat acclimation is associated with down regulation of genes associated with energy metabolism, food intake, mitochondrial energy metabolism, and cellular maintenance processes and upregulation of genes that are linked with immune responsiveness.122 The HSPs are the most extensively studied heat-inducible proteins and show faster

Subjects experiencing syncope

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MALIGNANT HYPERTHERMIA 1

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Days of heat acclimation FIGURE 10-12  Incidence of syncope among 45 subjects who lived in and trained at cool ambient temperatures and could complete a physical training regimen without mishap. Then they were relocated to a hot environment where they carried out the same physical training regimen. (Modified from Bean WB, Eichna LW: Performance in relation to environmental temperature: Reactions of normal young men to stimulated desert environment, Fed Proc 2:144, 1943; and Hubbard RW, Armstrong LE: The heat illness: Biochemical, ultrastructural, and fluid-electrolyte considerations. In Pandolf KB, Sawka MN, Gonzalez RR, editors: Human performance and environmental medicine at terrestrial extremes, Indianapolis, 1988, Benchmark Press, pp 305-359.)

transcriptional response and elevated cellular reserves (HSP 72 specifically) in heat-acclimated versus nonacclimated individuals.122,123,193,200 That is, whereas nonacclimated individuals require de novo HSP 72 synthesis for cellular protection, individuals who reside in hot climates maintain elevated HSP 72 levels.190 The cellular mechanisms of heat acclimation are not fully understood but are thought to involve global and tissue-specific changes in genes involved in thermal responsiveness, DNA repair and synthesis, free radical scavenging, and apoptosis.122

Genetic Polymorphisms Heatstroke susceptibility is influenced by complex interactions between environmental and host genetic factors. Emerging molecular technologies have improved our understanding of the genetic mutations and polymorphisms that may predispose to heat illness or inhibit resolution of SIRS. It is anticipated that the ability to prescreen individuals for genetic polymorphisms that may prevent resolution of SIRS will help in developing more effective therapies to alleviate morbidity/mortality in these individuals.

SINGLE NUCLEOTIDE POLYMORPHISMS Single nucleotide polymorphisms (SNPs) are variations in the nucleotide sequence of DNA that can affect physiologic responses to environmental stimuli. SNPs have been implicated in a variety of diseases, including sepsis, type 1 diabetes, arthritis, inflammatory bowel disease, and rheumatic fever.79,136,250,296 The

MH is a genetic disorder that causes muscle rigidity, hyperthermia, tachycardia, and metabolic acidosis during exposure to volatile anesthetics or depolarizing skeletal muscle relaxants. Exercise, heat stress, and emotional stress also trigger reactions in approximately 5% to 10% of MH patients.58,326 MH reactions are a result of a massive release of calcium from the type 1 ryanodine receptor (RyR1) of the sarcoplasmic reticulum, which overwhelms cellular mechanisms of calcium homeostasis and activates actin–myosin filaments to cause muscle rigidity and hyperthermia.238 RyR1 is the most common mutation in skeletal muscle, but additional isoforms have been identified in B and T cells, thalamus, hippocampus, and heart.163,202,300 Activation of the RyR1 by a variety of pharmacologic compounds, including caffeine, halothane, and the muscle relaxant 4-chloro-m-cresol, has led to the development of an in vitro contracture test of skeletal muscle biopsies to identify MH individuals.266,345 Dantrolene is used to treat MH reactions by lowering intracellular calcium stores, decreasing muscle metabolic activity, and preventing hyperthermia. The use of dantrolene, in combination with improved monitoring standards and early detection using the in vitro contracture test, has helped to reduce mortality rates from greater than 70% to less than 5% in MH patients.186 MH has been identified in several animal species, including dogs,231 boars,278 cats,14 and horses,3 but the most common experimental animal is a porcine MH model that possesses a single mutation in the skeletal muscle RyR1 gene. These animals develop the MH syndrome in response to inhalational anesthetics, exercise, heat, and other stressors.314 Mild exercise exacerbates MH symptoms in response to anesthetics in MH pigs, suggesting that inflammatory mediators released by skeletal muscle may contribute to the MH syndrome.314 MH patients show an approximately fivefold higher expression of IL-1β when stimulated with caffeine and 4-chloro-m-cresol compared with control cells.94 Recent development of a transgenic mouse model that overexpresses the RyR1 receptor has proved useful to study the MH/EHS link and could shed light on the role played in this syndrome by inflammatory cytokine production from skeletal muscle or other organs.69 Association of RyR1 mutations with EHS incidence suggests that screening young, healthy individuals (e.g., athletes, military personnel) for the MH mutation could be a powerful tool to determine heatstroke susceptibility.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 10  Pathophysiology of Heat-Related Illnesses

identification of SNPs in the promoter region of genes suggests that disease susceptibility may be affected by altered transcription of immune determinants of clinical outcome. SNPs have been identified in IL-1, IL-2, TNF, IFNγ, IL-10, IL-1ra, TLR-2, and TLR-4. The risk for death from sepsis is significantly increased in patients with a genetic polymorphism in the TNF-α or TNF-β gene.83 Even for those cytokine polymorphisms located distal to a critical promoter region that do not directly affect gene transcription rates, coinheritance of multiple immune-responsive genes by a process known as linkage disequilibrium can alter immune function. Some TNF-α polymorphisms exist in linkage disequilibrium with HLA haplotypes that encode cell-surface antigens. Coinheritance of these genes may ultimately be responsible for poor sepsis outcome.138,296

20

CHAPTER 11 

Clinical Management of Heat-Related Illnesses KAREN K. O’BRIEN, LISA R. LEON, AND ROBERT W. KENEFICK

This chapter discusses the clinical manifestations, management, and prevention of heat-related illnesses. The spectrum of injury ranges from milder conditions such as heat cramps to fatal manifestations such as arrhythmias; it involves complications such as rhabdomyolysis and multiorgan dysfunction syndrome, and it may result in death from overwhelming cell necrosis caused by a lethal heat-shock exposure. Exertional heat stroke (EHS) is commonly characterized by development of mental status changes or collapse during physical activity in a warm environment. The severity of heat illness depends on the degree and duration of the elevation in core temperature (Tco). Heat stroke is an extreme medical emergency that can be fatal if it is not treated promptly with rapid cooling. To prevent and minimize complications and save lives, proper prevention, management, and clinical care are essential.

Exertional Heat Illness Dehydration and heat exposure can impair exercise performance and contribute to various illnesses. Exertional heat illnesses are comprised of minor and serious disorders. Minor heat and dehydration-related illnesses include heat cramps, erythromelalgia, and heat syncope. Heat cramps are characterized by intense muscle spasms, typically in the legs, arms, and abdomen. Heat cramps result from fluid and electrolyte deficits and occur most often in persons who have not been fully acclimated to a combination of intense muscular activity and environmental heat. Individuals who are susceptible to heat cramps are often believed to be profuse sweaters who sustain large sweat sodium losses.13,106 Heat syncope (fainting) is characterized by dizziness and weakness during or after prolonged standing or after rapidly standing up from a lying or sitting position during heat exposure. Heat syncope results from blood pooling in the cutaneous and skeletal vasculature, and it occurs most commonly in dehydrated and inactive persons who are not acclimated.93 Erythromelalgia is characterized by pain and swelling in the feet and hands that is triggered by exposure to elevated temperatures.64 Serious illnesses include exertional heat injury (EHI) and EHS. These illnesses have many overlapping diagnostic features; it has been suggested that they exist along a continuum on the severity scale.17 Heat exhaustion is characterized by inability to sustain cardiac output in the presence of moderate (>38.5° C [101° F]) to high (>40° C [104° F]) body temperatures, and is frequently accompanied by hot skin and dehydration. EHI is a moderate to severe illness characterized by injury to an organ (e.g., liver, kidneys, gut, muscle) and that usually (but not always) involves a high Tco of more than 40° C (104° F). EHS is a severe illness that is characterized by central nervous system dysfunction (e.g., confusion, disorientation, impaired judgment) and that is usually accompanied by a Tco of more than 40.5° C (105° F). EHI and EHS can be complicated by cardiac arrhythmia, liver damage, rhabdomyolysis, coagulopathy, fluid and electrolyte imbalances, and kidney failure. Rhabdomyolysis is most often observed with novel and strenuous overexertion. Clinical evidence suggests that dehydration increases the likelihood or severity of acute renal failure associated with rhabdomyolysis.19,91 Among U.S. soldiers who have been hospitalized for serious heat illness, 25% had rhabdomyolysis, and 13% had acute renal failure.22 EHS is usually associated with prolonged exertion in a warm climate; however, in many instances, EHS occurs within the first 2 hours of exercise and not necessarily at high ambient 232

temperatures.17,37 This is because exertion and environmental heat stress during the 72 hours that precede such an event strongly influence the individual’s susceptibility to heat illness.40 Using a Tco of 40.5° C (104.9° F) as a critical temperature to initially diagnose EHS is arbitrary. Mental status changes in an individual who is performing exertion in the heat should be the defining characteristic of heat stroke unless the individual has sustained head trauma. At the stage of collapse, profuse sweating is still likely to be present unless heatstroke develops in an already anhidrotic individual. Dry skin may be evident either in situations in which the climate is very dry and sweat evaporates easily or when heatstroke coincides with a severe degree of dehydration.36 Heat stroke is often categorized as either “classic” or “exertional,” with the former primarily observed in elderly individuals or otherwise sick or compromised populations and the latter in apparently healthy and physically fit persons.

ON-SITE EMERGENCY MEDICAL TREATMENT The early diagnosis of heat illness can be critical to therapeutic success. Early warning signs include flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion.74 If the patient is alert and has no mental status changes, he or she can rest in the shade or indoors, and oral rehydration can be instituted with cold water or an electrolyte-replacement beverage. The concentration of carbohydrates in such a beverage should not exceed 6%; otherwise, gastric emptying and fluid absorption by the intestines may be delayed. Responders should target an intake of 1 to 2 L (0.9 to 1.8 qt) over 1 hour. If the patient does not improve or in fact worsens, he or she should be evaluated by a medical provider. All persons with suspected heat injuries should be observed to ensure that decompensation does not occur. The victim should continue to rest and drink over the next 24 hours. As a general rule, for every pound of weight lost by sweating, 0.5 qt (2 cups or 500 mL) of fluid should be consumed. It may require 36 hours to completely restore lost electrolytes and fluid volume to all body compartments via oral intake. After the acute episode, a medical provider should determine any possible host risk factors for heat illness and review with the victim the signs of heat illness and preventive measures to consider. Any athlete who is performing exercise in warm weather and who develops mental status changes in the absence of trauma should be treated as an EHS victim until proved otherwise.36 EHS is a medical emergency. Rapid reduction of elevated Tco is the cornerstone of EHS management; the duration of hyperthermia may be the primary determinant of outcome.59,100 Cooling should not be delayed so that a temperature measurement can be obtained. Cooling measures should only be minimally delayed for vital resuscitation measures. Nevertheless, it is important to follow the ABCs (airway, breathing, and circulation) of stabilization while cooling efforts are initiated; see Box 11-1 for basic first aid information. Before 1950, the mortality rate with EHS was 40% to 75%.6,35 Long-term survival is directly related to rapid institution of resuscitative measures.49 In the field, the sick individual should be placed in the shade, and any restrictive clothing should be removed. There are multiple ways to cool victims in the field, with cold-water immersion (CWI) being the most effective modality.24,86 In a remote setting, this can be accomplished by using a small children’s pool filled

1. Place the patient in the shade. 2. Assess airway, breathing, and circulation. 3. Initiate cardiopulmonary resuscitation if the patient is pulseless or apneic. 4. Remove any restrictive clothing. 5. Initiate rapid cooling measures. 6. Activate emergency medical services. 7. Measure the patient’s rectal temperature to confirm the diagnosis 8. Evacuate the patient to the nearest medical facility via emergency medical services.

with iced water. The victim should be submerged up to the shoulders and kept under immediate hands-on supervision at all times. Another expedient method in the field is to keep bed sheets soaked in a cooler full of iced water; the victim can then be wrapped in the cold sheets. Particular care should be given to covering the head and to resubmerging the sheets every few minutes to recool them.79 Ice packs can be applied to the groin, axillae, sides of the neck, and head to augment iced-sheet cooling. Cooling should continue until emergency medical services providers arrive. Nonmedical first responders should not attempt to evacuate heat stroke patients themselves, because this may distract from cooling efforts. If CWI or iced sheets are not available, the victim should be kept wet by applying large quantities (20 to 30 L [5.3 to 7.9 gal]) of tap water or water from any source, and the victim’s body should be constantly fanned. Cooling blankets are generally ineffective as a single modality for inducing the rapid lowering of body temperature required for treating heatstroke.

EMERGENCY MEDICAL SERVICES TREATMENT During evacuation, CWI is often not a viable method for treatment. Iced sheets and ice packs can be easily used en route during transport. Many EMS vehicles now carry refrigerated intravenous (IV) fluid to initiate induction of therapeutic hypothermia in cardiovascular emergencies. When used, chilled IV fluid (4° C [39° F]) should be peripherally administered.63 Vascular access should be established without delay by inserting a 12- or 14-gauge IV catheter. Administration of normal saline or lactated Ringer’s solution should be started. Recommendations vary regarding administration rate of fluids. Some clinicians advise a rate of 1200 mL (1.26 qt) over 4 hours,78 whereas others encourage a 2-L (2.11-qt) bolus over the first hour and an additional liter of fluid per hour for the next 3 hours.98 Patients should be placed on a cardiac monitor. Administration of supplemental oxygen may help to meet the victim’s increased metabolic demands, and it may also be used to treat hypoxia that is commonly associated with aspiration, pulmonary hemorrhage, pulmonary infarction, pneumonitis, or pulmonary edema.34,67 A blood glucose determination should be performed, and adults with blood sugar level less than 60 mg/dL should be treated with 1 ampule of 50% IV dextrose solution. Children should be treated with 2 to 4 cc/kg of 25% IV dextrose solution. The use of antipyretics is not effective and may potentially be harmful to heatstroke victims. Aspirin and acetaminophen lower Tco by normalizing the elevated hypothalamic set point that is caused by pyrogens; in heatstroke, the set point is normal, with Tco elevation reflecting a failure of normal cooling mechanisms. Furthermore, acetaminophen may induce additional hepatic damage, and administration of aspirin may aggravate bleeding tendencies. Alcohol sponge baths are inappropriate under any circumstances, because transcutaneous absorption of alcohol may lead to poisoning and coma. In a comatose victim, airway control should be established by inserting a cuffed endotracheal tube. Positive-pressure ventilation is indicated if hypoxia persists despite supplemental oxygen administration.

The victim’s altered mental status may adversely affect the ability of emergency department personnel to obtain a detailed history of precipitating events. Lack of such information may also delay diagnosis. Emergency medical transport personnel should attempt to obtain this history before evacuating the victim and should communicate the information to medical staff. Of particular importance is the duration—and, when available, the maximum degree—of hyperthermia.

HOSPITAL EMERGENCY MEDICAL TREATMENT Patients with suspected heat stroke should be placed in a large treatment room to accommodate the needed number of staff. Patients are often combative and disoriented before reestablishing their baseline mental status. Aggressive cooling measures should continue until mental status returns to normal and Tco is 39° C (102° F).24 After discontinuation of cooling, Tco should be monitored every 5 minutes to ensure that it does not increase. The Tco reported in the field for heatstroke victims may be significantly higher (e.g., 41.1° C [106.9° F]), than those documented in the hospital emergency department (e.g., 37.8° C [100° F]), because Tco may fall during transport to the hospital.99 Documenting only a mild elevation in Tco on arrival does not exclude the diagnosis of heatstroke. Central nervous system (CNS) disturbances (i.e., coma, convulsions, confusion, or agitation) that accompany hyperthermia may also result from CNS infections, sepsis, or other disease processes. Other diagnoses should be considered when the patient does not regain normal mental status when the Tco is normalized in less than 30 minutes. When Tco remains elevated for a longer time, there is a decreased likelihood that mental status will normalize with euthermia.17 Tco can be measured at several anatomic sites, but oral, tympanic, esophageal, and rectal temperatures show regional variations as a result of differences in tissue metabolic activity, local blood supply, and temperature gradients between neighboring tissues. During exercise, active skeletal muscle temperature differs dramatically from that of other areas of the body that are not directly involved in the activity. Oral temperature is considered to be similar to blood temperature as a result of the rich blood supply of the tongue, but it is also influenced by hyperventilation and drinking fluids. Rectal temperature is a highly reliable indicator of body temperature, but it has a slower response rate and gives slightly higher readings than do other sites in the body. The comparison of oral and rectal temperature values in heatstressed underground miners showed a difference of approximately 1° C (2° F), with oral temperatures underestimating rectal values.108 Tympanic temperature responds more rapidly to cooling or heating than does rectal temperature, but it is influenced by changes in the skin temperature of the head and neck.44,68 The ear should be insulated from the environment to prevent cool ambient temperatures (<30° C [86 ° F]) from affecting this measurement. Esophageal temperature is the most accurate and responsive to changes in blood temperature, but its instrumentation is impractical in severely injured or unresponsive patients. If airway control was not previously established and if the patient is still unconscious, a cuffed endotracheal tube should be inserted to protect against aspiration of oral secretions. Supplemental oxygen—and, when hypoxia (PaO2 <55 mm Hg) or hypotension is present, positive-pressure ventilation—should be provided. Overly vigorous fluid resuscitation may precipitate pulmonary edema, so careful monitoring is indicated. Ideally, 1 to 2 L (1.05 to 2.11 qt) of fluid should be administered during the first hour after collapse, and additional fluids should be administered until satisfactory urine output (0.5 cc/kg/hr in an adult and 1.0 cc/ kg/hr in a child) is established.38 Most heatstroke victims arrive with a high cardiac index, low peripheral vascular resistance, and mild right-sided heart failure with elevated central venous pressure. Only moderate fluid replacement is indicated if effective cooling results in vasoconstriction and increased blood pressure. Providers should consider noninvasive intravascular volume monitoring or the minimally invasive monitoring of systolic volume variation and pulse pressure variation. If these methods are not adequate, a Swan-Ganz pulmonary artery catheter may be 233

CHAPTER 11  Clinical Management of Heat-Related Illnesses

BOX 11-1  Basic First Aid for Heat Illnesses

PART 2  COLD AND HEAT

necessary to assess appropriate fluid supplementation. Some victims have a low cardiac index, hypotension, and elevated central venous pressure. These persons have been successfully treated with an isoproterenol drip (1 mg/min).78 Patients with a low cardiac index, low central venous pressure, hypotension, and low pulmonary capillary wedge pressure should receive fluid. Unless the patient has rhabdomyolysis, aggressive fluid hydration is seldom required after initial treatment. Cardiac monitoring should be maintained during at least the first 24 hours of hospitalization. Arrhythmia is most likely to occur during hyperthermia, but it may also occur as a result of electrolyte abnormalities. The use of norepinephrine and other α-adrenergic drugs should be avoided because they cause vasoconstriction, thereby reducing heat exchange through the skin. Anticholinergic drugs that inhibit sweating (e.g., atropine) should also be avoided. Cooling techniques are ineffective when the victim suffers seizures that increase storage of body heat; therefore, convulsions should be controlled. Intravenous benzodiazepines are preferred for their efficacy and renal clearance. Initial dosing is either 4 to 8 mg of IV lorazepam or 10 mg of IV diazepam. If seizures persist for more than 10 minutes after the first dose, an additional 4 mg of lorazepam or 10 mg of diazepam should be administered. As a result of drastic cooling, skin temperature may decrease enough to cause shivering. Administration of 12.5 mg of meperidine via slow IV push103 or of 5 mg of diazepam is effective to suppress shivering and to prevent an additional rise in Tco from metabolic heat production. If CWI is used, the increase in metabolic rate as a result of shivering will be more than offset by the high rate of heat transfer. Therefore the presence of shivering should not be a cause for concern when this method of cooling is used.24,83 Severe muscle cramping may be caused by electrolyte imbalances. Magnesium levels should be obtained. If magnesium levels are low, consideration may be given to the use of 50% IV magnesium sulfate (4 g in 250 mL of 5% dextrose injection at a rate that does not exceed 3 mL per minute).14,15 A Foley catheter should be placed to monitor urine output. Renal damage from myoglobinuria and hyperuricemia can be prevented by promoting renal blood flow by administering IV mannitol (0.25 mg/kg) or furosemide (1 mg/kg).98 If creatine phosphokinase (CPK) levels exceed 100,000 international units, alkalinize the urine of patients with exertional rhabdomyolysis; there is no advantage to alkalinization when levels are lower. Hemodialysis should be reconsidered if anuria, oliguria (<0.5 mL/ kg of urine per hr for >6 hr), uremia, or hyperkalemia develops. Cooling and hydration usually correct acid–base abnormalities; however, serum electrolytes should be monitored and appropriate modifications of IV fluids made. Glucose should be monitored repeatedly, because either hypoglycemia or hyperglycemia may occur after EHS.95 Oral and gastric secretions are evacuated via a nasogastric tube that is connected to continuous low suction. Although antacids, proton pump inhibitors, and histamine-2 blockers have been used to prevent gastrointestinal bleeding, no studies to date demonstrate their efficacy for heatstroke victims. Induced Hypothermia Induced hypothermia is increasingly being used for many neurologic and cardiovascular emergencies, including acute stroke, neonatal hypoxic–ischemic encephalopathy, and after cardiac arrest.9,50,76,94 This therapeutic modality has not been evaluated for effectiveness in individuals with EHS, but may have a role in cooling severe refractory cases of EHS. There may be a role for a period of induced hypothermia after severe EHS. Dantrolene No drug has been found to have a significant effect for reducing Tco. Antipyretics are ineffective, because the thermoregulatory set point is not affected in heatstroke. Furthermore, antipyretics might be harmful, because they cannot be readily metabolized in the heat-affected liver. However, dantrolene has been used quite successfully for the treatment of several hypercatabolic syndromes, such as malignant hyperthermia, neuroleptic malignant syndrome, and other conditions that are characterized by muscular rigidity or spasticity.107,114 Dantrolene stabilizes the 234

calcium (Ca2+)-release channel in muscle cells, thereby reducing the amount of Ca2+ released from cellular calcium stores. This lowers intracellular Ca2+ concentrations, muscle metabolic activity, muscle tone, and thus heat production.27,75 In some studies, dantrolene was claimed to be effective for the treatment of heatstroke, whereas in others it improved neither the rate of cooling nor survival.25,31,66,109 In six patients with rhabdomyolysis, intramuscular Ca2+ concentrations were 11 times higher than in controls, and dantrolene successfully lowered this elevated Ca2+.65 Collectively, the limited data available are at best inconsistent. Despite growing evidence for a possible benefit of dantrolene treatment in patients with heatstroke, justification for its routine use in such cases is not proved, although future clinical trials may change this assessment. Moran and colleagues71 studied dantrolene in a hyperthermic rat model, and found it to be effective as a prophylactic agent in sedentary animals only. Dantrolene induced more rapid cooling by depressing Ca2+ entry into the sarcoplasm; this led to relaxation of peripheral blood vessels with attenuated production of metabolic heat. Dantrolene may also be effective in treating heatstroke by increasing the cooling rate. However, in other animal models, dantrolene was not superior to conventional cooling methods.117 As such, dantrolene is not recommended.

CLINICAL MANIFESTATIONS Clinical manifestations of heatstroke vary, depending on whether the victim suffers from classic heatstroke, which is a common disorder of older adults during heat waves and occurs in the form of epidemics, or EHS,1 which occurs when excess heat generated by muscular exercise exceeds the body’s ability to dissipate it (Table 11-1). Some overlap in presentation may occur; treatment with a medication (e.g., antihypertensive or antipsychotic) that places an older adult at risk for classic heatstroke also places an exercising individual at risk for EHS. The clinical picture of heatstroke usually follows a distinct pattern of events

TABLE 11-1  Comparison of Classic and Exertional

Heatstroke

Characteristics

Classic

Exertional

Age group

Young children and older adults

Health status Concurrent activity Drug use

Chronically ill Sedentary Diuretics, antidepressants, antihypertensives, anticholinergics, and antipsychotics May be absent Usually absent; poor prognosis if present Usually absent Uncommon Uncommon Mildly elevated

Men between the ages of 15 and 45 yr Healthy Strenuous exercise Usually none

Sweating Lactic acidosis Hyperkalemia Hypocalcemia Hypoglycemia Creatine phosphokinase Rhabdomyolysis Hyperuricemia Acute renal failure Disseminated intravascular coagulation Mechanism

Usually present Common Often present Frequent Common Markedly elevated

Unusual Mild <5% of patients Mild

Frequently severe Severe 25-30% of patients Marked; poor prognosis

Poor dissipation of environmental heat

Excessive endogenous heat production and overwhelming heat-loss mechanisms

Modified from Knochel JP, Reed G: Disorders of heat regulation. In Kleeman CR, Maxwell MH, Narin RG, editors: Clinical disorders of fluid and electrolyte metabolism, New York, 1987, McGraw-Hill.

Acute Phase The acute phase of heatstroke is characterized by CNS manifestations. Because brain function is very sensitive to hyperthermia, this phase is present in all heatstroke patients. Early signs of CNS dysfunction are typically cerebellar and include ataxia, poor coordination, and dysarthria.116 Advanced signs of CNS depression include irritability, aggressiveness, stupor, delirium, and coma.2,21,102 Mental status changes usually resolve after return to a normal Tco. After a return to normothermia, persistence of coma is a poor prognostic sign.57,102 Other symptoms include fecal incontinence, flaccidity, and hemiplegia. Cerebellar symptoms may persist beyond the acute phase.69,102,116 Other common disturbances during the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dysfunction, including diarrhea and vomiting, often occurs. However, the latter may reflect translocation of toxic gram-negative bacterial lipopolysaccharide from the lumen of the intestines because of poor splanchnic perfusion as a result of hypotension caused by increased skin blood flow and from CNS impairment.18,41,102 Hyperventilation and elevation of Tco primarily lead to respiratory alkalosis, which in EHS may be masked by metabolic acidosis as a result of increased glycolysis and hyperlacticacidemia.26,74 Hypoxemia may be present in patients with respiratory complications.28,74,105 It should also be noted that oxygen consumption is elevated during hyperthermia, with a 10% to 13% increase for every ° C above euthermia.32 EHS shares many common findings with systemic inflammatory response syndrome (SIRS).17,97 Endotoxemia, hyperthermia, and other risk factors (e.g., preexisting infection) and stressors associated with EHS can trigger this exaggerated inflammatory response. Patients should be assessed for SIRS after admission with the use of the following criteria:16 (1) body temperature of less than 36° C (98.6° F) or of more than 38° C (100.4° F); a heart rate of more than 90 beats per minute, tachypnea, or an arterial partial pressure of carbon dioxide of less than 4.3 kPa (32 mm Hg); and a white blood cell count of less than 4000 cells/ mm3 (4 × 109 cells/L) or of more than 12,000 cells/mm3 (12 × 109 cells/L) or the presence of more than 10% immature neutrophils. When two or more of these criteria are met, SIRS can be diagnosed. The presence of systemic inflammatory response markers during the acute phase predicts the severity of subsequent phases. Hematologic and Enzymatic Phase Hematologic and enzymatic disorders peak 24 to 48 hours after collapse. In the hematologic and enzymatic phase of EHS, hematologic, enzymatic, and other blood parameters are altered. In humans and experimental animals, hyperthermia results in leukocyte activation46 and in changes in lymphocyte subpopulations, both in absolute numbers and in percentages.1 Leukocytes may range from 20 to 30 × 103/mm3 or higher.10,51 In severe cases, leukocyte activation is associated with the systemic activation of coagulation cascades.55 In one study, all fatal cases of EHS involved disturbances in the blood coagulation system.10,101 Prothrombin time, partial thromboplastin time, and the level of fibrin split products increased with a fall in thrombocytes.38 Clotting dysfunction peaked 18 to 36 hours after the acute phase of heatstroke; 2 to 3 days after heatstroke, prothrombin levels fell to 17% to 45% of normal. Depending on the severity of heatstroke, thrombocyte values ranged between 110 × 103/mm3 and 0.100,101 This systemic inflammatory response state resembles gramnegative bacterial sepsis, and it appears that lipopolysaccharide (a cell-wall component of gram-negative bacteria) participates in the pathophysiology of EHS.43 Enzymes One of the prominent and almost pathognomonic characteristics of EHS is the appearance of exceptionally high levels of certain cellular enzymes, which implies cell damage or death. Most patients with EHS show an elevation of serum CPK activity and myoglobinuria, which suggests damage to skeletal muscle.37 CPK values in the range of 103 to 104 international units were

commonly found, with peak values occurring 24 to 48 hours after collapse.30,96 At a Tco of 41.8° to 42.2° C (107.24° to 107.96° F), aspartate aminotransferase and alanine aminotransferase levels rose by factors of 25 and 8, respectively, and bilirubin levels approximately doubled to 1.56 mg/dL.82 These rises in enzyme levels are related to tissue damage, which in turn depends on both Tco and its rates of rise and duration.73 CPK was the most sensitive to increases in Tco, and this was followed by lactate dehydrogenase, which is an index of generalized tissue damage. CPK levels in EHI and EHS typically peak at 24 to 48 hours. Rising values after this point should alert the clinician to the possibility of an occult compartment syndrome. It is not uncommon for a victim of EHI to complain of lower-extremity pain that declares itself as a compartment syndrome. During the 1994 Hajj, 26 heatstroke victims admitted to a heatstroke treatment unit had elevated levels of CPK, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase; these levels remained high after 24 hours. Those who died had higher enzyme levels than did the survivors. Lactate dehydrogenase concentration was useful for distinguishing between those who died and those who had a rapid recovery. The enzymes were better prognostic indicators than were Tco, anion gap, and serum potassium level. Late Phase The late phase of heatstroke manifests 3 to 5 days after collapse, and is characterized by disturbances in renal and hepatic functions. These abnormalities are consistent with multiorgan dysfunction syndrome as a result of SIRS. Acute renal failure is a common complication of severe cases, and occurs in approximately 25% to 30% of patients with EHS patients.60,67,100 Oliguria and anuria are characteristic features. During this phase, urine has been described as being like machine oil, with a high specific gravity.81,84,92,100 Usually present in the urine are red and white cells, hyaline and granular casts, and mild to moderate proteinuria.92 The etiology involves multiple causes,81 but a major one is reduced renal blood flow caused by heat-induced hypotension, hypohydration, and peripheral vasodilation. In addition, direct thermal injury may also lead to widespread renal tissue damage.92 Myoglobinuria and elevated blood viscosity that result from disseminated intravascular coagulation may further contribute to acute oliguric renal failure.84,92,104,111 EHS is usually manifested by increased serum levels of liver enzymes, but acute liver failure has also been reported.115,39 High bilirubin levels, which may last for several days, reflect hepatic dysfunction and hemolysis. In most cases of EHS, liver injury is usually asymptomatic and exhibits reversible elevation in plasma aminotransferase levels.48 Acute liver failure is documented in 5% of patients with EHS.61 Hypophosphatemia (<0.5 mmol/L) at the time of admission may predict occurrence of acute liver failure.39 Despite limited experience and the observation that EHS patients with extensive liver damage may recover spontaneously, orthotopic liver transplantation had been suggested as a potential treatment.12,47,89 Among 16 reported cases of EHS-induced liver failure,45 three patients underwent liver transplantation. In the conservatively managed group, eight patients recovered spontaneously, and five died. Concomitantly, all three patients who received transplantation died. Hadad and co-workers45 concluded that, because of the poor and limited results of liver transplantation after heatstroke, the interpretation of prognostic criteria is crucial before listing a patient for such surgery.

SEQUELAE AND AFTERCARE The combination of the rapid reduction of Tco, control of seizures, proper rehydration, and prompt evacuation to an emergency medical facility results in a 90% to 95% survival rate in heatstroke victims, with morbidity directly related to the duration of hyperthermia.17,97 A poor prognosis is associated with Tco of more than 41° C (105.8° F), prolonged duration of hyperthermia, hyperkalemia, acute renal failure, and elevated serum levels of liver enzymes. Therefore misdiagnosis, early inefficient treatment, and delay in evacuation are the major causes of clinical deterioration. Full recovery without evidence of neurologic impairment has been achieved even after coma of 24 hours’ duration and 235

CHAPTER 11  Clinical Management of Heat-Related Illnesses

with three phases: (1) acute, (2) hematologic or enzymatic, and (3) late.38

PART 2  COLD AND HEAT

subsequent seizures.101 Persistence of coma after return to normothermia is a poor prognostic sign.102 Red blood cell apoptosis (i.e., cell blebbing, asymmetry, and shrinkage) on early peripheral blood smears is a very poor prognostic sign and may indicate extensive cellular necrosis. Neurologic deficits may persist, but usually only last for a limited period of 12 to 24 months and only rarely for longer. CNS dysfunction becomes increasingly severe with prolonged duration of hyperthermia and associated circulatory failure. Nevertheless, coma that persists for up to 24 hours, even with subsequent seizures, is usually followed by complete recovery without evidence of mental or neurologic impairment.2,88 However, chronic disability may prevail for several weeks or months in the forms of cerebellar deficits, hemiparesis, aphasia, and mental deficiency.2,60,88 Only in exceptional cases, when coma persisted for more than 24 hours, did mental and neurologic impairment become chronic and prevail for years. However, in one study of classic heatstroke, 78% of patients had minimal to severe neurologic impairment, such as ataxia or dysathria.30 Long-term EHS victims may have increased mortality from heart, liver, and kidney disease.113

PREVENTION Prevention of heat illness relies on an awareness of host risk factors, altering behavior and physical activity to match these risk factors and environmental conditions, and a requirement for appropriate hydration during physical exercise in the heat. More aggressive educational activity that explains heat illness and its prevention to the public is to be strongly promoted. Primary care physicians should incorporate this information into the anticipatory guidance of routine health assessment. Despite a wealth of medical literature about heat injury, some athletic coaches continue to use physical or psychological methods to force athletes to compete or train under intolerably hot conditions. This practice should be viewed as irresponsible, dangerous, and possibly criminally negligent. The importance of recognizing milder forms of heat illness cannot be overstated. Any time heat injuries occur, coaches and trainers should reassess all athletes and determine what other measures can be implemented to prevent more serious injuries from occurring. Awareness of Host Risk Factors Shapiro and Moran96 studied 82 cases of EHS in Israeli soldiers and concluded that at least one factor that predisposes an individual to heatstroke (e.g., diarrhea, lack of acclimatization, poor fitness) was associated with each case. Correcting those individual risk factors should lead to strategies that can prevent heatstroke. Any underlying condition that causes dehydration or increased heat production or that causes decreased dissipation of heat interferes with normal thermoregulatory mechanisms and predisposes an individual to heat injury. Older individuals are less tolerant to EHI than younger persons, and they are more susceptible to classic heatstroke because of decreased secretory ability of their sweat glands and decreased ability of their cardiovascular systems to increase blood flow to the skin. When healthy young adults exercise strenuously in the heat, EHS may occur despite the absence of host risk factors. Elite and professional athletes, the general public, and the military have widely used ergogenic aids (e.g., the herb ephedra [ma huang]) that contain ephedrine to improve performance and for weight loss. Because ephedra increases metabolic rate, it has caused numerous cases of heat illness and deaths worldwide, and it has been banned. Because there are no clear ergogenic benefits to the use of ephedra alone, use of ephedra-containing substances should be discouraged.80 The ratio of basal metabolic rate to surface area is higher in children than in adults. As a result, a child’s skin temperature is higher for any given Tco. Although the secretory rates of sweat glands are lower in children, children have greater numbers of active sweat glands per area of skin than adults and overall greater sweat rates per unit area.54 Any reduction in the rate of sweating puts children especially at risk. The primary mechanism for heatstroke in young children is hot vehicle entrapment. 236

Between 1998 and 2010, 462 children died from heatstroke as a result of vehicular hyperthermia. The primary means of heat dissipation is production and evaporation of sweat. Any condition that reduces this process places the individual at risk for thermal injury. Poor physical conditioning, fatigue, sleep deprivation, cardiovascular disease, and lack of acclimation all limit the cardiovascular response to heat stress.40,56 Obesity places an individual at risk as a result of reduced cardiac output, the increased energy cost of moving extra mass, increased thermal insulation, and altered distribution of heat-activated sweat glands.72 Older adults and younger individuals show decreased efficiency of thermoregulatory functions and increased risk for heat injury. Several congenital or acquired skin abnormalities affect sweat production and evaporation. Ectodermal dysplasia is the most common form of congenital anhidrosis. Widespread psoriasis, poison ivy, sunburn, scleroderma, miliaria rubra (i.e., “prickly heat,” which is caused by the plugging of sweat ducts with keratin), deep burns, and prior skin grafting may also limit sweat production. Dehydration affects both central thermoregulation and sweating. A mere 2% decrease in body mass through fluid loss produces an increase in heart rate, increase in Tco, and decrease in plasma volume. In an otherwise healthy adult, gastrointestinal infection with vomiting and diarrhea may cause sufficient dehydration to place the individual at risk for EHS. Chronic conditions that may contribute to heat illness include diabetes mellitus, diabetes insipidus, spinal cord injury, eating disorders (especially bulimia), and mental retardation. Alcoholism and illicit drug use are among the 10 major risk factors for heatstroke in the general population.58 An important effect of alcohol consumption is inhibition of antidiuretic hormone secretion, which leads to relative dehydration. Autonomic dysfunction, which is present with many chronic diseases, impairs thermoregulation.52 Despite evidence that hypohydration limits physical performance, voluntary dehydration continues to be routine in certain athletic arenas.5,7,20,110 Wrestlers, jockeys, boxers, and bodybuilders commonly lose 3% to 5% of their body mass 1 to 2 days before competition. In addition to restricting fluid and food, they use other pathogenic weight-control measures, such as self-induced vomiting, laxatives, diuretics, and exposure to heat (e.g., saunas, hot tubs, “sauna suits”). Athletes who are undergoing rapid dehydration are at risk not only for heat injury but also for other serious medical conditions, such as pulmonary embolism.29 Box 11-2 highlights common medications that interfere with thermoregulation. Special attention should be paid to the role of antihistamines in reducing sweating. This class of medications is commonly obtained over the counter, so the general population should be warned about the dangers of exercising in the heat when they are taking antihistamines. Although it has been widely believed that sustaining an episode of heatstroke predisposes the individual to future heat injury, this has been refuted in a recent study of heatstroke victims.8 Ten heatstroke patients were tested for their ability to acclimate to heat; BOX 11-2  Drugs That Interfere With Thermoregulation Drugs That Increase Heat Production • Thyroid hormone • Amphetamines • Tricyclic antidepressants • Lysergic acid diethylamide Drugs That Decrease Thirst • Haloperidol Drugs That Decrease Sweating • Antihistamines • Anticholinergics • Phenothiazines • Benztropine mesylate Data from references 12, 31, 50, 66, 105, and 107.

ADAPTATION TO ENVIRONMENTAL CONDITIONS Appropriate adaptation to hot environmental conditions encompasses many forms of behavior, including modifying clothing, the degree of physical activity, searching for shade, the anticipatory enhancement of physical conditioning, acclimation to heat stress, and paying attention to the level of hydration. Clothing Different regions of the body are not equivalent with regard to sweat production.53 The face and the scalp account for 50% of total sweat production, whereas the lower extremities contribute only 25%. When exercising under conditions of high heat load, maximal sweat evaporation is facilitated by maximal skin exposure. Clothing should be lightweight and absorbent. Although significant improvement has been made in the fabrication of athletic uniforms, the uniforms and protective gear required by certain branches of the military and public safety officers continue to add to the risk of heat injury. Developing protective clothing that permits for more effective heat dissipation is indicated. Uniforms should be modified to decrease the amount of extra protective equipment and head gear needed as much as is safely possible during the first week of training and during times of high heat stress conditions. Activity Behavioral actions can effectively minimize the occurrence of classic heatstroke. Lack of residential air conditioning places indigent persons at risk during heat waves. By sitting in a cool or tepid bath periodically throughout the day, the individual can decrease heat stress and thereby prevent heat injury. The more than 10,000 deaths during the 2003 heat wave in Europe could have been reduced by simple announcements by public health officials of this preventive measure. This type of “heat dumping” activity can also include taking cool showers instead of warm showers. In addition, the forearms and hands can be immersed into water that has been cooled to 10° to 20° C (50° to 68° F) for a period of 10 minutes. This action will achieve a reduction in Tco of 0.7° C (1.3° F) and provide the athlete with sustained capability to train in the heat.42 In addition to forearm and hand immersion in cool or cold water, the concept of cooling the palm by various devices, some of which add vacuum pressure to the palm in addition to cooling, has recently become popular. A comprehensive review23 of cooling rates of various cooling modalities has shown that this methodology is no more effective in lowering body core temperature than limb immersion in tap water (15° C [59° F]). Recent research on these devices has shown that the addition of negative pressure with cooling did not enhance any cooling effect.62 In addition, these devices have been shown to be ineffective in slowing the development of hyperthermia when used between exercise bouts4 and in the improvement of high-intensity, intermittent exercise.112 Cold or ice water has been reported to have a cooling power of 5 to 8 times greater than hand/palm cooling devices.23 Given the low cooling power of these devices, their use in a field or athletic setting, especially for treatment of heat injury or illness, should be questioned. This is also true when viewed in terms of cost vs. limb immersion modalities. Regarding use in a wilderness setting, these devices have additional drawbacks including the need for electrical power via batteries and the added weight of transport. Athletes should be placed in the shade whenever possible during periods of rest and instruction. If shade is not available in areas where warm weather training is routinely conducted, consideration should be given to constructing overhead shelters. If latrines are not easily accessed at training areas, consideration should be given to placing portable latrines nearby to prevent

TABLE 11-2  Determination of Wet Bulb Globe

Temperature Heat Index

Temperature (T, in ° F) Wet bulb T Dry bulb T Black globe T Heat index

Factor

Example

×0.7 ×0.1 ×0.2

78 × 0.7 = 54.6 80 × 0.1 = 8.0 100 × 0.2 = 20.0 82.6

Wet bulb reflects humidity, dry bulb reflects ambient air temperature, and black globe reflects radiant heat load; the heat index is the sum of the three. Alternative equation: Wet bulb globe temperature = (0.567 Tdb) + (0.393 Pa) + 3.94, where Tdb is dry bulb temperature and Pa is water vapor pressure.

voluntary fluid restriction. The authors recommend spacing runners widely apart during group runs to allow for optimal heat dissipation. Modification of physical activity should not be based solely on any individual parameter of ambient temperature (Tamb), relative humidity, or solar radiation, because all of these contribute to heat load. The wet bulb globe temperature (WBGT) is an index of heat stress that incorporates all three factors. This value may be calculated (Table 11-2), or it may be obtained directly from portable digital heat-stress monitors that measure all three parameters simultaneously to compute the WBGT. When heatstress monitors are used, care should be taken to ensure that they are calibrated yearly and that they are not left out in the heat for long periods of time without use. Care should also be taken to ensure that the device measures radiant heat, humidity, air movement, and shaded temperature to calculate WBGT. Devices that measure the heat stress index, relative humidity, and wind speed should not be used to estimate WGBT. Current recommendations from the American College of Sports Medicine for preventing exertional heat illness during workouts and competition are based on the WBGT.3 Most heat injuries occur during cooler WBGT periods as a result of cumulative heat exposure from preceding days. Some clinicians have proposed that heatwarning systems would base their warnings on cumulative heat stress rather than solely on the current WBGT.113 Other clinicians have suggested the use of syndromic surveillance to help alert the public about periods of high heat stress.11 Table 11-3 presents a suggested modification of sports activity that is also based on the WBGT. Although American College of Sports Medicine guidelines for the summer indicate that vigorous physical activity should be scheduled in the morning or evening, individuals should be cautioned that the highest humidity of the

TABLE 11-3  Modification of Sports Activity on the

Basis of Wet Bulb Globe Temperature

Index

Limitation

<10° C (50° F)

There is a low risk for hyperthermia but a possible risk for hypothermia. There is a low risk for heat illness. There is a moderate risk toward the end of the workout. Those at high risk for heat injury should not continue to train; all athletes should practice in shorts and T-shirts during the first week of training. Care should be taken by all athletes to maintain adequate hydration. Unacclimated persons should stop training; all outdoor drills in heavy uniforms should be canceled. Acclimated athletes should exercise caution and continue workouts only at a reduced intensity; they should wear light clothing only. Stop all training.

<18.3° C (65° F) 18.3°-22.8° C (65°-73° F) 22.8°-27.8° C (73°-82° F) 27.8°-28.9° C (82°-84° F) 28.9°-31.1° C (85°-88° F) 31.1°-32.2° C (88°-90° F) ≥32.2° C (90° F)

237

CHAPTER 11  Clinical Management of Heat-Related Illnesses

by definition, the ability to acclimate to heat indicates heat tolerance. Nine of the patients demonstrated heat tolerance within 3 months after the heatstroke episode; the remaining patient acclimated to heat one year after his heat injury. In no case was heat intolerance permanent. Although individuals may show transient heat intolerance after thermal injury, evidence for permanent susceptibility to thermal injury is lacking.

PART 2  COLD AND HEAT

day is usually during early morning. In 1999, Montain and coworkers70 updated the fluid replacement guidelines for warmweather training (see Chapter 70, Table 70-5). It is important to note that compliance with these recommendations does not remove all risk of heat injury. The development of another index of heat stress that provides a better basis for the prevention of EHS is indicated. Rav-Acha and colleagues85 assembled a case series of six fatal cases of EHS in the Israeli Defense Forces and examined the circumstances that led to the deaths. A significant association between the accumulation of predisposing factors and EHS totality was found. In almost all of the fatal cases, seven predisposing factors were noticed: (1) low physical fitness; (2) sleep deprivation; (3) high heat load; (4) high solar radiation; (5) physical exercise unmatched to physical fitness; (6) absence of proper medical triage; and (7) training during the hottest hours. These fatality factors primarily concerned organizational training regulations and not individual factors, which emphasizes the importance of proper guidelines and safety measures in a warm climate—rather than individual characteristics—for preventing EHS fatalities. It follows that a combination of predisposing factors that were already found to impair heat tolerance40 is a strong predictor of a grave prognosis. Dehydration was found in only two of the six cases reported. Conditioning The contribution of cardiovascular conditioning to thermoregulation is discussed in Chapter 4. Ideally, an individual should train under temperate or thermoneutral conditions before exercising in the heat. For the previously sedentary individual, an exercise regimen that incorporates 20 to 30 minutes of aerobic activity 3 to 4 days a week will improve cardiovascular function after 8 weeks. It is important to remember that even physically active individuals may lack physical conditioning relative to a particularly stressful competition or activity. Heat illness in runners commonly occurs when novices exceed their training effort during

238

races or when well-trained athletes increase their pace above normal during long-distance events. Acclimatization During initial exposure to a hot environment, workouts should be moderate in intensity and duration. A gradual increase in the time and intensity of physical exertion over 8 to 10 days should allow for optimal acclimatization.33 Early season high-school heatstroke deaths are most likely to occur during the first 4 days of practice87; children require 10 to 14 days to achieve an appropriate acclimatization response. Acclimatization can be induced by simulating hot environmental conditions indoors. Aerobic activity should be conducted during exposure to the hot environment so that the individual can achieve optimal acclimatization.90 If symptoms of heat illness develop during the acclimation period, all physical activity should be stopped and appropriate interventions begun. Acclimatization is not facilitated by restricting fluid intake; in fact, conscious attention to fluid intake is required to prevent dehydration. As with physical conditioning, there are limits to the degree of protection that acclimatization provides from heat stress. Given a sufficiently hot and humid environment, no one is immune to heat injury.

RESEARCH Areas for future research include improved clarification of when athletes can safely return to play; the role of autonomic nervous system dysfunction in EHS; the benefit of induced hypothermia for EHS treatment; and the role of clonidine, activated protein C, and antibiotics during initial treatment. We extend much appreciation to the previous authors of this chapter, Daniel S. Moran and Stephen L. Gaffin.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 12 

Wildland Fires: Dangers and Survival MARTIN E. ALEXANDER, ROBERT W. MUTCH, KATHLEEN MARY DAVIS, AND COLIN M. BUCKS

There can be few natural physical phenomena with the scope and complexity of a forest fire. The fuel that powers it is found in a huge range of sizes, quantities, and arrangements in space. The weather affects the current condition of this fuel array in a bewildering maze of drying and wetting effects, each fuel component responding to a “different drummer.” The combustion process itself, once under way, responds to a complex blend of fuel variation, moisture status, topography, wind speed, and other atmospheric factors. Its frontal intensity varies over an immense range, from tiny flickers easily stepped over, to dense sheets of flame whose fierce radiation keeps the observer at a distance. —VAN WAGNER (1985)

In describing the 13 wildland firefighter fatalities that occurred on the Mann Gulch fire near Helena, Montana, on August 5, 1949, author Norman Maclean275 wrote in his seminal book Young Men and Fire, published in 1992, that “They were still so young they hadn’t learned to count the odds and to sense they might owe the universe a tragedy.” Three years later, Canadian folksinger-songwriter James Keelaghan, inspired by Maclean’s book, paid tribute to the fallen firefighters in a haunting ballad entitled “Cold Missouri Waters.” The Mann Gulch fire has been called “the race that couldn’t be won.”403 Although the crew increased their pace ahead of the fire, the fire accelerated faster than they did until fire and people converged. Miraculously, three people survived the fire. Smoke jumper foreman Wag Dodge ignited an “escape fire” by burning off a patch of cured grass into which he tried to move all of his crew, whereas two others found a route to safety and escaped injury on a nearby rockslide. Many improvements in a firefighter’s odds of surviving an entrapment or burnover encounter with a wildland fire have occurred since 1949. These advances include improved understanding of fire behavior, increased emphasis on fire safety and fire training, and development of personal protective equipment. However, as incidents such as the 14 firefighter fatalities on the 1994 South Canyon fire in Colorado (Figure 12-1) have shown, tragedies continue to occur.170 Norman Maclean’s son, John, would in turn write about this fatal fire 50 years later.271 Grief over lost loved ones can sometimes lead to further tragedies. For example, one of the smoke jumpers killed on the 1949 Mann Gulch fire, Stan Reba, had been married less than one year. His widow grieved for him and never remarried, and then 10 years later took her own life.236,286 Wildland fires are a threat to human life, property, and natural resources in many regions of the world (Figure 12-2). Although the total number of deaths among the general public due to wildland fires in modern times pales in comparison with the death toll and destruction from other natural hazards (e.g., hurricane, tornado, flood, earthquake, tsunami, avalanche)83 and human-made disasters, the fatalities are frequent and devastating.470 There are very few comprehensive summaries of deaths due to wildland fires on a worldwide basis. The compilation of U.S. wildland firefighter fatalities begun in the early 1970s519 is unique.339 Statistics on the number of civilian or wildland firefighter fatalities due to being trapped or overrun by wildland fires on a global basis are unfortunately not kept in any 240

systematic manner.234 It is, however, well known that more than 300 deaths due to bushfire entrapments and/or burnovers occurred in the state of Victoria in Australia alone during the 20th century.248 On Saturday, February 7, 2009, Australia experienced a bushfire disaster of unparalleled portions:473 In the wake of a long drought, and on a day of high temperatures, strong winds and low humidity, bushfires swept through residential and farming communities in Victoria. Some 430,000 hectares [one million acres] of forest and farmland, countless homes and other buildings were burnt, and hundreds of millions of dollars damage were done to economic and community assets. Far more tragically, it was Australia’s worst civil disaster: 173 lives were lost. February 7th 2009 has become Black Saturday, to be (one imagines) seared into the Australian psyche for generations to come. That day, more than 300 fires were reported across the state. Fifteen of these developed into major incidents, with the most extensive damage and loss of life resulting from four fires.138,195,298 A royal commission was established soon afterward to investigate the causes and responses to these fires (http://www. royalcommission.vic.gov.au/). The commission’s final report, issued at the end of July 2010, sets out 67 recommendations for protecting human life, “designed to reflect the shared responsibility that governments, fire agencies, communities, and individuals have for minimizing the prospect of a tragedy of this scale ever happening again.”459 In their report, the commissioners offered a warning: It would be a mistake to treat Black Saturday as a ‘one-off’ event” for “ … the risks associated with bushfires are likely to increase.” Given the occurrence of other major wildland fire disasters involving significant loss of life in recent years—for example, Greece in August 2007525,526and Russia during the 2010 summer fire season—this prediction has global application. This chapter describes the current look at fire as a historical force and discusses fire management policies, the nature and scope of wildland fire hazards, behavior of fires, typical injuries, fatality fire statistics, several fatal fire incidents, and survival techniques. Although the emphasis is on North America, reference is made to other regions of the globe, most notably Australasia and Europe. Wildland fire, like many other disciplines and subjects, has its own unique terminology, so readers may need to consult glossaries.190,300,345

For online-only figures, please go to www.expertconsult.com

FIGURE 12-1  Flame front spreading upslope through Gambel oak (Quercus gambelii) and pinyon (Pinus edulis)–juniper (Juniperus monosperma) fuel complex during the major run of the South Canyon fire in western Colorado on the afternoon of July 6, 1994. Approximately two and a half minutes after this photograph was taken, the first of 14 firefighters was overtaken by the advancing flames that were estimated to have travelled upward of 110 to 165 m/min (360 to 540 ft/min). (Courtesy USDA Forest Service; photo by S. Archuleta.)

Wildland Fire Management and Technology Programs for dealing with the overall spectrum of fire are collectively termed fire management.55 They are based on the concept that fire and the complex interrelated factors that influence fire phenomena can and should be managed. The scientifically sound fire management programs that respond to the needs of people and natural environments must also maintain full respect for the power of fire.55 Since the early 1900s, federal, state, and local fire protection agencies in the United States, for example, have routinely extinguished wildland fires to protect watershed, range, and timber values, as well as human lives and property. The basic methods of fire suppression210,268 have changed very little, although new technologies have gradually come on board (Figure 12-3). However, improvements in fire detection, fire danger rating systems, and fire suppression methods have been developed by fire science laboratories and two equipment development centers maintained by the U.S. Department of Agriculture (USDA) Forest Service, as well other organizations (e.g., state agencies and universities). Patrol planes, some with infrared heat scanners, other fixed-wing aircraft (Figure 12-4), and helicopters (Figure 12-5), can deliver firefighters, equipment, and fire-retarding chemicals or water to the most remote fire. These firefighting resources are organized under an Incident Command System that

FIGURE 12-2  A wildland–urban interface fire in the Amarante region of Portugal on August 5, 2005. Drought conditions contributed to an exceptionally severe fire season in southern Europe during 2005. Twelve firefighters and 10 civilians were killed in Portugal. Eleven firefighters were killed in one separate incident in a nature reserve in the Guadalajara area east of Madrid, Spain, on July 17, 2005. (Courtesy Publico newspaper; photo by Paulo Ricca.)

241

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

can easily manage simple to complex operational, logistic, planning, and fiscal functions associated with wildfire suppression actions.113,184,332 Many other countries have followed a somewhat similar path in their evolution with regard to wildland fire suppression and supporting research and development.382-384,387 Modern fire suppression technology, however, cannot indefinitely reduce the area burned by wildfires, as demonstrated, for example, by numerous large fires and major fire seasons in the past 30 years or so in North America: Mack Lake fire in Michigan in 1980; the “Siege of ’87” in California in 1987; Silver Complex in Oregon in 1987; Greater Yellowstone Area fires in 1988; Stanislaus Complex in California in 1989; Foothills fire near Boise, Idaho, in 1992; Garnet fire near Penticton, British Columbia, in 1994; Millers Reach fire in Alaska in 1996; Virginia Hills fire in Alberta in 1998; Florida fires of 1998; Silver Creek fire in British Columbia in 1998; Cerro Grande fire in New Mexico in 2000; Valley Complex in Montana in 2000; Chisholm fire in Alberta in 2001; Biscuit fire in Oregon in 2002; Hayman fire in Colorado in 2002; Rodeo/Chedeski fire in Arizona in 2002; House River fire in Alberta in 2003; “Firestorm 2003” season in British Columbia; and record-setting fire seasons in Alaska and the Yukon Territory in 2004 (Figure 12-6, online), to name a few. Similar incidents have occurred in other regions of the world. The hard lesson learned from these and other fires is that wildfires are inevitable. Several factors have coincided to produce massive forest

PART 3  BURNS, FIRE, AND RADIATION

brome, in the arid regions of the western United States has increased the frequency of fires in desert shrublands.529 Wildland fires can benefit plant and animal communities. Evolutionary development produces plant species well adapted to recurrent fires. Fire tends to recycle ecosystems and maintain diversity.267,523 Thus, there is growing consensus that fire should be returned to many wildland ecosystems where appropriate to perpetuate desirable fire-adapted plant and animal communities and to reduce fuel accumulations.240 A landmark report in 1963 to the National Park Service by the Advisory Board on Wildlife Management259 described how the western slope of the Sierra Nevada had been transformed by fire protection:

A

When the forty-niners poured over the Sierra Nevada into California, those that kept diaries spoke almost to a man of the wide-spaced columns of mature trees that grew on the lower western slope in gigantic magnificence. Today much of the west slope is a dog-hair thicket of young pines, white fir, incense-cedar, and mature brush—a direct function of overprotection from natural ground fires. Not only is this accumulation of fuel dangerous to the giant sequoias and other mature trees, but the animal life is meager, wildflowers are sparse, and, to some at least, the vegetative tangle is depressing, not uplifting. It must also be acknowledged that in some cases, past logging practices contributed to the resulting fuel structure. Nevertheless, the board recommended that the Park Service recognize in management programs the importance of the natural role of fire in shaping plant communities.

WILDLAND FIRE MANAGEMENT POLICIES

B FIGURE 12-3  A helitorch or flying drip torch is a specialized aerial ignition device slung below and activated from a helicopter (A). It dispenses and ignites gelled fuel. The use of a helitorch in wildfire suppression operations can take many forms (e.g., to reduce the intensity, slow, or steer a fire; to remove potentially dangerous fuel concentrations; to widen and strengthen control lines; to expedite mop-up operations). Regardless of its specific purpose, the main objective of this application of “fighting fire with fire” is to speed up or strengthen control actions (B). Aerial backfiring and burning out with a helitorch can be one of the safest, most economic, fastest, and least damaging means of widening control lines and constitutes one of the major innovations in wildland fire suppression technology in the past 30 years. The helitorch is also used in prescribed burning operations. (Courtesy Alberta Sustainable Resource Development and Wildfire Consulting Ltd, Edmonton, Alberta; photos by O. Spencer and W. Bereska.)

mortality, including drought, epidemic levels of insects and diseases,239,319,324 and unnatural accumulations of fuels at the stand level and at a growing landscape scale in some but not necessarily all vegetation types241 as a result of attempted fire exclusion.16,211 This result in the dry forest types of the western United States was foreshadowed by a forester, Harold Weaver,499 in the early 1940s. Many agencies are now using prescribed fire more frequently, deliberately burning under predetermined conditions to reduce accumulations of fuels and to protect human life, property, and other values that are at risk by wildfire.301,320,354 Research has indicated that fires are not categorically bad. In fact, many plant communities in North America are highly flammable during certain periods in their life cycles.81 For example, annual grasses, ponderosa pine, and chaparral plant communities are flammable during almost every dry season. Other communities, such as jack pine or lodgepole pine forests, although fire resistant during much of their life cycle, eventually become fire prone when killed by insects, diseases, and other natural causes. The spread of non-native grasses, such as cheatgrass and red 242

Recent tragedies in the western United States have focused attention on the need to reduce hazardous fuel accumulations.443 The events associated with the 1994 fire season in particular created a renewed awareness and concern among federal land management agencies about wildfire impacts, leading to a combined review of fire policies and programs. The result was enactment

FIGURE 12-4  Specialized fixed-wing aircraft like the amphibious CL-415 “superscooper” are capable of delivering water and chemical fire retardants on or near a wildfire. Although such planes are used in sustained-action situations on isolated sectors of large fires, they are most effective in initial attack operations during the incipient phase of fire growth. In such cases, their primary purpose is to slow down the progress of the fire until such time as ground suppression resources are able to arrive and effect direct containment. Wing-tip vortices are created in the wake of low-flying aircraft. These vortices gradually dissipate as they descend to the ground level. They can cause a sudden, unexpected increase in fire activity as a result of the momentary wind gust. This can pose a threat to anyone located near the fire perimeter. (Photo by T. Nebbs.)

of a new interagency federal wildland fire management policy, which provided a common approach to wildland fire among federal agencies and called for close cooperation with tribal, state, and other jurisdictions.337 The principal points of the 1995 federal wildland fire policies are as follows: • Firefighter and public safety remains the first priority in wildland fire management. Protection of natural and cultural resources and property is the second priority. • Wildland fire, as a critical natural process, must be reintroduced into the ecosystem, accomplished across agency boundaries, and based on the best available science. • Where wildland fire cannot be safely reintroduced because of hazardous fuel accumulations, pretreatment must be considered, particularly in the wildland–urban interface. • Wildland fire management decisions and resource management decisions are connected and based on approved plans. Agencies must be able to choose from the full spectrum of actions—from prompt suppression to allowing fire to have an ecologic function. • All aspects of wildland fire management will involve all partners and have compatible programs, activities, and processes. • The role of federal agencies in the wildland–urban interface includes firefighting, hazardous fuel reduction, cooperative prevention and education, and technical assistance. Ultimately, the primary responsibility rests at the state and local levels. • Structural fire protection in the wildland–urban interface is the responsibility of tribal, state, and local governments.

PRESCRIBED FIRE AND WILDLAND FIRE USE Prescribed fire, the intentional ignition of grass, shrub, or forest fuels for specific purposes according to predetermined conditions, is a recognized land management practice.35,494,508 The objectives of such burning vary: to reduce fire hazards after 243

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

FIGURE 12-5  Several different sizes and models of rotary-wing aircraft or helicopters are used in a wide variety of direct roles as well as support functions in wildland fire suppression, including the dropping of water or fire-retarding chemicals directly on the fire. Helicopters  also create wake vortices while in forward motion, just like airplanes, but generally these vortices are much weaker. A more common safety issue with helicopters is the downward induced air flow or rotary downwash. Some downwash effects are unavoidable when helicopters are engaged in direct attack on the fire with water or chemicals. Anyone located near the fire perimeter during such operations could be at risk. Even with a “long line” delivery system operated from a Bell 212 helicopter, as illustrated here on the Anarchist Mountain fire near Osoyoos in southern British Columbia on July 16, 2003, rotary downwash can still be a significant issue. (Courtesy Alberta Sustainable Resource Development.)

• Federal agencies must better educate internal and external audiences about how and why we use and manage wildland fire. The 1995 U.S. federal wildland fire management policy was reviewed and updated in 2001,342 following a particularly severe fire season in the western United States the year before; about 2.8 million hectares (about 7 million acres) were burned over by about 89,000 fires during the 2000 fire season in the United States.479 Results of the 2001 review and update were defined in the “2003 Interagency Strategy for the Implementation of Federal Fire Management Policy.”254 This strategy broadened the scope of fire management to balance fire suppression with management for ecologic benefits and supports the use of the full range of fire management activities to achieve ecosystem stability, including fire use. The 2003 implementation strategy stresses the need to complete or revise fire management plans that are more effectively and directly integrated with other natural resource goals.78 One of the other outgrowths of the 2000 fire season was the National Fire Plan (http://www.fireplan.gov), which calls for the following actions: • Ensuring that necessary firefighting resources and personnel are available to respond to wildland fires that threaten lives and property • Conducting emergency stabilization and rehabilitation activities on landscapes and communities affected by wildland fire • Reducing hazardous fuels (dry brush and trees that have accumulated and increase the likelihood of unusually large fires) in the country’s forests and rangelands • Providing assistance to communities that have been or may be threatened by wildland fire • Committing to the Wildland Fire Leadership Council, an interagency team created to set and maintain high standards for wildland fire management on public lands It is clear from these objectives that one of the major foci of the U.S. National Fire Plan is the human dimension of wildfire (i.e., rural homeowners and communities).235,270 The 2003 implementation strategy was reviewed during a field test in 2008 and resulted in a 2009 policy revision. The revision removed the distinction between wildland fire use and wildfire.254 It provides the highest degree of flexibility ever afforded to managers and facilitates their ability to respond to changing conditions and complexities of a wildfire event. In 2005, the Canadian Council of Forest Ministers signed off on the Canadian Wildland Fire Strategy Declaration,107 which is based on principles of risk management and hazard mitigation. This strategy will strive to strike a balance between public safety, forest protection and health, and fire management expenditures that maintains a strong and effective fire suppression organization, but it also includes innovative hazard mitigation, preparedness, and recovery programs—in other words, a more holistic view of wildland fire envisioned some 40 years ago as land management agencies made the transition from fire control to fire management. This strategy recognizes the need for shared responsibility among the various stakeholders (i.e., property owners, industries, and local, provincial, and federal governments).230 One of the guiding principles of this new declaration was that “public safety—including the safety of firefighters—is paramount.” Fire management policies similar to those of the United States and Canada exist in other parts of the world.191 The Food and Agriculture Organization of the United Nations192 prepared a generic set of fire management guidelines to serve as a basis for developing policies. The Fire Paradox project, a research initiative supported by the European Commission from 2006 to 2010 (http://www.fireparadox.com), examined wildland fire from multiple perspectives as a basis for influencing policies regarding integrated fire management.426

PART 3  BURNS, FIRE, AND RADIATION

logging, expose mineral soil for seedbeds, regulate insects and diseases, perpetuate natural ecosystems, and improve range forage and wildlife habitat.307,500 In some areas managed by the National Park Service, USDA Forest Service, and Bureau of Land Management, naturally ignited fires may be allowed to burn according to approved prescriptions; fire management areas have been established in national parks and wildernesses from the Florida Everglades to the Sierra Nevada in California (Figure 12-7, online). Planned-ignition prescribed fires are also carried out. Similar policies exist in Canadian National Parks.224 Visitors are increasingly aware that wildland fires can be an important part of the natural cycle of an ecosystem and that the future health of parkland may depend in part on today’s managed fires.

Wildland–Urban Interface: New Look of a Historical Problem Just as resource agencies are attempting to provide a more natural role for fire in wildland ecosystems, the general public is increasingly living and seeking recreation in many of these areas. The area where houses and other human-made structures meet or are intermingled with wildland vegetation is regarded as the wildland–urban interface or intermix, although other names have been used (Figure 12-8, online). It is a growing problem from a wildland fire perspective in the United States73,391,467 and many other regions of the world.228 As mentioned earlier, past fire exclusion practices in the United States have allowed abnormal fuel accumulations in some forest types and regions, and this fact has combined with the sacrifice of relatively safe perimeter fire suppression strategies in favor of directly protecting people and their possessions.518 Direct suppression actions within the fire’s perimeter place firefighters at a greater disadvantage from a safety standpoint. The new interagency policy that emphasizes firefighter and public safety as the first priority will result in less effort to save structures in dangerous situations. Thus, what is known of fire behavior and fire survival principles must be readily available to emergency medical personnel, wildland dwellers, and recreationists. In fact, fire protection agencies and others have been making such information more readily available to the general public for some time now,114,162,193,501 although much more needs to be done.17

NATURE OF THE PROBLEM Hot, dry, and windy conditions annually produce high-intensity fires that threaten or burn homes where wildland and urban areas converge (Box 12-1). Can the historical levels of destruction, injury, and fatality be repeated today in the face of modern fire suppression technology? The answer to this question requires an analysis of the conditions that created such high-intensity fire behavior events in the forests of northern Idaho and northwestern Montana during late August 1910 (Figure 12-9, online) in which 85 people (Figure 12-10), including 78 firefighters, were killed.135,179,385,438 The earliest fire incident of note involving a large loss of human life was the series of conflagrations in the Miramichi region of New Brunswick and adjacent areas in Maine in early October 1825, in which at least 160 people139,374 perished.471 This was followed by several fatality fires in the U.S. Lake States region, including the Peshtigo and area fires in eastern Wisconsin in October 1871 (about 1300 fatalities),227,260,510 the Lower Michigan fires of September 1881 (169 fatalities),232 the Hinckley fire in east-central Minnesota in September 1894 (418 fatalities),252 the Baudette fire in northern Minnesota in October 1910 (42 fatalities),374 and the Cloquet fire in Minnesota in October 1918 (538 fatalities).108,232 The western United States experienced other fatality fires, such as in western Washington and Oregon in midSeptember 1902 (38 fatalities).77,296 Canada suffered similar tragedies. For example, the province of Ontario experienced several significant settler-related wildfire fatalities in 1911, 1922, and 1938, including the 1916 “Matheson Holocaust” in which as many as 400 people were killed.53,159,295 In 1908, a forest fire destroyed the city of Fernie, British Columbia. Twenty-two people were reported killed.276 244

Other countries, such as New Zealand299 and France,193 are reported to have suffered similar but varying losses in the 20th century. In Australia, for example, possessing some of the world’s most fire-prone environments,115 71 lives were lost in the state of Victoria on “Black Friday” in January 1939.193,351 On August 1, 1959, 48 people were reported killed by a forest fire northeast of Massif des Aures, Algeria.234 In early September 1963, forest fires swept about 2 million hectares (about 4.9 million acres) in Paraná State in southern Brazil, destroying more than 5000 homes and killing 110 people.434 More than 100 people were killed by extensive forest and savannah fires in Cote D’Ivoire (Republic of Ivory Coast) on the southern coast of western Africa during the 1982-1983 fire season.415 On October 8, 1871, the same day that fire wiped out the town of Peshtigo, Wisconsin, and surrounding communities, the Great Chicago fire devastated urban Chicago.510 Comparative statistics for those two fires highlight the destructive potential of wildland fires. In every way, the Peshtigo conflagration was far worse than the Chicago blaze. The Peshtigo fire covered about 518,000 hectares (about 1,280,000 acres) and killed about 1300 people, whereas 906 hectares (2240 acres) burned and some 200 lives were lost as a result of the Chicago fire.217 The Great Chicago fire is generally acknowledged as the birthplace of modern urban fire prevention. As Lloyd265 notes, “mention the name Peshtigo to most people and all you get is a blank stare. Mention Mrs. O’Leary’s cow to the same person and they will think right away of the Great Chicago fire” and “Some of the same social misconceptions that allowed Peshtigo to be all but forgotten persist today.” So, it is perhaps fitting to consider the following poem entitled “The Peshtigo Calamity:”232 As the years roll along and the ages have sped O’er the charred, blackened bones of the Peshtigo dead, And the story is told by the pen of the sage, In letters immortal on history’s page— No fancy can compass the horror and fright The anguish and woe of that terrible night. The August 1910 wildfires in northern Idaho and Montana had several elements in common with the Peshtigo fires of 1871: many uncontrolled fires burning at one time; prolonged drought, high temperatures, and moderate to strong winds; and mixed conifer and hardwood fuels with slash from logging and land clearing. These large fires occurred primarily in conifer forests north of the 42nd meridian, or roughly across the northern quarter of the contiguous United States.77 One of these critical elements that is not as likely to occur today as formerly is the

FIGURE 12-10  Burned ruins of the foundry in Wallace, Idaho, furnish mute testimony to the destructive force of the 1910 fires. The cottage on the terrace was the only one left standing in that part of town. Of the 85 people reported killed in the “big blowup of 1910,” 78 were firefighters. (Courtesy USDA Forest Service; photo by R.H. McKay.)

D. Blasor-Bernhardt68

B12-1  Tok, Alaska, July 1, 1990, 15 to 30 minutes after the lightning strike that started the Tok fire. (Photo by D. Blasor-Bernhardt.)

July 1, 1990, started out like any other Sunday, but it quickly turned Tok, Alaska, into a near raging inferno. I was working at the Chamber of Commerce Main Street Visitor Centre when an otherwise beautiful day suddenly turned black and foreboding. Blowing in, a huge thundercell hung just southeast of town. I stepped outside just in time to see a long, crooked finger of electricity split from an ominous cloud and drill its way into Earth. Minutes later, where the lightning had hit, a mushroom-shaped cloud began to grow. I grabbed my camera and snapped a few shots. Five days later, and in spite of several thousand firefighters and equipment from all over Alaska, Canada, and the States, Tok was completely under siege and at risk of being cremated. The wind-blown inferno licked greedily at several unoccupied dwellings, then consumed them. East-side residents were evacuated. We, on the west side, were told to pack our things, to be ready to leave, and to await further instructions. Tok was enveloped on two sides by fire—from the eastern and northern directions. My log home was about a mile from the north front of the fire. I stood on the cabin’s sod roof, watching the fire,

when the kids and extended family converged there about the same time, looking to me for instructions. All day, I had the sprinklers and hoses running full blast over the cabins, garage, and surrounding area. By now, the area looked like a swamp. Good. I’d leave them on, even if we evacuated, in the hope that it would help save some of our place from destruction. Smoke stifled each breath. Helicopters screamed back and forth carrying people, equipment, and large buckets of water. There was no fear, no panic, in anyone—just resignation. And there was no way our town would be destroyed. I told the kids to first pack up whatever was closest to their hearts—it didn’t matter how silly an item seemed if that made them feel good. The first thing I placed in my own car was my late husband’s ashes. I couldn’t bear to leave him behind. Next, we would take irreplaceable things: photo albums, mementos. Then down to brass tacks: the necessary things for survival and rebuilding in the event we were burned out. Bombers loaded with retardant flew directly overhead. We were in a war zone—man against fire. The girls loaded their cars with personal items. Mine was loaded with blankets, groceries, and clothing. The boys readied our tandem-axle trailer, loading it with items from the garage— chainsaws, tools, portable generator, water jugs. If the fire drew too near and we had to evacuate, the plan was for the girls and I to load our pets while the boys quickly cut the trees down around the cabins, hopefully providing a bare, wet perimeter between them and the fire. Fully loaded, we assembled in the driveway, ready for word to come. Besides myself, six young adults, a baby, half a dozen dogs, numerous cats, a snake, six vehicles, and a trailer comprised the Bernhardt entourage. We were ready. We waited in the foul air, our eyes smarting from the smoke. An ember hit me on the shoulder, burning a hole though my shirt. Sadly, I turned to look at our homes one last time. Tomorrow they would be gone. Imperceptibly at first, a slight shift in the wind began. I held my breath. “Mom?” my son said. “Yes,” I answered, “but I’m afraid to hope.” The wind, definitely shifting now, was no longer blowing toward us. A sweet, light rain began to fall. While the eight of us stood together, soaking wet in the rain, a trooper came by to tell us the worst was over. In all, the fire burned 109,501 acres (44,314 hectares) at a cost of over $35 million (U.S.), yet not one person had been injured, not one occupied dwelling destroyed, and Tok had been spared by a miracle wind.

From Blasor-Bernhardt D: A town that nearly went … up in smoke, Guide to the Goldfields and Beyond (Harper Street Publishing, Dawson City, Yukon Territory) Summer: 52, 1997.

simultaneous presence of many uncontrolled fires. The effectiveness of modern fire suppression organizations is now able to reach even the most remote wildland locations. High-velocity winds and more than 1600 individual fires contributed to the spread of the fires in 1910; it is unlikely that a multifire situation of that magnitude would occur today.80,115 However, multiple fire starts are still possible owing to human-caused ignitions (e.g., arson, power lines). For example, on October 16, 1991, 92 separate fires occurred in the Spokane region of eastern Washington329 in the space of a few hours under the influence of exceedingly strong winds.31 Prolonged drought, high winds, and flammable fuel types, however, remain significant to the behavior of high-intensity fires. Some of the fires most potentially damaging to human lives and property occur in areas rich in chaparral shrub fuel in southern California. Wilson518 and Phillips372 described the severe 1970 fire season in California, in which official estimates showed that 97% of 1260 fires occurring between September 15 and November 15 were held to less than 121 hectares (300 acres). The other 3% of the fires, fueled by a prolonged drought and fanned by strong Santa Ana winds, produced 14 deaths, destroyed 885 homes, and burned about 243,000 hectares (about 600,000 acres), as chronicled in the 1971 film Countdown to Calamity. Ten years later, the situation recurred over 9550 hectares (23,600 acres) in southern California, the Panorama fire in November 1980, which

resulted in the deaths of 4 people and loss of more than 325 structures.104 On October 20, 1991, a devastating fire “of unprecedented force blew out of control”4 in the hills above Oakland and Berkeley, California. Burning embers carried by high winds from the perimeter of a small fire resulted in a major wildland–urban interface conflagration. The impact on people and their possessions was enormous.4,453 The fire resulted in direct deaths of 25 people, including a police officer and a firefighter, injured 150 others, destroyed 2449 single-family dwellings and 437 apartment and condominium units, burned about 650 hectares (about 1600 acres), and did an estimated $1.5 billion in damage.328 The scenario for disaster included a 5-year drought that had dried out overgrown grass, shrubs, and trees, making them readily ignitable. Other factors included untreated wood shingles, unprotected wooden decks that projected out over steep terrain, low relative humidity, high temperatures, and strong winds that averaged 32 km/hr (20 mph) and gusted up to 56 to 80 km/hr (35 to 50 mph). The area had not experienced any rain for 67 days before the major fire run, although mean monthly maximum temperatures in the 6 months preceding the fire were not appreciably high (i.e., 18° to 23° C, or 64° to 73° F).32 These severe conditions produced a voracious fire that consumed 790 homes in the first hour. Winds lessened to 8 km/hr (5 mph) by the first evening, which assisted with the containment of the fire. 245

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

BOX 12-1  What Is It Like to Experience a Wildland–Urban Interface Fire? A Town That Nearly Went…Up in Smoke by

PART 3  BURNS, FIRE, AND RADIATION

wildfires is the result of a small percentage of fires.446 Thus, on some days, adverse fuel and weather conditions, coupled with an ignition source, will conspire to produce conflagrations that occur in spite of our best fire prevention, detection, and initial attack efforts. Climate change will only exacerbate the situation.188 Recent research involving simulations of evacuations in response to a threatening wildfire has revealed that strategic planning is essential.152-154,163 Communities need to ensure that they are fully prepared well in advance of a threatening wildfire occurrence by developing individual and local government emergency action plans.364 Taylor455 has emphasized that managing the fire risk at the wildland–urban interface is a shared responsibility involving both private citizens and numerous government agencies. Past fire experiences in Australia360,501 have demonstrated that quite often “houses protect people and people protect houses.” Research had demonstrated that a well-prepared house can provide protection from fire and that the presence of people prepared to defend against their home burning down is the most significant factor in determining its survival (Table 12-1). Obviously, zones of defendable space around homes must be established in advance of fires; the young, older adults, and infirm are generally encouraged to leave well ahead of the fire. Communities at risk from wildfires should be encouraged to be responsible for their own safety, because fire service personnel may not be available when burning conditions are severe. The major issue is whether able-bodied residents should stay and defend or “fight” for their homes, or “flee” in the hopes of escaping an advancing fire.516 In the late 1990s, the Tasmania Fire Service had a policy that provided guidance on bushfire safety and evacuation decision making called “Prepare, Stay, and Survive.”205 When there was a threatening wildfire, people were told to go home and assist in the protection of their property. Because human lives and property values are at risk when threatened by wildfires, exemplary cooperation and teamwork are required to ensure adequate safety margins. Team members identified for reducing the loss of life and property include state agencies, local government, the communities, and individuals. The “Stay or Go” policy concerning evacuation was advocated by the Australasian Fire Authorities Council (AFAC)45

Firefighters had the situation under control by the fourth day, but not before they had been given an awful glimpse of the nature of fires in the future. In late October 2003, fires in southern California burned over 300,000 hectares (742,000 acres) in 1 week alone, taking 23 lives and destroying more than 3300 homes.103,242,322 In recent times, wildland fire fatalities among the general public have not been restricted to just California, or the United States for that matter. Four civilians were killed as a result of the massive forest conflagration that converged on the outskirts of Canberra, Australia, in January 2003.3 During the summer of 2003 in Portugal, 21 people lost their lives in 18 different fire incidents.488,493 On January 11, 2005, 9 people (including 4 children and 2 firefighters) perished on the Eyre Peninsula of South Australia as a result of being overrun by an extremely fast-spreading grass fire in what is now referred to as “Black Tuesday” in the state.125,430,437 Mutch and Keller323 give a compelling account of the wildfires that occurred in Texas and Oklahoma during late 2005 and the early part of 2006, in which 19 civilians and 6 firefighters lost their lives. In many parts of the world, but especially in the United States and Canada, the primary response has been to evacuate all people threatened by wildfires.1,136,390 For example, more than 200,000 people were evacuated in Canada between 1980 and 2007 in more than 500 separate incidents67 The pros and cons of evacuation are extensively discussed in Chapter 12 of Webster’s seminal work,501 The Complete Bushfire Saftey Book, entitled “The Decision—Evacuate or Stay? Safety or Suicide?” In this regard, Phil Cheney,119 a renowned Australian bushfire research scientist, feels that “What it comes down to is a civil right to risk your own life to save your house. I personally am in favor of people taking risks in their lives provided that they also bear the responsibility for the consequences.” Some amazing logistic feats have taken place to date without incident using both ground and air transportation. A good example of the latter occurred in early June 1995 as the residents of Fort Norman and Norman Wells in Canada’s Northwest Territories were airlifted to Yellowknife, the territorial capital.160 However, statements later on from the public like “I think they took us away just in time” suggest that this approach is not infinitely infallible. Coupled with this reality is the fact that modern fire records indicate that the vast majority of area burned by

TABLE 12-1  Approximate Probabilities of a House Surviving a Wildland Fire* Scenario Scenario Scenario Scenario

A: Total disregard for any fire safety precautions B: Fire safety precautions taken only in regard to fuels surrounding house C: Fire safety precautions taken only in regard to the house itself D: All reasonable fire safety precautions to and near the house taken Without Persons in Attendance Fire Intensity Class (kW/m)

Scenario

500-1,500

1,500-10,000

With Persons in Attendance Fire Intensity Class (kW/m)

10,000-60,000

Scenario

A 14.4% 1.2% 0.3% B 16.0% 4.9% 1.0% C 26.1% 8.7% 1.9% D 59.1% 28.1% 7.4% kW/m × 0.29 = BTU/sec-ft The following attributes were considered in the above scenarios:

A B C D

500-1500

1500-10,000

10,000-60,000

29.9% 63.6% 76.5% 93.0%

10.3% 32.1% 46.8% 78.2%

2.3% 8.9% 15.3% 42.6%

Scenario House and Surrounding Fuel Conditions

A

B

C

D

Flammable objects nearby (e.g., firewood heap)? Wooden shingle roof? Nonwooden or nontile roof with pitch >10°? External walls made of brick, stone, or concrete? Trees (5+ m high) within 40 m of house?

Yes Yes No No Yes

No Yes No No No

Yes No Yes Yes Yes

No No Yes Yes No

From Alexander ME: Proposed revision of fire danger class criteria for forest and rural areas in New Zealand, ed 2, Christchurch, New Zealand, 2008, Scion Rural Fire Research Group. http://www.scionresearch.com/fire. m × 3.3 = ft. *Based on a logistic regression model as developed from an analysis of 455 houses, which were completely destroyed, threatened, or sustained minor damage by the bushfire that swept through the township of Mount Macedon in Victoria, Australia on the evening of Ash Wednesday (February 16) in 1983.515,517

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*References 87, 89, 221, 225, 266, 464.

where houses are able to survive fires even when fire services personnel are not available. The “team” would consist of the effective partnership between the fire services and home dwellers. The “theme” would comprise the dual strategy of adequate defensible space coupled with the home dweller’s motivation to remain on site as an important factor in suppressing fires initiated by ember attack. In order for this approach to work, rural homeowners must understand that although wildfires can be dangerous, with proper precautions, people can remain with their homes and be an important part of the solution to the wildland– urban interface fire problem. Empowering communities at risk from wildfire to play an active part in their own protection is viewed as a viable long-term strategy to enable safe and harmonious coexistence with fire as an element of nature.117 During the 2000 fire season in western Montana, some individuals took it upon themselves to stay with their homes as flame fronts advanced. They created defensible space, installed sprinkler systems, engaged in fire suppression activities, and provided local intelligence to incoming fire service personnel. No home was lost as people demonstrated responsibility for their personal well-being. A similar “prepare, stay, and defend” action was successfully carried out during the 2003 fire season on the Wedge fire along the North Fork of the Flathead River in western Montana. The property was prepared in advance to be “fire safe,” the homeowner remained with volunteer fire department officials, and the home survived the passage of a high-intensity crown fire (Figure 12-11). Wildland fires that threaten human lives and property are not exclusively located in southern California because the exodus to wildland regions has become a national phenomenon. Fires burned about 81,000 hectares (about 200,000 acres) in Maine in October 1947, killing 16 people;100,172 another area of about 81,000 hectares (about 200,000 acres) burned in New Jersey in April 1963.52 Wildland fire disasters have not always been large

A

B FIGURE 12-11  Homeowners and firefighters (A) successfully prepared, stayed, and defended this rural home in western Montana from a high-intensity flame front (B) associated with the Wedge fire in July 2003. (Courtesy Big Fork Volunteer Fire Department.)

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as a fundamental component of community bushfire safety in Australia.222 Variants to this general theme exist (e.g., “prepare, leave early, or stay and defend”). However, the essence of the approach urges people to make the decision to prepare themselves and their properties to “stay” and defend when a wildfire is likely, or to “go” well before a fire is likely to arrive. Although early evacuation may contribute to increased personal safety, bushfire property losses are likely to increase. Conversely, late evacuation may put people at greater risk than had they stayed in the house as the fire passed around them. An evaluation of this policy is the focus of Project C 6— Evaluation of Stay or Go Policy currently being undertaken by the Australian Bushfire Cooperative Research Centre (http:// www.bushfirecrc.com/research/c61/c61.html), led by co–project leaders John Handmer, RMIT University, and Alan Rhodes, Country Fire Authority of Victoria. Fire management agencies and the public alike will no doubt find the final results of this research project of great interest. Preliminary results emerging from the project generally supported the 2005 AFAC position, while recognizing that implementation issues remained.* However, the fires of February 7, 2009, in Victoria, Australia, and in turn the Royal Commission’s report459 have changed the context for this approach quite significantly. There are a number of emerging issues (e.g., limit of validity), so the policy is most likely to evolve in coming years399in the aftermath of the Black Saturday fires, as evidenced by AFAC’s revised position on bushfire community safety based on emergency risk management principles.49 The 2009 Black Saturday fires have placed an urgent emphasis on the continuing debate over what constitutes the safest strategies for survival in the wildland–urban interface. The Victorian fires led to the creation of a catastrophic, or “Code Red,” level of fire danger. When this category of fire danger is forecast for the next day, it is recommended that people in a high-risk bushfire area leave the night before or in the early morning (http:// www.cfa.vic.gov.au/firesafety/bushfire/danger-warnings.htm). At the next two lower levels (i.e., “Extreme” and “Severe”), it is recommended to stay only if one’s home is well prepared, well constructed, and can be actively defended. Testimony by John Handmer before the 2009 Victorian Bushfires Royal Commission,459 coupled with analyses produced by him and his research team,220 indicate that only a small percentage of homes and property were adequately prepared to be fire resistant. Without preparing a fire-resistant home and property in advance, the only prudent course of action is to evacuate early. This issue of whether to “prepare, stay, and defend” or evacuate early is a subject considered worthy of more open debate and discussion in North America.17,294,325,365,442 Two communities in the United States—Painted Rocks in Montana and Rancho Sante Fe in California—have adopted variations of the original Australian model of “Prepare, Go Early or Stay and Defend.”325 Both communities have had the “Stay and Defend” practice successfully tested by wildfires. Both U.S. communities are carefully monitoring the lessons learned from the 2009 Black Saturday fires to determine if any change is needed in their approach. Meanwhile, Ready, Set, Go! (RSG) was rolled out as a full-scale pilot program by the Ventura County Fire Department and the Orange County Fire Authority for the 2009 fire season in Southern California. Other fire departments, such as Los Angeles County,151 Los Angeles City, San Bernardino County, Riverside County, Santa Barbara County, and Cal Fire, have adopted the basic approach. The RSG approach involves preparing one’s house to withstand a wildfire, preparing one’s family for evacuation, and finally, leaving earlier. The program is now endorsed by the International Association of Fire Chiefs (http://www.iafc.org/displaycommon. cfm?an=1&subarticlenbr=1229). In many regions of the world, people are warned that wildfires are dangerous and that they always need to evacuate. This scare tactic approach reinforces the concepts that wildland fires are always dangerous and that people must leave their homes. Perhaps one solution to dealing with fires in the wildland–urban interface in the future would be to embrace the concept of “A Dream, a Team, and a Theme.”321 The “dream” would be one

PART 3  BURNS, FIRE, AND RADIATION

in size. On September 26, 1936, most of the coastal town of Bandon in western Oregon was destroyed, and 11 people were killed by a wildfire that covered probably no more than about 4000 hectares (about 10,000 acres).232 The prevalence of gorse (Figure 12-12), a non-native plant, was considered a key contributing factor to the resulting devastation. More recently, on July 16, 1977, the Pattee Canyon fire in Missoula, Montana, destroyed 6 homes and charred about 500 hectares (about 1200 acres) of

A

B

C FIGURE 12-12  Old man’s gorse (Ulex europaeus) is probably the worst fuel type (A) in the world from the standpoint of wildland fire management for two main reasons. The density of the vegetation and its sharp spines or thorns (B) make it extremely difficult if not nearly impossible to physically engage in any kind of fire suppression activity. Vigorous stands grow outward, crowding out all vegetation and forming a center of fine, dry, dead, elevated fuel. This fuel structure, coupled with the plant’s oil content, readily contribute to the development of high-intensity flame fronts even under relatively mild fire weather conditions (C). Gorse is native to central and western Europe, where it has long been cultivated for hedgerows. It has been introduced to Australia, New Zealand, the west coast of the United States (California, Oregon, and Washington), and southwestern British Columbia. It has also been reported in Costa Rica and the Hawaiian Islands. In the northeastern United States, it has established itself along the Atlantic Coast from Virginia to Massachusetts. (Courtesy Ensis Bushfire Research Group, New Zealand.)

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forests and grasslands in only a few hours.187 Similarly, more than 70 homes were damaged or destroyed by fires in the southern Cape Peninsula region of South Africa that burned about 8000 hectares (about 19,800 acres), during January 16 to 20, 2001.105,486 A whole host of other cases have occurred in North America231 and are steadily accumulating. Fires at the wildland–urban interface are also increasing internationally. For example, the Ash Wednesday fire disaster in southeastern Australia on February 16, 1983, burned about 340,000 hectares (about 840,000 acres) of urban, forested, and pastoral lands in the states of Victoria and South Australia, killing 77 people, injuring some 3500, and destroying more than 2500 homes.57,226,352 Phenomenal fire spread rates in both forests and grasslands occurred,243,393 and flame heights of almost 200 m (650 feet) were observed.454 In May 1987, wildfires in northeastern China409 added a new perspective regarding the devastating impact wildland fires may have on human lives, property, and natural resources. These fires reportedly burned about 1.34 million hectares (about 3.31 million acres), killed 212 people, seriously injured another 226, and left about 56,000 homeless.166 Clearly, it was a disaster of major proportions. These fires resulted from a combination of heavy dry fuels, sustained drought, and strong winds.448 Rates of spread during the major runs reached 20 km/hr (12 mph). Protecting lives and property from wildfires at the wildland–urban interface represents one of the greatest challenges faced by wildfire protection agencies. Large forest fires during the intense El Niño drought conditions of 1997 and 1998 focused public and media attention once again on the need to evaluate public policies and practices in the forestry and nonforestry sectors that directly or indirectly contribute to the impact of wildland fires. The size and damage attributed to these fires were so immense that the Christian Science Monitor termed 1998 “The Year the Earth Caught Fire.” At times, that seemed to be literally true, as smoke palls blanketed large regional areas, disrupted air and sea navigation, and caused serious public health threats.206,389,414,522 At least 60 people were killed in Mexico as a result of the fires,468 and ecosystems that generally are not subjected to fires, such as the Amazon rain forest and the cloud forest of Chiapas, Mexico, sustained considerable damage. A global fire conference sponsored by the Food and Agricultural Organization of the United Nations in October 1998 brought together specialists from 33 countries to review the serious nature of worldwide fires.191 Participants at the conference in Rome concluded that governments needed to enact more sustainable land use policies and practices to reduce the impacts of wildfires on people and natural resources. It is becoming increasingly rare to have a wildland fire situation or incident that does not involve people and their homes. However, people are not fully aware of the fire risks and hazards of living and traveling in or near wildlands.62,214 Risk, in the jargon of the wildland fire specialist, is the probability that a fire will occur. Hazard is the likelihood that a fire, once started, will cause unwanted results. Risk deals with causative agents or ignition sources; hazard deals with the fuel complex.197 The results of two surveys carried out in the western United States during the 1970s indicated a general feeling of overconfidence by most residents toward the potential danger or threat of a wildland fire. Eighty percent of Seeley Lake, Montana, forest residents interviewed thought that the forest fire hazard was low to moderate in their area.196 Seventy-five percent of Colorado residents interviewed thought that the forest fire hazard was low or moderate in mountain subdivisions of their state.233 Forest fire hazards in these two areas were much higher than these public estimates. In a survey of attitudes toward bushfires in the Dandenong Ranges of Victoria, Australia, it was found that people who had experienced bushfires tended to rank their area with a higher rating than did people without such experience.175 However, the survey also revealed that 40% of the people with recent severe bushfire experiences still did not rate bushfires as one of the three most important environmental problems in their area. Dr. Sarah McCaffrey,293 a research social scientist with the USDA Forest Service who has been studying the social dynamics of fire management for nearly a decade, has suggested that the general public is far better informed of the issues dealing with the wildland–urban fire problem interface than was the case during the 1970s and

starts, were unlikely to take all possible steps to safeguard their own properties, and exhibited a negative view of prescribed fire to the extent that it could preclude its use as a risk management tool. There is a growing need for the general public, emergency medical personnel, and fire suppression organizations to be well prepared to deal with wildland fire encounters (Box 12-2). As Reitz and Geissler396 have recently noted, “The old model of individual homeowners and neighborhoods depending solely on government provided firefighting resources is gone. Recent wildland fires have demonstrated that community firefighting resources are easily outpaced when multiple structures are burning simultaneously. The cure is to move most structure protection responsibility to the homeowner and community.” In 2000, 450 residents of Strathcona County, Alberta, Canada, were randomly selected to test which three educational methods would produce the greatest change in homeowner behavior with respect to the wildland–urban interface.444 The study showed that residents could be influenced to change their behaviors when provided with the information materials that enabled them to select between fire-safety alternatives. A recent study evaluated workshops for the adult public featuring experimental learning about wildland fire.363 Participants used hands-on activities to investigate fire behavior and ecology and to assess hazards in the wildland–urban interface. Effectiveness was examined using a pretest, a post-test following the program, and another post-test 30 days later. Participants’ knowledge increased after the workshop, and attitudes and beliefs became more supportive of fire management. The study concluded that hands-on activities can help adults become better informed about wildland fire and more positive about fire management.

BOX 12-2  Recommendations to Reduce Loss of Life and Property in the Wildland–Urban Interface Fire Protection Services • Remember that firefighter and public safety is the first priority in every fire management activity. • Ensure that all personnel receive regular cross-training in fighting wildfires and structural fires. • In urban departments, in particular, recognize the need to extinguish fires in wildland fuels by using thorough mop-up procedures. • Recognize the need for close coordination of response efforts among neighboring departments or agencies. • Develop specific mutual-aid plans for coordinating resources to attack fires in the wildland–urban interface. • Schedule and conduct regular mutual-aid training exercises. • Regularly schedule and conduct fire prevention and fire preparedness education programs for the general public and homeowners. • Conduct an assessment of fire risks, and prepare a strategic plan to reduce these risks. • Work effectively with lawmakers and other government officials to help prevent unsafe residential and business development. Legislators • Examine existing laws, regulations, and standards of other jurisdictions that are applicable locally in mitigating hazards associated with wildland fires. • Adopt National Fire Protection Association (NFPA) guidelines in the form of NFPA 1144, (formerly NFPA 299, 1991 edition) Standard for the Protection of Life and Property From Wildfire.330 The purpose of this standard is to provide criteria for fire agencies, land use planners, architects, developers, and local government for fire-safe development in areas that may be threatened by wildfire. NFPA 1144 provides minimum planning, construction, maintenance, education, and management elements for the protection of life, property, and other values that could be threatened by wildland fire. It is designed to assist local, state, and federal fire agencies in dealing with the escalating challenges presented by the proliferation of

wildland–urban interface communities and the monetary losses of structures in wildland–urban interface areas. These guidelines address the following topics: assessment and planning; access, ingress, egress, and evacuation; fuel modification area; water supply; and residential development design, location, and construction. • Provide strong building regulations that restrict untreated wood shingle roofs and other practices known to decrease the fire safety of a structure in the wildlands. Planners and Developers • Create a map of potential problem areas based on fuel type and known fire behavior. • Evaluate all existing or planned housing developments to determine relative wildland fire protection ratings and advise property owners of conditions and responsibilities. • Ensure that all developments have more than one ingress– egress route. • Offer options for fire-safe buildings. • Provide appropriate firebreaks, fuel breaks, or greenbelts in developments. • Ensure that adequate water supplies exist in developments. • Follow specifications in NFPA 1144 Standard for the Protection of Life and Property From Wildfire.330 Public and Homeowners • Determine the wildfire hazard potential of the immediate area before buying or moving into any home. • Contact federal, state, and local fire services for educational programs and materials regarding fire protection. • Provide a fuel-modified area or defensible space around vulnerable structures to reduce the likelihood of ignition by an advancing wildfire. • Design and build nonflammable homes. • Urge lawmakers to respond with legislative assistance to require appropriate fire safety measures for communities.

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1980s.290,291 She attributes this fundamental change to programs like Firewise, fire safe councils, and media coverage. No doubt the large number of conflagrations in the past 20 years has also contributed to an increased awareness regarding the realities of wildland fire. In more recent surveys carried out in Florida and Minnesota348 of homeowners’ preferences for vegetation and defensible space near their homes, people interviewed recognized the wildfire threat but varied in their perceptions of effective wildfire prevention measures and willingness to take actions to reduce the potential threat to themselves and their homes. Most supported the use of planned fire to reduce fire potential, especially if wildland fire experts who understand the local ecology and fire behavior conducted the prescribed burns. In-depth interviews conducted with homeowners along the northern part of the Colorado Front Range revealed that these people face difficult decisions regarding implementation of wildfire mitigation measures.76 Perceptions of wildfire mitigation options were found to be possibly as important as perceptions of risk in determining likelihood of implementation. These mitigation options were often viewed as tradeoffs between wildfire risk and preferred landscapes. The study participants also reported, however, that one-on-one information sharing with wildland fire experts, as well as increased understanding of the flexibility of mitigation options, encouraged implementation. Personalized contact appears to be a key factor in educating homeowners about the realities of living in a wildland environment.292 Participants in a survey conducted in Michigan521 considered wildland fires as inherently uncontrollable and the resulting damage essentially random. Thus, they only weakly supported investments in fire suppression infrastructure but strongly supported fire prevention programs that reduced the number of fire

PART 3  BURNS, FIRE, AND RADIATION

WILDLAND FIRE LESSONS Recommendations to reduce the loss of life and property in the wildland–urban interface will be useless unless they are implemented at the grassroots level by all stakeholders. An excellent example of a community-based program is one implemented at Incline Village and Crystal Bay in the Lake Tahoe basin.431 The objective of this program is to “reduce the potential for natural resource, property, and human life losses due to wildfire by empowering the communities’ residents with the knowledge to address the hazard, providing the resources necessary to correct the problem, and encouraging the cooperative efforts of appropriate agencies.” The three major components of this defensiblespace program include neighborhood leader volunteers, a slash removal project, and agency coordination. The key to protecting life and property in the wildland–urban interface is property owners’ realization that they have a serious problem and that their actions embody a significant part of the solution. In the Incline Village and Crystal Bay community fire plan, neighborhood leader volunteers are trained in defensible-space techniques and are expected to teach these techniques to their neighbors and to coordinate neighborhood efforts. Such concerted community action will greatly minimize threats from the southern California type of “fires of the future” as discussed earlier. It is also wise to have sensible land development practices, because tragedies arise not only from ignorance of fuels and fire behavior (Figure 12-13) but also from a greater concern for the aesthetics of a home site than for fire safety.331 Several aspects of development detract from fire safety in the wildland–urban interface:137,187 • Lack of access to adequate water sources • Firewood stacked next to houses • Slash (i.e., branches, stumps, logs, and other vegetative residues) piled on home sites or along access roads • Structures built on slopes with unenclosed stilt foundations • Trees and shrubs growing next to structures, under eaves, and among stilt foundations • Roads that are steep, narrow, winding, unmapped, unsigned, unnamed, and bordered by slash or dense vegetation that makes them extremely difficult if not impossible for fire appliances to negotiate • Subdivisions on sites without two or more access roads for simultaneous ingress and egress • Roads and bridges without the grade, design, and width to permit simultaneous evacuation by residents and access by

FIGURE 12-13  This permanent residence, located in west-central Alberta, Canada, is unlikely to survive exposure to even a low-intensity wildland fire, and it would be difficult to stay and defend it for a number of reasons. There is dense forest vegetation immediately adjacent to the structure. Cedar shakes have been used for roofing. This has been shown time and time again to be the “kiss of death” in wildland–urban interface fires (at the time this photo was taken in 1997, the shingles were in such bad shape that they had lichens growing on them). The homeowner also liked to store flammable materials under his deck. (Courtesy Yukon Wildland Fire Management; photo by A.K. Beaver.)

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firefighters and emergency medical personnel and their equipment • Excessive slopes, continuous or heavy fuel situations, structures built in box canyons, and other hazardous situations • Lack of constructed firebreaks and fuel breaks around home sites and in subdivisions • Living fuels that have not been modified by pruning, thinning, landscaping, or other methods to reduce cured vegetation and litter that readily contribute to spot fire development and fire intensity • Homes constructed with flammable building materials (e.g., wooden shake shingles) • Propane tanks exposed to the external environment • Inability to deliver water effectively before and during passage of a fire front around the home property (e.g., lack of proper equipment, such as sprinklers) In a lot of cases, simply cutting the grass and keeping the yard cleaned up will dramatically increase the chances of the house surviving a wildfire.126

WHAT SOME ORGANIZATIONS HAVE TO OFFER The National Disaster Education Coalition is a group of U.S. federal agencies and nonprofit organizations that support common goals in disaster and hazards education. This group worked hard with the nation’s leading social scientists in this area to produce a state-of-the-art guide for public risk education. The group developed a standardized guide327 on hazard safety messages, providing information that all organizations agreed on for national use. The guide covers many different hazards, including wildland fires, as well as general preparedness issues. Firewise Communities is a national mitigation planning pro­ gram that encourages communities to include land use planning, building codes, landscaping codes, zoning, and fire protection in developing new communities and in retrofitting existing communities.51,376 Firewise Communities is a national initiative designed to reach beyond the fire service and involve homeowners, community leaders, planners, developers, and others in the effort to protect people and property from the dangers of wildland fire. Firewise Communities programs include the Firewise Communities Workshop series, Firewise Communities/USA Recognition Program, and support for fire organizations and community groups. The Firewise Communities program is part of the Wildland–Urban Interface Working Team of the National Wildfire Coordination Group (NWCG), a consortium of wildland fire agencies that includes the USDA Forest Service, Department of Interior, National Association of State Foresters, U.S. Fire Administration, Federal Emergency Management Agency, and National Fire Protection Association. Firewise Communities emphasizes that everyone in every community is responsible for fire protection. Firewise Communities workshops help define responsibilities for a network that includes many partners. The intent is to undertake planning and actions to ensure that people live more compatibly in every neighborhood situation in a wildland fire environment. Toward this end, a website has been developed (http://www.firewise.org), and several publications and books331,428 have been published to assist homeowners living in the wildland–urban interface. A team of scientists from across the United States has been visiting communities to identify the activities they need to undertake to increase their wildfire preparedness and the resources necessary to support these activities. This research is funded by the National Fire Plan and is led by the Social and Economic Dimensions of Ecosystem Management Research Work Unit of the USDA Forest Service’s North Central Research Center. Research partners include the USDA Forest Service’s Pacific Northwest Research Station, University of Minnesota, Southern Oregon University, and University of Florida. Sixteen community preparedness case studies were completed between 2002 and 2004 in a variety of locations throughout the continental United States (jfsp.fortlewis.edu).509,514 Partners in Protection, based out of Alberta, Canada, is a coalition of professionals representing national, provincial, and municipal associations and organizations committed to raising

Fire Behavior URBAN AND WILDLAND FIRE THREATS Safety precautions for wildland firefighting crews are continually upgraded as new knowledge is gained about fire behavior and human behavior. The sites where people were injured or killed by fire are routinely examined284,315,512 afterward to assess fuel conditions, terrain features, probable wind movements at the time of the fire, and actions of firefighters (Figure 12-14). In this regard, author Norman Maclean275 has noted: It is hard to know what to do with all the detail that rises out of fire. It rises out of a fire as thick as smoke and threatens to blot out everything. Some of it is true but doesn’t make any difference. Some of it is just plain wrong. And some doesn’t even exist, except in your mind, as you slowly discover long afterwards. Some of it, though, is true—and makes all the difference. The information gleaned from past wildland firefighter fatalities, as well as data about hazards in the wildland–urban interface, are now included in training programs and safety briefings. In reviewing many past wildland fire tragedies, a sobering observation is that crew members are almost always experienced and well-equipped firefighters, trained to anticipate “blowup” fire

C

B

A FIGURE 12-14  In an attempt to avoid the intense heat of this brush fire in southwestern Colorado, four firefighters took refuge in the fire line, in the foreground at point A. Affected by intense convective and radiant heat and dense smoke, one individual ran into the fire and died at point B. Another individual ran about 300 m (1000 feet) down the ridge, where his body was found at point C. The third fatality was a person who remained at point A; he died a short time after this position was overrun by fire. The only survivor also remained in a prone position at point A with his face pressed to the ground. At one point he reached back and threw dirt on his burning pants legs. The survivor sustained severe burns to the backs of his legs, buttocks, and arms. The deaths of the other three individuals were attributed to asphyxiation. (Courtesy USDA Forest Service.)

conditions (i.e., a temporary escalation in fire behavior). However, when visibility is lowered to 6 m (20 feet), noise levels preclude voice communication, eyes fill with tears, and wind blows debris in all directions, a person’s judgment is badly impaired. For many members of the general public, the first wildland fire they may experience will in all likelihood be a high-intensity conflagration. As Cheney118 notes: The approach of a major fire can appear ominously threatening to those directly in its path, but is often viewed with curiosity and with little concern if it appears that the wind will direct the fire past their properties. Thus, when a combination of circumstances, often associated with a frontal wind passage, exposes residents to a high-intensity fire environment, they are very much unprepared. Their senses are assaulted by sudden darkness, thick blinding and choking smoke, buffeting winds and unexpected calm periods, searing heat and flames which illuminate the smoke-obscured scene and a roaring noise of wind and explosive combustion. In all this activity they observe flames which change from a metre or two to engulfing whole trees. In such a dramatic and emotional situation, many people are apt to invent phenomena (such as, houses exploding, the air burning, fantastic spread rates and the like) to explain the extent of the devastation that confronts them when the smoke clears away. Even for experienced firefighters, previous training can give way to panic-like attacks and poor decision making, leading to actions that can result in serious injury or death.356 This scenario is most evident in urban fires; the pattern of hysteria affecting people trapped in burning buildings is all too familiar to urban firefighters.435 The way fire kills in the urban setting can be compared with wildland fires, as shown here:359 • Heat rises rapidly to upper stories when a fire starts in the basement or on the ground floor. Toxic gases and smoke rise to the ceiling and work their way down to the victim—a vital lesson for families planning protective measures. Smoke poses the double problem of obscuring exit routes and contributing to pulmonary injury and oxygen deprivation. • As the fire consumes oxygen, the ambient oxygen content drops, impairing neuromuscular activity. When the oxygen content drops below 16%, death by asphyxiation will ensue 251

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

awareness, providing information, and developing forums with a view to encouraging proactive, community-based initiatives with respect to fires at the wildland–urban interface. Partners in Protection has produced a comprehensive manual with respect to the wildland–urban interface fire problem entitled FireSmart: Protecting Your Community From Wildfire.364 This well-illustrated guide focuses on how individuals and communities can work together to reduce the risk for loss from fires in the wildland– urban interface. It provides practical tools and information for use by residents and by individuals and organizations that operate in the wildland–urban interface. The primary topics are description of interface issues, evaluation of hazards, mitigation strategies and techniques, emergency response for agencies and individuals, training for interface firefighters, community education programs, and regional planning solutions. The manual, available in both book form and CD-ROM, can be viewed online at the Partners in Protection website (http://partnersinprotection. ab.ca) and covers nearly every facet of fire preparations in the wildland–urban interface. In the chapter on communications and public education, for example, several principles are cited for effective communication: • Begin with clear, explicit objectives. • Do not make assumptions about what people know, think, or want done. Take time to find out what people are thinking by using surveys, focus groups, or other research. • Involve all parties that have an interest in the issue. Identify and address the particular interests of different groups. • Identify with your audience. Put yourself in their place, and recognize their emotions. • Take time to coordinate with other organizations or groups. • Choose your spokespeople carefully, and ensure they have the training to communicate your messages effectively. • Practice and test your messages. • Do not either minimize or exaggerate the level of risk. • Promise only what you can do. Do what you promise. • Plan carefully, and evaluate your efforts. Kumagai and colleagues250 also offer some excellent advice with respect to wildland fire education and communication with the general public. Nowadays most local, state, provincial, territorial, and federal fire management agencies have some sort of outreach program related to the wildland–urban interface. For example, the State of Alaska offers teachers both face-to-face wildland fire workshops and an online training course.450 Beginning in 1993, the Country Fire Authority of Victoria, Australia, developed a program called “Community Fireguard,” which assists communities in developing wildfire survival strategies.71

PART 3  BURNS, FIRE, AND RADIATION

unless the victim is promptly evacuated. Asphyxiation, not fire itself, is the leading cause of fire deaths. • Ambient temperatures may rise extremely rapidly from even small fires. Temperatures of 150° C (300° F) will cause rapid loss of consciousness and, along with toxic gases, will severely damage lung tissues. Warning devices may offer the only possibility for survival owing to the rapid onset of debilitating symptoms. Obvious similarities and differences are seen between wildland fires and urban fires: • Smoke, heat, and gases are not as concentrated in wildland situations as in the confined quarters of urban fires. • Flames are not a leading killer in either the urban or wildland situation, although admittedly there is a general lack of autopsies being performed, so this assertion awaits confirmation. • Although oxygen levels may be reduced near wildland fires, there is usually sufficient replenishment of oxygen in the outdoor environment to minimize deprivation. Asphyxiation, however, can also be an important cause of death in wildland fires. • Inhalation of superheated gases poses as serious a threat to life in wildland fires as in urban fires. • Wildland smoke does not contain toxic compounds produced by combustion of plastics and other household materials, but it does impair visibility, contains carbon monoxide, and carries suspended particulates that cause severe physical irritation of the lungs. • Sprinkler systems and automatic early-warning devices to detect smoke or heat may protect people from serious injury or death in the urban environment, but in the wildland environment, people must rely on their experience, senses, knowledge, and skills or ingenuity to provide early warning of an impending threat to life. The general public needs to appreciate that fires occurring under certain fuel, weather, and topographic situations may result in explosive fire growth on an area basis (Figure 12-15, online). The fire that burned through Faro, Yukon, on June 13, 1969, is a good example of this type of behavior.244 The Faro fire, which burned about 15,500 hectares (about 38,300 acres) resulted from a lightning strike that occurred 8 km (5 miles) west of town at 5:04 PM. The fire started to spread fairly quickly in an easterly direction. Fire crews were dispatched from town by vehicle to take suppression action, but little could be done because of crowning activity. By 8:30 PM, the fire had burned through town and was continuing to spread farther east. In other words, the fire had traveled 8 km (5 miles) in less than 3.5 hours. This equates to a rate of spread of around 2.3 km/hr (1.4 mph) or 40 m/min (131 ft/min). This would not be considered an unusual situation in many regions of the North American boreal forest.29,155 How wide would the fire have likely been when it hit the edge of town? A rough rule of thumb is to divide the separation distance by a factor of 2 to 4 based on an assumed wind-driven fire shape.458 The fire would have thus been roughly 2 to 4 km (1.2 to 2.5 miles) wide when it hit the western edge of Faro. Fire Behavior Knowledge: A Wildland Fire Early-Warning System Fire behavior is defined as the manner in which fuel ignites, flame develops, and fire spreads and exhibits other related phenomena as determined by the interaction of fuels, weather, and topography. The science of fire behavior describes and predicts the performance of wildland fires in terms of ignition probabilities, rates of spread, intensity levels, spotting distances and densities, and crowning potentials. To the lay person, a wildland fire can be a perplexing event. As Countryman and Schroeder note:150 A casual observer seeing a forest fire for the first time would probably decide there is little rhyme or reason to the way a fire burns. Its sudden variations in direction of travel, its quick change from a seemingly mild, slow-burning fire to a raging inferno, all seem to add up to erratic behavior without local explanation. Actually a fire behaves in accord with changes in its surroundings—the character and condition of the 252

burnable vegetation, the topography, and the meteorologic factors—that affect fuel flammability, fire intensity, and fire spread. This complex of environmental factors that control the behavior of fire is what we call “fire environment.” Understanding one’s fire environment145 is considered a key factor for safe and effective action in dealing with wildland fires. For example, 4 of the 32 civilians killed in Victoria during the 1983 Ash Wednesday fires in southeastern Australia were caught outside their homes tending to or attempting to herd up livestock,248 apparently unaware of the change in wind direction and speed that accompanied passage of the cold front through their area.393 In such situations in southeastern Australia, the strong prefrontal winds are from the northwest. With the passage of the front, the wind direction changes sharply to the southwest, and winds increase markedly in strength. Had these people understood or been aware of the implications of the cold front passage on fire behavior and received some information on the timing of the change, they may have chosen to stay inside their homes.248 An excellent overview of the fire environment concept has been prepared by the National Wildfire Coordinating Group.336 Experienced firefighters routinely monitor the fire and the fire environment and assess the probable behavior of fires using fire behavior guidelines and experienced judgment based34,54 on current and expected fire weather conditions in relation to local fuel type information, topographic conditions, and moisture levels.85,261,458 This is also referred to as “situational awareness” (i.e., understanding what the fire is doing and what you are doing in relation to the fire and being able to predict where the fire and you will be in the future).377 In the conclusions to their detailed case study report on the 1994 South Canyon fire, USDA Forest Service fire researchers96 noted: None of the findings and observations discussed in this study represent new breakthroughs in wildland fire behavior understanding. Rather, the findings support the need for increased understanding of the relations between the fire environment and fire behavior. We can also conclude that fire managers must continue to monitor and assess both present fire behavior and potential future fire behavior given the possible range of environmental factors. The emergency medical person, backcountry recreationist, and wildland homeowner must also understand certain basic fire behavior principles to provide for adequate personal safety. A cardinal rule in wildland fire suppression is to base all actions on current and expected fire behavior.287,308 Attention to simple principles, indicators, and rules should enable wildland users to anticipate and avoid wildfire threats. Heat, oxygen, and fuel are required in proper combination before ignition and combustion will occur54,201 (Figure 12-16, online). If any one of the three is absent, or if the three elements are out of balance, there will be no fire (Box 12-3). Fire control actions are directed at disrupting one or more elements of this basic fire triangle.14 Physical Principles of Heat Transfer Heat energy is transferred by conduction, convection, radiation, and spotting, but generally only the last three processes are significant in a wildland setting.102 Although conduction through solid objects is important in the burning of individual logs,54 this process does not transfer much heat outward from a flaming front, unless there is a substantial accumulation, such as is found in blowdown.200 Convection, or the movement of hot masses of air, accounts for most of the heat transfer upward from the fire. Convective currents usually move vertically unless a wind or slope generates lateral movement (Figure 12-17). Convection preheats fuels upslope and in shrub and tree canopies, which contributes further to a fire’s spread and the onset of crowning forest fires. Through radiation, heat energy is emitted in direct lines or rays; about 25% of combustion energy is transmitted in this manner. Radiated heat on exposed skin can cause discomfort and severe pain (Figure 12-18), and even death at elevated

Certain universal principles apply to all spreading fires in vegetation, living or dead. These really have nothing to do with biology but are based purely on the physics and chemistry of combustion: 1. There must be sufficient fuel of appropriate size and arrangement in space. 2. This fuel must be of sufficient dryness to support a spreading combustion reaction. 3. There must be an agent of ignition. In practical terms, the primary requirement is a continuous layer of finely divided fuel or minor vegetation on the surface of the ground. This material may be conifer needles, hardwood leaves, grass, lichen, moss, finely divided shrubs, or other minor vegetation. However, it must be present and it must be continuous, or the possibility of spreading fire does not really exist. The second requirement is that the material be dry enough. The maximum moisture content at which fire will spread is hard to specify; for any given fuel or vegetation complex, it will depend on the amount of fuel, its arrangement in space, and   the wind speed. Thus, fire spreads poorly or not at all in surface litter of various kinds at moisture contents over 25% or 30% (dry weight basis), whereas fine shrubby fuels or conifer foliage may support fast-spreading fires at moisture contents of 100%   or more. The two limiting criteria common to all spreading fires are as follows: 1. The fire must transfer enough heat forward to dry out the unburned fuel and raise it to ignition temperature by the time the flame front arrives. 2. Enough fuel must pass through the moving flame front to produce a continuous solid flame. The behavior of any fire is the result of a complex process that results in a dynamic equilibrium among all elements of mass and energy flowing in and out of the flame zone. However difficult this whole process may be to describe and predict, the above two criteria run like threads through the whole range of fires in vegetation, whether the fuel itself is dead or live. From Van Wagner CE: Fire behaviour in northern conifer forests and shrublands. In Wein RW, MacLean DA, editors: The role of fire in northern circumpolar ecosystems, Chichester, England, 1983, J. Wiley & Sons.

levels.114,142 The amount of radiant heat transferred decreases inversely with the square of the distance from a point source. More radiant heat is emitted from a line of fire than from a point source. Radiant heat travels in straight lines, does not penetrate solid objects, and is easily reflected. It accounts for most of the preheating of surface fuel ahead of the fire front and poses a direct threat to people who are too close to the fire (see Figure 12-17). Most organized fire suppression crews in the United States carry protective fire shelters39,40,368 as part of their personal protective equipment (PPE) (Figure 12-19).369 These aluminized “pup tent” type of structures are intended to protect against radiant heat.99,380 The U.S. Forest Service fire shelter was never designed to mitigate against sustained, direct flame contact.303 Certain materials that fail when in direct contact with flames, such as “emergency space blankets,”193 are also not appropriate for use in wildland fires84 and in fact could cause serious burn injuries. Similarly, “emergency evacuation smoke hoods,” intended for use in urban situations or other human-made environments (e.g., airplanes), have absolutely no application in a wildland fire environment despite manufacturers’ suggestions to the contrary. Spotting is a fire spread or mass transport heat transfer mechanism by which wind currents carry flaming firebrands or glowing embers land beyond the main advancing fire front to start new fires (Figure 12-20). In this manner, fire spread may accelerate very quickly, unexpected new fire starts can occur, and fire intensity and in-draft winds can dramatically increase as spot fires coalesce (Figure 12-21). High-density, short-range spotting up to 100 m (328 ft) is a common feature of many wildfires, especially

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

BOX 12-3  Requirements for Wildland Fire Spread

A Wind

B FIGURE 12-17  Fuels and people upslope (A) or downwind (B) from a fire receive more radiant and convective heat than on the downslope or upwind sides of a spreading fire. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)

when fine fuels are very dry.37 Low-density, intermediate- to medium-range spotting up to about 1 to 2 km (0.6 to 1.2 miles) is a common occurrence with high-intensity crown fires.29 Longer-range spotting occurs very infrequently in most fuel types. Firebrand material being transported up to 16 km (10 miles) from its source has been reported in North America.38 The native eucalyptus forests of Australia have a notorious reputation when it comes to spotting behavior owing to the bark characteristics of many species, including an authenticated spot fire distance of 30 km (19 miles) or more.269

FIGURE 12-18  Most of the heat felt from a fire is radiant heat, which is largely a function of the height, depth, and angle of the flame front. Wildland firefighters work far enough from the radiating flames to avoid pain to exposed skin (e.g., face and ears). This also limits the amount of radiant heat absorbed through clothing. Wildland firefighters working near an active fire edge with hand tools typically adjust their distance from the flames so that the radiant heat they receive from the fire is little more than that of direct sunlight. (Courtesy British Columbia Forest Service.)

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PART 3  BURNS, FIRE, AND RADIATION

C

A

B

D

FIGURE 12-19  The personal protective equipment for a firefighter includes hard hat and safety goggles, fire-resistant shirt and trousers, leather boots and gloves, and an aluminized fire shelter carried in a waist pouch (A). Firefighters also carry canteens to ensure an adequate water supply in a heat-stressed environment. The fire shelter (B) is deployed (C) by firefighters as a last resort to provide protection from being exposed directly to radiant heat and superheated air (D). (Courtesy USDA Forest Service.)

FUNDAMENTAL WILDLAND FIRE BEHAVIOR CHARACTERISTICS One important aspect of fire behavior that distinguishes urban or structural fires from wildland fires is the latter’s horizontal spread potential. Although urban or structural fires may exhibit some vertical fire spread potential, for practical purposes, they are considered stationary fire sources. Wildland fires on the other hand characteristically involve moving flame fronts, sometimes advancing with astonishing speed (Figure 12-22). Whereas ground or subsurface fires may spread very slowly (about 1 m [3 feet] per hour),507 surface fires in open grown forests can reach rates of about 15 to 25 m/min (50 to 80 ft/min); conversely, surface fires in closed forest types typically spread at 5 to 6 m/

FIGURE 12-20  Fires can easily cross narrow canyons. Fuels and people on the slope opposite a fire in a narrow canyon are subject to intense radiant heat and spot fires from airborne embers. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)

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min (16 to 20 ft/min) before the onset of crown combustion. Crowning forest fires generally advance at rates between 30 and 60 m/min (100 to 200 ft/min), occasionally higher.29,155 Grass fires spread at rates up to around 385 m/min (1263 ft/min) or 23 km/ hr (about 14 mph).125,350 It is thus quite possible for forest fires to advance up to 80 km (50 miles) in a single day7,405 and for grass fires to travel correspondingly even farther. The threat to life and property largely depends on a fire’s residence time (Table 12-2). This represents the length of time any object overrun by a fire will be heated by direct flame contact. Coupled with the fire’s rate of spread, the residence time determines the depth of the active or continuous flaming front (Figure 12-23). The length of time that a fire will continue to burn by smoldering combustion depends on the composition, compaction, moisture content, and quantity of fuel present.194 The most basic features of a wildland fire are that (1) it spreads or moves, (2) it consumes or “eats” fuel, and (3) it produces heat energy and light in a visible flaming combustion reaction.6 Byram101 defined fire intensity as the rate of heat energy release per unit time per unit length of fire front, regardless of its depth. Numerically, it is equal to the product of the quantity of fuel consumed in the flaming front, a fire’s rate of fire spread, and a fuel heat combustion value. Flame size is its main visual manifestation. The fastest spreading part of a fire is the head; the back of the fire is the slowest spreading part, with the flanks being intermediate between the two (Figure 12-24). It is for this reason that the fire intensity, flame length, and flame height (see Figure 12-23) are greatest at the front of the fire and least at the rear109 (Figure 12-25). The amount of radiation received from a flame front is determined by the size and geometry (e.g., height, depth, and tilt angle) of the flame front. Radiation levels coupled with residence times determine the nature of burn injuries.84,173 Environmental Factors Influencing Wildland Fire Behavior A wildland fire behaves according to variations in the fire environment (i.e., fuels, weather, and topography). Some of the fire environment factors associated with adverse burning conditions that can signal the potential or onset for severe fire behavior are listed in Box 12-4. These factors or indicators are subject to assessment, measurement, and observation.

B

C

D

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

A

FIGURE 12-21  The occurrence of numerous spot fires is a direct indication that the moisture content of fine fuels has attained a critically dry level and in turn an early warning signal that the potential for extreme fire behavior exists or is imminent. This sequence of photos (A to D) spanned a period of just over 100 seconds taken late in the afternoon of July 9, 2005, near Coimbra, Portugal. The fuel type is a blue gum  (Eucalyptus globulus)–maritime pine (Pinus pinaster) stand. (Courtesy Associação para o Desenvolvimento da Aerodinâmica Industrial; photos by M. G. Cruz.)

When a person encounters a wildland fire, the first step should be to review the principles and indicators of fire behavior, sizing up the situation in terms of fuel, weather, topographic factors, and observed fire behavior. After the fire’s probable direction and rate of spread are estimated, travel routes that avoid hazards to human life can be planned (see Figure 12-24). The direction of the main body of smoke is often a good indicator of the direction the fire will take.

Fuel.  Because wildland fuels vary so widely in their distribution, their physical characteristics or properties (i.e., moisture content, size and shape, compactness or arrangement, load, horizontal and vertical continuity, chemical content), and their effect on fire behavior, some means of classification is needed for their systematic assessment. Fuels are commonly classified into four groups or strata (Figure 12-26). Some fuel types may exhibit only one or two of the strata (e.g., grasslands, shrublands, and logging slash lack the ladder and crown fuel stratum). An increase in fuel available for combustion affects fire intensity. In other words, the more fuel that is burning, the greater the heat energy released by the fire. As Brown and Davis77 noted:

Flame flashes

Prevailing wind Flame length

Ash FIGURE 12-22  A novel approach to reminding people of the capricious nature of wildland fire spread. This sign is located at Betty’s Bay on the South African coast near Cape Town. The vegetation type is fynbos—a highly flammable Mediterranean shrubland fuel complex.485 (Courtesy CSIR Natural Resources and the Environment, Stellenboch, South Africa; photo by B.W. van Wilgen.)

Flame height

Flame angle

Flame depth

Compact surface layer

FIGURE 12-23  Cross-sectional view of a stylized free-burning fire in a grass fuel bed. (From Cheney P, Sullivan A: Grassfires: Fuel, weather and fire behaviour, ed 2, Collingwood, Victoria, Australia, 2008, CSIRO Publishing.)

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PART 3  BURNS, FIRE, AND RADIATION

TABLE 12-2  Nominal Residence Times for Four Broad Fuel Complexes and Computed Maximum Theoretic Flame

Depths* Associated With Variable Rates of Fire Spread

Rate of Fire Spread

Broad Fuel Complex Grassland Shrubland Forest stand Logging slash

Residence Time

10 m/min (33 ft/ min) Flame Depth

20 m/min (66 ft/ min) Flame Depth

40 m/min (131 ft/ min) Flame Depth

(sec)

(min)

(m)

(ft)

(m)

(ft)

(m)

(ft)

10 20 45 90

0.17 0.33 0.75 1.5

1.7 3.3 7.5 15

5.6 10.9 24.6 49.2

3.4 6.6 15 30

11.2 21.7 49.2 98.4

6.8 13 30 60

22.3 42.7 98.4 196.8

*Numerically equal to residence time multiplied by the rate of fire spread (in compatible units).

The ignition, buildup, and behavior of fire depend on fuels more than any other single factor. It is the fuel that burns, that generates the energy with which the fire fighter must cope, and that largely determines the rate and level of intensity of that energy. Other factors that are important to fire behavior (that is, moisture, wind, etc.) must always be considered in relation to fuels. In short, no fuel, no fire! Certain types of fuel, such as chaparral, pine, and eucalyptus, burn more intensely because their foliage contains flammable oils and resins (see Figure 12-12). The size and arrangement of fuel also influence fire behavior. Small, loosely compacted fuel beds, such as dead grass, long pine needles, and shrubs, burn more rapidly than does tightly compacted fuel. Large fuels burn best when they are arranged so that they are closely spaced, such as logs in a fireplace. Scattered logs with no small or intermediate fuel nearby seldom burn unless they are decomposed. Seasonal changes in the moisture content and live-to-dead ratio (e.g., degree of curing in grasslands) of conifer tree foliage, shrubs, grasses, and other herbaceous plants can result in gradual changes in fuel flammability over the course of a fire season.147,269 Wildland fire research has identified a wind speed threshold in fuel types with a discontinuous, combustible surface layer (e.g., due to the presence of areas of bare, mineral soil).82,86 In these discontinuous fuel types, fire spread is exceedingly limited until a certain or threshold wind speed level is attained, and then

Finger

Head

Left flank

the rate of advance can be quite unexpectedly rapid199 (Figure 12-27, online). This kind of situation could lead a person into a false sense of security regarding fire potential, until unfortunately it is often too late. Various weather phenomena (e.g., wind, hail, snow, ice, and frost) and insect and disease epidemics can drastically elevate the flammability of a fuel complex, creating decidedly new fire safety concerns.33 For example, on July 9, 1999, heavy rains and winds in excess of 145 km/hr (90 mph) blew down about 181,000 hectares (about 447,000 acres) of sub-boreal forest in northeastern Minnesota, resulting in heavy dead and downed woody fuel loads.200 Weather.  The greater the wind, the more rapid the spread of fire. Thunderstorm downdrafts and winds associated with dry cold frontal passages can be especially hazardous.125,411 Low relative humidity and high air temperatures decrease the moisture content of fine, dead fuels and thereby increase ignition ease and rate of spread. Prolonged drought makes more medium and heavy fuels available for combustion, leading to increased intensity levels. When fuels reach critically dry levels, fires become very responsive to minor changes in wind and slope. Fires tend to burn more vigorously under unstable atmospheric conditions. The North American continent has been classified into 15 fire climate regions based on geographic and climatic factors411 (Figure 12-28). Major fire seasons, or periods of peak fire activity, can be used to warn emergency medical personnel and wildland users of the most probable times for life-threatening situations. Exceptions occur. For example, rapidly spreading grass and forest fires can occur during the winter months in the northern latitudes, such as happened in southwestern and west-central Alberta on December 14, 1997, under Chinook conditions and

Spot fire

Rear Wind direction

Pocket Finger Right flank Unburned island

FIGURE 12-24  The parts of a fire are described in terms of its left flank, right flank, head, and back or rear. There may also be unburned islands within the fire and spot fires ahead of the fire. The safest travel routes generally involve lateral movement on contours away from the fire’s flank or movement toward the rear of the fire. Moving in front of a head fire should be avoided. The burned area inside the fire’s peri­ meter can offer a safe haven provided smoldering or glowing combustion levels are low and the flaming perimeter can be safely penetrated by an individual; falling trees or snags and rolling rocks could, however, still pose a hazard. (Modified from Mobley HE, Moore JE, Ashley RC, et al: Planning for initial attack, rev ed, Forestry Report SA-FR-2, Atlanta, Ga, 1979, USDA Forest Service, Southeastern Area State and Private Forestry.)

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FIGURE 12-25  Elliptical fires resulting from multiple, wind-driven, point source ignitions associated with a prescribed burning operation in a southeastern U.S. pine plantation. As indicated by the smoke drift, the winds are blowing roughly from lower right to the upper left. (Courtesy USDA Forest Service; photo by C.W. Adkins.)

Fuel • Continuous fine fuels, especially fully cured (dead) grasses • Large quantities of medium and heavy fuels (e.g., deep duff layers, dead-down logs) • Abundance of bridge or ladder fuels in forest stands (e.g., branches, lichens, suspending needles, flaky or shaggy bark, small conifer trees, tall shrubs extending from ground surface upward) • Tight tree crown spacing in conifer forests • Presence of numerous snags • Significant amounts of dead material in elevated, shrubland fuel complexes • Seasonal changes in vegetation (e.g., frost kill) • Fire, meteorologic or insect and disease impacts (e.g., preheated canopy or crown scorch; snow-, wind-, or icedamaged stands; drought-stressed vegetation; or mountain pine beetle–killed stands) Weather • Extended dry spell • Drought conditions • High air temperatures • Low relative humidity • Moderately strong, sustained winds • Unstable atmosphere (visual indicators include gusty winds, dust devils, good visibility, and smoke rising straight up) • Towering cumulus clouds • High, fast-moving clouds • Battling or shifting winds

no snow cover.213 One of the grass fires advanced 33 km (20.5 miles) in less than 4 hours for a spread rate of around 8 km/hr (about 5 mph), seriously threatening the community of Granum.70 A forest fire near the town of Hinton in west-central Alberta on the same day posed a similar threat. Although the fire season for the southern Pacific coast is shown in Figure 12-28 as June through September, critical fire weather can occur year-round in the most southerly portion. Fire

• Sudden calm • Virga (i.e., a veil of rain beneath a cloud that does not reach the ground) Topography • Steep slopes • South- and southwest-facing slopes in the northern hemisphere • North- and northeast-facing slopes in the southern hemisphere • Gaps or saddles • Chutes, chimneys, and narrow or box canyons Fire Behavior • Many fires that start simultaneously • Fire that smolders over a large area • Rolling and burning pine cones, agaves (a desert plant found in the southwestern United States), logs, hot rocks, and other debris igniting fuel downslope • Frequent spot fires developing and coalescing • Spot fires occurring out ahead of the main fire early on • Individual trees readily candling or torching out • Fire whirls that cause spot fires and contribute to erratic burning • Vigorous surface burning with flame lengths starting to exceed 1 to 2 m (3 to 6 feet) • Sizeable areas of trees or shrubs that begin to readily burn as a “wall of flame” • Black or dark, massive smoke columns with rolling, boiling vertical development • Lateral movement of fire near the base of a steep slope

seasons are most active during spring and fall in the Great Plains, Great Lakes, and North Atlantic regions. The pattern of seasonal fire occurrence in Australia has also been mapped,269 as has the frequency of large fire occurrences.115 Topography.  The steeper the slope, the more rapid the spread of fire. Fire usually burns uphill, especially during daylight hours. Changes in topography can cause rapid and violent changes in

Crown fuels

Ladder fuels Surface fuels

Ground fuels Mineral soil

FIGURE 12-26  Profile of a stylized forest stand showing the location and classification of fuel complex strata. Wildland fuels contain energy, stored over extended periods through photosynthetic processes, that is released rapidly, occasionally explosively, in combustion. (Modified from Brown AA, Davis KP: Forest fire: Control and use, ed 2, New York, 1973, McGraw-Hill.)

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BOX 12-4  Early Warning Signals or Indicators Associated With Extreme Fire Behavior Potential

PART 3  BURNS, FIRE, AND RADIATION FIGURE 12-28  Fire climate regions of North America, based on geographic and climatic factors: (1) interior Alaska and the Yukon, (2) north Pacific Coast, (3) south Pacific Coast, (4) Great Basin, (5) northern Rocky Mountains, (6) southern Rocky Mountains, (7) Southwest (including adjacent Mexico), (8) Great Plains, (9) central and northwest Canada, (10) sub-Arctic and tundra, (11) Great Lakes, (12) Central States, (13) North Atlantic, (14) Southern States, and (15) Mexican central plateau. The bar graphs show the monthly and annual precipitation for a representative station in each of the fire climate regions. Months on the map indicate fire seasons. The graph for Decatur, Illinois, obscures the provinces of Newfoundland and Prince Edward Island on the map. (Modified from Schroeder MJ, Buck CC: Fire weather, Agriculture Handbook 360, Washington, DC, 1970, USDA Forest Service.)

fire behavior (Figure 12-29). On steep terrain, rolling firebrands may cause a fire to initially spread downhill, followed by upslope runs. Mountainous terrain can modify wind speed and direction and in turn influence fire behavior in exceedingly complex ways.411 Slope exposure or aspect has a very pronounced diurnal effect on fine-fuel flammability, a fact directly incorporated into the Campbell Prediction System of wildland fire behavior (http:// www.dougsfire.com).106 Extreme Fire Behavior Extreme fire behavior is generally considered a level of fire activity that often precludes any fire suppression action by conventional means.300 It usually involves one more of more of the following characteristics: 258

• High rates of spread and intensity • Active crowning • Prolific spotting • Presence of large fire whirls • Well-established convection column Fires exhibiting such phenomena often behave in an apparent erratic, sometimes dangerous manner. Fire whirls appear frequently in and around wildland fires.144 Most fire whirls are small and short-lived, but occasionally one becomes large and strong enough to do tornado-like damage and cause serious injury, such as occurred at Mt Kuki, Japan in 1977;181 death is also a distinct possibility. Their occurrence is commonly associated with unstable air, moderate winds, and large heat sources created by plentiful and dry fuel

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL FIGURE 12-29  Chutes, chimneys, and box canyons created by sharp ridges provide avenues for intense updrafts (like a fire in a woodstove) and rapid rates of spread. People should avoid being caught above a fire under these topographic conditions. (Modified from Barrows JS: Fire behavior in Northern Rocky Mountain forests, Station Paper No. 29, Missoula, Mont, 1951, USDA Forest Service, Northern Rocky Mountain Forest and Range Experiment Station.)

concentrations (Figure 12-30) or terrain configurations that concentrate the heat from the fire (e.g., lee side of a ridge).207,218 These fire-induced tornado-like whirlwinds can travel up to 2.5 km (1.6 miles) from the main fire441 and can cause considerable damage and even lead to fatalities. On March 7, 1964, a fire whirlwind that formed on the Polo fire near Santa Barbara, California, cut a 1.6-km (1-mile) path, injuring four people, destroying two houses, a barn, and four automobiles, and wrecking a

FIGURE 12-30  Large fire whirl associated with the burning of logging slash debris near Whitecourt, Alberta. (Courtesy University of Alberta; photo by M.Y. Ackerman.)

100-tree avocado orchard.373 The fringe of the fire whirl passed over a fire truck and sucked out the rear window of the vehicle. A firefighter standing on the rear platform of the vehicle was pulled up vertically so that his feet were pointing to the sky while his hands clasped the safety bar. A small piece of plywood was rammed 7.6 cm (3 inches) into an oak tree. Several years of drought combined with a national forest health issue that has produced many dead and dying forests set the stage for extreme fire behavior conditions that threaten people, property, and natural and cultural resources. Protection from these conditions requires understanding of the crown fire process. Crowning involves a fire spreading horizontally as a “wall of flame” from the ground surface up through and above the canopies of trees (Figure 12-31) or tall shrubs. The first views inside a crown fire were documented on videotape during the International Crown Fire Modelling Experiment near Fort Providence in Canada’s Northwest Territories in 1997.457 The onset of

FIGURE 12-31  Experimental crown fire in a northern jack pine (Pinus banksiana) and black spruce (Picea mariana) forest near Fort Providence, Northwest Territories. The average height of flames from crowning forest fires is generally one to one and a half times taller than the tree height. Flame flashes will extend considerably higher into the fire’s convection column. (Courtesy Canadian Forest Service.)

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PART 3  BURNS, FIRE, AND RADIATION

crowning is significant from both a safety and suppression perspective. At a minimum, when a fire crowns, the rate of spread and intensity doubles, and the area burned quadruples.12 Author Norman Maclean274 gives an indication of how crown fires were handled in the early part of the 20th century by the USDA Forest Service: By the time they reached the fire, it had spread all over the map, and had jumped into the crowns of trees, and for a lot of years a prospective ranger taking his exam had said the last word on crown fires … When asked on his examination, “What do you do when a fire crowns?” he had answered, “Get out of the way and pray like hell for rain.” This wisdom seems still valid today. Rothermel402,404 described the conditions that produce a crown fire: 1. Dry fuels 2. Low humidity and high temperatures 3. Heavy accumulations of dead and downed fuels 4. Small trees in the understory, or “ladder fuels” 5. Steep slope 6. Strong winds 7. Unstable atmosphere 8. Continuous crown layer The two most prominent behavior patterns of crown fires are wind driven and plume (or convection) dominated. Each type of crown fire poses a distinct set of threats to people. Free-burning wildland fires are seldom uniform and well behaved, so these descriptions of wind-driven and plume-dominated crown fire behavior may not be readily apparent. The behavior of these types of fires can be expected to change rapidly as environmental, fuel, and topographic conditions change.402 Wind-Driven Crown Fire.  A running crown fire can develop when winds increase with increasing elevation above the ground, driving flames from crown to crown (Figure 12-32). Steep slopes can produce the same effect. Spread rates in conifer forests can reach up to 12 km/hr (7.5 mph) for brief periods of time243,427 and are possibly faster in mountainous terrain,402 especially in open forest or nonforested or shrubland fuel types.96,129 A running crown fire is accompanied by showers of firebrands downwind, fire whirls, smoke, and rapid development of a tilted convection column. As long as the wind remains fairly constant from one direction, the flanks of the fire can remain relatively safe. The greatest threat is to people who are immediately at the head, or

downwind side, of the fire, although medium- and long-distance spot fires can also pose an unexpected risk.5,66 Plume-Dominated or Convection-Dominated Crown Fire.  An alternative form of crown fire develops with relatively low wind speeds or when wind speed decreases with elevation above the ground. This type of crown fire is referred to as plume dominated or convection dominated because it is characterized by a towering convection column that stands vertically over the fire (Figure 12-33). This type of fire poses a unique threat to people because it can produce spot fires in any direction around its perimeter. It can also spread rapidly as the combustion rate accelerates. One form of a plume-dominated crown fire that can be especially dangerous is when a downburst of wind blows outward near the ground from the bottom of the convective cell. These winds can be extremely strong216 and can greatly accelerate a fire’s spread. This type of wind event occurred during the major run of the Dude fire near Payson, Arizona, on June 26, 1990, when six firefighters were killed.208 Some indicators help signal the onset of a downburst from a plume-dominated crown fire. The surest indicator is the occurrence of precipitation of any amount, even a light sprinkle, or the appearance of virga (evaporating rain) below the base of a cloud formation.402,411 Another indicator is rapid development of a strong convection column above the fire, or nearby thunder cells. A third and very short warning is the calm that develops when the in-draft winds stop before the turnabout and outflow of wind from the cell. This brief period of calm may be accompanied by a humming sound just before the reversing wind flow arrives. If any of these indicators is present, the area should quickly be evacuated and a safe refuge sought. The downburst may also break or uproot trees, creating an additional hazard for people.402 Value of Fire Danger Ratings Forest fire control in the early days before organized protection was relatively simple. As Williams513 explains: One tried to keep wild fires out of the settlements and in the woods where they belonged. There was no planning—fire was fought wherever it could not be avoided. Later, as forest fire control became organized, specific plans for fire control action became an obvious necessity. To form the basis for such plans, a reliable measure of the day-by-day state of forest flammability was needed.

Wind

Heading fire

Backing fire

1

2

3

Ignition point

3

2

1

FIGURE 12-32  Cross-sectional view of a wind-driven crown fire, illustrating the various stages of combustion: preignition (1), ignition and flaming combustion (2), and glowing or smoldering combustion (3). People are most at risk on the downwind side and upper flanks of such a free-burning fire. This type of fire is caused by winds that increase in velocity with increasing elevation above the ground. (Modified from Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain Press Publishing Co.)

260

Died in Tasmanian Fires, February 7, 1967

Location

No. of Deaths

Mustering stock Firefighting Traveling in a vehicle Escaping from and found at some distance from houses Within a few meters of houses In houses

2 11 2 11 10 17

From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer.

FIGURE 12-33  Cross-sectional view of a plume-dominated or convection-dominated crown fire. People are at risk around the complete perimeter of this type of fire because it has the potential to spread intensely or spot in any direction around its perimeter with little or no warning. This form of crown fire develops when wind velocities are relatively low or when velocities decrease with elevation above the ground coupled with critically dry and abundant fuel conditions. The convective plume associated with this type of fire may rise to 7600 to 9100 m (25,000 to 30,000 feet) above the ground. (Modified from Cottrell WH: The book of fire, ed 2, Missoula, Mont, 2004, Mountain Press Publishing Co.)

To help fill that need, full-time research into the systematic measurement of forest flammability or “fire danger” began in the United States and Canada in the 1920s and has continued more or less uninterrupted since that time.22,77 Fire management agencies employ fire danger rating systems to help them gauge ignition and fire behavior potential based on fuel characteristics, past and current weather conditions, and certain topographic variables that encapsulate fire behavior knowledge garnered from research.23,269,456 Such systems have been demonstrated to be of value in accurately predicting fire behavior in the wildland–urban interface.10 In commenting on the historic fatality fires around the turn of the 20th century, Brown and Davis77 pointed out that in general terms, these situations reflected the public’s indifference to forest fires that had persisted for so many years and still lingers on to some degree today. They noted: The Maine fires of 1947 were a sobering reminder in this respect. They occurred at a time when fire danger measurement was well understood and means for mass public dissemination of this information were well developed. Responsible officials were aware of the mounting fire danger. Nonetheless, some fifty fires were reported to have been burning in Maine at the time the major break occurred on October 23. A contributing circumstance was the general feeling that, as it was late October, the fire season was over. Fire danger rating outputs are being applied directly to the task of community fire safety and protection, including early warning or alert systems linked to fire weather forecasts that operate during the fire season, such as those developed for the Northwest Territories, Canada.30 This information is now commonly accessible to the general public on the Internet regarding

countries like the United States (http://www.fs.fed.us/land/wfas), Canada (http://cwfis.cfs.nrcan.gc.ca), New Zealand (http://nrfa. fire.org.nz/fire_weather), the European Union (http://www.effis. jrc.ec.europa.eu), and many other countries (see http://www.fire. uni-freiburg.de). Forecasts of fire weather conditions are by themselves useful; the information can also be used to forecast fire danger indexes and potential fire behavior characteristics.61,156,411 In Australia, television and radio are relied on extensively to alert the public of “total fire ban” days (i.e., extreme fire danger) based on current fine-fuel moisture levels, drought status, and forecasted fire weather conditions.123 Fire danger rating and fire behavior predictions can be used to judge whether evacuations are required or to assist people with preparing for the eventuality of a fire arriving.229 Evacuation routes must be established in advance, and the actual time taken to evacuate to a safe zone needs to be determined in much the same manner as a wildland firefighter uses an escape route to reach a safety zone or an urban dweller evacuates a building fire using preidentified travel routes and exit locations.

Fire-Related Injuries and Fatalities Few would argue that battling wildland fires is physically arduous work that occurs in austere conditions and includes inherent dangers. As a result, injuries and death occur infrequently but regularly. In the United States, statistics for wildland fire–related serious injuries and deaths have been maintained for decades and have provided useful data in developing protocols for safe firefighting practices. The nature of these fatalities can be broadly categorized as deaths directly by fire in burnover or entrapment situations and deaths resulting from fire suppression activities. Most fatalities in wildland fire burnover situations occur on days of extreme fire danger when people are exposed to abnormally high heat stress caused by weather or proximity to fires. Loss of life is dramatically highlighted under extreme burning conditions; however, many more people are injured than are killed by fires. One of Australia’s worst bushfire disasters occurred on February 7, 1967, when 62 people died in Tasmania.288,511 Analysis of the locations and ages of 53 individuals at the time of death are instructive (Tables 12-3 and 12-4). Most people whose bodies were found within or near houses were old, infirm, or physically disabled. More than one-half of the houses vacated by the 11 people who traveled some distance before being killed were not TABLE 12-4  Age Distribution of 53 Persons Who

Died in Tasmanian Fires, February 7, 1967

Age Group (yr) 1-25 26-50 51-75 76-88

No. in Group

Average Age (yr)

1 13 26 13

23 38 64 82

From McArthur AG, Cheney NP: Report on Southern Tasmania Bushfires of 7 February 1967, Hobart, Australia, 1967, Government Printer.

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CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

TABLE 12-3  Location of Bodies of 53 Persons Who

PART 3  BURNS, FIRE, AND RADIATION

burned. Most of these victims would probably have survived if they had remained in their homes. Most of the 11 firefighters who died were inexperienced. Many might have survived if they had observed fire behavior and safety rules. Krusel and Petris248 investigated the circumstances surrounding the 32 civilian deaths that occurred during the 1983 Ash Wednesday bushfires in Victoria. As a result, they identified three categories of victims, suggesting ways to address the deficiencies in the manner in which individuals respond to the wildfire threat: • Victims who recognized the real threat to their safety with enough time to save their lives, but chose an ineffective survival strategy • Victims who did not recognize the real threat to their safety in time to implement an effective survival strategy • Victims who were physically incapable of implementing an effective survival strategy. Similar situations have been reported around the world. For example, during the 1993 fire season in the Tarragona Province of eastern Spain, five people were killed trying to escape from their home, built in the woods and surrounded by a fire; four of the victims were older adults and did not dare to flee until it was impossible to escape.487 In 2007, the National Wildfire Coordinating Group published an analysis of 310 wildland firefighter fatalities that occurred in the United States from 1990 to 2006.281 During this 17-year period, burnover situations constituted only the fourth most common cause of death, and the number of these incidents declined during the surveyed years. A total of 64 deaths, or 20.6%, were attributed to burnovers during this time period. By comparison, 72 deaths (23.2%) resulted from aircraft accidents, 71 deaths (22.9%) were caused by vehicle accidents, and 64 wildland firefighters (21.9%) died from heart attacks. The remaining percentages were classified as deaths resulting from falling trees, snags, or rocks (3.9%), other medical causes (2.9%), and miscellaneous causes (4.5%). Thus the top three leading causes of deaths related to wildland firefighting activity were not the result of individuals being burned over or entrapped by a wildland fire, although five firefighters were killed at a single location on the 2006 Esperanza fire in southern California.484 Reports for 2007-2009, in which 49 wildland firefighters died, showed similar trends.283 Interventions are possible to reduce the number of firefighter fatalities associated with aircraft and vehicle accidents, as well as those linked to heart attacks (Box 12-5).279,282 There have been more than 160 wildland fire suppression– related fatalities in Canada during the 70-year period between 1941 and 2010.24 Although the causes for all these firefighter

fatalities are not precisely known, certainly aircraft-related fatalities have been far more common in recent decades compared with earlier years of recordkeeping. It is much more difficult to gather accurate information regarding the incidence of minor to moderate injuries and episodes of illness among wildland firefighters. There are a number of reasons why these statistics do not exist. In general, the field draws individuals with a “can-do” attitude who are willing to work through many hardships that would cause workers in a general workforce to take time off for rest. Secondly, the vast majority of the care happens informally either on the fire lines as work continues or at base camps at temporary, low-level medical facilities where formal records are not maintained. Firefighters will often wait until they leave a fire to seek treatment from a private provider for an ongoing problem, and the injury or illness will not be tracked as a workplace-related incident. In the United States, the Bureau of Land Management has guidelines outlining the nature of burn injuries that require transport to and evaluation at a specialized burn center.237 This protocol largely corresponds to the guidelines of the American Burn Association (http://www.ameriburn.org/). By comparison, other medical protocols are region dependent. Fire suppression crews frequently have one or two medics, usually trained to the Emergency Medical Technician (EMT)-Basic level, among their members. The skill set of these medics depends on whether they are active, professional medical providers when they are not fighting wildland fires or if they maintain the certification solely for the position on the crew. Larger incidents may employ additional medical personnel to survey personnel on the fire lines or at portable medical tents/trailers in the base camp. Midlevel providers, such as paramedics, nurse practitioners, and physician’s assistants, usually staff these facilities. The availability of a medical command physician varies by region in the United States. When a firefighter requires evaluation and care outside the scope of first responders, the patient must be transported from the incident. The nature of the problem dictates if this transport requires specialized care at a trauma or burn center or if the local hospital closest to the incident can provide care. When large fires require hundreds to thousands of personnel, a small local hospital in a rural area may be overburdened by the temporary additional population. Transport protocols are determined on a regional basis and may use ground ambulances or air medical service (via rotary- or fixed-wing aircraft) depending on the nature of the incident and availability of resources.

BOX 12-5  21st-Century Common Denominators for

COMMON DENOMINATORS OF FIRE BEHAVIOR ON FATALITY FIRES

More than 20% of fatalities during wildand firefighting operations continue to concur in burnovers and entrapments. Carl Wilson’s original common denominators519 are just as important in the 21st as they were in the 20th century However, as the major causes of firefighter fatalities shift, it has suggested that additional factors need to be considered: • Firefighters are most likely to die in an aircraft accident. Before every flight, fire managers must ask, “Is this flight essential?” and “Is everyone onboard essential to the mission?” • Firefighters are nearly as likely to die in a motor vehicle accident as in an aircraft accident. Driving too fast for the conditions, failure to wear seat belts, rushing to a fire, and driving home while exhausted from firefighting kills firefighters. • Firefighters can reduce their risk for dying from heart attack on the job by staying fit, maintaining their ideal body weight, and having regular medical checkups. • Unexpected events such as falling snags, rolling rocks, downed power lines, and lightning strikes cause more than 8% of fatalities during wildland firefighting operations. Firefighters and fire managers can reduce fatalities by learning to expect these unexpected events.

A review of wildland firefighter fatality records between 1926 and 1976 shows that 145 men died in 41 fires from fire-induced injuries.339,340,519 Besides the 1949 Mann Gulch and 1990 Dude fires, large losses occurred on the 1933 Griffith Park fire in California (29 deaths and 150 others injured),174 the Blackwater fire in Wyoming in 1937 (15 deaths),75 the Pepper Hill fire in Pennsylvania in 1938 (8 deaths),413 the Hauser Canyon fire in California (11 deaths),110,432 the Rattlesnake fire in California in 1953 (15 deaths),272 the 1956 Inaja fire in California (11 deaths),412,474 the 1966 Loop fire in California (12 deaths),148 and the 1968 Canyon fire in California (8 deaths).149 Wilson’s review519 of people killed by wildfires in areas protected by other federal, state, county, and private agencies indicated 77 fire-induced fatalities in 26 fires during this same time period. The United States is not the only country to have had firefighters killed by entrapments and burnovers. For example, 25 soldiers were killed while involved in wildland firefighting operations near Lisbon, Portugal, on September 6, 1966.234 Australia has experienced a number of firefighter fatality incidents.115,234 For example, on December 2, 1998, five volunteer firefighters were killed near the town of Linton, Victoria, when the tanker they were traveling in was overrun by fire.140 From his analysis of the incidents in the United States during the period 1926 to 1976, Carl Wilson519 identified several common features associated with fatal fires: 1. Most of the incidents occurred on relatively small fires or isolated sectors of larger fires.

Wildland Fire Fatalities

Modified from Mangan R: Wildland firefighter fatalities in the U.S.: 1990-2006, National Fire Equipment System Publication PMS 841, Boise, Idaho, 2007, National Interagency Fire Center, National Wildfire Coordinating Group, Safety and Health Working Team.

262

NATURE OF INJURIES AND FATALITIES Fire-related injuries and fatalities are a direct consequence of heat, flames, smoke, critical gas levels, or indirect injuries280,316 (Figure 12-34, online). Injuries and fatalities associated with wildland fires fall into one of five categories: heat (direct thermal injury, inhalation, and heat stress disorders), flames (direct thermal injury and inhalation), smoke (inhalation and mucous membrane irritation), critical gas levels (oxygen, carbon monoxide, and carbon dioxide), and indirect effects (acute and chronic medical disability and trauma). Intense fires that produce very high temperatures generally last for only a short time. The duration of intense heat increases with fuel load, being greater in a forest fire where heavy fuels452

are burning than in a grass125 or shrub fire (see Table 12-2). Temperatures near the ground are lower because radiant heat is offset somewhat by inflow of fresh air and the fact that gases of combustion rise and are carried away by convection.114 Close to the ground, within a few meters of flames reaching up to 11 m (36 feet), air temperatures may be less than 15° C (59° F) above ambient temperature. The breathing of heated air can be tolerated for 30 minutes at 93° C (199° F) and for 3 minutes at 250° C (482° F).269 Death or severe pulmonary injury occurs when these limits are exceeded. Thermal injuries of the respiratory tract frequently contribute to the clinical picture of smoke inhalation. People trapped in a fire may have no choice but to breathe flame or very hot gases. This usually injures the tissues of the upper airway and respiratory tract, most commonly the nose, nasopharynx, mouth, oropharynx, hypopharynx, larynx, and upper trachea. These injuries may result in edema that obstructs the airway and produces asphyxia or that causes tracheitis and mediastinitis. Signs of thermal injury to the airway include thermal injuries to the head, face, and neck; singed facial hair; burns of the nasal, oral, or pharyngeal mucosa; and stridor or dysphonia.312,449,528 Associated with a history of exposure to flame and hot gases in a closed space, these clinical findings strongly suggest the presence of a thermal injury to the airway. With the potential for acute airway obstruction, there is obvious urgency in establishing this diagnosis. Most experts who treat thermal injuries of the tracheobronchial tree advocate early visualization of the vocal cords by laryngoscopy and bronchoscopy.313 Bronchoscopy is a useful predictor of the clinical course and urgency of intensive care unit intervention. In addition, one report shows a significantly greater incidence of pneumonia and late mortality in people with facial burns than in those without them.524 Burns of the lower trachea are rarely reported. In fact, injuries to and beyond the carina are difficult to produce when the trachea is cannulated and hot gases are delivered in the anesthetized dog.310,527 Air has a very low specific heat and is therefore a poor conductor of thermal energy. In addition, the thermal exchange systems of the upper airway are quite efficient. The hot gas or flame is cooled sufficiently in the upper airway so that it does not burn the bronchi or more distal structures. However, although water or steam in the hot gas mixture is probably rare, it is a far more efficient conductor of heat and permits significant thermal injury to the lower trachea and bronchi. A delayed onset (2 to 24 hours after smoke inhalation) of pulmonary edema and adult respiratory distress syndrome is widely reported and should be anticipated. Heat stress169,417 occurs when air temperature, humidity, radiant heat, and poor air movement combine with strenuous work and insulative clothing to raise body temperature beyond safe limits. Sweating cools the body as moisture evaporates. When water lost through sweating is not replaced, physiologic heat controls can deregulate, and body temperature may rise, leading to heat exhaustion or heatstroke (see Chapters 10, 11, and 70). Direct contact with flames causes thermal injury, and death is inevitable with exposure for long periods. Burns may be superficial, partial, or full thickness (see Chapter 13). Immediate death results from hypotension, hyperthermia, respiratory failure, and frank incineration. As mentioned earlier, the common cause of asphyxia in wildland fire is smoke. Danger increases where smoke accumulates because of poor ventilation, as in caves, box canyons, narrow valleys, and gullies. Dense, acrid smoke is particularly irritating to the respiratory system and eyes. Excessive coughing induces pharyngitis and vomiting. Keratitis, conjunctivitis, and chemosis may make it impossible to keep the eyes open. There are concerns about the levels of oxygen, carbon monoxide, and carbon dioxide associated with wildland fires. Critical levels readily occur in a closed space and near burning or smoldering heavy fuels, but the open space associated with wildland fires usually contributes to continual mixing of air. Misconceptions or myths about lack of oxygen or excessive carbon monoxide and carbon dioxide in a wildland fire abound in the popular literature.125 Flaming combustion can be maintained only at oxygen levels that exceed 12%, a level at which life can also be supported.114,269 263

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

2. Most of the fires were innocent in appearance prior to the “flare-ups” or “blow-ups.” In some cases, the fatalities occurred in the mop-up stage. 3. Flare-ups occurred in deceptively light fuels. 4. Fires ran uphill in chimneys, gullies, or on steep slopes. 5. Suppression tools, such as helicopters or air tankers, can adversely modify fire behavior (helicopter and air tanker vortices have been known to cause flare-ups). Many firefighters were surprised to learn that tragedy and near-miss incidents occurred in fairly light fuels, on small fires, or on isolated sectors of large fires, and that the fire behavior was relatively quiet just before the incident, even in the cases involving aircraft.149,161,215 Many have been led to believe that it is the conflagration or large, high-intensity crown fire in timber and heavy brush that traps and kills firefighters. Yet, with some exceptions, most fires were innocent appearing just before the fatal moment. Case studies of wildland firefighter fatality incidents from other regions of the world suggest similar patterns and circumstances—for example, the 25 fatalities at Puerto Madryn, Argentina, on January 21, 1994164; 10 fatalities in the Sabie district of the Mpumalanga Province of South Africa in 1994165; and 5 fatalities associated with three different incidents that occurred in Portugal during the 1999 and 2000 fire seasons.492 Wildland firefighter fatalities have been reported in Italy, Spain, Portugal, and Croatia in the last decade.489,491 Wilson concluded that the hairline difference between fatal fires and near-fatal fires was determined by the individual’s reaction to a suddenly critical situation. Escapes were due to luck, circumstances, advance planning, a person’s ability to avoid panic, or a combination of these factors. Frequently, poor visibility and absence of concise fire information threatened survival opportunities by creating confusion and panic. For many years, Wilson’s findings were summarized in a popular booklet, published initially by the USDA Forest Service and in later years by the National Wildfire Coordinating Group.338 This information has now been incorporated into the 2010 edition of the Incident Response Pocket Guide, published by the National Wildfire Coordinating Group.346 The British Columbia Forest Service found many of the same factors identified by Wilson in their investigation of a number of close calls or near misses that occurred during the 1994 fire season.50 Although there have been few wildland firefighter fatalities in Canada due to entrapments or burnovers,36,463 those that have occurred are also in alignment with Wilson’s findings.60 Most fatality fires are the result of a temporary escalation in fire spread, an increase in flame dimensions, crowning and spotting activity, or the development of large fire whirls, often occurring suddenly and with very little warning. A gentle surface fire will rapidly develop into a high-intensity fire. This could occur, for example, as a result of thunderstorm downdraft winds,125,411 a change in fuel types,50 fire-whirl development upon the fire reaching a ridgeline with an opposing gradient wind,144 or a “slope reversal” (e.g., fire slowly backs down a northerly aspect, crosses the drainage, and then rapidly spreads up the southfacing slope),388 such as documented with time-lapse photography on the 1979 Ship Island fire in central Idaho.336 As the moisture content of dead and live fuels decreases, fires become increasingly more responsive to slight changes in wind strength and slope steepness. Once “critically” dry levels are reached, fire behavior becomes exceedingly unstable.28,85,269

PART 3  BURNS, FIRE, AND RADIATION

With continued in-drafts of air that feed the flames, a fresh source of oxygen is usually present. Even mass fires, in which large tracts of land are burning, rarely reduce oxygen to hazardous levels. Low oxygen levels may occur, however, where there is little air movement, such as in caves or mine shafts (Figure 12-35) or in burned-over land that continues to smoke from smoldering fuels. Concentrations of carbon monoxide exceeding 800 parts per million (ppm) can cause death within hours. Most fires produce small quantities, but atmospheric concentrations rarely reach lethal levels because of air movement. High concentrations appear to be associated with smoldering combustion of heavy fuels, such as fallen trees or slash piles, and carbon monoxide may also collect in low-lying areas or underground shelters (e.g., root cellars).116 Outdoors, the danger lies in continual exposure to low concentrations that can increase blood carboxyhemoglobin levels. Prolonged exposure affects the central nervous system, resulting in headache, impaired judgment, progressive lethargy, decreased vision, and other psychomotor deficits.519 Carbon monoxide levels of 50 ppm were measured close to a prescribed burn in grass.143 In another estimate, concentrations of 30 ppm were found roughly 61 m (200 feet) from the fire front. Studies on the 1974 Deadline and Outlaw forest fires in Idaho showed that firefighters were exposed to levels above the standards proposed by the National Institute of Occupational Safety and Health (35 ppm over an 8-hour period).465 However, more recent measurements of carbon monoxide levels and particulates made on wildfires between 1992 and 1995394 indicate that wildland firefighters are seldom exposed to smoke that exceeds the Occupational Safety and Health Administration’s permissible exposure limits.395 Decreased ambient oxygen may contribute to hypoxia and the overall picture of smoke inhalation (Table 12-5). This mechanism is at least variably operant. When standing gasoline was ignited in a closed bunker, the fire self-extinguished, whereas the ambient oxygen level remained at 14%, a survivable level.310 Injecting burning gasoline or napalm into bunkers produced nearly complete and prolonged exhaustion of ambient oxygen. Conflicting

TABLE 12-5  Human Response to Decreased

Ambient Oxygen at Sea Level

Ambient Oxygen (%)

Human Response

20.9 16-18 12-15

Normal function Decreased stamina and capacity for work Dyspnea with walking; impaired coordination; variable impaired judgment Dyspnea at rest; consciousness preserved; impaired judgment, coordination, and concentration Loss of consciousness; death without prompt reversal Death in 6 to 10 minutes

10-12 6-8 <6

data make it difficult to classify definitively situations in which decreased ambient oxygen and subsequent hypoxia of exposed individuals contribute to the clinical picture of smoke inhalation. Studies in which ambient oxygen was measured by scientists did not show significant depletion at the scene of the fire.209 Few data are available on levels of carbon dioxide around wildland fires. Although it may be produced in large quantities, it apparently never reaches hazardous concentrations, even in severe fire situations.114,269 The quantity of burning fuel and type of topography affect levels of oxygen and toxic gases. Danger is greater in forest fires where heavy fuels burn over long periods of time than in quickmoving grass and shrub fires. Topography has a major influence: caves, box canyons, narrow canyons, gulches, and other terrain features can trap toxic gases or hinder ventilation, thereby preventing an inflow of fresh air. Although most fatalities result from encounters with smoke, flames, and heat, critical gas levels can induce handicaps sufficient to render the victim more vulnerable to other hazards. Whereas respirators285 are not routinely used on wildland fires or on wildland–urban interface fires, they could possibly play a role in the future as a means of protection against airborne toxic materials.

WILDLAND FIRES, AIR TOXINS, AND HUMAN HEALTH

FIGURE 12-35  USDA Forest Service Ranger Ed Pulaski led 42 men and two horses to this mine tunnel near Placer Creek in northern Idaho to seek refuge from the 1910 firestorm. One man failed to get into the tunnel and was burned beyond recognition. All the men in the tunnel were evidently unconscious for a period of time. Five died inside, apparently from suffocation. The remainder of the crew was evacuated to the hospital in Wallace, where all recovered. For a fuller account of this incident, see reference 384. (Courtesy USDA Forest Service; photo by J.B. Halm.)

264

In the United States each year, about 80,000 firefighters are involved with suppression activities on about 70,000 wildland fires that burn an average of more than 0.8 million hectares (2 million acres). In 1988, more than 2 million hectares (5 million acres) of land were burned, with a total combined suppression cost exceeding $600 million. The firefighting effort has another cost that has not been quantified: the effect of smoke on firefighter health and productivity. Over the 4 months of the Greater Yellowstone Area fires, about 40% of the 30,000 medical visits made by wildland firefighters were for respiratory problems. More than 600 firefighters required subsequent medical care. In the Happy Camp area during the Klamath fire complex in California in 1987, ambient concentrations of carbon monoxide measured as high as 54 ppm on a volume basis.497 A better understanding of the long-term effects of wildland fire smoke on people is clearly needed, although “firefighters just keep coming back year after year,” notes Dr. Brian Sharkey,422 a wildland firefighter health and safety specialist with the USDA Forest Service’s Missoula Technology and Development Center (MTDC) who coordinated an 8-year study of the health hazards of smoke on wildland firefighters.418,420 Combustion of wildland fuels produces many by-products in a variety of concentrations, depending on the type of fuel and the nature of the fire characteristics.357 The impact of these byproducts is very difficult to assess. Short-term studies have been inconclusive, and long-term studies are enormously complex and essentially absent from the literature. Completion of a prospective epidemiologic study would be highly informative. The combustion products of concern include these classes of materials: • Particulate matter • Polynuclear aromatic hydrocarbons

“camp crud,” especially late in the fire season, suggest a classic infectious outbreak pattern. Other infectious outbreaks that have spread through the wildland fire community include a series of methicillin-resistant Staphylococcus aureus (MRSA) outbreaks in fire camps during the 2008 and 2009 seasons in the United States.264,482,483 Infectious illness shared among firefighters is likely promoted by a variety of factors, including close working and living proximity, challenged immune conditions resulting from strenuous work and nutritional demands, hygiene conditions dictated to some degree by the environment, and potentially firefighters’ access to seasonal vaccinations. Identifying possible interventions to decrease the burden from infectious illness would be beneficial to improving firefighter wellness and productivity. The epidemiologic data collected for wildland firefighting are very sparse, either for analysis of short-term outbreak situations or long-term health and wellness.

Wildland–Urban Interface Fire Survival Principles and Techniques History has demonstrated repeatedly that individuals simply were not prepared to make correct choices of survival alternatives under stressful situations. At least 437 wildland firefighters were killed in the United States between 1910 and 2009 as a direct result of a burnover or entrapment by a free-burning wildfire.339,281,283 Overconfidence, complacency, ignorance, bad habits, lack of preparation, poor decision making, and a whole host of other human factors quickly lead to improper and unsafe actions during fire emergencies.356,504,519 “Learning from mistakes” in these settings is not a reasonable education strategy because second chances are frequently unavailable in the wildland firefighting profession. The USDA Forest Service organized a task force in 1957 to “study how we might strengthen our ways and means of preventing firefighting fatalities.”309 A major recommendation was to adopt service-wide standard firefighting orders. Ten standard firefighting orders287,308 summarize the fundamental principles of safety on the fire line (Box 12-6). Although these were written for wildland firefighters, they apply to all people working, living,

BOX 12-6  Ten Standard Firefighting Orders Adapted

for the General Public

1. Keep informed of fire weather conditions, changes, and forecasts and how they may affect the area where you are located. 2. Know what the fire is doing at all times through personal observations, communication systems, or scouts. 3. Base all actions on current and expected behavior of the fire. 4. Determine escape routes and plans for everyone at risk, and make certain that everyone understands routes and plans. 5. Post lookouts to watch the fire if you think there is any danger of being trapped, of increased fire activity, or of erratic fire behavior. 6. Be alert, keep calm, think clearly, and act decisively to avoid panic reactions. 7. Maintain prompt and clear communication with your group, firefighting forces, and command and communication centers. 8. Give clear, concise instructions, and be sure that they are understood. 9. Maintain control of the people in your group at all times. 10. Fight fire aggressively, but provide for safety first. (Nonqualified or untrained and improperly dressed or equipped persons should engage in firefighting operations only when it is absolutely necessary to assist injured persons. Wildland firefighting is a physically demanding task and should not be attempted by persons who are not in good physical condition.)

265

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

• Carbon monoxide • Aldehydes • Organic acids • Semivolatile and volatile organic compounds • Free radicals • Ozone • Inorganic fraction of particles Large variances are associated with the development of smoke combustion products and exposure to the materials of concern.497 Ward and colleagues498 indicated that the toxicity of the combination of combustion products depends on the relative concentrations of the individual compounds, as well as the overall concentration and length of exposure. Individual toxicities are associated with many of the compounds found in smoke. The combined toxicity of these substances is not known. A detailed set of studies is being carried out to provide answers so that risk management options can be exercised. One of these studies suggested that wildland firefighters experience a small cross-seasonal decline in pulmonary function and an increase in several respiratory symptoms.407 Eye irritation, nose irritation, and wheezing were associated with recent firefighting. The strenuous work of fighting or escaping a fire magnifies chronic illnesses, age disabilities, exhaustion, and cardiovascular instability. Common trauma is induced by falling trees or limbs, rolling logs or rocks, vehicular accidents, poor visibility, panic, falling asleep in unburned fuels that later ignite, and leaving the safety of buildings and vehicles. Cuts, scrapes, scratches, lacerations, fractures, and eye injuries (foreign particles, smoke irritation, sharp objects) are other common afflictions. Poison oak, poison ivy, stinging insects, and poisonous snakes are additional sources of trauma during wildland fires. To avoid fire-related injuries and fatalities, a person must keep attuned to mental and physical stress levels and be aware of cumulative effects.417 Ignorance of this simple principle is disastrous. Accurate statistics have not been collected to document the frequency and nature of injuries and illnesses over the course of different fire seasons. The common afflictions listed above are inherent to completing strenuous work under adverse conditions. Overall, the infrequency of major traumatic injuries speaks to the success of firefighters’ adhering to established safety protocols. A range of occupational and overuse injuries consistently emerges over the course of the fire season. Blisters and foot problems occur frequently early in the season, especially if offseason fitness has fallen by the wayside. As with other soft-tissue injuries, these can be complicated if not promptly addressed with standard first aid. Muscle strains, back problems, and tendinitis often follow particularly intense work periods. These maladies are best prevented by firefighters’ maintaining off-season fitness regimens to endure the physical rigors of firefighting.264 Research and development carried out by the MTDC of the USDA Forest Service have led to invaluable contributions regarding the health and safety of wildland firefighters, including the following: • Optimal work-rest patterns • Firefighter nutrition and hydration requirements and regimens • Heat stress and uniform/personal protective equipment design • Tool testing to optimize firefighter efficiency • The relationship between firefighter nutrition and immune function These studies have informed U.S. firefighting protocols to improve productivity and firefighter safety.168,419,421,423,424 The informal surveys conducted of wildland firefighter health demonstrate a pattern of increasing respiratory symptoms over the course of the fire season. This pattern has become common enough that firefighters have coined a term—”camp crud”—to describe the range of symptoms shared throughout the camps. The severity and frequency of symptoms can have legitimate safety and productivity consequences. Smoke exposure has been considered as one factor contributing to the frequency of respiratory illness44 and decreased respiratory function over the course of the fire season,198 but there is no consensus on how interventions could be feasibly instituted to reduce smoke exposure in wildland fire suppression. Regular occurrences of the flulike

PART 3  BURNS, FIRE, AND RADIATION

Lookout(s)

Hazard (Fireline hazards such as fire entrapment or falling or rolling objects are inherent in the wildland fire environment)

Communication(s)

X

Escape routes

Firefighters

Route 1

Route 2

Safety zone(s)

FIGURE 12-36  Concept of the LCES wildland fire safety system. (From Gleason P: LCES: The key to safety in the wildland fire environment, Fire Manage Notes 52:9, 1991.)

or traveling near wildland fires and are adapted here to remind emergency medical personnel, wildland homeowners, and recreationists of safety precautions to be taken around wildland fires. Much of this material is summarized in the handy Incident Response Pocket Guide.346

LCES: THE KEY TO SAFE PROCEDURES IN WILDLAND FIRE ENVIRONMENTS LCES stands for lookout(s), communication(s), escape routes, safety zone(s).203 These variables are key components in evaluating the threat posed by fire-line hazards and determining the best course of action (Figure 12-36). Some fire management agencies have added an “A” to LCES, thus LACES, for a variety of meanings—attitude, awareness, and anchor points.251,461 The Australasian Fire Authorities Council has, for example, adopted the LACES wildland fire safety acronym with the proviso that the “A” stands for awareness.46 Most Canadian fire management agencies have taken the “A” in LACES to connote anchor point.460 The importance of an anchor point is quite vividly highlighted in the video A Firefighter’s Return From a Burnover: The Kelly York Story, which details the severe burn injuries received by a volunteer firefighter while attempting to suppress a grass fire in central California during the 1995 fire season.177 As Australian fire management and research pioneers Harry Luke and Alan McArthur269 state in their seminal reference book Bushfires in Australia, fire suppression “must at all times start from an anchor point.” The wildland fire environment’s basic hazards are lightning, volcanoes, falling of fire-weakened trees and snags, rolling rocks and logs, entrapment by free-burning fires, respirable particulates, air toxins, and heat stress. When these hazards exist, there are two options: 1. Do not enter the environment, or 2. Adhere to safe procedures according to LCES. LCES should be viewed from a “systems” point of view, stressing their interdependence. For example, the best safety zone is worthless if the escape route does not offer access at the point of need. People must be familiar with the LCES plan well before it is needed. In addition, the nature of wildland fires dictates that LCES be redefined in pace with changing conditions. The LCES wildland fire safety system is implemented as follows: • Lookout(s): Fixed lookouts or roving lookouts must be where both the hazard and the people can be seen. A lookout is trained to observe the wildland fire environment and to recognize and anticipate changes in fire behavior. 266

When the hazard becomes a potential threat or danger, the lookout relays this information so people can depart for the safety zone. • Communication(s): Communication refers to alerting people to the approaching or pending hazard. Promptness and clarity are essential. • Escape routes: These paths lead from a currently threatened position to an area free from danger. More than one escape route must be available. Escape routes are probably the most elusive component of LCES because they change continuously. Timely access to safety zones is the most important component.63 Research on wildland firefighter travel rates27,56,97,408 suggests that, although civilians could momentarily advance at a rate in excess of what most wildland fires are capable of achieving, even the most fit individuals would not be able to sustain such a pace for more than a few minutes before being burned over by an advancing fire, especially on steep slopes—escaping uphill is thus a very questionable concept, unless a safety zone is known to be very nearby. Furthermore, some fire researchers believe there is a common tendency to overestimate the distance to a fire when observing through the forest, which may lull firefighters into thinking there is more time available for an orderly exit than is actually the case.124 • Safety zone(s): In a safety zone, threatened persons find adequate refuge from danger. The size of the safety zone must be sufficient to provide protection from flames, radiant heat, convective heat, falling trees and snags, and rolling rocks and logs. The necessary size varies with changes in fuels, topography, wind conditions, and fire intensity. The question of whether a previously burned area will serve as a safety zone depends not only on the size of the area but also on the degree of completeness of fuel consumption, both vertically and horizontally.96,366 What constitutes a safety zone varies widely among individuals.440 Based on theoretic consideration for radiation emitted from a “wall of flame” under idealized conditions (e.g., level terrain, steady-state fire conditions),93 it has been suggested, from the standpoint of flame radiation, that a safety zone should be large enough that the distance between the human occupants and flame front be at least four times the maximum expected flame height at the edge of the safety zone95 (Table 12-6). It should be emphasized that in deriving this rule of thumb, several assumptions had to be made that could ultimately limit the usefulness of this simple guide,451 although some field verification has been accomplished.94 Furthermore, both the modeling and resultant TABLE 12-6  Minimum Safety Zone Separation

Distances and Sizes (Circular Shape) in Relation to Flame Height*

Flame Height

Separation Distance

Area†

Meters

Feet

Meters

Feet

Hectares

Acres

2 5 10 20 40 60

6.5 16 33 66 128 262

8 20 40 80 160 240

26 64 132 264 512 1048

0.02 0.13 0.5 2.0 8 18

0.05 0.31 1.2 5.0 20 45

*For a single person on flat topography based on the “four-times-flame-height” rule of thumb for radiant heat only (i.e., no convection) and no allowance for flame impingement or other fire line hazards.93,95 It is assumed that the person is standing upright and is properly clothed, including headgear and gloves. † Assuming the area of a circle is equal to approximately 3.14159 times the square of the separation distance, where the separation distance is deemed to be the radius of a circle. For perspective, a typical North American ice hockey rink is 0.16 hectare (0.39 acre) in size, whereas Canadian and American football fields are about 0.6 hectare (1.5 acre) and 0.4 hectare (1.1 acres) in size, respectively. In turn, the maximum sizes of outdoor soccer and rugby fields would be approximately 0.8 hectare (2.0 acres) and 1.0 hectare (2.5 acres), respectively. A full-size basketball court is about 0.04 hectare (0.1 acre) in size.

EIGHTEEN “WATCH OUT!” SITUATIONS IN THE WILDLAND FIRE ENVIRONMENT The following list of 18 “Watch Out!” situations, adapted from the wildland fire community’s safety guidelines,306,311,429 are of particular relevance to emergency medical personnel and wildland users; each of these situations has come about as a result of one or more wildland firefighter fatalities: 1. You are moving downhill toward a fire, but must be aware that fire can move swiftly and suddenly uphill. Constantly observe fire behavior, fuels, and escape routes, assessing the fire’s potential to run uphill. 2. You are on a hillside where rolling, burning material can ignite fuel from below. When below a fire, watch for burning materials, especially cones and logs, that can roll downhill and ignite a fire beneath you, trapping you between two coalescing fires. 3. Wind begins to blow, increase, or change direction. Wind strongly influences fire behavior, so be prepared to respond to sudden changes. 4. The weather becomes hotter and drier. Fire activity increases, and its behavior changes more rapidly as ambient temperature rises and relative humidity decreases.

5. Dense vegetation with unburned fuel is between you and the fire. The danger in this situation is that unburned fuels can ignite. If the fire is moving away from you, be alert for wind changes or spot fires that may ignite fuels near you. Do not be overconfident if the area has burned once because it can reignite if sufficient fuel remains. 6. You are in an unburned area near the fire where terrain and cover make travel difficult. The combination of fuel and difficult escape makes this dangerous. 7. Travel or work is in an area you have not seen in daylight. Darkness and unfamiliarity are a dangerous combination. 8. You are unfamiliar with local factors influencing fire behavior. When possible, seek information on what to expect from knowledgeable people, especially those from the area. 9. By necessity, you have to make a frontal assault on a fire with tankers. Any encounter with an active line of fire is dangerous because of proximity to intense heat, smoke, and flames, along with limited escape opportunities. 10. Spot fires occur frequently across the fire line. Generally, increased spotting indicates increased fire activity and intensity. The danger is that of entrapment between coalescing fires. 11. The main fire cannot be seen, and you are not in communication with anyone who can see it. If you do not know the location, size, and behavior of the main fire, planning becomes guesswork, which is an unfavorable response. 12. An unclear assignment or confusing instructions have been received. Make sure that all assignments and instructions are fully understood. 13. You are drowsy and feel like resting or sleeping near the fire line in unburned fuel. This may lead to fire entrapment. No one should sleep near a wildland fire. If resting is absolutely necessary, choose a burned area that is safe from rolling material, smoke, reburn, and other dangers or seek a wide area of bare ground or rock. 14. Fire has not been scouted and sized up. 15. Safety zones and escape routes have not been identified. 16. You are uninformed on strategy, tactics, and hazards. 17. No communication link with crew members or supervisors has been established. 18. A line has been constructed without a safe anchor point. Humorous artwork has even been developed to help illustrate or visualize the 10 standard fire orders and 18 “Watch Out!” situations.317

FIFTEEN STRUCTURAL “WATCH OUT!” SITUATIONS FOR THE WILDLAND–URBAN INTERFACE Continuing development creates ever more wildland–urban interface; therefore fires are tending to occur more often in that interface. These 15 structural “Watch Out!” situations have been defined to increase awareness of structural fire dangers:466 1. Access is poor (e.g., narrow roads, twisting, single lane with inadequate turning). 2. Load limits of local bridges are light or unknown; the bridges are narrow. 3. Winds are strong, and erratic fire behavior is occurring. 4. The area contains garages with closed, locked doors. 5. You have an inadequate water supply to attack the fire. 6. Structure windows are black or smoked over. 7. There are septic tanks and leach lines. These are found in most rural situations. 8. A house or structure is burning with puffing rather than steady smoke. 9. Inside and outside construction of structures is wood with shake-shingle roofs. 10. Natural fuels occur within 9 m (30 feet) of the structures. 11. Known or suspected panicked individuals are in the vicinity. 12. Structure windows are bulging, and the roof has not been vented. 13. Additional fuels can be found in open crawl spaces beneath the structures. 267

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

radiation-based guide do not consider flame impingement or horizontal reach into a clearing, fire whirls, or any allowance for convective heat transfer, which will be significant under windy conditions in sloping terrain.125,401 Obviously, further study, including field measurements, and development are warranted (e.g., allowance for convective heating on a slope), which is indeed the case.90 Nevertheless, while acknowledging these limitations, this rule of thumb has been incorporated into existing operational guidelines,346 training course material,463 and computer programs.41 According to Butler and Forthofer,98 additional modeling (e.g., radiation on a sloping surface), subsequent observations, and other field measurements support “four times flame height” for minimum safety zone size, although research is continuing on this matter.91 While serving as the ignition boss during the International Crown Fire Modelling Experiment (ICFME) in the Northwest Territories,18,445 one of the authors (MEA) was able to informally evaluate the Butler and Cohen93,95 safety zone guideline. Based on observations and the experience of being on the backside or upwind edge of all the ICFME experimental crown fires,447,457 the four-times-flame-height rule of thumb seems to be reasonably valid. As Butler and Forthofer98 point out, “It’s important to realize that this should be considered a minimum—meaning that in all cases larger is better.” In using Butler and Cohen’s rule of thumb93,95 for safety zones or in turn Table 12-6, the logical question is: How does one go about estimating flame height in advance of a fire’s occurrence? On the basis of various fire behavior observations and various analyses, we can say with some degree of certainty that the maximum flame heights in grasslands, shrublands, and hardwood stands would vary, depending on the burning conditions, from about 2 to 10 m (7 to 33 feet). Thus a separation of at least 40 m (130 feet) should be adequate in most fuel types that do not contain conifer trees. The average flame height of crown fires in conifer forests is generally 2 to 2.5 times the stand height.447 Any area smaller than a safety zone should be regarded as a possible “survival zone” or site. Unfortunately, no quantitative description of what constitutes a survival zone presently exists. The FPInnovations–Feric Wildland Fire Operations Research Group (http://fire.feric.ca) and the University of Alberta are currently engaged in a project to better define the criteria for survival zones in wildland fires.25,26 Nevertheless, specific case study examples (e.g., 1937 Blackwater fire in Wyoming, 1958 Wandilo fire in South Australia, and 1990 Dude fire in Arizona) suggest that survival is possible in relatively small areas even when exposed to a highly hostile thermal environment provided a person maintains a prone position and uses every possible bit of protection against radiation, convection, and direct flame contact. Movement within the survival zone may also be possible and necessary as the flame front surrounds the site.

PART 3  BURNS, FIRE, AND RADIATION

14. Firefighting is taking place in or near chimney or canyon situations. 15. Elevated fuel or propane tanks are present. These are also known as the “Wildland–Urban Watch Outs!”346

TAKING REFUGE IN VEHICLES, BUILDINGS, AND PROTECTIVE FIRE SHELTERS USED BY WILDLAND FIREFIGHTERS The radiant energy of a fire, although highly intense at a given location, typically lasts for only a short time. Because radiant heat travels in straight lines, does not penetrate solid substances, and is easily reflected, seeking refuge in vehicles, buildings, or protective fire shelters should be viewed as a lifesaving solution. Vehicles Wildland firefighters have survived severe fire storms or the passage of fire fronts by taking refuge in vehicles.278,289,361,362 Sadly, there are reported cases in which civilians would have survived or avoided serious injury had they remained in their vehicles.234,358 Bereska65 has indicated that he and two others were forced to drive a 3 4 -ton Dodge 4 × 4 truck at a moderate speed (25 to 30 km/hr or 16 to 19 mph) through the flame front of a grass fire during a prescribed burning operation carried out in northcentral Alberta in early April 1980. Winds at the time of the incident were light (less than 12 km/hr [7 mph]), and the flames, although high (3 to 4 m [10 to 13 feet]), were not deep (1 to 2 m [3 to 7 feet]). He remembers “it got very hot instantly and as we came out of the flames we opened the windows and appreciated the cool fresh air.” The following three U.S. case histories serve as examples of intense burning situations in which lives were saved because people stayed inside vehicles while the fire front passed by their location:429 • In 1958, a veteran field section fire warden and two young men were fighting forest fires that burned in heavy fuels near the Bass River State Forest in southern New Jersey. A 90-degree wind shift transformed the flank fire into a broad head fire, with the advancing flames reaching up to 12 m (40 feet) in height. The men entered their vehicle, a Dodge W300 Power Wagon, which stood in the middle of a 4-m (13-foot) wide sand road. Simultaneously, the engine and radio failed. The fire warden repeatedly admonished the crewmen, who wished to flee, to stay in the truck. Subsequently, the truck was rocked violently by convection currents and microclimatic changes generated by the flames. The men could neither see nor breathe because of smoke, and the cab began to fill with sparks that ignited the seat. The men stayed with the truck for only 3 or 4 minutes during passage of the head fire, but they indicated later that the interval involved seemed more like 3 or 4 hours. At the first opportunity, all of them left the vehicle on the upwind side and crouched beside it to escape the searing heat and burning seats. The warden proceeded to burn his hand severely while disposing of a flaming gas can located in the truck bed. Although the young men escaped virtually unscathed, the older man suffered lung damage and remained on limited duty for 5 years. He has since recovered completely and subsequently retired. • In a 1962 California Division of Forestry fire in Fresno County, three men, followed by a flank fire that had turned into a head fire, raced back to their truck only a few feet ahead of the flames. The truck would not restart. After the main body of flames passed over the vehicle, the men jumped out to breathe because the truck was burning. Almost completely blinded by smoke and heat, they stumbled headlong into matted fuels, and two received first- and second-degree burns. One man was not burned but had to be treated for smoke inhalation. The truck was a loss. • In 1976 a firefighter died while fighting a grass fire near the town of Buhler in Reno County, Kansas. A flashover occurred from buildup of gases on the lee side of a windbreak. A fire truck was caught in the flashover, and the firefighter working from the back of the vehicle ran and 268

was killed. Although the truck burned, the driver was not seriously hurt. Sitting in a vehicle during a passing fire front is often perilous, but when a person is trapped, it is almost certain doom to attempt escape by running from the fire. The preceding case histories illustrate a few facts that, if remembered, may prevent panic-like reactions: • The engine may stall and not restart. • The vehicle may be rocked by convection currents. • Smoke and sparks may enter the cab. • The interior, engine, or tires may ignite. (Tires exploded during the Crank fire burnover in California in August 1987 involving several wildland fire engines.334 This is obviously unsettling in an already stressful situation that could lead to panic-like reactions.) • Temperatures increase inside the cab because heat is radiated through the windows. • Metal gas tanks and containers rarely explode. • If it is necessary to leave the cab after the fire has passed, keep the vehicle between you and the fire. The type of vehicle determines the amount of protection afforded. Two travelers died in a fire in 1967 in Tasmania, Australia, when they were caught in a canvas-topped vehicle.269 A later fire in Australia led to further research on various vehicles’ protection and the explosiveness of gasoline tanks. In 1969 near Lara, Victoria, Australia, a fast-moving grass fire crossed a fourlane expressway.193,269 Several cars stopped in the confusion of smoke and flames. Seventeen people left the safety of their cars and perished. Six people stayed inside their vehicles and survived, even though one car ignited. Investigations were carried out by the Forest Research Institute (now the Commonwealth Scientific and Industrial Research Organization [CSIRO], Division of Forestry and Forest Products) in Canberra, Australia, to collect accurate data and dispel the misconceptions that make people flee a safe refuge if trapped by fire.114 Cars were placed between two burning piles of logging slash to study a car’s ability to shield against radiation.269 The test was a hotter, longer-duration fire than would normally be encountered in a wildland setting. Car bodies halved the external radiation transmitted at the peak of the fire, but a person inside would have suffered severe burns to bare skin. Although air temperatures inside the car did not reach hazardous levels until well after the peak radiation had passed, smoke from smoldering plastic and rubber materials would have caused discomfort and made the car uninhabitable. In this study, metal gasoline tanks did not explode, whether intact on cars or separated and placed on a burning pile of slash. Apparently, when tanks are sealed, the space above the liquid contains a mixture too deficient in oxygen vapor to support an explosion. Several years ago, Cheney114,116 offered the following general advice for survival when in a car and trapped by fire: • If smoke obstructs visibility, turn on the headlights and drive to the side of the road away from the leading edge of the fire. Try to select an area of sparse vegetation offering the least combustible material. • Attempt to shield your body from radiant heat energy by rolling up the windows and covering up with floor mats or hiding beneath the dashboard. Cover as much skin as possible. • Stay in the vehicle as long as possible. Unruptured gas tanks rarely explode, and vehicles usually take several minutes to ignite. • Grass fires create about 30 seconds (maximum) of flame exposure, and chances for survival in a vehicle are good. Forest fires create higher-intensity flames lasting 3 to 4 minutes (maximum) and lowering chances for survival. Staying in a vehicle improves chances for surviving a forest fire. Remain calm. • A strong, acrid smell usually results from burning paint and plastic materials, caused by small quantities of hydrogen chloride released from breakdown of polyvinyl chloride. Hydrogen chloride is water soluble, and discomfort can be relieved by breathing through a damp cloth. Urine is mostly water and can be used in emergencies.

Buildings The decision to evacuate a house or remain and defend it is not an easy one. Fire services generally prefer that residents evacuate the threatened area so that agencies can concentrate on protecting structures. Authorities also agree that evacuation of older adults and very young, infirm, and fearful people is usually a good idea.248 People should evacuate only if it can be accomplished safely, well in advance of any danger. If not, then it is

BOX 12-7  Guidance for People in a Vehicle During a

Wildland Fire

Advance Preparation • Always carry woolen blankets, leather gloves, and a supply of water in the vehicle. • Dress in suitable nonsynthetic clothing and shoes, including a hat. Encountering Smoke or Flames • If you see a wildland fire in the distance, carefully pull over to the side of the road to assess the situation. If it is safe to do so, turn around and drive to safety. • If you have been trapped by a wildland fire, find a suitable place to park the car and shelter from the fire. Positioning Your Car • Find a clearing away from dense bush and high ground fuel loads. • Where possible, minimize exposure to radiant heat by parking behind a natural barrier, such as a rocky outcrop. • Position the car facing toward the oncoming fire front. • Park the car off the roadway to avoid collisions in poor visibility. • Do not park too close to other vehicles. Inside Your Car • Stay inside your car—it offers the best level of protection from radiant heat as the fire front passes. • Turn headlights and hazard warning lights on to make the car as visible as possible. • Tightly close all windows and doors. • Shut all the air vents, and turn the air conditioning off. • Turn the engine off. • Get down below the window level into the foot wells, and shelter under woolen blankets. • Drink water to minimize the risks of dehydration. As the Fire Front Passes • Stay in the car until the fire front passes and the temperature has dropped outside. • Fuel tanks are unlikely to explode. • As the fire front approaches, the intensity of the heat will increase, along with the amount of smoke and embers. • Smoke gradually gets inside the car, and fumes will be released from the interior of the car. Stay as close to the floor as possible to minimize inhalation, and cover mouth with a moist cloth. • Tires and external plastic body parts may catch on fire. In more extreme cases, the car interior may catch on fire. • Once the fire front has passed and the temperature has dropped, cautiously exit the car. (Be careful—internal parts will be extremely hot.) • Move to a safe area such as a strip of land that has already burned. • Stay covered in woolen blankets, continue to drink water, and await assistance. Modified from Australasian Fire Authorities Council: Guidelines for people in cars during bushfires, East Melbourne, Victoria, Australia, 2008, AFAC.

safer to shelter in place. Several principles should guide the evacuation decision:501 • A fire within sight or smell is a fire that endangers you. • Occupants are often quite effective in preventing their house from burning down. The more they understand the dynamics of fire behavior and have prepared for a fire occurrence, the easier and safer this task will be. • Evacuation when fire is close is too late; evacuation must only be done when it is certain that it is safe to do so. • More people are injured and killed in the open than in houses. • Learn beforehand about community refuges. • Evacuate only to a known safe refuge only when it is safe to do so. Whether people can find refuge in buildings depends on construction materials, house design detail, and proximity of fuels around the structure. If a home is constructed amid flammable vegetation, plans and procedures to safeguard the home and its occupants are essential. A building usually offers protection while the fire passes, even if it ignites during or after the fire’s passage, because it shields against radiant heat and smoke. After the fire passes, it may be necessary to exit if the building is burning. Either attempt to suppress the fire or to move onto burned ground. Numerous wildfire case histories from Australia, starting with the 1939 Black Friday fires in Victoria,258 demonstrate that homes provide safe havens.248,269,358,517 In 1967 in Tasmania, 21 people left their houses as fire approached. All died, and some were within a few meters of the buildings. Many houses did not burn and would have been refuges. When taking refuge in a building, give people useful jobs, such as filling vessels with water, blocking cracks with wet blankets, and tightly closing windows and doors. If possible, assign lookouts to keep watch for spot fires on and within the building throughout the fire event. Before fire approaches the house, plan to have taken the following precautions:257,429 • If you plan to stay, evacuate your pets and livestock and all family members not essential to protecting the home well in advance of the fire’s arrival. • Be properly dressed to survive the fire. Wear long pants and boots, and carry for protection a long-sleeved shirt or jacket made of cotton fabrics or wool. Synthetics should not be worn because they can ignite and melt. Wear a hat that can offer protection against radiation to the face, ears, and neck areas. Wear leather or natural fiber gloves and have a handkerchief handy to shield the face, water to wet it, and safety goggles, if possible. • Remove combustible items from around the house, including lawn and poolside furniture, umbrellas, and tarp coverings. If they catch fire, the added heat could ignite the house. • Ensure that anything that might be tossed around by strong fire-induced winds is secured (e.g., sheet metal, lumber, and plywood). • Ensure that the areas around any external propane tanks are fuel free for a considerable distance. Ensure that the tanks are properly restrained and the pressure relief value is directed away from buildings and access ways. • Close outside attic, eave, and basement vents to eliminate the possibility of sparks blowing into hidden areas within the house. Close window shutters. • Place large plastic trash cans or buckets around the outside of the house and fill them with water. Soak burlap sacks, small rugs, and large rags to use in beating out burning embers or small fires. Inside the house, fill bathtubs, sinks, and other containers with water. Toilet tanks and water heaters are an important water reservoir. • Place garden hoses so that they will reach any place on the house. Use the spray gun type of nozzle, adjusted to spray. Avoid laying the hose over or adjacent to combustible objects. • If you have portable gasoline-powered pumps to take water from a swimming pool or tank, make sure they are operating in place and well protected from nearby combustible elements. 269

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

Subsequent experiences,88 coupled with new research carried out by the Australian Bushfire Cooperative Research Centre,256 have lead to more definitive guidelines (Box 12-7).48

270

Home destruction No

Expected

Not expected

Not expected

Expected

Yes

Yes

No

High-intensity wildfire

PART 3  BURNS, FIRE, AND RADIATION

• Place a ladder against the roof of the house opposite the side of the approaching fire. If you have a combustible roof, wet it down or turn on any roof sprinklers. Turn on any special fire sprinklers installed to add protection. Do not waste water. Waste can drain the entire water system quickly. Where possible, divert water from gutters back into the firefighting supply. • Back your car into the garage, and roll up the car windows. Disconnect the automatic garage door opener (otherwise, in case of power failure, you cannot remove the car). Close all garage doors, and seal them with wet rags where possible. Avoid storing combustible elements in a garage that cannot adequately be sealed from ember attack. • Place valuable papers and mementos inside the car in the garage for later departure following passage of the fire, when it is safe and may become necessary to do so. In addition, place all pets in the car. • Close windows and doors to the house to prevent sparks from blowing inside. Close the damper on the fireplace to prevent smoke and embers from entering the house. Leave the doors inside the house open. This will enable occupants to remain vigilant throughout the exposure. If a room or area in the house ignites and develops beyond the occupants’ ability to contain it, then doors can be closed in the house to manage smoke spread. Begin to plan an exit to the outside, bearing in mind the state of the fire outside the house. The approach should be to retreat to a room with an exit door that opens onto a region with little fuel. Turn on a light in each room to make the house more visible in heavy smoke. Have a backup plan for when the electricity supply fails by having flashlights handy. • Turn off the main gas supply to stoves and furnaces. • If you have time, take down drapes and curtains. Close all Venetian blinds or noncombustible window coverings to reduce the amount of heat radiating into the house. This provides added safety in case the windows give way because of heat or wind. • As the fire front approaches, go inside the house. Stay calm; you are in control of the situation. Continually move around inside the house, monitoring its state and the progress of the fire outside. Avoid spending time in the areas that have only one way of exiting the space. If practical, include monitoring of the roof cavity. Goggles will prove handy in dealing with any smoke that enters the house. • After the fire passes, check the roof immediately. Extinguish any sparks or embers. Then check the attic for hidden burning sparks. If you have a fire, enlist your neighbors to help fight it. For several hours after the fire, recheck for smoke and sparks throughout the house. It is worth noting that research in this area by the Australian Bushfire Cooperative Research Centre is continuing under Project D1—Building and Occupant Protection (http://www.bushfirecrc. com/research/d11/d1123.html) under the leadership of Justin Leonard, CSIRO Sustainable Ecosystems. If a person expects to take refuge in his or her home and in turn survive to ensure its defense, then it is critical that steps are taken to reduce the ignition potential of the structure as much as possible. Recent research on home ignition involving field experiments, coupled with modeling and observations of recent wildland–urban interface fire incidents, has provided valuable new insights into the means of ensuring home survival.130,131,133 The research has shown that the characteristics of the home (e.g., exterior building materials) and in an area referred to as the “home ignition zone” located within 30 to 60 m (100 to 200 feet) of the home (e.g., surface fuel accumulations immediately adjacent to the structure that would be receptive to ignition by airborne firebrands) principally determines its ignition potential and thus its survivability during exposure to a wildland fire (Figure 12-37), videos that summarize this research are available from Firewise Communities.132,185,186 It is quite conceivable, for example, that a home could have little or no natural surface fuel within the immediate vicinity of the dwelling, but because cedar shake shingles were used in the roof construction, it is vulnerable to ignition from airborne embers or firebrands from an approaching wildfire. If such a burning structure is not handled

FIGURE 12-37  Expectations of home destruction as a result of exposure to a wildfire. Home survival is expected if low fire intensities occur (lower right cell) and unexpected if the home is destroyed (lower left cell). Conversely, home survival is not expected if high fire intensities occur (upper left cell) and unexpected if the home survives (upper right cell). (From Cohen JD: Home destruction. In Graham RT, technical editor: Hayman fire case study: Summary, General Technical Report RMRS-GTR-115, Fort Collins, Colo, 2003, USDA Rocky Mountain Research Station.)

soon after ignition, it can contribute to the demise of neighboring houses if left unattended314 or push the limits of fire protection to effectively keep up if too many structures become involved.134 The use of external sprinkler systems on a home141,349,436 should not be viewed as a panacea for a lack of fuel treatment in the home ignition zone and beyond or the use of flammable building materials. There is a perception that sprinklers should be capable of providing thermal protection from a high-intensity wildfire assault when in fact their real value is in preventing ignitions from airborne firebrands,304 direct flame contact, and radiation. The FPInnovations–Feric Wildland Fire Operations Research Group has been engaged in a number of research studies related to the use of sprinkler systems for home and cabin protection since 2002, including outdoor field trials, using simulated structures, involving both prescribed and experimental fires.495,496 According to the group’s leader, Ray Ault,43 he and his colleagues maintain that the greatest use of commercially available Rain Bird types of sprinklers and small portable pumps for individual home structure protection is in applying water in sufficient quantities and locations to inhibit external ignitions from airborne firebrands by an approaching or passing wildfire well in advance. If the presoaking or application of water for wetting down fuels is applied for too long, it can lead to other problems (e.g., flooded basements). Irrigation systems have also been occasionally applied to the task of wildland–urban interface protection. Other more elaborate systems have been devised. For example, the Saskatchewan Fire Management and Forest Protection Branch has successfully adapted and applied operationally a manure drag hose transportation system to the task of creating wet “breaks or belts” in values protection or to facilitate backfiring or burnout operations.249

PROTECTIVE FIRE SHELTERS USED BY WILDLAND FIREFIGHTERS The concept of a protective fire shelter for wildland firefighters described earlier (see Figure 12-19) was originally conceived by Australian bushfire researchers in the late 1950s.245,269 The USDA

States in the mid to late 1960s and became a required PPE item for federal wildland firefighters in 1977. More than 1200 U.S. wildland firefighters have deployed their fire shelters to date (up to and including the 2010 fire season).370 The fire shelter is credited with having saved the lives of more than 320 firefighters and preventing at least 315 serious burn injuries,370 although it is not known with any degree of certainty how many would have actually survived and suffered no burn injuries without the fire shelter. Some personal accounts of fire shelter deployments (Box 12-8) have been published.112,397 Why protective fire shelters work well was demonstrated dramatically on August 29, 1985, when 73 firefighters were forced

BOX 12-8  What Is It Like to Experience a Wildfire Entrapment in a Protective Fire Shelter?

B12-2  Shelter deployment on the Shelley fire, Gila National Forest, June 24, 1989. (Photo by Mark Erickson, copyright 2006.) Mark Erickson, a freelance photographer from Silver City, New Mexico, was unexpectedly involved along with 40 wildland firefighters in a fire shelter deployment associated with the major run of the Shelley fire that took place in the Gila National Forest on June 24, 1989. He recently recounted the experience:182 Dr Bruce Hayward, a biologist from Silver City, and I had been putting together a joint effort about the Gila Wilderness, he doing text and I covering the photography. It was decided that during the fire season that I should get out and get some images of fire because of its importance as ecological process in the area. The Shelley fire was started by lightning on June 16, 1989 but I didn’t visit the fire site until June 23. I initially went out to the Sheep Corral area toward Goose Lake to photograph the slurry bombers dropping fire retardant but decided to return the next day and get on the line. Jim Turner from the Shasta Ranger District in California was assigned to go with me and we headed up to the Snow Creek spike camp being manned by the local National Guard. The troops had a water tender and some miscellaneous stores with which to resupply the firefighters. We left our vehicle at the spike camp and headed down the fireline in a northeasterly direction. The fire had been turned over to a Class I Incident Command Team and an infrared imaging aircraft had been brought in to determine the location of hotspots. There was major concern down the valley near Lake Roberts about the many structures that could conceivably be in the path of the fire if the current fire suppression efforts were to fail. I photographed many of the hotshot crew members as they built fireline and felled snags near the line. It is hot, dirty work, especially when air temperatures are already high and there is little or no humidity.

Working our way along Panther Canyon, we noticed that there was a large column of smoke in the direction from which we had just come. Apparently the fire was heading right for the Snow Creek spike camp where the National Guardsmen were being hurriedly schooled on the use of fire shelters. A slurry bomber went over just as the Sacramento Interagency Hotshot Crew came up the fireline from the south. I took a few photographs of the hotshots with the “blowout” in the background and we turned and headed back toward a deployment zone or area on the fireline. The guardsmen were spared having to deploy as the fire made another turn and started toward us instead. Entering the deployment zone, the crew began to take care of the business of stowing gear such as chainsaws and fuel bottles on the perimeter of the area. Cubitainers of water were brought to the center of the deployment zone and personal gear was laid out. Last minute clearing was taking place as the fire began chugging its way closer to us. Even though there was some “good” black between us and the advancing fire front, the noise created by the crowning was incredible as it got closer to our location. Someone gave the order to deploy the fire shelters and all of us retreated underneath. Located in the center of the deployment zone, I continued to photograph the fire as it crowned around us. Comments from the firefighters about the reverberating sounds created by the fire were prevalent. The winds created by the fire were truly amazing and I was glad that the folks at the Technology and Development Center in Fort Missoula had seen fit to add straps to the fire shelters so that they wouldn’t fly away. Cinders from the fire were making small pin holes in the shelter, resulting in a planetarium effect as the flames surrounded the deployment area. The worst of all was the smoke. Everyone was chattering back and forth checking on their buddies. The duff was really burning when the fire decided to come back on us. We were ordered to move in the opposite direction and ended up laying in the smoldering pine needles. Thank heavens for Nomex as we all ended up with lots of holes in our clothing, but nothing burst into flame. I wish we would have had more time to rake the area before the fire hit our deployment zone. One could really feel the radiant heat from the shelters and I was really glad that we had them. There were many comments about being done on one side and “could we turn over to the other?” The fire finally moved on down the canyon, but we stayed in the shelters for an hour it seems. Finally we stuck our heads out to a smoke-filled environment where it was difficult to see more than 10 feet. I continued to take photographs as I thought folks wouldn’t really believe it if I just told them about this. A few of the crew were having some respiratory problems, but everyone was mobile. The cubitainers had been stripped of their cardboard casings and cases of MREs (meals ready to eat) were burnt to the ground. The handles on the fire tools were history, but the chainsaws and fuel bottles were intact. The deployment zone was still smoldering. I’m amazed how small it felt during the peak period of fire activity. Our shelters were fairly well spent and we tossed them into a pile—an unwise decision if we had had to deploy later again that day—and we headed down to the spike camp. General observation: cool heads keep a situation from escalation.

271

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

Forest Service equipment development center in Missoula, Montana (now the MTDC) initiated research and development of protective fire shelters around the same time as the Australians,475 and this work has continued to this day99,380 with a view to reducing the number of serious burn injuries and fatalities among firefighters who become trapped while fighting wildland fires.39 Shelters designed in the shape of a pup tent protect the firefighter by reflecting radiant heat. Constructed of an aluminum-foil and fiberglass cloth laminate, the shelter reflects about 95% of the radiant heat emanating from a fire. These shelters were never designed for direct flame contact. Fire shelters were first introduced operationally on the wildland fire scene in the United

PART 3  BURNS, FIRE, AND RADIATION

to take refuge in their shelters for about 1.5 hours following passage of a high-intensity, active crown fire that swept over and around their location.8,326,406 The incident took place during the Butte fire in the Salmon National Forest in central Idaho. Observers described the crown fire that overran the firefighters as a standing wall of flame that reached about 60 m (about 200 feet) above the treetops. Within the shelters, firefighters experienced extreme heat for as long as 10 minutes. Shelters were so hot that they could be handled only with gloves. After leaving the shelters, some firefighters showed symptoms of possible carbon monoxide poisoning, including vomiting, disorientation, and difficulty breathing. Emergency medical technicians administered oxygen to several individuals before evacuation from the site after the incident. Five firefighters were hospitalized overnight for heat exhaustion, smoke inhalation, and dehydration. The consensus of those interviewed was that without the shelters, none would have survived.333 It should be emphasized that the fire shelter was intended to be used as a last resort when it became impossible to escape to a safety zone before being overrun by a fire. However, despite the emphasis placed on this basic tenet and extensive training in entrapment avoidance over the years,306,308,335,341,463 the results from a recent study74 suggest a possible link to what has been suspected for many years—that some firefighters are likely to engage in behavior that neutralizes the gain in safety afforded by fire shelters. In other words, fire shelters can lead to additional risk taking410 or what’s called “risk homeostasis.”202 Putnam378 maintains that “you are always better with a fire shelter in an entrapment situation than not.” That is fair enough advice, so it seems. Fire shelters are, after all, relatively light to carry—the current model weighs 1.9 to 2.2 kg (4.2 to 4.8 lb) depending on the size40,367—and a minor inconvenience to carry around. Even when fire shelters become compromised, they still provide some protection. One of the entrapment survivors of the 1990 Dude fire, Dave LaTour, deployed his fire shelter before the arrival of the fire front and stayed under his shelter even after a hole was kicked in it by one of the firefighters who got out of his shelter and attempted to evade the flames.343 This allowed hot gases to enter his shelter. Despite this development, LaTour stayed down on the ground as flat as possible. He did sustain some burn injuries but fully recovered. LaTour was able to mentally concentrate his attention on his family to help him through the ordeal of being burned over by the passage of a highintensity flame front. One of the authors (MEA)11 is of the opinion that the main issue regarding their use, beside not knowing what constitutes an adequate clearing size for a shelter deployment in a particular situation,11,247 is the time taken for their efficient deployment.64 In trying to avoid a wildland fire entrapment or burnover, seconds can mean the difference between life and death.377 Without a regular, formalized training program, carried out under realistic environmental conditions, the precious time taken to deploy a shelter might be better spent attempting to evade the fire’s encroachment on one’s position to reach a safer location.11 The British Columbia Forest Service is the only Canadian fire management agency to have ever formally included protective fire shelters as part of a firefighter’s PPE. In 2005, it undertook an associated risk analysis59 and as a result decided to no longer have its firefighters carry fire shelters,223 relying instead on situational awareness and entrapment avoidance. The Australasian Fire Authorities Council has adopted a similar position on the grounds that fire shelters cannot guarantee firefighter survival and may result in firefighters placing themselves at greater risk in the belief that a fire shelter will protect them.47

EMERGENCY PROCEDURES DURING A WILDLAND FIRE ENTRAPMENT OR BURNOVER The danger of being entrapped or burned over and possibly killed or seriously injured by a wildfire is a very real threat for people living, working, or visiting480 in rural areas subject to wildfires. Arnold “Smoke” Elser,180 an accomplished Montana outfitter, described how he helped guests avoid entrapment by a forest fire in the mid-1960s: 272

The fire began at the bottom of the canyon and proceeded up canyon as fires do. However, the wind currents carried the smoke to the east and not up the drainage to the north; therefore, we received no warning of the fire. The Monture Creek trail goes through some very old mature timber which was not burning as we approached. As my stock, the guests, and I arrived at the fire site and realized that we were in danger, we felt we should fall back and try to flank the fire to the east. Starting back toward this trail, we found a ground fire that made it very hazardous to travel in this direction. Because of my knowledge of the trail and terrain, I knew that our best bet would be to wet down the stock, guests, saddles and outer clothing and try to break through the head of the fire. We successfully did this, receiving only a few minor burns on the horses and the loss of some apparel tied to the backs of the saddles. Some lessons that I learned in this experience were that in handling livestock in a fire situation you must have a very close, firm hand on them. It is also very important that no one panics or shows any excitement, as this alarms the livestock and begins the panic run that is so well known. I found that by talking in very low monotone, keeping the pack stock and saddle stock very close together (head to tail), and moving on a good trail, we were able to come through this fire with virtually no harm. Elser180 had these additional suggestions for wildland recrea­ tionists: Campers, whether they be livestock-oriented, hikers, or boaters, should know where to camp to provide adequate fire barriers around campsites. All campers should consider at least one, and preferably two, safe escape routes and havens (such as rock piles, rivers, and large green meadows) away from heavy fuel areas. Campers should be alert to canyon air current conditions in critical fire seasons. The safety of many recreationists is threatened by nylon and other synthetic fabrics used in the manufacture of most backpacking equipment. These materials melt upon contact with heat. The very nature of good horse packing equipment is a deterrent to fire; canvas mantles that cover the gear and the canvas pack saddles are easily wet down. Leather items such as chaps, good saddle bags, and western hats [that] can shield against heat blasts all provide important protection for the horse user. Sometimes there may be no chance to easily escape an approaching wildfire. Injuries can be minimized or avoided and possible death adverted by adhering to certain fundamental principles and procedures (Box 12-9). There are, however, four simple concepts that one must try to adhere to at all times:42,114,121,501 • Select an area that will not burn—the bigger the better—or, failing that, with the least amount of combustible material, and one that offers the best microclimate (e.g., depression in the ground). • Use every means possible (e.g., boulders, rock outcrops, large downed logs, trees, snags) to protect yourself from radiant and convective heat emitted by the flames. • Protect your airways from heat at all costs, and try to minimize smoke exposure. • Try to remain as calm as possible. The first requirement will limit the flame dimensions and in turn the potential heat energy from flame radiation. It will also limit the time of exposure, an important factor in thermal injuries. Radiant heat can kill you long before direct flame contact.142,501 The more exposed skin, the greater the likelihood of death. Obviously, the last requirement—to remain as calm as possible—may seem difficult to establish and maintain. The expectation that people will panic (i.e., a sudden uncontrollable fear or alarm leading to unthinking behavior) during an emergency situation such as wildfire entrapment or burnover is very strong. Admittedly, with the benefit of 20/20 hindsight, it is easy to point to some decisions that were not optimal and played a negative role in the outcome of the fire.356 Structural fire researchers feel that most people faced with a fire situation react in a rational manner considering the ambiguity of the initial cues about the fire, their limited knowledge about fire development and

or Burnover

When entrapment or burnover by a wildland fire appears imminent, injuries or death may be avoided by following these basic emergency survival principles and procedures. • Acknowledge the stress you are feeling. Most people are afraid when trapped by fire. Accept this fear as natural, so that clear thinking and intelligent decisions are possible. If fear overwhelms you, judgment is seriously impaired, and survival becomes more a matter of chance than good decision making. • Protect yourself against radiation at all costs. Many victims of forest fires actually die before the flames reach them. Radiated heat quickly causes heatstroke, a state of complete exhaustion. Find shielding to reduce heat rays quickly in an area that will not burn, such as a shallow trench, crevice, large rock, running stream, large pond, vehicle, building, or the shore water of a lake. Do not seek refuge in an elevated water tank. Avoid wells and caves because oxygen may be used up quickly in these restricted places; consider them a last resort. To protect against radiation, cover the head and other exposed skin with clothing or dirt. • Regulate your breathing. Avoid inhaling dense smoke (which can impair both your judgment and eyesight). Keep your face near the ground, where there is usually less smoke. Hold a dampened handkerchief over the nose. Match your breathing with the availability of relatively fresh air. If there is a possibility of breathing superheated air, place a dry, not moist, cloth over the mouth. The lungs can withstand dry heat better than moist heat. • Do not run blindly or needlessly. Unless a clear path of escape is indicated, do not run. Move downhill and away from the flank of the fire at a 45-degree angle where possible. Conserve your strength. If you become exhausted, you are much more prone to heatstroke and may easily overlook a place of safe refuge. • Burn out fuels to create a safety zone if possible. If you are in dead grass or low shrub fuels and the approaching flames are too high to run through, burn out as large an area as possible between you and the fire edge. Step into the burned area and cover as much of your exposed skin as possible. This requires time for fuels to be consumed and may not be effective as a last-ditch effort, nor does this work well in an intense forest fire. • Lie prone on the ground. In a critical situation, lie face-down in an area that will not burn. Your chance of survival if the fire overtakes you is greater in this position than standing upright or kneeling. • Enter the burned area whenever and wherever possible. Particularly in grass, low shrubs, or other low fuels, do not delay if escape means passing through the flame front into the burned area. Move aggressively and parallel to the advancing fire front. Choose a place on the fire’s edge where flames are less than 1 m (3 feet) deep and can be seen through clearly, and where the fuel supply behind the fire has been mostly consumed. Cover exposed skin and take several breaths, then move through the flame front as quickly as possible. If necessary, drop to the ground under the smoke for improved visibility and to obtain fresh air.

fire dynamics, and the restricted time to make a decision and to take action.435 Panic is viewed as being synonymous with a frightened, scared, nervous, or anxious response.435 In actual fact, panic in the form of irrational or crazed behavior (e.g., aimlessly trying to flee) is rare during fires. Social scientists long ago rejected this concept to explain human behavior in urban fires.127,375,435 Instead of panic, what is commonly observed is an increased level of stress. Stress is not panic. As Dr. Guylene Proulx, a human factors specialist with the National Research Council Canada’s structural fire research program, suggests, “This stress is not an abnormal reaction or a negative response; on the contrary, stress is regarded as a necessary state to motivate reaction and action” and that

“Decision-making under stress is often characterized by a narrowing of attention and focusing on a reduced number of options. This explains why training is so important because the person is unlikely to develop new solutions under heightened stress; a well-run decision plan learned and practiced beforehand is easier to apply under stress.” There are four fundamental or basic survival techniques or options (see Box 12-9) available to an individual who is caught out in the “open” and is likely to be entrapped or burned over by a wildfire and is not able to take refuge in a vehicle or building193,269,501 or have a protective fire shelter. These four survival options are as per follows:19,21,416 • Retreat from the fire and reach a safe haven. • Burn out a safety area. • Hunker in place. • Pass through the fire edge into the burned-out area. These four survival options are presented in no particular order of priority. Such factors as the size of the fire, the fire environment, the size and location of safety areas or zones, the prevailing fire behavior, and the location of the person with respect to the head of fire will ultimately dictate which option or options (should the first one of these options selected become compromised) should be selected. Each of these options has its own unique advantages and disadvantages. Survival Option 1: Retreat From the Fire and Reach a Safe Haven When people are under pressure, they fall back on habitual, first-learned, and overlearned responses.504 The natural tendency when a person is threatened by a hazard such as a wildfire is to try and move away from the danger as quickly as possible to a place of safe refuge. If the distance between the fire and safe area is short, the fire’s advance slow, the path to the safe area easily traversed, and the person able bodied, then selection of this survival option is appropriate. Bear in mind that a safe refuge may be very nearby, so one should not avoid the most obvious place even though it may temporarily be uncomfortable to reach owing to smoke or low to moderate radiation levels, for example. In some cases, this might mean just taking a few steps into the “black” or recently burned-over ground. The question of whether a previously burned area will serve as a safety zone will depend not only on the size of the area but also on the degree of completeness of fuel consumption, both vertically and horizontally.96,366 Furthermore, a recently burned-over area may not immediately serve as a safe refuge owing to the burnout time of woody fuels and duff,452 in contrast to grassland fuels in which a person can enter the recently burned area in a matter of a few seconds.125 There are a good many cases in which firefighters have escaped injury and death by being able to outpace or outma­ neuver a spreading fire.366,463 There have also been many wellpublicized cases or incidents during which attempting to initially outpace and then ultimately outrun an advancing flame front have ended in tragedy, including several incidents already mentioned in this chapter (i.e., 1938 Pepper Hill fire, 1949 Mann Gulch fire, 1953 Rattlesnake fire, 1956 Inaja fire, 1966 Loop fire, 1968 Canyon fire, and 1994 South Canyon fire). Sadly, there are many other examples,398 one of the most recent being the 2003 Cramer fire in central Idaho involving two firefighter fatalities.129 Dr. Ted Putnam,379 a retired wildland fire safety specialist with the USDA Forest Service, considers that many of the abovenoted fatality fires were in fact escapable had better decision making been employed (e.g., dropped tools and packs earlier on to maximize rate of advance, put the fastest pacesetters at the lead, and used fire shelters as shields against radiant and convective heat). Similar incidents involving civilians have also taken place. For example, on November 30, 1957, four members of a group of nine young hikers perished while trying to outrun a bushfire in the Blue Mountains of New South Wales, Australia, as it advanced upslope.193,269 Another incident occurred on August 26, 1995, near the community of São Domingos in the district of Sandtarém, Portugal.490 Three civilians who had been assisting local firefighters in suppression operations eventually ended up being killed while trying to run ahead of the fire when it blew up. A fourth 273

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

BOX 12-9  Surviving a Wildland Fire Entrapment

PART 3  BURNS, FIRE, AND RADIATION

individual received severe burns to his feet, which eventually led to them being amputated, and he died some months later. Simulations carried out by the FPInnovations-Feric Wildland Fire Operations Research Group based on their research on firefighter travel rates,157 coupled with case study information gleaned from the 1949 Mann Gulch and 1994 South Canyon fires,97 clearly indicate that a person is not able to sustain a maximum pace for even a relatively short period of time without being overrun by a rapidly advanced flame front, even on a moderately steep slope.27,56 For example, a fire spreading at 60 m/min (197 ft/min) up a 26% slope would, depending on the fuel type, overrun someone in about 6 to 7.5 minutes or after about 360 to 460 m (1200 to 1500 feet) once the “race” had started. Chandler and colleagues112 state, “In most firefighter fatalities … the unsuccessful strategy has been to try and run away from the fire and continue running until exhaustion or the radiant heat load from the fire front fells the victim and allows the flame front to pass over him or her.” Thus trying to outpace a fire for any significant distance, but especially uphill, is “courting disaster.”269 For this reason, escape routes involving travel upslope should generally not be selected. Survival Option 2: Burn Out a Safety Area Burning out fuels to create an area of safety or to enlarge an existing burned area is a viable survival technique or option in some situations (e.g., light fuels and having sufficient time to implement). As Luke and McArthur269 have noted, “Carrying a box of matches is part of survival planning” (in this regard, a windproof type of matches would be ideal); most wildland firefighters carry fuses, which would be infinitely more reliable and effective than a match. Undoubtedly the most publicized example of this survival strategy being used in modern times occurred on the 1949 Mann Gulch fire, mentioned at the start of this chapter.275,403 However, the technique was known to have been used by American Indians in the early 1800s381,476 and undoubtedly by aboriginals in other parts of the world, as depicted, for example, in the 1989 movie, The Gods Must Be Crazy II. Wag Dodge described his escape fire during his testimony at the board of review investigation into the 1949 Mann Gulch fire as follows: After setting a clump of bunch grass on fire, I made an attempt to start another one, but the match had gone out and upon looking up, I had an area of 100 feet square that was ablaze. I told the man nearest to me that we would wait a few seconds to give it a chance to burn out inside, and then we would cross through the flames into the burned area, where we could make a good stand and our chances of survival were more than even. Interestingly, Dodge’s statement was printed in the letters to the editors section of the September 1949 issue of Life magazine following publication of an article on the Mann Gulch fire entitled “Smokejumpers Suffer Ordeal by Fire” from the previous issue. In that letter, the reader stated, “I am sure that there are many people throughout the country who would appreciate and perhaps benefit sometime by a more detailed account of how Foreman Wagner Dodge, who kept calm and did not become panic-stricken, saved himself.” It has been estimated that Dodge’s escape fire was about 37 m (121 feet) long and 26 m (85 feet) wide at the time that his “island” of survival was engulfed by 3-m (10-foot) tall flames associated with the main fire front.25 Survival Option 3: Hunker in Place When caught in the open, survival may depend on taking advantage of every possible source of cover or protection from radiant and convective heat (e.g., depressions in the ground, large rocks or logs).193 If a cave (see Figure 12-35) or root cellar520 is used as a refuge, it is important to vacate into the open at the earliest opportunity owing to potential problems associated with accumulations of smoke and carbon monoxide. In selecting this option, the importance of staying as flat as possible with one’s nose and mouth pressed down into the ground cannot be overemphasized, because the reduction in radiation received is considerable.26 Lying prone not only 274

minimizes one’s radiation profile, but cooler, denser air will always be present at ground level. In selecting this option, bear in mind the following advice:121 When a fire passes over a point, the air temperature near the ground is higher than the air above it and remains higher for longer. So if someone is sheltering from radiation at ground level, they need to stand up as soon as possible after the fire passes to breathe cool, fresh air. This is most apparent in grass fires where air at ground level is hot and smoky for several minutes whereas at 2 m [6.6 feet] it is cool and breathable within 10 to 15 seconds of the flames passing. Although there have been reported cases of firefighters surviving on large rockslides during a wildfire entrapment or burnover, most notably two smoke jumpers on the 1949 Mann Gulch fire,275,403 there have also been instances in which these apparently safe, fuel-free areas contained enough combustible materials to cause injury or death (e.g., Shephard Mountain fire in western Montana on September 4, 1996). Four firefighters died on a rockslide during the 2001 Thirtymile fire in north-central Washington, due in part to the accumulation of duff and rotting wood lodged in the rock crevices that ignited from airborne firebrands.79,273,478 In selecting this option, maximum use should be made of any clothing or other readily nonburnable material to protect exposed skin. You may have to improvise.477 Synthetics should not be used because they readily melt when exposed to flame radiation. During the 1983 Ash Wednesday fires in Victoria, Australia, two individuals wearing only summer clothing who covered themselves with a synthetic blanket perished, while two other individuals right next to the two victims covered themselves with a wet woolen blanket and survived the burnover.248 A good example of using this option was the Wandilo fire that occurred in an exotic pine plantation near Mount Gambier, South Australia, on April 5, 1958. Eleven firefighters found themselves trapped on a narrow firebreak during a “blowup.”269,289 Eight in the group attempted to run back along the firebreak, but perished after exposure to extreme radiant heat levels and direct flame contact. Of the three who survived, two remained in the cab of their firefighting truck to shelter from the worst of the firestorm and only left this cover when the vehicle was well alight and the fire’s peak intensity had abated. The remaining survivor sheltered in a deep wheel rut in the soft sand of the firebreak with his coat over his face during the peak period of extreme fire behavior. Taking refuge in a natural water body such as a pond, lake, or river must be done with caution, but for other reasons (e.g., swimming ability). For example, in 1986, three firefighters in the province of Quebec, Canada, drowned as a result of being forced to enter a lake with a steep drop-off when their camp location was overrun by fire.13 The risk for hypothermia must also be considered.98 Dion167 described an incident that occurred in westcentral Saskatchewan, Canada, in May 1919 in which 11 Cree Indians perished because they were not able to reach a nearby lake or find deep enough water to avoid radiation burns. Of the 12 who survived the ordeal, 11 “bore the marks of their burns for life.” One adult member of the group “escaped severe burns by staying under the water” as much as was possible. It has been suggested that the minimum depth of water should be 0.45 to 0.6 m (1.5 to 2 feet) deep.344,433 Survival Option 4: Pass Through the Fire Edge Into the Burned-Out Area Luke and McArthur269 have suggested that “running through flames cannot be generally recommended and should certainly not be attempted when flames are more than 1.5 m [5 feet] in height or depth.” Nevertheless, a number of firefighters have done this very thing and survived (e.g., 1991 Tikokino grass fire in New Zealand392). In fact, the five members of the group of young hikers that survived the 1957 bushfire in the Blue Mountains of New South Wales mentioned earlier did so successfully but suffered considerable discomfort. A similar incident occurred on the Warm Springs Indian Reservation in central Oregon in June 1985. Wildland fire behavior analyst Jim Roessler400 has

Convection

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

indicated that those individuals who tried to outrun a grass fire on a moderately steep slope were killed, whereas at least one person who passed through the flame front survived. In contrast, during the blowup of the 1937 Blackwater fire, the “five horsemen” made the decision to move downhill through the advancing flames.75 Three did not make it, no doubt due in part to the heavy fuel conditions. Of the two who did survive, one died later of burn injuries. A group of 41 on another section of the fire rode out the blowup in a ridgeline clearing as the fire progressed upslope; 3 were badly burned and eventually died of their injuries. It has been suggested that a person could theoretically survive passing through flames 3  m (9.8 feet) high and 37  m (121 feet) in depth and still survive.112 It is presumed that the person would be immersed in flames for less than 7.5 seconds and would require ideal running conditions (e.g., good footing, no obstructions) and be properly clothed to withstand the direct flame contact. Although it is reasonable to expect a person to be able to hold his or her breath for this long, the very notion of attempting such a drastic or draconian112 feat seems unimaginable. Nevertheless, it is worth noting that firefighters have lived, albeit while suffering severe burns as a result, by running through high-intensity flame fronts. One of the most notable examples of this involved a prescribed fire (PB-3/79) in heavy logging slash near Geraldton, Ontario, Canada, on August 22, 1979.35,297,318 As a result of a complex set of unforeseen circumstances, eight members of the firing crew found themselves encircled by fire. One member of the party, a local fire technician, realizing that there was no other option except to run through the advancing flame front or face what appeared to be certain death, tried to get seven seasonal employees to follow him. They failed to heed his urgings and were eventually engulfed by the fire, whereas he survived but did suffer serious burn injuries. This outcome is hauntingly reminiscent of the 1949 Mann Gulch fire and Wag Dodge’s escape fire in which 15 firefighters failed to follow his lead and 13 ended up perishing. In this regard, Dr. Karl Weick,505 a renowned professor of organizational behavior and psychology, points out that there is good evidence to support the notion that when people are threatened, their thinking becomes much more rigid and difficult to change. Furthermore, they tend to seek out and talk to only those who are most familiar to them.425 The survival technique or option of moving through the flame front to previously burned ground would logically be most suitable in light, discontinuous fuel types that fail to produce deep, uniform flame fronts, and significant postfrontal smoldering or isolated flaming, such as that afforded by certain grasslands (e.g., heavily grazed areas). Furthermore, if one has the good fortune to take advantage of a lull in the wind, this would lessen the momentary rate of spread and in turn the flame depth (see Table 12-2). An area along the flanks of the fire (see Figure 12-24) would be preferable to the head. One may only have to travel a relatively short distance before reaching previously burned ground that has “cooled” down sufficiently to serve as a safe area. Having reached the burned area, a person would still have to be cognizant of the danger posed by fire-weakened trees and falling snags, hot ash pits and burned-out stump holes, and rolling rocks or logs.263 This would apply to the other survival options as well. It is worth emphasizing that wildland firefighters as well as members of the general public have been killed and seriously burned while engaged in using fire as a land management tool.35,302,441,488,493 Thus the survival principles and options discussed earlier are equally applicable to prescribed fires or controlled burns. Although radiant heat emanating from a wall of flame is generally viewed as the principal killer in wildland fire entrapments and burnovers,142 under certain conditions convective gases or superheated air can have lethal consequences with little or no warning, most notably upslope of a fire source. Under strong winds, a fire’s convection column will not lift away from the surface of a steep slope.125 As slope steepness increases, flames gradually “attach” themselves (Figure 12-38), thereby enhancing fire spread by both direct flame contact and convective heat transfer.401 This is the very reason that fires spread faster

Weak indraft Strong indraft

Flame detached from slope

A

SHALLOW SLOPE

Convection

Indraft Flame attached to slope

B

STEEP SLOPE

FIGURE 12-38  Effect of slope steepness on degree of flame attachment and convective heat transfer for shallow sloping (A) and steep sloping (B) terrains. (Redrawn from Rothermel RC: Fire behavior considerations of aerial ignition. In Mutch RW, technical coordinator: Prescribed fire by aerial ignition: Proceedings of a workshop, Missoula, Mont, 1985, Intermountain Fire Council.)

upslope than on level ground given the same fuel and weather conditions.

Wildland Fires and Human Behavior As discussed earlier, the reality of human behavior in fires is somewhat different from the panic scenario “nourished by the media and movie industry who like to play on strong emotional images.”375 What is regularly observed in urban fire situations is a lethargic response to fire alarms or even the initial cues of a fire (e.g., smoke and visible flame). What has been most troubling to the wildland fire community in recent years is the fact that the same mistakes seem to be made time and time again,170 rather than using “the lessons of the past so we don’t have to keep relearning them the hard way.”340 Since the mid-1990s, there has been a growing recognition among the wildland fire community of the role that human factors play in firefighter fatalities.92,171,377 Morse311 considered the development of a mental “scotoma” among firefighters to be a major contributing factor in many wildland fire fatality incidents, noting, “Scotoma is, literally, a blind spot. In a psychological sense, it is that condition which occurs when a person tends to block out from his or her 275

PART 3  BURNS, FIRE, AND RADIATION

consciousness anything considered not important—or critical—to survival.” In other words, blindness to danger perceived as routine takes hold and blocks out sensitivity to hazardous events or conditions present in the wildland fire environment. The smoke jumpers involved in the 1949 Mann Gulch fire would appear to have suffered from a psychological scotoma or overconfidence.503 By the time they had landed and gathered their gear together, it was nearly 5:00 PM. At the time, “They did not feel the fire threatened them then.”403 Less than an hour later, 12 smoke jumpers and a local firefighter were overrun and killed by the fire. Air temperatures reached a maximum of 36° C (97° F) on the day in question, and in turn, the fully cured grasses were in a critically dry state.403 It was a day of extreme fire danger.15 One of the survivors, Bob Sallee, commented afterwards:403

A

I took a look at the fire and decided it wasn’t bad. It was burning on top of the ridge and I thought it would continue on up the ridge. I thought it probably wouldn’t burn much more that night because it was the end of the burning period (for that day) and it looked like it would have to burn down across a little saddle before it went uphill any more. One crew member was reported to have been taking photographs of the fire less than 10 minutes before the first fatalities occurred.275,403 Similarly, photographs were being taken by firefighters on the line just moments before the 1994 South Canyon fire blowup,96 in which 14 of their fellow firefighters were overrun and killed (see Figure 12-1). Even on the major run of the Thirtymile fire in north-central Washington on July 10, 2001,79,273 the firefighters behaved more as spectators than as potential victims until it was too late for some. A total of 16 people (14 firefighters and 2 civilians) were entrapped and required to deploy protective fire shelters. Four firefighters were killed, and 2 were injured, 1 with severe burns. Earlier during the day in question, the feeling was that the fire was “basically a mop-up show.”79 Some of the firefighters who were overrun by the fire “spent time taking photos or making journal entries” just a half hour before the incident.79 Although wildland firefighters may be subject to a whole host of human failings or other psychological phenomena,129,355,504 openly acknowledging and constantly being aware of the potential for entrapment or a burnover, regardless of the situation, is the initial key step in reducing the risk for injury or death from wildland fires. Complacency may be the most difficult factor to overcome.316 The late Paul Gleason,204 a veteran wildland firefighter and accomplished rock climber, noted that three major causes of climbing accidents are ignorance, casualness, and distractions. Although firefighters are expected to engage a wildfire, civilians are not. Nevertheless, the general public could also become complacent about wildfires and fail to fear the worst, until, unfortunately, it is too late. This may be due in part to a fascination with fire in general (Figure 12-39, online), denial, indifference, or a complete ignorance about free-burning fire behavior. In any case, there is a perception that there is no real sense of urgency until the threat is imminent. As Proulx375 points out, “People are often too cool during fires, ignoring or delaying their response to the initial cues of an actual emergency. Once occupants decide that the situation requires moving to an area of safety, the time left could be minimal.” This is probably best exemplified by an urban fire case study. On May 11, 1985, 56 people burned to death and more than 200 were injured when a rapidly growing fire, caused by a cigarette, engulfed the wooden main grandstand at Valley Parade Stadium in Bradford, England, during a soccer match. Filmed documentation of the fire indicates that the blaze spread the entire 88-m (289-foot) length of the stand in less than 5 minutes—a rate of 18 m/min (59 ft/min). Although people in the immediate vicinity of the developing fire moved toward exits, “Persons in remote sections of the grandstand continued to watch the match, apparently unconcerned about (or perhaps unaware of) the developing fire.”246 One of the seven factors that contributed to the loss of life was “The failure of patrons to perceive the danger of the developing fire in the early stages and begin evacuation.”246 276

B FIGURE 12-40  Fires in fully cured grasslands are very responsive and can attain exceedingly rapid rates of spread. The flank of a grass fire, with a change in wind direction, can quite quickly become the head and catch the unwary off guard. This scene from the multifire situation that occurred in the Spokane, Washington, area on October 16, 1991 (A), reinforces the importance of having well-established escape routes that can be easily navigated (B) to a designated safety zone. (Courtesy Spokane Statesman Review/WorldPictureNews; photos by K. King.)

It is hard sometimes to believe that a wildland fire could become life threatening, especially if it is far away from the observer or small in size and is not burning very vigorously at the time. However, danger is inherent in every wildland fire occurrence, be it a wildfire or a prescribed fire. Some wildland fire situations are simply more hazardous than others and can catch a person or persons off guard (Figure 12-40), possibly leading to severe injuries or even death.54,85 Tom Leuschen262 is an experienced fire manager and wildland fire behavior analyst who worked for many years in north-central Washington, within sight of the area struck in 2001 by the Thirtymile fire. He was involved in the accident investigation and had the following to say about the incident: When I stand at the deployment site and look at their pictures, knowing what I know about the fuels, barriers, and interactions between fires, I honestly do not expect that they will have to shelter either. I am as wrong as they were. Things got very complex as the fires joined at their location. The obvious lesson is that we must prepare for the worst when trapped, regardless of what we may anticipate. They were entrapped at 1634 and deployed at 1724. They had time to get organized. Anyone involved in a wildland fire can become a victim of an entrapment or burnover at any time given the precarious nature of wildland fires and their environmental influences. People need to be constantly mindful or conscious of this fact because, as Weick502,504 says, “safety is not bankable” and it is “an ongoing struggle for alertness.” Plan for and expect the worst every time out. This may be difficult, because a blatant disregard for worst-case scenarios is one of the common, yet least studied, human traits111 (Box 12-10).

Weick’s Book Review of Cerulo’s Never Saw It Coming: Cultural Challenges to Envisioning the Worst*

Karen Cerulo argues that people have a clear preference, culturally shaped, for paying attention to best-case scenarios and casual attention to worst-case scenarios. Whether people render the worst-case invisible or vague or recast the worst case as positivity in disguise, the result is that they are unable to envision the worst case and unprepared to avoid it or deal with it. Thus, the plaintive phrase provides the title of this work, “we never saw it coming.” The reader comes away from this book with a new appreciation of the need for mindful attention, resilient action, and skills of improvisation. With these three resources as part of an action repertoire, we will go a long way toward acknowledging and preparing for worst-case scenarios. *From Weick KE: Book reviews: Never saw it coming: Cultural changes to envisioning the worst, Am J Sociol 113:1762, 2008.

PROPER CLOTHING There are documented cases in which homeowners, who were seemingly prepared to stay and defend their property, have died because they were not properly dressed to do so (e.g., clad only in shorts or a bathing suit and slippers).501 Clothing protects against radiant heat, embers, and sparks, so it is sensible to dress appropriately.141,358 The cover of a recent book on the wildland– urban interface fire situation in southern California219 depicts a lightly clad homeowner on the roof of his house presumably attempting to extinguish sparks or embers with a garden hose as a high-intensity flame front approaches (Figure 12-41). This is a potential recipe for disaster in many respects. This person is not properly attired to stay and defend his property, nor is this the correct approach. Closely woven material is more resistant to radiation and less likely to ignite than is open-weave material. Natural fibers are

best. Wool is more flame resistant than cotton, although cotton can be improved by chemical treatment to retard flammability. As mentioned earlier, synthetic materials are a poor choice because they readily absorb heat or, worse yet, can ignite and melt onto the skin.371 Closely woven materials that provide protection also restrict airflow, so clothes should fit loosely so that they do not interfere with dissipation of body heat. Cotton long johns or undergarments absorb sweat, aid evaporation, and do not melt; however, underwear made of synthetic materials does melt. Wearing excessive layers of clothing generally contributes to heat stress. As little skin as possible should be exposed to fire. Long trousers and a long-sleeved shirt should be worn. For maximum protection, the shirt should be kept buttoned with the sleeves rolled down. Brightly colored (yellow or orange) coveralls or shirts are worn by organized firefighting crews. These colors improve safety and communications because they are visible in smoke, vegetation, and blackened landscapes. Other essential apparel includes a safety helmet (hard hat), gloves (leather or natural fiber), leather work boots, woolen or cotton socks, a warm jacket for night wear, goggles, and a handkerchief. Clothing, backpacks, tents, and other camping equipment made of synthetics should be discarded when a person is close to a fire.

WATER INTAKE Sweating is the primary method for body cooling, although exhaling warm air and inhaling cooler air also decreases body temperature (see Chapter 70). Because the cooling effect of sweat evaporation is essential for thermoregulation, fluids lost during strenuous work must be replaced. In firefighting, water losses of 0.5  L/hr (1  pt/hr) are common, with losses of up to 2  L/hr (2  qt/hr) under extreme conditions.269 Unless water is restored regularly, dehydration may contribute to heat stress disorders, reluctance to work, irritability, poor judgment, and impatience. Thirst is not a good indicator of water requirements during strenuous work, so additional drinking of small quantities of water at regular intervals is recommended. A useful signal of dehydration is dark, scanty urine. An excessive amount of electrolytes may be lost through sweating, leading to nausea, vomiting, and muscle cramps. When meals are missed or unseasoned foods are eaten, electrolyte supplements may be needed to replace lost salts. Sweetened drinks should be used as a source of energy if solid food is not available.

PERSONAL GEAR Some rescue and medical missions take a few days. Therefore it is necessary to be prepared for extended periods and changing conditions in the backcountry (Box 12-11).

HOW TO REPORT A WILDLAND FIRE TO LOCAL FIRE PROTECTION AUTHORITIES

FIGURE 12-41  An inappropriately clad and positioned homeowner attempting to defend his property from ember attack during a wildfire in Rancho Penasquitos, San Diego, California, on August 25, 1995. The fire at the moment appears largely dominated or supported by a plentiful fuel source. However, given the capricious nature of fire and winds, this fire could have easily turned into a more wind-dominated event at any time. Thus this individual could have been incapacitated by a momentary blast of superheated air from the convection or radiant heat produced by the spreading fire. In the absence of any outside assistance, this would then have left him vulnerable to burning by direct flame contact along with his home. Fortunately for this individual, shortly after the photo was taken, an air tanker dropped a load of fire retardant near the advancing flames and effectively nullified the fire’s spread and intensity. (Courtesy California Chaparral Field Institute; photo by R.W. Halsey.)

A caller should be prepared to provide the following information when reporting a fire: • Name of person giving the report • Where the person can be reached immediately • Where the person was at the time the fire was discovered • Location of the fire; orient the fire to prominent landmarks, such as roads, creeks, and mileposts on highways • Description of the fire: color and volume of the smoke, estimated size, and flame characteristics if visible • Whether anyone is fighting the fire at the time of the call The phone number to call varies locally. For example, in Alberta, Canada, the number for reporting wildland fires is 310FIRE or 310-3473 in both the northern and southern halves of the province, even though they have different area codes. In other locations, it may simply be 9-1-1. Rural homeowners should make a point of finding out the number to call before the beginning of fire season. 277

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

BOX 12-10  Envisioning the Worst: An Extract From

PART 3  BURNS, FIRE, AND RADIATION

BOX 12-11  Personal Gear for a Rescue Mission on

a Wildland Fire Incident

• Boots (leather, high-top, lace-up, nonslip soles, extra leather laces) • Socks (cotton or wool, at least two pairs) • Pants (natural fiber, flameproof, loose fitting, hems lower than boot tops) • Belt or suspenders • Shirt (natural fiber, flameproof, loose fitting, long sleeves) • Gloves (natural fiber or leather, extra pair) • Hat (hard hat and possibly a bandanna, stocking cap, or felt hat) • Jacket • Handkerchiefs or scarves • Goggles • Sleeping bag and ground cover • Map • Protective fire shelter • Food • Canteen • Radio (AM radio will receive better in rough terrain; FM is more line-of-sight; emergency personnel should have a two-way radio) • Bolt cutters (carried in vehicles to get through locked gates during escape from flare-ups or in the rescue of trapped people) • Miscellaneous items (mess kit, compass, flashlight, extra batteries, toilet paper, pencil, notepaper, flagging tape, flares, matches (windproof), can opener, washcloth, toiletries, insect repellent, plastic bags, knife, first-aid kit, and lip balm)

PORTABLE FIRE EXTINGUISHERS People should know which extinguisher to select for a specific hazard in the home or recreational vehicle and be trained in its use. When a fire is discovered, first evacuate occupants to safety and promptly report the fire to the appropriate authorities. If the fire is small and poses no direct threat, an extinguisher should be used to fight it. The three major classes of fires are as follows: • Class A fires: fueled by ordinary combustible materials, such as wood, paper, cloth, upholstery, and many plastics • Class B fires: fueled by flammable liquids and gases, such as kitchen greases, paints, oil, and gasoline • Class C fires: fueled by live electrical wires or equipment, such as motors, power tools, and appliances The right type of extinguisher must be used for each class of fire. Water extinguishers control Class A fires by cooling and soaking burning materials. Carbon dioxide or dry chemical extinguishers are used to control class B fires by smothering flames. Multipurpose dry chemical or liquefied gas extinguishers control class A, B, and C fires by a smothering action. Liquefied gas extinguishers also produce a cooling effect. A dry chemical or liquefied gas extinguisher is recommended for recreational vehicles.

BASIC WILDLAND FIRE MATERIALS, TRAINING COURSES, AND OTHER INFORMATION RESOURCES A large number of reference or textbooks on wildland fire suppression currently exist, many of which have been cited or referenced in this chapter. Wildland Fire Fighting for Structural Firefighters is a comprehensive text written specifically for firefighters whose primary focus is fighting structure fires, but who also have wildland and wildland–urban interface responsibilities. 278

This book210 provides an excellent overview on wildland fire behavior, fire apparatus and communications equipment for wildland fires, wildland firefighting tools and PPE, extinguishing agents, wildland incident management, fire suppression methods, wildland and interface fire suppression, firefighter safety and survival, fire prevention and investigation, and fire protection planning. The booklet Planning for Initial Attack published by the USDA Forest Service305 is a handy reference on basic fire behavior and fire suppression principles. Other reference books on the basics of wildland fire suppression exist.268 For a good general reference book on forest fires, see the recent contribution by Omi.353 Managing Fire in the Urban Wildland Interface is the most comprehensive professional guide on the wildland–urban interface fire problem.69 Wildfire magazine, the official publication of the International Association of Wildland Fire, is an excellent source of information on current fire management topics (http://www.iawfonline.org), as is International Forest Fire News (http://www.fire.uni-freiburg. de/iffn/iffn.htm) and Fire Management Today (http://www. fs.fed.us/fire/fmt). Other information that would be valuable to emergency response personnel includes reference materials and materials associated with the Publications Management System (PMS) and “S,” or suppression skills, training courses available through the U.S. National Wildfire Coordinating Group’s National Fire Equipment System (NFES) based at the National Interagency Fire Center in Boise, Idaho.347 These include, for example, “Firefighter Training” (S-130, 2003), “Look Up, Look Down, Look Around” (PMS 427, 1992),335,336 “Lookouts, Communications, Escape Routes and Safety Zones (LCES)” (S-134, 2003), “Fire Operations in the Wildland–Urban Interface” (S-215, 2003), and “Lessons Learned: Fatality Fire Case Studies” (PMS 490, 1998)340,341 The latter course uses nine past fatality fires as a learning tool to help fire line tactical decision makers avoid similar mistakes. It is worth noting that some NFES publications are available online (http://www.nwcg.gov). The WFSTAR (Wildland Fire Safety Training Annual Refresher) website (http://www.nifc.gov/ wfstar/index.htm) is an excellent resource for the latest information on wildland firefighter safety. The Wildland Fire Staff Library (http://www.fireleadership/gov/toolbox/staffride/index. html), developed by the National Wildfire Coordinating Group, is also a highly useful source of information on past firefighter fatality incidents. There are also several CD-ROM–based training courses available on fire line safety,36,463 fire behavior,462 and fire danger rating.439 For additional information on introductory to advanced wildland fire training courses available at the local area, geographic area, and national levels in the United States, visit the Wildland Fire Training website (http://www.nationalfiretraining. net). For national wildland fire training courses in Canada, visit the website of the Canadian Interagency Forest Fire Centre (http://www.ciffc.ca). One of the initiatives of the U.S. National Wildland–Urban Interface Fire Program was a firefighter safety program in the wildland–urban interface series. This training package, which includes three videos, was developed for small community fire departments to address the problems faced by structural and wildland firefighters when fighting fires, especially those threatening structures in the wildland–urban interface.255 Copies can be ordered from Firewise Communities online catalog. The Wildland Fire Lessons Learned Center (http://www. wildfirelessons.net) is a good source for information on nearly all aspects of wildland fire management. An annotated reading list and bibliography on wildland firefighter safety management are available253 on their “My Fire Community” website (http:// www.myfirecommunity.net). The Fire Research Institute library (http://www.fireresearchinstitute.org/), which provides online search capability, is a good source of scientific and technical wildland fire literature.212 Wildfire Today (http://www.wildfiretoday.com) and the Global Fire Monitoring Center (http://www.fire.uni-freiburg.de) are popular websites for the latest news in wildland fire management. Wildland Fire: Home of the Wildland Firefighter (http:// www.wildlandfire.com) is another unique website serving the global wildland fire community.

Fire suppression efforts in the late 1800s and early 1900s were largely ineffective because of limited access, absence of trained firefighting organizations, and lack of a fire detection network. During these times, many residents and numerous firefighters died in wildland fires in the United States and Canada. In the recent past, firefighters were more vulnerable to injuries and fatalities from wildfires than was the general public. Today, with many people living and seeking recreation in wildlands, the odds for serious fire encounters are shifting toward an inexperienced populace. Large property losses and direct injuries are being reported in increasing numbers in the wildland–urban interface. It has now become not a question of “if” a wildfire will come or of it “can’t happen here,” but rather “when and where” the next major wildland–urban interface conflagration will take place (Figure 12-42, online). Emergency medical personnel will probably have increasing exposure to wildland fires in the future and will need to know more about fire-related injuries, fire safety, and fire survival. Many wildland firefighters are in turn feeling compelled to save homes,189 in part as a result of the expectations placed on them by the general public and homeowners in particular, coupled with a culture derived from more than a century of wildland fire suppression.58 Not surprisingly, many wildland firefighter fatalities in recent years have been associated with wildland–urban interface incidents (e.g., the 2003 Cedar fire in southern California).103 Given even the best practices,277 there is an overwhelming need to impress on rural homeowners that no home is worth a firefighter’s life. Although wildland fires have not yet posed a serious threat to backcountry recreationists in the United States to any appreciable degree, the prospect for such confrontations is growing. For example, two recreationists were involved in entrapment and burnover associated with the major run of the 2001 Thirtymile fire178; fire investigators concluded they would probably not have survived, although they did suffer minor injuries, had they not joined up with the firefighters just before (about 14 minutes) their location was overrun.480 Many years of practical experience with wildland fires allow us to conclude the following: • Many indicators point to the fact that financial support and programs that address only emergency responses to wildfires will result in more damaging and expensive wildfire emergencies in the future. Public policies and public education that link sustainable land use practices with emergency preparedness are likely to be most successful in the long run. • Residential shifts to the wildland–urban interface will increase exposures to life-threatening situations. • Expanded use of fire in managing national parks and wilderness areas will increase the likelihood that backcountry recreationists will encounter free-burning fires. • By and large, the general public tends to underestimate existing fire hazards and for the most part is usually not experienced in avoiding wildfire threats. • In some instances, attempted fire exclusion practices have contributed to development of hazardous wildland fuel situations in terms of quantity and continuity, setting the stage for extreme fire behavior in some plant communities. The national ecosystem health issue has compounded this problem by producing vast expanses of dead and dying forests, increasing the threat to people from fast-moving, high-intensity fires. • Knowledge of fire behavior principles and survival guidelines will prepare people to take appropriate preventive measures in threatening situations. The general public must share responsibility with suppression organizations to minimize fire hazards created by humans. Care with fire, proper cleanup of debris, fuel reduction efforts on wildland property, fire-safe construction guidelines, and application of survival skills will minimize fire threats. Such precautions should become as commonplace in the wildland environment as smoke alarms and fire extinguishers have become in urban settings. Every community should undertake, as part of the risk management

process associated with the wildfire threat, an assessment of their fire environment in terms of potential fire behavior. A good example of this type of analysis has been completed for over a hundred communities in northern Saskatchewan, Canada.158 Sadly, major disasters are commonly required for fundamental changes to occur. Disasters do not simply happen.470 They usually involve an “incubation period” that involves “the accumulation of an unnoticed set of events that are at odds with the accepted beliefs about hazards and the norms for their avoidance.”469 Wildland fire suppression agencies will continue to provide fast, safe, and energetic initial attack responses to protect human life, property, and natural resources.14 Many fires will start and burn under environmental conditions that permit their control at a very small size. However, in certain situations (e.g., critically dry fuels or strong winds), some fires9,31,32 will defy control until burning conditions ameliorate. The major runs of the 1985 Palm Coast fire in south Florida2 and the Millers Reach fire that occurred near Anchorage, Alaska, on June 2, 1996,128 are good examples of this kind of fire behavior and associated suppression problems. No radically new concept of fire suppression for stopping the head of a hot, fast-running wildland fire should be anticipated in the future.146 In his book, An Introduction to Fire Dynamics, Drysdale173 points out that “Further major advances in combating wildfire are unlikely to be achieved simply by continued application of the traditional methods. What is required is a more fundamental approach which, can be applied at the design stage … Such an approach requires a detailed understanding of fire behavior.” Strategic fuel management and land use planning could potentially reduce the total number and size of wildfire occurrences, as well as influence their geographic distribution, and thereby mitigate the impacts of too much of the “wrong kind of fire.”386 Science-based-only solutions211 are considered insufficient; effective wildland fire policy must integrate ethics, economics, aesthetics, and values.386 Furthermore, as Cheney118 points out, if we are to encourage people to live safely in the wildland environments, they need to be fully aware of the full potential for fire behavior and what can be done to protect themselves and their assets. He goes on to say that “they must be individually persuaded to recognize what constitutes the fuel for a forest fire and be convinced that, since they own the fuel, they also own the fire it produces and are responsible for the damage they or others nearby incur.” The public and fire management agencies themselves must fully appreciate that fuel management is not a panacea for conflagration mitigation, but rather a prerequisite to aid in successful fire suppression.20,72,122,472 An excellent source of information on fuel management is the USDA Forest Service Fuels Synthesis Project (http://www.fs.fed.us/fire/tech_ transfer/synthesis/synthesis_index).481 After the 1983 Ash Wednesday fires in southeastern Australia, the editor of Australian Forestry commented on what could be learned from studying such wildland fire disasters:176 Advances in technical areas will be of great value. It would be valuable too to make comparable advances in the areas of public policy. People forget, community attitudes change and policies erode. Perhaps one of the greatest challenges, given the realities of southeastern Australia, is to learn how to ensure the permanence of public interest policies where permanence is required. Twenty years later and following the bushfires that engulfed Canberra, Australia, in 2003 (http://www.en.wikipedia.org/ wiki/2003_Canberra_bushfires), Cheney120 offered some advice on this matter: … I believe that there is strong evidence that the policies and institutional arrangements of organizations, both those directly related to fire management and those completely unrelated, will have the result of perpetuating major fire disasters. I also believe that the legal framework in which we’re working is one that [militates against] individuals taking responsibility for their own actions and lifestyle choices. In this country wildfire is inevitable but the impact 279

CHAPTER 12  WILDLAND FIRES: DANGERS AND SURVIVAL

Concluding Remarks

of disastrous fires can be reduced. But this will only be achieved if policies focus on the physics of fire spread and foster a climate of awareness where fuel reduction, from the backyard to beyond, is encouraged and supported by legislation. At the end of the day, though, what can an individual do to improve matters when it comes to living with fire? Kaufmann, Shlisky, and Marchand238 offer some very practical advice: • Get involved in a community-based conservation group working on local landscape restoration projects. • Educate yourself about the role of fire in your local ecosystems. • Provide feedback on agency land management plans. • Consult with regional experts on how to safely reintroduce fire on to your land holding. • Participate in local workshops (e.g., Firewise Communities) to learn how to treat fuels around your home and create defensible space.

Their final suggestion: “Start simply. But start.” Local forestry and fire management agencies are more than willing to offer technical advice and information. Just give them a call to get started today before wildfire comes knocking!183 Acknowledgments. The authors hereby thank the following individuals for their candid comments on various sections of the chapter: M. Ackerman, A. Beaver, K. Brauneis, B. Butler, D. Campbell, P. Cheney, J. Cohen, M. DeGrosky, T. Greer, M. Heathcott, J. Leonard, T. Leuschen, S. McCaffrey, J. McLevin, B. Mottus, P. Murphy, S. Otway, G. Proulx, T. Putnam, D. Quintilio, A. Rhodes, B. Sharkey, R. Smith, D. Thomas, R. Thorburn, K. Weick, and T. Zimmerman. The assistance of the following individuals in the preparation of this chapter is also duly noted: B. Bereska, M. Campbell, M. Cruz, M. Erickson, J. Handmer, T. Petrilli, G. Pearce, and O. Spencer.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 13 

Emergency Care of the Burned Victim MICHAEL J. MOSIER AND DAVID M. HEIMBACH

Epidemiology Each year in the United States, approximately 2 million individuals are burned seriously enough to seek the care of a physician, and about 70,000 of these require hospitalization. Fortunately, the number of deaths attributable to burns decreased from 12,000 in 1979 to 4000 in 2009. Although treatment facilities would like to take credit for this decrease, the most likely reason is the widespread use of smoke detectors in both public and private dwellings. It has been estimated that more than 90% of burns are preventable and that most are caused by carelessness or ignorance. During the next few years, the biggest contributions in decreasing burn mortality and morbidity may come not from medical scientists but rather from improved engineering design and more successful programs in teaching burn prevention to the public. Like other forms of trauma, burns frequently affect children and young adults. The hospital expenses and the social costs related to time away from work or school are staggering. Although most burns are limited in extent, a significant burn of the hand or foot may prevent a manual laborer from working for a year or more and in some cases may permanently prevent a return to former activity. The eventual outcome for the burned victim is related to the severity of the injury, individual physical characteristics of the victim, motivation toward rehabilitation, and quality of treatment of the acute burn. Most persons with burns who are seen by physicians visit emergency departments, where judgment in triage, care plan for small burns, and initial management for major burns can influence survival of the victim and eventual cosmetic and functional results. Because most victims are young and about one-third are children, they will live with the consequences of the acute treatment for an average of 50 years. The decisions made at the initial contact with the victim require answers to the algorithm shown in Figure 13-1. This chapter describes first-responder care for major burns and is organized to guide assessment of burn severity and initial 280

management of serious burns, as well as to provide an initial treatment plan for minor burns.

Physiology For burns other than chemical burns, the primary events of injury occur during the time of heat contact. Coagulation necrosis takes place within cells, and denaturation of collagen occurs in the dermis. Either blood vessels are completely destroyed or the endothelium is damaged severely enough to cause clotting, which leads to ischemic necrosis of remaining viable cells. The burn wound is not static. Surrounding the zone of coagulation is a zone of capillary and small vessel stasis. Red cells form into rouleaux, platelet and white cell aggregates form, and the circulation becomes stagnant. Over the next hours or even days, the ultimate fate of the burn wound depends on resolution or progression of this zone of stasis. Cells and tissue stroma release mediators to initiate the inflammatory response. Histamine, serotonin, prostaglandin derivatives, and the complement cascade all have roles. In victims with burns of less than 10% of the total body surface area (TBSA), the actions of these mediators are generally limited to the burn site itself. Capillary permeability increases, neutrophils marginate, and additional inflammatory cells (monocytes, macrophages) are attracted by chemotaxis to the site of injury, initiating the healing process. As burns approach 20% TBSA, the local response becomes systemic. The capillary leak, permitting loss of fluid and protein from the intravascular compartment into the extravascular compartment, becomes generalized. Cardiac output falls as a result of markedly increased peripheral resistance, decreased intravascular fluid volume from the capillary leak, and accompanying increase in blood viscosity. Decreased blood volume and cardiac output, accompanied by an intense sympathetic response, lead to decreased perfusion to the skin and viscera. Decreased flow to the skin can convert the zone of stasis to one of coagulation, increasing the depth of the burn. The capillary leak and depressed cardiac output lead to depressed central nervous system (CNS)

<5% TBSA

>5% TBSA

Superficial or deep but very small

Burn covering >50% of hand or foot

Smoke inhalation without burn Burn ≤20% TBSA Eye involvement

Smoke inhalation with burn Burn >20% TBSA Electrical burn

First aid See MD if not healed in 3-5 days

First aid See MD by day 2

Ground transfer to community hospital

Immediate transfer to burn center

FIGURE 13-1  Algorithm for decision making at the scene. TBSA, Total body surface area.

function, and in extreme cases they result in severe cardiac depression with eventual cardiac failure in healthy patients or in myocardial infarction in patients with preexisting coronary artery disease. The first sign of CNS change is restlessness, followed by lethargy and finally coma. Without adequate resuscitation, burns of 30% TBSA frequently lead to acute renal failure, which in a victim with a severe burn almost invariably leads to a fatal outcome. Cardiovascular changes begin immediately after a burn. The extent of these changes depends primarily on the size of the burn and to a lesser extent on the depth of the burn. Most victims with uncomplicated burns of less than 15% TBSA can undergo oral fluid resuscitation with some salt-containing solution. As the burn extent passes 20% TBSA, massive shifts of fluid and electrolytes occur from the intravascular into the extravascular (extracellular) space. Reversal of the shifts begins during the second postburn day, but normal extracellular volume is not completely restored until 7 to 10 days after the burn. Unless the intravascular volume is depleted, classic hypovolemic shock occurs. An untreated person will die of cardiovascular collapse; if treatment is poor, irreversible acute tubular necrosis and renal failure will develop.

Types of Burns SCALD BURNS In civilian practice, scalds, usually resulting from hot water, are the most common cause of burns. Water at 60° C (140° F) creates a deep partial-thickness or full-thickness burn in 3 seconds. At 68.9° C (156° F), the same burn occurs in 1 second. Freshly brewed coffee from an automatic percolator is generally about 82° C (179.6° F). Boiling water always causes deep burns, and soups and sauces, which are thicker in consistency, remain in contact longer with the skin and often cause deep burns. In general, exposed areas tend to be burned less deeply than areas covered with thin clothing. Clothing retains the heat and keeps the liquid in contact with the skin for a longer time. Immersion scalds are deep and severe burns.18,28,92 Although the water may be cooler than with a spill scald, the duration of contact is longer, and these burns frequently occur in small children or older adult victims with thin skin. Consequently, many states have passed legislation to set home and public hot water heaters to maximum temperatures well below 60° C (140° F). Scald burns from grease or hot oil are generally deep partial thickness or full thickness. Cooking oil and grease, when hot enough to use for cooking, may be in the range of 204.4° C (400° F). Tar and asphalt burns are a special kind of scald. The “mother pot” at the back of the roofing truck maintains tar at a temperature of 204.4° to 260° C (400° to 500° F). Burns caused by tar directly from the mother pot are invariably full thickness. By the time the tar is spread on the roof, its temperature has

FIGURE 13-2  Tar burn of hand. (Courtesy Paul S. Auerbach, MD.)

decreased enough that most of the burns are deep partial thickness (Figure 13-2). Unfortunately, the initial evaluator cannot usually examine these burns because of the adherent tar. The tar should be removed by application of a petroleum-based ointment (such as Vaseline) under a dressing. In the field, mayonnaise may serve this purpose (Figure 13-3). The dressing may be removed and the ointment reapplied every 2 to 4 hours until the tar has dissolved. Only then can the extent of the injury and the depth of the burn be accurately estimated.40,91

FLAME BURNS Flame burns are the next most common burn injuries. Although injuries in house fires have decreased with the advent of smoke detectors, a significant number of burn injuries still result from careless smoking, improper use of flammable liquids, automobile accidents, and clothing ignited from stoves or space heaters. Victims whose bedding or clothes have been on fire rarely escape without some full-thickness burns. Outdoor misadventures result from using cooking stoves fueled by white gasoline, taking lanterns into tents, smoking in a sleeping bag, and starting (or improving) charcoal fires with gasoline or kerosene. Most accelerants, whether gasoline, kerosene, propane, or diesel, behave similarly with ignition temperatures of 210° to 280° C (410° to 536° F) and therefore burn at a high temperature with rapid tissue injury and full-thickness burns.

FLASH BURNS Flash burns are next in frequency. Explosions of natural gas, propane, gasoline, and other flammable liquids cause intense heat for a very brief time. For the most part, unignited clothing protects the skin in flash burns. Flash burns generally have a distribution over all exposed skin, with the deepest areas facing the source of ignition. Flash burns are partial thickness, with the depth dependent on the amount and kind of fuel that explodes. Although such burns generally heal without requiring extensive

FIGURE 13-3  Mayonnaise used to dissolve tar off a hand burn. (Courtesy Paul S. Auerbach, MD.)

281

CHAPTER 13  Emergency Care of the Burned Victim

Burn

PART 3  BURNS, FIRE, AND RADIATION

skin grafts, they may be very large and associated with significant thermal damage to the upper airway.

CONTACT BURNS Contact burns result from hot metals, plastic, glass, or hot coals. Such burns are usually limited in extent but are deep. Victims involved in industrial accidents commonly have both severe contact burns and crush injuries, because these accidents often occur from presses or from hot, heavy objects. With the increased use of wood-burning stoves, an increasing number of toddlers are burned each year. The most common injuries are deep burns on the palms because the child falls with hands outstretched against the stove. Contact burns, especially in unconscious persons or those dealing with molten materials, are frequently fourth degree.16,53,80 In the wilderness setting, the most common contact burn is from hot coals, which are often as hot as 537.8° C (1,000° F). Intoxicated campers dance around and then into the campfire, architects of “river saunas” mishandle hot rocks, children fall into fires, and beach walkers may sustain deep burns when coals are buried in sand overnight. Even though the injured areas may be small, they can be deep and devastating when the hiker must walk a considerable distance on burned feet.24

ELECTRICAL BURNS Electrical burns are actually thermal burns from very highintensity heat. As electricity meets the resistance of body tissues, it is converted to heat in direct proportion to the amperage of the current and the electrical resistance of the body parts through which it passes. The smaller the body part through which the electricity passes, the more intense is the heat and the less it is dissipated. Therefore fingers, hands, forearms, feet, and lower legs are frequently totally destroyed, whereas larger-volume areas, such as the trunk, usually dissipate the current enough to prevent extensive damage to the viscera, unless the contact point is on the abdomen or chest. Although cutaneous manifestations may appear limited, massive underlying tissue destruction may be present because muscle, nerves, blood vessels, and bones can be burned beyond recovery.15,33,34,66 Arc burns occur when current takes the most direct path rather than the one of least resistance. These deep and destructive wounds, which may be initiated at extremely high temperature, occur at joints that are in close apposition at the time of injury. Most common are burns of the forearm to the arm when the elbow is flexed, and from the arm to the axilla if the shoulder is adducted when current passes from the upper extremity to the trunk. Electrical burns cause a particular set of other injuries and complications that must be considered during the initial evaluation. As mentioned previously, injuries related to a fall are common. The intense associated muscle contractions may cause fractures of the lumbar vertebrae, humerus, or femur and may dislocate shoulders or hips. Electrical cardiac damage may have symptoms like those of a myocardial contusion or infarction. Alternatively, the conduction system may be deranged. There can be actual rupture of the heart wall or of a papillary muscle, leading to sudden valvular incompetence and refractory cardiac failure. Household current at 110 volts generally either does no damage or induces ventricular fibrillation. Alternating current is more likely to induce fibrillation than is direct current. If no cardiac abnormalities are present when a victim is first seen after shocks of 110 to 220 volts, the likelihood that they will appear later is small. The nervous system is particularly sensitive to electricity. The most severe brain damage occurs when current passes through the head, but spinal cord damage is possible any time current passes from one side of the body to the other.44,48 Myelinproducing cells are susceptible. The devastating effects of transverse myelitis may develop days or weeks after injury. Conduction remains normal through existing myelin, but as the old myelin wears out, it is not replaced and conduction stops. Peripheral nerves are commonly damaged and may demonstrate severe permanent functional impairment.20,30 Every victim with an 282

electrical injury must have a thorough neurologic examination as part of the initial assessment. Myoglobinuria is a frequent accompaniment of severe electrical burns. Disruption of muscle cells releases cell fragments and myoglobin into the circulation to be filtered by the kidneys. If untreated, this can lead to permanent renal failure. Lightning strikes are discussed in Chapter 3, and reviews are available.*

CHEMICAL BURNS Chemical burns, usually caused by strong acids or alkalis, are most often the result of industrial accidents, home use of drain cleaners, assaults, and other improper use of harsh solvents.† In contrast to thermal burns, chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue or by dilution by flushing with water. Although individual circumstances vary, acid burns may be more self-limited than are alkali burns. Acid tends to tan the skin (as leather is tanned), creating an impermeable barrier that limits further penetration of the acid. Alkalis combine with cutaneous lipids and saponify the skin until they are neutralized. A full-thickness chemical burn may appear deceptively superficial, appearing as only a mild brownish surface discoloration. The skin may appear intact during the first few days after the burn and then begin to slough spontaneously. Unless the observer can be absolutely certain, chemical burns should be considered deep partial thickness or full thickness until proved otherwise.

Clinical Presentation Cutaneous burns are caused by the application of heat or caustic chemicals to the skin. When heat is applied to the skin, the depth of injury is proportional to the temperature applied, duration of contact, and thickness of the skin. The severity of the burn injury is related to the size of the burn, depth of the burn, and part of the body that is burned.

ESTIMATION OF BURN SIZE Burns are the only quantifiable form of trauma. The single most important feature in predicting mortality, need for specialized care, and the complications expected from the burn is the overall burn size in proportion to the victim’s TBSA. Treatment plans, including initial resuscitation and subsequent nutritional requirements, are derived directly from the size of the burn. A general idea of burn size is provided by the “rule of nines.” Each upper extremity accounts for 9% TBSA, each lower extremity accounts for 18%, the anterior and posterior trunk each account for 18%, the head and neck account for 9%, and the perineum accounts for 1% (Figure 13-4). Although the rule of nines provides a reasonably accurate estimate of burn size, a number of more precise charts have been developed. A diagram of the burn can be drawn on a chart so that a relatively precise calculation of burned area can be made from the accompanying TBSA estimates given. Children less than 4 years old have much larger heads and smaller thighs in proportion to body size than do adults. In an infant, the head accounts for approximately 18% of the TBSA; body proportions do not fully reach adult percentages until adolescence. To further increase accuracy in burn size estimation, especially when burns are in scattered body areas, the observer might calculate the unburned areas on a separate diagram. If the calculations of the unburned areas and the burned areas do not add up to 100%, the observer should begin again with a new diagram to recalculate the burned areas. For smaller burns, an accurate assessment of burn size can be made by using the victim’s hand. The hand amounts to 2.5% TBSA. The dorsal surface accounts for 1%, the palmar surface for 1%, and the vertical surface for 0.5% (including the fingers).

*References 21, 22, 25, 26, 54, 66. † References 23, 35, 59, 62, 73, 76, 82.

9% 9%

9%

18%

1%

9%

9%

9%

A

18% 9% 9% 18% 13.5%

18% 1%

13.5%

18%

9%

B

DEPTH OF BURN An understanding of burn depth requires an understanding of skin anatomy (Figure 13-5). The epidermis, an intensely active layer of epithelial cells under layers of dead keratinized cells, is superficial to the active structural framework of the skin, the dermis. Although metabolically very active, the dermis has no regenerative capacity, and epithelial cells must eventually cover the surface of the dermis before the burn is healed. The skin appendages (hair follicles, sebaceous glands, and sweat glands) all contain an epithelial cell lining, so when the surface epidermis has been killed, epithelial covering must take place from overgrowth of the epithelial cells lining the skin appendages. As these cells reach the surface, they spread laterally to meet their neighbors, creating a new epithelial surface. As the burn extends deeper into the dermis, fewer and fewer appendages remain, and the epithelial remnants must travel farther to produce a new surface covering, sometimes taking many weeks to produce coverage. When the burn extends beyond the deepest layer of

the skin appendages, the wound can heal only by epithelial ingrowth from the edges, by wound contraction, or by surgical transplantation of skin from a different site. The thickness of skin varies both with the age and sex of the individual and with the part of the body considered. Although the thickness of the living epidermis is relatively constant, keratinized epidermal cells may reach a height of 5 mm (0.2 inch) on palms of hands and soles of feet. The thickness of the dermis, on the other hand, may vary from less than 1 mm (0.04 inch) on eyelids and genitalia to more than 5 mm (0.2 inch) on the posterior trunk. Although the proportional thickness of skin in each body area is similar in children, infant skin thickness in each specific area may be less than one-half that of adult skin; the skin does not reach adult thickness until adolescence. Similarly, in patients older than 50 years, dermal atrophy causes all areas of skin to become quite thin. Burns are classified by increasing depth as first degree, superficial partial thickness, deep partial thickness, full thickness, and fourth degree. The following descriptions appear to separate

FIGURE 13-5  Skin anatomy.

Epidermis Dermis Subcutaneous tissue Muscle Bone

First degree Partial thickness Full thickness

283

CHAPTER 13  Emergency Care of the Burned Victim

FIGURE 13-4  Rule of nines used for estimating burned surface area. A, Adult. B, Infant.

PART 3  BURNS, FIRE, AND RADIATION

FIGURE 13-7  Deep partial-thickness burn. Note cherry-red color.

scarring, particularly in pigmented individuals and children, becomes inevitable. Full-Thickness Burns FIGURE 13-6  Superficial partial-thickness burn. Note pink color and moist surface.

burns into clearly defined categories, but many burns have a mixture of characteristics that give the observer an imprecise diagnostic ability. Considerable research is under way to devise instruments that will more precisely measure the depth of injury. Much of current burn treatment depends on knowledge of the depth of the burn. First-Degree Burns First-degree burns involve only the epidermis. The prototype is mild sunburn. First-degree burns do not blister. They become erythematous because of dermal vasodilation and are quite painful, both spontaneously and when touched. The erythema and pain subside over 2 to 3 days. By the fourth day, the injured epithelium desquamates in the phenomenon of “peeling.” Superficial Partial-Thickness Burns Superficial partial-thickness burns (Figure 13-6) include the upper layers of dermis and characteristically form blisters with fluid collection at the interface of the epidermis and dermis. Blistering may not occur for some hours after injury. Burns initially thought to be first degree may therefore be diagnosed as superficial partial thickness by day 2. When blisters are removed, the wound is pink and wet, and it is quite painful when contacted by currents of air. The wound is hypersensitive to touch and blanches with pressure, and blood flow to the dermis is increased over that of normal skin. If infection is prevented, superficial partialthickness burns heal spontaneously within 3 weeks without functional impairment. They rarely cause hypertrophic scarring, but in pigmented individuals the healed burns may never completely match the color of the surrounding normal skin. Deep Partial-Thickness Burns Deep partial-thickness burns (Figure 13-7) also blister, but the wound surface is usually a mottled pink and white color immediately after the injury. Alternatively, the burned dermis may be dry, with a cherry red color. The victim complains of discomfort rather than pain. When pressure is applied to the burn, capillary refill returns slowly or may be absent. The wound is often less sensitive to touch than is the surrounding normal skin. By the second day, the wound may be white and is usually fairly dry. If infection is prevented, such burns heal in 3 to 9 weeks but invariably do so with considerable scar formation. Unless active physical therapy is continued throughout the healing process, joint function may be impaired and hypertrophic 284

Full-thickness burns (Figure 13-8) involve all layers of the dermis and can heal only by wound contracture, epithelialization from the wound margin, or skin grafting. Full-thickness burns are classically described as leathery, firm, depressed when compared with the adjoining normal skin, and insensitive to light touch and pinprick. Unfortunately, the difference in depth between a deep partial-thickness burn and a full-thickness burn may be less than 1 mm (0.04 inch). Full-thickness burns are easily misdiagnosed as deep partial-thickness burns, because the two types have many of the same clinical findings. For example, they may be mottled in appearance. They rarely blanch with pressure and may have a dry, white appearance. The burn may be translucent with clotted vessels visible in the depths. Some full-thickness burns, particularly immersion scalds, have a red appearance and can be confused with superficial partial-thickness burns. However, these red, full-thickness burns do not blanch with pressure. Fullthickness burns develop a classic burn eschar. An eschar represents the structurally intact but dead and denatured dermis that, over days to weeks, separates spontaneously from the underlying viable tissue. Fourth-Degree Burns Fourth-degree burns involve not only all layers of the skin but also subcutaneous fat and deeper structures. These burns almost always have a charred appearance. Frequently, only the cause of the burn gives a clue to the amount of underlying tissue destruction.

FIGURE 13-8  Full-thickness burn. Note thick, leathery, white eschar.

CARE AT THE SCENE Flame Burns The first responder must remove the injured person from the source of heat. Because of the potential dangers of smoke inhalation in closed areas, the rescuer in a fire must take extreme caution not to become a victim. Persons with burning clothing should be prevented from running and should be made to lie down to keep flames and smoke away from the face. If water is not immediately available, the flames can be smothered with a coat or blanket. If nothing is available to douse or cover the flames, the victim should be rolled slowly on the ground. Once the burning has stopped, the clothes should be removed; some fabrics will continue to smolder and synthetic fabrics may melt, leaving a hot adherent residue on the victim that will continue the burning process. Scalds and Grease Burns The victim of a scald or grease burn must be removed from the source of heat. Any wet clothing or wrap should be removed, because fabric retains moist heat and may continue to burn skin that is in contact with the hot material. Accidents resulting from cooking indoors with grease are particularly hazardous. The startle response to a grease splatter may cause the victim to drop a pan of grease onto the fire, starting a kitchen fire that can rapidly become a dwelling fire. Airway Once flames are extinguished, primary attention must be directed to the airway. Any person rescued from a closed space or involved in a smoky fire should be considered at risk for smoke inhalation injury. If compressed oxygen is not available, a victim who is coughing independently should be encouraged to continue to do so. If the victim is unconscious or the airway status is in question, the victim should be placed supine and the airway manipulated manually via the chin lift or jaw thrust maneuver. When smoke inhalation is suspected, 100% oxygen should be administered by a tight-fitting mask. If the victim is unconscious and if personnel are trained to insert an endotracheal tube, such a tube should be passed and attached to a source of 100% oxygen. If the airway has to be supported by a tight mask, the rescuers must be aware of the significant danger of aspiration of gastric contents. Air forced into the stomach distends it and causes vomiting. The mask prevents expulsion of the fluid, and the victim rapidly aspirates vomitus into the tracheobronchial tree. No unconscious supine victim should ever be left unattended. Other Injuries and Transport Once an airway is secured, the first responder should quickly assess for other injuries and then transport the victim to the nearest hospital.8,20,66 Victims should be kept flat and warm and should be given nothing by mouth. Aside from establishment of an airway, further resuscitation is unnecessary if the victim will arrive at a hospital within 30 minutes. For transport, the victim should be wrapped in a clean, dry sheet and blanket. Sterility is not required. Cold Application Smaller burns, particularly scalds, may be treated with immediate application of cool water in the hope of limiting the extent of injury. The application of cold water is controversial, but immediate cooling decreases pain, possibly by a decrease in thromboxane production. By the time several minutes have passed, or after arrival in the emergency department, further cooling is not likely to alter the pathologic process. Ice water should not be used except on the smallest burns. Using ice on larger burns can easily induce systemic hypothermia and associated cutaneous vasoconstriction that can extend the thermal damage. Swelling During transport, constricting clothing and jewelry should be removed from burned and distal parts, because local swelling begins almost immediately. Constricting objects increase the

swelling, and removing tight jewelry in the presence of distal edema is time consuming once swelling has occurred. Electrical Burns Electrical burns are particularly dangerous, both to the victim and to the rescuer. If the victim remains in contact with the source of electricity, the rescuer must avoid touching the victim until the current can be turned off or the wires cut with properly insulated wire cutters. Once the victim is removed from the source of current, airway, breathing, and circulation must be checked. Ventricular fibrillation or standstill is a common accompaniment to a major transthoracic current; cardiopulmonary resuscitation should be instituted if carotid or femoral pulses are not palpable. If pulses are present but the victim is apneic, mouth-to-mouth resuscitation alone may be lifesaving. Cardiopulmonary resuscitation should continue until a cardiac monitor can be obtained, which will direct treatment for cardiac standstill or ventricular fibrillation. Once an airway is established and pulses return, a careful search must be made for associated life-threatening injuries. Electrocuted victims frequently fall from heights and may have serious head or neck injuries. The intense tetanic muscle contractions associated with electrocution may fracture vertebrae or cause major joint dislocations. Patients with high-voltage electrical injuries should be treated with spinal precautions and splints if necessary, until fractures can be ruled out. Chemical Burns Whenever possible, chemical burns should be thoroughly flushed with copious amounts of water at the scene of the accident. Chemicals will continue to burn until removed; washing for 5 to 10 minutes under a stream of running water may limit the overall severity of the burn. No thought should be given to searching for a specific neutralizing agent. Delay deepens the burn, and neutralizing agents may cause burns themselves; they frequently generate heat while neutralizing the offending agent, adding a thermal burn to the already potentially serious chemical burn. Hydrofluoric acid is commonly used as a cleaning agent in the petroleum industry or for glass etching. As an acid it causes coagulation necrosis, and the fluoride ion then chelates positively charged ions such as calcium and magnesium, causing an efflux of intracellular calcium, which results in cellular death.65 Fluoride ion is also a metabolic poison that inhibits sodium-potassium adenosine triphosphatase (ATPase), allowing efflux of potassium.55 Hydrofluoric acid burns are classified based on the concentration of the solution according to the National Institutes of Health Division of Industrial Hygiene.94 Concentrations above 50% cause immediate tissue destruction and pain. Concentrations of 20% to 50% create a burn that is apparent within several hours of exposure; exposures with concentrations less than 20% may take as long as 24 hours to become apparent. Systemic symptoms of hypocalcemia or hypomagnesemia are usually absent, although cardiac dysrhythmias may develop and, once present, are difficult to restore to a normal rhythm. QT prolongation is the typical electrocardiogram finding when present. Treatments of hydrofluoric acid exposure are designed to neutralize the fluoride ion and prevent systemic toxicity. Topical calcium gluconate gel (3.5  g of 2.5% calcium gluconate mixed with 5  oz of water-soluble lubricant applied to the wound 4 to 6 times a day for 3 to 4 days) can be used after the wounds are copiously irrigated.57 Pain relief with this approach is often quite rapid. Return of pain is often a sign to repeat the dressing change. Phosphorus can be found in both military and civilian settings. It is an incendiary agent found in hand grenades, artillery shells, fireworks, fertilizers, and some homemade explosives. White phosphorus ignites in the presence of air and burns until the entire agent is oxidized or the oxygen source is removed (such as immersion in water). Treatment should consist of irrigation with large amounts of water, removal of easily identifiable pieces of phosphorus, and moist dressings for transport. Ultraviolet light can be used to identify embedded particles through phosphorescence, allowing for improved removal. Hypocalcemia, hyperphosphatemia, and cardiac arrhythmias have been reported.90 285

CHAPTER 13  Emergency Care of the Burned Victim

Treatment

PART 3  BURNS, FIRE, AND RADIATION

First Aid at the Scene for Smaller Burns Not all burns need immediate medical attention. Burns less than 5% TBSA (excluding deep burns of the face, hands, feet, perineum, or circumferential extremity) can be treated successfully in a wilderness setting if adequate first-aid supplies are available and wound care is performed diligently. Except for the very shallow burn that heals within a few days, most burns should be seen by a physician within 3 to 5 days after injury. Burns should be washed thoroughly with plain soap and water and dried with a clean towel. The water used should be suitable for drinking, but it need not be sterile or bottled. Any obviously dead skin should be peeled off (which may be painful) or trimmed with sharp manicure scissors (usually painless). Large (greater than 2.5 cm [1 inch]), thin, fluid-filled blisters should be drained and the dead skin trimmed to prevent a potential closedspace infection. Deep burns, as from a flame, are firm and leathery, usually do not blister, and do not require immediate debridement. A small tube of silver sulfadiazine cream and tubes of bacitracin or Neosporin antibiotic ointment should be available in the first-aid kit. Either may be used and should be spread lightly over the wound. The wound may then be wrapped in dry, clean gauze, which need not be sterile. Simple dressings (one type of topical cream, plain gauze) are sufficient. Some patients prefer nonadherent dressings, such as Telfa or Adaptic (sometimes known as “greasy gauze”), because they are less likely to stick to the wound during dressing changes. The same effect can be achieved by soaking (with water) a plain gauze dressing that appears stuck to the wound, waiting a few minutes, and then removing the dressing with additional water if necessary. Other dressings (hydrogels, silver-coated dressings, silicone gel sheets, calcium alginate) designed to minimize the frequency of dressing changes and promote healing are available but are not necessary. The authors recommend simple antibiotic ointments such as silver sulfadiazine or bacitracin and plain gauze dressings rather than “specialty” dressings for inclusion in first-aid kits because they are simple, cheaper, and effective. Although patients may prefer one dressing over another for various reasons, no dressing has been shown conclusively to accelerate the healing of burn wounds. As such, the first-aid kit should be stocked with general-use supplies, which are less expensive and easier to replenish. Mobility of the wound area must be actively maintained, and concentrated efforts should be made to avoid dependent positioning, especially when the victim is resting or sleeping. Focal edema in a small burn wound can be painful and alarming and should be prevented with extremity elevation and active rangeof-motion exercises several times a day. Wound care should be performed once a day if the outer dressing remains dry. A wet, sticky outer dressing needs more frequent wound care to keep up with drainage from the wound. If only the outer dressing is dirty, whether soiled from food, dirt, or other substance, it may be changed as often as needed to maintain a clean dressing and aid in patient comfort. For the quickest healing of superficial burns, daily wound care should remove all exudates and crust, both of which significantly retard wound healing. Once a wound has epithelialized or is nearly epithelialized, a moisturizing lotion is recommended to aid in hydration and decrease scarring. Vitamin E, aloe, and oat beta glucan are often used for their antiinflammatory and soothing properties. Melaleuca is a topical antibacterial and antifungal tea tree oil that Australian aboriginal people have used for a variety of medicinal purposes. It is the active ingredient in Burnaid, a popular cream used for superficial partial-thickness burn injuries. When determining the type of dressing to apply to a burn wound, the following considerations are important: • The dressing should cover the entire burned area (an enclosed dressing), leaving no burned skin exposed to air or air currents. • The burn wound surface should stay moist, whereas the unburned skin surrounding the burn should not macerate. • The dressing should be relatively light and not bulky; it should not limit the patient’s ability to actively flex and extend all burned extremities and digits. Frequent flexion 286

FIGURE 13-9  Contact burn from stepping on hot coals. Small, flat blisters do not require debridement.

and extension prevent the burned skin from tightening and thereby assist with pain control and prevention of edema. These principles are far more important than the choice of topical agent to cover the burn. Commonly used topical agents that might be carried in first-aid kits include antiseptic and antibiotic ointments and creams (e.g., bacitracin, Neosporin, Polysporin, double antibiotic ointment, triple antibiotic ointment, silver sulfadiazine) and nonantibacterial ointments (e.g., Aquaphor, Vaseline, A+D ointment). All of these agents are acceptable and the use of a topical antimicrobial is not essential in the early postburn setting. Technique of Burn Wound Debridement.  Small intact blisters do not need debridement (Figure 13-9). The blister environment serves as a sterile biologic dressing, preventing desiccation and (usually) pain. The intact blister should be protected from trauma and observed every few hours to ensure that the blister has not popped. If the blister opens, debridement is usually recommended because the leaking blister fluid may lead to crusting that can effectively “seal over” the wound, leading to a closedspace infection (Figure 13-10). Debridement of blisters is essentially painless so long as the blistered skin is cut and not peeled or torn. The burn should be washed with soap and water. Forceps are used to grasp the blistered skin, and small (manicure) scissors can be used to cut off the blister roof (Figure 13-11). Care should be taken to remove as much of the blistered skin as possible, leaving a uniform surface that can then be treated with a topical agent (Figure 13-12). There will be no bleeding during this procedure. To ensure that the procedure will be painless, the body part to be debrided should be stabilized against a solid surface. This prevents motion on the part of the patient, and it optimizes control for the person performing the procedure.

FIGURE 13-10  Contact burn from stepping on hot coals. Leaking blisters that have burst should be debrided (see text).

CHAPTER 13  Emergency Care of the Burned Victim

BOX 13-1  Baxter (Parkland) Formula First 24 Hours—Ringer’s Lactate • 4 mL /kg/% burn in 24 hours One-half in first 8 hours One-half in second 16 hours • Example: 70-kg (154-lb) man with 50% burn 4 mL × 50% × (70 kg) = 14,000 mL in 24 hours 7000 mL in hours 1 to 8 3500 mL in hours 8 to 16 3500 mL in hours 17 to 24

A

Second 24 Hours—Albumin or Plasma at Maintenance • Maintain normal vital signs • Adequate urine output • Example: 70-kg (154-lb) man with 50% burn 250 to 500 mL plasma 2000 to 2500 mL D5W D5W, Dextrose 5% in water.

B FIGURE 13-11  Partial-thickness burn to the dorsal hand from hot oil while cooking at camp. A, Blister is debrided 5 days after the injury. B, Bacitracin ointment is applied. (Courtesy Tim Platt-Mills, MD.)

EMERGENCY DEPARTMENT CARE The primary rule for the emergency physician is to “forget about the burn.” Although a burn is usually readily apparent and is often a dramatic injury, a careful search for other life-threatening injuries must take priority. Only after an overall assessment of the victim’s condition should attention be directed to the specific problem of the burns. Assessment of the nonthermally injured victim is presented in Chapter 21; the following paragraphs consider the specific problems encountered in the victim with burns. Resuscitation Since the 1970s, more than a dozen resuscitation plans have been suggested. The goal of all of them is to complete treatment with a living victim who has normally functioning kidneys and does not have cardiac failure or pulmonary edema. Nearly all of these plans use a combination of colloid and crystalloid solutions, but they vary considerably in the ratio of colloid to crystalloid, timing

FIGURE 13-12  The burn seen in Figure 13-9, after debridement.

of colloid administration, sodium concentration of crystalloid solution, and, to a much lesser extent, total volume of fluid given.* Some require frequent changing of solutions, others require mixing of solutions, and some require careful monitoring of the victim’s electrolytes. Intense controversy rages over which resuscitation plan is best, but this need not concern the physician without a special interest in burn physiology. There is general agreement on a few facts. A victim with very large burns will probably need both colloid and crystalloid. Initially, capillaries are permeable to both crystalloid and colloid solutions. The capillary leak to albumin and other large molecules repairs itself between hours 6 and 24 after injury. The choice of formulas for initial resuscitation is probably of relatively little consequence as long as the rate of fluid administration is modified according to the victim’s changing requirements as the hours pass. Because of its simplicity, ease of administration, and need for little blood chemistry monitoring, the formula developed by Baxter, known as the Baxter formula, or Parkland formula, has been adopted by most experts and recommended officially by the American College of Surgeons Committee on Trauma. According to the Baxter formula, crystalloid is given during the first 24 hours, while the capillaries are still permeable to albumin, and then colloid is given during the second 24 hours, when the capillary leak has presumably sealed. Rapid administration of crystalloid solution results in early expansion of depleted plasma volume, which will return cardiac output toward normal. Once the capillary leak has sealed, colloid (usually in the form of albumin) remains the most effective solution to maintain plasma volume without further increasing edema. The Baxter formula was derived to provide specific replacement of known deficits measured by simultaneous determinations of red blood cell volume, plasma volume, extracellular fluid volume, and cardiac output during burn shock. The first 24-hour and second 24-hour calculations are shown in Box 13-1. The formula calls for the administration of lactated Ringer’s solution, 4 mL/kg body weight per percentage of body surface burned during the first 24 hours after the injury. One-half of this fluid should be given in the first 8 hours and the second one-half during the next 16 hours. Fluid therapy during the second 24 hours consists of the administration of free water in quantity sufficient to maintain a normal serum sodium concentration, as well as plasma (or other colloid) to maintain a normal plasma volume. The adequacy of resuscitation can best be judged by frequent measurements of vital signs, central venous pressure, and urine output and by observation of general mental and physical responses. Despite myriad new monitoring devices, urine output *References 4, 13, 29, 32, 38, 56, 60, 63.

287

PART 3  BURNS, FIRE, AND RADIATION

remains one of the most sensitive and reliable assessments of fluid resuscitation. In the absence of myoglobinuria, a urine output of 0.5 mL/kg/hr in adults and 1 mL/kg/hr in children weighing less than 10 kg (22 lb) ensures that renal perfusion is adequate. The victim’s sensorium gives an indication of the state of cerebral perfusion and oxygenation. The victim should be alert and cooperative; confusion and combativeness are signs of inadequate resuscitation or warn of other causes of hypoxia, and supplemental oxygen should be provided in addition to fluid resuscitation. Patients with burns that involve less than 10% TBSA generally do not require fluid resuscitation. They should stay well hydrated but should not be encouraged to force fluids. Patients with burns that involve between 10% and 20% TBSA usually do not require intravenous (IV) fluid resuscitation. They should be encouraged to drink fluids that contain electrolytes (e.g., Gatorade) and should be discouraged from drinking large amounts of water or sodas. Hydration status in these patients should be monitored simply by ensuring that the oral mucous membranes are moist and that urine output is brisk with light-colored urine. Patients with burns that involve more than 20% TBSA should receive IV fluid resuscitation with crystalloid solution until they reach a facility where medical professionals can evaluate the need for other types of fluids. Victims with burns of less than 50% TBSA can usually be resuscitated with a single large-bore peripheral IV line. Because of the high incidence of septic thrombophlebitis, lower extremities should be avoided as IV portals. Upper extremities are preferable, even if the IV line must pass through burned skin. Victims with burns larger than 50% TBSA or who have associated medical problems, are at the extremes of age, or have concomitant smoke inhalation should have additional central venous pressure monitoring. Because of the extremely unstable state of the circulation in victims with burns over 65% TBSA, such victims should be monitored in an intensive care setting where a SwanGanz catheter for measuring pulmonary capillary wedge pressure and cardiac output is available. The presence of myoglobinuria alters the resuscitation plan. Myoglobinuria results from destruction of muscle cells, with release of myoglobin (the red muscle pigment). This is most often a problem when there are associated crush injuries, electrical burns, or extremely deep thermal burns. Characteristic colacolored urine is an indication to increase the amount of fluid given and to establish a diuresis of 70 to 100 mL of urine per hour. An initial bolus of 25 g of mannitol in adults or 0.5 to 1 g/ kg in children with a repeat dose in 15 to 30 minutes should be considered. Escharotomy Careful monitoring of the peripheral circulation is required in victims with circumferential full-thickness burns of the extremities. The edema that forms beneath inelastic eschar increases tissue pressure to a point at which it exceeds lymphatic pressure, thereby further increasing edema. When the edema exceeds venous pressure and eventually approaches arterial pressure, it stops all circulation to the extremity distal to the constricted area. The classic findings of compartment syndrome, usually considered to be pain, paresthesias, pulselessness, and tense swelling, may or may not be present in the burned extremity. Therefore distal pulses should be carefully monitored with Doppler ultrasound. If any of the clinical signs mentioned earlier occur, or if Doppler signals disappear, an escharotomy should be performed immediately. Escharotomy performed in the hospital does not require an anesthetic, because only an insensate full-thickness burn is incised. An incision is made through the eschar into subcutaneous tissue, first along the lateral aspect of the extremity and, if symptoms or signs do not improve, along the medial aspect (Figure 13-13). The incisions need not be as deep as the investing muscle fascia, and bleeding can usually be easily controlled with electrocautery and topical clotting agents. If arrival to the hospital will be within 6 hours, escharotomies should not be done in the field because the victim may bleed to death without proper equipment to control bleeding. 288

FIGURE 13-13  Deep full-thickness flame burns to the bilateral lower extremities and buttocks requiring medial and lateral escharotomies. (Courtesy Michael J. Mosier, MD.)

Circumferential full-thickness burns of the trunk in small children occasionally demand an escharotomy to improve pulmonary function. Chest wall escharotomies are made in the anterior axillary line bilaterally, extending from the clavicle to the costal margin. If the abdomen is involved with the burn, the inferior margins of the escharotomy may be connected transversely (Figure 13-14). Fasciotomies are rarely needed in victims with thermal burns. However, if distal pulses do not return after medial and lateral escharotomies, fasciotomy should be considered. On the other hand, victims with electrical injuries frequently need fasciotomy. Careful monitoring is mandatory for all victims with electrical burns and with burns associated with soft tissue trauma or fractures. In these circumstances, loss of pulses is a strong indication for urgent fasciotomy under general anesthesia in the operating room. The need for escharotomy in the burned hand is somewhat controversial. Fingers burned badly enough to require escharotomy are frequently mummified, and the lack of muscles in the fingers puts less tissue at ischemic risk. Escharotomy done in fingers that may not require it runs the risk of exposing the interphalangeal joints (Figure 13-15), leading to subsequent infection that may ultimately require joint fusion or finger amputation. Both the palmar arch and the digital vessels should be monitored with Doppler ultrasound in any significant hand burn. If the signals disappear over the palmar arch or in the digital vessels, consideration should be given to performing a dorsal interosseous fasciotomy.

FIGURE 13-14  Full-thickness flame burns to the anterior torso and left upper extremity. Escharotomies were performed along the flank, sternum, clavicle, costal margin, and abdomen to release the restricting eschar and allow improved chest and abdominal wall compliance. (Courtesy Michael J. Mosier, MD.)

FIGURE 13-15  Full-thickness flame burns to the right hand with escharotomies in a fan pattern between metacarpals to adequately release pressure from edema formation. (Courtesy Michael J. Mosier, MD.)

Burn Wound Management The burn wound should be cleansed initially with a surgical detergent. All loose, nonviable skin should be gently trimmed. Debridement should be done gently; small doses of IV narcotic are usually sufficient analgesia for this procedure. General anesthesia and operating room debridement should be avoided until resuscitation is complete, unless other surgical procedures are necessary. Once the wound is cleansed, a topical chemotherapeutic agent should be applied. A detailed description of all the agents available is beyond the scope of this chapter, but those most commonly used in the United States and other industrialized countries contain silver sulfadiazine. It comes as a white cream, is soothing to the wound, has a good antimicrobial spectrum, and has almost no systemic absorption or toxicity.6,37,77,85 The victim should be carefully questioned about allergy to sulfa drugs before its use, however, because allergic reactions are encountered in about 3% of patients. These reactions may be manifested clinically as pain after application rather than the soothing feeling that silver sulfadiazine usually provides. If an allergy is suspected by history, a small (10 × 10 cm [4 × 4 inch]) patch of silver sulfadiazine should be applied as a test. The remainder of the wound can be dressed in bacitracin. If no local reaction occurs after 2 to 4 hours, an allergy is unlikely and silver sulfadiazine is the dressing of choice. If an allergy is confirmed, the victim should be referred to a burn center, where the next choice of topical antimicrobial would probably be silver nitrate solution.

OUTPATIENT BURNS The vast majority of victims with burns do not require hospitalization. In many cases, the burn, if merely kept clean, heals spontaneously in less than 3 weeks with acceptable cosmetic results and no functional impairment. Unfortunately, good results in treating superficial minor burns may entice the unwary physician to treat more complex burns by the same methods. For the victim, the consequences of such a mistake can be the need for subsequent hospitalization, joint dysfunction, and hypertrophic scarring that may be difficult to correct, as well as considerable loss of time from work or school. First-Degree Burns Although first-degree burns are very painful, victims rarely seek medical attention unless the burned area is extensive. These victims do not require hospitalization, but control of the pain is extremely important. Aspirin or codeine may be adequate for small injuries, but for large burns, liberal use of a more potent narcotic for 2 to 3 days is indicated. For topical medication, the authors recommend one of the many proprietary compounds containing extracts of the Aloe vera plant in concentrations of at least 60%. Aloe vera has antimicrobial properties and is an effective analgesic.46,74 Anecdotal

Superficial Partial-Thickness Burns Treatment of superficial partial-thickness burns presents little problem. If the wound is kept clean, the victim is kept comfortable, and the joints are kept active, these wounds heal in less than 3 weeks with minimal scarring and no joint impairment. Initially, the wound should be cleansed and debrided as described previously. Small blisters may be left intact. Biochemical analysis of the protein-banding pattern of burn blister fluid, obtained by polyacrylamide gel electrophoresis, has shown it to be similar to that of serum.88 The authors suggest that the fluid is an exudate mainly from the vascular system, that it provides a good environment for the fibroblasts in the damaged site, and that it facilitates the healing process. Larger blisters are difficult to protect, however, and blister fluid is a rich culture medium for bacteria that live in the skin appendages. Therefore large blisters and small blisters in large burns should usually be totally removed with forceps and scissors. In some instances the blister fluid can be aspirated with a large-bore needle, allowing the blistered epidermis to remain on the wound as a biologic dressing. This dead epidermis, however, is fragile, tends to contract, and rarely stays in place except over small areas. After debridement, these wounds can sometimes be managed with one of the newer synthetic dressings that contain elemental silver. There are several on the market (Aquacel Ag, Acticoat, Mepilex Ag) that can be applied and left in place for a week or until the burn is healed at about 2 weeks. However, the most commonly used treatment is wound coverage with silver sulfadiazine and application of a light dressing to promote active range of motion. Some very small burns do not require topical agents. For small facial burns, bacitracin ointment may be a better choice than silver sulfadiazine cream because it is less drying. Pain is managed as for first-degree burns, and the patient usually should return every 2 to 3 days until the wound heals or the patient has demonstrated the ability to manage the wound without supervision. If silver sulfadiazine is used, an appropriate home treatment regimen is to have the patient cleanse the wound once daily with tap water and reapply the topical agent and light dressing. During dressing changes, and as often as possible, all involved joints should be put through a full range of motion. The dressing may be unnecessary while the patient is at home, but the patient should dress the wound before leaving the house. This method is highly successful, but it is inconvenient and fairly painful and requires good patient cooperation. The “exposure” method has little to recommend it. This method involves leaving the wound open, allowing the wound drainage to desiccate and form a scab. Controlled studies in animals have shown that desiccation and crust formation interfere with wound healing. Our experience has also shown that crusts crack over joints, cause considerable discomfort, and can hide infection. Deep Partial-Thickness and Full-Thickness Burns Treatment of deep partial-thickness and full-thickness burns is a matter of grave concern. Full-thickness burns heal only by contraction and epithelialization from the periphery. Epithelium does not begin to migrate until the eschar is removed; the growth rate then is only about 1 mm (0.04 inch)/day. Thus healing of even a small full-thickness burn may involve many weeks of discomfort and disability. Deep partial-thickness burns may take 4 to 8 weeks to heal and then leave an unacceptable scar. If a joint is involved, some loss of joint function is the rule. The authors have adopted a policy of early excision and grafting for such wounds. 289

CHAPTER 13  Emergency Care of the Burned Victim

evidence suggests that it may decrease subsequent pruritus and peeling. Burns from ultraviolet rays (sunlight, sunlamp) may initially appear to be only epidermal, but the injury may in fact be a superficial partial-thickness burn with blistering apparent only after 12 to 24 hours. Therefore the victim with such a burn should be cautioned about blisters and should be asked to return if they form, because wound management then becomes more important because of the potential for infection and subsequent scarring.

PART 3  BURNS, FIRE, AND RADIATION

Initial outpatient treatment can be followed by elective surgery as soon as it can be scheduled. Small wounds can be treated through day surgery; larger wounds located over dynamically important areas can be closed with only a day or two of hospitalization. Excision and grafting procedures should be done by a surgeon experienced in tangential wound excision. The advantages of this aggressive approach—a pain-free patient with normal joint function, better cosmetic result, and a rapid return to work or school—more than compensate for the brief hospitalization and the very small risk associated with a minor operation. Should the excision and grafting plan be unacceptable to the patient or treating physician, the standard method of daily cleansing and application of silver sulfadiazine cream is used. Most full-thickness burns need grafting at about 3 to 4 weeks after the injury. Deep dermal burns should be seen by the physician frequently during the healing process, and active physical therapy is crucial to ensuring a successful outcome.

REHABILITATION Physicians who regularly care for people with burn injuries recognize that treatment goals extend far beyond healing of the wounds and survival of the victim. The aim is to return victims at least to their preburn functional status physically and to ensure smooth and timely reentry into family and social situations, including work or school. Awareness that recovery from burn injury often depends on a number of nonphysician health care workers is essential. Depending on the severity of the burn and associated social situation, participation is commonly required of nurses, nutritionists, occupational therapists, physical therapists, recreational therapists, social workers, vocational rehabilitation counselors, psychologists, pain management specialists, and clergy. Burn rehabilitation should be initiated by the first physician to see the victim. Once all systemic and wound issues have been addressed, proper positioning of wounded extremities or digits should be assessed by an occupational therapist who has been specially trained in burn management. Splints should be made immediately if deemed appropriate. Range-of-motion exercises should be started on the day of injury, and frequent follow-up by a physical therapist is essential. The best functional outcomes result from meticulous attention to early mobility. Patients almost universally choose not to move a burned body part, and an active ancillary burn staff is essential for satisfactory results. Burn scars require approximately one year to fade, soften, and mature. Physical therapy may be required throughout this time period or longer. Pressure garment therapy may be used in certain cases in an attempt to prevent hypertrophic scars from deve­ loping. The interested reader is referred to books dealing with acute burn care, reconstructive plastic surgery, and burn rehabilitation.1,7,11

Inhalation Injury Of the nearly 500,000 fire victims admitted to hospitals each year, smoke or thermal damage to the respiratory tree may occur in as many as 30%.68 Carbon monoxide poisoning, smoke poisoning, and thermal injury are three distinctly separate aspects of clinical inhalation injury. Inhalation injury rarely occurs in an outdoor setting.

CARBON MONOXIDE POISONING Pathophysiology Carbon monoxide (CO) is a colorless, odorless, tasteless gas that has an affinity for hemoglobin 200 times greater than that of oxygen. The most simply explained mechanism of action of CO is reversible displacement of oxygen on the hemoglobin molecule. Although worsening hypoxia is important, and the percentage of carboxyhemoglobin (COHb) in the blood represents in large measure the degree of victim hypoxia, this simple mechanism cannot account for all of the experimental and clinical findings seen with exposure to CO. For example, an 290

experimental group of dogs was exchange-transfused with blood containing 80% COHb. They showed no symptoms. In a control group with COHb levels of 80% produced by inhalation of CO, all animals died. Furthermore, the degree of enzyme and muscle impairment may not correlate accurately with the levels of blood COHb.12,17,27,47 In vitro, CO combines reversibly with cardiac muscle myoglobin and heme-containing enzymes, such as cytochrome oxidase (a3).12 Despite its intense affinity, it readily dissociates according to the laws of mass action. The half-life of COHb in humans breathing room air is 4 to 5 hours. In humans breathing 100% oxygen, the half-life is reduced to 45 to 60 minutes.51 In a hyperbaric oxygen chamber at 2 psi, the half-life is 30 minutes, and at 3 atm in a chamber it is reduced to 15 to 20 minutes.87 Clinical Presentation Blood levels of COHb provide a laboratory measure to correlate with associated symptoms of CO poisoning. Levels less than 10% do not cause symptoms, although victims with exercise-induced angina may show decreased exercise tolerance. At levels of 20%, healthy persons complain of headache, nausea, vomiting, and loss of manual dexterity. At 30%, they become confused and lethargic and may show depressed ST segments on an electrocardiogram. In a fire situation, this level may lead to death because the victim loses both the interest and the ability to flee the smoke. At levels between 40% and 60%, the victim lapses into coma, and levels much above 60% are usually fatal. Therapy Victims who have not been unconscious and who have a normal neurologic examination on admission almost always recover completely without treatment beyond administration of 100% oxygen. Victims who remain comatose once COHb levels have returned to normal have a poor prognosis, and in the authors’ experience they rarely awaken. Although enthusiasts for hyperbaric oxygen treatment (HBOT) (see Chapter 76) consider it a standard of care for CO poisoning,2,3,49,58 other physicians are skeptical.75 One controlled study indicated that hyperbaric oxygen made no difference for moderate poisoning, and multiple treatments were no better than a single treatment for victims with severe poisoning.69 Furthermore, when associated with a major burn, transport to a chamber delays definitive care and is associated with numerous complications, including emesis, seizures, eustachian tube occlusion, aspiration, hypocalcemia, agitation requiring restraints or sedation, arterial hypotension, tension pneumothorax, and cardiac arrhythmia or arrest.31,83 The issue of whether, and at what time in the progression of CO poisoning, HBOT may be of value will undoubtedly continue to be studied and debated.

THERMAL AIRWAY INJURY Pathophysiology The term pulmonary burn is a misnomer. True thermal damage to the lower respiratory tract and lung parenchyma is extremely rare unless live steam or exploding gases are inhaled. The air temperature near the ceiling of a burning room may reach 540° C (1004° F) or more, but air has such poor heat-carrying capacity that most of the heat is dissipated in the nasopharynx and upper airway. Heat dissipation in the upper airway, however, may cause significant local thermal injury. Clinical Presentation Victims who have been in explosions (propane, natural gas, or gasoline) and have burns of the hands, face, and upper torso are particularly at risk for pharyngeal edema (Figure 13-16). Therapy Maintenance of the airway is the main concern with potential thermal airway injury. Victims injured in explosions should be examined for oropharyngeal erythema and edema. If these are present, the victim should be intubated for 24 to 72 hours until edema subsides. A simple test to determine if intubation should continue is to see if the victim can breathe around the

endotracheal tube when the cuff is deflated. If so, the airway edema has probably resolved, and extubation should be safe. If doubt exists, extubation should be performed over a fiberoptic bronchoscope or nasogastric tube, which allows easy replacement of the endotracheal tube if necessary. Because this is not a pulmonary parenchymal injury, the purpose of intubation is to protect the airway and not necessarily to assist with ventilation. Ventilator settings should be adjusted accordingly, and vigorous pulmonary toilet should be instituted to prevent the pulmonary problems (atelectasis and pneumonia) commonly seen in intubated victims.

SMOKE POISONING Pathophysiology Some 280 separate toxic products have been identified in wood smoke. Modern petrochemical science has now produced a wealth of plastic materials in homes and automobiles that when burned produce nearly all of these and many other products not yet even characterized.42,64,81,95 Prominent by-products of incomplete combustion are oxides of sulfur, nitrogen, and many aldehydes. One such aldehyde, acrolein, causes severe pulmonary irritation and edema in concentrations as low as 10 ppm. Although the chemical mechanisms of injury may be different with different toxic products, the overall end-organ response is reasonably well defined.* There is immediate loss of bronchial– epithelial cilia and decreased alveolar surfactant. Microatelectasis, and sometimes macroatelectasis, results in and is compounded by mucosal edema in small airways. Wheezing and air hunger are common symptoms at this time. After a few hours, tracheal and bronchial epithelia begin to slough and hemorrhagic tracheobronchitis develops. In severe cases, interstitial edema becomes prominent, resulting in a typical picture of the adult respiratory distress syndrome (ARDS). Pulmonary alveolar macrophages are poisoned, causing severe impairment of chemotaxis, which undoubtedly contributes to the high incidence of late pneumonia seen in victims with associated cutaneous burns. The activated neutrophils release superoxides and free radicals of oxygen, which together with other inflammatory mediators aggravate alveolar–capillary damage, leading to increased interstitial edema and impaired oxygenation. Clinical Presentation Any victim who has been indoors or in an enclosed space with a smoky fire and has a flame burn should be assumed to have smoke poisoning until proved otherwise. The acrid smell of smoke on the victim’s clothes should raise suspicion. Rescuers are often the most important historians and should be carefully questioned. *References 9, 14, 36, 39, 50, 51, 72, 79, 93, 95.

Therapy All victims burned in an enclosed space or having any suggestion of neurologic symptoms should be given 100% oxygen while awaiting measurement of COHb levels. This should be administered through a tight-fitting mask in the field. If the victim demonstrates labored breathing or if a prolonged transport time is anticipated, endotracheal intubation should be performed by trained personnel. Oxygen at 100% can then be administered by ventilator. Mucosal burns of the mouth, nasopharynx, and larynx respond with edema formation and may lead to upper airway obstruction

FIGURE 13-17  View of the proximal airway on bronchoscopy, demonstrating a moderate amount of erythema and carbonaceous debris, consistent with a grade 2 inhalation injury by bronchoscopic criteria. (Courtesy Michael J. Mosier, MD.)

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CHAPTER 13  Emergency Care of the Burned Victim

FIGURE 13-16  Deep full-thickness flame burns to the face and neck with emergent cricothyroidotomy secondary to the inability to perform oropharyngeal intubation. (Courtesy Michael J. Mosier, MD.)

Careful inspection of the mouth and pharynx should be done early. Hoarseness and expiratory wheezes are signs of potentially serious airway edema or smoke poisoning. Copious mucus production and carbonaceous sputum are sure signs, but their absence should not raise false hopes that injury is absent. COHb levels should be obtained; elevated COHb levels or any clinical symptoms of CO poisoning are presumptive evidence of associated smoke poisoning. In very smoky fires, COHb levels of 40% to 50% may be reached after only 2 to 3 minutes of exposure.87 Anyone with suspected smoke poisoning should have a set of arterial blood gases drawn. One of the earliest indicators is an improper ratio of arterial partial pressure of oxygen (PaO2) to fraction of inspired oxygen (FIO2) (the P/F ratio). Normally the ratio is 400 to 500, whereas patients with impending pulmonary problems have a ratio of less than 300 (e.g., a PaO2 of less than 120 mm Hg with an FIO2 of 0.40). A ratio of less than 250 is an indication for vigorous pulmonary therapy and not an indication for merely increasing the inspired oxygen concentration. A number of authorities suggest the routine use of fiberoptic bronchoscopy10,52,71,77 (Figure 13-17). It is inexpensive, quickly performed by an experienced clinician, and useful for accurately assessing edema of the upper airway. Aside from the presence of tracheal erythema, however, it does not materially influence the treatment for smoke poisoning. Therefore, it should be used only when the diagnosis is in doubt or for experimental studies. We have correlated by multivariate analysis a constellation of history, signs, and symptoms with bronchoscopic findings in 100 consecutive patients with suspected smoke inhalation admitted to the University of Washington Burn Center in Seattle. If the patient had the combination of history of closed-space fire, carbonaceous sputum, and a COHb level greater than 10%, there was a 96% correlation with positive bronchoscopy. Presence of two of the above features dropped correlation to 70%, and if only one was present, the correlation dropped to 36%. As discussed previously, upper airway edema was best correlated with an explosion (flash burn) that involved both the face and upper torso. Nearly 50% of such victims had significant upper airway edema and underwent prophylactic airway intubation.

PART 3  BURNS, FIRE, AND RADIATION

at any time during the first 24 hours after the burn. Red or dry mucosa or small mucosal blisters should alert the observer to the possibility of subsequent airway obstruction; they also should raise suspicion that significant smoke inhalation may have occurred. Any victim with burns of the face should have a careful visual inspection of the mouth and pharynx; if abnormalities are found, the larynx should be examined immediately on arrival at the hospital. The presence of significant intraoral and pharyngeal burns is a clear indication for early endotracheal intubation, because the progressive edema may make later emergency intubation extremely hazardous, if not impossible. The mucosal burns themselves are rarely full thickness and can be successfully managed with good oral hygiene. Once inserted, the endotracheal tube should remain in place for 2 to 5 days until the edema subsides. Pulmonary functions early in the course of smoke poisoning are variably affected. Typically, there are decreased lung volume (functional residual capacity) and vital capacity, evidence of obstructive disease with reduction in flow rates, increased dead space, and rapid decrease in compliance. Surprisingly, much of the variability in pulmonary response appears to correlate with severity of the associated cutaneous burn.11 Without associated burns, mortality from smoke poisoning is low, the disease rarely progresses to ARDS, and symptomatic treatment usually leads to complete resolution of symptoms in a few days. In the presence of burns, smoke poisoning appears to approximately double the rate of mortality from burns of any size. Pulmonary symptoms (hypoxia, rales, rhonchi, wheezes) are seldom present on admission but may appear 12 to 48 hours after exposure. In general, the earlier the onset of symptoms, the more severe the disease.86 No standard treatment has evolved to ensure survival after smoke poisoning; each recommended treatment modality is tempered by opinion and the individual experience of the treating physician. In the presence of increasing laryngeal edema, nasotracheal or orotracheal intubation is indicated. A tracheostomy is never an emergency procedure and certainly should be avoided as initial airway management in victims with burns to the face and neck. A soft-cuffed endotracheal tube should be left in place for 3 to 5 days until the generalized oropharyngeal edema subsides. Mild cases of smoke poisoning are treated with highly humidified air, vigorous pulmonary toilet, and bronchodilators as needed. Blood gases are drawn at least every 4 hours, and the P/F ratio is calculated. Worsening symptoms, difficulty in handling secretions, and a falling P/F ratio are all indications for intubation and respiratory assistance with a volume ventilator. If oxygenation is impaired (P/F ratio 250 or less), positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) is initiated and increased by increments of 3 to 5 cm H2O until no further improvement in the P/F ratio occurs or there is evidence of decreased cardiac output. The physician must carefully search for other mechanical causes of poor ventilation (e.g., restricted chest wall motion from full-thickness burns, pneumothorax from high ventilator pressures, or mechanical difficulties with the endotracheal tube). Prophylactic antibiotics have no value in this chemical pneumonitis, and the subsequent burn management and treatment of eventual bacterial pneumonia can be made more difficult by development of resistant organisms if antibiotics are used early. Corticosteroids are commonly used in victims with severe asthma. Clinicians dealing with smoke poisoning often use them for their spasmolytic and antiinflammatory actions. Several authors have studied the use of corticosteroids, but a most convincing study comes from Moylan,61 who showed in a prospective blinded study of patients with smoke poisoning and associated major burns that the rates of mortality and infectious complications were higher in the corticosteroid-treated patients. In patients with associated burns, Robinson and Seward73 found that corticosteroids did not alter the hospital course of patients admitted to the hospital after the MGM Grand and Hilton Hotel fires in Las Vegas in 1981. The decision for hospital admission and need for specialized care rest on the severity of symptoms from the smoke and the presence and magnitude of associated burns. Any victim who 292

shows symptoms of smoke inhalation and has more than trivial burns should be admitted. If the burns are greater than 15% TBSA, the victim should probably be referred to a special care unit. In the absence of burns, admission depends on the severity of symptoms, presence of preexisting medical problems, and social circumstances of the victim. Otherwise healthy victims with mild symptoms (only a few expiratory wheezes, minimal sputum production, COHb level less than 10%, and normal blood gas levels) can be watched for an hour or two and then discharged if they have a place to go and someone to stay with them. Victims with preexisting cardiovascular or pulmonary disease should be admitted for observation if they have any symptoms related to the smoke. Victims with moderate symptoms (generalized wheezing, mild hoarseness, moderate sputum production, COHb levels 5% to 10%, and normal blood gas levels) may be admitted for close observation and treated as for asthma. The patient with severe symptoms (air hunger, severe wheezing, and copious [usually carbonaceous] sputum) requires immediate intubation and ventilatory support in an intensive care unit setting.

Other Considerations Burns are tetanus-prone wounds. The need for tetanus prophylaxis is determined by the victim’s current immunization status. The treating physician should follow the recommendations of the American College of Surgeons. All victims undergoing IV resuscitation should have an indwelling urinary catheter placed for hourly monitoring of urine output. Arterial lines are useful in victims who need frequent assessment of blood gas levels or who will need repeated blood sampling. Necessary laboratory work during the resuscitation phase is relatively minimal. Blood should be drawn for baseline blood chemistries. If major operative procedures, such as fasciotomy or multiple escharotomies, are expected, blood should be sent for type and crossmatching in anticipation of needing several units of whole blood. Determination of blood gas levels is mandatory in any victim with a suspected inhalation injury, and arterial pH measurement is useful as an assessment of the overall treatment of shock. If the Baxter formula is used for resuscitation, frequent electrolyte determinations are not necessary because levels will remain in the normal range. By 48 hours, however, careful monitoring of serum sodium and potassium levels becomes important. High levels of circulating aldosterone result in an increase in renal potassium excretion. Evaporative water loss to varying degrees through eschar dramatically increases the free-water requirements of burned victims. Hemoglobin and hematocrit levels are initially high and remain high or normal until the third or fourth postburn day. Blood glucose level is commonly elevated because of the glycogenolytic effect of elevated catecholamines, gluconeogenetic effect of elevated glucocorticoid and glucagon levels, and relative insulin resistance.41,78,89,96 This well-described “stress diabetes” can become a problem in normal patients if glucose-containing solutions are given during resuscitation, and is frequently a serious problem in patients with preexisting diabetes. All diabetic patients require careful monitoring of blood and urine glucose levels, and most require supplemental insulin during resuscitation. All medications during the shock phase of burn care should be given intravenously. Subcutaneous and intramuscular injections are unreliably absorbed systemically, and their use should be avoided. Pain control is best managed with small IV doses of morphine until pain control is adequate without affecting blood pressure. Before the discovery of penicillin, 30% of burn victims died during the first week after their injury from overwhelming β-hemolytic streptococcal sepsis. The availability of penicillin decreased streptococcal infections but had no influence on mortality or the incidence of bacterial sepsis. Victims then survived the first postburn week only to die of gram-negative penicillinresistant bacterial sepsis during the second or third week after the burn. The advent of effective topical chemotherapeutic agents applied directly to the burn wounds made possible the control of streptococcal infection, obviating the need for prophylactic penicillin. The use of prophylactic antibiotics in outpatient burns

BURN SEVERITY AND CATEGORIZATION Severity of injury is proportionate to the size of the total burn, depth of the burn, age of the victim, and associated medical problems or injuries. Burns have been classified by the American Burn Association and the American College of Surgeons Committee on Trauma into categories of minor, moderate, and severe.5 Moderate burns are defined as partial-thickness burns of 15% to 25% TBSA in adults (10% to 20% in children), full-thickness burns of less than 10% TBSA, and burns that do not involve the eyes, ears, face, hands, feet, or perineum. Because of the significant cosmetic and functional risk, all but very superficial burns of the face, hands, feet, and perineum should be treated by a physician with a special interest in burn care in a facility that is accustomed to dealing with such problems. Major burns, as described previously, most full-thickness burns in infants and older adults, and burns combined with diseases or injuries should also be treated in a specialized facility. Moderate burns can be treated in a community hospital by a knowledgeable physician as long as the other members of the health care team have the resources and knowledge to ensure a good result. Adoption of early excision and grafting or creative use of local tissue rearrangement to achieve early wound closure have made burn care more complex, and an increasing number of victims with small but significant burns are being referred to specialized care facilities to take advantage of these concepts. The criteria for admission to the hospital of victims with minor and moderate burns vary according to physician preference, the victim’s social circumstances, and the ability to provide close follow-up. In some circumstances, superficial burns as large as 15% can be successfully managed on an outpatient basis. In other circumstances, burns as small as 1% may require admission because of the victim’s inability or unwillingness to care for the wound. In general, the threshold for admission of older adults and infants should be low. Any victim (child or adult) who the physician suspects has been abused must be admitted.

TRANSPORT AND TRANSFER PROTOCOLS Once an airway is established and resuscitation is under way, burn victims are eminently suitable for transport.8,19,43 Resuscitation can continue en route, because for the most part patients

remain stable for several days. This was well proved during the Vietnam War, when burn victims were transported from Vietnam to Japan and then from Japan to the military burn center in San Antonio, Texas. The transport was generally accomplished during the first 2 weeks after the burn, with few complications occurring in about 1000 patients transferred. Hospitals without specialized burn care facilities should decide where they will refer patients and work out transfer agreements and treatment protocols with the chosen burn center well in advance of need. If this is done, definitive care can begin at the initial hospital and continue without interruption during transport and at the burn center. In general, transfer should be from physician to physician, and contact should be established between them as soon as the patient arrives at the initial hospital. The mode of transport depends on vehicle availability, local terrain, weather, and the distances involved. For distances of less than 80 km (50 miles), a ground ambulance is usually satisfactory. For distances between 80 and 241 km (50 and 150 miles), many people prefer helicopter transport. It should be noted, however, that monitoring, airway management, and any changes in therapy are more difficult to achieve in a helicopter. All victims transported by air should have a nasogastric tube inserted and be placed on dependent drainage, because nausea and vomiting usually result during the flight. Two large-bore IV lines should be functional in case one stops working. For distances over 241 km (150 miles), fixed-wing aircraft are usually satisfactory. Modern air ambulances are completely equipped flying intensive care units, and the personnel are usually well trained for both critical care and the peculiarities of victim care during the flight (see Chapter 40). The referring physicians must ensure that the victim’s condition is suitable for a long transport and prepare the victim for the flight. The victim’s airway must be secure. At 9144 m (30,000 feet), planes can be pressurized to an altitude of about 1676 m (5500 feet). Although supplemental oxygen can be given in flight, if the victim’s oxygenation is marginal, performing intubation and starting mechanical ventilation before the transport may be preferable. Intubation is difficult en route, so if there is any question of upper airway edema, the victim should be intubated at the referring hospital. Burned victims have difficulty maintaining body temperature, and should be wrapped warmly before transport. Bulky dressings, a blanket, and a Mylar sheet (usually available from the flight team) can help maintain body temperature. In case the victim has any cardiac irregularities, the plane must be equipped with electronic monitoring capability, because noise and vibrations in flight make clinical monitoring difficult. Only after all other assessments are complete should attention be directed to the burn itself. If the victim is to be transferred from the initial hospital to a definitive care center during the first postburn day, personnel at the referring hospital can leave the burn wounds alone, merely calculating the size of the burn for resuscitation, and monitoring pulses distal to circumferential full-thickness burns. The victim can be wrapped in a clean sheet and kept warm until arrival at the definitive care center.

REFERENCES Complete references used in this text are available online at www. expertconsult.com.

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has not been carefully evaluated, so opinion is divided regarding its utility in victims not requiring hospitalization. Stress ulceration of the stomach and duodenum was once a dreaded complication, occurring in nearly 30% of victims with burns. Protection of the gastric mucosa by immediate feeding through a small nasogastric tube or, failing that, decreasing gastric acidity with histamine2 (H2) receptor antagonists, proton pump inhibitors, or coating the gastric mucosa with sucralfate has made stress ulcers rare.45,58,67,70,84 Psychosocial care should begin immediately. The victim and family must be comforted, and a realistic outlook regarding the prognosis of the burns should be given, at least to the victim’s family. In house fires, the victim’s loved ones, pets, and many or all possessions may have been destroyed. If the family is not available, some member of the team, usually the social worker, should find out the extent of the damage in hopes of comforting the victim. If the victim is a child and the circumstances suggest that the burn may have been deliberately inflicted or resulted from negligence, physicians in most states are required by law to report their suspicion of child abuse to local authorities.

CHAPTER 14 

Exposure to Radiation From the Sun  ANDREW C. KRAKOWSKI AND LEE A. KAPLAN

Sun exposure, sun damage, and sun protection are increasingly the focus of medical, scientific, and public attention. Adverse effects of sunlight overexposure are well documented,84,147 but the relative value and safety of sun-protective strategies are debated. These issues are of particular concern to wilderness enthusiasts, who spend considerable time in the sun. Sun protection against acute phototrauma, especially sunburn, is more easily judged than is protection against chronic phototrauma such as photoaging, cataracts, and photocarcinogenesis. However, these chronic effects are increasingly relevant to modern societies with demographically aging populations. The economic concerns are huge; billions of dollars are spent annually in the cosmetic and medical industries to repair photodamage, photoaging, and skin cancer. Consumer interest in photoprotection is rapidly expanding. With better sunscreens and photoprotective clothing, even more investment in the future will be focused on sun protection.

Solar Radiation ELECTROMAGNETIC SPECTRUM The sun produces a continuous spectrum of electromagnetic radiation (Figure 14-1). The most energetic rays, which are those with wavelengths that are shorter than 10 nm (i.e., cosmic rays, gamma rays, and x-rays), do not appreciably penetrate Earth’s surface. Phototrauma is primarily the result of ultraviolet radiation (UVR). UVR (10 to 400 nm) accounts for about 10% of the incident radiation at Earth’s surface; visible light (400 to 760 nm) accounts for about 50%; and infrared (IR; 760 to 1700 nm) accounts for about 40%.84 UVR has four components. Vacuum UVR (10 to 200 nm) is readily absorbed by air and does not penetrate Earth’s atmos­ phere. Ultraviolet C (UVC; 200 to 290 nm) is almost entirely absorbed in the stratosphere, which is 15 to 50 km (9.3 to 31.1 miles) above Earth’s surface, and by oxygen and ozone. Manmade sources of UVC (e.g., germicidal lamps, arc-welding devices) are rarely medically relevant. Ultraviolet B (UVB; 290 to 320 nm) is biologically quite active and principally responsible for tanning, burning, and nonmelanoma skin cancer (NMSC) formation.4,147 Beneficial effects of UVB include vitamin D production from a cutaneous precursor, 7-dehydrocholesterol, to form previtamin D3, which is quickly converted to vitamin D3 (cholecalciferol). It is first hydroxylated in the liver into 25-hydroxyvitamin D3 and subsequently in the kidneys into 1,25-dihydroxyvitamin D3; this is the active metabolite, which stimulates calcium absorption from the gut.131 Approximately 90% of 25-hydroxyvitamin D3 is formed in this manner.237 Of the UVR that reaches Earth’s surface, UVB accounts for roughly 10%, whereas ultraviolet A (UVA; 320 to 400 nm) accounts for about 90%, depending on the season and the time of day. UVA is typically subdivided into “near UVA” or UVA II (320 to 340 nm) and “far UVA” or UVA I (340 to 400 nm). Although these subdivisions are somewhat arbitrary, they are based on photobiologic responses. UVA is biologically active, and it contributes to tanning, burning, photoaging, and carcinogenesis. UVA penetrates the skin more deeply than does UVB, with less energy lost in the superficial layers of the stratum corneum and the epidermis. In addition, UVA is the principal trigger for photo-drug reactions. Longer-wavelength visible light and IR may also cause cutaneous phototrauma, albeit rarely. Solar urticaria has been reported to occur with exposure to visible 294

wavelengths. IR alone—as well as in combination with UVR— may produce epidermal and dermal alterations.152

ENVIRONMENTAL INFLUENCES ON UVR EXPOSURE Exposure to UVR is substantially affected by latitude, altitude, season, time of day, solar zenith angle, albedo (reflectivity), clouds, atmospheric pollution, ozone levels, and personal factors, including occupation and personal behaviors.* Most UVR reaches Earth around midday: 80% between 9 AM and 3 PM and 65% between 10 AM and 2 PM.84 UVB peaks at midday, when the sun is at its zenith.179 UVB is absorbed, reflected, and scattered by the atmosphere, and, at midday, it has less atmosphere to traverse. During early morning and late afternoon, when the sun nears the horizon, UVB decreases considerably. Latitude and season have similar effects: peak UVB exposure is approximately 100 times greater in June than in December.179 For each degree of latitude away from the equator, UVB intensity decreases an average of 3%. UVA varies considerably less than UVB with latitude, time of day, and season, as predicted by Rayleigh’s law: Atmospheric light scattering ∝ 1/λ4, where λ is the wavelength. The shorter the wavelength, the greater is the atmospheric scattering, so UVB is scattered much more readily than is UVA. In addition, UVA (but not UVB) is transmitted through window glass, thus allowing for indoor exposure to UVA but not to UVB. UVR may be increased by surface reflection. Surprisingly, water is a relatively poor reflector. UVR at midday penetrates water up to 60 cm (23.6 inches), so submerged skin is not necessarily protected.179 Reflection from water may increase as the sun nears the horizon, but, at that time, there remains little UVB to reflect because of atmospheric attenuation. Ice and snow are considerably better reflectors. Clean snow may reflect up to 85% of UVR,179 which accounts for oddly distributed sunburns in spring skiers. Grass, sand, metal, concrete, salt flats, and other surfaces reflect UVR to varying degrees. The importance of surface reflection was demonstrated in a 2010 study that was conducted in Spain, which showed that a blue-and-white painted canvas beach umbrella with a radius of 0.8 m (2.6 ft) and a height of 1.5 m (4.9 ft) effectively blocked direct UV radiation; however, sensors positioned at the base of that same beach umbrella still measured 34% of the incident horizontal irradiance found “in the open.”297 Clouds may attenuate UVR exposure. Absorption by clouds varies from 10% to 80% but rarely exceeds 40%.147 Polluted clouds, which contain the greatest concentration of hydrocarbons, are the most effective at absorbing UVR. Clouds are more effective at absorbing heat in the form of infrared radiation, occasionally seducing hikers and bathers into excessively lengthy midday exposures. Wind and water augment sunburn. In mice, exposure to wind plus UVR results in more erythema than does exposure to UVR alone.226 In humans, wind may reduce heat perception, thereby encouraging longer exposure. Water increases UVR exposure because moist skin reflects less UVR, thereby resulting in greater *References 181, 198, 102, 205, 228, 293.

For online-only figures, please go to www.expertconsult.com

Does not reach Earth’s surface

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CHAPTER 14  Exposure to Radiation From the Sun

nm = 10–9 m = 10 Å

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FIGURE 14-1  The electromagnetic spectrum.

absorption of UVB. Consequently, swimmers and hikers in humid environments may be at risk for increased UVR absorption.84 Altitude profoundly influences UVB exposure. Until recently, it was generally accepted that UVB exposure rises 4% for each 305-m (1000-foot) rise above sea level. However, Rigel and colleagues247 demonstrated an 8% to 10% increase in UVB for each 305-m (1000-foot) rise above sea level. Beginning at the 3353-m (11,000-foot) summit of a ski run in Vail, Colorado, these investigators measured UVB readings every 152 m (500 feet) as they skied to the base of the run at 2500 m (8200 feet). This study showed that UVB exposure readings in Vail, Colorado (latitude 39 degrees North) at 2591 m (8500 feet) approximated readings made under similar conditions—but 772 miles nearer the equator—at Orlando, Florida (latitude 28 degrees North, elevation 18 m [60 feet]). Snow, wind, and altitude may act simultaneously to greatly augment UVB exposure for skiers and climbers. Singh and coworkers271 reported that 36% of climbers (24 of 67) developed significant sunburns during three consecutive expeditions up to 7000 m (23,400 feet) in the western Himalayas, despite the application of sunscreen. During a year-long study of professional Alpine mountain guides with the use of continuous dosimetry monitoring, Moehrle and colleagues210 confirmed exceedingly high cumulative UVR exposures. These data emphasize the difficulties of providing appropriate UVR protection for high-altitude outdoor enthusiasts.

OZONE DEPLETION AND ULTRAVIOLET RADIATION EXPOSURE Stratospheric ozone, which lies 15 to 50 km (9.3 to 31.1 miles) above Earth’s surface, provides a thin and fragile shield against UVR. The combination of ozone and oxygen absorbs virtually the entire incidence of UVC. Ozone attenuates UVB and modestly reduces UVA II, but it allows the transmission of all UVA I.323 Ozone is continuously created and removed from the stratosphere by natural physicochemical processes that are in turn significantly affected by manmade pollution. Molina and Rowland211 first suggested that chlorofluorocarbons (CFCs) could cause ozone depletion. CFCs are organic chemicals that contain carbon, chlorine, and fluorine that were initially developed during the 1970s as refrigerants. Since then, CFCs have been used in several technologies and industrial processes, including air-conditioning systems, insulation, cleaning solvents, degreasing agents, and metered-dose inhalers. Related compounds known as halons contain bromine, which also depletes stratospheric ozone. Halons arise from seawater, fire extinguishers, and various industrial processes.128 CFCs and halons belong to the group of chemicals known as halocarbons.

The remarkable stability of CFCs allows them to rise into the stratosphere, where, when catalyzed by solar radiation, they release chlorine (Cl−) and chlorine monoxide (ClO−), which in turn degrade ozone. One prominent chemical pathway by which CFCs deplete ozone is as follows:128 Cl − + O3 → ClO− + O2 O3 + UVR → O + O2 ClO− + O → Cl − + O2 Net reaction: 2O3 + UVR → 3O2 Note that Cl− is preserved in this reaction. The half-life of Cl− is approximately 75 years,309 although CFCs may reside in the stratosphere for 50 to 200 years.128 During that time, each Cl− ion may destroy 100,000 molecules of ozone.309 Over Antarctica, additional and augmented ozone-depleting mechanisms may be operative; molecular halogens coat the surface of ice clouds, thereby making them even more reactive and able to degrade ozone.128 Ozone losses were first reported over Antarctica in 198576 by the British Antarctic survey. Ozone showed large declines in the austral springtime (September/October), and it decreased a total of 35% during the springtimes that occurred from 1975 to 1984.128 Ozone depletion is now documented at all latitudes except the equator. This depletion is uneven, with more loss at the poles and less at the middle latitudes.309 There is also a well-documented “waxing and waning” that occurs with the seasons. With the use of its total ozone mapping spectrometer in satellite orbit, the National Aeronautics and Space Administration has documented ozone depletion over continental Europe, North and South America, South Africa, New Zealand, and Australia.169 Significant increases in UVB have been documented, even near the middle latitudes, because of ozone depletion. In Toronto from 1989 to 1993, Kerr and McElroy151 documented surface UVB increases of 35% per year in winter and 7% per year in summer, which corresponded with ozone decreases of 4% per year and 1.8% per year, respectively. Their experimental design allowed for assignment of all of the UVB increase to ozone depletion rather than to cloud coverage or pollution. Similar increases in ground-level UVB that parallel decreases in stratospheric ozone have been documented in Scotland.215 Typically, in the northern hemisphere’s middle latitudes, ozone losses are greater during winter (i.e., about 6% per decade) than during summer (i.e., about 3% per decade).128 Ironically, pollution (e.g., smog, particulates) may mitigate UVR increases by absorbing UVB.309 295

PART 3  BURNS, FIRE, AND RADIATION

The effects of ozone depletion on the biosphere and human skin cancer rates have been estimated. Although these estimates vary, data suggest that, for every 1% decrease in ozone, there is a corresponding 2% increase in the incidence of basal cell carcinoma (BCCa) and 3% increase in the incidence of squamous cell cancer (SCCa).59 Melanoma incidence may increase by 1%.309 However, even if UVB triples near the poles, as is suggested in worst-case scenarios, polar areas will still receive less UVB than current equatorial levels.309 Ozone depletion may have its greatest effects on nonhuman biosystems. Plant and plankton yields may be diminished significantly, causing an uncertain and potentially severe detriment to terrestrial and marine life.323 To prevent ecologic disturbances and to restore ozone levels, international agreements have been negotiated. The Vienna Convention in 1985 and subsequent Montreal Protocol in 1987 were among the first and most notable. The Montreal Protocol, which has now been signed by 184 of the 191 United Nations member nations,299 agreed to limit and then reduce CFC production, which led to a 50% reduction by 1998.128 Three later amendments were made to accelerate progress in response to increasing awareness of ozone depletion in the middle latitudes. The London Amendment in 1990 required the complete phaseout of halocarbon production. The Copenhagen Amendment in 1992 accelerated the timetable for complete phaseout, stopping production in developed countries by 1996 and in undeveloped nations within 10 years; it also extended the protocol to include hydrochlorofluorocarbons. The Vienna Amendment in 1995 revised the phaseout schedule of hydrochlorofluorocarbons.128,273 Although the Montreal Protocol is working—CFC production has been decreased by 90%299—its modest limitations would allow elevated stratospheric chlorine levels through most of the 21st century.128 By contrast, the stricter limitations of the Copenhagen Amendment will result in ozone levels rising again within the first decade of the 21st century.273 Among the remaining sources of CFC production are metered-dose inhalers and cleaning agents for rocket motor manufacturers.128 American factories could produce 53,500 tons of CFCs annually for export until 2005.23 CFC substitutes are more costly, with an estimated 22,000 tons being produced in 1994.23 This led to an international black market in CFCs. A significant portion of this black market is in Freon that is smuggled to automobile air-conditioner rechargers. In 1996, an estimated 10,000 tons of CFCs were smuggled into the United States from Mexico and elsewhere.83 Despite these black-market sources, initial projections suggested that atmos­ pheric chlorine would begin to fall in this decade, with resultant UVB levels gradually falling by 2050 to levels that were recorded during the 1950s. Unfortunately, recent data suggest that current global warming trends exacerbate ozone depletion and may delay the recovery of the ozone layer.299

Acute Effects of Ultraviolet Radiation on Skin: Sunburn and Tanning The effects of UVR on skin depend primarily on wavelength, length of exposure, intensity of exposure, repetition of exposure, age at time of exposure, site of exposure, and genetic factors of the individual who is exposed. To have a biologic effect, UVR must be absorbed. Absorbing molecules in the skin are known as chromophores, and different wavelengths of UVR are absorbed by different chromophores. Among these are nucleic acids (especially pyrimidine bases), various amino acids in cutaneous proteins, and lipoproteins in cell membranes. These chromophores are at varying depths in the skin, accounting in part for the differing photobiologic responses to UVR. To date, there is only imprecise—but improving—knowledge of how a given photochemical reaction results in a specific biochemical product, thereby leading to an observable clinical change.

ULTRAVIOLET C RADIATION UVC has no appreciable impact on human health, as it is effectively screened from Earth’s surface by stratospheric ozone and 296

oxygen. Even with continued ozone depletion, levels of UVC are not expected to rise. As mentioned, manmade sources of UVC such as germicidal lamps and arc-welding devices have been only rarely associated with cutaneous pathology as might be predicted, because UVC is effectively absorbed by the stratum corneum, which is the outermost cutaneous layer.84

ULTRAVIOLET B RADIATION UVB acutely induces a cutaneous inflammatory response that is at least partially definable clinically, histologically, and biochemically.137 Clinically, erythema or sunburn is the hallmark of acute overexposure to UVB. The action spectrum for erythema peaks with UVB.217 Generally, UVB is considered to be 1000-fold more effective than UVA for induction of erythema. In a human model, 300-nm UVB is 1280-fold more effective at inducing erythema than 360-nm UVA.324 Erythemogenic doses are usually defined as multiples of the minimal erythema dose (MED), which is the lowest dose that elicits perceptible erythema. In a typical fairskinned individual, the MED might range from 15 to 70 mJ/cm2 for UVB and from 20 to 80 J/cm2 for UVA. For example, 1 MED of UVB for a typical fair-skinned individual would require 20 minutes of midsummer exposure in San Diego, whereas 1 MED of UVA would require 2 to 3 hours of exposure. In a day’s time, a person can receive 15 MEDs of UVB but only 2 to 4 MEDs of UVA.200 Consequently, although people are exposed to 10-fold to 100-fold more UVA than UVB, more than 90% of sunlight-induced erythema is attributable to UVB. The erythema action spectrum, which peaks in UVB, is remarkably similar to the absorption spectrum of DNA,217 which suggests that DNA is a principal target chromophore for UVBinduced erythema325 and pyrimidine dimer formation. Supporting this is the finding that pyrimidine dimer yields correlate with erythema.116 Sunburn reflects a local vascular reaction. The causes are multifactorial: DNA damage, prostaglandin activation, cytotoxicity, and other mechanisms are implicated. UVB erythema has its onset 2 to 6 hours after exposure; it peaks at around 12 to 36 hours and fades after 72 to 120 hours.84,137,147 Acute histologic changes that accompany UVB exposure include edema with vasodilation of the upper dermal vasculature137 and endothelial cell swelling, most likely as a result of vasoactive mediators being released.112 Delayed histologic changes include the appearance of sunburn cells in as little as 30 minutes after exposure. These dyskeratotic cells have enlarged nuclei and vacuolated cytoplasm. Initially, sunburn cells are localized in the lower one-half of the epidermis; however, after 24 hours, they are also found in the upper half. These sunburn cells may represent actively cycling and proliferating basal cells that cannot adequately repair UVR-induced DNA lysosomal damage.55 Beginning 1 hour after exposure, stainable Langerhans’ cells (i.e., cutaneous antigenpresenting cells) are reduced by 25%; by 72 hours after exposure, only 10% remain.137 In mice that are exposed to repetitive suberythemogenic doses of UVB, normal numbers of Langerhans’ cells return by 8 days after exposure.137 Vacuolization of melanocytes is seen after 1 hour and returns to normal 4 to 24 hours after exposure.137 Mast cells decrease in number and granularity within 1 hour, returning to normal after 12 to 72 hours.137 By 24 to 48 hours after exposure, there is increased melanin synthesis, epidermal proliferation, and thickening of the stratum corneum. Functionally, the epidermal permeability barrier diminishes after UVB exposure because of the altered kinetics of lamellar-body– containing cells in the exposed epidermis.133 Biochemical changes that accompany sunburn include increased levels of histamine,137 which return to normal within 74 hours. However, histamine is unlikely to be the sole or even the principal mediator of vasodilation and erythema, because antihistamines are ineffective in preventing sunburn. UVR induces increased phospholipase activity, with accompanying increases in prostaglandins (PGs). PGD2, PGE2, PGF, and 12-hydroxyeicosatetraenoic acid are increased in suctioned blister aspirates immediately after UVB exposure, and peak after 18 to 24 hours.137 Topical and intradermal indomethacin, which is a prostaglandin inhibitor, blocks UVB-induced erythema for 24 hours after exposure,275 thus supporting the thesis that

ULTRAVIOLET A RADIATION UVA penetrates more deeply into the skin than does UVB. Whereas 95% of incident UVB is reflected or absorbed by the epidermis, nearly 50% of UVA reaches the dermis.75 UVA contributes modestly to sunburn and may cause clinical erythema. Prolonged daily UVA exposure can approach 125 J/cm2, which significantly exceeds the threshold erythema dose of 20 to 80 J/ cm2.278 Clinically, UVA erythema has an onset within 4 to 6 hours; it peaks after 8 to 12 hours and fades after 24 to 48 hours.137,147 Erythema that results from UVA may have a distinct pathophysiologic mechanism. UVA-induced erythema may be caused by keratinocyte cytotoxicity.137 Histologically, UVA erythema displays more epidermal spongiosis, fewer sunburn cells, and more dermal changes than does UVB-induced erythema, with a denser and deeper mononuclear cell infiltrate and more vascular damage.137

INFRARED RADIATION IR radiation plays a less well-defined role in photodamage. Near-IR preirradiation prevents UVR-induced cytotoxicity,200 which suggests that a possible evolutionary protective mechanism for IR is the daily preparation of skin cells to resist UVRinduced damage. However, no data indicate whether IR protects against UVR’s mutagenic and carcinogenic effects.

SUNBURN TREATMENT Sunburn is self-limited, and its treatment is largely symptomatic, involving local skin care, pain control, and antiinflammatory agents (Box 14-1).15 Studies that have assessed the treatment of sunburn can be divided into those that evaluated the agents used immediately after UV exposure (i.e., before symptoms have manifested) and those that evaluated the agents for the actual treatment of acute sunburn reactions.121 Cool-water soaks or compresses may provide immediate relief, and topical anesthetics are sometimes useful. It is generally preferable to use the nonsensitizing anesthetics menthol,

BOX 14-1  Sunburn Treatments Pain Control Acetylsalicylic acid Nonsteroidal antiinflammatory drugs Skin Care Cool soaks and compresses Nonmedicated moisturizers Topical anesthetics Pramoxine (Prax) lotion Menthol plus camphor (Sarna) anti-itch lotion Anti-itch concentrated lotion (Pramoxine) plus camphor plus calamine (Aveeno) Lidocaine plus camphor (Neutrogena Norwegian Formula) soothing relief moisturizer Steroids Topical (e.g., triamcinolone 0.1% cream applied twice daily when erythema first appears) Systemic

camphor, pramoxine, and lidocaine rather than the potentially sensitizing anesthetics that contain benzocaine and diphenhydra­ mine. Refrigerating topical anesthetics before application provides added relief. A legion of topical remedies have been suggested anecdotally. These include aloe, baking soda, and oatmeal, but controlled studies are lacking. Topical steroids, with their vasoconstrictive effects, are often considered “first-line” treatment for acute sunburn; however, their efficacy remains controversial. A randomized, double-blind clinical trial of 20 patients with Fitzpatrick skin types I, II, and III compared erythema reactions in areas that were treated with either topical moderate-potency corticosteroid (hydrocortisone-17-butyrate) or high-potency corticosteroid (clobetasol propionate) 30 minutes before and 6 or 23 hours after exposure to UVB (i.e., a bank of TL12 fluorescent tubes); only the areas that had been treated with high-potency corticosteroid 30 minutes before UVB exposure demonstrated clinically significant results.78 Diclofenac gel, which is a topical nonsteroidal antiinflammatory drug, alleviates pain, erythema, and edema for up to 48 hours when it is applied after exposure.152 Oral nonsteroidal antiinflammatory drugs provide analgesia and may reduce sunburn erythema.84 According to a recent Medical Letter, the combined use of topical steroids and oral nonsteroidal antiinflammatory drugs slightly decreases erythema during the first 24 hours if these drugs are administered before exposure or shortly after exposure, before sunburn becomes clinically apparent.238 Few published studies support the value of systemic steroids, but they enjoy considerable anecdotal support. In a metastudy of all published articles related to sunburn treatment from 1966 to 2001, Han and Maibach121 found no therapy to be unequivocally or consistently effective and no consensus for the treatment of sunburn. Moreover, education for acutely sunburned patients is lacking. Warnings regarding skin cancer are rarely given to sunburned patients when they are seen in the emergency department.15

TANNING Tanning, like sunburning, is caused by UVR. Consequently, persons who are seeking a tan risk sunburn. Tanning is biphasic. After sun exposure, there is immediate pigment darkening within minutes, followed by delayed pigment darkening (DPD) in 3 days. Immediate pigment darkening is predominantly the result of the action of UVA on preformed melanin precursors; it occurs in as little as 5 minutes after exposure, peaks in 60 to 90 minutes, and then fades quickly. However, DPD represents new melanin synthesis within melanocytes and the subsequent spread of the richly melanized melanosomes into surrounding keratinocytes. After UVB exposure, DPD is notable by 72 hours, peaks after 5 to 10 days, and then slowly fades. DPD is primarily a response to UVB. Most tanning studies have been performed with erythemal doses of UVR. However, multiple suberythemal exposures to UVA are significantly more melanogenic than is similarly dosed UVB.20 The mechanism of DPD is uncertain, but it is likely to be multifactorial. UVB stimulates tyrosinase release and arachidonic acid metabolites, and it releases α-melanocytestimulating hormone from keratinocytes.7 It also increases the binding affinity of melanocytes for melanocyte-stimulating hormone, thereby resulting in increased melanocyte proliferation, melanization, and arborization.29 UVB increases melanocytes in both exposed and protected human skin,282 which suggests the possibility of a UVR-stimulated circulating factor that promotes melanocyte proliferation.

Chronic Phototrauma NATURAL DEFENSES AND SKIN TYPE Absence of erythema does not preclude cutaneous photoreactions. Chronic exposure to UVR is accompanied by insidious cumulative biologic and clinical changes. Although some of these changes are the result of broadband UVR, UVA and UVB often have distinct and different effects on the epidermis, dermis, extracellular matrix, cytokines, and immune response.311 In response to UVB, the stratum corneum thickens110 and melanin increases; both of these are protective mechanisms to mitigate 297

CHAPTER 14  Exposure to Radiation From the Sun

eicosanoids (PGs and leukotrienes) are significant mediators of UVR-induced inflammation.160 UVB stimulates induction of proinflammatory and mutagenic cytokines: tumor necrosis factor-α and interleukins 6 and 12.133 UVR generates free radicals in the skin that probably contribute to the sunburn reaction193 by causing peroxidative chromosomal, membrane, and protein damage.16 Topical antioxidants may mitigate sunburn when they are applied before but not after exposure. Melatonin16 and vitamin C57 act protectively by scavenging UVR-generated free radicals; however, neither absorbs UVR.

PART 3  BURNS, FIRE, AND RADIATION

BOX 14-2  Skin Types I Always burns; never tans II Often burns; tans minimally III Sometimes burns; tans moderately IV Burns minimally; tans well V Rarely burns; tans deeply; moderately pigmented (brown) VI Never burns; deeply pigmented (black)

further UVB photodamage. The stratum corneum, which is the outermost layer of skin, is composed of flattened anucleate keratinocytes. It reflects, scatters, or absorbs up to 95% of incident UVB, depending largely on its thickness.123 With repeated exposure to UVB, the stratum corneum can increase its thickness up to sixfold.84 As a consequence, the stratum corneum is the main photoprotective factor in whites.110 Repeated UVA exposures may cause some thickening,178 but to a much lesser degree. Consequently, UVA tans are not as photoprotective as are UVB tans. Melanin reflects, scatters, and absorbs throughout the UVR spectrum; it acts as an antioxidant, and it reduces UVR-induced photoproducts.157 Consequently, constitutive (racial) skin color is a principal determinant of an individual’s erythemal response to UVR. Although blacks and whites have similar numbers of melanocytes, these pigment-forming cells are differently melanized and distributed in black and white skin. Increased melanin in blacks can decrease the dermal penetration of UVR up to fivefold53 and increase the MED up to 30-fold. By contrast, tanning is much less protective. After an entire summer of tanning, the MED in whites increased only 2.3-fold.53 Clinically, these racial differences in melanization are reflected in lower rates of burning, photoaging, and skin cancer in blacks. Susceptibility to photodamage is typically defined by six distinct skin types (Box 14-2). Racial pigmentation alone does not account for differences in skin type. Some redheads tan easily, whereas some blacks burn readily. Reporting errors (typically involving the overstating of sun tolerance) are common, thus further complicating the interpretation of skin types.239 Skin type correlates well with MED. Additional factors that influence MED include age and anatomic site. Lower MEDs are recorded in the very young and the very old.147 Differences in stratum corneum thickness and melanocyte concentration may account for body-site–specific differences in MED. For example, the MED of the back is typically less than the MED of the lower leg. Chronic suberythemal UVA exposures also cause photodamage. Repetitive low-dose exposures to UVA result in histologic changes,170,178 including the thickening of the stratum corneum and of the granular and stratified cell layers, decreased elastin, vascular dilation, and inflammation. Aside from the thickened stratum corneum and increased pigmentation, intrinsic mechanisms of photoprotection include antioxidants, such as the glutathione peroxidase-reductase system, that mitigate damage from UVR-induced reactive oxygen species. DNA repair enzymes correct most UVR-induced mutations. Carotenoids stabilize biologic membranes from singlet oxygen attack. Urocanic acid absorbs some of the UVR that penetrates the stratum corneum.58

Chronically sun-exposed sites have fewer Langerhans’ cells. Keratinocytes and fibroblasts from sun-damaged skin have diminished life spans in culture.104 The most notable histologic change with chronic UVB exposure is deposition of thickened amorphous elastic fibers high in the dermis, which is demonstrable in photoexposed white skin by the age of 30 years. In a transgenic mouse model, UVB but not UVA produces this solar elastosis.294 Another mouse model suggests that the action spectrum for “photosagging” peaks in UVA at 340 nm122 and that this action spectrum is remarkably similar to that of the generation of singlet oxygen by the excitation of transurocanic acid. The authors of that study concluded that UVA causes photoaging because of its interaction with transurocanic acid, which releases reactive oxygen species. With photoaging, elastin gene expression appears to be activated, although data are conflicting. Tropoelastin and fibrillin synthesis actually diminish with chronic UVB exposure,310 whereas transcription of other extracellular matrix genes is enhanced. In particular, photoaged skin demonstrates increased matrix metalloproteinases, which are potent mediators of connective tissue damage.80 These arise within hours of UVB exposure and even after suberythemal exposure.79 Interestingly, tretinoin inhibits induction of these UVB-induced proteinases,79,80 perhaps explaining in part its clinical usefulness against photoaging.223,308 Tretinoin also normalizes photoaltered epidermal differentiation and deposits new type I collagen in the upper dermis.115

OCULAR EFFECTS Acute overexposure to UVB may cause photokeratitis (snowblindness), especially in skiers and climbers,326 whereas chronic exposure to UVR may cause or contribute to pterygia, cataracts, and macular degeneration. A full discussion is presented in Chapter 28.

A

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PHOTOAGING Long-term repetitive exposures to sunlight result in photoaging.80 This process, known as dermatoheliosis, is distinctive clinically and histologically from chronologic aging; it is not merely accelerated chronoaging. Photoaged skin is characterized by dryness, roughness, mottling, wrinkling, atrophy, and pebbling, and it may be studded with precancers (actinic keratoses) or cancers (Figure 14-2). Most of what we consider “old-looking” skin is in fact the result of photoaging rather than chronoaging. Although age can be estimated from observing sun-exposed sites, it cannot be estimated from photoprotected sites.307 The action spectrum for photoaging includes UVB, UVA, and IR.178 298

FIGURE 14-2  Phototrauma. A, Tan and peeling after sunburn. B to D, Dry, mottled, wrinkled, and pebbled skin with photoaging.

CHAPTER 14  Exposure to Radiation From the Sun

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D

FIGURE 14-3  A, Actinic keratoses: thin, vague, and scaly papules. B, Basal cell carcinoma: smooth, pearly papule. C, Squamous cell carcinoma: keratotic red and tan papule. D, Melanoma: note the asymmetry, border irregularity, color variegation, and diameter of more than 6 mm (0.24 inch).

SUN AND SKIN CANCER Actinic keratoses (solar keratoses) are considered by many dermatologists to represent in situ dysplasias that result from exposure to solar irradiation. The majority of these lesions are characterized clinically as being 0.3 to 2 cm (0.12 to 0.79 inch) in size, multiple, sharply bordered, irregularly shaped pink papules with adherent scale. It is often easier to appreciate actinic keratoses as “rough spots” via direct palpation than by visual detection alone. A hypertrophic type exists and may lead to cutaneous horn formation, especially on the dorsal surfaces of the hands and the extensor forearms. Actinic keratoses may be tender when rubbed or shaved over with a razor. They are predominantly located in chronically sun-exposed areas. Actinic keratoses tend to be more common in lighter skin, and they typically appear in people who are more than 50 years old, although fair-skinned patients who live in areas of high solar irradiation may develop them much earlier (i.e., at the age of 20 to 40 years). Actinic keratoses may be prevented by sun avoidance and a diet that is low in fats. Treatment strategies range from cryosurgery and topical chemotherapy with 5-fluorouacil or imiquimod to chemical peels, laser resurfacing, and photodynamic therapy. The consideration of skin biopsy is warranted when the lesion is larger than 0.6 cm (0.24 inch), if there is a palpable dermal component, or when the lesion persists despite appropriate therapy. Like precancerous actinic keratoses, true skin cancers (Figure 14-3) are believed by most dermatologists to be overwhelmingly caused by UVR exposure. In particular, UVR is the principal cause of NMSC (i.e., BCCa and SCCa), which is the most common of all cancers. UVR also contributes significantly to melanoma, but it is not a sine qua non. The incidence of skin cancer is staggering. One in five Americans247 and two-thirds of all Australians13 born today will develop skin cancer. In addition, the incidences of both NMSC108 and melanoma continue to increase.246 Three causative factors seem to predominate: • Lifestyle trends, including sun exposure, sunbathing, and tanning bed use

• Aging of the population • Ozone depletion Since the 1890s, epidemiologic evidence has accumulated that links sun exposure with NMSC in humans. The incidence of skin cancer increases with increasing proximity to the equator.54 NMSC has a far greater incidence in whites than in blacks, and occurs primarily on sun-exposed areas. Risk for NMSC increases with increasing sun exposure, and repeated sunburn is an independent risk factor.164 Adopting a sun-protected lifestyle is associated with decreased risk.130 Patients with xeroderma pigmentosum (XP), which involves a deficient ability to repair UVR-induced DNA damage, have a 1000-fold greater risk of developing NMSC, typically at a very early age.160 During the 1920s, laboratory data confirmed that UVR induces and promotes NMSC in mammalian animal models.147,287 UVC and UVB are effective inducers of SCCa in mice.137 Although UVB is primarily implicated, UVA augments UVB-induced carcinogenesis,287 and can be a carcinogen on its own. Development of NMSC in humans is related to the time and intensity of exposure. Sun exposure during childhood and adolescence is more predictive of later BCCa.88 British immigrants to Australia assume the much higher Australian risk of NMSC only if they emigrate before the age of 18 years; after that time, these immigrants retain the lower British risk.189 A separate study suggests that risk decreases after the age of 10 years.163 Gallagher and co-workers88 found that BCCa is associated with sun exposure up to the age of 19 years but that it is not associated with mean annual cumulative summer sun exposure. In this study, risk for BCCa was also associated with fair complexion and freckling. Kricker and colleagues164 suggest that intermittent (rather than continuous) sun exposure in poor tanners is the most important factor in development of BCCa. Clinically, BCCa includes a heterogeneous group of low-grade malignant cutaneous tumors that are characterized by differentiation markers that are usually associated with hair-follicle development. BCCa is the most common cancer in the United States, and, although it can be locally aggressive, it is almost never 299

PART 3  BURNS, FIRE, AND RADIATION

FIGURE 14-5  Basal cell carcinoma demonstrating characteristic “rolled” borders and central ulceration.

FIGURE 14-4  Pink, pearly papule with a rolled border and overlying telangiectasias located on the right pectoral area of a 55-year-old surfer from San Diego; biopsy revealed a basal cell carcinoma.

metastatic. These lesions are most commonly found on the head and neck (Figure 14-4), but any part of the body may be involved. Interestingly, in contrast with SCCa, BCCa is relatively uncommon on the dorsal surface of the hand, where solar radiation exposure is high. Several clinical morphologies of BCCa exist, and the diagnosis depends on the astute clinician recognizing the many forms that are taken by this cancer. Nodular BCCa, which comprises the majority of BCCa, may manifest as one or a few small, pearly papules with a central depression and “rolled borders” (Figure 14-5). Telangiectasias may be seen coursing through the lesion; the lesions are usually friable, and they frequently bleed when rubbed with a cotton-tipped swab. Pigmented BCCa is similar to nodular BCCa, but this morphologic type appears brown or black because of the presence of pigment. Cystic BCCa manifests as bluish-grey, dome-shaped cystic papules or nodules that are similar in appearance to hidrocystomas. Morpheaform BCCa manifests as a white sclerotic plaque, usually without the characteristic findings of a pearly, “rolled” border; for this reason, it is often missed or misdiagnosed as a scar. Superficial BCCa, which is the most common pattern seen in patients with human immunodeficiency virus, is another common form of BCCa that favors the trunk and distal extremities; it usually manifests as a superficial, dry, scaly lesion that can resemble patches of slow-growing eczema or psoriasis, although close examination reveals the raised border. Rodent ulcer is a neglected BCCa that has ulcerated; consequently, the “rolled” border of the lesion may not be present or recognizable.

A

SCCa, which is the second most common form of skin cancer, manifests clinically as dull-red, superficial, indurated, welldemarcated plaques that arise on sun-exposed areas such as the face and dorsal surfaces of the hands. Lower-lip lesions may develop with actinic cheilitis; in these cases, a history of repeated sunburns and smoking are predisposing factors. As the lesions grow over the course of months, they become deeply nodular and ulcerate (Figure 14-6, A and B). The ulcer may be hidden by an overlying crust that, when removed, reveals a discrete, indurated, and elevated base. Careful examination of regional lymph nodes is warranted in suspected cases. The rate of metastasis from all skin sites ranges from 0.5% to about 5%; risk factors that can increase this rate include a location that involves the temples, scalp, ear, or lip; recurrence after prior treatment; size and depth of the primary lesion; histologic findings; and host immunosuppression. The relationship of photoexposure and SCCa is distinct and different from that of the sun and BCCa. There is a significantly increased risk of SCCa with chronic occupational exposure, especially during the 10 years before diagnosis.89 Although cumulative lifetime photoexposure and SCCa are not associated, risk factors include periodic recreational exposure, pale complexion, and red hair. Persons who develop SCCa seem to be phenotypically sensitive to UVR, with chronic exposure as adults. Household and office exposure to nonsolar UVR does not increase the risk of BCCa and SCCa.14 In select mouse models, suberythemal UVR has caused SCCa.217 In these models, gradual suberythemal exposures to UVR may actually be more carcinogenic than are erythemal doses.87 This may be relevant to humans, and it may explain why persons without any prior sunburns may develop SCCa.

MELANOMA Melanoma includes a number of different clinicopathologic types. Nodular melanomas are typically smooth, dome-shaped, and

B

FIGURE 14-6  Squamous cell carcinoma. A, Neglected squamous cell carcinoma on lateral and posterior shoulder. B, Closer image of the same carcinoma.

300

FIGURE 14-7  Melanoma on the posterior helix, which made early selfdetection difficult.

FIGURE 14-8  “Yin-yang”–shaped melanoma on back demonstrating asymmetry, color variegation, and a diameter of more than 6 mm  (0.24 inch). The location made early self-detection difficult.

a prior sunburn than are age-matched controls, and they are three times as likely to relate a history of multiple prior sunburns.73 Persons who tan poorly and burn readily are at higher risk for melanoma.180 The distribution of melanomas on the trunk (in both sexes) and the lower legs (in women) is consistent with the hypothesis that intermittent sun exposure is provocative. However, melanomas also arise in sun-protected sites, especially in nonwhite populations, which suggests an additional cause that is separate from sun exposure. A high level of outdoor activity during college is associated with a fourfold risk of later melanoma.72 Servicemen who served in the Pacific theater during World War II have a higher risk of melanoma than do those who served in Europe.39 The incidence of melanoma is increased in indoor workers with higher socioeconomic status, again reflecting the role of intermittent intense sun exposure.149 Fluorescent lights raise some concern,305 but they do not significantly increase melanoma risk, especially when these lights have covers or diffusers.135 Sunburns in childhood may be particularly relevant to the later development of melanoma. Celtic migrants to Australia who arrived before the age of 10 years assume the high melanoma risk of native Australians; migrants who are more than 15 years old on arrival have only one-fourth that risk.255 Europeans who live more than 1 year in a sunny climate have an increased relative risk (i.e., 2.7) of melanoma, and the risk increases substantially (i.e., 4.3) if they arrive before the age of 10 years.10 However, one study suggests that childhood sun exposure contributes a serious risk only if there is subsequent and significant sun exposure as an adult.8 This association of increased melanoma risk with sun exposure during youth may be in part attributable to the effect of sun on the development of melanocytic nevi (moles) in children. Several studies confirm that the number of nevi in children increases with increasing acute and chronic sun exposure.* In Australia, the number of nevi up to the age of 12 years increases with increasing proximity to the equator.150 Increased nevus counts with sun exposure are demonstrable at early ages. In Queensland preschoolers between the ages of 0 and 35 months, increased nevus counts are associated with more time spent outdoors and a history of sunburn.125 These children have the highest number of nevi in the world, and, not surprisingly, Queensland has the highest incidence of melanoma in the world126 at 55.8 per 100,000 for males and 42.9 per 100,000 for females.13,25 The number of nevi is a strong predictor of melanoma risk. Melanoma increases with increasing numbers of benign acquired nevi. In a large European case-controlled study, the most important risk factors for melanoma are the number of nevi and the number of atypical nevi.93 Established nevi may develop histologic changes transiently, thus simulating melanoma *References 37, 92, 93, 125, 126, 302.

301

CHAPTER 14  Exposure to Radiation From the Sun

friable lesions that most commonly occur on sun-exposed areas of the head, neck, and trunk. They are twice as common in men as in women. Lentigo maligna manifests as a tan macule on sundamaged skin, typically among older patients who live in sunny climates; this type of melanoma may darken and spread so slowly that patients are often unaware of changes (Figure 14-7). Superficial spreading melanoma has no known preference for sundamaged skin, and affects adults of all ages. Color variegation (i.e., dark brown, black, red, white, blue) is common with this type of melanoma (Figure 14-8). These lesions may arise de novo or in association with a preexisting nevus; a new papule or nodule may develop as the vertical growth phase develops. Acral lentiginous melanoma, which is the most common type of melanoma in dark-skinned and Asian populations, may begin as a light brown and uniformly pigmented macule or patch that gradually darkens, thickens, and ulcerates with time. Subungual or plantar lesions are often present, and Hutchinson’s sign (i.e., a black discoloration of the proximal nail fold at the end of a hyperpigmented linear streak) portends melanoma in the matrix of the nail. Amelanotic melanoma is difficult to discern clinically, because it lacks pigment and may mimic a benign inflammatory papule or BCCa. Other types include ocular, mucosal, polypoid, desmoplastic, and soft-tissue melanomas. Melanoma has a less well-defined relationship with sun exposure; clearly, however, sun exposure plays a significant role in its development.6 The ultraviolet action spectrum for melanoma remains uncertain, with different results in different animal models. In Monodelphis domestica, a South American marsupial, both UVA and UVB are implicated63; in Xiphophorus (platyfish and swordtails), UVA, UVB, and visible (blue) light are causative63; and in transgenic mice Tyr-SV40E (C57BL/6 strain), UVB is the etiologic waveband.153 In humans with XP, the 1000-fold increased incidence of melanoma strongly supports UVB as a causative agent.161 A unique and elegant laboratory experiment documented that UVB induces melanocytic hyperplasia, atypia, and melanoma in newborn human foreskin xenografts on RAG-1 (immunodeficient) mice.7 Melanoma incidence increases with proximity to the equator in white populations149 in the United States, Australia, and Scandinavia as well as in the nonwhite population of India.167 In the U.S. Surveillance, Epidemiology, and End Results Program from 1992 to 2001, the incidence of melanoma increased with lower latitudes in non-Hispanic whites; no association was noted in Hispanics or blacks.69 In contrast, Hu and co-workers138 noted a positive association of lower latitude and UVR exposure with melanoma in blacks and Hispanics in the United States, although statistical significance was reached for black men only. Intermittent intense exposures pose a particularly high risk for melanoma.71 A meta-analysis of 57 studies published before September 2002 supports a significantly increased risk of melanoma with a history of intermittent sun exposure and sunburn.91 In contrast, there is only a small increased risk for total sun exposure, and there is decreased risk with heavy occupational exposure.73,91 Patients with melanoma are twice as likely to relate a history of

PART 3  BURNS, FIRE, AND RADIATION FIGURE 14-9  Melanoma on the back demonstrating the ABCDEs: asymmetry, border irregularity, color variegation, diameter of more than 6 mm (0.24 inch), and evolving features (i.e., the patient’s wife had noticed that the area at 9 o’clock was “growing out from the rest of it”).

after a single UVR exposure;291 some data suggest that sunburn can induce malignant transformation in benign nevi.47 In the United States, melanoma incidence has increased since records were first kept in the 1930s, rising 121% in the 20 years between 1973 and 1994.117 An estimated 68,130 Americans (29,260 women and 38,870 men) will have developed new cases of invasive cutaneous melanoma in 2010; an additional 46,770 cases of melanoma in situ will have been diagnosed that year as well.143 Today, the lifetime risk of melanoma for a male child born in the United States is 1 in 57; for a female child, the risk is 1 in 81.4 Similarly, large increases in melanoma incidence have been noted in Europe, Australia, and even Japan.149 However, melanoma incidence and death rates show signs of stabilizing and perhaps decreasing for younger cohorts,106,117,149 probably as a result of improved sun-protective behaviors. Significant national efforts have been made to educate and protect populations at risk. In Australia, taxes have been removed from sunscreen sales, hats are typically required for children when they are playing outdoor sports, and artificial shade is increasingly available in public parks. In addition to improved photoprotection, early detection has been widely promoted. The Skin Cancer Foundation encourages monthly self-examinations, with special attention to pigmented lesions that display atypical clinical features, which are the so-called ABCDEs of melanoma:235 asymmetry; border irregularity; color variegation; diameter of more than 6 mm (0.24 inch); and evolving features (Figure 14-9). Nevi with these clinical features, symptomatic nevi, or nevi that bleed should be evaluated by a dermatologist.

MOLECULAR BASIS OF PHOTOCARCINOGENESIS Several photomolecular events are associated with NMSC. UVR causes characteristic photoinsults at sites of adjacent pyrimidines on DNA.36,213,324 UVR photons are absorbed at the 5-5 double bonds, which results in cyclobutane dimers if both bonds open and 6-4 (pyrimidine-pyrimidone) photoproducts if a single bond opens.36 Cyclobutane dimers predominate 3:1, with thymine (T-T) dimers being the most common.160 Suberythemal and erythemal doses of UVR can induce T-T dimers.325 High-performance liquid chromatography can quantitatively measure these UVB photoproducts.42 Such measurements indicate 30-fold interindividual variation in photoproduct yields.42 Resultant UVR-induced mutations have a distinctive signature: two-thirds display cytosine → thymine (C → T) substitutions at dipyrimidine sites, and 10% show CC → TT substitutions.36 These mutations are relatively unique to UVR damage and allow UVR-induced mutations to be distinguished from chemical mutations.36 Data suggest that cyclobutane dimers and 6-4 photoproducts are primarily responsible for the mutagenic171 and carcinogenic160 properties of UVR. Many genes, including genes that are involved 302

in tumor suppression and promotion, may be targets for UVR mutations. Tumor-suppressor genes (TSGs) that are known to play a role in photocarcinogenesis include p53, p16, and PTCH.35,134 A mutation of p53, which is the most common genetic alteration identified in human cancers,134 is found in nearly 50% of all cancers.36,160 Approximately 50% of BCCa, 60% of actinic keratoses, and 90% of SCCa contain p53 mutations.36,328 Although p53 mutations may be found in non–sun-damaged skin at a low frequency, 10−2 to 10−3, mutations are much more common in sun-exposed sites.36 Normal p53 protein is a transcription factor that regulates the cell cycle. DNA damage stimulates p53 protein production, which leads to cell-cycle arrest in G1 (a premitotic phase), thereby allowing time for DNA repair.36 Irreparable damage leads to apoptosis or programmed cell death. Sunburn cells are examples of apoptotic cells.328 Cells with mutated p53 are more resistant to apoptosis with subsequent UVR exposures, which explains why p53 inactivation reduces sunburn cells in irradiated mouse skin.328 Within the p53 gene there are “hot spots:” these are codons where mutations frequently occur.36,43 Most p53 mutations result in a single amino-acid substitution, typically cytosine to thymine (C → T).328 Although normal, wild-type p53 has a short half-life and is generally unstable and unstainable, mutated p53 is significantly more stable and consequently stainable by immunohistochemical techniques.43,247 Both UVA and UVB upregulate p53 expression in human skin.46 After a single UVR exposure to the forearms, p53 protein expression peaks in 24 hours and returns to baseline after 360 hours.119 Mutations in p53 occur as an early initiating event in photocarcinogenesis.160 In actinic keratoses, unique p53 mutations are present throughout the lesion,328 which confirms that they occur before (rather than after) lesion formation. Different actinic keratoses display different p53 mutations, again supporting the role of p53 mutations as initial causative events that are followed by the clonal expansion of mutated cells to form clinically visible lesions of precancerous actinic keratosis.328 Altered p53 provides a survival advantage to mutated cells. In response to chronic UVR, neighboring nonmutated cells become apoptotic and die, thereby allowing space for the further expansion of the mutated clone with ongoing UVR exposure36 and ultimately resulting in development of actinic keratosis or SCCa. However, p53 mutations alone may be insufficient to produce NMSC. Patients with Li-Fraumeni syndrome, who inherit a mutated form of the p53 gene, have increased incidence of sarcomas, adenocarcinomas, and melanomas, but not NMSC.160 Consequently, other factors, such as decreased DNA repair and UVR-induced immunosuppression, must play a permissive role. For example, in patients with XP, there are increased numbers of p53 mutations36 and defective gene repair mechanisms as well as greatly increased numbers of NMSC. DNA repair may also be defective in normal patients who do not have the syndrome who develop BCCa at an early age306 as well as in older adult patients,213 who have a higher incidence of NMSC. Cutaneous lymphomas may also show a higher frequency of UVR signature p53 mutations.197 In mycosis fungoides, these mutations are found in the tumor stage but not the plaque stage,197 which suggests that UVR promotes the clinical progression of this lymphoma. These findings are particularly interesting in the light of epidemiologic data that demonstrate increased incidence of non-Hodgkin’s lymphoma among those who live closer to the equator.1 Other TSGs are less well studied but have increasingly defined roles in photocarcinogenesis. In melanoma, p16 is frequently inactivated139 and increasingly downregulated as melanoma progresses.277 Another TSG, PTCH, which is also located on chromosome 9, is frequently mutated in both familial and sporadic BCCa. Mutations of PTCH are especially notable in patients with XP and multiple BCCa.139 In addition to downregulating TSGs, UVR can activate protooncogenes to form functional oncogenes.139 Included in this group are the proto-oncogenes bcl-2, c-fos, and ras. In response to UVR, the bcl-2 protein is overexpressed, with resultant suppression of apoptosis and consequent permissive expansion of malignant clones. In addition, UVR alters c-fos, thereby disrupting transcription of nuclear proteins that are involved in cell

PHOTOIMMUNOLOGY UVR produces local and systemic immunosuppression.219 Locally, UVB depletes Langerhans’ cells, which are immunocompetent antigen-processing cells, for up to 2 weeks after exposure.208 In addition, UVB functionally alters Langerhans’ cells by interfering with their presentation of antigens to T cells,111 thereby diminishing helper T cell 1 responses (which promote contact hypersensitivity) while preserving helper T cell 2 responses257 (which suppress contact hypersensitivity), thereby effectively converting Langerhans’ cells from immunogenic to tolerogenic. Antigenspecific suppressor T cells arise; their appearance is possibly mediated by the UVR-induced synthesis of interleukin 10 from keratinocytes.257 As a consequence, contact hypersensitivity and mixed lymphocyte reactions are diminished with UVR exposure. This may at least partially explain why UVR-induced skin cancers, which are antigenic, progress to clinical lesions. In mice, this UVR-induced immunosuppression can be transferred with irradiated T lymphocytes.219 Other proposed mediators of UVR-induced immunosuppression include cis-urocanic acid,54 tumor necrosis factor-α, prostaglandins,217 and DNA photoproducts.209 Immunoregulatory failure contributes to formation of skin cancer.165 Skin cancer is often more aggressive and occurs at an earlier age among immunosuppressed patients.74,224 In Australia, 45% of kidney transplant patients develop skin cancer within 11 years, and 70% develop it within 20 years.32 For heart transplant patients in Australia, the incidence of skin cancer is 31% at 5 years and 43% at 10 years; skin cancer accounts for 27% of patient deaths in this group after the fourth post-transplant year.224 In these patients, the ratio of SCCa to BCCa is 3:1, which is the precise opposite of the ratio that is present in nonimmunosuppressed patients. These figures are unusual only because most studies suggest that the risk of skin cancer is higher after heart transplant than after kidney transplant because of higher doses of immunosuppressive drugs with the former. Chronic sun exposure and fair complexion further increase risk of skin cancer in transplant patients,224 possibly as a result of the overexpression of p53.99

Photoprotection SUNSCREENS Chemical sunscreens were discovered in 1926. By 1928, the first commercial sunscreen, which contained benzyl salicylate and benzyl cinnamate, was marketed in the United States.82 Subsequent sunscreen evolution was primarily directed toward UVB protection to mitigate development of sunburn from overexposure to the sun. Para-aminobenzoic acid (PABA) was first advocated as a sunscreen in 1942; it was patented in 1943 and made commercially available in 1960. By then, national advertisements for sunscreens were promoting the message that people would be able to tan without burning. Sun protection factor (SPF) 15 formulations became available around 1980. More recently, as

TABLE 14-1  Sunscreening Agents Approved in the

United States

Sunscreen Aminobenzoic acid Avobenzone Cinoxate Dioxybenzone Ecamsule* Homosalate Menthyl anthranilate (meradimate) Octocrylene Octyl methoxycinnamate (octinoxate) Octyl salicylate (octisalate) Oxybenzone Padimate O Phenylbenzimidazole sulfonic acid (ensulizole) Titanium dioxide Trolamine salicylate Zinc oxide

Maximal Screen (%) 15 3 3 3 2 15 5 10 7.5 5 6 8 4 25 12 25

Modified from the U.S. Food and Drug Administration: Sunscreen drug products for over-the-counter human use: Final monograph, Fed Reg 64:27666, 1999. *Approved by the U.S. Food and Drug Administration on July 21, 2006.

UVA photodamage has been increasingly appreciated, UVA sunscreening agents such as avobenzone have been introduced. Micronized preparations of titanium dioxide (TiO2) and zinc oxide (ZnO) have become popular, and they provide broadspectrum protection throughout the UVR range. Previously considered “physical” (reflective) as opposed to “chemical” (absorptive) sunscreens, these micronized preparations blur the traditional distinctions. Micronized TiO2 and ZnO are largely transparent and absorb, reflect, and scatter UVR.159 Consequently, chemical and physical labels for sunscreens are of diminishing value and perhaps should be dropped. In the United States, sunscreens are regulated over-the-counter drugs. The U.S. Food and Drug Administration’s (FDA) Final Overthe-Counter Drug Products Monograph on Sunscreens, which was published in the Federal Register on May 21, 1999, established the allowable sunscreening agents, testing procedures, and labeling claims for efficacy, water resistance, and safety.295 On June 17, 2011, the FDA published a final rule that updated the labeling claims and testing procedures of the 1999 Final Monograph.296 The current FDA-approved sunscreening ingredients are listed in Table 14-1. Two names are sometimes given for the same agent, because the U.S. Pharmacopeia changed the names of several sunscreening agents (effective September 1, 2002) to better conform to international standards.297 PABA is an effective UVB absorber that has fallen out of favor. Poorly water soluble, PABA must be formulated in an alcohol vehicle. On the skin, it binds epidermal proteins, thus enhancing its resistance to water removal (substantivity) but provoking contact and photocontact dermatitis in approximately 4% of exposed subjects. Further limiting its acceptability, PABA can permanently stain fabrics a dull yellow color. As a consequence, PABA has been largely replaced by PABA esters such as amyl dimethyl PABA (padimate A) and octyl dimethyl PABA (padimate O). These absorb well in the UVB range, are easier to formulate in nonalcoholic vehicles, and are less staining and less allergenic. Cinnamates are the next most potent UVB absorbers. They often replace PABA in PABA-free sunscreens, but octyl methoxycinnamate (octinoxate; Parsol MCX) is an order-of-magnitude less potent than padimate O.175 Octocrylene, which is a cinnamate derivative, is a weak UVB absorber that also absorbs UVA modestly up to 360 nm. Cinnamates are poorly bound to the stratum corneum and may cause contact dermatitis. Cinoxate is the most frequent contact sensitizer, with cross-sensitization to related cinnamates in coca leaves, balsam of Peru, and cinnamon oil.65 Salicylates, including homosalate and octyl salicylate (octisalate), are relatively weak absorbers of UVB, and they are consequently most often used in combination with other sunscreening agents. They have the advantages of being nonsensitizing and water insoluble, and they help to solubilize benzophenones in commercial products.84 303

CHAPTER 14  Exposure to Radiation From the Sun

proliferation. UVB also causes mutations in ras, thereby disrupting mitogenic signaling pathways. In particular, mutations in BRAF, which is a critical component of the ras protein kinase pathway, are found in a large percentage of nevi168 and melanomas,231 especially melanomas that arise on intermittently sunexposed skin.186 However, BRAF mutations occur only rarely in melanomas that arise in chronically sun-exposed or completely sun-protected skin,186 which suggests multiple genetic pathways for melanoma induction. Moreover, mutations of BRAF and p53 may interact to form melanoma.231 Oxidative damage is another mechanism, in addition to mutation, by which UVR contributes to photocarcinogenesis. Although UVA is less directly mutagenic than is UVB, it is more potent with regard to causing cellular oxidative damage by producing reactive molecular oxygen and nitrogen species that in turn damage DNA, proteins, and lipids. This damage contributes to carcinogenesis via inflammation, immunosuppression, and, ultimately, mutation.120 In addition, a group of zinc-dependent enzymes, known as matrix metalloproteinases, increase in response to UVR by altering the cutaneous extracellular environment to favor tumor invasion and spread.38,139

PART 3  BURNS, FIRE, AND RADIATION

Anthranilates are similarly weak UVB absorbers that also filter UVA. They display peak absorption at 340 nm.175 The single commercially available agent from this class is methyl anthranilate (meradimate). Phenylbenzimidazole sulfonic acid (ensulizole) is a unique UVB absorber. Unlike other chemical absorbers, which solubilize in the oil phase of emulsion formulations, phenylbenzimidazole sulfonic acid is water soluble. This physiochemical property has resulted in its increasing use in oil-free cosmetic sunscreens.175 Benzophenones are broader-spectrum sunscreening agents, with good absorption in the UVB and UVA ranges up to 360 nm.175 The three benzophenones available in the U.S. market are oxybenzone, dioxybenzone, and sulisobenzone. In the United States, dibenzoylmethanes are represented by a single agent: avobenzone (Parsol 1789, butyl methoxydibenzoylmethane). It is a potent UVA absorber, with little or no absorption in the UVB range.175 Its absorption peak at 358 nm falls nearly to zero at 400 nm.252 Concerns have been raised that photodegradation may limit its effectiveness. Under simulated solar light, avobenzone can be degraded 36% in as little as 15 minutes.261 However, these data are disputed, and there is debate regarding whether any significant decrease occurs with typical use, especially given the mitigating effect of combined sunscreening agents in commercially available preparations.261 For example, a patented complex known as Helioplex—a combination of avobenzone, oxybenzone, and diethyl 2,6-naphthalate—is remarkably photostable.51 In addition, select stabilizing compounds such as vitamin C, vitamin E, and iron chelators may retard photodegradation.199 Ecamsule (Mexoryl SX) is the newest sunscreening agent to be approved by the FDA, although it has been available in Europe and elsewhere for several years. It is an excellent UVA filter, with maximal absorbance at 345 nm and with modest absorption in the UVB range as well. Ecamsule is distinguished by being highly photostable and thermostable. It effectively protects skin from repeated exposures to UVA, thereby preventing the histologic changes associated with photoaging.267 Physical sunscreens traditionally refer to opaque agents that primarily reflect, scatter, and, to a lesser extent, absorb UVR. These include calamine, ichthammol, iron oxide, kaolin, red veterinary petroleum, starch, talc, TiO2, and ZnO. In the wilderness, extemporaneous physical blockers can be made from ashes, mud, and leaves. A sunscreen with a physical filter typically protects throughout the UVR and visible spectra and may even protect against IR-induced erythema.227 However, classic physical blockers are messy, uncomfortable, and cosmetically undesirable. Preparations of TiO2 and ZnO with a submicron (i.e., nano) particle size are now widely available. In contrast, with normal TiO2 and ZnO size ranges (150-300 nm for TiO2 and 200-400 nm for ZnO), in which the larger size permits these particles to reflect and scatter light, the submicron dimensions (typically 20-150 nm for TiO2 and 40-100 for ZnO) make these particles more soluble in their vehicle base and minimally reflective of visible light. Cosmetically, this is an advantage, because it makes them more transparent (or nearly so) in thin coats. The lower refractive index of ZnO in the visible range makes it less white and more transparent than TiO2.207 However, submicron-sized preparations significantly absorb UVR, thereby providing broad-spectrum protection from UVB and UVA and blurring the distinction between chemical and physical sunscreens, as mentioned previously.64,175,260 TiO2 and ZnO are sometimes marketed as “chemical-free” sunscreens, which is clearly a misnomer. In addition, products that contain “physical” sunscreening agents are often marketed as “sunblocks,” which is a misleading term that was eliminated in the 1999 FDA Final Monograph.295 Of note is that metal oxide nanoparticles, with their potential to be absorbed through the skin, have received a great deal of media attention in recent years but have not been comprehensively evaluated with regard to their potential longterm effects on human health. Likewise, the ecologic impact of product use and disposal and the fate and toxicity of nanoparticles in the environment will most likely be influenced by a number of factors (e.g., aggregation, stability, transport, sedimentation, biouptake) that remain to be rigorously studied.225 New sunscreens are on the horizon, with imaginative observation leading to future sources of sunscreening agents. For example, Saikawa and colleagues258 determined that the viscous 304

“red sweat” of the hippopotamus is an excellent broad-spectrum sunscreen, with absorption in the 200 to 600 nm range.258 Sunscreen Vehicles Sunscreen vehicles affect efficacy and acceptability. The ideal vehicle spreads easily, maximizes skin adherence, minimizes interaction with the active sunscreening agent, and is noncomedogenic, nonstinging, nonstaining, and inexpensive. In practice, the best vehicle is highly dependent on personal preference. Creams and lotions (emulsions) are most popular. Both are oilin-water or water-in-oil preparations, although lotions spread more easily. Most sunscreening agents are lipid soluble, which results in an objectionable greasy feel. Increasingly popular “dry lotions” minimize the lipid component and often include at least one water-soluble sunscreening agent to reduce oiliness.175 In contrast, sunscreen oils contain only a lipid phase. Oils spread easily but thinly, thus limiting the achievable concentration of active sunscreening agent and thereby limiting protectiveness. In addition, oils are oily and cosmetically less acceptable. Other anhydrous vehicles, such as ointments and waxes, may be desirable for climbers and winter campers by reducing the risks of chapping and frostbite. Gels are generally nongreasy but tend to wash or sweat off easily. In addition, gels seem to produce more stinging and irritation. Sticks typically incorporate sunscreening agents into wax bases, but applying stick preparations to larger areas is not easy. Aerosols can cover large areas quickly but tend to be wasteful, with spray lost to the air, and they usually form an uneven film175; they also need to be rubbed in to provide adequate and uniform protection.18 Sunscreens are increasingly being incorporated into cosmetics, including foundations, lipsticks, and moisturizers. Sun Protection Factor The ability of a sunscreen to protect the skin from UVR-induced erythema is measured by the SPF. The SPF is defined as the ratio of UVR required to produce minimal erythema (1 MED) in sunscreen-protected as opposed to sunscreen-unprotected skin.147,295 It can be represented by the following formula: SPF =

MED of sunscreen-protected skin MED of unprotected skin

Testing conditions are standardized by the FDA.295 The agent to be tested is applied at a standard concentration of 2 mg/cm2. Testing is performed indoors with a solar simulator on the back between the beltline and the scapulae. The SPF is typically determined on a panel of 20 (or a maximum of 25) subjects with skin types I, II, or III (see Box 14-2). The mean is then determined to be the approved SPF. Although indoor testing with a solar simulator is more reproducible than outdoor natural sun exposure, it may yield a falsely high SPF value. In outdoor testing of more than 30 sunscreens labeled SPF 15, none were found to actually have an SPF of more than 12.230 Several factors are responsible for lower SPF values with outdoor testing, including sweating; clothing, towel, and sand abrasion; and application variability. In addition, solar simulators generally have reduced outputs of UVA as compared with sunlight.261 SPF determinations use erythema as their measurable endpoint. Erythema is predominantly a result of UVB and not UVA exposure. Consequently, SPF is primarily a measure of UVB protection. The relationship of SPF to UVB absorption is given in Table 14-2. How high an SPF is necessary? Given that SPF 15 blocks 93% of UVB, some argue that SPF 15 is sufficient187 and that higher labeling claims are misleading and costly for consumers. However, in several studies, higher SPF sunscreens conferred clinical and histologic benefits. In children on Florida beaches, a single application of SPF 25 sunscreen protected just as well as multiple applications of SPF 15 for up to 6 hours of exposure.221 Histologically, an SPF 30 sunscreen provides better protection against sunburn cell formation than does an SPF 15 sunscreen.145 Sunscreen Application Perhaps the most persuasive argument in favor of higher-SPF sunscreens derives from variations in application technique. The

B Radiation Absorption

Sun Protection Factor 2 4 8 15 30 50

Ultraviolet B Radiation Absorption (%) 50.0 75.0 87.5 93.3 96.7 98.0

protection provided by sunscreen is related to the amount of product that is applied.263 In the real world, sunscreens are applied at much lower concentrations than the 2 mg/cm2 at which they are tested. When used ad lib, sunscreens are typically applied in concentrations of 0.5 to 1 mg/cm2.21,262 The resultant SPF is considerably reduced, typically to about 50% of the labeled SPF for chemical sunscreens.40 Some suggest that the reduction is even greater and that the actual SPF is only 20% to 50% of the labeled value.283 Physical sunscreens tend to be applied even more thinly, typically at two-thirds the concentration of chemical sunscreens, most likely because of their cosmetic visibility.62 For TiO2 products, application concentrations of 0.65 mg/cm2 result in SPF values of only 20% to 30% of the intended labeled value.283 Not surprisingly, persons who burn more easily tend to apply thicker concentrations of sunscreen.62 There is no difference in the applied concentrations of higher versus lower SPF formulations. Uneven application further reduces sunscreen protection. With the use of a fluorescent dye, a pattern of spotty use emerges. Individuals typically cover the forehead adequately, but the temples, ears, and posterior neck are often undertreated or missed entirely.99,177,244 Newly available sunscreens that contain disappearing colorants are popular because they provide visible assurance of complete coverage. Adequate coverage of just the chronically exposed areas (i.e., the face, ears, and dorsal surfaces of the hands) requires 2 to 3 g (0.07 to 0.11 oz) of product per day;175 this requires the use of an 8-oz bottle of sunscreen every 80 to 120 days. Application delay imposes a further decrease in protectiveness. In a study of families on Chicago beaches in the summer,249 sunscreen was applied only after arriving at the beach in 98% of families. The median delay from arrival to sunscreen application to the last family member was 51 minutes. Underapplication, uneven application, and delayed application of sunscreens result in unnecessary photoexposure and photodamage. In addition, for hikers, the concomitant use of sunscreen and insect repellent that contains diethyltoluamide lowers the effective SPF by 34%.212 In an effort to balance these issues with consumer concerns about SPF inflation, the FDA set a labeling limit of SPF 30+ in the 1999 Final Monograph295 that was effective May 21, 2001. This was subsequently extended to December 31, 2002, and later deferred indefinitely until the FDA develops a more comprehensive set of requirements to address both UVA testing and labeling. It is expected that the FDA will announce these changes officially in October 2010. Ultraviolet A Radiation Protection Factors With increased understanding of UVA-induced photodamage and the recent addition of better UVA-blocking agents (e.g., avobenzone, ecamsule, micronized TiO2 and ZnO), more attention has been focused on measuring UVA protection. Several measures of UVA protectiveness have been suggested, but none have been widely accepted or used. Among them are the UVA protection factor, which is analogous to SPF.253 The principal drawback of UVA protection factor determination is related to the lengthy exposure times required to induce erythema. A second method, the phototoxic protection factor, shortens exposure times by sensitizing skin to UVA with oral or topical psoralens. However, the relevance of phototoxic protection factor data to real-world conditions has been challenged. Other UVA protection factors involve measuring UVA-induced immediate pigment darkening, suppressing UVA-induced sunburn cell formation in psoralen-treated skin, and UVA-induced photocurrent transmission through various

media.84 In its 1999 Final Monograph, the FDA chose not to impose a specific UVA protection factor but allows a sunscreen to make UVA protection claims as long as it contains an approved UVA sunscreening agent.295 However, Rosenstein and co-workers255 found that sunscreens with a labeling claim of UVA protection allow for transmission of 6% to 52% UVA. Proposed New Sun Protection Factor and Ultraviolet A Radiation Labeling Requirements The FDA revised sunscreen labeling and effectiveness testing standards in a final rule, published in the Federal Register on June 17, 2011.296 Prepared in response to nearly 2900 public submissions, the FDA’s final rule represents the most significant changes to sunscreen labeling and testing in more than a decade. Effective for all products with annual sales less than $25,000 by June 17, 2013, and for all other products by June 18, 2012, the final rule establishes labeling and effectiveness testing for over-the-counter sunscreen products marketed without an approved application under Section 505 of the Federal Food, Drug, and Cosmetic Act. It does not address issues related to sunscreen active ingredients or certain other issues regarding the Generally Recognized as Safe and Effective (GRASE) determination for sunscreen products. The FDA chose to publish this final rule, even as it continues to work toward a comprehensive final monograph, with the immediate goals of public health in mind. More specifically, the FDA hopes the new rule will provide the following services to the public: • Help ensure currently marketed products be appropriately labeled and tested for both UVA and UVB protection • Promote proper use of these sunscreens and greater consumer protection from the damaging effects of UV radiation • Identify claims that render a product “misbranded” or claims that are not allowed on any over-the-counter sunscreen drug product marketed without an approved application; for example, terms like “sunblock,” “sweatproof,” and “waterproof” have been deemed misleading and are no longer permitted The final regulations establish new testing parameters that reduce the number of subjects required in SPF testing from 20 to 10 subjects, and require only a single in vitro test to demonstrate broad spectrum protection. Performance is determined on a pass/fail basis using a critical wavelength of 370 nm. The critical wavelength is defined by FDA as the wavelength at which the integral of the spectral absorbance curve for a particular sunscreen product reaches 90 percent of the integral over the UV spectrum from 290 to 400 nm:

Where λc = critical wavelength, A(λ) = mean absorbance at each wavelength, and dλ = wavelength interval between measurements.297 Products that pass testing (i.e., possess a mean critical wavelength ≥ 370 nm) will be labeled Broad Spectrum and SPF 15 (or higher) on the front, demonstrating protection against both UVB and UVA radiation. The new labeling will also inform consumers on the back of the product that sunscreens labeled as both Broad Spectrum and SPF 15 (or higher) not only protect against sunburn, but, if used as directed with other sun protection measures, can reduce the risk of skin cancer and early skin aging. For these broad spectrum products, higher SPF values also indicate higher levels of overall protection. Conversely, sunscreen products that are not broad spectrum, or that are broad spectrum with SPF values from 2 to 14, will be labeled with a warning that reads: “Skin Cancer/Skin Aging Alert: Spending time in the sun increases your risk of skin cancer and early skin aging. This product has been shown only to help prevent sunburn, not skin cancer or early skin aging.” The FDA also now requires that instructions for reapplying sunscreen at least every two hours, after swimming or sweating, and immediately after towel drying be included on labels. Likewise, a new “direction statement” will be included that states: 305

CHAPTER 14  Exposure to Radiation From the Sun

TABLE 14-2  Skin Protection Factor and Ultraviolet

PART 3  BURNS, FIRE, AND RADIATION

Sun Protection Measures: Spending time in the sun increases your risk of skin cancer and early skin aging. To decrease this risk, regularly use a sunscreen with a Broad Spectrum SPF of 15 or higher and other sun protection measures including:   Limit time in the sun, especially from 10 a.m.-2 p.m.   Wear long-sleeved shirts, pants, hats, and sunglasses. Required warnings on all covered over-the-counter products will also include the following (Figure 14-10, online): • “Do not use on damaged or broken skin.” • “When using this product keep out of eyes. Rinse with water to remove.” • “Stop use and ask a doctor if rash occurs.” Concomitant to announcing its final rule for sunscreen labeling and testing, the FDA also released three additional regulatory documents that may affect future sunscreen regulations. The proposed rule would limit the maximum SPF value on sunscreen labels to “50+” because, according to the FDA, there is not sufficient data to show that products with SPF values higher than 50 provide greater protection for users than products with SPF values of 50; the proposal creates the opportunity for the submission of data to support the inclusion of higher SPF values in the final rule. The advance notice of proposed rulemaking will allow the public a period of time to submit requested data addressing the effectiveness and the safety of sunscreen sprays, and to comment on possible directions and warnings for sprays that the FDA may pursue in the future among other issues regarding dosage forms for sunscreens. Finally, the Draft Enforcement Guidance for Industry outlines information to help sunscreen product manufacturers understand how to label and test their products in light of the new final rule and other regulatory initiatives. Substantivity The ability of a sunscreen to resist being washed off by water is referred to as substantivity. The FDA’s 2011 final rule changed testing and labeling requirements significantly in order to make it clearer and easier for consumers to understand water resistance as part of their purchase decision. Of interest, the new testing requirements were based on marketing data that indicated individuals at the beach or pool spend an average of 21 minutes in the water, and go into the water an average of 3.6 times per outing.296 Conditions for testing substantivity are set by the FDA. Freshwater immersion is required in an indoor fresh water pool, whirlpool, or hot tub maintained at 23° to 32° C (73° to 90° F). Fresh water is defined as clean drinking water that meets Environmental Protection Agency standards established in 40 CFR, part 141. Sunscreens that are newly labeled “water resistant (40 minutes)” or “water resistant (80 minutes)” will have passed testing requirements that include water immersion (with moderate activity) for 20 minutes with 15-minute drying times (no towel drying), repeated once or thrice, respectively.296 The conditions under which substantivity testing is performed raise some concern for “real world” relevance and applicability. For example, the effect of relative humidity, sunscreen dosage (i.e., amount applied), immersion time, and activity level should be considered. Similarly, the MED for skin that has been bathed in salt water is less than the MED for skin that has been bathed in fresh water, and both are lower than the MED of dry skin.90 Furthermore, cold churning water, sand abrasion, and toweling may add to sunscreen loss, which begs the question of whether water-resistant sunscreens are truly surf-resistant. The concerns about saltwater substantivity, which have been amplified by surfer folklore, have led to an almost cultish market of “surf shop” sunscreens, although few published data indicate whether these products are more substantive in a saltwater environment. Select sun screening agents, primarily PABA and PABA esters, are intrinsically substantive as a result of bonding to stratum corneum proteins. Other sunscreens must be incorporated into vehicles that confer substantivity. By applying sunscreen 15 to 30 minutes before water exposure, substantivity can be increased. Reapplication after swimming or sweating helps to ensure protection. Today dozens of affordable, UVA- and UVB-protective, water-resistant sunscreens are commercially available (Table 14-3). 306

Stability Photostability, which is a sunscreen’s ability to remain intact and effective after sun exposure, has been questioned for a number of sunscreens, most notably avobenzone. Questions regarding photostability have also been raised about octyl dimethyl PABA and octyl methoxycinnamate. Marot and colleagues190 demonstrated that photodegradation of octyl methoxycinnamate allows histologic and enzymatic injury to the skin and that failure of a photolabile sunscreen may result in genotoxicity.191 In a European study of 27 photoprotective lipsticks, 14 showed photoinstability; in other words, they became partially photoinactive after moderate UVR exposure.185 Twelve were photolabile in the UVA range, one was in the UVB range, and one in both the UVA and UVB ranges. Photostability can be significantly improved with the use of combinations of sunscreening agents. For example, octocrylene stabilizes avobenzone in a number of sunscreen formulations, whereas 4-methylbenzylidene camphor can be used to stabilize octyl methoxycinnamate.30 Vehicle formulations also affect stability; butyloctyl salicylate and butyloctyl benzoate contribute to photostability.30 There are few published data regarding packaging, storage, and shelf life of sunscreens. Packaging may affect sunscreen acceptability and stability. For example, octyl methoxycinnamate turns polyvinyl chloride a bright yellow color. In a recent study by Santoro and co-workers,259 benzophenone-3 and octyl methoxycinnamate maintained stability for 60 days in both glass and plastic containers at room temperature (25° C [77° F]) and at 35° C (95° F), with only minor changes in concentrations seen at 10° C (50° F) and 45° C (113° F). The generally accepted wisdom is to keep sunscreens out of glove compartments and similar locations where they are exposed to extremes of temperature for long periods. Shelf life is presumed to be at least 1 year or more for most commercially available sunscreens, although data are lacking. Sunscreen Prevention of Chronic Photodamage Sunscreens prevent sunburns in addition to mitigating UVRinduced histologic damage, UVR-induced immunosuppression, photoaging, and photocarcinogenesis. Sunscreens reduce UVRinduced DNA damage,300 but not entirely.44 Reductions are seen in pyrimidine photoproducts in humans44 as well as in UVRinduced p53 mutations and skin cancer in mice.5 Sunscreen nearly eliminates the overexpression of p53 in mice after acute236 and chronic90 UVR exposure. In humans, an SPF 15 sunscreen reduces p53+ cells by 33% after chronic UVR exposure.24 The published effects of sunscreen on immunosuppression are contradictory, largely resulting from the complex relationships of UVR dosing and sensitivity in different experimental models. SPF is not a reliable measure of a sunscreen’s ability to block UVRinduced immunosuppression; two sunscreens with identical SPF values may vary considerably with regard to their immunoprotectant effects.242 SPF and immune protection factor are not synonymous or equivalent.322 Overall, sunscreens mitigate but do not abrogate UVR-induced immunosuppression. In mice, sunscreens prevent the UVR-induced depletion of Langerhans’ cells, with higher-SPF sunscreens conferring greater protection.19 However, earlier studies noted little or no immunoprotectant effect from sunscreens.19 A broad-spectrum SPF 15 sunscreen prevents the UVR-induced suppression of contact hypersensitivity to dinitrochlorobenzene, a potent topical allergen, in humans.268 In C3H mice transplanted with NMSC, sunscreen blocks UVR-induced immunosuppression, thereby allowing for tumor rejection and again demonstrating increased protection with higher SPF values.248 However, in susceptible mice that have been injected with melanoma, sunscreens fail to adequately suppress UVB enhancement of melanoma growth.313 This finding has been overinterpreted and misinterpreted by some to support a peculiar antisunscreen stance. However, the most appropriate interpretation is that sunscreens by themselves are not sufficient to prevent all of the immunosuppressive sequelae of UVR exposure and that sunscreens should be used as part of a larger sun-protective strategy that includes avoidance and clothing protection. Sunscreens reduce sunburn cell formation and solar elastosis33 in humans. The histologic changes of photoaging in mice are

Product

Sun Protection Factor

High Sun Protection Factor Waterproof Broad-Spectrum Creams and Lotions Bain de Soleil Oil-Free Protecteur Sunscreen Lotion Banana Boat Sport 50 Blue Lizard Australian Sunscreen Lotion Bullfrog SuperBlock Lotion Coppertone Sport Ultra Sweatproof Dermatone Sunscreen Lotion DuraScreen Lotion Hawaiian Tropic Ozone Sunblock Kiss My Face Sunblock Lotion Neutrogena Ultra Sheer Dry-Touch Sunblock Ocean Potion Anti-Aging Sunblock Ombrelle Sunscreen Lotion Extreme Panama Jack Sunscreen Lotion Sea & Ski Sport SolBar PF Cream TI Screen Moisturizing Sunscreen Lotion Water Babies Sunblock Lotion High Sun Protection Factor Gels Bullfrog Quik Gel Coppertone Sport Sunblock Gel Pre-Sun Ultra Gel Ti-Screen Sports Gel High Sun Protection Factor Sprays Banana Boat Sport Quik Block Sunblock Spray Bullfrog Fast Blast Spray Sunblock Coppertone Sport Sunblock Spray Neutrogena Healthy Defense Oil-Free Spray Ti-Screen Sunscreen Spray High Sun Protection Factor Sticks Banana Boat Sport Sunscreen Stick Bullfrog Quik Stick Hawaiian Tropic Ozone Oil-free Sunblock Stick Neutrogena Healthy Defense Sunblock Stick Ocean Potion Sport Stick Shade Sunblock Stick Specialty Sunscreens AloeGator Super Waterproof Gel Bullfrog Surfer Formula Gel Dermatone Skin Protector Pomade SolRx ProSport Lip Screens Banana Boat Aloe Vera Lip Balm Coppertone Sport Lip Guard Dermatone Medicated Lip Balm Hawaiian Tropic Aloe Vera Sunblock Lip Balm Neutrogena Lip Moisturizer Ti-Screen Lip Protectant “Physical” Sunscreens Neutrogena Sensitive Skin Sunblock Lotion Pre-Sun Sensitive Skin Sunblock Vanicream Sunscreen Moisturizers Containing Higher-SPF Sunscreens Anthelios SX Daily Moisturizing Cream Aveeno Positively Radiant Daily Moisturizer Eucerin Extra Protective Moisture Lotion Lubriderm Daily Moisture Lotion Neutrogena Healthy Defense Daily Moisturizer Oil of Olay Complete Defense Daily UV Moisturizer Purpose Dual Treatment Moisture Lotion

Active Ingredients

35 30 30+ 45 30 36 30 70 30 55 50 40 45 50 50 30 45

A, B, OC, S B, C, OC, S B, C, OC, ZO B, C, MA, OC, S, TI B, C, S C, PBSA, ZO B, C, PBSA, S, TI B, C, PB, S, TI C, TI A, B, OC, S A, B, C, S A, B, OC, S B, C, OC, S B, C, S, ZO B, C, OC, S A, B, C, OC, S B, C, S

36 30 30 20

B, C, OC, S A, B, OC, S A, B, C, S B, C, S

48 36 30 30 23

A, B, C, OC, S B, C, OC, S B, C, S A, C, S B, C, MA, OC

30 36 50+ 30 60 30

B, C, OC, S B, C, OC, S A, B, OC, S A, C, S A, B, S B, C, S

40+ 36 23 44

B, B, B, B,

30 15 23 45+ 15 15

B, C, PB, S B, C B, PB C, OC, S B, C B, C

30 28 15

TI TI TI, ZO

15 15 30 15 30 30 15

A, E, OC A, C, S C, OC, PBSA, TI, ZO B, C, S C, OC, PBSA, ZO C, OC, S, ZO C, MA, TI

C, C, C, C,

OC, S OC PB OC, S

A, Avobenzone; B, benzophenones; C, cinnamates; E, ecamsule; MA, methyl anthranilate (meradimate); OC, octocrylene; PB, para-aminobenzoic acid or paraaminobenzoic acid ester; PBSA, phenylbenzimidazole sulfonic acid (ensulizole); S, salicylates; TI, titanium dioxide; ZO, zinc oxide.

prevented by pretreatment with SPF 15 sunscreen.155 In mice that have been exposed to UVB for 10 to 20 weeks, subsequent sunscreen use prevents further photodamage and promotes repair of previous damage, even with continued exposure.156 Higher-SPF sunscreens provide increasing protection against UVB-induced wrinkling in mice.28 Similarly, histologic and clinical

signs of UVA-induced photoaging are prevented by broadspectrum sunscreens.124 Sunscreen use reduces formation of precancerous actinic keratoses216,289 and promotes resolution of preexisting lesions.289 In a 2-year trial of sunscreens in humans with actinic keratoses, those who benefited most had the greatest number of keratoses at 307

CHAPTER 14  Exposure to Radiation From the Sun

TABLE 14-3  Select Sunscreen Products

PART 3  BURNS, FIRE, AND RADIATION

enrollment,216 thereby underscoring the value of continuing sunscreen use in adults. Daily use of SPF 15 sunscreen in adults reduces the incidence of SCCa but not of BCCa.114 Stern and colleagues281 estimated that using an SPF 15 sunscreen from birth until the age of 18 years would reduce the lifetime risk of NMSC by 78%. Liquid base makeup, even without sunscreen, provides an SPF of approximately 4 because of the pigments used in the foundation.175 For women who use lipstick, the incidence of SCCa is lower than in nonusers and men.234 Sunscreens, Melanoma, and Vitamin D Controversy regarding the effects of sunscreen use on the incidence of melanoma has intensified as melanoma incidence and sunscreen sales have both risen over several decades. Previous epidemiologic studies have, in general, failed to demonstrate conclusive evidence of decreased melanoma incidence with sunscreen use. Paradoxically, several studies have suggested an increased risk of melanoma with sunscreen use.12,63 In 1996, Donawho and Wolf 63 reviewed retrospective studies that evaluated melanoma risk in sunscreen users; only one showed decreased risk,135 whereas seven showed increased risk. Subsequent studies have continued to show contradictory results; a case-control study in southern Spain, which was published in the same year as the meta-study by Donawho and Wolf, showed decreased melanoma risk with sunscreen use in a Mediterranean population.251 In 1993, Garland and co-workers94 proposed that sunscreens, by primarily blocking UVB and sunburn, permit longer exposures to UVA in sunlight and that this increased UVA exposure results in increased incidence of melanoma. Confounding all of these studies, however, are the following points: • Persons who are at the highest risk for melanoma (i.e., those with fair complexions who burn easily) may be precisely the same persons who use sunscreens. • Earlier sunscreen products had lower SPFs and narrower spectrums. Modern sunscreens are typically more substantive, with higher SPFs, and substantially broader and better UVA protection. • Because sun exposure during childhood appears to be the most provocative for melanoma, surveying adults about their sunscreen habits may be irrelevant and misleading. Importantly, in 2010, Green and co-workers113 published a large, community-based study that provides strong evidence that daily application of sunscreen may directly reduce melanoma risk. Between 1992 and 1996, 1,621 randomly selected residents of Queensland, Australia, ages 25 to 75 years, were randomized into two groups. In the “daily” sunscreen group, participants were given free and unlimited supply of broad-spectrum sunscreen (SPF 16) and asked to apply it each morning to their head, neck, arms, and hands, with reapplication advised after heavy sweating, bathing, or long sun exposure. Participants in the “discretionary” group continued using sunscreen of any SPF at their usual discretionary frequency, which could include no use at all. Participants were also independently randomized to receive either 30 mg beta carotene or placebo supplements. The groups were then observed for incidence of primary melanoma and followed for an additional 10 years. By the end of the study, risk for developing any first primary melanoma was reduced by 50% (P = 0.051) and risk for invasive melanoma was reduced by 73% (P = 0.045) in “daily” users compared with “discretionary” users. There were no significant between-group differences in either in situ melanomas or melanomas at prescribed application sites. No direct effects of beta carotene were observed. Limitations of the study include the borderline significance of the risk reductions (though a discussion of the rigorous statistical methods are reviewed in an accompanying editorial by Gimotty and Ganz107) and the study’s applicability to different geographical locations and populations (i.e., different skin types). When considered in total, however, the results of this uniquely ambitious study provide support for sunscreen use as a means of helping to reduce the risk of melanoma. The effect of sunscreens and clothing protection on the numbers of nevi in children and adolescents, which is a prominent risk factor for melanoma,93 is controversial as well. In Australian children between the ages of 0 and 35 months, 308

sunscreen use is associated with modestly decreased nevus counts.125 However, in a study of adolescent twins in the United Kingdom,302 sunscreen use did not decrease nevus counts. In fact, there was a modest increase in benign nevi in adolescents who regularly used high-SPF sunscreens, possibly because of increased exposure times among sunscreen users. In this U.K. study, clothing protection had no effect on nevus counts. However, in a separate study of first- and fourth-graders in British Columbia, those who regularly used sunscreens developed fewer nevi, especially on intermittently sun-exposed sites.173 It remains unclear why intermittent sun exposure, especially during childhood, is associated with an increased risk of melanoma, whereas chronic occupational exposure is partially protective.91 An increasingly popular explanation is that vitamin D, which is formed by the action of sunlight on the skin, may be protective. Data are amassing to support this hypothesis. Mortality rates of several common cancers in the United States (e.g., breast, colon, prostate) increase with increasing latitude.68 In 1990, Garland and colleagues95 suggested that decreased cutaneous synthesis of vitamin D at higher, less-sunny latitudes might explain increased mortality from breast cancer in the northern states. Recently, Smedby and co-workers274 reported that sunlight reduces the risk of non-Hodgkin’s lymphoma. Among men in the Navy, Garland and colleagues96 determined that regular sun exposure reduces melanoma risk. In a population-based study of 528 patients with melanoma, Berwick and co-workers25 found that increased survival is associated with sun exposure. These data suggest that melanoma may be among the tumors for which vitamin D has a salutary effect. Supporting this hypothesis are laboratory data that demonstrate the presence of vitamin D receptors on melanoma cells, with growth inhibition occurring in response to this vitamin.52 In a case-control study of 502 melanoma patients and 565 control patients, Millen and colleagues202 found that diets rich in vitamin D and carotenoids were associated with a reduced risk of melanoma. These findings beg the following question: Do sunscreens, by absorbing UVB, reduce vitamin D levels sufficiently to pose an increased risk of melanoma and perhaps other cancers as well? Holick131 states that there is an “unrecognized epidemic” of vitamin D deficiency in the United States. Nonetheless, concerns regarding sunscreen-induced vitamin D depletion may not be warranted. Although regular sunscreen use can decrease cutaneous synthesis of vitamin D3194 and the circulating levels of measurable 25-hydroxyvitamin D,195 even the most conscientious sunscreen users appear to maintain normal levels of vitamin D. Using an SPF 17 sunscreen throughout an Australian summer 113 subjects maintained adequate vitamin D levels,188 and 24 subjects who were using SPF 15 sunscreen for 2 years maintained normal parathyroid hormone levels and normal bone metabolic markers.77 Moreover, eight patients with XP maintained normal vitamin D levels for the 6 years that they were observed, despite rigorous photoprotection with sunscreens, clothing, and sun avoidance.276 Part of the controversy surrounding vitamin D stems from unclear or varying recommendations regarding the recommended dietary allowance (RDA) and the difficulty involved with getting adequate amounts from diet and supplements. For example, in 2008, the American Academy of Pediatrics published guidelines that recommended a daily intake of vitamin D of 400 IU per day for all infants and children beginning during the first few days of life; these updated guidelines were based in part on new clinical trials, and effectively doubled the dose recommended in the previous 2003 guidelines.303 Human milk typically contains a vitamin D concentration of 25 IU/L or less, therefore supplementation is recommended for all breast-fed infants. If an infant is weaned to vitamin-D–fortified infant formula and consuming at least 1000 mL per day, or if a child who is 1 year of age or older is weaned to vitamin-D–fortified milk, then further supplementation is not necessary, according to the American Academy of Pediatrics report and the U.S. Centers for Disease Control and Prevention. Some authors advocate for more aggressive supplementation to meet physiologic need, particularly for individuals who are deprived of sun exposure. This is important as vitamin D’s role in the maintenance of innate immunity and the prevention of

thiazides, sulfonamides, benzocaine, and hair dyes that contain paraphenylenediamine may occur.245 Paradoxically, sunscreens have become the leading cause of photoallergic contact dermatitis.290 Oxybenzone is the most commonly implicated. In 283 cases of photodermatitis, 35 people were photoallergic to oxybenzone, and 17 were allergic to PABA.286 In a separate study of 108 patients with photodermatitis, four were photoallergic to oxybenzone, and four were allergic to other sunscreening agents.290 Stinging or burning without accompanying erythema, scaling, or dermatitis is common, especially in periocular areas and particularly in patients with rosacea, although the addition of skin “protectants” (i.e., dimethicone or cyclomethicone) to the sunscreen vehicle can mitigate this.218 Certain vehicles (e.g., alcoholic gels) may be more stinging. Even when periocular application is avoided, perspiration, water immersion, and rubbing may cause sunscreen to migrate, thus producing symptoms. Comedogenicity is primarily related to ingredients in the vehicle base. Certain common excipients (e.g., almond oil, cocoa butter, isopropyl myristate, isopropyl palmitate, olive oil) are possible comedogens. TiO2 and ZnO can generate reactive molecular species, called free radicals, with sun exposure.64 TiO2 is more photoactive than is ZnO.207 Electromagnetic radiation with wavelengths of less than 412.5 nm has sufficient energy to excite TiO2 electrons from the valence band to the conduction band.159 Photoactivated TiO2 can damage DNA in vitro.129 In vivo, however, it is unlikely that TiO2 particles penetrate the stratum corneum to reach underlying epidermal cells that contain DNA. Transmission electron microscopy fails to demonstrate TiO2 penetration of the stratum corneum.66 Data also demonstrate that ZnO is not absorbed and that Zn levels are unchanged after application.98 Coating TiO2 or ZnO with silicone halts photoproduction of reactive species.64 Still, some concerns have been raised regarding the use of these agents on broken skin. Some sunscreening agents have weak estrogenic or anti­ androgenic activity.266 In particular, benzophenone-3, octylmethoxycinnamate, and 3-(4-methylbenzylidene) camphor may have estrogenic effects on human breast cancer cells in culture.265 To assess their endocrinologic safety, Janjua and co-workers141 studied the whole-body application of these three sunscreening agents on humans daily for 1 week with the use of a liberal concentration of 2 mg/cm2. Plasma and urine levels of all three agents were detectable in men and postmenopausal women; luteinizing hormone and follicle-stimulating hormone were unchanged, and there were only minor changes in testosterone and estradiol (in men only). The authors concluded that these endocrinologic alterations are clinically insignificant and that these sunscreen products are safe for use, at least for adults.

Sunscreens and Herpes UVB is a potent stimulus for the reactivation of herpes labialis in outdoor enthusiasts.141 Although sunscreen is ineffective for preventing recurrences in skiers on the slopes,204 it is quite effective for preventing recurrences in the clinical laboratory,254 which perhaps reflects a difference in application techniques.

CLOTHING PROTECTION

Sunscreen Side Effects Sunscreen side effects are generally mild and limited. In a prospective study of 603 subjects who applied SPF 15 sunscreen or vehicle control,81 19% in both groups had adverse reactions. Most reactions were irritant in nature, and fewer than 10% were allergic. More than one-half of the individuals who developed irritation were atopic. These data support the notion that most contact irritant dermatitis to sunscreens is attributable to excipients. Similarly, allergic reactions to sunscreens are more often the result of preservatives and fragrances than of active sunscreening agents.65 As a consequence—and contrary to popular belief— higher-SPF sunscreens are not more irritating than lower-SPF sunscreens.269 Nonetheless, most sunscreening agents can cause allergic or photoallergic contact dermatitis.147 For example, PABA is now rarely used, because it sensitizes approximately 4% of exposed subjects. After an individual is sensitized, cross-sensitization with

Clothing is a crucial part of sun protection, and provides substantial coverage to broad surface areas. However, clothing varies considerably in its ability to block UVR. Robson and Diffey250 determined the SPF of 60 different clothing fabrics, ranging from 2 (polyester blouse) to 1000 (cotton twill jeans). The most important factors for determining SPF are the tightness of the weave101,179,250 and then the actual fabric. An extreme example of this is Lycra, which blocks nearly 100% of UVR when lax and only 2% when maximally stretched.179 Other determinants include wetness and color. Dry and dark fabrics have a higher SPF than otherwise identical but wet and white fabrics.101 A typical dry white cotton T-shirt has an SPF of 5 to 9. Accumulating data show that clothing prevents chronic photodamage. In European children, clothing coverage is associated with fewer nevi.9 Blue denim reduces UVR-induced p53+ cells twice as effectively as does an SPF 15 sunscreen.24 Denim greatly reduces the formation of skin cancers in patients with XP.22 Standardized testing of clothing fabrics has produced a new measure, the ultraviolet protection factor, which is analogous to the SPF for sunscreens. A collimated UVR source is passed through flat, tensionless fabric, with resultant transmission measured by a spectroradiometer or broadband sensor.101,250,327 However, the resultant ultraviolet protection factor is generally 309

CHAPTER 14  Exposure to Radiation From the Sun

diseases such as diabetes and certain cancers comes to light.264 Given the remarkably brief sun exposures that are needed to synthesize vitamin D,132 Holick suggests an approach of sensible sun exposure, which involves 5 to 10 minutes of exposure two or three times weekly in conjunction with the dietary intake of vitamin D and vitamin supplements.131 This recommendation has raised considerable controversy and concern in the dermatologic community, where the rise in melanoma incidence and sunscreen use has been considered a reflection of increased recreational sun exposure.217 Weighing in on the debate, the Institute of Medicine, at the request of agencies of the U.S. and Canadian governments, assembled an expert panel of 14 scientists to review the increasing body of research on vitamin D and update its 1997 Dietary Reference Intakes (DRIs). After systematic review of the data was performed, the expert committee, on November 30, 2010, concluded that bone health was the only outcome for which causality and sufficient dose-response evidence were established. Importantly, vitamin D’s role in cancer prevention was not found to be conclusively demonstrated. In addition, the group formally recognized the limitations of 25-hydroxyvitamin D as a biomarker of effect, pointing out that more aggressive vitamin D dosing regimens are based on higher target serum 25-hydroxyvitamin D levels that, in these experts’ opinions, were not justified by the evidence. In total, the new RDA for vitamin D, which assumes minimal sun exposure, suggests the following: • 1 to 70 years, 600 IU per day • 71 years or older, 800 IU per day The committee continued to recommend 400 IU per day as the adequate intake (AI) reference value for infants 0 to 12 months of age. The group also established tolerable upper intake levels (UL) for vitamin D, taking into account emerging evidence of U-shaped associations (i.e., increased risk at both low and high levels and lowest risk at moderate levels of serum 25-hydroxyvitamin D) for all-cause mortality, cardiovascular disease, vascular calcification, pancreatic cancer, falls, frailty, and fractures. The recommended UL for vitamin D is as follows:140 • 9 years and older, 4000 IU per day • 4 to 8 years, 3000 IU per day • 1 to 3 years, 2500 IU per day • 6 to 12 months, 1500 IU per day • 0 to 6 months, 1000 IU per day Scientific literature demonstrates that vitamin D plays a clear role in older adults who are at higher risk for osteopenia and fractures,109 and for infants at risk for rickets (especially breast-fed infants, who may get inadequate vitamin D in human milk).97,162 What still lacks are long-term studies that prove causation and dose-response for what role—if any—vitamin D plays in skin cancer prevention. Further research in the field will help put an end to this dermatologic controversy.

PART 3  BURNS, FIRE, AND RADIATION

much lower than the values seen with actual use, because natural sunlight is scattered and reflected to a far greater extent than a collimated beam.241 In the United States, sun-protective clothing is regulated as a medical device (Figure 14-11, online). Several manufacturing strategies are used to achieve high SPFs. One approved product, Solumbra, is made of tightly woven nylon with an SPF of 30 or more. In hairless mice, this fabric is significantly better than cotton for reducing formation of UVR-induced SCCa.201 In contrast, SolarKnit uses chemically treated cotton and cotton– synthetic blends to achieve an SPF of 30 or more. Rayosan, which is a UVR-absorbing agent, bonds to various fabrics and increases their SPF by up to 300%; it stays on the clothing through several washings.179 A unique chemical UVR protectant, Tinosorb FD, may be incorporated into detergents to increase the SPF of clothing with each wash. Ladies’ hosiery provides a surprisingly low SPF: black hose has an SPF of 1.5 to 3, and beige hose has an SPF of less than 2.270 Perhaps this explains in part why skin cancers are more common on the lower legs of women than those of men. Hats are also protective, with protection varying as a function of brim diameter and wearing style. Small-brimmed (<2.5 cm [≈1 inch]) hats adequately protect the forehead and the upper nose; medium-brimmed (2.5 to 7.5 cm [≈1 to 3 inches]) and wide-brimmed (>7.5 cm [≈3 inches]) hats protect increasing proportions of the nose, cheeks, chin, and neck,61 with largebrimmed hats providing an equivalent SPF of 7 for the nose, 3 for the cheeks, and 2 for the chin. Baseball-style caps are especially useful as a part of an overall sun-protective strategy for children. When these hats are used to protect the forehead and periocular areas, sunscreen application can be limited to areas below the cheekbones, thus mitigating the risk of stinging from application near the eyes. Glasses, contact lenses, and sunglasses protect the corneas from most UVB and from variable amounts of UVA.256 Surprisingly, price is unrelated to protection.3 A complete discussion of this is provided in Chapter 28.

SUN AVOIDANCE An indoor lifestyle is protective but undesirable for most persons. More practical is the avoidance of excessive midday sun (i.e., from 10 AM to 3 PM), which significantly reduces UVB exposure.177 Shade provides variable and often less protection than is generally assumed. In one study, shade beneath leafy trees provided an SPF of less than 4.229 Shade cloths allow significantly more UVB exposure than does clothing of the same fabrics, largely because of atmospheric scattering and surface reflection.314 Automobile windshields block UVB and some UVA, whereas side windows typically block only UVB.292 This may explain why photodamage is more prominent on the left side of the face of Americans (and on the right side of the face of Australians) who drive a great deal.272 Factors that affect UV-protective properties of glass include color, type, coating, and interleave between layers of glass. Transparent plastic films that meet legal requirements in all 50 states can be applied to block more than 99% of UVR (e.g., LLumar UV Shield).

SUNLESS TANNING Bronzers Most artificial tanners and bronzers contain dihydroxyacetone (DHA). DHA reacts with amino groups of keratin proteins via the Maillard reaction to form brown-pigmented products known as melanoidins.174 With DHA, bronzing can occur in as little as 1 hour. Often, however, it requires multiple applications to achieve the desired depth of color. Maintaining this bronzed look requires reapplication every few days, because the stained stratum corneum is shed from the skin surface. The depth of color is related to the thickness of the stratum corneum and the amount and frequency of application.175 Cosmetic complaints include difficulty with obtaining an “even” tan and yellowing of the palms. DHA plus lawsone (a henna dye) was previously used as a sunscreening agent. However, DHA alone is an inadequate 310

sunscreen. It absorbs no UVB; rather, DHA absorbs higherwavelength UVA I and lower-wavelength visible light,85 which makes it useful for select photosensitivity disorders, such as porphyrias and polymorphous light eruption. Some commercial bronzing products now contain sunscreen in addition to DHA. Although the artificial tan produced by these combination products lasts for days, the photoprotection lasts for only hours. Consequently, the FDA Final Monograph requires that bronzers without sunscreens display a warning that they do not protect against sunburn. Certain other products to promote indoor tanning have been used, but few are safe and effective. Tan accelerators that contain melanin precursors such as tyrosine have no discernible benefit.142 Sunscreen preparations that containing psoralens (most commonly 5-methoxypsoralen [oil of bergamot]) are available in Europe. Although these stimulate melanin synthesis, they are tumorigenic in mice.48 Psoriasis patients who have been treated with psoralen plus UVA (PUVA) have a higher incidence of SCCa279 and, with prolonged use, melanoma.280 Users of psoralencontaining sunscreen have an increased risk of subsequent melanoma.12 Oral carotenoids, especially canthaxanthin, have been promoted as tanning pills. However, these are potentially toxic and consequently not approved in the United States. Tanning Salons Although precise data are lacking, approximately 25 million North Americans—many of them adolescents—use tanning salons each year.285 In a survey of high school students in St Paul, Minnesota, 34% admitted to using tanning salons at least four times during the previous year.222 Tanning has even been evaluated as a possible dependency in certain populations.220 Until 1980, most sunlamps emitted mostly UVB.12 Today’s tanning salons make use of high-output UVA tanning beds and market their services as a way to tan without burning, with a subtle but incorrect message that such tans are safe. In fact, chronic suberythemal UVA contributes to photoaging, immunosuppression, and carcinogenesis. In addition, there is significant variation in the radiation output of tanning beds. In a study of 50 tanning beds in England,317 UVA output varied by a factor of 3, and UVB output varied by a factor of 60. Typically, tanning bed outputs are contaminated with 2% to 10% UVB,304 which is more than the average UVB content of natural sunlight. In 38 Scottish tanning units, 10 minutes of exposure yielded the same carcinogenic risk as did 30 minutes of peak summer sun at the same latitude.214 Tanning bed exposure for 15 to 20 minutes induces DNA damage in fibroblasts.315 Several case-control studies document a positive association between tanning bed use and the later development of melanoma.10,305,312 In a Swedish study of 400 patients and 640 controls, persons who used sunbeds or sunlamps before the age of 30 had a 7.7-fold increased risk of melanoma.312 In 420 patients from Germany, France, and Belgium, melanoma risks increased 8.97-fold when sunlamps or sunbeds were used for tanning.11 Ironically, UVA tans are less effective than are natural tans for conferring protection against subsequent sunburn.146 In addition, maintaining a yearlong tan provides no protection against subsequent melanoma development.135 Too often, tanning salons ignore photosensitizing risks in their patrons.41 Furthermore, the damage from tanning salons is insidious. Public awareness of the danger needs to be heightened, and health and government regulators are now taking the lead.316 Recently, the World Health Organization stated that no one less than 18 years old should use tanning beds. Increasingly, states and individual counties within the United States are restricting access to tanning parlors by minors. Currently, a majority of states regulate the use of tanning facilities by minors. Several states have banned access to indoor tanning facilities to anyone younger than 14 years of age unless medically necessary.49,288 Melanin and Thymine Dimers Cyclobutane T-T dimers, which are produced by the action of UVR on skin, stimulate melanin synthesis and subsequent pigmentation.105 Eller and co-workers70 exposed melanocyte cultures to synthetic T-T dimers and noted twofold to threefold increases in tyrosinase messenger ribonucleic acid and sevenfold

UNIQUE PHOTOPROTECTANTS Systemic Sunscreens Safe and effective oral sunscreens remain elusive. Clearly, these would have an advantage with regard to convenience, coverage, and substantivity. Several oral agents have been evaluated, but few are significantly effective or have favorable risk-to-benefit ratios in normal individuals. However, three botanicals appear promising: green tea, turmeric, and extracts of the fern Polypodium leucotomos.243 Currently, a few oral agents are used for patients with photosensitivity disorders: beta-carotene is helpful for individuals with erythropoietic protoporphyria, chloroquine is used for patients with lupus erythematosus, and psoralens helps those with polymorphous light eruption. Antioxidants UVR exposure results in reactive oxygen species that contribute to DNA damage232 and peroxidative destruction of membrane lipids.137 These effects contribute to DNA structural abnormalities, inflammation, and immune alterations. Protecting the skin from reactive species are various natural antioxidants (vitamins A, C, and E; reduced glutathione; urocanic acid; melanin) and enzymatic systems (catalase, superoxide dismutase).137 However, chronic exposure to UVR depletes the skin of these antioxidants.183 Applying antioxidants before UVR exposure delays skin damage in hairless mice.27 Select forms of vitamin E, especially tocopherol sorbate, diminish photoinduced free radicals and skin wrinkling in mice.144 Topical application of vitamins C and E provide protection against the histopathologic changes of photodamage in swine skin.57 In this animal model, sunscreen plus vitamins C and E provide more protection than does sunscreen alone.57 Although vitamin C does not act as a sunscreen (it does not absorb UVR), it protects against erythema and sunburn cell formation by quenching free radicals that are at least partially causative.56 The beneficial effect of topical vitamin C in swine skin persists for 72 hours after application, which suggests a potential strategy for longer-term photoprotection. Resveratrol, which is a potent antioxidant found in grapes, nuts, and red wine, mitigates the UVB-associated damage in mouse skin. It reduces UVB-induced edema, inhibits lipid peroxidation, and decreases production of enzymes associated with tumor promotion.2 Silmarin, which is a flavonoid derived from milk thistle, also has antioxidant, antiinflammatory, and salutary immunomodulatory effects when applied topically.148 Topical applications of aloe and tamarind xyloglucan have similarly been shown to protect against UVR-induced immunosuppression by acting as antioxidants rather than sunscreens.284 Oral antioxidants may also be of value for preventing photodamage. In humans, a combination of 2 g of vitamin C in combination with 1000 IU of vitamin E given orally for 8 days increased MED, albeit modestly.67 A more recent and larger study of human volunteers involving the use of a combination of oral vitamins C and E for 3 months documented a significant decrease in the clinical signs of sunburn and thymine dimer formation after UVB irradiation.233 In a mouse model, dietary addition of lutein, which is a carotenoid antioxidant, decreased edema and suppression of contact hypersensitivity after UVB exposure.172 Green tea given orally to mice reduced cutaneous oxidative damage and abnormal matrix metalloproteinase formation in response to UVB.301 There are some concerns about the routine use of antioxidants. For example, topical vitamin E may provoke contact sensitization and may occasionally serve as a tumor promoter.206 In addition, both topical and oral antioxidants might interfere with the normal functioning of p53 protein to produce apoptosis of photodamaged keratinocytes via oxidative enzymes. Repair Enzyme T4 Endonuclease V There has been considerable interest in postexposure therapy for sunburn with the topical application of the DNA repair enzyme

BOX 14-3  Common Oral Photosensitizing Medications Antihistamines Fluoroquinolones Nonsteroidal antiinflammatory drugs Oral contraceptives Phenothiazines Sulfonamides Sulfonylureas Tetracyclines Thiazides Tricyclic antidepressants

T4 endonuclease V (T4N5). When it is applied in liposomes, T4N5 localizes in the epidermis and the appendages,320 thereby enhancing repair of UVR-induced DNA damage in mice and humans.318 T4N5 prevents UVR-induced immunosuppression166 and reduces UVR-induced skin cancer in mice.319 In a study of 30 patients with XP, T4N5 in a liposomal base significantly reduced the incidence of new actinic keratoses and basal cell carcinomas after 1 year.321 Given these qualities, T4N5 may serve in the future as a “morning-after” cream.

Photosensitivity Disorders ENDOGENOUS PHOTOSENSITIVITY DISORDERS Sun protection is especially important for persons with endogenous photosensitizing disorders, persons who take photosensitizing medications (Box 14-3), and persons who are exposed to topical photosensitizers (Box 14-4). The most common endogenous photodermatosis is polymorphous light eruption, which affects 10% to 14% of whites and predominantly females who are less than 30 years old. Clinically, this manifests with pruritus, erythema, macules, papules, or vesicles on sun-exposed skin arising 1 to 2 days after exposure and resolving spontaneously over the next 7 to 10 days. It is most common with initial sun exposures during the spring or early summer; “hardening” of the skin may occur with subsequent exposures. The action spectrum is unclear, although it is most commonly 290 to 365 nm.84 Patient education is very important for persons with this group of disorders. Sun avoidance and protective clothing are critical. Liberally applied sunscreens are helpful; a broad-spectrum sunscreen that contained padimate O and avobenzone was quite effective in one study.86 For medication-related photosensitization disorders, identifying the specific causative agent is crucial, and discontinuation or substitution, whenever possible, should be considered. For polymorphous light eruption, super- or highpotency topical steroids in several daily to weekly pulses— frequently in combination with systemic antihistamines (e.g., diphenhydramine, hydroxyzine, doxepin)—can help to manage pruritus and control the eruption. Hardening of the skin in the spring with UVB, narrow-band UVB, or PUVA can be very effective. Systemic antimalarials (e.g., 200 to 400 mg/day of hydroxychloroquine sulfate, started in late winter) are generally less effective than phototherapy; beta-carotene has been used with varying success. For patients with severe issues, azathioprine, cyclosporine, thalidomide, and mycophenolate mofetil may be considered. Lupus erythematosus may be exacerbated by sunlight. Although UVB is typically causative, UVA can contribute to this condition in some patients. Consequently, broad-spectrum sunscreens in combination with sun avoidance and clothing protection are most appropriate. A broad-spectrum sunscreen that contained padimate O and avobenzone diminished clinical severity in a 4-week study.45 Systemic antimalarials may also be used in more serious cases. Porphyrias are caused by inherited abnormalities in heme synthesis. Clinical manifestations vary with the genetic subtype, but photosensitivity is common with this group of disorders. Typically, the action spectrum is in the Soret band at 400 to 311

CHAPTER 14  Exposure to Radiation From the Sun

increases in melanin production. Topical application to guinea pigs increases pigmentation. This raises the question of whether the induction of protective pigmentation in humans might be possible with T-T dimers.

PART 3  BURNS, FIRE, AND RADIATION

BOX 14-4  Topical Phototoxins and Photoallergens Topical Phototoxic Compounds Dyes Eosin Methylene blue Medications Phenothiazines Sulfonamides Psoralens Methoxypsoralen Trimethylpsoralen Tars Creosote Pitch Topical Phototoxic Plants Angelica Carrot Celery Cow parsley Dill Fennel Fig Gas plant Giant hogweed Lemon Lime Meadow grass Parsnip Stinking mayweed Yarrow Topical Photoallergenic Compounds Antiseptics Chlorhexidine Hexachlorophene Fragrances Methylcoumarin Musk ambrette Phenothiazines Salicylanilides Sulfonamides Sunscreens Benzophenones Cinnamates Dibenzoylmethanes Para-aminobenzoic acid Para-aminobenzoic acid esters

410 nm. Consequently, sunscreens other than “physical” blockers are generally inadequate, although topical DHA and oral betacarotene may be useful adjuncts to sun avoidance and protective clothing. Chronic actinic dermatitis manifests as persistent macules and plaques that are often infiltrated and lichenified on chronically sun-exposed sites on older men. These patients may demonstrate dermatitic flares on involved areas with even modest photoexposure to UVR and shorter-wavelength visible light. Histologically the disorder can demonstrate progression from dermatitis to T-cell lymphoma. Broad-spectrum sunscreens, sun avoidance, and clothing protection (including the wearing of brimmed hats) are essential. For advanced cases, therapy with azathioprine, cyclosporine, PUVA, and retinoids has been used. Persons with persistent light reaction display a peculiar and persistent overreaction to sun exposure as a result of a prior topical photoallergy. Musk ambrette, which is found in many 312

perfumes, has been reported to provoke persistent light reaction.245 UVB is most often causative, although UVA may be involved as well. Broad-spectrum sunscreens, sun avoidance, and clothing protection provide appropriate prophylaxis. For disorders in which melanocytes are defective or absent (e.g., albinism, vitiligo) and for disorders in which DNA repair mechanisms are deficient (e.g., XP), the protective triad of sunscreens, sun avoidance, and clothing protection is required.

PHOTOTOXICITY Most oral photodrug eruptions are phototoxic, and they clinically manifest as exaggerated sunburn on exposed skin. Typically, there are sharp cutoffs at the “V” of the neck and the short-sleeve line. Less commonly there may be photo-onycholysis, which causes the distal fingernails to separate from their underlying beds. Photodrug eruptions are usually triggered by UVA. The most common offending drugs are listed in Box 14-3. Topical photosensitizers may cause phototoxicity, photoallergy, or both. Phototoxicity results in an exaggerated sunburn that is typically followed by postinflammatory pigmentation. Phototoxicity is nonimmunologic. The action spectrum for most topical phototoxic sensitizers is in UVR. A surprisingly large number of plants contain photosensitizers that can produce phototoxic reactions in exposed human skin (see Box 14-4), which results in a condition known as phytophotodermatitis. The most common chemical precipitants are furocoumarins, especially psoralens, which are found in limes, lemons, and certain other plants (Figure 14-12). Phytophotodermatitis is common among farmworkers, bartenders, cannery packers, and vacationers to sunny climates. Oil of bergamot, which contains 5-methoxypsoralen, is a frequent cause of phototoxicity related to perfumes (berloque dermatitis). Streaks of erythema and subsequent pigmentation on exposed skin of the face, neck, and wrists typify this eruption. Meadow-grass dermatitis among hikers is another example of phytophotodermatitis. Various common weeds, including meadow parsnip, contain furocoumarins, which cause whiplike erythematous streaks and pigmenting on skin after exposure to sunlight. Psoralens have been incorporated into sunscreens in Europe to promote tanning, although their use is associated with increasing risks of burns and carcinogenicity.48 PUVA is used therapeutically for psoriasis and select other dermatoses.

PHOTOALLERGY Although phototoxic reactions may occur in anyone, photoallergic reactions occur only in previously sensitized individuals. Photoallergic reactions are uncommon. They are typically provoked by interaction of UVA with a topical proallergen, and result in contact dermatitis within 48 hours. Unlike phototoxic reactions, which are limited to exposed skin, photoallergic reactions can spread to sun-protected adjacent sites. Sunscreens are

FIGURE 14-12  Phytophotodermatitis on a teenager after a “lime fight” that took place during an outdoor summer picnic.

Changing Attitudes Toward Photoprotection During the 20th century, a tan became desirable. It was equated with health, wealth, and stylishness. Characterizing the times was Coco Chanel’s pronouncement in 1929 that “a golden tan is the index of chic.” Sadly, this attitude led to dangerous behaviors and resulted in an epidemic of skin cancer. Psychological and attitudinal barriers remain some of the most challenging to overcome. Several studies have documented current attitudes toward photoprotection. In a study of Connecticut beachgoers, 70% said that they were there to obtain or maintain a tan.330 College students who were questioned in North Carolina stated that they rarely if ever used sunscreens.298 In a U.S. study of 2459 whites, 59% admitted to sunbathing, and 25% stated that they had sunbathed more than 10 times during the preceding year.158 Among spring skiers, only two-thirds used sunscreens, and of those, one-third were sunburned at the time of the survey.199 A survey in Leicester, England found that onehalf of all children were sunburned at least once a year.31 A 2003 Fact Sheet from the Centers for Disease Control and Prevention reported that 43% of white children who were less than 12 years old in the United States had one or more sunburns within the prior year.118 Even patients with sun-related problems often do not adopt adequate sun-protection habits. One study documented that patients with dysplastic nevus syndrome, who are at higher risk for melanoma, do not avoid sunburning.34 Among Israeli patients 1 year after treatment for BCCa, only 49% wore hats or long sleeves in the summer, and 62% used less than two bottles of sunscreen per year.127 Sunscreen use correlates with knowledge of the harmful effects of sun exposure and an understanding of SPF values.26 In a survey of 1001 adults in the United States, only 42% were aware of the term melanoma, and only 34% knew that it was some type of skin cancer.203 Many mistakenly use sunscreens in the belief that sunscreens will promote tanning. Clearly more education is needed. For 146 college students in Southern California, a 12-minute videotape about photoaging in conjunction with ultraviolet facial photography resulted in improved sunprotective behaviors 1 month after the education.184 In Australia, where a significant educational effort is under way, three-fourths of adults visiting their family physicians reported that they used sunscreens.192 Australian state-sponsored and privately sponsored programs stress sun avoidance and clothing protection over sunscreens, and increasingly Australian fashion magazines feature more hats and more models who are less tan.50 Prevention and early diagnosis programs have yielded results: sun-seeking behaviors and sunburns have decreased. More importantly, the incidence of melanoma has decreased, and melanoma survival has increased in younger Australian cohorts.196 Photoprotection education needs to begin during childhood. Considerable sun exposure occurs by the age of 18 years,

and childhood exposure may be more significant than lifetime exposure for determining the subsequent risks of BCCa and melanoma. Children who use or who are compelled to use sunscreens at an early age are more likely to use sunscreens as adolescents.17 However, sun-protection policies in U.S. schools are lacking, with one 2006 study demonstrating that only 10% of the 484 secondary schools in 27 cities surveyed had a formal policy in place.42 This situation thus requires the education of parents. Sadly, parents too often ignore or are ignorant of photoprotective measures. On beaches in Galveston, Texas at midday in July, only 42 of 82 parents interviewed had applied sunscreen to their children.182 Only a history of prior painful sunburns was correlated with sunscreen use, and this finding was documented in other studies as well.329 Physicians should try to alter parental behavior through education, beginning with the first well-baby visit. In the Galveston study, photoprotection was discussed during only 18% of well-baby checkups. Sun avoidance and clothing protection should be advocated for infants who are less than 6 months old, and sunscreen should be added to the photoprotective regimen for older toddlers and children. Consistent use of sun protection during childhood would decrease the number of sunburns and provide lifelong reduction in photoaging and NMSC.281 Advertisers and the fashion industry continue to glorify tanning with the use of bronzed models. Even sunscreen advertisements seem to have a dual and medically incompatible message: tan beautifully while protecting your skin. No wonder the public is confused by oxymoronic enticements regarding a “healthy tan.”240 Recently in the United States there has been a glimmer of progress toward photoprotection education in the public media. In a review of models in six popular American fashion magazines between 1983 and 1993, there was a trend toward lighter tans, more sunscreens, and more articles about sun awareness, although men’s magazines did not demonstrate this trend.100

Conclusion Sun exposure is associated with both acute and chronic deleterious sequelae. Sun protection significantly mitigates these sequelae. Appropriate sun-protective strategies include a combination of sun avoidance, clothing protection, and sunscreens. Sunscreens have evolved to become increasingly elegant and effective. Despite occasional concerns, sunscreens have enjoyed an excellent safety record for more than 5 decades.103,176 Still, some issues remain controversial and unanswered. For example, further research is needed to answer concerns about vitamin D deficiency with strict sun protection. It is conceivable that minimal and “sensible” sun exposure in adults may be part of that answer. For now, the best advice remains to use sun protection. Sun protection should begin during infancy and continue throughout life; educating parents and children is key to the success of this plan. With the introduction of high-SPF, broad-spectrum, waterproof sunscreens and high-SPF clothing fabrics, the wilderness enthusiast can enjoy the outdoors more safely.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 14  Exposure to Radiation From the Sun

paradoxically the current leading cause of photoallergy.60,136 During the 1970s, the fragrance 6-methylcoumarin, which was added to a tanning product, was responsible for a number of cases of photoallergy.245 During the 1960s, there was a virtual epidemic of photoallergic reactions that resulted from antibacterial salicylanilides used in soaps.245 Prevention requires excellent UVA protection, including use of broad-spectrum sunscreens.

CHAPTER 15 

Volcanic Eruptions, Hazards, and Mitigation JOANNE N. FELDMAN AND ROBERT I. TILLING

Volcanic eruptions are spectacular, violent, and often quite dangerous expressions of Earth’s dynamic internal processes (Figure 15-1). More than 80% of the earth’s surface above and below sea level is of volcanic origin, and gaseous emissions from volcanoes helped form the earth’s oceans and atmosphere.22 On average, about 60 to 70 eruptions occur worldwide each year; half of these are continuations of previously erupting volcanoes, and the others are new eruptions.63,69 There are approximately 600 active volcanoes in the world and probably another 800 that have erupted at least once during the past 10,000 years.69 Some volcanoes erupt only once in their lifetime, whereas others erupt repeatedly or even continuously. The largest explosive eruptions occur infrequently; in general, the longer the time interval between eruptions, the larger the next eruption tends to be. Some of the worst volcanic catastrophes in history have occurred at volcanoes believed to be extinct, including the famous eruption of Vesuvius in AD 79, which destroyed the cities of Pompeii and Herculaneum (see later).69 In fact, in the past two centuries, 12 of the 17 largest eruptions were the first eruptions known in historical times.57,63 Table 15-1 lists some notable historical eruptions, the most recent of which occurred at Chaitén Volcano in southern Chile, coming back to life after being inactive for 9400 years.37 The Chaitén eruption, which began in May 2008, has continued nonexplosively into June 2010. This eruption has special volcanologic significance, because it is the world’s first major rhyolitic eruption since the 1912 eruption of Novarupta, Alaska—the largest in the 20th century (Figure 15-2; see Table 15-1). Volcanic eruptions have been responsible for the deaths of approximately 300,000 people in the past 400 years. In recent

years, the average is two to four fatal volcanic events per year.64 Causes of death and number of fatalities are not well documented.64 Most deadly of the volcano hazards, pyroclastic flows have claimed the most lives, whereas tephra is the most common killer (Box 15-1). Long after the eruption, famine and disease epidemics are responsible for up to one-third of the total fatalities attributed to explosive eruptions (Tables 15-2 and 15-3).64 Compared with other natural disasters, volcanic eruptions occur infrequently, affect few people, and are responsible for only a small percentage of fatalities. Only some 2% of all natural disasters are from volcanic activity.33,65 The deadliest volcanic eruption in history, Tambora, Indonesia, in 1815, killed approximately 60,000 people, whereas 1 million people were killed in the worst hurricane (Ganges Delta in Bangladesh, 1970) and 830,000 were killed in the worst earthquake (Shaanxi earthquake in China, 1556).36,62,69 Nevertheless, volcanoes have the potential to unleash one of the most destructive forces on Earth. Approximately 74,000 years ago, an Indonesian volcano named Toba

A

B

FIGURE 15-1  Eruption of Mt St Helens on May 18, 1980. (Courtesy Robert M. Krimmel, U.S. Geological Survey.)

314

FIGURE 15-2  A, Satellite view of an ash plume produced during the explosive phase of the ongoing eruption of Chaitén Volcano, southern Chile; plume is drifting downwind across Argentina and dissipating over the Atlantic Ocean. B, Aerial oblique view in January 2010 of the actively growing 2008-2010 lava dome within Chaitén’s 3-km (1.9-mile)wide summit caldera. (A MODIS/NASA image, May 3, 2008; B courtesy John Pallister, U.S. Geological Survey.)

For online-only figures, please go to www.expertconsult.com

Volcano

Country

Year

Significance

Santorini

Greece

1650 BC

Vesuvius

Italy

AD

Laki

Iceland

1783

Tambora

Indonesia

1815

Krakatau

Indonesia

1883

Montagne Pelée Novarupta

Martinique United States

1902 1912

Mt St Helens

United States

1980

El Chichón

Mexico

1982

Nevado del Ruiz

Colombia

1985

Mt Pinatubo

Philippines

1991

Chaitén

Chile

2008

One of the largest explosive eruptions on Earth; may have contributed to the decline of Minoan civilizations First major historical eruption to occur within range of major cities; first eruption to be well documented by an eyewitness (Pliny the Younger) Largest historical lava flow eruption on Earth; catastrophic impact on Iceland’s population from famine caused by loss of livestock from poisoning by hydrogen fluoride emissions Largest historical volcanic eruption on Earth; highest estimated eruption column (43 km [27 miles]); largest known death toll of over 60,000 (12,000 directly by pyroclastic flows* and tephra*; 48,000 indirectly from starvation and disease); global sulfuric acid aerosols caused worldwide climate change resulting in the “Year Without a Summer” in 1816; abnormally low temperatures in the northern hemisphere caused famine from widespread crop failure First large eruption of the modern age; two-thirds of the island destroyed; tsunami* killed 36,000 people living in adjacent coastal areas Classic example of a moderate-sized eruption causing severe loss of life: 29,000 people died Largest eruption in the world in the 20th century; occurred in uninhabited part of Alaska; no fatalities First major explosive eruption to be monitored intensively with modern technology; worst volcanic disaster in U.S. history; $1 billion worth of damage but only 57 people died because timely forecasting prompted evacuation Erupted violently three times; first eruption came as a complete surprise; pyroclastic flows killed 2000; worst volcanic disaster in Mexican history Example of small eruption causing severe loss of life; lahar* caused 23,000 deaths and $212 million of damage; worst volcanic disaster in Colombian history; disaster demonstrates that in densely populated areas, even very small eruptions can cause widespread devastation and kill thousands Second-largest eruption of the 20th century; major societal impact in Philippines; important but temporary global atmospheric effects; despite its huge size, eruption directly caused only 300 deaths because of timely evacuations prompted by precise forecasts by scientists Largest eruption in the 21st century to date; volcano had been dormant for 9400 years before abrupt onset of eruption in May 2008; activity is continuing nonexplosively through mid-June 2010; lahars and ashfalls caused relatively few deaths but severe socioeconomic impacts in southern Chile and downwind neighboring Argentina

79

Data from Sigurdsson H: The history of volcanology. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press; Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; Clemens JA: Volcano! Evacuation and military medical implications, ADF Health 3:25, 2002; and Lara LE: The 2008 eruption of Chaitén Volcano, Chile, Andean Geology 36:125, 2009. *See definitions in Box 15-1.

exploded and ejected 2800 km3 (672 cubic miles) of ash, dust, and volcanic gases high into the stratosphere, where it was carried around the world by high-altitude winds. The particulate matter interfered with solar radiation and is thought to have led to a 10° C (22° F) temporary global cooling of the earth’s surface.62,77 Such a degree of cooling today would be catastrophic on a global scale. We can expect more fatalities from volcanic eruptions as human settlements inexorably encroach on areas with high-risk volcanoes.4 Current estimates suggest that about 500 million people, or 10% of the world’s population, live within 100 km (62 miles) of a volcano that has been active in the historical record.4,53 Auckland, New Zealand, occupies an area of young volcanoes. Seattle–Tacoma, Washington, is on land that could be devastated by mudflows from an eruption of Mt Rainier. Naples, Italy, is built on the flanks of Vesuvius, where in the first minutes of a major eruption more than 100,000 people could be

BOX 15-1  Glossary of Terms Lahar Lava Magma Pumice Pyroclastic flow Tephra Tsunami Volcanologist

Volcanic mudflow Magma that has erupted at the earth’s surface Molten rock inside the earth Lightweight solidified fragments of magma ejected explosively from an eruption Ground-hugging ash and rock clouds that sweep down slopes at hurricane speeds Explosively erupted airborne volcanic material such as ash, pumice, and rocks Seismic sea wave generated by an earthquake or eruption Scientist who studies volcanoes

killed (Figure 15-3).4,9,57 Latin America and the Caribbean are areas of particularly high risk because of population density. During the 20th century, 76% of all fatalities from volcanic eruptions occurred in this region, and in the past 10 years, one-half of the most powerful eruptions occurred in this area. In general, most fatalities occur in densely populated, less developed countries (Table 15-4).53 Although volcanic eruptions constitute a significant natural hazard, other processes and products of volcanism can be highly beneficial to society, explaining in part why so many people live on or near volcanoes.62 Volcanic ash rejuvenates soil and can prevent the loss of phosphorus, resulting in highly productive agricultural land (Figure 15-4, online). Volcanic ore deposits supply diamonds, copper, gold, silver, lead, and zinc. Products of volcanic activity are used as building materials, as abrasive and cleaning agents, and for many chemical and industrial uses.22 Geothermal heat and steam can drive turbines to generate electricity, heat homes and industries directly, and be enjoyed by people at hot spring resorts (Figure 15-5, online). The beauty of volcanoes and volcanic activity also generates income for communities through tourism.

Vesuvius,

AD

79

The best-known volcanic eruption was Vesuvius on August 24, AD 79. This eruption killed thousands of people, devastated the surrounding countryside, and destroyed at least eight towns, most notably Pompeii and Herculaneum. Before this eruption, Vesuvius was seen as a benign mountain with lush vineyards planted on the slopes and human settlements on the mountain’s flanks. Unlike the nearby often-erupting volcanoes Etna and Stromboli, Vesuvius was not considered volcanic. Even a series of preeruption earthquakes, as is typical before eruptions, did little to raise concern that Vesuvius was an active volcano. The eruption was witnessed and documented by Pliny the 315

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

TABLE 15-1  Notable Historical Eruptions

PART 3  BURNS, FIRE, AND RADIATION

TABLE 15-2  Causes of Fatalities From Notable Volcanic Disasters Since 1000 AD No. of Deaths According to Primary Cause Volcano

Country

Year

Pyroclastic Flow

Merapi Kelut Vesuvius Etna Merapi Awu Oshima Cotopaxi Makian Papadayan Laki Asama Unzen Mayon Tambora Galunggung Nevado del Ruiz Awu Cotopaxi Krakatau Awu La Soufrière Montagne Pelée Santa María Taal Kelut Merapi Lamington Hibok-Hibok Agung Mt St Helens El Chichón Nevado del Ruiz

Indonesia Indonesia Italy Italy Indonesia Indonesia Japan Ecuador Indonesia Indonesia Iceland Japan Japan Philippines Indonesia Indonesia Colombia Indonesia Ecuador Indonesia Indonesia St Vincent Martinique Guatemala Philippines Indonesia Indonesia Papua New Guinea Philippines Indonesia United States Mexico Colombia Totals: GRAND TOTAL

1006 1586 1631 1669 1672 1711 1741 1741 1760 1772 1783 1783 1792 1814 1815 1822 1845 1856 1877 1883 1892 1902 1902 1902 1911 1919 1951 1951 1951 1963 1980 1982 1985

1000 — — — 300 — — — — 2960 — 1150 — 1200 12,000 — — — — — — 1560 29,000 6000 1330 — 1300 2940 500 1900 57 >2000 — >65,197

Lahar

Tsunami

Lava Flow

— 10,000 — — — 3200 — 1000 3000 — — — — — — 4000 1000 3000 1000 — 1530 — — — — 5110 — — — — — — >25,000 >57,840

— — — — — — 1480 — — — — — 15,190 — — — — — — 36,420 — — — — — — — — — — — — — 53,090 >261,467

— — 18,000 10,000 — — — — — — — — — — — — — — — — — — — — — — — — — — — — — 28,000

Posteruption Starvation — — — — — — — — — — 9340 — — — 48,000 — — — — — — — — — — — — — — — — — — >57,340

Modified from Tilling RI: Volcanic hazards and their mitigation: Progress and problems, Rev Geophys 27:237, 1989; and Tanguy J-C, Ribière C, Scarth A, et al: Victims from volcanic eruptions: A revised database, Bull Volcanol 60:137, 1998.

Younger. In two letters written to the Roman historian Tacitus, Pliny wrote that the first explosion began in the early afternoon and ended in the evening of the following day. At first, Vesuvius produced an enormous eruption cloud that ejected ash, pumice, and volcanic gases vertically up to 30 km (19 miles) high. Then, from a darkened sky, ash and pumice rained down on the towns of Pompeii and Straide, causing roofs to collapse under the weight of the ash fall and burying the towns (Figure 15-6, online). The town of Herculaneum, lying at the foot of Mt Vesuvius on a cliff overlooking the sea, was initially spared from burial. The prevailing wind blew away from the town and toward TABLE 15-3  Fatalities From Volcanic Eruptions,

1783-2000

Fatalities Volcanic Hazard Posteruption famine and disease epidemics Pyroclastic flows Lahars Volcanogenic tsunamis Debris avalanches Volcanic ash Volcanic gases Lava flows TOTAL

No. 75,000 67,500 42,500 42,500 10,000 10,000 1750 750 250,000

TABLE 15-4  Fatalities From Volcanic Eruptions by

Region, 1600-1982

% 30 27 17 17 4 4 <1 0.3 —

Modified from Baxter PJ: Impact of eruptions on human health. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press.

316

Pompeii. But in the early hours of August 25, Vesuvius exploded again, this time ejecting hot gases, ash, and pumice down the mountain’s slopes as a pyroclastic flow. Herculaneum was destroyed, buried beneath more than 20 m (66 feet) of pumice and ash. Whatever remained of Pompeii was also destroyed at that time.56 At about that time, Pliny the Younger wrote of the death of his uncle, Pliny the Elder, who probably died of asphyxiation from being caught too close to a pyroclastic flow.4 The remains of more than 2000 people found amid the ruins offer clues as to the causes of death. People unwilling or unable to flee their homes were instantaneously suffocated as hot volcanic ash and gases entered buildings. Others had multisystem trauma as the force of the explosion and pyroclastic flows scooped up rocks and building materials and smashed them into anything in their path. Skeletons recently uncovered in beach

Fatalities Region Indonesia Caribbean Japan Iceland Everywhere else TOTAL

No.

%

161,000 31,000 19,000 9400 19,000 239,400

67 13 8 4 8 100

Modified from Blong RJ: Volcanic hazards: A sourcebook on the effects of eruptions, Orlando, Fla, 1984, Academic Press.

THEORY OF PLATE TECTONICS

B

C FIGURE 15-3  A, Mt Eden, one of 50 geologically young but dormant volcanoes in the Auckland Volcanic Field, within the city of Auckland, New Zealand. B, Mt Rainier sits just 137 km (85 miles) southeast of Seattle–Tacoma, Washington. C, Bay of Naples, Italy, with Mt Vesuvius in the background. (A courtesy Lloyd Holmer, Institute of Geological and Nuclear Sciences, New Zealand; B courtesy Lyn Topinka, U.S. Geological Survey; C courtesy Robert I. Tilling, U.S. Geological Survey.)

The global distribution of volcanoes, as well as the origin and distribution of mountain ranges and earthquakes, are explained by plate tectonics.54,69 This theory suggests that the earth’s outermost layer is broken into a number of rigid plates that move relative to one another as they float atop the hotter, semisolid, more mobile material of the mantle. The nature and distribution of volcanic activity depend on the formation, movement, and destruction of these plates at their margins (Figure 15-10). When two tectonic plates move away from each other, or diverge, new crust is created as molten rock pushes up from the mantle and oozes out onto the earth’s surface or the seafloor. One well-known, mostly oceanic, divergent boundary, the MidAtlantic Ridge, is a submerged mountain range in the Atlantic Ocean that extends from the Arctic Ocean to beyond the southern tip of Africa. Along the Mid-Atlantic Ridge are numerous volcanoes, including those that rise above sea level in Iceland (Figure 15-11). Another prominent divergent boundary, entirely continental, is the 11,000-km-long (6835-mile-long) Great African Rift. About 75% of Earth’s volcanism occurs unseen along divergent boundaries, deep on the ocean floor. Two plates can also move toward one another, or converge. How two converging plates interact depends on the type of crust—continental or oceanic. Continental parts of plates, composed largely of granitic rocks, are relatively lightweight compared with the much denser and heavier oceanic parts of plates, which are composed of basalt. When two continental plates collide, both buckle upward to form a mountain range. The Himalaya Mountains are the result of the Indian plate colliding against the Eurasian plate (Figure 15-12). Few volcanoes are located in zones of continental collisions.

caves in Herculaneum suggested that the cause of death was the intense heat, roughly 500° C (932° F) (Figure 15-7).12,44,67

Volcanoes and Their Global Distribution Different images are associated with the word volcano—for example, a violently erupting Mt St Helens, a peaceful-looking snow-capped Volcán Villarrica in Chile, or rivers of lava flowing down the flanks of Kilauea Volcano in Hawaii (Figure 15-8). Volcano also means the opening, or vent, in the earth’s crust through which molten rock, ash, and gases are ejected. Molten rock, while underground, is called magma. It becomes lava once it reaches the surface. Whether a volcano erupts explosively (like Vesuvius or Mt St Helens) or nonexplosively (like the lava flows of Kilauea) depends on the magma—its composition, temperature, gas content, viscosity, and crystal content.62 Magma that is fluid and hot tends to erupt frequently (every few years) and generally nonexplosively. This type of volcano most commonly produces fountains or rivers of red-hot lava.72 In contrast, magma that is less fluid and cooler, and that contains trapped gases, tends to rise sluggishly and can plug up the volcanic vent. If enough pressure builds up as trapped gases

FIGURE 15-7  The “Garden of the Fugitives,” in Pompeii, Italy, reveals 13 adults and children huddled together in a futile attempt to shield themselves from pyroclastic flows from the eruption of Vesuvius in AD 79. The human casts are obtained by filling cavities left in hardened ash with liquid chalk. (Courtesy Lancevortex.)

317

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

A

expand during ascent, the pent-up pressure can blow the plug, abruptly unleashing the expanding gases and producing a violent eruption.35 The most volcanically and seismically active zone in the world, called the Ring of Fire, coincides roughly with the borders of the Pacific Ocean (Figure 15-9).35 The volcanically active countries in this zone include Russia, Japan, the Philippines, Indonesia, Papua New Guinea, New Zealand, and the countries on the Pacific coasts of North, Central, and South America. Volcanoes are also scattered in the Atlantic and Pacific Oceans—in Hawaii, Iceland, and the Galapagos.

PART 3  BURNS, FIRE, AND RADIATION

A

B

C

FIGURE 15-8  A, Violently erupting Mt St Helens on May 18, 1980. B, Villarrica Volcano, Chile, looks peaceful and even has a ski lift on its flanks, but the mountain is actually the most active volcano in Chile. C, A long river of lava flowing downhill from Kilauea Volcano in 1983. It ultimately enters the ocean 12 km (7.5 miles) away. (A courtesy Keith Ronnholm; B courtesy Robert I. Tilling, U.S. Geological Survey; C courtesy J. D. Griggs, U.S. Geological Survey.)

Many of the world’s volcanoes are located at the convergent boundary between a continental plate and an oceanic plate. When these plates converge, the heavier oceanic plate dives, or subducts, below the lighter continental plate. This produces tremendous pressure and heat, melting the rock deep in the mantle. This molten rock, or magma, traps gases, such as carbon dioxide (CO2) and sulfur dioxide (SO2), making it buoyant in the surrounding denser, solid rock, and it begins to rise through the surrounding solid rock. Magma movement causes earthquakes that can be recorded with sensitive volcano-monitoring equipment. If the rising magma finds an area of weakness at the earth’s surface, a volcano is created either just inland from the coast—for example, the volcanoes in eastern Russia, the Cascades in North America, and the Andes in South America— or just off the coast, such as the volcanic island arcs of the Aleutian Islands in Alaska,

FIGURE 15-9  The Ring of Fire, a zone of frequent earthquakes and volcanic eruptions encircling the Pacific Ocean. Where the plates come together, they form deep oceanic trenches (green). (From Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office.)

318

and Indonesia (Figure 15-13). Because of their proximity to a continent’s coastline or to an island, subduction volcanoes are often near populated regions and thus can have a significant human impact. Eruptions tend to be violent and explosive, such as the 1980 eruption of Mt St Helens or the 1991 eruption of Mt Pinatubo in the Philippines.62 Some volcanoes are found far from plate boundaries. The Hawaiian volcanoes are more than 3200 km (1988 miles) from the nearest plate boundary, and Yellowstone, with over 10,000 geysers, hot springs, and boiling mud pools, is located in the interior of the North American plate. At both of these locations, an inferred hot spot below the plate melts overriding rock to produce magma that can rise toward the surface and ultimately erupt onto the seafloor or land. It has been assumed that the hot spot is stationary, whereas the tectonic plate above it moves. However, recent studies have questioned the fixedness of hot spots, prompting substantial debate among Earth scientists. Examination of oceanic hot spots shows that in a series of islands created by plate movement, the islands farthest from the hot spot are the oldest. For example, a 6000-km (3728-mile) chain of volcanoes stretches from the older Emperor Seamounts (underwater sea mountains) off Alaska to the younger Hawaiian Islands. These were all created by passage of the Pacific Plate over the Hawaiian hot spot. This hot spot, currently located under the Big Island of Hawaii, has remained stationary for about 45 million years, whereas the Pacific Plate has been slowly moving to the northwest. According to the stationary-hot-spot model, as the plate continues to move over the hot spot, a new Hawaiian island will eventually emerge above sea level. In fact, just 35 km (22 miles) southeast of the Big Island there is an underwater volcano, Loihi, that has risen 3 km (1.9 miles) above the seafloor and is within 1 km (0.6 miles) of the ocean surface (Figure 15-14). At hot-spot volcanoes, eruptions tend to be nonexplosive and are rarely life threatening.35 Huge volumes of fluid lava pour out, often creating large volcanic mountains, such as Mauna Loa, the largest single volcano in the world, standing 8851 m (5.5 miles) above the sea floor.

Types of Volcanoes As erupted material accumulates around a volcanic vent, a volcano is formed and progressively grows. Classified by

Isl

Oc

an d

Convergent plate boundary

ea

Tr

c

Shield volcano

en

ar

tle pla

M an

te

ng

ti uc

Lithosphere Asthenosphere

Moho Hotspot

bd

nc h

Oceanic crust

Sub

Continental crust Ma ntl Moho ting e plat e

duc

Mantle Mantle plume ?

Su

Tre g

ch

Stratovolcano

nic rid spre ge ad in

Continental rift zone (young divergent plate boundary)

Ex tra te ob rrestr jec t ial

Divergent plate boundary

Not to scale

Schematic cross section of plate tectonics

FIGURE 15-10  Cross section of the main types of plate boundaries. (From “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory.)

Divergent boundary

Oc

ea

ni c rid spr ge ead i

Tre n

ch

ng

structure, the most common types of volcanoes are composite volcanoes, calderas, shield volcanoes, subglacial volcanoes, and flood basalts. These can be roughly grouped as either explosive or nonexplosive volcanoes. However, volcanoes can show both explosive and nonexplosive behavior during their lifespan. For example, Kilauea typically erupts nonexplosively, spewing out fountains and rivers of lava, yet a 1924 eruption was spectacularly explosive, and new studies show that Kilauea’s explosive eruptions are as frequent as those of Mt St Helens.

GENERALLY EXPLOSIVE VOLCANOES Lithosphere Oceanic crust

Asthenosphere

A

B

C

FIGURE 15-11  A, Cross section of an oceanic divergent boundary. B, Map of the Mid-Atlantic Ridge, along which the Eurasian and African plates are pulling away from the North American and South American plates. Note the ridge rising above sea level in Iceland. C, Exposed segment of the Mid-Atlantic Ridge at Thingvellir, Iceland. Left of the fissure, the North American Plate is pulling westward away from the Eurasian Plate (right of the fissure). (A from “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory; B and C from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office.)

Composite Volcanoes Composite volcanoes, or stratovolcanoes, have steep sides and are typically associated with subduction zones at converging plate boundaries. Mt Fuji in Japan, Mt Pinatubo in the Philippines, and Mt Rainier in the United States are classic examples. However, composite volcanoes can also be formed at divergent plate boundaries (e.g., Hekla in Iceland and Mt Kilimanjaro in Tanzania) or at hot spots (e.g., Mt Erebus in Antarctica and Tenerife of the Spanish Canary Islands).56,57 The steep-sided shape results from the deposition of viscous lava flows alternating with pyroclastic flows and ashfall deposits. The explosive nature of composite volcanoes comes from the high viscosity and volatility of the magma (Figure 15-15). Calderas Formed by the collapse of a volcanic structure, calderas are circular or elliptical depressions, generally over 1 km (0.62 mile) in diameter. Crater Lake in the U.S. Cascade Range is a large, partially filled caldera 10 km (6.2 miles) in diameter and 600 m (1970 feet) deep, formed when Mt Mazama exploded 7700 years ago. Krakatau, in Indonesia, was created by an 1883 eruption that involved rapid emptying of the magma chamber and subsequent collapse of the volcano.56 Kilauea Crater is another well-known caldera (Figure 15-16). Very large calderas fed by huge active magma chambers have been called supervolcanoes and are capable of producing enormously explosive eruptions. Yellowstone Caldera, 85 km (53 miles) long by 45 km (28 miles) wide, the largest and most worrisome in the United States, has a magma chamber that is 40 km (25 miles) long, 20 km (12 miles) wide, and 10 km (6 miles) deep.57 Yellowstone has produced explosive eruptions 1000 times larger than the 1980 Mt St Helens eruption. Two other geologically young, large calderas located in the United States are Long Valley Caldera in California and Valles Caldera in New Mexico. Outside the United States, very large calderas include Campi Flegrei in Italy, Kamari Caldera on the island of Kos in the eastern Aegean, and Rabaul Caldera in Papua New Guinea. Fortunately, very large caldera-forming eruptions were rare events, occurring approximately once in hundreds of thousands of years (Figure 15-17, online).57 319

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

Transform plate boundary

Convergent plate boundary

Hig hp late au

ou

e

ng

ra

M

Continental crust

Continental crust

Lithosphere

Lithosphere

A

Asthenosphere

Ancient oceanic crust

B

FIGURE 15-12  A, Cross section of two continental parts of plates converging, resulting in the formation of a mountain range. B, The snow-capped Himalayas and the Tibetan Plateau are produced by the collision of the Indian-Australian Plate (left) against the Eurasian Plate (right). (A from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B courtesy NASA, photo STS41G-120-22. http://eol.jsc.nasa.gov/sseop/EFS/printinfo.pl?PHOTO=STS41G-120-22.)

GENERALLY NONEXPLOSIVE VOLCANOES

of Hawaii, are classic examples of shield volcanoes (Figure 15-18).

Shield volcanoes have gentle slopes and are formed almost exclusively of layers of lava that have often flowed great distances from the eruptive vents. The magma, unlike that of explosive volcanoes, is predominantly of low viscosity and low volatility. Shield volcanoes are mostly formed at hot spots, although some are located at convergent or divergent plate boundaries—for example, Erta Ale in Ethiopia and Mt Etna in Italy. The largest volcanoes on Earth, Mauna Loa and Mauna Kea

Subglacial Volcanoes Historically active volcanoes located under glaciers, called subglacial volcanoes, are known only in Iceland and Antarctica. They can erupt explosively, but thick ice cover generally inhibits material from being ejected high into the atmosphere. Instead, lava flows out, often melting ice and creating subglacial lakes and rivers. If this subglacial water suddenly escapes onto the glacier’s surface (a glacial burst, or jökulhlaup), a huge river can form

Tr en

Volca n

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ic arc

Shield Volcanoes

Oceanic crust

Kronotsky Volcano

Continental crust

Lithosphere

Lithosphere

Ocean

Asthenosphere

Oceanic crust Lithosphere

Pacific

rc da an Isl

nc

h

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Tr e

PART 3  BURNS, FIRE, AND RADIATION

nt

ain

Continental crust

B

Lithosphere

Asthenosphere

C

D FIGURE 15-13  A, Cross section showing subduction of an oceanic plate resulting in the formation of continental volcanoes and mountains. B, Kronotsky Volcano, at 3525 m (11,570 feet) above sea level, lies at the margin of the Pacific Ocean on the Kamchatka Peninsula of Russia. It was formed from the subduction of the Pacific Plate (right) under the Eurasian Plate (left). C, Cross section illustrating subduction of an oceanic plate with formation of volcanic island arcs. D, View of steep-sided, symmetric Carlisle volcano on Carlisle Island in the central Aleutian Islands. The 1620-m (5315-foot)-high stratovolcano has erupted several times since the late 1700s. (A and C from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B modified from NASA, photo STS61A-45-0098. http://eol.jsc.nasa.gov/sseop/EFS/photoinfo.pl?PHOTO=STS61A-45-98; D courtesy M. Harbin, University of Alaska Fairbanks, U.S. Geological Survey.)

320

TE PLA

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Zone of magma formation Fixed "Hot Spot"

A

B FIGURE 15-14  A, Cross section of the Hawaiian hot spot. B, Map of the 6000-km (3728-mile)-long Emperor Seamount–Hawaiian Ridge formed by the passage of the Pacific Plate over the Hawaiian hot spot over a span of 70 million years. (A from Kious WJ, Tilling RI: This dynamic Earth: The story of plate tectonics, Washington, DC, 1996, U.S. Government Printing Office; B from “This Dynamic Planet,” a wall map produced jointly by the U.S. Geological Survey, the Smithsonian Institution, and the U.S. Naval Research Laboratory.)

and destroy anything in its path. Grímsvötn volcano, in Iceland, lies largely beneath the vast Vatnajökull icecap. The caldera lake is covered by an ice shelf 200 m (656 feet) thick, and only the southern rim of the 6- by 8-km (3.7- by 5-mile) caldera is exposed (Figure 15-19).57 Eyjafjallajökull, a subglacial volcano 120 km

Flood-Basalt Plateaus Flood-basalt plateaus are massive areas of hardened lava produced from the largest volcanic events known on Earth.29 Found on all continents and ocean floors, flood-basalt plateaus are created when basaltic magma erupts rapidly from fissures to form sheets of lava flows, typically tens of meters thick and covering tens of thousands of square kilometers.29 Good examples are the Columbia River Plateau (Figure 15-20, online) and the Deccan Plateau of India. The rate of erupting lava can be 20 times the average eruption rate of a hot-spot volcano, and the eruption is on average 1000 times bigger than that of a supervolcano.57 Not surprisingly, the copious release of volcanic gases during the eruptions of flood basalts can severely affect the climate, and there is a strong correlation between mass extinction on Earth and the eruption of flood basalts (see Figure 15-20).57 Undersea Volcanoes Most undersea volcanoes are found at oceanic divergent plate boundaries. Others are found at undersea hot spots or near island arcs at convergent plate boundaries. Where two plates diverge, magma is injected along the space created. If the magma reaches the seafloor, pillow lava (from slow effusions) or sheets of lava (from more rapid effusions) form. Sometimes, if the magma supply to a single point is sufficiently large and persistent, a cone-shaped volcano, called a seamount, rises from the seafloor. Seamounts found at undersea hot spots become island shield volcanoes, like the Hawaiian volcanoes, if they rise above sea level. Seamounts at subduction zones become island-arc volcanoes, like the volcanoes of Indonesia, above sea level. It is not uncommon for hot-spot seamounts to emerge above sea level and then later sink as the seamount moves away from the hot spot and the seafloor subsides under the weight of the lava. Atolls, found in equatorial regions, are the coral reefs around drowning island volcanoes, after they become inactive and sink below sea level (Figure 15-21, online).57

Volcano Hazards Some volcanic eruptions cause injury, death, and destruction within minutes to hours. Others produce hazards that pose risks to human life, livestock, and the environment for months to years after the eruption. Explosive and nonexplosive

Central vent Pyroclastic layers Lava flows

A

B

FIGURE 15-15  A, Cross section of a composite volcano (also called a stratovolcano). B, Mt Fuji, Japan, is a perfect example of a composite volcano. (Courtesy Thomas C. Pierson, U.S. Geological Survey.)

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CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

IFIC PAC

(75 miles) from Reykjavik, Iceland, began to erupt on March 20, 2010, after being dormant since 1823. During the eruption, hot lava melted the overlying glacial ice and generated jökulhlaups (see Figure 15-19, C ) that caused destructive flooding and prompted evacuation of more than 800 inhabitants. Then, on April 14, the eruption entered a much more explosive phase and propelled an enormous ash plume more than 8 km (5 miles) into the atmosphere.61 The easterly drift of this plume over northern Europe provides an illustrative example of the potential hazards of volcanic ash for aviation safety (see Volcanic Ash, later). As of June 2010, the Eyjafjallajökull eruption is continuing, although at a reduced level of activity.

PART 3  BURNS, FIRE, AND RADIATION

B

I

C II

III Lake

IV

D

A FIGURE 15-16  A, Cross section of the formation of a caldera. B, Crater Lake, Oregon, was formed by the caldera-forming eruption of Mt Mazama 7700 years ago. C, When that mountain erupted cataclysmically, the summit collapsed, forming a caldera that eventually filled with water to form Crater Lake. D, Kilauea Caldera, Hawaii, in 1954 after an eruption within the caldera (dark area is the new lava). (B courtesy Peter Dartnell, U.S. Geological Survey; C courtesy Crater Lake Natural History Association; D courtesy U.S. Geological Survey.)

volcanoes generate unique hazards, but explosive eruptions are usually associated with much larger numbers of deaths.

HAZARDS FROM EXPLOSIVE VOLCANOES Volcanoes with explosive characteristics are extremely dangerous. They can cause thermal injury from hot gases and ash; mechanical injury from mud flows, debris avalanches, and falling tephra; chemical injury from toxic gases, and, rarely, electrical injury from lightning or ionizing radiation injury from radon gas (Figure 15-22).4 Most volcano-related deaths, injuries, and psychosocial effects occur because the volcano erupts violently and rapidly, leaving little or no time for people to escape or take shelter.50 However, significant fatalities have been associated with mud flows and release of toxic gases during noneruption periods. Unfortunately, the global distribution of explosive volcanoes, mostly along convergent plate boundaries, places them in densely populated areas.7 Fortunately, explosive eruptions occur infrequently, and technologic advances have increased the ability of 322

volcanologists to predict an eruption. Before the 1980 and 2004 eruptions of Mt St Helens and the 1991 eruption of Mt Pinatubo, high-risk zones around the volcanoes were evacuated because of timely warnings. Pyroclastic Flows and Surges Commonly, when an explosive volcano erupts, a volcanic cloud of gas, ash, and lava fragments rises vertically into the atmos­ phere. If this rising eruption cloud becomes denser than the surrounding air, it collapses and falls back toward the ground. Such gravitational collapse of the cloud leads to the formation of a hot, high-speed avalanche of ash, volcanic gases, lava fragments, and heated air, called a pyroclastic flow.56 Pyroclastic surges are similar to flows but are more dilute and less dense (Figure 15-23) and can travel farther.4 There is little chance for survival in the direct path of a pyroclastic flow or surge traveling at 300 km/hr (186 mph) or even greater, with temperatures of 600° to 900° C (1112° to 1652° F).57 Everything living is carbonized by the extreme

Summit caldera

Magma reservoir

A

has been rebuilt, but the population now is only 5000, much below the 1902 level (Figure 15-24). Mitigation.  Mitigation of future disasters from pyroclastic flows depends on evacuation before an impending eruption. Failure for any reason to evacuate in time will result in many deaths. Unfortunately, many countries with human settlements close to active volcanoes do not have the resources to closely monitor volcanic activity, as the United States did for Mt St Helens. In Latin America and the Caribbean alone, nearly 60% of all deaths from volcanic eruptions are caused by pyroclastic flows.53 Survival is possible without evacuation far from the volcano, if there is adequate shelter to protect against high temperatures, asphyxiating gases, falling trees, and projectiles. Once persons are sheltered, windows, doors, and dampers should be closed. Skin should be completely covered, the head swathed in cloth and, to prevent severe lung damage, the breath should be held during the seconds to minutes when the hot cloud passes by. Emergency medical personnel should be prepared to treat burns and blunt trauma injuries.

Ice cap

B

Subglacial lake

A

FIGURE 15-18  A, Cross section of a shield volcano. B, Snow-capped Mauna Loa as seen from the Hawaiian Volcano Observatory on the Big Island of Hawaii. (B courtesy Robert I. Tilling, U.S. Geological Survey.)

temperatures and swept away by the hurricane force of gas, ash, and rock sweeping downhill. Most human victims die as a result of asphyxiation (from breathing overwhelming amounts of ash or from oxygen deprivation), exposure to the intense heat, or burial under volcanic debris. Moreover, fatal traumatic injuries can result from associated devastating winds that can flatten trees and throw rocks. Survivors might have severe and extensive burns to their skin and respiratory tracts, or blunt trauma injuries.53 Although the main impact only lasts a few minutes, pyroclastic deposits can remain extremely hot for weeks and pose a lingering danger.4 Subsequent fires could cause further injury and death. Some of the most famous volcanic disasters have involved pyroclastic flows and surges. The AD 79 eruption of Vesuvius sent pyroclastic flows down the volcano flanks, killing thousands in nearby towns. The 1980 eruption of Mt St Helens created a pyroclastic surge cloud that enveloped over one hundred people as it moved at locally supersonic speeds. The 57 people closest to the crater died. Many were buried by volcanic debris, and others died from exposure to intense heat or from asphyxia. One man was killed by a falling tree and another by a rock that flew through his car windshield. Two men died in the hospital from lung injury (acute respiratory distress syndrome) caused by inhaling fine ash.4 Two others, near the edge of the pyroclastic surge, survived with minimal injury. More people would have died, but the area surrounding Mt St Helens had been evacuated after swarms of earthquakes and changes in the shape of the mountain signaled an impending eruption. Two weeks after the eruption, ash deposits on the volcano were still 300° to 400° C (572° to 752° F).70 Gophers were the only animals to survive, because they were below ground. The most devastating eruption of the 20th century occurred on May 8, 1902, when Montagne Pelée, on the Caribbean island of Martinique, sent pyroclastic flows moving greater than 100 km/ hr (62 mph) down the mountainside. Within minutes, the city of Saint-Pierre, 6 km (3.7 miles) away, was annihilated and 29,000 people were killed. Only two survived in the town. At sea, ships were capsized and demasted, and people burned by hot air fall.57 Since then, Montagne Pelée has been relatively quiet. Saint-Pierre

B

C FIGURE 15-19  A, Cross section of a subglacial volcano. B, Subglacial volcano Grímsvötn in Iceland lies largely beneath the vast Vatnajökull icecap. The caldera lake is covered by a 200-m (656-foot)-thick ice shelf. A volcanic plume rises, during the November 2004 eruption, from the exposed southern rim of the 6- by 8-km (3.7- by 5-mile) caldera. C, Aerial view of jökulhlaups from the 2010-to-present eruption at Eyjafjallajökull, Iceland (see text). (B courtesy Freysteinn Sigmundsson, Nordic Volcanological Center.)

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CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

Central vent

PART 3  BURNS, FIRE, AND RADIATION

Eruption cloud (volcanic ash cloud)

Prevailing wind Eruption column

Tephra (ash) fall Acid rain

Debris avalanche (landslide)

Ballistic projectiles (bombs, blocks)

Lava dome collapse Pyroclastic flow Mud or debris flow (lahar) Lava flow

Lava dome

Vent

Pyroclastic flow Pyroclastic surge Fumaroles

Ground water

FIGURE 15-23  Pyroclastic flow sweeping rapidly downslope from Unzen Volcano, Japan, in 1991. (Courtesy Shigeru Suto, Geological Survey of Japan.) Crack

Magma

(After Myers et al., 1998)

FIGURE 15-22  Common volcanic hazards. (Modified from Bobbie Meyers, U.S. Geological Survey.)

Lahars (Volcanic Mudflows) Lahars, the Indonesian term for volcanic mudflows, can accompany most active, explosive volcanoes (particularly those with snow or ice cover), and historically they have been almost as devastating as pyroclastic flows.53 They occur when hot or cold volcanic debris mixes with water. Because the mixture has a high proportion of sediment, lahars behave like liquid cement and may cover 20 times the area of equivalent rock avalanches.35 The

mass of rock, mud, ash, and water sweeps down valleys, and when it reaches lowland plains, it slows down and spreads out to cover hundreds of square kilometers. Lahars destroy buildings, bridges, and other structures and leave thick deposits behind (Figure 15-25, online). Most fatalities occur when victims are caught in the flow and are killed by trauma resulting from this destruction, by flying debris, and by burial.4 More deaths occur later from famine and disease as people are displaced from their homes and local water sources become contaminated. Lahars are especially dangerous because they come unheralded. They can form during or after an eruption, or they may be completely unrelated to eruptive activity.4 Water is the key ingredient. Lahars need at least 10% water by weight to become mobile.57 During an eruption, hot pyroclastic material can melt glacial ice or snow, producing water that mixes with ash on the volcano’s flank. The water may come from a crater lake drained during an eruption or from the volcano’s own subsurface geothermal system. A subglacial eruption can form a subglacial lake that subsequently breaks out to the surface and mixes with glacial debris. Heavy rainfall occurring during an eruption can initiate

A

B

C

FIGURE 15-24  A, City of Saint-Pierre, Martinique, with Montagne Pelée in the background, before the 1902 eruption. B, City of Saint-Pierre showing the destruction from pyroclastic flows from Montagne Pelée, May 8, 1902. C, Seven months later, another, smaller pyroclastic flow sweeps down the flank of Montagne Pelée on December 16, 1902. (A from an anonymous source; B and C courtesy Academy of Sciences, France.)

324

FIGURE 15-26  Armero, Colombia, after devastating lahars from Nevado del Ruiz swept down the steep-sided valley (top center) on November 13, 1985. (Courtesy Richard Janda, U.S. Geological Survey.)

lahar formation. Shortly after an eruption, when new volcanic material is on the volcano’s flank and there is no ground cover, rainfall can mix with the ash to create a lahar. Even long after an eruption, under circumstances such as a sustained intense rainfall, water may mix with ash and a lahar (now called a secondary lahar) can start to flow. Posteruption secondary lahars have caused more fatalities than during the catastrophic eruption of Mt Pinatubo, in the Philippines, on June 15, 1991. Lahars can flow far from the site of the eruption. It is not necessarily the largest ones that produce the highest fatality rate; other factors include the victims’ proximity to the hazard and the efficacy of a warning system. The greatest volcano tragedy of recent times began late at night on November 13, 1985, with a small eruption of the Colombian volcano Nevado del Ruiz. Small pyroclastic flows melted the snow cap and glacial ice on the mountain at 1656 m (5433 feet). The water mixed with volcanic ash, forming lahars that swept down the steep valleys and destroyed the town of Armero 50 km (31 miles) away, killing 23,000 inhabitants (Figure 15-26). Around midnight, the first lahar struck the town, which was completely unaware of the danger, and covered it with 3 to 4 m (10 to 13 feet) of mud, burying three quarters of the population.4 Causes of death included suffocation from mud aspiration, trauma, hypovolemic shock, and, later, gangrene. Of the 834 survivors, 578 (69.3%) had lacerations, 343 (41.1%) had penetrating injuries, 312 (37.4%) had fractures, and 272 (32.6%) had eye injuries; many had multiple injuries.76 Armero had been rebuilt on the site of previous settlements destroyed by similar lahars in 1595 and 1845. Local officials were warned by an on-site scientific team but failed to act. Another devastating lahar occurred in 1953 when Ruapehu volcano in New Zealand claimed 151 lives after an ash and ice dam retaining its crater lake collapsed. The resultant lahar swept away the Tangiwai railway bridge just minutes before the arrival of the Wellington-Auckland express, and five train cars plunged into the river.57,72 Mitigation.  For communities at risk for being struck by a lahar, evacuation is as important as when the threat is a pyroclastic flow. Early warning systems include using trip wires stretched across lahar channels, seismic instrumentation (e.g., acoustic flow monitors), video cameras, automated rain gauges, and human observers. Also, lahars might be partly diverted or contained by creating channels, and they might be held back by dams and retention basins.57 To reduce the water source, reservoirs or crater lakes can be lowered in level. Survival is possible without complete evacuation if the population at risk can be quickly moved to higher ground. Caution should be taken when crossing bridges. Emergency medical personnel in high-risk areas need to be prepared to treat blunt and penetrating trauma (crush injuries, lacerations, fractures, eye injuries), hypovolemic shock, and wounds with gangrene complications. Access to victims buried in the thick cement-like mud can be difficult and prolonged.

Tsunami, the Japanese term for harbor wave, is a seismic sea wave triggered by an earthquake or by volcanic activity. Specific triggers include major earthquakes along subduction zones, submarine landslides, underwater explosions, eruptions of island volcanoes, and avalanches on the flanks of a volcano.35 Waves can move at speeds of more than 800 km/hr (497 mph), and travel hundreds or even thousands of kilometers away from the source. In deep water, a tsunami is generally less than 1 m (3 feet) high and of no threat, but as the wave approaches the shore, its speed falls and its height increases until it becomes a steep breaking wave or an enormous surging wall of water. Though relatively infrequent, tsunamis pose a severe risk that cannot be ignored, as was illustrated by the 2004 Indian Ocean Banda Aceh undersea earthquake, magnitude 9.0, which generated a tsunami that devastated the shores of Indonesia, Sri Lanka, India, Thailand, and other countries, with waves of up to 15 m (49 feet) high, killing approximately 228,000 people, although it is hard to know the exact figure (Figure 15-27). Tsunamis caused by volcanic activity have directly killed more than 42,500 people, which is as many as have been killed by lahars. Tsunamis, like lahars, can come unheralded to settlements close to the source but can also affect distant coastal regions. Fortunately, many of these distant communities can now receive forewarning from the Pacific Tsunami Warning System and the newly established Indian Ocean Tsunami Warning System. Death and destruction occur when a tsunami slams ashore and destroys low-lying coastal communities (Figure 15-28, online). Fatalities associated with volcanogenic tsunamis include those triggered by Mt Unzen, Japan, in 1792 and Krakatau, Indonesia, in 1883. Mt Unzen, on the Japanese island of Kyushu, is an island-arc volcano created above a subduction zone. In 1792, part of the volcano collapsed, probably as a result of seismic activity. The subsequent debris avalanche swept 6 km (3.7 miles) down the volcano to devastate the city of Shimabara, killing over 9500 people. Most of the debris then emptied into the sea and triggered a tsunami that struck much of the seacoast of Ariake, killing another 5000 people in villages and on farms, even those

FIGURE 15-27  Hundreds of dead bodies and debris are piled along the coast, a dramatic demonstration of the devastation caused by tsunamis affecting the Indian Ocean basin, this one triggered by the Banda Aceh earthquake, December 26, 2004. (Photographer unknown.)

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CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

Tsunamis

PART 3  BURNS, FIRE, AND RADIATION

A

B

FIGURE 15-29  A, Tsunami buoy contains pressure sensors for determining a wave’s size by gauging the weight of the water column passing over it. B, “TsunamiReady” sign. (Courtesy National Oceanic and Atmospheric Administration.)

as high as 30 m (98 feet) above sea level, along nearly 100 km (62 miles) of coastline.56 The famous eruption of Krakatau in 1883, involving volcano collapse and sending pyroclastic flows into the sea, set off a series of tsunamis that washed away 165 coastal villages on Java and Sumatra, killing 36,000 people.35,57 Mitigation.  Volcanic islands at risk for being hit by a tsunami include the islands of Hawaii, the Marquesas, the Canaries, Tristan da Cunha, and Réunion.57 Other low-lying coastal regions are at risk. Key to mitigation is a worldwide tsunami warning system similar to the Pacific Tsunami Warning System, which was created in 1965 to warn of impending tsunamis in the Pacific Basin. In Hawaii, the warning system consists of sirens throughout the islands. Lobbies of coastal high-rise buildings are designed to allow water to pass through them without causing structural damage.57 In addition, tsunami-warning-system buoys are scattered throughout the Pacific Ocean, and many coastal communities are educated to flee to high ground in case of earthquake or volcanic eruption (Figure 15-29). As a result of the 2004 Indian Ocean Banda Aceh undersea earthquake and tsunami, three more tsunami warning systems have been established. The Indian Ocean Tsunami Warning System became active in June 2006, whereas the other two, the Caribbean Sea and Adjacent Regions Tsunami Warning System and the Northeastern Atlantic, the Mediterranean and Connected Seas Tsunami Warning System, have been established but are not operational. The United Nations Intergovernmental Oceanographic Commission, through the International Tsunami Information Center, coordinates the four systems. Evacuation to higher ground is essential to reduce the morbidity and mortality associated with tsunamis, and effective evacuation depends on public education of the officials and inhabitants of coastal communities. Emergency medical personnel need to be prepared to treat near drownings, the effects of trauma, and disease epidemics. Debris Avalanches Volcanoes, especially steep-sided composite volcanoes, can be the site of catastrophic debris avalanches at any time.56 In 1792 at Mt Unzen, mentioned previously, it was a debris avalanche that swept down the side of the volcano, killing thousands before emptying into the sea and setting off a devastating tsunami.56,57 Also in Japan, in 1888, an avalanche from the north flank of Bandai volcano sent 1.5 km3 (0.36 cubic mile) of debris down the mountainside, killing 400 people below.56,57 A debris avalanche also contributed to the eruption of Mt St Helens in 1980. 326

Triggered by an earthquake, a debris avalanche on the north flank of the mountain removed rock overlying a shallow magma chamber. Pent-up volatile gases in the magma, no longer contained by the overlying pressure of the rock, quickly expanded, causing explosive fragmentation of the magma and the first eruption. Mitigation.  Mitigating danger from debris avalanches includes mapping the zones of potential slope collapse and avoiding travel to and high-density development within those areas. Fatalities and injuries are associated with blunt trauma and burial beneath rock debris. A victim caught in a rock fall should immediately seek some sort of shelter, and roll into a ball to protect the head. Health care professionals need to be prepared for victims of blunt trauma. Tephra Tephra is the general term for fragmented rock of any size (volcanic blocks, glass shards, pumice, ash) ejected into the air by volcanic explosions. Tephra can range in size from large ballistic ejecta (over 1 m [3 feet]) to ash (less than 2 mm). The largest tephra fall back to the ground at high speeds in the immediate vicinity of the volcano. Smaller fragments stay airborne longer, and the smallest are carried away by prevailing winds before ultimately being deposited, even at distances of many hundreds of kilometers from the volcano. Ballistic Ejecta.  An erupting volcano can eject huge ballistic fragments at high velocities (Figure 15-30). They can travel kilometers away from the volcanic vent and can cause significant damage (skull injuries, lacerations, blunt trauma of the chest and abdomen) to humans on impact.4,57 The zone of damage from volcanic ballistics is generally limited to about 5 km (3 miles)— the maximum recorded range—so this is rarely a major human health hazard.4 However, in Italy in 1944, three men were killed at Terzigno by falling volcanic rocks from Mt Vesuvius 5 km (3 miles) away. In 1924, an explosive eruption at Kilauea knocked a photographer down with flying stones and severed his leg. He died later that day, probably from toxic gas exposure.9 Fire is a more common hazard, because hot flying ejecta can set fire to wooden structures, forests, or grassland. Volcanic Ash.  Smaller-sized tephra, especially ash, pose a much greater danger than do blocks and bombs. Drifting volcanic ash can be deposited hundreds to thousands of kilometers downwind from a volcano. Heavy accumulations of ash fall can collapse

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

A

B

FIGURE 15-30  A, Spectacular explosive spray of ballistic ejecta when hot lava from Kilauea Volcano entered the ocean in 2008 in Hawaii; observers (left corner) give scale. B, A large ballistic block thrown up onto the shore from a previous lava entry into the ocean in the 1980s. (A courtesy Michael Poland, U.S. Geological Survey; B courtesy Christina Heliker, U.S. Geological Survey.)

roofs, interfere with driving, clog machinery, and damage vegetation (Figure 15-31). A layer of ash only 10 cm (4 inches) thick is enough to collapse a flat roof, especially if it is wet with rainfall.53,57 Approximately 10,000 fatalities have been directly associated with ash fall, and the majority of these are from collapsed roofs. In 1991, Mt Pinatubo in the Philippines erupted during an untimely typhoon. Subsequent ash mixed with rain collapsed roofs and killed at least 300 people.57 Decreased visibility from airborne ash and slippery ashcoated roads pose a danger to drivers of motor vehicles. During and after an eruption, the incidence of motor vehicle accidents and associated injuries rises. Moderate amounts of ash fall can also directly damage motors and other machinery, as fine ash clogs engine filters and lubrication systems.57 Damaged machinery is rarely a risk to human health, except in the case of jet engines. Volcanic ash clouds contain a combination of fine rock and glass particles. If a jet aircraft flies into a volcanic ash cloud, even thousands of kilometers away, the ash can damage engines, avionics, and airframes. Ash particles can block fuel nozzles, air filters, and external navigational equipment. Abrasion damage can badly scratch cockpit windows, landing lights, and turbine blades. Volcanic glass sucked into the engine will melt in the heat, accumulate and solidify into a glassy layer that chokes fuel nozzles, coats turbine engines, and interferes with sensors, leading to reduced engine performance and ultimately total engine failure. High levels of static electricity in volcanic material can also interfere with radio communication. Comprehensive summaries of the damage and impacts of volcanic ash on aircraft operating and support systems are described in works by Casadevall13 and Miller and Casadevall.46 In the last 30 years, over 80 commercial aircraft have accidentally flown into eruption clouds, and 7 of these encounters caused in-flight loss of jet engine power.48 In 1982, two jetliners

flew into the eruption cloud from Galunggung volcano on Java. The first, a British Airways jumbo jet carrying 240 people, lost all four engines and plummeted 7500 m (24,600 feet) in 16 minutes before cold air chilled and shattered the volcanic glass and the engines could be restarted. The jet made an emergency landing at Jakarta airport with three functioning engines and flying blind because the windshield was opaque from ash abrasion. A few weeks later, a Singapore Airline jumbo jet flew into a volcanic ash cloud from the same volcano, lost three engines and dropped 2400 m (7874 feet) before one engine restarted, and the aircraft made an emergency landing (Figure 15-32).9 Fortunately, to date no lives have been lost from aircraft–volcanic ash encounters. However, in mid-April 2010, the high eruption cloud from the Eyjafjallajökull eruption (Figure 15-33, A) and its easterly drift over northern Europe (Figure. 15-33, B) raised serious concerns of possible damaging encounters between commercial aircraft and volcanic ash. As a precautionary measure, aviation officials closed many airports and grounded flights in the United Kingdom, France, Germany, Norway, Sweden, Finland, and Spain; many Europe-bound flights from the United States were also cancelled. The airport closures and flight cancellations resulted in the biggest disruption in commercial aviation since that caused by the September 11, 2001, terrorist attacks on the United States. Heavy ash can strip vegetation from leaves and coat surviving leaves. Destroyed vegetation and crops result in starvation of animals and can ultimately lead to famine in areas dependent on agriculture for subsistence. Famine from ash-related destruction of crops was the number one cause of fatalities associated with volcanic eruptions before the 20th century. With global communication and world relief organizations, famine is less common. Most volcanic ash poses little direct danger to humans. Eye irritation may cause conjunctivitis and corneal abrasion, especially in persons wearing contact lenses, but treatment is 327

PART 3  BURNS, FIRE, AND RADIATION

disease.47,59 For example, after Mt St Helens erupted in 1980, there was a fourfold increase in the number of asthma patients and a twofold increase in the number of bronchitis patients visiting emergency departments in two large hospitals.6 However, no study has shown significant long-term consequences of regularly breathing ash, even in the densely populated regions around Mt Sakurajima in Kyushu, Japan, where eruptions occur hundreds of times each year.75 Some studies have shown some types of ash, especially ash with a high content of the mineral cristobalite, can cause lung inflammation, but there is no evidence of any fibrogenic lung changes.31,38,60

A

B

Mitigation.  To prevent injury from large tephra, danger zones around the volcano should be mapped, and they should be closed when eruption is a possibility. If closure is not possible, concrete shelters can be built in danger zones for the public to access. Hard hats should be worn at all times, and anyone caught near an erupting volcano should watch for missiles and dodge them.4 Emergency medical personnel need to be prepared for blunt trauma to the head and torso and for burn victims. To minimize injury from ash, drive slowly, minimize engine use, and wear eye protection and a dust mask. All vehicles and machinery should be put inside a garage or barn. Animals and livestock should be brought into closed shelters. Consider evacuating children and high-risk individuals (asthmatics and persons with chronic bronchitis) until ash levels are lower. Although communities used to be advised to keep flat roofs clear of ash buildup, this is not now recommended, as people have been injured or killed from falling off roofs while cleaning off ash (Figure 15-34). Health care professionals should be ready for an increase in emergency visits from motor vehicle collisions, eye injuries, and respiratory problems. To mitigate the dangers associated with aircraft travel near volcanic ash clouds, air traffic is routed away from eruption

C FIGURE 15-31  A, An enormous ash cloud from the 1980 eruption of Mt St Helens passing over the small town of Ephrata, Washington, 233 km (145 miles) to the west. B, Ash-covered village of Parentas, Java, after one of the eruptions of Galunggung Volcano in 1982. C, In the city of Yakima, central Washington, ash made roads slippery and decreased visibility after the 1980 eruption of Mt St Helens. (A courtesy Douglas Miller; B courtesy Maurice Kraft; C courtesy U.S. Geological Survey.)

simple.34,53 Inhalation of ash, typically thought to be a significant health hazard, is for the most part benign, except for people with preexisting lung disease, and heavily exposed workers, such as gardeners, road workers, and police.* Most ash particles are too large to be respired, high-dust concentrations are of brief duration, and ash is biologically inert.53,72 However, fine ash particles of less than 10 µm in diameter can irritate the lungs. They are especially dangerous for people with asthma and chronic bronchitis, and they result in increased visits to emergency departments for exacerbation of chronic lung *References 6, 8, 10, 14, 24, 43, 58, 75.

328

A

B FIGURE 15-32  A, Eruption cloud from Rabaul Volcano, New Britain Island, Papua New Guinea, September 1994. Note the difference  in appearance between the eruption cloud and the ordinary mete­ orologic clouds. B, Aircraft damage after flying into an eruption cloud from Redoubt Volcano in Alaska, December 1989. (A cour­ tesy NASA, photo STS064-116-47, http://eol.jsc.nasa.gov/sseop/EFS/ photoinfo.pl?PHOTO=STS064-116-47; B courtesy Joyce Warren.)

B FIGURE 15-33  A, A high-rising eruption cloud from the explosive phase of the ongoing eruption of the subglacial volcano Eyjafjallajökull in Iceland. B, The airspace of northern Europe affected by the drifting eruption ash cloud from Eyjafjallajökull Volcano ( ). (Courtesy U.K. Met Office.)

clouds based on the analyses of a global system of Volcanic Ash Advisory Centers. These centers—-working with volcanic observatories—coordinate and disseminate information on atmospheric volcanic ash clouds that may endanger aircraft. In addition, if aircraft accidentally fly into an ash cloud, pilots are now trained in what to do at the first sign of engine failure. Pilots will turn around the plane to fly out of the eruption cloud and will try to cool the engines by idling. With engine cooling, the glassy coating will break off, thus preventing total engine failure. Volcanic Gases Gases dissolved in magma can separate explosively or passively from the molten rock and be discharged into the atmosphere. During an explosive eruption, 10 million to a billion tons of volcanic gases can be released into the atmosphere over a period of a few hours to a few days. During noneruptive periods, gas can also escape continuously from fissures, geysers, and other sites of volcanic activity. The most abundant gas released from magma is water vapor (H2O). Second is CO2, closely followed by SO2. Carbon monoxide, hydrochloric acid, hydrogen, and hydrogen sulfide (H2S) are other common gases released in appreciable quantities.56 CO2 and H2S are by far the most dangerous. Because they are both denser than air, they collect in lowlying areas and cause harm if inhaled by unsuspecting individuals.53 CO2 is an asphyxiant, and at concentrations higher than 20%, even a few breaths can very quickly lead to unconsciousness and death from acute hypoxia, severe acidosis, and respiratory paralysis. H2S, the colorless gas that smells like rotten eggs, is so toxic that a high-level exposure can kill a human after a single breath.57 H2S, much like cyanide, arrests cellular respiration and thus aerobic metabolism. There are numerous accounts of fatalities associated with CO2 emissions from volcanic activity. Perhaps the most lethal tragedy occurred in 1986 at Lake Nyos, Cameroon, when dangerous amounts of dissolved CO2, once trapped in the lower

FIGURE 15-34  Ash removal in Moses Lake, eastern Washington, after the 1980 eruption of Mt St Helens. Keeping roofs clear of ash is not advised because of the risk of falling off. (Photographer unknown.)

329

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

A

levels of this volcanic crater lake, suddenly rose to the surface and were abruptly released like champagne suddenly uncorked.28 The gas rose 80 m (262 feet) before the CO2 settled to the ground and rolled down valleys and into villages up to 20 km (12 miles) away, instantly suffocating 1746 people and 3000 livestock. About 1500 others survived and suffered transiently from burns, headache, nausea, vomiting, cough, dyspnea, hemoptysis, and chest pain (Figure 15-35, online).1 Only 2 years earlier, at nearby Lake Monoun, a similar but smaller cloud of CO2 welled up from the lake, flowed downhill, and killed 39 people.28 In Indonesia, in 1979, a release of CO2-rich volcanic gas from Sinila Crater (Dieng Plateau) killed 142 local inhabitants as they evacuated the area via a low-lying valley.39 Less dramatically, CO2 leaking from underground volcanic systems in Italy has been linked to the deaths of animals and two children. In the Mammoth Lakes region in eastern central California, accumulation of volcanic CO2 trapped under snow may have contributed to the death of a cross-country skier as well as three ski patrol members.11,27 There are a few reports of H2S-associated fatalities. Six downhill skiers on Kusatsu-Shirane volcano in Japan died in 1971, and four hikers who wandered into the lowest part of the summit crater on Adatara volcano in Japan died in 1997. Neither volcano was erupting at the time.30,57 Chronic low-level H2S exposure may also have deleterious health effects. In Rotorua, New Zealand, where 30% of the city’s population lives downwind of an actively degassing geothermal field, preliminary findings indicated there is a spatial relationship between exposure and an increase in respiratory symptoms, especially in individuals with chronic obstructive pulmonary disease.21 SO2 is an irritant to mucous membranes, can induce respiratory distress, and can have an adverse effect on pulse rate and blood pressure, but it has never been proved to directly cause death.2,40-42,57 However, in Japan, SO2 emissions from Mt Oyama on the island of Miyake forced evacuation of Miyake’s 3900 residents to the mainland from September 2000 to February 2005.16 Since the return of residents to the island of Miyake, despite ongoing SO2 emissions, research has showed a relationship

PART 3  BURNS, FIRE, AND RADIATION

between SO2 concentrations and acute respiratory symptoms such as cough, sore throat, and shortness of breath.32 Similarly, there are no fatalities associated with hydrogen fluoride (HF), but indirectly HF was responsible for the death of 10,000 Icelanders in 1783. HF from the prolonged Laki fissure eruption poisoned much of the pastureland and crops, causing the death of half the livestock and crop failure, which ultimately led to famine and death.55-57 Mitigation.  Mitigating the danger associated with toxic volcanic gases depends on the type of gas and how it is released. Since the Lake Nyos disaster, scientists have placed 12 pipes into the lake at different depths to allow CO2 to escape continuously rather than accumulating to dangerously high levels. Danger zones can be mapped, and warnings signs can be posted. Equipment can be stationed to monitor gas emissions. Recreationists should be educated to avoid certain activities at times of gas release or buildup under snow. Low-lying areas where poisonous gases can collect should be avoided. Emergency medical personnel should remove victims from the source of toxic gases, place them on high-flow oxygen, and treat other injuries accordingly.

2:58 PM, July 2, 1983

A 3:11 PM, July 2, 1983

HAZARDS FROM NONEXPLOSIVE VOLCANOES In general, nonexplosive volcanoes pose little direct danger to humans. Few fatalities are associated with them because lava usually flows slowly enough for people to avoid it.4,5 Generally, those who died either lingered to watch the lava or returned to their homes too early. On the other hand, rivers of lava can cause significant property damage as they set fire to, knock down, or bury buildings and roads. On rare occasions, flows of lowviscosity lava have been witnessed to travel down steep slopes at speeds as high as 100 km/hr (62 mph). Lava Flows Fatalities associated with lava flows account for only about 0.3% of total deaths from volcanic activity. The most deadly lava flow took place at Mt Nyiragongo, Congo.4 Nyiragongo is among the few volcanoes with an active lava lake inside its summit crater, and during an eruption in 1977, this lake suddenly drained through fissures in the crater wall. A very fluid lava flow, estimated to be traveling at 100 km/hr (62 mph), swiftly engulfed small towns, killing hundreds of people.4,51,56,57 In 1947, a scientist filming a lava flow at Mt Hekla in Iceland was killed by a glowing lava block rolling downslope.9 Other hazards include methanefueled explosions when lava overruns vegetation, and explosions or scalding steam when lava flows over ice or snow or into water (Figure 15-36).57 Mitigation.  Because lava flows rarely pose a significant health hazard during volcanic activity, they are not a high priority for health planning.53 However, to limit property damage, lava-flow diversion is a possibility. In 1973, after 6000 years of inactivity, Eldfell volcano on the island of Heimaey in Iceland reawakened and lava poured out, threatening the most important port of the Icelandic fishing industry. To stop or divert the lava flow, cold seawater was sprayed onto the advancing lava front, and after 2 weeks of nonstop work, the port was saved.56,57 Other attempts at diversion, including building rock and dirt barriers, and aerial bombings,69 have not been successful. Health care professionals should be prepared to treat burns from contact with lava or scalding steam. Jökulhlaups A jökulhlaup is a large outburst flood associated with the eruption of a subglacial volcano. The heat from the volcano melts overlying ice, forming a subglacial lake. As the lake rises, the overlying glacier is lifted and begins to melt, forming a subglacial river. If this river bursts to the surface, disastrous flooding can occur. When this happened in 1996 from a subglacial eruption at Grímsvötn in Iceland, water escaped from a 3.5-km (2.2-mile) crevice at a maximum rate of 45,000 m3/sec (12 million gal/sec) to form, temporarily, the second-largest river on Earth.57 Miles of road and bridges were destroyed. A smaller jökulhlaup emerged 330

B FIGURE 15-36  A rapidly advancing lava flow from Puu Oo vent, Kilauea Volcano, Hawaii, engulfs vehicles. (Courtesy Robert W. Decker, U.S. Geological Survey.)

in November 2004, from volcanic activity at Grímsvötn, with a peak discharge of up to 4000 m3/sec (1 million gal/sec), but this time no roads or bridges were destroyed.66 In 2010, jökulhlaups of the Eyjafjallajökull eruption (see Figure 15-19, C ) caused substantial destruction of roads and infrastructure locally, but fortunately no deaths or injuries.

POSTERUPTION HAZARDS Major eruptions can be hazardous long after the eruption is over. Large quantities of gas released into the atmosphere can cause air pollution, produce acid rain, and deplete ozone, possibly affecting global climate for a few years.4 Water supplies can be contaminated and crops destroyed, leading to disease epidemics and famine.3 Moreover, overcrowding and poor sanitation conditions—commonly associated with temporary evacuation camps—pose health hazards and sometimes lead to disease epidemics. After the eruption of Mt Pinatubo in June 1991, a measles outbreak, diarrhea, and respiratory infections resulted in the death of hundreds of children from an isolated tribe forced to live in evacuation centers.23 Ongoing smaller eruptions can also cause problems (Figure 15-37, online). In Italy, Mt Etna is the largest continuous source of volcanic SO2 globally, and Stromboli is probably the second largest in Europe.20 During the 8 months that the Laki fissure in Iceland was erupting in 1783, at least 122 million metric tons (MT) of SO2, 7 MT of hydrogen chloride, and 15 MT of HF were released into the atmosphere.73 HF poisoned Icelandic sheep and destroyed crops, contributing to the death of about one-fifth of Iceland’s entire population.55 In addition, the Laki eruptions were probably responsible for the death of more than 10,000 people in England during the summer of 1783 and winter of 1784.55,73 Noting that the mortality rate was 16.7% above normal for this time period, experts in the United Kingdom suggest that a cloud of volcanic gases and particles swept south from Laki into England and was responsible for the very hot 1783 summer and subsequent severe winter.55,73 Combing climatic data, burial records, and written accounts, they read of a summertime “volcanic haze” or “dry fog” that shrouded the moon and sun, reduced visibility, withered vegetation, and caused health problems.20,55 Like smog, the dry fog caused headache and eye irritation, exacerbated lung disease,

Risk Reduction From Volcanic Hazards Humans are vulnerable to severe, unpreventable volcanic eruptions. Risk reduction starts with comprehending the seriousness of volcanic hazards and being prepared for the associated dangers. Nearly 99% of fatalities associated with volcanic eruptions are from pyroclastic flows and lahars, yet one-tenth of the world’s population lives in cities and homes near volcanoes, sometimes on the volcano slopes or on the remains of a previous pyroclastic flow, lahar, or debris avalanche.53,57 Fortunately, most volcanic eruptions are preceded by premonitory events, such as earthquakes and other measurable phenomena, far enough in advance to enable scientists and emergency workers to plan for disaster. However, a few of the most severe eruptions have occurred with little or no warning, and most of the world’s dangerous volcanoes are in densely populated countries that lack the resources or political interest to monitor them.5,69 Nevertheless, emergency planning for an eruption, including creation of hazard-zone maps and hazard evaluation, should be routine for all populated areas near volcanoes, regardless of their location or apparent state of activity.5 Risk reduction includes volcano monitoring, eruption prediction, and effective coordination between volcanologists, scientists, health care professionals, and the community at risk. In addition, with tourism increasing to volcanic destinations, the tourist industry, practitioners of travel medicine, and adventure travelers need to educate themselves and others about the potential health hazards when in volcanic environments.25

VOLCANO MONITORING Scientists monitor volcanoes for seismic activity (earthquakes), changes in volcano shape (ground deformation), surface temperature, magma level, gas emissions, and other chemical and physical attributes (Figure 15-38, online).50 Earthquakes and ground

deformations are the most reliable diagnostic observations for helping scientists predict when a volcano might erupt or when it is no longer likely to erupt.45,68 The importance of monitoring cannot be overstated. During the last half of the 20th century, most eruptions from monitored volcanoes were anticipated weeks or months in advance. These include the eruptions of Mt St Helens in 1980 and 2004 and Mt Pinatubo in 1991 (see next). Often, the problem is not predicting when the volcano will erupt but convincing government officials to act on the warning. Before 1985, authorities in Armero, Colombia, were warned that lahars could devastate their town, but the warning was disregarded, and the eruption at Nevado del Ruiz and the subsequent lahars destroyed the town and killed over 25,000 people.57

ERUPTION PREDICTION AND MT PINATUBO: EFFECTIVE VOLCANIC-EMERGENCY RESPONSE In April 1991, the Philippine volcano Mt Pinatubo began to erupt weakly for the first time in recorded history. Ultimately, the activity escalated into the world’s largest eruption in the preceding eight decades, yet only 300 people were killed, even though at least 600,000 people lived in cities, villages, and military bases around the volcano. The larger tragedy was prevented by effective cooperation between local authorities and scientists of the Philippine Institute of Volcanology and Seismology (PHIVOLCS) and the U.S. Geological Survey (USGS). Two months before the climactic eruption on June 15, PHIVOLCS consulted the USGS’s Volcano Disaster Assistance Program (VDAP), a mobile volcano-response team (i.e., an eruption SWAT [special weapons and tactics] team) of experienced volcanologists and other scientists who rapidly respond to a developing volcanic crisis with state-of-the-art portable monitoring equipment (Figure 15-39, online). The request for assistance came after there was an increase in the number of earthquakes, up to 500 per day, explosions, and new cracks opening in the volcano. The VDAP team set up a base camp at Clark Air Force Base and began to monitor and interpret seismic activity, ground deformation, and gas emissions. They also gathered data about Pinatubo’s previous eruptions to predict the types of hazards that could be expected and to create a map of the area, delineating zones at risk during an eruption. Finally, the PHIVOLCS-USGS team worked with local authorities to develop an evacuation plan and educate the people. A 30-minute video, “Understanding Volcanic Hazards,” produced after the tragedy of Armero, Colombia, in 1985, was shown to local officials and populations to raise awareness of hazardous volcanic processes. On June 7, a month and a half after the USGS team arrived, a warning was sent out of a possible major eruption within 24 hours. Villages and cities were evacuated. Five days later, the first in a series of powerful explosive eruptions began. An eruption cloud rose 19 km (12 miles) into the air, and small pyroclastic flows started down to the north and northwest. Additional eruptions took place over the next 2 days. On June 15, a cataclysmic eruption took place during a typhoon. The eruption cloud rose 12 km (7.5 miles) into the atmosphere and spread out like an umbrella more than 200 km (124 miles) in all directions. Wet ash covered a 4000-km2 (1544-square-mile) area, burying crops and collapsing roofs, and many destructive lahars were generated.15 Ash fell as far away as the Indian Ocean. The warning saved at least 5000 lives and a great deal of property damage.

COORDINATION BETWEEN VOLCANOLOGISTS AND HEALTH CARE PROFESSIONALS Coordination between geologists, other scientists, and health care professionals is essential to prepare communities for volcanic emergencies. Planning for future eruptions requires determining the history of a volcano’s past eruptions and their impacts, developing a hazard-zone map, anticipating when a volcano might erupt, and describing the types of hazards to be expected and their potential effects on health (Figure 15-40). Furthermore, health care professionals need to identify high-risk populations, prepare for disaster victims, and help volcanologists educate the community about potential health effects for each volcanic hazard.50 Evacuation of communities, especially in low-lying 331

CHAPTER 15  Volcanic Eruptions, Hazards, and Mitigation

and irritated mucous membranes. Wintertime deaths were associated with unusually cold temperatures. Benjamin Franklin, U.S. ambassador to France in Paris at the time, was the first to link the effect of Laki’s eruption on climate, and presented a scientific paper on the topic. Eruption clouds that penetrate the upper atmosphere can spread volcanic particles and gases across an entire hemisphere.57 During the 3 months it can take fine ash particles to settle out, solar heating is reduced and the lower atmosphere is cooled. The 1991 eruption of Mt Pinatubo in the Philippines created a large volcanic cloud that drifted around the world and caused a temporary average global temperature drop of 0.5° C (0.9° F).35 The largest eruption in recorded history, in 1815 at Tambora, Indonesia, reduced the average global temperature by 3° C (5.4° F) for several years.35 This eruption directly or indirectly caused the death of an estimated 60,000 people in Indonesia and was responsible for a typhus epidemic in Great Britain, cholera in India, and mass migration from northern Europe and Russia. It ruined farms in New England and spurred westward migration.57 The greatest eruption since humans evolved was that of Toba in Indonesia, about 74,000 years ago. The global temperature dropped 5° C (9° F) for many years, causing a global environmental catastrophe. It may have resulted in an estimated decrease in the population of Homo sapiens from over 100,000 to less than 2000.57 Some volcanic soils may also pose a health risk. Nonfilarial elephantiasis, otherwise known as podoconiosis or mossy foot, appears to be caused by chronic exposure of unprotected feet to irritant alkalic red clay soils rich in volcanic particles. Microscopic particles absorbed through abrasions in the feet penetrate the lymphatic system, causing inflammation, lymphatic fibrosis, and ultimate blockage. As the lymphatics are obstructed, the lower extremities swell, resulting in elephantiasis. Podoconiosis is predominately found in high-altitude areas (>1,250 m [4101 feet]) of tropical Africa, Central America, and North India.17-19,49,71,74 Fluoride leached from volcanic rocks into drinking water can also cause disease. In eastern Turkey near Tendurek Volcano, mottled enamel from high levels of fluoride, called endemic dental fluorosis, has been observed in humans and livestock since the 1950s.52

PART 3  BURNS, FIRE, AND RADIATION

TABLE 15-5  Casualties Caused by Pyroclastic Flows in 20th-Century Explosive Eruptions Eruption

Year

Deaths (N)

Ratio of Dead to Injured

Montagne Pelée, Martinique La Soufrière, St Vincent Taal, Philippines Lamington, Papua New Guinea Mount St Helens, United States Unzen, Japan Merapi, Indonesia Soufrière Hills, Montserrat

1902 1902 1911 1958 1980 1991 1994 1997

28,000 1565 1335 2942 58 43 63 19

230 : 1 11 : 1 10 : 1 44 : 1 16 : 1 5 : 1 3 : 1 4 : 1

Survivors After Treatment 163 treated, 123 survived 194 treated, 120 survived Not known 70 treated, 67 survived 130 airlifted, 9 treated, 7 survived 17 treated, 4 survived (minor burns) 86 treated, 11 dead on arrival 7 treated, all survived

From Baxter PJ: Impact of eruptions on human health. In Sigurdsson H, Hougthon BF, McNutt SR, et al, editors: Encyclopedia of volcanoes, San Diego, 2000, Academic Press.

areas and river valley regions, is of utmost importance. Goggles and masks should be distributed, especially to individuals who must work in dusty conditions.

EMERGENCY MEDICAL RESPONSE Emergency medical care plays a small role in severe volcanic eruptions. The number of injured who could benefit from treatment is much smaller than the number of victims killed within minutes of a catastrophic eruption (Table 15-5).5 Therefore prevention is of utmost importance, and evacuation is the key to decreasing morbidity and mortality.5 Health care professionals should be prepared to treat a variety of medical problems in persons who survive (Box 15-2), and they must be aware that access to victims will be limited by high ash conditions, burial beneath volcanic debris, and ongoing hazards. Transient increases in emergency department visits and hospital admissions will require additional resources.8

GEOTOURISM With the increased interest in visiting volcanic environments, the numbers of injuries and illnesses are increasing. Areas like Hawaii Volcanoes National Park have experienced a high rate of injuries and illness because of inexperienced hikers entering high-risk environments and disregarding warning signs.26 People working or traveling near an active volcano or volcanic environment should heed these safety recommendations: • Read about the volcanic environment, including past eruptions and accidents. • Know the current volcano warning level, and obey local authorities.

BOX 15-2  Summary of Health Effects From Volcanic

Eruptions

Physical • Blunt trauma from pyroclastic material, lahars, debris avalanches, tsunamis, and tephra • Burns, wounds, and gangrene complications • Asphyxiation from lack of oxygen or inhaled ash • Acute irritation of the respiratory tract caused by ash • Exacerbation of prior respiratory disease caused by inhaled particles • Respiratory tract and lung burns caused by inhalation of hot steam • Conjunctivitis and corneal abrasions • Toxic effects of gases such as CO2, H2S, SO2, HF, CO, and radon • Gastroenteritis • Skin irritation from acid water • Drowning in lahars or tsunamis Psychological • Depression • Anxiety • Nightmares • Psychomotor disorders • Irritability • Insomnia • Confusion • Neurosis • Stress Modified from Zeballos JL, Meli R, Vilchis A, et al: The effects of volcanoes on health: Preparedness in Mexico, World Health Stat Q 49:204, 1996. CO2, Carbon dioxide; CO, carbon monoxide; HF, hydrogen fluoride; H2S, hydrogen sulfide; SO2, sulfur dioxide.

• Travel with a guide experienced in local conditions. • Leave travel details with a responsible person. • Wear a hard hat and take a gas mask, if appropriate. • Beware of the sources of danger on a volcano: • Rock falls • Avalanches • Hazardous gases • Look for warning signs of an eruption. • Immediately leave the area if it becomes dangerous. • Do not approach lava flowing through vegetation. FIGURE 15-40  First of a series of powerful explosions beginning on June 12, 1991, Pinatubo Volcano, Philippines (see text); note within the yellow oval a farmer and buffalo plowing. (Courtesy David Harlow, U.S. Geological Survey.)

332

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 16 

Injury Prevention: Decision Making, Safety, and Accident Avoidance EUNICE SINGLETARY AND DAVID S. MARKENSON

For many, it is the wild in wilderness that fuels a passion for the wilderness experience. Wilderness areas are considered the last areas that humans do not control and have not developed. This lack of human control in undeveloped terrain, combined with the enthusiasm of wilderness explorers, is an ideal recipe for unintentional injury. Managing the risk through sound decisions and efforts to improve safety and reduce accidents is a critical component of wilderness medicine and the focus of this chapter. Contributing to overall risk for injury is the growing feasibility of exploration by wilderness novices, children, elders, and persons with disabilities or chronic health issues by using offroad vehicles, watercraft, and aircraft or via improved access. For persons who venture into the wilderness, there are growing technologic advances in communications equipment, global positioning systems, sporting equipment design, water purification and disinfection, and food processing and preservation techniques, all of which extend the duration of expeditions and permit exploration of remote wilderness once accessed by only the most skilled and experienced persons. Environmental hazards, such as exposure to cold, heat, snow, or altitude, can be minimized through proper planning and training. Wilderness sports activities, such as hunting, snowmobiling, and backcountry ski touring, are safer today not only because of advances in technologic and safety equipment, but because of efforts to educate the public about associated risks and how to manage or reduce these risks and efforts to train the public in wilderness first-aid and medicine (Figure 16-1, online). Despite the growth in numbers of practitioners of wilderness medicine and improved ability to provide care for many injuries and illnesses in remote settings, evacuation of injured victims from the wilderness remains daunting and can turn a minor problem into a major medical situation with a protracted rescue. There are 78 million hectares (193 million acres) of land in the U.S. National Forests and Grasslands. Thousands of rivers and lakes are parts of the National Forests, and there are 247,000 km (153,000 miles) of trails, primarily for nonmotorized use. It is estimated that 178 million people recreate each year in the national forests.152 Sixty-four percent of 446 million visits to national parks in 2009 were considered recreational, with 1.9 million categorized as backcountry overnight visits.97 The National Sporting Goods Association estimates that between 1994 and 2004, the number of Americans involved in backpacking and wilderness camping climbed from 10.2 million to 13.3 million. During the same time period, the number of hikers increased from 25 million to 29.8 million.98 With increased access comes the potential for higher numbers of injuries, illnesses, and fatalities. According to the Centers for Disease Control and Prevention (CDC), in 2005 a total of 173,753 injury-related deaths occurred in the United States, and during 2006 an estimated 29,821,159 persons with nonfatal injuries were treated in U.S. hospital emergency departments.26 The number of injuries and injury-related deaths as a result of wilderness activities is unknown and can only be extrapolated, particularly from National Park Service (NPS) data. Between 2003 and 2006, there were 12,337 search and rescue (SAR) operations in national parks, involving 15,537 visitors and involving 522 fatalities and 4860 ill or injured visitors.60 From a public health point of view, the physical, financial, and emotional consequences of injury can 334

be wide ranging, devastating, and long lasting. The CDC’s National Center for Injury Prevention and Control (Injury Center) was formed partially as a result of a recommendation of the 1985 Institute of Medicine report Injury in America, which concluded that supporting injury research is necessary to substantially reduce injury rates.30 The Injury Center strives to prevent injury and reduce its consequences, using a public health approach that describes the problem, identifies risk and protective factors, develops and tests prevention interventions and strategies, and promotes widespread adoption of effective interventions and strategies. Although the Injury Center includes intentional as well as unintentional injuries in its focus on injury prevention, their efforts and approach may prove to be a model for future research and methods for injury reduction in the wilderness setting. This chapter reviews basic principles of injury applied to the wilderness environment. Individual (human/host) factors and behavior and how they apply to injury risk and prevention are detailed, including preparation, planning, anticipation of problems, and errors of omission or commission. Problems are approached from the perspective of environmental hazards, rather than from a particular activity, because many hazards are common to different wilderness activities. Throughout this chapter, prevention of injury is the focus. Details of pathophysiology and treatment are found in the referenced chapters throughout this text.

Principles of Wilderness Injury and Prevention THE INJURY FIELD: BASIC PRINCIPLES Injury prevention is a key component of public health and medical care. It is a long-held belief of physicians and public health practitioners that injury prevention is far superior to injury treatment. Underlying injury prevention is the concept that when an injury occurs it is usually the result of a series of events under specific circumstances that had they been identified in advance might have been avoided, addressed, and/or eliminated to prevent or mitigate the injury. In the field of injury prevention, accidents are defined as unpredictable acts of fate or chance events, whereas injuries are defined as damages resulting from a sequence of accidents or intentional actions. Injuries are prevented by stopping or reducing the number of accidents causing them and/or eliminating the intentional actions and situations that lead to them. By applying this principle, practitioners of injury prevention estimate that 90% of all injuries are predictable and preventable. For example, by inspecting, testing, and replacing equipment, individuals may prevent accidents related to equipment failure. The need for this approach is even greater in wilderness medicine than in many other fields of medicine. In medicine we attempt to prevent injury, but if that prevention fails, we then provide emergency care and rehabilitation to limit the lasting effects of injury and return the person to good health. In the case of wilderness injuries, which may occur in areas with limited immediate care and often with significant distance and time to reach definitive care, our ability to limit the extent of injury is less, magnifying the need for prevention.

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Injury prevention can occur at many points along the continuum, beginning before injury through rehabilitation. In classic injury prevention and epidemiology, opportunities for prevention are divided into primary, secondary, and tertiary phases. Primary prevention avoids development of a disease. Most population-based health promotion activities are primary preventive measures. In addition, many environmental or regulatory controls are primary. Secondary prevention activities are aimed at early disease detection, thereby increasing opportunities for interventions to prevent progression of disease and emergence of symptoms. In the field of injury prevention this would include early recognition of injury to limit the extent and impact of an injury should it occur. An example in wilderness medicine is early recognition of foot blisters and use of protective coverings or footwear alteration to prevent skin breakdown and further extension of blisters or infections. Wearing protective equipment is both primary and secondary if it limits the extent of injury. Interventions may cross multiple stages of prevention. Tertiary prevention reduces the negative impact of an already established disease by restoring function and reducing diseaserelated complications. In the field of injury prevention, this traditionally includes prompt and appropriate medical rehabilitation. An example is early splinting of a fracture in the field to prevent further injury and to limit swelling and associated complications. Quaternary prevention is the set of health activities that mitigate or avoid the consequences of unnecessary or excessive interventions within the health system. This stage is the latest addition to the classic three stages of prevention and is not always included in descriptions of injury prevention.

EPIDEMIOLOGIC FACTORS: HUMAN OR HOST, AGENT, AND ENVIRONMENT One of the most commonly used methods of categorizing the factors that lead to injury is “human (host), agent, and environment.” Numerous human factors can lead to injury and be used as opportunities for prevention. Examples include predisposition to injury, such as osteoporosis predisposing to fractures; behaviors that may be high risk for injury, such as alcohol consumption and intoxication; decision making, such as a choice to proceed on an icy trail; and different body habitus, ages, or conditions, such as pregnancy. The next factor is the agent. Broadly defined, the agent is what causes the injury. Although this may seem straightforward, the lines can be blurred. For example, if someone decides to strike a branch with his or her hand to break it, is the branch the agent or is the human who made the decision the agent? Most would agree the branch is the agent and the human factor was the decision to strike it. Classic descriptions of agents would be propelled objects, items that strike people, falls from heights, or malfunctioning mechanical devices. In the wilderness, the items include failing ropes or belts when climbing, branches and rocks when falling, wet ground causing a slip, a poorly positioned or inappropriately worn backpack leading to back injury, or a hot object that causes burns. The last factor is the environment, which includes the situation in which the injury occurred. This might be temperature conditions, such as extremes of heat or cold, but may also include a situation where there is only one option for moving forward through less-than-ideal terrain without the option to turn back.

CONCEPTUAL MODELS A more comprehensive conceptualization for intervention and prevention can be done by combining stages of injury prevention with the host, agent, and environment approach. This combination was proposed by Dr. William Haddon, Jr., who is widely considered the father of modern injury epidemiology. Haddon’s matrix is an injury prevention brainstorming tool originally designed for motor vehicle safety that combines the epidemiology triangle (host, agent, environment) and levels of prevention. This combination allows planning for injury interventions and prevention strategies by phases in time of the event.

In addition to planning interventions, this matrix can also be used to collect data to determine the factors that cause injuries. The following are the steps to complete Haddon’s matrix: 1. Assess the contributing factors or characteristics of an injury from the perspective of the following: • Host or human factors • Agent of energy or vehicle (such as crashworthiness of a vehicle) • Physical environment (such as roadway design or safety features) • Social environment (such as passage and enforcement of seat belt laws) 2. Then combine them with time phases: • Pre-event: What factors affect the host before the event occurs? • Event: What are factors related to the crash phase? • Postevent: What are factors related to the postevent crash phase? 3. Place the items with the possible intervention in the appropriate location in Haddon’s matrix. Haddon’s 10 Strategies for Reducing Injuries In addition to developing the matrix, Haddon also proposed strategies for reducing injuries. These strategies have been grouped into 10 specific approaches, commonly known as Haddon’s 10 Strategies (with examples): 1. Prevent creation of the hazard. • Perform preparticipation musculoskeletal physical examination to identify underlying pathologic problems of the knee joints. • Provide treatment and rehabilitation before sports participation. • Provide warm-up programs involving neuromuscular and proprioceptive training to stabilize the knee. 2. Reduce the amount of the hazard. • Limit the physical areas for activities. Provide limitations on activities or exposure to the environment. 3. Prevent the release of the existing hazard. • Ensure that waste is kept properly distant from potable water sources. 4. Modify the rate or partial distribution of release of the hazard from its source. • Limit activity to an individual’s ability. • Substitute individuals as necessary during a specific activity. 5. Separate, in time or space, the hazard and that which is to be protected. • Limit climbing to certain weather conditions. • Perform strenuous activity only when ambient conditions are appropriate. 6. Separate the hazard and that which is to be protected by interposition of a material barrier. • Use well-fitted gear. • Employ protective gear. 7. Modify basic relevant qualities of the hazard. • Avoid surfaces that increase the potential for injury. 8. Make what is to be protected more resistant to damage. • Provide fitness training, including stretching, strengthening, and improving balance and movement. 9. Begin to counter the damage already done by the hazard. • Seek and receive prompt medical care as soon as the injury is noted. 10. Stabilize, repair, and rehabilitate the object of the damage. • Provide rehabilitation, and use stabilization devices, such as knee braces.

ENVIRONMENTAL, EDUCATIONAL, AND ENFORCEMENT APPROACHES TO INJURY PREVENTION In addition to describing possible interventions using Haddon’s matrix approach, it may be helpful to characterize the type of intervention. One way to categorize injury prevention efforts is by the three E’s: 335

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THE CONTINUUM OF INJURY PREVENTION

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• Environment makes the environment or product safer. • Education provides information to individuals. • Enforcement relies on change through laws. Comprehensive injury prevention projects employ strategies that include all of these. Environmental Approach The environment includes physical surroundings (e.g., roadway), products (e.g., vehicles), and the social environment (e.g., societal attitudes toward drinking and driving). The environmental approach is a strategy that does not depend on action by those being protected; it is passive, automatic, and constant in its protective effects. As a result, this approach is considered the most effective strategy. In some cases, there is the technology available to make products safer, but industry has not adopted it, often because of economic disincentives. In classic injury epidemiology, environmental interventions refer to the following: • Physical surroundings • Product design, protocols, and practices • Social environment The following are key concepts for environmental modifi­ cation: • Design safer surroundings • Pool fencing • Handrails • Antislip surfaces • Playground surfaces • Roadways • Bike/walking paths • Design safer products • “Kill switches” • Childproof packaging • Crib slat spacing • Flame-resistant sleepwear • Vehicle design • Protocols and practices • “Traffic calming” • Walk-light timing at crosswalks • Bus stop placement • Lighting for crime reduction • Factory settings for water heaters • Social environment • Alcohol consumption and operating motorized devices while drunk • Domestic violence • Violence on television • Safety devices Educational Approach Preventive measures defined as an educational approach involve education of large populations, targeted groups, or individuals and efforts to alter specific injury-related behaviors. Many injuries result less from lack of knowledge than from failure to apply what is known. Three goals of educational interventions are as follows: 1. Provide information regarding injury risks and how to avoid them. 2. Change attitudes away from risks and toward safer practices. 3. Alter behaviors. It is not enough to know that seat belts save lives, but one must actually use the seat belt for it to be effective. An educational approach may be appropriate in the following instances: • New knowledge about a risk is needed (e.g., defective equipment, better approaches to an activity, newer and safer technology available) • No other approach exists (e.g., an activity that is inherently unsafe and avoidance is the only strategy) • To influence decision makers, lawmakers, and design engineers • To teach specific behaviors and skills (dialing 9-1-1, crawl under smoke, self-care of injuries) 336

Limitations of the educational approach include the following: • It uses an active approach. Passive approaches are pre­ ferred. • It may be an inappropriate message for the target audience. Targeted, at-risk populations are not always reached through mass-media educational campaigns. • There are variations in learning style among adults and possible language barriers. In education, “one size doesn’t necessarily fit all.” There are variations in learning styles unique to children and adults, cultures, and socioeconomic status. • There may not be cultural acceptance of the message. Messages should be tested with a focus group to be certain that they are not offensive. Enforcement Approach This approach uses a strategy that seeks to require change in behavior, the environment, or product by enacting law and policy. Enforcement initiatives and laws are directed toward individuals, products, and environmental conditions. The following are examples of laws targeted to individuals: • Requiring: • Seat belts • Child restraints • Helmet use • Prohibiting: • Drunk driving • Excessive speed The following are examples of laws targeted to products: • Requiring: • Motor vehicle standards • Helmet standards • Childproof packaging • Prohibiting: • Fully automatic weapons • Flammable fabrics The following are examples of laws targeted to the environment • Requiring: • Swimming pool fence • Smoke detectors • Prohibiting: • Firearms in airports/schools • Rigid structures on highways Characteristics of successful laws include the following: • There are few exceptions to compliance. • Detection is easy (measuring speed with radar, observing helmet use). • Punishment is certain, swift, and sure. • There is publicity about enforcement. Enforcement and laws can have a much greater impact on changing behavior when enforcement is highly visible and media are used to let the public know about enforcement campaigns. Controversies arise when legislation is perceived to restrict personal freedoms.

SOCIAL-ECOLOGIC MODEL In addition to the classic epidemiology approach of host, agent, and environment enhanced by the stages of prevention and articulated by Haddon in his matrix, another conceptual model attempts to describe injury prevention but with more focus on the interplay of different factors. The social-ecologic model has its foundation in human development and has been refined to apply to injury prevention and epidemiology. The social-ecologic framework was created by Urie Bronfenbrenner19 in the context of understanding human development and is very compatible with a broader view of public health.76 Social-ecologic theory defines various levels of the social environment, depicting the nested roles of intrapersonal factors, interpersonal factors, institutional elements, and cultural elements. This social-ecologic framework enhances the standard public health model of agent-host-environment.88,120,135 With respect to understanding injury prevention, intrapersonal factors include both developmental and sociobehavioral features

RISK AND EFFECT MODIFICATION IN INJURY PREVENTION EPIDEMIOLOGY Two basic epidemiologic concepts are risk and effect modification. Risk is the likelihood of disease occurrence and is often operationalized as relative risk to aid in decision making. This is a method to describe how one option versus another option may lead to different disease outcomes. In injury prevention, one always must consider risk. Some activities are inherently risky, and all one can do is provide interventions that protect the individual or minimize the impact of a potential injury. In other cases, there may be several options each with different risk, so that one can determine the relative risk. Major human risk factor examples are age, gender, and experience. Another basic epidemiologic concept that can be applied to injury prevention is that of effect modification. An effect modifier is a variable that lies in the pathway from independent/main explanatory variable and the dependent/outcome variable. When applying this to injury prevention, one can think of an effect modifier as something that lies in the pathway between the event and the injury, and that can alter the injury outcome from similar events. An example might be wearing a helmet, so that when thrown from a horse the injury to one’s head is less than if not wearing a helmet. Human factors can be considered from the perspective of effect modifiers. For example, when caught in bad weather, the more experienced hiker will be less likely than the novice to be injured.

ACTIVE VERSUS PASSIVE INJURY PREVENTION STRATEGIES Before proceeding to implement methods of injury prevention, it is important to recognize that injury prevention strategies are either active or passive.112 Active injury prevention strategies require change in behaviors by individuals before or when exposed to risks.145 For example, individuals must be convinced that wearing seat belts reduces the risk for injury and then must take the action of buckling up. Passive injury prevention

strategies are preferable because they require no action on the part of the individual.54,72 For example, recent advances in automotive safety have been gained by placement of air bags. A more classic passive approach has been referred to as environmental controls. An example of this is a fence placed around a pool to prevent entry of unsupervised children, thus reducing drowning incidents.

MORBIDITY AND MORTALITY STATISTICS FOR WILDERNESS INJURY The difficulties of obtaining data about injury prevention in the wilderness are the diversity of activities covered and lack of a single source for the data. As a result, data are often only for a selected activity and in a single location. Some data involve several activities. An example is a CDC study released in 2008 of nearly 213,000 people who had been treated each year in emergency departments for outdoor recreational injuries from 2004 to 2005.44 Of those injured, about 109,000 (51.5%) were young people between the ages of 10 and 24. For both men and women of all ages, the most common injuries were fractures (27.4%) and sprains (23.9%). Of these, most injuries were to the arms or legs (52%) or to the head or neck (23.3%). Overall, 6.5% of outdoor injuries treated were diagnosed as traumatic brain injury. Researchers found that snowboarding (25.5%), sledding (10.8%), and hiking (6.3%) were associated with the highest percentage of injuries requiring emergency department visits. The study points out that wilderness injury prevention begins with planning, preparation, and problem anticipation, which are discussed later in this chapter. An example of event-specific data is for backpacking and camping. Data reveal that more than 11 million people participated in backpacking or wilderness camping in 1990. The morbidity and mortality figures from eight national parks in California between 1993 and 1995 are 1708 injuries and 78 fatalities.95 Another event-specific activity for which there are data is scuba diving. There are more than 9 million certified scuba divers in the United States, with approximately 650,000 annual certifications.35 The Divers Alert Network37 at Duke University Medical Center (Durham, NC) reported approximately 1000 serious diving-related injuries and approximately 90 diving-related fatalities annually between 1995 and 2002. In addition to event-specific data, one can examine equipmentbased data, which can include data based on certain types of vehicles. For example, from 1990 through 1995, an estimated 32,954 persons were involved in injuries related to personal watercraft.18 Lastly, one may search data to learn about specific types of injuries or deaths. An example of this type of data is a western Washington study of 40 pediatric wilderness-activity related deaths between 1987 and 1996.100 Ninety percent of the victims were male, and 83% were 13 to 19 years of age. The most common cause of death was drowning (55%), followed by closed head injury (26%). Injuries or deaths resulted from lack of preparation, lack of training for wilderness activities, and inadequate basic safety equipment; alcohol use and rescue delays were contributing factors. Of note, the presence of adults did not appear to be significant in reducing the incidence of mortality.

PUTTING INJURY PREVENTION INTO PRACTICE Planning Careful planning is the foundation for a safe activity that minimizes risk and avoids injury. Planning begins by gathering all relevant data for the planned activity. This includes up-to-date information regarding weather, trail, and campground conditions, best times to travel, permit requirements, equipment needed, and special considerations unique to the activity. After gathering all available information, one develops a plan for activities. The plan may be very brief and purely a mental exercise for some activities such as brief hikes, camping trips, rock climbing, or day diving. For longer excursions, the planning phase will include a detailed, written plan. Planning activities may include activity-specific 337

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of individuals (i.e., the host), for example, a young child’s curiosity and exploratory behaviors through touching, tasting, and crawling; an adolescent’s propensity to take risks and the varied responses to parent and peer influences; or an older adult’s suicide risk due to a sense of hopelessness in the face of an incurable chronic disease, or avoidance of walking in certain locations because of fear of falling or assault. Likewise, biologic features of the host, such as a young child’s lack of balance and strength, high center of gravity, and small size, relate to some of the hazards encountered. For an older adult, biologic characteristics such as bone brittleness; reduced visual acuity, reaction time, and balance; and thinner skin all increase susceptibility to injury events such as traffic crashes, pedestrian injuries, falls, and burns. Interpersonal factors are those that result from the interactions between two persons, for example, intimate partners, parent and child, employer and employee, or adolescents. In the injury sphere, this relates to intentional injury as a result of behaviors associated with disciplinary practices or conflict resolution. Institutional elements are those that reflect organizations in which individuals function, for example, schools, places of worship, and workplaces. How these organizations promote or control activities and environments can affect injury risks. Work sites contain many hazards and adopt many types of safety practices, whereas places of worship may either encourage or discourage certain safe or unsafe practices. Prehospital trauma care and inpatient health care systems are institutions that affect injury outcomes.105 Cultural elements include broad social values and norms as well as governmental policies that guide or mandate behaviors of individuals or organizations. Examples are values placed on individual freedom; social norms about drinking or corporal punishment; and laws, policies, and regulations about producing, selling, and storing firearms. Any health problem can be viewed as resulting from and being alleviated by the interactions among these dynamic factors.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

planning that addresses unique risks or needs. For example, to plan for a climb that includes high altitude, allowance is made for ascent and descent to allow time for acclimatization. Planning may include provision of equipment specific to the activity, such as scuba gear or helmets. Two of the most important planning factors are personal limitations and required preparation. It is important to establish criteria under which the activity can be undertaken safely. The level of detail is based on the risks. For events with high risk or multiple risks, these criteria need to be detailed. There are many factors that figure into a “go” or “no-go” decision plan. Some factors, such as weather, local conditions, physical conditioning for the activity, sleep, and wellness, may apply to all activities, but others may be activity specific, such as water conditions for rafting and kayaking. Once the criteria are established, the most important thing is to adhere to them. Injuries often occur when the desire to perform an activity causes someone to participate in a situation that is either unsafe or exceeds personal abilities. At a minimum, one must address the following: • Predetermined “go” or “no-go” criteria, which may include the following: • Weather and environmental conditions at the activity site • Personal criteria such as sleep, preparation time, preexisting illness, departure time and window • Required participants • Equipment • Comprehensive equipment checklist • Timeline • Alternative plans • Communication methods, including emergency communi­ cations • Emergency procedures, including the following: • Medical emergencies • Unexpected weather or local conditions • Equipment failure Preparation After planning, the next step in a good injury prevention approach is to prepare for the activity so as to minimize risk and put into place factors that are targeted at the human, agent, and environmental issues that can lead to injury. Preparation activities can be grouped into human factors (physical and mental preparation) and material factors, such as equipment preparation. Physical Preparation.  Physical preparation includes maintaining excellent fitness and health in anticipation of the activity and the added stresses over daily activities. This may include conditioning, medical evaluation for physical abilities and health to undertake the activity, better medication adjustment for persons with chronic illness, and/or disability-specific planning for those with disabilities. In addition to general physical preparation there are unique considerations for physical preparation related to the genitourinary tract (see Injury Prevention for the Genitourinary Tract, later). Mental Preparation.  Mental preparation emphasizes thinking through the plan, ensuring that one is well rested, focusing on the activity, and being confident about the activity. Mental preparation also includes proper education and training. This should include training specific to the activity and emergency medical training. Discuss and agree on a travel route. Select a leader, and review each member’s capabilities and what equipment and supplies are necessary. Equipment Preparation.  Material preparation involves acquiring proper equipment (both routine and for emergencies and unplanned events), testing and organizing equipment, and having backup equipment. Carry sufficient equipment to survive for extended periods if unforeseen changes occur and under the worst possible environmental conditions for the season. This includes ensuring that preventive maintenance has been performed for equipment and that equipment is in good working condition. Review each person’s responsibility for equipment. Make sure that equipment and weight are properly distributed, taking into 338

account abilities. Equipment should be appropriate for the activity and the environment (e.g., waterproof, ruggedized). Selecting battery-powered items that require the same size and type of batteries minimizes items to be carried. Maintain an equipment checklist. If using specialized equipment, know its proper use and maintenance. Courses are available through retail outlets, clubs, and wilderness organizations to prepare and train participants for most outdoor activities. The minimum equipment list should include, but is not limited to the following: • Emergency equipment • Emergency blankets • Emergency bag • First-aid kit • Flashlight • Maps, compass, navigation equipment • Communication and emergency communication equipment • Footwear • Skin and eye protection • Backpack • Water, extra food • Extra clothing • Timepiece • Survival/unplanned conditions equipment may include the following: • Fire starter, matches • Shelter (e.g., emergency tube tent) • Survival whistle • Water • Water disinfection system • Avalanche beacon • Personal locator beacon, rescue laser, ground insulation Problem Anticipation Even with good planning and preparation, problems occur. For most activities and trips, major problems can be anticipated. A good exercise before undertaking any activity (and during the activity at various times) is to think through the five most likely problems and the two rare but significant problems, to both plan and prepare for them. Standard problem anticipation approaches include bringing adequate protection from environmental and recreational hazards, having all the appropriate immunizations, safe drinking and food hygiene practices, and ensuring that everyone has a working knowledge of first aid. Physical Disabilities (see Chapter 102) For persons with disabilities, it may be a great challenge to access wilderness. In federally designated wilderness areas, Congress reaffirms in the Americans with Disabilities Act that nothing in the Wilderness Act prohibits use of a wheelchair in the wilderness by a person whose disability requires its use. There are 54 million persons with disabilities in the United States, and this number is expected to grow. The challenge for the future will be ensuring that persons with disabilities have the same opportunity to participate in wilderness activities and programs as do persons without disabilities, without necessarily making wilderness access easier.153 The principles of injury prevention apply to people with disabilities who participate in wilderness activities. Their preparation, planning, and anticipation of problems must take into account the specific disability and unique physical and mental challenges of that disability.

Individual Factors and Injury Prevention SPECIFIC TOOLS FOR PLANNING AND PREPARATION IN THE WILDERNESS Maps and Orienteering People should have the ability to tell where they are and where they are going. A single wrong turn can have disastrous consequences. Maps are useful tools for planning, and the Global Positioning System (GPS) gives an accurate determination of actual location. Traditional two-dimensional maps, such as road maps, identify a sampling of features on the ground, with symbols

Global Positioning System Devices The GPS is a U.S. space-based global navigation satellite system that provides continuous positioning, navigation, and timing services to users from anywhere on Earth. Use of a GPS device requires an unobstructed view of four or more GPS satellites, each of which broadcasts signals that GPS receivers use to provide absolute locations in three dimensions (latitude, longitude, and altitude), velocity of movement and orientation, and precise time. GPS receivers have become commonplace for navigation on ground, air, and water. Modern GPS receivers often overlap graphic displays of terrain or nautical features to further assist navigation. A GPS unit can assist SAR organizations with recovery of lost or stranded travelers. Because line of sight is required for GPS receivers to function, their use may be limited in dense forests or jungles or below steep cliffs or rock overhangs. In addition, they are sensitive to extremes of temperature, moisture or humidity, and mishandling. They depend on battery power, so users should carry spare batteries. They should not be used as total replacement for traditional maps or compasses for navigation and positioning or use of natural references, such as sun position, wind, or topography. Communication Devices Traditionally, emergency communications from wilderness settings have been limited to signaling with devices such as a mirror or other reflector, whistle, fire, smoke, or flare (Figure 16-2). Newer laser devices encased in waterproof housings have been found to be very effective in identifying people during aerial searches, particularly at night. Commercially available “rescue laser flares” are small, lightweight, and rugged handheld laser devices that project a wide line, rather than the pinpoint light normally associated with a laser. They allow the user to sweep across an area with a dispersed red or green light beam that can be seen from up to 30 miles away (3 miles in daylight). The device is powered by lithium batteries that when used continuously will last for up to 72 hours, depending on the model.111 The international distress signal (SOS), which can be used with many signaling devices, consists of three short signals, followed by three long signals, and then three short signals, repeated at

intervals. Signals may communicate the general location of an injured person, but to provide more detailed information about injuries or illness, some form of vocal or written communication is needed. Vocal communication allows rescuers to obtain an accurate, on-site victim report with descriptions of injuries, mechanism of injury and the specific location of the victim. Ongoing communications with a reporting party can help guide rescuers to the victim and allow them to provide advice about first aid before their arrival. Cell phone technology is useful only when travel is within an area with cell phone relay stations, making its use limited in the wilderness. Wireless access for cell phone use is becoming more common inside U.S. national parks but is limited to the more populated areas where the park service often provides audio tours. Signals may be weak or unreliable. Cell phones in national parks are controversial: Conservationists argue that parks run the risk of becoming too civilized. Critics argue that the presence of cell phone towers in wilderness areas and national parks creates a false sense of security. Despite the controversies, cell phones are being used increasingly within national parks to notify authorities of mountaineering and recreational accidents. If a cell phone is used within a park, it is best to program in the direct number for park dispatch, because dialing 9-1-1 will often reach a county sheriff, who must then relay the call. Once dispatch is reached, state your location and call-back number early in the conversation in case of connection failure. A member of a party may need to hike to the nearest trailhead to obtain cell phone service. Completion of a standard incident report form before leaving the scene will allow the caller to provide critical information about the nature of the incident, location, and initial care provided. Cell phones with GPS (E911) technology can be useful for providing the location of an injured person. As a result of a mountaineering accident with three fatalities on Mt Hood in 2007, the Oregon state legislature proposed bills that mandate electronic signaling devices (personal locator beacons, mountain locator beacon, GPS receiver with cell phone/two-way radio) for all climbs above 3048 m (10,000 feet) on Mt Hood. Although local rescue personnel and climbers are reported to encourage the use of such equipment, they do not believe its use should be required.127 One survey of climbers found that 14% of them always carry a cell phone. Twenty-one percent of climbers who reported carrying a cell phone indicated that they had used it to report an accident.8 If a cell phone or GPS unit is carried into the wilderness, consider using a waterproof box or case to prevent damage from crushing, dropping, or water, along with a backup battery. In most cases, portable radios serve as a good choice for communication between party members. When carrying a portable radio, determine which frequencies are allowed for personal use and which frequencies are monitored in your area. Radiofrequency interference from transmitting cell phones (code division multiple access [CDMA]) or two-way radios can cause interference with some avalanche beacons. Playing an iPod at close range has also been found to cause radio frequency interference in all beacons.38 A common intermediate (processing) frequency for cell phones or digital cameras is 455 kHz, which is very close to the 457 kHz radio frequency of avalanche beacons. In addition, false signals may be produced in some beacons from cell phones cycling their transmission to “handshake” with their cell. To ensure there is no radio frequency interference, electronic equipment, including cell phones and digital cameras, should be turned off while doing an avalanche transceiver search with any brand of digital or analog transceiver.149 Satellite phones connect with orbiting satellites and have the potential to be used worldwide. The size and weight of early “sat phones” once limited their use in the wilderness, but current versions are as small as a “smartphone” or mobile PDA (Figure 16-3, online). The cost of newer satellite phones can top $1000, prohibiting their use by many wilderness adventurers. In addition, most satellite phones will only work with a corresponding network and cannot be used if the network is switched. Depending on the type of satellite phone service used, there may be a delay in transmission of voice or data. Geostationary satellite phone systems depend on line of sight for service. 339

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to represent physical objects. Topographic maps, also known as “topo” maps or contour maps, use contour lines or shaded relief to represent the shape of land surface. Contour lines connect contiguous points at the same altitude. Topo maps usually depict significant bodies of water, forest cover, or other features and are prepared using interpretation of aerial photography or remote sensing techniques. The U.S. Geological Survey (USGS) produces several series of national topographic maps, the largest and best known of which is the 7.5 minute, 1:24,000 scale, quadrangle nonmetric scale map, each of which covers an area of 0.125° latitude by 0.125° longitude spaced 7.5 minutes apart (an area of about 49 to 64 square miles). The 7.5 minute series of maps has been abandoned recently in favor of The National Map, a collaborative effort of the USGS and federal, state, and local agencies to improve topographic information in the United States and contributing to the development of a new generation of digital topographic maps.141 An accurate graphic information system (GIS), such as a digital elevation (terrain) model, allows wilderness explorers to extract and analyze additional information via three-dimensional digital representation of surface terrain or topography. An offshoot of GIS is location-based services, which allows GPS-enabled mobile devices (such as cell phones, personal digital assistants [PDAs] and laptop computers) to display their location in relation to fixed or mobile assets (such as a gas station or police car) or to relay their position back to a central server for display or other processing. This is a potentially useful future application in national parks. GIS has led to the explosion of Internet mapping services, such as Google Maps and MapQuest, which allow users access to aerial satellite imagery useful in the planning and preparation stage of wilderness travel. Whether a two-dimensional planimetric, topographic, or graphic display map is used for wilderness travel, it is essential that the user carry the map and know how to use it. In addition, ingress points, checkpoints, and egress points should be established before traveling.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

D

E

FIGURE 16-2  A, Smoke signal. B, Handheld flare. C, Marking location with flare. D, Rocket flare. E, The Rescue Laser Flare Magnum. (A to D courtesy Eunice Singletary; E copyright Greatland Laser, Anchorage, Alaska. http://www.greatlandlaser.com.)

Low-Earth-orbit systems (<2000 km [1243 miles] above the earth’s surface) depend less on line of sight. Two such systems in the United States are Globalstar (http://www.GlobalstarUSA.com) and Iridium (http://www.Iridium.com). Globalstar does not provide coverage of the polar caps because of the inclination of their orbiting satellites; Iridium claims worldwide coverage. Satellite phones are banned in a number of countries, such as North Korea and Myanmar, because their use bypasses local telecommunication systems, hindering efforts at censorship. In disaster situations, large spikes in call volumes may lead to cascading failures of a network, similar to cell phone network failures noted in past disasters. Protective Gear Engineering accomplishments have improved protective equipment for wilderness travel and recreational activities. Clothing.  Waterproof and breathable fabrics, sealed seams, lightweight high-loft insulation, quick-dry material, and material with sun-blocking properties have been at the forefront of outdoor clothing offerings. Sometimes referred to as technical clothing, these fabrics have temperature regulation properties embedded in the yarns and retained with washing. Microfiber materials are used as an alternative to down for insulation in sleeping bags and clothing, because they retain heat when damp or wet. Microfiber material wicks moisture and sweat away from the body and keeping wearers drier and warmer in cold weather and cooler in hot weather. A combination of yarn selection, fabric 340

construction, and finishes is used to create sun-blocking protection, which is often rated with the Ultraviolet Protection Factor (UPF) system.7 A rating of 15 earns a product a rating of “good”; a rating of 30, “very good”; and a rating of 40 or 50+, “excellent.” Foot and Hand Wear.  Ideal footwear in the wilderness accommodates environmental factors (extremes of heat, cold, terrain), user comfort, and protection needs. Proper fit and hygiene are crucial for comfort and to prevent “hot spots,” blisters, or toenail problems. The purposes of footwear are protection, cushioning, support, and grip. Selecting, fitting, breaking in, and caring for footwear help it last a long time and maximize comfort. It is important to properly size footwear, including accommodating for swelling that may occur during prolonged activities. Each foot should be properly fitted. When sizing footwear, it is important to consider not only the length and width, but the ball-to-heel (arch) length. For hiking, wear shoes that extend above the ankle to reduce likelihood of an ankle sprain. Footwear should fit comfortably with moderate tension on the laces, so that they can be tightened or loosened as needed. To avoid blister formation, seams should not rub against any part of the foot. The tongue of the footwear should be aligned and laced properly. Otherwise, the tongue can slide into an incorrect position and cause blisters. Ankles should be comfortably supported by stiff heel counters or heel cups and should not slip with toe flexion, causing blisters because of repetitive rubbing. With the foot on the ground, there should be no more than 6 to 12 mm (0.2 to 0.5 inches) of heel lift.

Helmets.  Helmets are used for many wilderness and remote activities, including mountain biking, skiing and snowboarding, rafting, kayaking, and climbing. Most helmets are designed for specific activities. The use of helmets by recreational bicyclists dates back to the mid-1970s. Early helmets had polycarbonate hard shells with an expanded polystyrene liner and little or no ventilation. Helmets for children were not introduced until 1984. Since the 1990s, bicycle helmet design has evolved, with incorporation of vents—critical for cooling in high-exertion riding— and cradles to fit the head more precisely. Bicycle helmets today come in either a hard shell design or a soft/micro shell. Helmets for racers often have a streamlined, elongated back (Figure 16-4). The back of the head is covered less with bicycle helmets than with other helmets. For this reason, bicycle helmets are not appropriate for skating, skateboarding, and other activities in which falls backward are more common. The Snell Memorial Foundation131 created the first standards for helmet design in 1985. Today, the U.S. Consumer Product

FIGURE 16-4  Bicycle helmets with varying designs. (Courtesy Eunice Singletary.)

Safety Commission (CPSC)140 requires standards for helmets sold in the United States. CPSC standards have been criticized as being less stringent than current Snell B95 standards and as having weakened over time.144 The trend in bicycle helmet design today is to make them thinner and with larger vents, which may compromise the ability of certain helmets to protect against head injury. In addition, there is concern that the liners of many bicycle helmets are too rigid to properly cushion and protect the head.31 One of the most important elements of helmet selection for any activity is proper fit. One study showed that 96% of helmets were improperly fitted.104 Fit can be adjusted on helmets using cushioned pads, or by use of a band inside the helmet that may be adjusted with a tightening wheel or plastic clips. The chinstrap can be adjusted to help with fit, and it should be kept fastened under the chin to help keep the helmet in place during falls. Should a helmet be damaged by a fall, or should the helmet exceed 5 years of age (or less according to the manufacturer), the Snell Memorial Foundation recommends replacement.4 Helmets are not without criticism. Laws mandating use for bicyclists have been paradoxically blamed for a decrease in use. Helmets have been blamed for an increase in accidents, because some feel they restrict peripheral vision and decrease hearing. It is speculated that use of a helmet encourages risky behavior. Goggles.  Goggles provide a thermal barrier and help protect eyes from wind, snow, rain, dryness, and ultraviolet (UV) or bright light. Sunglasses provide some protection from the elements and UV light, especially when they “wrap” the face or have plastic or leather side guards. Goggles should fit well on the wearers face. The foam on the frame should fit uniformly and snugly around the entire goggle, because gaps increase airflow and contribute to drying of the eyes. Depending on the activity of the wearer, other desirable features may include helmet compatibility, polychromatic or interchangeable lenses for varying light conditions and to improve contrast, and prescription lens inserts. Fogging lenses are a common problem. Most goggles are vented to help prevent fogging, and many have antifog coatings. Goggles with a spherical double lens provide high-quality optics and fog-free vision. In general, ski goggle design has changed little over the years. Zeal Optics has recently designed a new goggle (Transcend GPS) with an integrated heads-up display system that shows GPS, speed, altitude, vertical odometer, time, and temperature, all of which can be viewed on the spherical polarized lens by scrolling with buttons on the side of the goggle. Although more expensive than traditional goggles, this new design may have applications for backcountry snow-sports enthusiasts. Future plans for the goggle include trail maps, text messaging, emergency calling, buddy tracking, and music controls. Body Armor.  Once popular with football players and dirt bike enthusiasts, body armor and padded clothing are promoted for water sports, snow sports, cycling, and other outdoor sports. Snowboard gloves or mittens with integrated wrist guards are purported to decrease the risk for hand, wrist, and forearm 341

CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

Thermal insulation is the most important factor in footwear designed for protecting feet from cold and is influenced greatly by moisture control. Although foot comfort is affected by the interaction of sock, sole, and shoe, the choice of footwear is influenced by factors such as intended activity, fit, shoe weight, insulation, vapor barrier, waterproofing, protection, flexibility, and durability. Mechanical injuries to the toes can be avoided with shoes or boots with integrated steel caps and soles. Sole design can prevent slippage; the design should be based on the intended use. Materials with good friction at moderate temperatures tend to become hard with cold temperatures and to lose their grip. On wet ice, virtually all shoe materials become slippery. Insulation is an important factor with low ambient temperatures. Adding heat sources such as disposable chemical foot and toe warmers, warm air or water circulation, or battery powered electrical heaters can reduce heat loss. Additional heat sources generally reduce volume inside the shoe or boot, potentially compromising fit and maneuverability, and also add weight. A 100-g (3.5 oz) increase in the weight of footwear has been shown to increase oxygen consumption by 0.7 to 1.0%, the equivalent of adding five times that weight carried on the torso.70,71,83 Insulating qualities of footwear largely depend on air being trapped inside the fabric of the shoe and between the sole of the foot and the shoe, and can be increased by addition of socks, so long as the footwear is large enough to accommodate the socks without becoming too tight.78 Socks play a large role in moisture management by absorbing sweat. Sweat rates vary widely in the foot, with lower rates in cold weather of 3 g/hr at rest. Newer synthetic materials, such as polypropylene, Capilene, and Thermax, wick moisture quickly, making them good choices for an inner layer. Pile or fleece socks do not wick moisture very well. Wool offers many advantages. It is warm in winter, cool in summer, absorbs and wicks sweat, and keeps the feet warm when wet. Furthermore, during long trips, it rinses well in cold stream water, can be worn for days at a time without wear, and does not mat down like cotton socks with terry loop liners. Impermeable or semipermeable footwear materials prevent external moisture from entering footwear and wetting insulation. Moisture from sweat inside a shoe reduces insulation qualities and increases heat loss by 5%. Walking and the subsequent pumping effect of moving air in footwear removes moisture and in ordinary shoes removes about 40% of humidity.78 Footwear requires drying to retain insulation and protect feet from the cold. Moist socks and insoles should be changed, and shoes with removable liners should have the liners removed. Placing footwear in a warm, well-ventilated location will assist with drying. Hand protection from cold requires gloves or mittens with insulation, moisture barrier, and adequate space for air trapping. Mittens allow more air trapping and heat retention than do gloves, but with a tradeoff for dexterity. Mittens with glove liners or finger inserts allow improved dexterity without loss of insulation and may include pockets for placement of disposable chemical heaters. For other wilderness activities where gloves are needed but dexterity is critical (such as fly-fishing or climbing), fingerless gloves may be appropriate.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

injuries in snowboarders, but may increase the risk for elbow, upper arm, and shoulder injuries.55,121 Knee and elbow pads, padded pants or shorts, spine and back protectors, and upper body protectors are promoted to offer protection from injury, but with little evidence of effectiveness outside of football.90 Such gear is often articulated, thermal-formed, or soft foam-padded clothing or wraps designed to be lightweight and flexible, usually fitting underneath underwear or outerwear. Some gear includes molded plastic plating or shoulder cups. Mouth Guards.  The efficacy of mouth guards in preventing or reducing dental trauma is debated. There are studies that show significantly lower rates of dental injuries and soft tissue injuries among users of mouth guards in football and basketball than among nonusers.43,79 Other studies have found no significant difference in oral, head, or neck injuries between users and nonusers of mouth guards.16 Although the American Dental Association reports that mouth guards can reduce the severity and incidence of oral injuries, they also recommend further research on currently available models.2 The CDC has pointed out the need for high-quality research into the effectiveness of mouth guards.24 Avalanche-Specific Protective Gear.  According to the Colorado Avalanche Information Center,29 there has been an annual average of 25 deaths in the United States due to avalanches over the past 10 winters, with 36 fatalities in the 2009-2010 season. Avalanche fatalities most commonly involve backcountry snowmobilers, skiers, and snowboarders, but ice climbers, snowshoers, and hikers are also occasionally killed (Figure 16-5, online). Fatalities from avalanches are most commonly due to asphyxiation, followed by trauma with asphyxiation, or trauma alone.91 The key to reducing the risk for being caught in or killed by an avalanche is not safety equipment, but rather education and training, along with avalanche awareness and smart decision making. The skills acquired require repeated practice. Traveling in avalanche country with a trusted and trained partner is a key element of avalanche safety. Additional tools that may help one avoid or survive an avalanche include a digital or analog transceiver; a lightweight shovel for digging test pits or for recovering a buried victim; and a collapsible probe to pinpoint the exact location of a buried victim following a transceiver search.128 Snowshoers and snowmobilers tend to underestimate avalanche danger when traveling in backcountry.129 The RECCO Rescue System (http://RECCO.com) was introduced in 1983 and is used by over 600 rescue organizations worldwide, including more than 100 ski areas, rescue organizations, and helicopter companies in the North America. It consists of a RECCO detector used by search organizers and a reflector permanently integrated into the helmet, boots, or clothing of the wearer. The system uses harmonic radar to pinpoint a victim’s exact location. The reflector has advantages of requiring no batteries or training, but it is not designed for self-rescue or as a replacement for traditional avalanche transceivers. It is an additional tool for search and rescue that compliments transceivers when worn in an area where the RECCO detector is readily available. More recent technologic advances are designed to improve the chances of survival by an avalanche victim. The AvaLung is a 9-oz sling type of apparatus worn over the shoulder that prolongs the time a victim can breathe while trapped under snow. Two other devices use one or two inflatable air bags holding up to 45 L of gas to allow a victim caught in an avalanche to float to the surface, avoiding burial and enhancing visibility for searchers. The ABS system deploys two air bags from a backpack when a handle is pulled. Nitrogen canisters that inflate the bags are replaceable, allowing the system to be reused. Snowpulse SA markets an air bag in a backpack that when released, envelops the head, providing similar flotation along with head protection. Snowpulse cartridges for air bag inflation are refillable (see Chapter 2). Training and Education William Haddon’s strategy for reducing the magnitude and burden of injuries involves the pre-event phase, the event phase, 342

and the postevent phase.137 The pre-event phase focuses on prevention. Education and training in this phase includes courses that provide wilderness explorers the ability to recognize and avoid dangers in the environment and courses that teach acquisition of basic skills and techniques necessary to safely perform activities in the wilderness. Such courses include topics such as avalanche awareness and safety, rock and ice climbing, rope use, caving, mountaineering, map reading, orienteering, and kayaking. Courses are available through clubs, colleges, and specialty organizations that represent these activities. The Outdoor Wilderness Leadership School, the National Outdoor Leadership School (NOLS), and Outward Bound are examples of organizations that offer instruction in many different wilderness activities, as well as courses for instructor development. Education and training for wilderness medical care or SAR techniques are a component of the third (postevent) phase of Haddon’s injury matrix. Salvaging people and property is the focus of this phase. Initial (field) emergency care SAR operations, extrication, and transportation to advanced medical care for victims of wilderness injuries all fall into this phase. Different levels of providers may provide emergency care in the wilderness. As the popularity of wilderness excursions and wilderness medicine have grown, so have the number and variety of courses in wilderness emergency care. Although there is no national standardized curriculum or certification for wilderness first aid, courses are available through organizations such as the American Red Cross, Wilderness Medical Associates, and the Wilderness Medical Institute. These courses are generally 16 hours in duration.147 Some organizations offer a 36-hour advanced wilderness first-aid course and are ideal for wilderness enthusiasts without medical backgrounds. Guides, SAR team members, and outdoor educators without medical backgrounds complete courses with more comprehensive curricula and practical training, such as a 70-hour wilderness first responder course or a wilderness emergency medical technician (EMT) course. Unlike standard first responder and EMT courses, these programs include content that prepares an individual to deliver emergency medical care in harsh environments, when evacuation times may be lengthy, and when equipment may need to be improvised. Wilderness EMT courses are designed for EMS personnel working in search and rescue, on expeditions, in disaster situations, or in remote settings. For medical professionals with Advanced Life Support certification, a 36-hour Wilderness Advanced Life Support course is offered by Wilderness Medical Associates and other organizations. Supervision and Buddy Systems.  The number of children and adolescents exploring backcountry wilderness areas has steadily increased, accounting for 25% of backpackers and wilderness campers in the United States.98 Children and adolescents typically enter wilderness areas either in a family group or through a sponsored group youth expedition or outing (Figure 16-6). Groups are accompanied and supervised by adults trained as instructors in various recreational disciplines or in wilderness emergency care. There are few studies looking at wilderness injuries or fatalities in children or adolescents. A retrospective study of visitor fatalities at all NPS units for 2003 and 2004 found that of 356 fatalities, 13% (46) occurred in children and adolescents 19 years or age or younger.62 A second study found that children and adolescents account for 21.2% of all NPS visitors nationwide requiring SAR assistance.59 The most common activities reported at the time of request for SAR were hiking, mountaineering, and boating. A study in Washington State identified 40 recreational wilderness fatalities among children and adolescents between 12 months and 19 years, with hiking and swimming the most common activities preceding death. Four out of five pediatric fatalities in this study involved children drowning after falling out of boats or into water while playing at a campsite.100 Supervision of children or lack thereof in wilderness fatalities or injuries is rarely mentioned in these retrospective studies, although a lack of personal flotation devices was noted for nonscuba drowning fatalities in the latter study. For supervised expeditions, one study found that only 13% of all 1646 reported health problems were related to trauma,33 whereas a study by Sadnicka122 found that 10% of medical problems among 2915

travelers between 15 and 18 years of age in 250 expeditions to multiple countries were the result of trauma. Organizations such as NOLS strive for safety in outdoor activities. Through their risk management program, NOLS decreased the number of injuries to a rate of 1.18 per 1000 program days for the years 2002 to 2005. NOLS attributes this reduction to prevention strategies that include reduced (11-kg [25-lb]) backpack weights, carefully planned course routes, avoiding overly demanding terrain early in a trip, emphasizing warm-up and stretching before hiking and strenuous activities, and deliberately teaching students how to hike on rugged and uneven terrain.92 Just as risk management programs and supervision of participants in organized group wilderness recreation activities may potentially decrease the incidence of injury, use of a buddy system is desirable for individual activities. People who engage in climbing, backcountry skiing, snowmobiling, and other solo activities in the wilderness are encouraged to do these activities with a buddy (Figures 16-7 and 16-8). The buddy should be someone with whom they are familiar. If unfamiliar with a buddy, one should use a half-day outing at a lower level of activity to become acquainted with their skills, styles, and physical condition. Wilderness partners need to be aware of each other’s previous experience for the planned activity; level of training in pertinent topics such as avalanche fundamentals, companion rescue, or wilderness emergency medical care; and what medical supplies are being carried. Additional points that should be addressed include the following: • What gear, specialty equipment, personal clothing, food, water, communications, and safety equipment are being carried? • Maps and route of travel. What are the potential hazards and current condition of the planned route? What is the weather forecast? What are the contingency plans in case a route or access conditions have deteriorated? What will be the turn-around or pull-out time, and how will you decide whether to continue on or turn back? • In the event of a serious event or injury, what is the emergency plan, and what resources are available? Emergency contact information and pertinent medical information should be shared with each other and with a nontraveling contact. Once wilderness travel plans have been decided, it is best not to change them at the last minute. Likewise, it is a good idea not to change buddies or to add additional travel partners in haste. Problem Anticipation: Acute Illness and Injury Even with the best preparation and planning, acute illnesses and injuries occur. When primary prevention fails, one needs to be prepared to address illnesses and injuries and minimize their impact. This is accomplished through medical clearance and vaccinations, first-aid training and ensuring that one has proper first-aid supplies, medical supplies, and medications. Because supplies may be limited as a result of availability or what one can carry in the wilderness, one must be ready to improvise.

FIGURE 16-7  Lone kayaker surfing the falls. Having a buddy or spotter to accompany individuals in solo wilderness activities is advisable. (Courtesy Haley Buffman.)

First-Aid Training.  Every adult participating in wilderness activities at a minimum should have training in cardiopulmonary resuscitation (CPR) and have completed a basic first-aid course that covers common illnesses and injuries. Additional training beyond first aid may be needed, depending on the activity, distance to more definitive medical care, and underlying medical conditions of participants. For example, if one is participating in a remote area with delayed time to further medical care, at least one person needs to have completed a formal wilderness first-aid training program with emphasis on remote conditions and prolonged care.

FIGURE 16-8  Wilderness treks are more fun and less risky with a buddy. (Courtesy Haley Buffman.)

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CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

FIGURE 16-6  Children in wilderness activities are typically supervised by excursion guides, parents, or both. (Courtesy Eric Becker.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Medical Clearance.  Before participating in any athletic activity, it is prudent to obtain medical clearance. This is especially important for the following: • Activities in remote areas • High-risk activities and extreme sports • Person with chronic illness and/or physical limitations The purpose of medical clearance is to determine appropriate activities, personal limits, and go/no-go decisions. For persons with chronic medical conditions, the goal may be to optimize these conditions. An example is a diabetic with projected increased physical activity and projected altered meal schedule needing to alter the insulin regimen, or a patient on a medication that increases photosensitivity having to adapt to a sunny environment. Vaccinations and Prophylaxis.  Tetanus vaccination should be current. If the intended activity requires travel to remote areas or areas subject to endemic diseases, then individuals should consult with a health care provider regarding the need for vaccination and/or drugs for prophylaxis. An example is the need for prophylaxis if hiking or camping in a malaria-risk area. First-Aid/Emergency Medical Supplies.  For most activities a first-aid kit should be available. For brief activities with low injury risk that do not require an overnight stay or travel to remote areas, a basic first-aid kit is appropriate. The contents of commercially available first-aid kits vary greatly. In general, a kit should contain the items listed in Table 16-1.146 These recommendations are expanded for more remote locations. For certain extreme sports or very distant locations, extrication equipment may be necessary. Medications.  Prescription medications may need to be considered for wilderness activities. At a minimum, bring medications prescribed for those participants sufficient for the entire trip and include an additional supply to cover unforeseen trip extension. For a single-day trip, a rule of thumb is 2 days of medications; for prolonged trips or remote environments, 1 week’s extra should be taken. Additional medications to consider are the following: • Antibiotics • Epinephrine autoinjector • Intravenous fluids

TABLE 16-1  Wilderness First-Aid Kit Item Dressings and Wound Care Adhesive bandage (Band-Aid) Adhesive tape (2-inch roll) Conforming gauze bandage (Kling 3-inch roll) Elastic bandage (Ace 3-inch wrap) Moleskin (l5.5-square inch sheets) Spenco 2nd Skin (3-inch × 4-inch pads) Sterile gauze compresses (4 inches × 4 inches) Equipment Scissors Thermometer Tweezers Oral OTC Preparations Antacid (chewable tablet) Antihistamine (diphenhydramine 50 mg) Bismuth subsalicylate (Pepto-Bismol chewable) Ibuprofen (200-mg tablets) Topical OTC Preparations Alcohol swabs (for cleaning equipment) Antiseptic ointment (Neosporin 0.9-g packets) Hydrocortisone 1% cream (30-g tube) Povidone-iodine solution (individual swabs) Tincture of benzoin (30-mL bottle) OTC, Over-the-counter.

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Quantity 12 2 2 1 2 4 6 1 1 1 6 6 6 6 10 6 1 8 1

• Oxygen • Resuscitation medications Improvisation in Treatment.  In many instances, drugs and supplies are inadequate. One may need to rely on improvisation to address these situations. Planned improvisation refers to situations where a specific piece of emergency equipment cannot be brought, but there is a predetermined plan to improvise the device. The classic example is extrication equipment for a patient whose size and weight are prohibitive. Therefore one must preplan how to convert existing equipment, such as backpack frames, should the need arise. Unplanned improvisation is exemplified by a major injury leading to uncontrolled bleeding. A tourniquet may be required but might not be standard equipment. In such a case, form a tourniquet from nontraditional material, such as a belt. Injury Prevention for the Genitourinary Tract.  To prevent genitourinary infections during outings, individuals should maintain attention to genital hygiene and hydration. Infections and irritation of the genitourinary tract are more common in women than in men because the female urethra is shorter, leaving the bladder more vulnerable to colonization by bacteria. The risk for infection can be exacerbated during wilderness activity because of infrequent urination and urethral trauma from vigorous activity or bruising from a bike seat, saddle, or climbing harness. One should provide adequate padding, allow for adequate bathroom breaks, and minimize urethral trauma. To avoid vaginitis, women should keep themselves cool and dry by wearing loose-fitting clothing that maximizes air circulation and minimizes the optimal conditions for bacterial and fungal growth. Avoid nylon undergarments, because they retain humidity. Cotton undergarments or underwear made from a material such as polyester that wicks moisture and is fast drying, are ideal. Women may need to consider sanitary protection for menstruation. If menstruating while in the wilderness, women should change tampons or sanitary napkins just as frequently as at home to avoid infection. Women who handle tampons should make sure that hands are scrupulously clean before insertion. For environmental reasons, tampons with cardboard rather than plastic applicators should be used if wilderness disposal is a possibility. Injury Prevention for the Feet.  Proper footwear, including careful selection of shoes and socks, helps prevent problems such as blisters. The soles should be protected with layers of cushioning thick enough to prevent bruising, but pliable enough to allow natural heel-to-toe flexion. Thick soles insulate against cold and heat. The tread provides grip. Support comes from a fit that stops the foot from slipping inside the shoe, but that is not so tight that it prevents the foot from expanding when it swells. Check socks for loose threads, knots, or harsh stitching that might cause blisters or sore spots. Flat seams at the toes are important. Bulky seams rub and cause blisters. Consider wearing one pair of fairly heavy socks (rag wool) and one pair of light liner socks next to the skin. With one sock, the boot and the outer sock tend to move as a unit. They rub against the heel and the tops of the toes at the metatarsal heads. A lightweight liner sock tends to cling to the foot. As the boot moves, the socks rub against each other, not against foot skin. Consider using powder to keep the feet dry. Some boots feature sock liners or booties made from vapor-permeable membranes, such as Gore-Tex and Sympatex, hung between the lining and outer aspect of the boot. These may be appealing initially because of the ability to prevent leaks, but over time they may leak. Their lack of breathability means that water vapor cannot penetrate the barrier, resulting in hot, sweaty feet. In addition to appropriate footwear and socks, one must practice proper foot hygiene. Keep toenails short and cut square. Keep feet dry to avoid skin softening. Immediately stop walking and attend to the first sign of a sore or “hot spot” to prevent further injury. Carry supplies, such as moleskin, tape, or Molefoam, to allow protection of any reddened areas. The covering should extend beyond any redness.

A

The Physical Environment and Injury Prevention The event phase of injury begins when physical forces exert themselves unfavorably on people or property. Prevention of injury at this stage involves intervention to prevent the harmful effects when excessive mechanical, thermal, chemical, electrical, or ionizing radiation energy is contacted. Harmful effects of excessive energy may occur acutely, as with thermal burns, or as a result of prolonged exposure with extended wilderness stays.

ULTRAVIOLET EXPOSURE UV light is the main cause for most skin cancers and cataracts. Anyone who has ever experienced a severe sunburn or solar keratitis is aware of the significant, even disabling pain associated with acute burns to skin and corneas from UV light. Even on a cloudy day, UV light can cause a serious burn. In the wilderness setting, injury from UV light is largely preventable. Photoprotection begins with behavioral changes. Limiting exposure to UV light is an essential prophylactic element and begins with avoiding exposure at peak times of the day (10 AM to 4 PM) and with covering the skin and eyes with UV-blocking clothing and sunglasses. The photoprotective properties of clothing depend on its thickness, weight, and color, with darker fabrics having greater photoblocking ability. Lightweight fabrics treated to enhance UV protection are especially useful in the wilderness setting. Hats provide photoprotection for the scalp, face, and neck; the amount of skin covered varies with the style of hat (Figure 16-9). Sunglasses protect the eyes from the discomfort of bright lights, but not all sunglasses provide UV protection. In the United States, there is an American National Standards Institute (ANSI) standard for sunglasses that includes impact resistance and UV protection.5 ANSI Z80.3 1996 standards require that a lens should have a UV-B (280 to 315 nm) transmittance of no more than 1% and a UV-A (315 to 380 nm) transmittance of no more than 0.3 times the visual light transmittance. When purchasing sunglasses with UV protection, choose a pair labeled “meets ANSI Z80.3 1996 [normal] or [strictest] UV blocking requirements” or “lenses block [X] % of UV-A and [X] % of UV-B” (as close as possible to 100%). Because of the intensity of light at altitude and the reflection of light off snow and ice, sunglasses used in winter

B FIGURE 16-10  Examples of traditional (A) and contemporary (B) sunglasses with side guards to help reduce ultraviolet light at altitude. (Courtesy Julbo.)

wilderness settings often include leather blinders on the sides or broad temple arms to further block light transmission (Figure 16-10). Sunglasses worn for travel at altitude on snowpack or in polar regions should transmit 5% to 10% of visible light and block up to 100% of UV radiation. Some sunglasses also block highenergy visible, or “blue” light, which is postulated to contribute to macular degeneration.52 The best optic quality is achieved with glass lenses, but in the wilderness, glass lenses are easily broken or shattered. Plastic lenses are lighter and more resistant to breaking, but they scratch easily. The lightest and most shatterproof plastic lenses for sunglasses are made of polycarbonate. Polarizing lenses reduce glare and are popular with fishing enthusiasts because they allow one to see below the sunlit surface of water. Sunglasses designed for water sports are constructed for greater impact resistance and flotation and include a nose cushion and retaining strap to hold in place. Lens color, polarizing characteristics, and price do not relate to UV protection, so sunglasses should be sought that meet the requisite UVA and UVB protection. Sunscreens are topical or oral products designed to protect the skin from the harmful effects of UV light by absorbing, scattering, or reflecting UV radiation. Topical “shielding” sunscreens are the most effective at preventing sunburn. Prevention of photoaging depends more on blocking low-energy UV light. Some topical sunscreens have been shown in animal models to also repair preexisting damage from UV radiation exposure.75 Sunscreens are rated by their sun protection factor (SPF), with a higher number correlating generally with greater protection. Faircomplected individuals should use a sunscreen of SPF 30 or higher. Look for a product with broad UV-A and UV-B protection. It is important to apply an adequate amount of the product (approximately 1 oz for the uncovered skin of an average 150-lb adult), to apply the product 15 to 30 minutes before exposure, and to reapply the product 15 to 30 minutes after exposure begins.36 When maximum protection from UV exposure is needed, a topical sunblock should be used. These products contain titanium dioxide or zinc oxide and are more opaque than are sunscreens. When sunscreens are needed on or in the water, use a product that is water resistant. Water resistance does not mean waterproof. The products will resist loss of protection from UV exposure after swimming or with sweating but may still require reapplication.

TEMPERATURE EXTREMES

FIGURE 16-9  Hat with extensions to shade the neck offer increased protection from sunburn. (Courtesy Eunice Singletary.)

Cold Injury The spectrum of cold injuries ranges from localized cold injury (frostbite) to systemic hypothermia. A complete discussion of the pathophysiology and treatment for cold injury is found in 345

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If primary prevention fails to prevent blister formation, try to prevent rupture and infection. Relieve external pressure by applying a doughnut-shaped piece of Molefoam. A blister should not be unroofed unless absolutely necessary. If this is required, wash the area with soap and water, and insert a decontaminated needle (“sterilized” by a flame or with rubbing alcohol) into the edge of the blister. Gently press out the fluid. Apply a sterile dressing. If the blister has already broken, cleanse and cover the area. Topical antiseptic ointment may be beneficial.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Chapters 4 to 9. Prevention of cold injury begins in the pre-event phase with preparation and planning. Weather forecasts should be studied and excursions or expeditions timed to avoid hazardous weather. Climbing, hiking, and backcountry skiing partners or groups should have a travel plan that includes turn-around times and an emergency/crisis plan for potential cold injury. Proper cold-weather clothing (above), including waterproof and windproof outerwear, and dressing in layers are essential for wilderness travel in extreme cold. For short periods of travel, some clothing, including fleece jackets, vests, gloves, and foot beds, are available with wire or carbon microfiber heating elements (ActiVHeat, Therm-ic, Hotronic) that provide up to 5 hours of supplemental heat. Batteries are rechargeable or replaceable, making these garments impractical for excursions lasting more than a day or two, unless spare batteries or a source for recharging are carried. Disposable chemical heaters are available for use in gloves, mittens, shoes, or boots, as well as in pockets. Duration of heat varies; temperature for most brands is high enough to cause burns if placed on bare skin.123 Proper nutrition and hydration are essential for endogenous heat generation. Following an accident when a person has limited mobility, or during long excursions with extreme weather, clothing and nutrition may not be enough to keep a person warm. In these cases, shelters must be used (Figure 16-11, online) or improvised, and a source of exogenous heat is necessary. Sleeping bags offer additional insulation, and a second person in the bag will offer additional warming or protection from heat loss. The heat escape lessening position (HELP) is taught to prevent hypothermia in cold water and involves putting one’s knees together and hugging them close to the chest with both arms. A group of people can gather in this position. A similar position can be used in outdoor settings when no shelter is possible. Figure 16-12 is a risk management process for preventing cold injury applicable to the wilderness setting.23 Heat Illness Heat illness is a spectrum of illnesses ranging from minor cramps and edema to heat exhaustion and life-threatening heatstroke. Heat illness results when heat gain overwhelms the body’s heatloss mechanisms and body temperature rises. In terms of wilderness travel and reducing the risk for heat illness, sources of heat gain include strenuous physical activity and environmental acquisition through conduction, convection, and radiation. Dissipation of excess heat occurs primarily by radiation through the skin and is influenced by clothing. In high ambient temperatures, evaporation becomes the most effective means of heat loss. This is enhanced with sweating. Evaporation is less effective with high ambient humidity. Heat dissipation is hampered by dehydration, cardiovascular dysfunction, skin conditions, certain medications, lack of acclimatization, reduced sweating capability, extremes of age, and hypothalamic dysfunction. When planning for wilderness trips, each participant needs to evaluate his or her risk based on age, presence of preexisting illnesses, and medications (Figure 16-13, online). If traveling during a period of high ambient temperatures and humidity, acclimatization takes 7 to 10 days, so activity level initially needs to be limited. Plan to carry enough water and electrolytecontaining fluids and to wear loose-fitting, lightweight, and lightcolored clothing that enhances evaporation by wicking, while providing shade and protection from the sun (Figure 16-14). Avoid strenuous exertion during the hottest part of the day, and take frequent breaks for hydration and cooling. NOLS guidelines for hydration call for 0.5 L of ingested liquid before strenuous exercise and 0.25 L every 20 minutes during exertion.125 Wilderness excursion leaders who supervise group activities need to emphasize preventive measures, recognize the signs and symptoms of heat illness, know when evacuation is necessary, and be able to provide emergency care. Signs of impending heat illness include headache, dizziness, fatigue, and concentrated urine. Immersion (Trench) Foot and Pernio (Chilblains) Immersion foot and chilblains are nonfreezing cold injuries. Immersion foot is seen when feet have been exposed to moisture at ambient temperatures near or above freezing for prolonged periods.138 Dependent positioning of the feet and overly tight 346

1. Identify/assess hazard How cold is it?

Air temperature Wind Rain Solar load Immersion Sea-state Altitude

2. Identify/assess contributing factors Analyze game/training requirements Determine uniform and equipment available for each person Identify high-risk athletes

Work rates Load carried Duration Availability of clothing/shelter Food and water Experience Fitness Fatigue Health Body fat Nutritional status Time of day

3. Develop controls Implement cold mitigation

Obtain appropriate weather information Train in cold conditions Provide proper clothing and equipment Provide warming facility Provide food and water Implement exposure/rewarming schedules Mandatory clothing changes

4. Implement controls Adopt and implement controls into plans

Changing weather plan Develop standing operating procedures (SOPs) for: Self checks Buddy checks Leadership checks

5. Supervise Evaluate and correct controls

Enforce controls Modify behavior

FIGURE 16-12  A risk management process for preventing cold injury that is applicable to the wilderness setting. (From Castellani JW, Young AJ, Ducharme MB, et al: American College of Sports Medicine position stand: Prevention of cold injuries during exercise, Med Sci Sports Exerc 38:2012, 2006.)

boots are believed to contribute. Keeping the feet dry for at least 8 hours a day often prevents this injury. Pernio (chilblains) is a vasculitis that follows exposure to damp, nonfreezing temperatures, most commonly below 10° C (50° F).107 It is characterized by red to violaceous lesions on exposed skin and is most common in young to middle-age women with Raynaud’s phenomenon or systemic lupus erythematosus. Keeping exposed skin to a minimum and exchanging wet or damp gloves, socks, and face and neck gaiters for dry wear will help prevent this injury.

WIND AND RAIN Wind has a primary effect of increasing convective heat loss, causing an exposed person to cool toward ambient temperature more rapidly than without wind. With moderate to strenuous exer 2 max ]), cise (intensity >60% maximum oxygen consumption [ VO heat production exceeds heats loss at a temperature of 5° C (41° F) in wet clothes with wind velocity of 5 m/sec, and body temperature is maintained. With light or no exercise, heat loss exceeds heat production, and core temperature declines. Exercise in rain leads to rapid declines in core temperature.22,106,109 Wind reduces the insulating value of clothing. Wind-blocking outerwear can counter much of this effect (Figure 16-15, online).

A

WATER

B FIGURE 16-14  A and B, Plan to carry enough water and electrolytecontaining fluids to hydrate adequately in warm weather. (A courtesy Haley Buffman; B courtesy Eunice Singletary.)

Windchill is the apparent temperature felt on exposed skin and depends on wind speed and air temperature. The “windchill factor” is always lower than the ambient temperature; when apparent temperature (what it feels like) exceeds ambient temperature, a heat index is used. Windchill tables have been available through the National Weather Service since the 1970s, with the most recent revised index published in 2001. The index applies to temperatures of 10° C (50° F) or below and wind speeds above 3.0 mph, calculates wind speed at 5 feet (typical height of a human face), and assumes no impact from the sun. Figure 16-16 shows a windchill chart from the National Weather Service.99 Windchill is useful for planning wilderness travel in order to anticipate appropriate clothing and insulation. Wind

Between 2003 and 2006, there were 12,337 reported SAR operations in NPS units, involving 15,537 park visitors. The combined lake, ocean, and river environments accounted for 35% of the total SAR environments—nearly double the number within mountain environments. Motorized boating, swimming, and nonmotorized boating (e.g., canoeing, kayaking, rafting) were three of the top six activities reported by visitors at the time SAR operations were initiated.60 An evaluation of visitor fatalities at all NPS units between 2003 and 2004 found that of 356 fatalities, 16% involved boating incidents or swimming. More than one-half of the swimming fatalities involved rip currents, river currents, and large waves, whereas one-half of boating fatalities involved boats capsizing (Figure 16-18). The most significant risks associated with water immersion or recreational activities on the water are drowning, hypothermia, and trauma from striking an object. Hypothermia is a significant risk from immersion, considering that convective heat loss in water is 25 times greater than that in air, and heat loss by conduction increases as thermal gradients increase in cold water.51 The greater the surface area of a body that is immersed, the greater the heat exchange area and the faster the decline in core temperature.81 Endurance athletes and swimmers are not immune to core temperature drop but can often partially compensate by adapting through cold-water training and by use of wetsuits. When people fall from a boat, kayak, or raft, they usually do not have the advantage of prior cold-water training or a wetsuit. A recent review of U.S. Coast Guard annual boating statistics reports for 1997 to 2006 found that although canoeists and kayakers accounted for 13% of total reported recreational boating deaths, they accounted for 29% of deaths due to hypothermia and 17% of deaths due to drowning (Figure 16-19). In the canoeist/kayaker group, failure to wear a personal flotation device was the primary factor in accidental drowning, and capsizing precipitated two-thirds of injuries or fatalities.103 A

FIGURE 16-16  Windchill chart. (From National Weather Service: NWS windchill chart, 2001. http://www.weather. gov/os/windchill/index.shtml.)

Wind (mph)

Calm 5 10 15 20 25 30 35 40 45 50 55 60

40 36 34 32 30 29 28 28 27 26 26 25 25

35 31 27 25 24 23 22 21 20 19 19 18 17

30 25 21 19 17 16 15 14 13 12 12 11 10

25 19 15 13 11 9 8 7 6 5 4 4 3

20 13 9 6 4 3 1 0 -1 -2 -3 -3 -4

15 7 3 0 -2 -4 -5 -7 -8 -9 -10 -11 -11

Frostbite Times

Temperature (° F) 10 5 0 -5 -10 1 -5 -11 -16 -22 -4 -10 -16 -22 -28 -7 -13 -19 -26 -32 -9 -15 -22 -29 -35 -11 -17 -24 -31 -37 -12 -19 -26 -33 -39 -14 -21 -27 -34 -41 -15 -22 -29 -36 -43 -16 -23 -30 -37 -44 -17 -24 -31 -38 -45 -18 -25 -32 -39 -46 -19 -26 -33 -40 -48 30 minutes

-15 -28 -35 -39 -42 -44 -46 -48 -50 -51 -52 -54 -55

10 minutes

-20 -34 -41 -45 -48 -51 -53 -55 -57 -58 -60 -61 -62

-25 -40 -47 -51 -55 -58 -60 -62 -64 -65 -67 -68 -69

-30 -46 -53 -58 -61 -64 -67 -69 -71 -72 -74 -75 -76

-35 -52 -59 -64 -68 -71 -73 -76 -78 -79 -81 -82 -84

-40 -57 -66 -71 -74 -78 -80 -82 -84 -86 -88 -89 -91

-45 -63 -72 -77 -81 -84 -87 -89 -91 -93 -95 -97 -98

5 minutes

Wind chill (° F) = 35.74 + 0.6215T – 35.75(V0.16) + 0.4275T(V0.16) Where, T=Air temperature (° F) V=Wind speed (mph)

Effective 11/01/01

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speeds do not reflect man-made wind. For instance, a snowmobiler traveling 35 mph on a calm day will be exposed to wind speed of 35 mph across his or her body. In addition, wet skin exposed to wind chills faster than does dry skin. If wet skin is exposed to wind, the ambient temperature used in the windchill chart should be 10° C (18° F) lower than measured actual ambient temperature.17 When windchill temperature falls below −27° C (−17° F), frostbite can occur in 30 minutes of less. Travelers in mountain terrain should presume that wind speed would likely increase as altitude increases and natural barriers to wind (trees) become more sparse. Wind-blown snow is a potential travel hazard. Reduced visibility from blowing snow can cause a person to become disoriented, lost, and even to fall off rocky precipices or into a crevasse (Figure 16-17). Wind makes securing of shelters significantly more difficult and can turn natural and man-made objects into trauma-inflicting missiles.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Figure 16-20). If a fall is into swift water, contact with rocks or downed trees (streamers) increases the chance of additional trauma or becoming trapped underwater and drowning (Figures 16-21 and 16-22). Prevention of drowning from falls off boats or rafts begins with use of a personal flotation device. A water-activated light is useful for locating a person in a nighttime rescue. In swift-water boating activities, most wilderness excursion companies and leaders require a helmet to be worn (Figure 16-23, online). If

A

B A

C FIGURE 16-17  A, Wind from blowing snow can reduce visibility and cause climbers or hikers to become lost or fall off rocky precipices. B and C, Wind can make posing for pictures on cliff edges especially precarious. (A courtesy Haley Buffman; B and C courtesy Eunice Singletary.)

B

C FIGURE 16-18  Large waves and river currents are commonly involved in water-related fatalities. (Courtesy Haley Buffman.)

348

FIGURE 16-19  A, B, and C, Canoeists and kayakers account for 13% of the total reported recreational boating deaths in the United States. (Courtesy Haley Buffman.)

FIGURE 16-20  A fall into water can be associated with traumatic injuries to the head or spine with subsequent drowning (Courtesy Eric Becker.)

people fall into swift water, they are instructed to position themselves so that they travel downstream feetfirst, which allows them to avoid hitting their head on rocks and to see and avoid objects in the water (Figure 16-24, online). Alcohol ingestion is associated with a higher relative risk for death while boating, even with lower levels of blood alcohol. The risk is the same for passengers as for operators.25,39,130 One of the greatest preventive measures for both operators and passengers engaged in watercraft activities is to abstain from drinking.

SNOW To a wilderness enthusiast, nothing can be more delightful than fresh snow, and yet nothing can be potentially more dangerous. Snow becomes a hazard when it slides (avalanches), when it accumulates in heavy snowstorms to such great depths that a person can asphyxiate following a fall, and when a wilderness adventurer becomes wet, cold, or unable to see due to blowing snow. Non–avalanche-related snow immersion death was described by Cadman20 in 1999. Asphyxiation associated with snow immersion occurs when skiers or snowboarders fall upside down into a snow bank or into a tree well around a conifer. It has been

proposed that snowboarders are at higher risk than are skiers from asphyxiation because of the lack of releasable bindings on snowboards. Preventing injury or death from non–avalanche snow immersion begins with basic precautions. Always ski or ride with a partner; in very deep snow following a snowstorm, always ski or ride a slope within eyesight or voice contact of your partner; ski or ride one at a time on slopes using a spotter; and avoid tree wells on glady slopes.142 In case of accidental submersion, attempt to release bindings; if a ski pole is available, it may be the only means of releasing a binding short of twisting out. Several products designed for surviving avalanche burials are potentially useful to backcountry and sidecountry recreationalists to improve chances of surviving snow immersion. The AvaLung (see above) and the Snow Snorkel may increase survival time under snow by diverting expired air away from the face.150 Inflatable air bag type of devices marketed for improving survival in avalanches (e.g., Snow Pulse) may help prevent snow immersion asphyxiation by allowing a skier or snowboarder to remain in a “head-on-top” position following a fall in deep snow.

HYDRATION If fluid intake is less than fluid loss, dehydration may result. Many individuals do not drink an adequate amount of fluids in the wilderness. In a cold environment, this is because when skin temperatures fall significantly, thirst is less noticeable compared with during hot weather.73 In cold temperatures, moderate fluid loss may not be as important for exercise performance as during hot weather.27 If cold-weather clothing maintains skin and core temperature to what would be expected during exercise in a temperate or hot environment, then dehydration will likely

A

B

C

FIGURE 16-22  A, B, and C, Removal of logs and branches from rivers can lessen the risk for injury or death after falling from a raft or kayak. (Courtesy Haley Buffman.)

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CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

FIGURE 16-21  Downed trees or branches (streamers) increase the chance of additional trauma or becoming trapped underwater and drowning. (Courtesy Haley Buffman.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

negatively impact performance.49 Individuals with hypohydration or hyperhydration who are exposed to intermittent exercise with normobaric hypoxia demonstrate greater physiologic-strain hypoxemia and acute mountain sickness (AMS) symptoms than do individuals with euhydration.110 Hydration status can be monitored in the wilderness by observing the color (and thus concentration), volume, and frequency of urine output. Oral fluids containing sodium have been shown to aid in fluid retention over several days of cold exposure, as well as in wildland firefighters in heat-stress conditions.32,115 During wilderness excursions, a source of water needs to be readily available and easily reached to permit frequent, ad libitum fluid intake. Severe exercise-associated hyponatremia (EAH) from overzealous hydration is a well-described problem in endurance sports participants, particularly women, individuals with low body weight, and those taking nonsteroidal antiinflammatory drugs (NSAIDs).50,65,66,101 In general, EAH is not frequently encountered in the wilderness setting, although there are reports of EAH in hikers, trekkers, climbers, cold weather endurance athletes, and long-distance cyclists.* Symptoms reflect noncardiogenic pulmonary edema and cerebral edema and include nausea, vomiting, and headache followed by neurologic symptoms such as confusion, disorientation, seizures, or coma. A recommended preventive measure to be considered, especially by those at risk (women, low body weight, planned prolonged exercise duration, extremes of heat), is to refrain from using NSAIDs while participating in sustained physical activity in the wilderness setting. In addition, moderate fluid intake is recommended based on the perceived need (ad libitum) rather than a specific amount. Any fluid intake during prolonged exercise that exceeds combined urine and sweat output (800 to 1000 mL/hr) should be considered high risk for development of EAH.114 Wilderness excursion leaders need to educate and advise their group members on appropriate fluid intake and be able to recognize early symptoms of EAH. There are many marketed hydration systems. These systems use bags (“bladders” or reservoirs) to hold water or other liquid inside an insulated carrier or are integrated into a backpack. Water is sucked through a bite valve from a dispensing tube extending from the reservoir up over the shoulder or through the inside of an insulated shoulder strap. “Wearable” hydration includes garments, such as cycling jerseys, that contain concealed reservoirs. Some hydration system manufacturers use antimicrobial compounds in the reservoir and bag to inhibit bacterial growth. Hydration systems are more difficult to clean than are water bottles but have the advantage of allowing a person to easily carry large amounts of liquids needed for maintaining hydration during prolonged physical activity.

ALTITUDE Wilderness adventurers most commonly encounter changes in altitude during travel through mountainous terrain. As travelers ascend to higher altitude, barometric pressure decreases. Although the fraction of oxygen in the atmosphere remains constant, the partial pressure of oxygen decreases with ascent. Hypoxia is the physiologic insult that is responsible for altitude illness. The altitude where symptoms of altitude illness occur varies between persons. One study of tourists in Colorado found that 71% experienced symptoms of altitude illness following arrival at altitudes of 2103 to 2957 m (6900 to 9700 feet), which represents the elevation of many ski areas.67 There is no absolute elevation where altitude illness can be predicted; rather, it is influenced by the rate of ascent, the altitude reached and where sleep occurs, duration of exposure to altitude, and level of physical activity. Individuals with a prior history of altitude illness are prone to future altitude illness,143 and adolescent girls have a higher incidence than do boys.34 Prevention begins with education. Only just over one-half of respondents on a survey at a major U.S. ski area were aware of the existence of AMS, and one-third were unaware that it could *References 9, 14, 77, 119, 134, 151.

350

be prevented. One-half the respondents preferred to receive information about AMS from the Internet. This suggests that the Internet may be an effective means of educating the public about AMS symptoms and means of prevention.57 Because slow, gradual ascent allows time for acclimatization to altitude, this is the primary means of prevention, particularly when ascending to high or extremely high altitude. If symptoms develop during ascent, additional time is needed for acclimatization before resuming ascent. If symptoms do not abate, then descent to an altitude 305 to 914 m (1000 to 3000 feet) lower, particularly for sleep, may be needed. The use of acetazolamide 125 to 250 mg twice daily beginning 1 day before travel and continuing for several days at altitude has been shown to prevent symptoms of AMS.1,28,42 While at high altitude, a dose of 250 mg every 8 hours has been shown to dramatically reduce symptoms.46 Dexamethasone has also been found to prevent symptoms of AMS.41,113 Risk factors and susceptibility for high-altitude pulmonary edema (HAPE) are similar to AMS and include a prior history of HAPE, rapid ascent, and higher altitudes. Additional risk factors include male gender, intense exercise, cold ambient temperatures, and preexisting respiratory tract infection.40,68,132 Preexisting primary pulmonary hypertension and intracardiac shunt, such as ventricular or atrial septal defect, or patent foramen ovale, may predispose to HAPE.3,74,148 As for AMS, primary prevention of HAPE is by gradual ascent. Ascent rate should be limited to no more than 300 to 350 m (984 to 1148 feet) per day above 2500 m (8202 feet) (sleeping altitude) with an additional day of acclimatization added for every 600 to 1200 m (1969 to 3937 feet) above 2500 m (8202 feet).11 Pharmacologic prophylaxis aimed at preventing altitude-induced pulmonary hypertension is most commonly achieved with the calcium channel blocker nifedipine, 30 mg extended release daily or twice daily.12 Sildenafil and tadalafil, both phosphodiesterase-5 inhibitors and pulmonary vasodilators, have been evaluated for prophylaxis and treatment of HAPE but have the potential side effect of causing significant headache. When taken beginning a day before ascent, dexamethasone reduced the incidence of HAPE by 78% and was superior to tadalafil in its efficacy. However, side effects may limit its use as a prophylactic agent.13,86 For individuals who are prone to development of HAPE, the β-agonist salmeterol 125 mcg inhaled twice a day has been found to reduce the incidence of HAPE by 50%. Side effects, notably tachycardia, are similar to those of other β-agonists. Studies do not conclusively support the use of acetazolamide for prevention of HAPE.85 Because of its safety profile and lack of serious side effects other than reflex tachycardia, nifedipine remains the prophylactic drug of choice for individuals with a prior history of HAPE.133 High-altitude cerebral edema (HACE) is the presence of a change in mental status and/or ataxia in a person with AMS, or the presence of both mental status change and ataxia in a person without AMS.136 Symptoms typically occur at night, and after several days at altitude; many persons with HACE also have HAPE or AMS. Without rapid treatment, HACE progresses to coma, and death occurs by herniation. There are no studies showing a benefit to prophylactic treatment. However, slow ascent and prophylaxis against AMS are likely beneficial.

BITES AND STINGS The incidence of wilderness-acquired bites and stings and their fatalities is difficult to ascertain, especially because many injuries go unreported, but there is likely a resemblance to statistics maintained by the American Association of Poison Control Centers (AAPCC). Between 2001 and 2005, an annual average of over 92,000 bites or stings were reported to the AAPCC. Over three-quarters (76%) were due to insects and spiders, 7.2% were from snakes, 6.9% from mammals, and 3% from aquatic animals (Figure 16-25, online). Twenty-seven fatalities were reported for the period, with 16 from snakebites.80 A study of long-distance hikers in Vermont found 6.6% of reported injuries in 155 hikers were due to insect bites. Heggie58 found that 7% of wilderness injuries in children under 18 years and 1% of injuries in adults in Mt Rainier and Olympic National Park in Washington were due to insect stings. Just over 2% of injuries reported by NOLS over a 4-year period were due to stings.82

FIGURE 16-26  Stings from hymenoptera commonly cause pain and local allergic reactions. (Courtesy Eunice Singletary.)

A

B FIGURE 16-27  A and B, Bells are frequently worn by hikers to produce noise and avoid startling a bear. Grizzly (A) and black bear (B). (Courtesy Eunice Singletary.)

hospitalization. The vast overall majority (69%) were due to rattlesnakes.102 Preventing snakebites begins with being aware of the presence of snakes and their typical habitats. Snakes tend to hide under debris, rocks, and other objects in the outdoors, so caution is urged when lifting up fallen wood or logs. It is important to not step on or near snakes. Use a flashlight to check for snakes in dark holes, and be aware that snakes can swim. If a snake is spotted, back away from it slowly and do not attempt to capture it. One study found that up to 67% of snakebites were the result of intentional interaction, and up to 40% of snakebite victims had consumed alcohol before the bite occurred.96 Snakes have a strike zone of one-third to one-half of body length. Since snakebites are typically to the lower leg, outfitters recommend specialized snake boots. Hiking boots and several layers of pants legs also help divert bites from many snakes. Keep tents zipped closed, and check inside sleeping bags and clothing before using. Mammalian attacks in the wilderness are unusual and typically provoked. Attacks by bears are a common preoccupation of hikers and campers, although the actual incidence of attacks is believed to be very low. Herrero63 found 77 people with reported injury from 66 incidents involving grizzly bears in North American national parks between 1900 and 1970, most involving bear sows with cubs. Attacks were frequently provoked either intentionally or unintentionally (i.e., surprising/startling a bear in its habitat); only 5 fatalities were reported. Attacks by black bear sows are much less common than those by brown bears (Figure 16-27). Hikers often wear bells to create noise while hiking to prevent inadvertently startling a bear and provoking an attack. Avoiding high-risk areas, such as where carrion or bear scat is located, is a way to avoid an encounter with a bear. It is recommended to keep food out of tents and in bear-proof containers and to burn garbage at least 300 feet downwind of a campsite. In the case of an encounter with a brown bear, it is best to avoid eye contact, to avoid running or turning away, and to assume a submissive posture (“play dead”) until the bear has left the area.53 Predatory encounters by a black bear should be dealt with by standing still, by attempting to intimidate and appear larger by raising one’s arms above the head, or by fighting back with any available 351

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Permethrin is a repellent that helps prevent bites from many crawling and blood-sucking insects. Some permethrin clothing formulations reportedly last up to 6 weeks, even with weekly laundering.124 In the United States, ticks transmit more diseases than do any other insects. When traveling in tick-infested country, wear long pants, bloused at the ankles and tucked into shoes or boots, and a long-sleeved, buttoned or pullover shirt tucked into pants and, if possible, covered with a jacket. Use of 0.5% permethrin spray on shoes and outer clothing is a barrier to ticks. Careful daily inspection of clothing and skin and removal of crawling insects while in tick-infested areas is recommended. Other precautions include avoiding sleeping on a cabin floor, not sleeping in a bed that touches the wall, and changing and laundering all bed linens before use if a cabin has been unoccupied.10 In general, mosquitos in North America cause little problem beyond minor itching and skin irritation. However, certain mosquitos transmit forms of encephalitis. Since 1999, West Nile virus has spread throughout the United States, infecting thousands and killing hundreds of people. Use of long pants and sleeves is a measure for preventing mosquito bites. Mosquito netting is effective for sleeping areas and is used on hats to protect the face and neck. N,N-diethyl-3-methylbenzamide (DEET) is an insect repellent used to reduce mosquito bites, including the species responsible for transmission of West Nile virus in the United States. The higher the percentage of DEET in a repellent, the longer and better the insect-repelling effect. Concentrations of at least 23.8% are highly effective in reducing mosquito bites for up to 5 hours.48 Newer formulations allow a lower percentage of DEET to be as effective as a higher-percentage formulation by mixing DEET in a controlled-release lotion vehicle that can last up to 20 hours. DEET can be absorbed through skin and should not be used on children under 2 years of age. Flies, gnats, and no-see-ums are not repelled as effectively as are other insects by DEET. When traveling in areas with these bothersome insects (coastal regions, southwestern United States), use a repellant containing di-Npropyl isocinchomeronate, or R-326. Some insect repellants are combined with sunscreens, but this may decrease the effectiveness of the repellant and/or the sunscreen. Certain spider bites cause significant morbidity. Prevention includes awareness of habitat; inspection of clothing, shoes, and sleeping bags; and shaking out items before use. Stings from hymenoptera cause local and allergic reactions (Figure 16-26). Limiting exposure to these insects is not easily accomplished. Wilderness travelers with known allergy to hymenoptera may prevent serious reactions to stings by prior desensitization therapy and should carry injectable epinephrine, oral antihistamines, and a corticosteroid. Avoiding brightly colored clothing, perfume or fruity scents, and walking barefoot in areas where stinging insects may be present are maneuvers to help prevent hymenoptera stings. Between 2001 and 2004, an estimated 9873 snakebites were treated each year in emergency departments in the United States, with nearly one-third due to venomous species, 18.7% while the patient was outdoors hiking or camping, and over 25% requiring

PART 4  INJURIES AND MEDICAL INTERVENTIONS

weapon or object.45 Pepper spray (5% to 10% capsicum oleoresin) may be an effective deterrent in the event of a charge by a bear.64 For some predatory species, such as mountain lions and wolves, it may be best to display aggressive behavior or fight back in the event of an attack.15,94 Other mammals that may inflict injuries or fatalities in the wild include bison, cougars, bats, deer and elk, coyotes, wolves, moose, porcupines, foxes, raccoons, skunks, and rodents (Figure 16-28). Human attacks by foxes are usually by rabid animals. One general method of preventing attacks by wild animals includes never approaching or attempting to capture or restrain an animal.

TOXIC EXPOSURES Exposure to inhaled toxins may stem from natural or man-made sources. The most common man-made exposures are most likely smoke from campfires. Fatalities are reported not infrequently from carbon monoxide (CO) inhalation due to accumulation inside of poorly ventilated tents after using camp stoves. Injury or death is preventable by being aware of the symptoms of CO poisoning, by ventilating tents, cleaning ice or snow off tent fabric, using maximum blue flames and avoiding low flames, and avoiding prolonged simmering.84 Wilderness travelers at altitude need to be especially alert to the symptoms of possible CO poisoning, because symptoms may be similar to those of altitude illness, although no relation has been found between increased CO exposure and AMS symptoms.117,118 Climbers on descent were found to have higher carboxyhemoglobin levels and an increased risk for CO exposure with increased hours of stove operation. Volcanoes are another source of possible toxic inhalation injury in wilderness adventurers. Volcanic laze is a dense plume of concentrated hydrochloric acid and seawater mist that forms when hot lava enters the ocean waters. It has been identified as the cause of two fatalities in Hawaii and is a risk for wilderness adventurers seeking close views of active volcanos.61 Volcanoes

A

release a number of potentially toxic gases, including sulfur dioxide, hydrogen fluoride, and carbon dioxide. Injury prevention includes avoiding standing under or downwind of a laze plume, avoiding depressions where carbon dioxide may settle, avoiding proximity to volcanic fumaroles, and avoiding exposure to volcanic ash.21 Poison ivy, oak, and sumac are common sources of allergic plant contact dermatitis caused by exposure to urushiol found throughout the plant (Figure 16-29, online). Exposure may be the result of direct contact, from inhalation of smoke particles from burning plants, and from contact with contaminated clothing, shoes, or gear. A skin protectant containing 5% bentoquatam (quaternium-18 bentonite) in a lotion form has been found to be effective at preventing allergic contact dermatitis from poison oak.89 When combined with skin cleansing using isopropyl and cetyl alcohol wipes and education to recognize offending plants, it may be especially effective at preventing contact dermatitis from Toxicodendron species.126 Prevention of adverse reactions from plants begins with being aware of potentially toxic plants that may be encountered in the area of planned travel, and being able to identify and avoid them. Wearing long-sleeved shirts and pants will help decrease exposure, but contamination is still possible from clothing. If contact with a potentially toxic plant is suspected, the area of contact should be washed thoroughly with water and mild soap and sun exposure to the area avoided. The opportunity to ingest poisons in the wilderness is practically limitless. Mushrooms, berries, roots, fruits, leaves, and other vegetation are tempting to many hikers or campers. Prevention involves being able to definitely identify toxic plants and to not ingest them in a harmful form.

WATER, GERMS, AND HYGIENE Water in wilderness areas is used for drinking, cooking, cleaning, and recreation. When wilderness travelers are concerned about possible water contamination in an area where they plan to drink that water, they should use a viable option for water disinfection. Perhaps the most important means of preventing infectious diarrhea in the wilderness is fastidious hand hygiene and education on hygienic techniques for food handling and preparation. Proper disposal of human waste in high-traffic alpine climbing routes, and all wilderness areas, is encouraged. Exposure to a travel or climbing companion with diarrhea increases the risk for developing infectious diarrhea.93 A revised three-bowl system of washing eating utensils was recently recommended for cleaning and reducing bacterial contamination on expeditions where running water is not available. The first bowl contains detergent to remove food residue and grease. A second bowl contains 20 mL of 4% bleach and is used to wash utensils until visibly clean, and a third bowl of drinkable water is used as a rinse to remove the smell and taste of disinfectant.56

Unique Risks of Select Wilderness Activities BACKPACKING

B FIGURE 16-28  A and B, Attacks by mammals, such as coyotes and porcupines, are uncommon. (Courtesy Eunice Singletary.)

352

The two basic types of backpacks are those with external frames and those with internal frames (Figure 16-30, online). The frames are designed to transfer the weight of the backpack from the shoulders and back to the hips and legs. An ideal backpack weight distribution is 20% on the shoulders and 80% on the hips. This distribution lowers the body’s center of gravity, making the fit more stable and places weight on the location best suited to carrying the weight. Backpack size is an important consideration for injury prevention. Individuals need to be sure that all equipment necessary for the duration of the trip can be carried without putting excessive strain on the shoulders and back muscles. In addition to backpack design, the prime concern regarding stress on the back and muscles is the proper amount of weight an individual can carry. This is determined by the size, body weight, and fitness level of the person. For multiday trips, where there is repetitive stress, a good rule of thumb is to limit the contents to 25% of body weight. To minimize the chance of back injury

Backpacks With External Frames A backpack with an external frame may be preferred because it allows a larger amount of weight to be carried, using a ladderlike frame commonly made of aluminum or plastic. A hip belt and shoulder strap are attached to the frame, usually with clevis pins and split rings. A backpack that is adjustable to fit the length of the spine is best. One should optimally select a design that prevents injuries. Lumbar padding and increased stability via a conical hip belt allow for comfort. Recurved shoulder pads/straps and a chest compression strap improve weight distribution and increase comfort. Additional advantages of a backpack with an external frame are allowing air space between the back and the pack, thus reducing sweating and skin breakdown; and weight carried higher in the pack, allowing for more upright posture. However, the pack may wobble side to side during walking, potentially compromising balance. Backpacks With Internal Frames The advantages of an internal frame backpack are that if well designed and fitted, it will conform more to the body, allowing for better balance, and can be worn comfortably for longer periods of time. With this advantage comes the absence of airflow, leading to problems with back perspiration and possible skin breakdown. Because the weight is carried lower, one must bend more, which in turn alters proper posture and can predispose to low back strain. Backpack Lifting Proper lifting techniques are the key to minimize injury. The least injurious method for donning a backpack is to have someone hold and stabilize the pack while the carrier slips his or her arms into the shoulder straps. If a second person is not available, the backpacker can lift and rest the backpack on an object that is waist high and then slip into it. If a backpack must be donned from the ground, the wearer should lift the backpack onto a bent knee and slide one arm through the shoulder strap. After adjusting the strap so that the backpack rests on the shoulder, the carrier should lean forward and rotate the body slightly, allowing the free arm to slide through the other shoulder strap. While still leaning forward with bent knees, the backpacker adjusts the second strap and hip belt. Backpacks and Children There are specially designed child carriers. Be certain to use a well-structured carrier that provides appropriate support and weight distribution. A child-carrying device should be equipped with restraints that prevent an active child from climbing out. One should not use an ordinary backpack to carry small children. Risks include strangulation if a child becomes entangled in the carrier’s harness, and head and body injury if a child wiggles out of the harness and falls or is struck by an overhead obstruction, such as a tree branch.

HIKING Environmental hazards to be anticipated during hiking include those common to many wilderness activities, such as altitude illness, temperature extremes, UV exposure, plant and insect exposure, and hygiene and water effects. Negotiating trails and uneven and hazardous terrain, including snow, ice, and mud, can be challenging. Because a trail is marked or exists on a map does not mean it is safe, clear, and well maintained. Plan to check actual conditions on the day of travel. The key to a safe and injury-free trip is ensuring proper balance. Watch for unstable rocks and boulders. Keep body weight over feet, with knees bent, and do not lean backward. When crossing rivers and streams, remember that water is very powerful. Use predefined crossing points, safety ropes, or watercraft and flotation devices.

A common injury during hiking and backpacking is low back pain. The most common reason for back injuries is carrying excessive or poorly distributed loads. Using a properly designed backpack and proper lifting techniques can help avoid these injuries. A useful injury prevention adjunct is a hiking pole or staff to provide stability on rough ground and diminish impact on knees and ankles. A staff can support a good walking rhythm and prevent imbalance when carrying a heavy load. Hiking poles allow for probing and identifying hidden rocks and deep spots and can hold back bushes, barbed wire, stinging plants, and other trail obstructions. Although one pole can be helpful, it can often lead to uneven balance and weight shift. Using two poles takes the load off the legs and hips and redistributes part of the weight to the upper body musculature. On a steep area, hiking poles enable tripoding, which is having three points of contact with the ground.

HAMMOCK SAFETY Hammocks safety issues exist. The priorities are strong and secure attachments with clear knowledge by the user of the weight tolerances for the hammock and the hanging hardware. A slight modification to the traditional hammock is the lightweight minihammock, which is popular for camping and backpacking. These hammocks have no spreader bars and can be folded easily. The CPSC warns that children can become trapped and strangle in certain mini-hammocks; two deaths and one nonfatal incident have involved mini-hammocks or backpacker hammocks. If a hammock is rigged too high off the ground, a child will have difficulty climbing into it and may become trapped or entangled, leading to strangulation. To prevent injuries, install a mini-hammock near the ground.139

HUNTING More than 35,000 firearm fatalities have occurred in the United States each year since 1989, and it is estimated that there are three nonfatal firearm injuries for each death associated with a firearm.6 The key elements to injury prevention while hunting are at a minimum the following: • Proper training for hunting and use of firearms, focusing on safety • Hunters wearing appropriate protective clothing; wearing international orange clothing articles when traveling in areas frequented by hunters; and ear and eye protection • Hunting only in approved areas and at safe distances from residential or populated areas • Compliance with all local and state laws and regulations Hunter safety courses are available in every state and are a prerequisite in most states to obtaining a hunting license. Key recommendations include warning nonhunters of hunting season, limiting hunting to designated hunting areas, and wearing international orange clothing articles when traveling in areas frequented by hunters. Hunters should always be sure of their target before shooting. A safety harness should be worn when using a tree stand. Care should be taken to use appropriate techniques when cleaning game to prevent lacerations. Eye protection with impact-resistant lenses should always be worn to prevent injury from ricocheting fragments and shotgun pellets. Ammunition should always be stored separately from guns. The greatest potential serious injury from hunting is a gunshot wound, but this is actually uncommon. A 9-year retrospective review of illnesses and injuries in hunters found that trauma accounted for only 45% of emergency department visits by hunters, with the majority of injuries being knife injuries associated with the field dressing of game. The most common medical visits were for cardiac signs and symptoms, and all emergency department deaths were due to cardiac causes.108 Cardiac evaluation of big game hunters with risk factors for cardiac disease should be considered.

HORSEBACK RIDING In 2005, an estimated 73,576 people were treated in hospital emergency departments for horseback-riding injuries.47 Horsebackriding injuries most frequently occur to the upper extremity as 353

CHAPTER 16  INJURY PREVENTION: DECISION MAKING, SAFETY, AND ACCIDENT AVOIDANCE

and allow better stability, the goal is distribution of the weight via maximal use of the frame. To achieve this goal, 50% of the weight should be in the upper one-third of the pack. To accomplish this distribution, lighter and bulkier items should be packed in the bottom and heavier items should be packed in the top close to the frame.

riders try to break a fall. Serious horseback-riding injuries involve the spine, pelvis, internal organs, and head. The following precautions should be taken to prevent horseback-riding injuries: • All riders should always wear riding helmets that meet proper safety standards. • Wear properly fitted, sturdy leather boots with a minimal heel. • Inspect all riding equipment for damage. • Be sure the saddle and stirrups are appropriate for your size and are properly adjusted. • Secure all riding equipment properly. • Amateurs should ride on open, flat terrain or in monitored riding arenas. • Jumps and stunts require a higher level of riding skill. Do not attempt these without supervision.

CLIMBING Climbing is a wilderness activity that poses risks common to many other wilderness activities, such as hypothermia, dehydration, heat illness, altitude illness, trauma from falls, and avalanches (Figure 16-31, online). Hand injuries, including fractures, tendon ruptures, and digital amputations, are common in climbers.87,116 Use of stiffer ropes, reducing rope slack, and grabbing rope in a controlled manner during a fall have all been suggested as means for preventing digital injuries in climbers.69

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 17 

Principles of Pain Management STEPHEN D. COLEMAN AND RAYMOND R. GAETA

Pain is ubiquitous in daily life, and multiple treatment modalities are available under normal circumstances. However, the wilderness setting presents significant challenges when available treatments are limited to those that are included with medical supplies for travel into remote locations. Many travelers have medical conditions that may restrict or limit the use of certain therapies. Some travelers may suffer chronic pain and are already receiving treatment with medications or implanted devices. The treatment of pain in remote and extreme environments is guided by patient characteristics, type of injury, and available therapies. Optimal treatment reduces the chances of further injury, decreases suffering, and improves the likelihood of successful rescue. The International Association for the Study of Pain4 defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition indicates that pain is not simply sensory input from tissue damage; rather, it is a complex experience that depends in varying degrees on an emotional component. The emotional component can vary markedly among individuals and circumstances; however, these factors may significantly affect physiology and dramatically alter the impact of pain on an individual patient. For example, fear and anxiety associated with injury in remote areas can exacerbate the situation. The optimal management of pain often requires a multimodal approach. This approach includes treatment of ongoing tissue damage, which may include interventions locally and systemically, non-narcotic medications, opioid and adjuvant medications, and awareness and management of psychological factors that affect an individual’s perception of pain.

Anatomy and Physiology of Acute Nociceptive Pain The early understanding of the transmission of sensation was that pain perception followed nerves that were simple conduits to the brain. As a greater understanding of pain has developed, it is clear that nociceptive pain, which is defined as the pain of tissue injury or potential tissue injury, is initiated by nociceptor activation in the periphery and modulated at multiple levels in the nervous system, thereby allowing for multiple targets for therapy. This sequence of events is categorized into four processes: 354

1. Transduction: Chemical, thermal, or mechanical energy is converted into an electrochemical signal. 2. Transmission: The signal is conducted to the central nervous system via Aδ and C fibers. 3. Modulation: The signal is altered by both positive and negative feedback loops in the spinal cord and the brain. 4. Perception: The signal is finally appreciated as pain. The skin, the periosteum, and the joint surfaces are abundantly populated with nociceptors that are activated by potential or actual tissue damage. Thinly myelinated Aδ and unmyelinated C fibers terminate in the skin as nociceptors and transmit nociception to the spinal cord. Fast-conducting Aδ fibers respond to mechanical stimuli and transmit sharp sensations. Slow-conducting C fibers respond to chemical, thermal, and mechanical stimuli and transmit burning sensations. Acute injury of the skin results in simultaneous transmission through Aδ and C fibers. Cell bodies of the Aδ and C fibers are located in the dorsal root ganglion, and they project fibers to the posterior horn of the spinal cord. Aδ and C fibers synapse with second-order neurons in the dorsal horn of lamina I to lamina V. These second-order neurons cross to the contralateral side of the spinal cord and ascend in the anterolateral spinal tracts to the thalamic nuclei, brainstem, and midbrain, where they synapse with third-order neurons and project to the cerebral cortex. The simple stimulation of nociceptors without tissue damage may result in transmission of an action potential to the spinal cord and higher levels of the nervous system, and this may eventually result in a perception. However, if stimulation results in tissue damage, a host of changes can occur; these include the local release of many chemicals near the site of the injury as well as chemical changes at the spinal cord and higher levels of the central nervous system. Locally released chemicals may be excitatory or inhibitory. Substance P and neurokinin A are excitatory neuropeptides that are released locally during tissue damage that may facilitate nociceptive transmission. Release of calcitonin gene-related peptide and substance P results in tissue edema and erythema by increasing vascular permeability in peripheral vasculature, thereby contributing to inflammation. There are proinflammatory substances released during tissue damage, including bradykinin, which can initiate pain transmission and sensitize nociceptors. Glutamate, nerve growth factor, serotonin, and histamine also potentiate the response of nociceptors. In addition, low pH may reduce the threshold of nociceptors. There are many additional sensitizing chemicals that act locally at the site of tissue injury as well as at the spinal cord level. The opposing system includes

Pain Measurement The experience of pain is completely subjective. Various scales have been introduced that attempt to quantify the level of pain; these include numeric scales (e.g., 0 to 10, with 10 being the worst pain), categoric scales (i.e., none, mild, moderate, or severe), and even face scales (i.e., smile, neutral, or frown). The visual analog scale appears to be more objective because the patient makes a mark along a 100-mm horizontal line that can then be measured to give a pain score of 73 mm, for example. The usefulness of any scale is best determined when making repeated measures for the same patient with the use of the same scale, especially in an acute setting. A baseline value establishes a set point from which higher pain scores should be interpreted as “worse” and lower pain scores interpreted as “better.” Infrequent measures (e.g., for a patient with a chronic condition) are somewhat less reliable. Interpatient reliability is even more problematic, because different people may experience the same injury differently.

Types of Pain The nomenclature of acute pain versus chronic pain is familiar to many, and relies on time as a determining factor; however, it adds little else to the understanding and treatment of pain. Understanding the mechanisms of pain allows pain to be treated on a continuum, with recognition that unmitigated acute pain can become chronic on the basis of physiologic changes that may occur within the nervous system rather than just with the passage of time. With this approach, the rationale for preemptive strategies and aggressive acute strategies comes into clearer view. Coexistence of acute and chronic pain in the same patient is thus treated in an integrated model. With an understanding of the common mechanisms of pain disorders, a rational approach to initial therapy can be developed with the use of three general categories that are based on pathophysiology. Pain may be considered nociceptive, inflammatory, or neuropathic, or it may be a combination of two or all three types with certain forms of injury (Figure 17-1). The categories and initial therapies are as follows:

Nociceptive

CHAPTER 17  Principles of Pain Management

release of pain-inhibitory substances such as endogenous opioids, β-endorphins, acetylcholine, γ-aminobutyric acid, and somatostatin; these substances impede nociceptive transmission. Modulating nociceptive input can inhibit or facilitate the transmission of signals. In addition to local and spinal cord effects of these chemicals, transmission of action potentials to the spinal cord may be modulated by the transmission of signals by other fiber types. A landmark publication by Melzack and Wall3 described the gate control theory, which operates at the spinal cord level. The authors described input from Aβ fibers, which transmit light touch and pressure and have an inhibitory modulation effect on transmission of nociception to the spinal cord. This description of the gate control theory may explain the mechanism for modulating nociception at the spinal cord level when transcutaneous electrical nerve stimulation (TENS) is applied. At the level of the spinal cord, nociception and the autonomic nervous system are under descending inhibitory control from supraspinal levels. A familiar example of descending inhibitory control is found in our normal disregard for the sounds of our heartbeat and respirations. Normally these signals are suppressed, but they are easily called into consciousness by cortical mechanisms. Similarly, the nociceptive system is also under descending inhibition from supraspinal systems, allowing us to ignore our pain at times during stressful situations. Serotonin and norepinephrine appear to be the primary neurotransmitters that regulate descending inhibitory control; however, others (e.g., α2 agonists, cannabinoids) may be involved. Thus the perception of pain involves not simply the transmission of signals from peripheral sensors to the brain. It is in fact a complex system that is initiated by stimulating peripheral nociceptors in the presence of a milieu of local mediators that facilitate or inhibit signal transmission. As transmission of the signal moves centrally, modulating influences exert their influence before the perception of the sensation occurs.

Inflammatory

Neuropathic

FIGURE 17-1  Categories of pain.

1. Nociceptive. Acute pain that is initiated by tissue injury in the form of a laceration, fractured bone, or crush injury is a type of nociceptive pain. It is a consequence of activating specific nociceptors within the skin, muscle, periosteum, joints, and probably the viscera. These receptors are likely the distal terminals of Aδ and C fibers; they may respond to specific stimuli, including chemical, thermal, and mechanical insults, or they may respond to more than one of these stimuli, in which case they are called polymodal receptors. Polymodal receptors represent the majority of nociceptors. The primary medications directed toward treating nociceptive pain are opioids. Opioids have their primary effects on the opioid receptors µ, δ, and κ. Their analgesic effect is produced in the periphery, at the dorsal horn of the spinal cord, and at supraspinal sites. 2. Inflammatory. Inflammatory pain is mediated by elaborating prostaglandins via the cyclooxygenase pathway. Sensitization of peripheral nociceptors is also mediated via this mechanism, which leads to hyperalgesia around the wound. Nociceptive pain and inflammatory pain generally coexist, because the pain stimulus provokes them both. Immunemediated inflammation with or without tissue injury also falls into this category. Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids are particularly effective for treating inflammation as well as mild to moderate pain. Peripherally decreased production of prostaglandins, including prostaglandin E2 (PGE-2), is the likely mechanism for decreased pain and inflammation. In addition to their peripheral actions, NSAIDs also appear to act on the dorsal horn of the spinal cord. Prostaglandin 2 at the level of the spinal cord is thought to cause release of glutamate both pre­ synaptically and postsynaptically. Glutamate may augment pain states and hyperalgesia. Inhibition of glutamate release at the spinal cord by reduction of PGE-2 as a consequence of NSAID administration involves a centrally acting mechanism in addition to the well-known peripheral mechanism. 3. Neuropathic. Neuropathic pain results from injury to the nervous system (e.g., peripheral nerve, spinal cord) that may occur as an acute injury of the nerve. Neuropathic pain may be the result of an isolated injury to the nervous system, or it may be the result of an injury that causes nociceptive or inflammatory pain. At the dorsal horn of the spinal cord, after peripheral nerve injury, release of cytokines and growth factors results in upregulation of nociceptive neurons. Although this is considered a broad category, various mechanisms are responsible for maintaining neuropathic pain, which results in multiple agents that are used to treat it. Antidepressants, anti­convulsants, antiarrhythmics, and local anesthetics are considered first-line agents 355

PART 4 INJURIES AND MEDICAL INTERVENTIONS

for treatment of neuropathic pain, and are given empirically. Gabapentin, which is commonly prescribed, was developed for treatment of epileptic seizures and designed to bind to γ-aminobutyric acid receptors. However, its analgesic effect is thought to be related to actions at the α2-δ subunit of L-type calcium channels that block the influx of calcium.

Pretravel Preparation Optimally a pretravel evaluation should assess the individual’s suitability for the wilderness experience and include an assessment of chronic medical conditions. A thorough history and physical examination should include the individual’s use of medications as well as any allergies and intolerances. Determining the use of chronic pain medications is important, because there are common and potential side effects to these medications. Some medications may cause cognitive impairment and psychomotor changes that may increase an individual’s risk for injury. Use of opioids may be associated with side effects including cognitive changes, constipation, and tolerance as well as withdrawal if the medication dose is significantly reduced or terminated abruptly. Termination of adjuvant medications—including antide­pressants (e.g., desipramine, duloxetine), benzodiazepines (e.g., lorazepam, alprazolam), and anticonvulsants (e.g., carbamazepine, gabapentin)—can also cause withdrawal-type syndromes. Individuals who are receiving chronic opioids or adjuvants for chronic pain may not have a predictable response to acutely administered analgesic medications for acute injuries. As management of chronic pain has become more complex and as more sophisticated implanted devices have become available, it has become more likely that individuals with chronic pain will be traveling in the wilderness. These devices include spinal cord stimulators, peripheral nerve stimulators, cortical and deep brain stimulators, and implanted intrathecal infusion devices. If an individual has one of these devices, it will be important for him or her to understand how to operate the device and to have contingency plans in case the device fails. For example, individuals with implanted pumps that deliver intrathecal medication require periodic refills of the reservoir, typically every 1 to 3 months. Persons who use these devices and persons with allergies should wear identification bracelets. Device manufacturers have a worldwide network of support that is accessible by telephone or e-mail, but this may not be practical in the wilderness, so written instructions should be available. Having the device information (i.e., the name of the manufacturer and the model number) and contact information for local health care providers and manufacturers will facilitate resolving difficulties when civilization is reached. When medications are transported internationally and specifically by air carrier, the Travel Security Administration in the United States may require specific handling of medications. Because regulations change periodically, one should check for updates before traveling. Medications should be properly labeled with appropriate prescription and patient identification information.

Treatment Modalities After injury, the patient should be assessed with regard to mechanism and severity of injury. Treatment modalities are available for management of acute pain; these include local, regional, and systemic techniques. Local physical modalities (e.g., cold, heat), local anesthetics, and topical medications may be effective. Regionally, nerve blocks of the extremities or other body parts may provide excellent analgesia or even anesthesia for many hours. Systemically, medications include opioids, NSAIDs, and antineuropathics for treatment of acute pain. Preparation of a pain first-aid kit for excursions into the outdoors allows for the greatest number of options for treatment of various maladies (Box 17-1).

PHYSICAL MODALITIES Rest minimizes additional pain and inflammation. If practical, maximize rest and minimize motion until pain is fundamentally 356

BOX 17-1  Pain Management First-Aid Kit* Basics Esmarch bandage, 3 × 36 inches Hot and cold packs Oral Medications Acetylsalicylic acid, 500 mg Acetaminophen, 500 mg Carisoprodol (Soma), 350 mg, or metaxalone (Skelaxin), 500 mg Diazepam (Valium), 5 mg Hydrocodone, 5 mg Injectable Medications Naloxone, two 0.4-mg ampules Ketamine, 50 mg/mL, 5 to 10 mL Lidocaine, 1%, 30 mL Procaine, 1%, 30 mL Midazolam (Versed), 5 mg/mL, 5-mL vial Morphine, 5 mg/mL, 5-mL vial Meperidine (Demerol), 50 mg/mL, 5-mL vial Topical Therapies Capsaicin ointment, 2-g tube Lidocaine ointment, 5%, 30 to 50 g Lidocaine patches, 5% Diclofenac, 1% gel, 100 g Diclofenac, 1.3% patch (Flector Patch) Additional Supplies Intravenous cannula, 20 gauge, three Intravenous cannula, 18 gauge, three Tourniquet Intravenous tubing sets, two Normal saline, 500 mL Intravenous 5% dextrose in lactated Ringer’s solution, 500 mL Acupuncture needles, 50 *Items in this list are subject to the individual’s training and scope of practice. This pain kit should be available in addition to a regular first-aid kit.

gone and the majority of function is restored. Ice or another cold application (e.g., immersing a sprained ankle in a cold stream) can reduce inflammation and pain from an acute injury. Ice should be applied intermittently (e.g., for 20 minutes per hour; by alternating ice with no ice in 20-minute intervals to avoid the risks of decreased blood flow to the region, which could result in decreased oxygen delivery, decreased clearance of cellular by-products, or even frostbite [further ischemia of the limb or local tissue may occur with prolonged contact with ice]). A towel or a similar material should be placed between the ice and skin, and tissue status should be closely monitored. Edema and swelling result from the acute inflammatory process and may cause significant pain and loss of function. As swelling in the extremities increases, there may be compression of the veins, which results in worsening bleeding and swelling. Further swelling may compress nerves and arteries (i.e., compartment syndrome), which will result in ischemia distal to the injury. Elevation reduces swelling by increasing venous return of blood and by minimizing tissue edema. Distended tissues increase pain. If possible, the injured site should be maintained above the level of the heart. If a bandage is applied to reduce swelling, an elastic bandage rather than a tight nonelastic bandage will help to prevent overly aggressive reduction of sufficient blood flow and, potentially, ischemia. Compression Analgesia Wrapping an extremity proximal to the site of injury to compress the relevant peripheral nerves can produce distal analgesia and anesthesia. This may occur intentionally or may be the consequence of placing a compression dressing over an injured site.

Topical Therapies Topical application of analgesic medications may be effective for treatment of mild to moderate pain. The advantages of using a topical preparation include eliminating the need for oral medication administration, beneficial metabolic interactions with other medications, reduced systemic adverse events, direct access to the site of pain, and ease of termination of treatment if a side effect occurs. Topical medications include NSAID gels and patches, lidocaine ointments and patches, and capsaicin creams, lotions, and patches. Topical application of NSAIDs is generally less effective than oral therapy; in addition, there may be localized skin irritation. Any topical analgesic medication should only be used on intact skin. In the United States, the only available topical NSAID is diclofenac, either as a 1% gel or a 1.3% patch. Outside of the United States, other topical NSAIDs may be available. Topical 1% diclofenac gel is applied four times daily over the site of pain, and is indicated for relief of osteoarthritis pain in joints that are amenable to topical therapy. The diclofenac patch (i.e., Flector Patch) is applied twice daily to the site of pain, and is indicated for acute pain that results from minor strains, sprains, and contusions. Topical lidocaine is available as 5% topical ointment, 4% topical cream, and 5% patch. Ointment and cream are applied up to three times per day. Up to three patches at a time may be applied, and the patches are to remain on the skin for no more than 12 hours during any 24-hour period. Lidocaine patches are indicated for postherpetic neuralgia; however, they may be effective for any localized pain condition. Capsaicin is available as a cream, lotion, or patch. Concentrations of capsaicin cream preparations range from 0.025% to 0.25%. A recently approved 8% capsaicin patch has limited usefulness outside of the clinic or hospital setting. Capsaicin results in burning pain at the site of application. Start with the least concentrated formulation of capsaicin, and apply it with lidocaine 5% ointment three or four times a day. Initially use three parts of lidocaine ointment to one part of capsaicin. As the application becomes more tolerable, increase to a one-to-one concentration; this will eventually be followed by full-strength capsaicin. Although the evidence for efficacy of capsaicin is the best for all of the topical agents, analgesia occurs approximately 7 days after the initiation of therapy, thereby limiting its use for acute pain.2 TENS can be an effective technique for management of painful stimuli. This therapy requires special equipment that users may easily bring into the wilderness. TENS is frequently used to treat chronic back pain with placement of electrode patches over the area of pain and then connecting them to the battery and controller. Clinical studies to demonstrate efficacy have been inconclusive. There are many criticisms of these studies, including the use of heterogeneous patient populations and nonstandard lead placement and stimulation parameters. Nonetheless many individuals report significant benefit while using TENS. The proposed mechanism is explained by the gate control theory. Peripheral stimulation of large afferent Aβ fibers by TENS inhibits nociceptive transmission in the dorsal horn. Some studies have noted release of endogenous opioids and serotonin.6,7 In addition, increases in opioid agonists in cerebrospinal fluid have been noted after TENS use. At least two patches are used. Patch placement requires experimentation to find the locations that provide the best analgesia. Pulse width, frequency, and intensity may be adjusted. TENS can be applied at high frequency (>50  Hz) with an intensity that is below motor contraction (i.e., “sensory intensity”) or at low frequency (<10  Hz) with an intensity that produces motor contraction. The device is adjusted to create a sensation at the site of the patch without causing muscle contraction or discomfort. In warm climates, the patches may require additional adhesive,

or else they might become dislodged, thereby limiting effectiveness. Regional Therapy Local anesthetics are membrane stabilizers. They reversibly decrease the rate of depolarization of neurons by inhibiting sodium ion channels in the neuronal cell membrane on the basis of chemical structure. Local anesthetic is considered either an amino ester or an amino amide. Familiar amino ester local anesthetics are procaine, chloroprocaine, and tetracaine. Amino amides include lidocaine, prilocaine, mepivacaine, bupivacaine, and ropivacaine. The principal differences between amino ester and amino amide are metabolic fate and potential for allergic reactions. Amide ester local anesthetics undergo hydrolysis; this results in production of para-aminobenzoic acid, which is more likely to precipitate an allergic reaction than are amino amides, which undergo hepatic metabolism. Local anesthetics also contain preservatives that may cause allergic reactions. An allergic reaction to a local anesthetic of one class does not increase the risk of an allergic reaction to the other class of local anesthetic, unless the reaction is to the preservative. The metabolism of amino amides is slower, so repeated dosing of these agents may result in increased systemic side effects with repeated exposure as compared with the amino esters. Systemic toxicity with local anesthetics is related to plasma concentrations of the drug. Local anesthetic may enter the systemic circulation by direct injection at the time that the block is placed or as a result of ongoing systemic absorption of drug in the tissue after placement of the block. Absorption of local anesthetic depends on the dose administered, vascularity of the site of injection, use of added epinephrine, and chemical properties of the anesthetic. Systemic toxicity with local anesthetics primarily involves the central nervous and cardiovascular systems. As plasma levels of local anesthetics increase, patients may experience perioral and tongue numbness followed by vertigo, tinnitus, and blurred vision. At higher plasma levels, seizures may occur. Intravenous benzodiazepines are effective to suppress seizures as a result of local anesthetic toxicity. Cardiac toxicity generally occurs at higher plasma concentrations than those that are necessary to produce central nervous system side effects. Cardiovascular toxicity results from relaxation of vascular smooth muscle and direct myocardial depression. Effects on the vascular smooth muscle may cause hypotension. Cardiac depression is thought to be related to sodium channel blockade. Slowed conduction can result in prolonged PR and QRS intervals and reentry ventricular dysrhythmias. Local anesthetics to consider having in a first-aid kit may include an amino amide, short-acting, rapid-onset local anesthetic such as 1% lidocaine; a slower-onset, longer-acting medication such as 0.5% bupivacaine or 0.5% ropivacaine; and, if there is need for a nonamide local anesthetic, an amino ester local anesthetic such as 1% procaine. Trigger Point Injections Pains from muscular spasm are readily identified. Palpation of the affected muscle group will localize sites of maximal tenderness, which are known as trigger points. Injecting 2 to 3  mL of local anesthetic will temporarily block pain and spasm. Care should be taken to avoid large volumes (i.e., >15  mL) of 0.5% bupivacaine, which is absorbed quickly from muscles.

NERVE BLOCKS Pain as a result of injuries to extremities may be amenable to placement of nerve blocks. The simplest of these is the field block, which involves local anesthetic being infiltrated around the wound. Injuries to the forearm and hand may be managed with an axillary nerve block (Figures 17-2 and 17-3). Injuries to the hand in an ulnar, radial, or median nerve distribution can be blocked at the wrist or in the forearm by blocking the respective nerves. Digital blocks may be placed for injuries to individual fingers or toes. More sophistication is required for blockade of a major nerve or plexus. With minimal training, the motivated individual can readily instill blocks, such as the femoral block near the inguinal ligament, for the lower extremities. Similarly 357

CHAPTER 17  Principles of Pain Management

In addition to providing analgesia, compression may result in loss of distal pulses, which should be monitored. Compression analgesia may result in development of paresthesias, thereby confounding the diagnosis of compartment syndrome. Therefore compression analgesia is not a recommended technique. However, it may be considered in rare circumstances, such as when a limb is not salvageable.

PART 4 INJURIES AND MEDICAL INTERVENTIONS

Median n.

Musculocutaneous n. Supraclavicular n. (lateral antebrachial (cervical plexus) cutaneous n.) Axillary n. Radial n. Radial n. (superficial br.) (inferior lateral brachial cutaneous n.) Humerus Axillary a.

(Palmar br.) Median n. Musculocutaneous n. Ulnar n. (palmar digital br.)

Median antebrachial Intercostobrachial and cutaneous n. medial brachial cutaneous n.

Radial n.

Ulnar n.

FIGURE 17-2  Ventral nerve distribution of the upper extremity. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

FIGURE 17-4  Axillary block. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

the entire foot can be blocked by placing local anesthetic at the level of the ankle joint in one of a combination of easily identifiable locations. The use of surface landmarks is adequate for anatomic localization of the appropriate nerves, because nerve stimulators and ultrasound machines are luxuries that are found only in the clinic or operating theater. Blunt-needle placement and administration of local anesthetic guided by paresthesias will usually suffice.

to the skin and then redirected inferior (medial) and deep to the artery, where the radial nerve is located; another 5 to 10 mL of local anesthetic are deposited. Finally, the needle is withdrawn to the depth of the axillary artery, where the ulnar nerve is located, and the remaining 5 to 10 mL of local anesthetic is deposited. During this procedure, the patient may experience paresthesias, which can be used to verify the location of the needle. However, this is not necessary. If the axillary artery is entered, continue to advance the needle through the artery, and then aspirate to make sure that the needle is deep to the artery (not intravascular) before depositing the local anesthetic. If the artery is entered, direct pressure should be maintained over the site for 5 minutes to limit bleeding. If 0.5% bupivacaine without epinephrine is used, the block duration will be 4 to 6 hours; with the addition of epinephrine, it may be 8 to 12 hours. Potential complications include intravascular injection of local anesthetic and vascular or nerve injury.

Axillary Block Sites distal to the elbow can be blocked by placing local anesthetic near the musculocutaneous, median, radial, and ulnar nerves at the distal axilla guided by the axillary artery pulse (Figure 17-4). This block is performed by having the patient supine with shoulder abducted to 90 degrees and externally rotated, with the elbow flexed. Stand or sit at the patient’s side caudal to the arm, and identify the axillary pulse over the proximal humerus. The site of entry is sterilized, and local anesthesia injected locally before a blunt needle is placed. (Blunt needles have a shorter bevel than do traditional hypodermic needles. These needles may be safer when performing nerve blocks, because they may be less likely to injure vascular and neural structures.) A 22-gauge blunt needle is then advanced superior to the pulse. The musculocutaneous nerve lies deep to the artery, and this is where 5 to 10 mL of local anesthetic is deposited. Superficial to the musculocutaneous nerve and the pulse of the axillary artery is the median nerve, where an additional 5 to 10 mL of local anesthetic are deposited. The needle is withdrawn Radial n. Median n.

Median antebrachial cutaneous n.

Ulnar n.

Axillary n.

(Posterior brachial (Posterior cutaneous n.) antebrachial cutaneous n.) (Inferior lateral brachial cutaneous n.)

Radial n.

Musculocutaneous n. Intercostobrachial (lateral antebrachial cutaneous n. cutaneous n.) Supraclavicular n. (cervical plexus)

FIGURE 17-3  Dorsal nerve distribution of the arm. (From Brown D: Atlas of regional anesthesia, Philadelphia, 1999, Saunders. Illustrations by Jo Ann Clifford.)

358

Wrist Block To accomplish a wrist block, it may be necessary to block one or two of the three nerves that innervate the hand. To perform this nerve block, the shoulder is abducted with the arm supported and the hand in a supine position. The ulnar nerve is located medial to the ulnar pulse at the level of the ulnar styloid. A blunt-beveled needle is advanced, a paresthesia may be obtained, and then 3 to 5 mL of local anesthetic is injected. If no paresthesia is obtained, the needle can be moved in a fanlike distribution while injecting local anesthetic to ensure nerve block. The median nerve is located between the ulnar styloid process and the distal radial prominence and between the flexor carpi radialis and palmaris longus tendons. With the wrist and fingers flexed, these tendons are easily identified. A blunt-beveled needle is advanced deep to the tendons, and 3 to 5 mL of local anesthetic is injected. The radial nerve is blocked by injecting 5 mL of local anesthetic subcutaneously as a field block over the radial aspect of the wrist proximal to the anatomic “snuff box.” The use of 1% lidocaine or 0.25% bupivacaine is sufficient to achieve good analgesia at each of these nerves. Digital Block The dorsal digital and proper palmar digital nerves are located over the medial and lateral aspects of the digits. To perform this block, the hand is pronated and supported. The skin is entered on the dorsal aspect of the digit. A blunt-beveled needle is inserted at the medial and lateral aspect of the proximal phalanx (Figure 17-5), and 1 to 2 mL of local anesthetic is injected on each side of the digit. The use of 0.25% bupivacaine or 1% lidocaine without epinephrine provides good analgesia. Femoral Block The sensory distribution of the femoral nerve includes the anterior and medial thigh and knee as well as the medial lower leg

Femoral nerve Femoral artery Femoral vein

Needle entry sites

Lateral femoral cutaneous nerve Rectus femoris muscle

Dorsal digital nerves Palmar digital nerves

FIGURE 17-5  Digital nerve block. (Courtesy Bryan L. Frank.)

in the saphenous nerve distribution (Figure 17-6). A femoral nerve block can be used for a femur fracture. With the patient supine, the inguinal ligament, anterior-superior iliac spine, pubic tubercle, and femoral pulse at the level of the inguinal ligament are identified. A 4-inch, 22-gauge, blunt-bevel needle is entered through the skin 1 cm lateral to the femoral pulse and advanced in the anterior-posterior plane. As the needle is advanced, a paresthesia may be elicited, although this is variable. A total volume of 20 to 40 mL of local anesthetic is injected while redirecting the needle from the initial medial position adjacent to the femoral artery to a more lateral position, thereby achieving a field block. The use of 0.25% bupivacaine will provide good analgesia; if motor block and anesthesia are necessary, 0.5% bupivacaine should be used. Because this is a field block, it may be slower in onset than other nerve blocks. The femoral artery is in close proximity to the injection site, so arterial puncture of the artery and intravascular injection are possible (Figure 17-7).

FIGURE 17-6  Distribution of the femoral nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)

Head of femur FIGURE 17-7  Femoral nerve block.

Common Peroneal Block A common peroneal block may be helpful for distal tibia and ankle trauma (Figure 17-8). With the patient in a lateral position, the fibular head is identified. A blunt-bevel needle is introduced just below the fibular head. A paresthesia can be elicited at a depth of 0.5 to 1 cm, and 5 mL of local anesthetic is deposited (Figure 17-9). Ankle Block To achieve analgesia of the foot, five nerves are blocked at the level of the ankle (Figure 17-10). Depending on the injury, one or more of the nerves may be blocked with local anesthetic. To block the posterior tibial nerve, a 22-gauge blunt-bevel needle is advanced at the level of the superior aspect of the medial malleolus from posterior to anterior, beginning just medial to the Achilles tendon. If a paresthesia is obtained, 5 mL of local anesthetic is injected. If a paresthesia is not elicited, the needle is advanced to the malleolus, and local anesthetic is injected. The sural nerve is blocked by entering the skin lateral to the Achilles tendon at the level of the superior aspect of the lateral malleolus. The needle is advanced from posterior to anterior until a paresthesia is obtained or the needle contacts the lateral malleolus, at which point 5 mL of local anesthetic is injected. The deep peroneal nerve is blocked by entering the skin lateral to the

FIGURE 17-8  Distribution of the common peroneal nerve. (From Obrien MD: Aids to the examination of the peripheral nervous system, ed 4, United Kingdom, 2008, Saunders.)

359

CHAPTER 17  Principles of Pain Management

Iliopsoas Sartorius muscle muscle

PART 4 INJURIES AND MEDICAL INTERVENTIONS

Semitendinosus m. Biceps femoris m.

Tibial n.

Popliteal v.

Popliteal a.

Common peroneal n. Fibular head

Tibia

FIGURE 17-9  Common peroneal block. (From Waldman SD: Atlas of interventional pain management. Philadelphia, 2009, Saunders.)

anterior tibial pulse, and then 5 mL of local anesthetic is injected. Field block of the superficial peroneal and saphenous nerves is performed by injecting 5 mL of local anesthetic medially and laterally from the point of entry for the deep peroneal block down to the malleoli.

SYSTEMIC THERAPY The use of various oral and parenteral analgesics forms the basis for the specific treatment of pain related to trauma in the

1 3 Extensor hallucis longus tendon

2

Superficial peroneal n.

Tibia

Posterior tibial a. Posterior tibial n.

Fibula

Flexor hallucis m. Peroneus brevis m. Sural n. Tendocalcaneus (Achilles tendon)

1 2

2

FIGURE 17-10  Ankle block.

360

Opioids Opioids that are effective for treatment of nociceptive acute pain are available in many forms and dosages to achieve various routes of administration. Although there can be differences in absorption of various opioids, the general rule of thumb is that titration to beneficial effect best suits the needs of patients. Oral administration remains the easiest form of delivery, and is accomplished with combination medications that contain hydrocodone and acetaminophen (e.g., Vicodin, Norco, Lortab). Care should be taken to avoid consuming more than 4 g of acetaminophen in 24 hours, because hepatic toxicity may occur above these levels. A step up from hydrocodone is oxycodone, which comes as both a sustained-release preparation (OxyContin) and as a shorter-acting agent (Roxicodone). Because there is no acetaminophen in these latter agents, the maximum dose is limited only by efficacy and side effects. Morphine remains the gold standard, and is available for both oral and parenteral use. Intravenous administration of opioids reduces variability introduced by oral administration and decreases the time to onset of analgesia. Intravenous administration can be by intermittent injection or continuous infusion. However, continuous infusion requires additional equipment, so intermittent bolus injections in remote locations are more practical. Intramuscular administration of opioids is feasible in remote areas, but drugs may have variable absorption from different muscle groups, thus making titration to effect and duration of action more difficult to determine. Management of nausea and vomiting, which are the most common side effects of these drugs, can be accomplished with antiemetics. Phenothiazines may cause undue sedation; therefore the use of a 5-hydroxytryptamine antagonist such as ondansetron (Zofran) is advised. Oversedation and respiratory depression are feared complications of opioid use. Naloxone is supplied in 1-mL vials that contain 0.4 mg/mL; when used judiciously in 40-mcg increments, naloxone can reverse many of the minor side effects, such as nausea, vomiting, pruritus, and sedation. Fulldose naloxone is still the appropriate treatment for respiratory depression. Nonsteroidal Antiinflammatory Drugs NSAIDs have both analgesic and antiinflammatory properties. Common agents such as ibuprofen and naproxen are readily available and offer first-line treatment for various minor aches and pains that may be encountered in the outdoors. They offer an inexpensive and effective means of treatment without concern about the possible adverse effects of opioids, and are generally free from regulation in foreign countries.

Deep peroneal n. Tibialis anterior tendon Saphenous n.

Ankle section

outdoors. Familiarity with multiple classes of medications is imperative. Their use should be guided initially on the basis of the mechanism of pain and whether pain is the result of nociceptive, inflammatory, or neuropathic causes (see Figure 17-1). Tables 17-1 and 17-2 list medications from various classes and doses that are calculated for a 70-kg (154-lb) man. Oral and parental doses are listed.

1

Anti-Neuropathic Drugs The efficacy of anti-neuropathic agents is variable because of the complexity of the mechanisms present within neuropathic pain states. Although antidepressants and antiarrhythmics can be effective, anticonvulsants (particularly gabapentin) offer a safe and reasonably tolerated therapy for the pain of nerve injury. Although it is sedating at higher doses, gabapentin that is started at 300 mg 3 times daily and then increased to 600 mg 3 times daily over the course of several days is usually well tolerated. Sedation is the major side effect, so dose escalation is not advised if the patient receives benefit at lower doses or cannot tolerate higher doses. Ketamine Ketamine is a powerful dissociative anesthetic that, when used in a small parenteral dose, can provide profound analgesia. As a centrally acting N-methyl-D-aspartate receptor antagonist, ketamine is effective for all types of pain in the short term. As little as 10 to 20 mg given intravenously or intramuscularly to an adult produces the desired analgesia. If needed, the dose may be

Drug

Dosage (mg)

Salicylates Acetylsalicylic acid

325-650

4-6

300-600

8-12

Gastrointestinal distress; inhibited platelet function; contraindicated in children with viral illness Similar to aspirin

300-1000

4-6

Hepatic toxicity with overdose

50 50-75 10

4-6 4-6 4-6

Similar to aspirin Similar to aspirin Similar to aspirin; use for 5 days or less because of the potential for gastrointestinal bleeding

4-6 4-6 6-8 8 6-8

Similar Similar Similar Similar Similar

Diflunisal Para-Aminophenol Acetaminophen Indoles Indomethacin Sulindac Ketorolac

Interval (hr)

Propionic Acids Fenoprofen 400-600 Ibuprofen 300-400 Ketoprofen 25-50 Dexketoprofen 25 Naproxen 200-275 Cyclooxygenase-2 Inhibitor Celecoxib 100-200 Narcotic Agonists (Oral) Codeine 15-60, with a maximum of 360 mg per 24 hr Hydrocodone 5-10 Hydromorphone 7.5 Levorphanol 4 Meperidine 300 Methadone 2.5-150 Morphine 30-60 Oxycodone 5-10 Extended release, 10

Risks and Precautions

12-24

to to to to to

aspirin aspirin aspirin aspirin, with less gastrointestinal distress aspirin

Gastrointestinal distress; skin rash

4-6

Narcotic side effects; note the cumulative acetaminophen dosage

4-6 3-4 6-8 2-3 4-12 3-4 4-6 12

Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic Narcotic

side side side side side side side

effects; note the cumulative acetaminophen dosage effects effects effects effects effects effects; note the cumulative acetaminophen dosage

From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002.

repeated every 2 to 3 hours. Titration to effect or to the presence of side effects is imperative. Psychomimetic effects (e.g., hallucinations, bad dreams) are seen with higher doses and may limit the use of this drug. A calm and quiet setting with minimal stimulation is the ideal setting for use. Benzodiazepines (e.g., midazolam, 2 mg intravenously) are effective for blunting this response.

Muscle Relaxants Muscle relaxants that are centrally acting are reasonable to use to treat acute muscle spasms related to injury. Sedation is a significant side effect that may limit the use of these drugs. Baclofen is a preferred agent because of its activity at the γ-aminobutyric

TABLE 17-2  Common Parenteral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults Drug

Dosage (mg)

Narcotic Agonists Codeine 15-75 IM Fentanyl 50-100 mcg Hydromorphone 1-2 IM Levorphanol 4 10-20 IM, 2.5 IV Morphine Meperidine 50-100 IM, 25-50 IV Oxymorphone 1 Narcotic Agonists and Antagonists 0.3-0.6 IM Buprenorphine 2-4 IM Butorphanol Dezocine 5-20 IM, 5-10 IV 10-20 IM, 1-5 IV Nalbuphine Nonsteroidal Antiinflammatory Drug 15-30 IM, 2-5 IV Ketorolac Dissociative Analgesic and Anesthetic 50-75 IM, 15-30 IV Ketamine

Interval (hr) 4-6 0.5-1 3-4 6-8 3-5 2-4

Risks and Precautions

3-4

Narcotic side effects Narcotic side effects; wide range of dosages Narcotic side effects; choose over morphine for a patient with hepatic impairment Narcotic side effects Narcotic side effects Narcotic side effects; active metabolite accumulates in patients with renal impairment and may cause seizures Narcotic side effects

6-8 3-4 2-4 3-6

May May May May

4-6

Similar to aspirin

2-4

Increased intracranial pressure

precipitate precipitate precipitate precipitate

narcotic narcotic narcotic narcotic

withdrawal withdrawal withdrawal withdrawal

From Burnham T, et al, editors: Drug facts and comparisons, St Louis, 1999, Facts and Comparisons Inc; and Emermann CL, Spenetta J: Pain management in the emergency department, Emerg Med Rep 23:53, 2002. IM, Intramuscularly; IV, intravenously.

361

CHAPTER 17  Principles of Pain Management

TABLE 17-1  Common Oral Analgesics: Dosage Recommendations for 70-kg (154-lb) Adults

PART 4 INJURIES AND MEDICAL INTERVENTIONS

acid B receptor; this makes it different from other agents that also act centrally but that have less specific sites of action, thereby resulting in less desirable side effect profiles. Carisoprodol (Soma), metaxalone (Skelaxin), and cyclobenzaprine (Flexeril) are examples of less preferred agents.

ALTERNATIVE THERAPIES Acupuncture Acupuncture has developed over the past 3 to 5 millennia in Asia, and has been practiced for the past several hundred years in the Western world. In many cases, acupuncture as an art and science was developed in geographic areas and under social and austere conditions that are familiar to wilderness travelers. The use of acupuncture by physicians to treat trauma and illness in wilderness settings has been described recently in the medical literature.1 When properly administered, acupuncture should have a very low risk of morbidity, and may be extremely effective for alleviating pain and restoring function to an injured wilderness traveler. It has been demonstrated that endorphin, enkephalin, monoamine, and adrenocorticotropic hormone are released after stimulation with acupuncture. Furthermore, the gate control theory of pain modulation and altered sympathetic activity may also apply. Clinically improved microvascular circulation may lead to decreases in tissue edema, which in turn may diminish pain and help with restoring function. Release of adrenocorticotropic hormone leads to increased circulating corticosteroids; decreased inflammation may contribute to decreased pain and improved healing. Contemporary medical acupuncturists are typically trained in a variety of styles and traditions. Many physicians make use of a combined approach of acupuncture point selections based on neuroanatomy and the points that are felt to have energetic effects within the body. In addition, acupuncture microsystems in which the entire body is represented in a small area (e.g., the ear, scalp, or hand) are often employed. These microsystems are often quite beneficial for acute pain relief. Sterile acupuncture needles are compact, lightweight, and easy to include in a daypack or a first-aid kit. Integration of acupuncture into the biomedical care of wilderness trauma, pain, and illness may dramatically enhance patient comfort and facilitate extrication from a remote setting. An energetic style of acupuncture that is especially useful for common trauma makes use of the tendinomuscular meridians of the acupuncture energetic subsystems. Indications for activation of the tendinomuscular meridians treatment include acute strains, sprains, abrasions, and hematomas. The method of activation for this style of treatment is to place a needle in the jing-well or ting point of one to three of the meridians involved in the lesion. This is followed by placing a needle in the “gathering point” of the meridians and then by placing needles around the area of induration, swelling, or bruising, approximately 1 cm (0.4 inch) out from the edge. All needles in this treatment are placed only 2 to 3 mm (0.08 to 0.12 inch) deep and are left in place for 20 to 45 minutes.

362

FIGURE 17-11  LI4 (ho gu) acupuncture site for headache.

Treatment of headaches is also amenable to acupuncture; a general point of insertion into the web space between the thumb and forefinger, known as LI4 (ho gu), is recommended (Figure 17-11).

PSYCHOLOGICAL TECHNIQUES Guided imagery or self-hypnosis is an often overlooked modality for pain management. The ability to transport the sensorium out of the painful experience into a different context is the aim of this technique. Although it is seemingly in the realm of a vaudeville show, self-hypnosis has been demonstrated to lessen the pain experience of patients with breast cancer, and is putatively felt to activate descending inhibitory pathways. Although these techniques are often thought of in the context of pain relief, their use to heighten the state of concentration has other uses in human performance, so learning the techniques before traveling is worth the investment of time. The mind is capable of extraordinary feats, as illustrated by the experience of Aron Ralston, whose arm was trapped between a rock and a canyon wall while canyon climbing alone in a remote area of Utah in 2004. Aron’s initial attempts to free himself produced excruciating pain. After reassessing his situation, relaxing, and making a plan, he touched his crushed hand and realized that it had lost sensation. This produced a sense that his arm was isolated from his body. He noted the disfigurement of this arm and observed that is was strange that he was not suffering pain. Unable to free himself and stranded alone with a limited water supply, he concluded that he needed to amputate his own arm and to focus all of his attention on this task. Not able to cut the bone, he levered the trapped arm, breaking the ulna and radius bones and thus freeing the arm. Although he felt a “blaze of pain” with the maneuver, he refocused on survival and was able to make his way to rescue.5 This is a story of an extraordinary person that illustrates the power of the human mind.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 18 



Taping and Bandaging DANIEL GARZA

Taping and bandaging are both useful skills in wilderness medicine. Taping can be used to support injured joints and soft tissues; bandaging is most often used to secure a wound dressing (Figure 18-1, online). In addition, bandaging with an elastic wrap is an alternative to taping, and, over larger joints such as the knee, it is often preferable. In general, taping requires practice and experience, but some simple techniques can be easily mastered. Taping is most often used for mild to moderate sprains and strains, with which some functional capacities (e.g., weight bearing, lifting), are maintained. Although taping offers dynamic support, it is in no way comparable with splinting, which is intended to immobilize an extremity. The most common tape that is applied is white athletic or “adhesive” tape, which is often used by athletic trainers in organized sports. Athletic tape may be applied to the skin, although it may lose adhesion if the body part is not shaved and if tape adhesive is not applied. Some keys to successful taping include the following: • Avoid leaving any gaps in the tape (i.e., allowing any skin to be visible), because these gaps will lead to blisters. Avoid excessive tension on tape strips that serve to fill such gaps. • Apply tape in a manner that follows skin contours to avoid wrinkles. • Try to overlap one-half of the width of the tape with each successive strip. Bandaging is accomplished with the use of either elastic wraps or gauze rolls of varying widths. After a dressing is applied to a wound, appropriate bandaging allows the patient to feel confident that the dressing will remain secure during reasonable amounts of activity. Regardless of the method used, it is important to remember that taping and bandaging—especially when circumferential— should not be so tight as to limit circulation.

Taping TYPES OF TAPE Athletic tape is composed of fibers that are woven into strips and that are coated with zinc oxide, which is an adhesive compound. Although athletic tape is most commonly colored white, it is available in many colors. Athletic tape is the most commonly used tape in sports and first aid for support and for the prevention of injuries. It is also available in many widths. Although the major advantage of athletic tape is versatility, its major disadvantage is the tendency of zinc oxide to lose adhesive properties with heat and moisture, thereby resulting in a loss of support when the patient sweats. A variety of techniques, which are described later in this chapter, are used to increase the durability of athletic tape under these conditions. Elastic tape (e.g., Elastikon) is cotton elastic cloth tape that incorporates a rubber-based adhesive. The elasticity of this tape allows for greater flexibility, so it is particularly useful for large joints such as the knees and shoulders.

SKIN PREPARATION Skin preparation involves measures that are intended to increase patient comfort as well as the longevity of tape adhesion. If tape is to be applied directly to skin, the area is usually first shaved to remove hair that may interfere with direct contact. Care must

be taken to avoid small abrasions in the skin when shaving, because these can serve as entry sites for infection. If the area cannot be shaved in a clean and deliberate manner, it is advisable to avoid shaving. Any obvious abrasion or other wound should be covered with a thin layer of gauze or a small adhesive bandage before taping. Some commercially available skin adhesives are available in aerosolized form. These preparations (e.g., Tuf-Skin) use benzoin as the adhesive. Skin adhesive is applied after the skin has been shaved and after all abrasions have been dressed. If the area is not shaved, a foam underwrap or prewrap is used to protect the patient’s body hair. Prewrap is available in 3-inch–wide rolls in many colors. After the application of a topical skin adherent (e.g., Tuf-Skin), prewrap is applied over the part to be taped in a simple and continuous circular wrap. The prewrap is sufficiently self-adherent and does not need to be taped. When tape is applied over bony prominences, it can create tension on the skin surface that leads to blistering. Heel-and-lace pads and foam pads are used to provide additional comfort by relieving potential pressure points. Heel-and-lace pads are prefabricated pieces of white foam that are adhered together with petroleum jelly and then applied to the anterior and posterior aspects of the talus when the ankle is taped. Pads of foam can be cut to size to fit over painful areas that need to be taped (e.g., for medial tibial stress syndrome) or used for support in special cases (e.g., for patellar subluxation).

ANKLE TAPING The most common injury to the lower extremity while hiking is a sprained ankle. It is usually the result of inverting the ankle on an unstable surface. Pain and swelling linger for several days, so taping can offer support if the patient is able to bear weight. Because most injuries occur to the lateral ligaments, taping supports the lateral surface by restricting inversion. In general, taping the ankle consists of anchor strips on the lower leg and foot, stirrups that run in a medial to a lateral direction underneath the calcaneus, and support from either a figure-8 or heel-lock technique (Figure 18-2). The heel lock requires expertise to perform, so most operators are initially more comfortable with the figure-8 technique.

TOE TAPING Taping toes that are sprained or fractured is simple and effective. This treatment involves “buddy taping” to the adjacent toe with one or two pieces of tape to provide support. A small piece of gauze, cotton, or cloth should be placed between the toes to avoid skin breakdown. A sprain of the first metatarsophalangeal joint, which is also known as turf toe, can be a painful and chronic condition. Taping for turf toe is done in an attempt to support and stabilize the joint (Figure 18-3).

LOWER-LEG TAPING Medial tibial stress syndrome, which is commonly referred to as shin splints, can be taped for support and comfort. Tape is brought from a lateral to a medial direction. A small foam pad can be placed to cover the area of tenderness. Underwrap should be used over a foam pad to secure the pad in place (Figure 18-4).

For online-only figures, please go to www.expertconsult.com

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A

B

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J

K

FIGURE 18-2  Ankle taping. A, With the ankle bent 90 degrees, apply anchors of 1.5-inch–wide tape at the lower leg and the distal foot. B, Apply three stirrups from a medial to a lateral direction in a slight fanlike projection. C, Fill in any gaps with horizontal strips. D, Begin the figure-8 technique. Apply tape across the front of the ankle in a left-to-right direction. E, Continue taping under the foot to the opposite side, and cross back over the top of the foot. F, Complete by wrapping tape around the leg, and end at the anterior aspect of the ankle. G, Apply heel locks for both feet (omit if not familiar with this technique). Start in a left-to-right direction, and apply tape across the front of the joint. H, Wrap tape around the heel (the bottom margin of the tape should be above the superior edge of the calcaneus) to form the first heel lock. I, Continue under the foot to the opposite side, and then cross back over the top of the foot. J, The tape is then brought back around the superior margin of the calcaneus and down and around the heel. K, Finish by wrapping the tape around the ankle. Repeat the figure-8 or heel-lock technique as desired.

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Place the first anchor around IP joint of first toe with 1-inch tape. Place the second anchor around midfoot with 11/2-inch tape. 2. Apply strip of 1-inch tape from distal to proximal anchor along medial aspect.

3. Continue with a strip of 1-inch tape from lateral edge of distal anchor along plantar aspect of first MTP joint to medial aspect of proximal anchor.

4. Cross with a strip of 1-inch tape extending from the medial aspect of the toe to the plantar aspect of the proximal anchor.

5. Begin dorsal strips by applying 1-inch tape from medial aspect of distal anchor across the dorsal aspect of the MTP joint to the proximal anchor.

6. Cross over the previous strip by applying 1-inch tape from lateral aspect of distal anchor to medial aspect of proximal anchor.

PATELLA TAPING Subluxation of the patella is exacerbated by the stress of walking long distances across uneven terrain. Incorporating a piece of foam into the taping of the knee can help to relieve symptoms. As with all taping around the knee, underwrap should not be used (Figure 18-6).

FINGER TAPING Injuries to the fingers are common in outdoor settings. Simple fractures and sprains can be initially treated by taping. The most common scenarios involve fingers that are hyperextended or that are “jammed.” Injuries in this scenario are often to the palmar ligaments and tendons. Patients may find it difficult to flex the finger against the resistance of an examiner’s finger, or they may demonstrate tenderness over the palmar aspect of the finger. Swelling is almost always present, so the precise injury may be difficult to diagnose. This presentation is also seen after reduction of a dorsal dislocation of the proximal interphalangeal joint. In all of these cases, it is always best to splint or tape the finger in slight flexion to avoid further injury to the flexor apparatus. Fingers are buddy taped to the adjacent finger, which serves as a splint (Figure 18-7). The second and third fingers and the fourth and fifth fingers are always paired. If the third and fourth fingers are paired, this makes injury to the second and fifth fingers more likely with subsequent activity. A small piece of gauze, cotton, or cloth should be placed between the fingers to avoid blistering or pressure on a tender joint. Strips of tape should be applied around the fingers but not over the joints. Although they are not as common, injuries of the extensor tendons can occur. These typically occur with hyperflexion, but they may also occur with hyperextension and axial loading.2 “Mallet finger” results from fracturing the base of the distal phalange, which is the site of attachment for the extensor tendon. The resulting inability of the distal phalange to fully extend results in a partially flexed finger. Injuries in which the extensor mechanism is clearly disrupted should be treated with the finger taped in full extension. A straight splint (e.g., a tongue blade, a

1. (Optional) Underwrap is applied over a foam pad.

7. Close with 1-inch strips around the toe and 11/2-inch tape around the forefoot.

FIGURE 18-3  Toe taping.

KNEE TAPING Because the knee is a large joint, taping requires expertise. Underwrap should not be used, because adequate traction to support the joint can only be achieved by taping directly to the skin. The patient’s knee should be shaved 6 inches above and below the joint line. Standard athletic tape should not be used, because it cannot provide sufficient support. Three-inch–wide elastic tape provides the foundation. Taping for injuries of the medial aspect of the knee is shown in Figure 18-5.

2. With the patient placing his or her heel on a rock or roll of tape, begin applying 11/2-inch tape from the superior margin of the malleoli to the calf.

FIGURE 18-4  Lower-leg taping.

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CHAPTER 18  Taping and Bandaging

1. Apply two anchors:

PART 4  INJURIES AND MEDICAL INTERVENTIONS

1. The patient maintains the knee in slight flexion (10 -15 degrees) by placing the heel on a small stone or cap of a spray can.

2. Apply two anchor strips of 3-inch elastic tape 6 inches above and below the joint line.

3. Apply a strip of 3-inch elastic tape from the anterolateral aspect of the lower leg, across the knee joint and up to the posteromedial aspect of the thigh.

1. Cut a piece of foam into a C shape, measured to encircle one-half of the patient’s patella.

2. The patient maintains the knee in slight flexion (10-15 degrees) by placing the heel on a small stone or cap of a spray can.

3. Apply two anchor strips of 3-inch elastic tape 4 inches above and below the patella.

4. Apply a second strip from the posterior calf to anterior thigh, forming an X.

5. Repeat steps 3 and 4 twice.

6. Apply two additional anchor strips of 3-inch elastic tape 6 inches above and below the joint for closure.

7. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the tape and provide additional support.

FIGURE 18-5  Knee taping.

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4. Apply the foam pad cut to fit the patient’s patella. Elastic tape (3-inch) is applied in a manner that reproduces the curvature of the foam pad.

5. Starting from the medial aspect of the lower leg anchors, bring the elastic tape around the lateral aspect of the patella and back to the medial aspect of the upper leg anchors.

6. (Optional) Wrap a 6-inch elastic bandage from mid-calf to mid-thigh to cover the taping and provide additional support.

FIGURE 18-6  Patella taping.

Bandaging Bandaging may be used to wrap and support an injury or to help dress a wound. Many of the techniques described in the previous sections about taping, such as the use of figure-8 patterns, are also used for bandaging.

TYPES OF BANDAGES FIGURE 18-7  Buddy taping of the fingers.

smooth stick) can be placed on the dorsal or volar surface and the finger taped to it for additional extensor support (Figure 18-8). Any significant injury to the fingers or hands should be evaluated by a physician, who can determine whether radiographs are necessary. Given the importance of maintaining optimal functioning of the hands for personal and professional activities, this point cannot be overemphasized.

THUMB TAPING The thumb is frequently injured when it is placed in extreme extension or abduction, which occurs when it is caught in the strap of a ski pole when a person is falling. Taping can prevent reproducing the mechanism of injury, particularly when the individual is grasping an object (Figure 18-9).

The type of bandage depends on the intended purpose. Elastic bandages (e.g., Ace wraps) come in many widths and are used to wrap injuries such as sprains and strains. These bandages generally are accompanied by separate clips or have built-in clips for the purpose of securing the bandage. Of note is that the double-length 6-inch–wide elastic bandage is quite useful for wrapping large joints, such as the knee and the shoulder. Bandaging wounds generally involves rolled gauze or cottonbased wraps that secure a dressing in place. These wraps are more desirable than are elastic bandages for wound care, because they do not place as much tension on the dressing. A triangular bandage, which is often used to create a sling, can be folded two to three times into a strap called a cravat (Figure 18-14). Cravat dressings are useful for applying pressure to a bleeding wound to promote hemostasis. In the discussion of bandaging different parts of the body that appears later in this chapter, the method for using an elastic bandage is described. When securing a wound dressing, the same methods may be used, except that rolled gauze or cotton

WRIST TAPING Wrist sprain generally occurs during a fall. It can initially be difficult to distinguish from a fracture. Although splinting is usually the most desirable treatment, there are two basic taping approaches that can be used, depending on whether the injury occurred with the wrist in hyperextension or hyperflexion. Anchors are first placed around the palm and the distal wrist. Support strips to prevent undesirable movements are placed on the palmar aspect for hyperextension injuries or on the dorsal aspect for hyperflexion injuries (Figure 18-10).

ELBOW TAPING The two most common soft-tissue injuries to the elbow result from hyperextension or excessive valgus force. Each of these injuries can result in significant ligament and tendon injuries. Taping techniques are intended to prevent reproduction of painful movements while maintaining function. Because these techniques allow for substantial joint movement, underwrap should not be used, and tape should be applied directly to the skin to allow for maximal adhesion. Taping for a hyperextension injury involves use of a fan of elastic or tape, which is similar to that used for the wrist, to prevent excessive extension (Figure 18-11). Individuals who have suffered valgus stress injuries require reinforcement with elastic tape placed on the medial aspect of the elbow (Figure 18-12).

A

SHOULDER TAPING Taping the glenohumeral joint is rarely performed, mostly because it results in such a significant restriction of movement that the patient cannot effectively function. Thus taping offers little advantage over a sling. However, taping the acromioclavicular joint can be effective in reducing pain and maintaining adequate function at the glenohumeral joint.

B FIGURE 18-8  A and B, Extension taping of the finger with a small splint.

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Injury to the acromioclavicular joint most commonly occurs when a patient falls on the lateral aspect of the shoulder. Sufficient force is transmitted through the acromioclavicular ligament to stretch or tear it, which results in an “AC sprain” or a “separated shoulder.” For this injury, tape should be applied directly to the skin (Figure 18-13).

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

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FIGURE 18-9  Thumb taping. A, With the use of 1.5-inch–wide athletic tape, wrap an anchor strip around the wrist. B, With the use of 0.75-inch– wide tape, start at the volar aspect of the wrist and continue along the dorsal aspect of the thumb toward the first web space. C, Allow the patient to crimp the tape as it comes across the web space, and then continue around the base of the thumb. D, Bring the tape around to the volar aspect of the wrist, and then tape at that point. To complete a thumb spica, apply several more strips of tape in succession. To reinforce this, rather than repeating a series of strips, continue as follows. E, Apply an anchor strip from the volar to the dorsal aspect of the wrist through the first web space; note the crimping. F, Apply a strip from the dorsal to the volar aspect of the anchor strip. G, Apply successive strips until the wrist is reached. H, Add a finishing anchor strip through the first web space. I, Complete the wrapping with an anchor strip at the wrist.

bandages should be substituted. If there is a special technique for wound care, it will be described separately.

SECURING BANDAGES Because bandages are not adhesive, they must be secured with tape or clips or by tying them to the body. Two techniques for tying off a bandage are as follows: 1. As you are finishing wrapping the body part with the bandage, bend the free end of the bandage backward over your fingers to create a loop. Double back around the body part, and then tie the remaining free end to the loop to secure the bandage1 (Figure 18-15). 2. As you are finishing wrapping the body part, tear or cut the remaining portion of the bandage lengthwise down the middle. Double back with one of the resulting strips, and then tie off the bandage.

ANKLE AND FOOT BANDAGING Ankle bandaging with a 2- to 3-inch–wide elastic wrap can be used to support a sprain. The bandage can be applied over a sock or directly to the skin. It is usually the most simple to use 368

a series of figure-8 wraps. One may also use a series of heel locks, which were described in the section about ankle taping. Anchors and stirrups are not used. When bandaging the foot, the same technique should be carried out to the metatarsophalangeal joint. Circumferentially bandaging the foot by itself often results in the bandage slipping, which does not occur when the ankle is also bandaged as part of the process.

KNEE BANDAGING A double-length 6-inch–wide elastic bandage can provide support to the knee. Ask the patient to hold the knee in slight flexion by placing his or her heel on a small stone or a piece of wood (Figure 18-16, A, online). The elastic wrap is then applied circumferentially from the mid quadriceps to the mid calf (Figure 18-16, B, online). If using gauze or a smaller-width elastic wrap to secure a dressing, a series of figure-8 wraps can be applied, with the patella left exposed.

THIGH AND GROIN BANDAGING Quadriceps, hamstring, and hip-adductor (i.e., groin) strains can all be treated with an elastic bandage in a hip-spica configuration.

C

CHAPTER 18  Taping and Bandaging

A

B

D

FIGURE 18-10  Wrist taping. A, With the hand wide open, apply one anchor across the palm of the hand and two to three anchors across the distal forearm. B, Measure out the distance between the two anchors, and then construct a fan of four strips at varying angles on a smooth surface. C, For hyperextension injuries, apply these support strips to the palmar aspect; for hyperflexion injuries, apply them to the dorsal aspect. D, Apply another set of anchors over the support strips.

The bandaging is modified slightly for a groin strain (Figure 18-17). Although the quadriceps and hamstring can be supported by wrapping only the leg with a 6-inch–wide elastic bandage, the hip spica helps to prevent slipping and provides additional support.

SHOULDER BANDAGING A shoulder spica is used to support shoulder sprains, strains, and subluxations (Figure 18-21). A triangular bandage can be used to dress a shoulder wound (Figure 18-22).

SCALP BANDAGING WRIST AND HAND BANDAGING Support to the wrist can be supplied with the use of a 2- to 3-inch–wide elastic wrap and a continuous wrapping technique (Figure 18-18). This same technique can be used with gauze to secure a dressing to a wound that involves the palm of the hand. A hand cravat bandage can be used for wounds that continue to bleed despite manual pressure1 (Figure 18-19).

FINGER BANDAGING Finger wounds are generally easily treated with adhesive bandages. However, if the size of the wound or the degree of bleeding necessitates a larger dressing, then the following method may be used. Fold a 1-inch–wide piece of rolled gauze back and forth over the tip of the finger to cover and cushion the wound (Figure 18-20). Next, wrap the gauze around the finger until the gauze is snug. On the last turn around the finger, pull the gauze over the top of the hand so that it extends beyond the wrist. Split this gauze tail lengthwise, and then tie the ends around the wrist to secure the bandage.

THUMB BANDAGING The application of a bandage or dressing to the thumb usually involves a thumb spica, as described in the previous section about taping. The gauze or elastic bandage should be looped continuously rather than applied in individual strips.

Wounds to the scalp often require a dressing to be placed over hair, which makes adhesion very difficult. The dressing can be secured with a triangular bandage in a method that allows for considerable tension if pressure is necessary to stop any bleeding (Figure 18-23).

EAR OR SIDE OF HEAD BANDAGING A wound to the pinna of the ear or other location on the side of the head may require a compression dressing. If the ear is involved, gauze should be placed both anterior and posterior to the ear to allow the ear to maintain its natural curvature. A cravat is used to secure the dressing (Figure 18-24). This method may be used for wounds anywhere along the side of the head or under the chin.

EYE BANDAGING When bandaging an eye, a shield is placed over the eye socket to protect the globe, and this is followed by the application of a bandage over the shield. The shield may be made of commercially available sterile pads, or it may be cut foam or felt, stacked gauze, or a shirt or cravat that has been fashioned into a doughnut shape (Figure 18-25). The bandage is fashioned from a cravat and a spare piece of 15-inch–wide cloth or a shirt. The spare cloth is placed over the top of the head from a posterior to an anterior direction so that the anterior portion lies over the unaffected eye. A cravat is then applied horizontally to hold the shield over the injured eye. To expose the uninjured eye, pull up both ends of the spare cloth, and tie it at the top of the head (Figure 18-26). 369

PART 4  INJURIES AND MEDICAL INTERVENTIONS

1. The arm is supinated and extended just short of where pain is experienced. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.

1. The arm is supinated and flexed to approximately 30 degrees. Apply anchors with 3-inch elastic tape 4 inches above and below the elbow.

2. Apply 3-inch elastic tape from distal to proximal anchors that form an X over the antecubital fossa. A total of four strips should be applied.

2. Apply 3-inch elastic tape that forms an X over the medial joint line.

3. Apply closure strips above and below the elbow over the original anchors.

The first strip begins at the posterior aspect of the proximal anchor and crosses to the anterior aspect of the distal anchor. The second strip begins at the anterior aspect of the proximal anchor and crosses to the posterior aspect of the distal anchor. Apply a total of four strips.

4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.

FIGURE 18-11  Elbow taping.

3. Apply closure strips above and below the elbow over the original anchors.

4. (Optional) Apply a 4- or 6-inch elastic bandage from distal to proximal to secure the taping.

FIGURE 18-12  Elbow taping for a valgus stretch injury.

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1. Apply three anchor strips with 3-inch elastic tape. Place the first anchor around the midhumerus. Place the second anchor beginning inferior to the nipple anteriorly and around to the inferior tip of the scapula posteriorly. Apply the third anchor from the anterior portion of the second anchor, over the trapezius and extending to the posterior portion of the second anchor. Note that a 3-inch gauze pad is incorporated into this anchor to protect the nipple. 2. Apply a longitudinal strip of 3-inch elastic tape from the anterior aspect of the first anchor, over the acromioclavicular joint and ending on the posterior aspect of the third anchor.

3. Apply the next strip overlapping two-thirds of the third anchor laterally. It should extend from posterior to anterior portions of the second anchor and cross over the acromioclavicular joint.

4. Apply the next strip from the posterior aspect of the first anchor, over the acromioclavicular joint and ending at the anterior aspect of the third anchor.

5. Repeat steps 2 through 4 two more times. (Optional) Wrap a 6-inch elastic bandage in a shoulder spica for additional support. (See Bandaging section.)

FIGURE 18-13  Shoulder taping.

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1. Wrap a double-length 6-inch elastic bandage around the mid-thigh in a medial to lateral direction and continue proximally.

2. At the groin crease, continue up and around the waist once to help anchor the bandage. FIGURE 18-14  Making a cravat from a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

3. Return to the thigh to complete the figure-8. For quadriceps and hamstring strains, concentrate on wrapping the leg, using an additional figure-8 bandage to anchor the wrap. For groin strains, concentrate on supporting the hip adductors by alternating wrapping the leg with figure-8 wraps.

A

B

FIGURE 18-15  A and B, Securing a bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy, Ski Patrol Magazine Winter:63, 2005.)

4. Finish wrapping leg.

FIGURE 18-17  Thigh and groin bandaging.

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FIGURE 18-18  Wrist bandaging. A, Begin by encircling the wrist with the bandage two to three times. B, Continue bandaging across the dorsum of the hand, through the first web space, and around the base of the proximal phalanges. C, Continue down and across the dorsum of the hand. D, Circle the wrist, and bring the bandage across the dorsum of the hand to form a figure-8. E, Repeat these steps, and make alternating figure-8 patterns on the dorsum of the hand. Secure the bandage at the wrist.

1. After dressing the wound, the patient closes his fist around rolled gauze.

2. Starting from the anterior aspect of the wrist, wrap one end around the dorsum of the hand, over the fingers and back to the wrist. FIGURE 18-20  To begin a finger bandage, place layers of gauze over the fingertip. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.) 3. With tension, wrap the other end around the dorsum of the hand, over the fingers and back to the wrist, creating an X.

4. Cross both ends around the wrist.

5. Tie the ends to secure the dressing.

FIGURE 18-19  Hand cravat bandage. (Redrawn from Donelan S: That’s a wrap: Wound bandaging made easy, Ski Patrol Magazine Winter:66, 2005.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

1. Begin by encircling the mid-humerus with a double-length 6-inch elastic bandage and continue proximally while wrapping. Once near the axilla, wrap over the acromioclavicular joint and around the posterior thorax.

2. Continue under the opposite axilla, across the chest and bring down over the acromioclavicular joint and onto the upper arm.

3. Repeat the figure-8 pattern as the length of the bandage allows and finish on the upper arm.

FIGURE 18-21  Shoulder bandaging.

1. Lay the base of the bandage over the shoulder with the apex pointed toward the arm. Tie the two free ends just anterior to the axilla.

1. Drape a triangular bandage just over the eyes and fold the edge 1 inch under to form a hem. Allow the apex to drop over the back of the neck.

2. Roll the apex up the arm to the desired point of coverage and tie off.

2. Cross the free ends over the back of the head and tie in a half-knot.

FIGURE 18-22  Shoulder bandaging with a triangular bandage. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

3. Bring the free ends to the front of the head and tie a complete knot. At the posterior aspect of the head, tuck the apex into the half-knot.

FIGURE 18-23  Scalp bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

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1. Place the cravat over the wound at the cravat’s midpoint. Wrap one end over the head and the other under the chin.

2. Cross the cravat just above ear level and wrap ends in opposite directions.

FIGURE 18-25  Bandaging for the injured eye. A cravat or cloth is rolled and wrapped to make a doughnut-shaped shield, which is then fixed in place over the eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

3. Tie off the ends.

FIGURE 18-24  Ear or side of head bandaging. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

FIGURE 18-26  To hold an eye patch in place with a cravat, hang a cloth strip over the uninjured eye. Hold the patch in place with the cravat, and then tie the cloth strip to lift the cravat off of the uninjured eye. (Redrawn from Auerbach PS: Medicine for the outdoors, ed 5, Philadelphia, 2009, Mosby.)

CHAPTER 19 



Splints and Slings MISHA R. KASSEL AND ALAN GIANOTTI

Splints and slings have been staples of medical care for thousands of years. For instance, orthopedic splinting was well documented in ancient Egypt more than 5000 years ago1,33 (Figure 19-1, online). First and foremost, splints and slings stabilize injuries by limiting movement (Box 19-1). Limiting movement minimizes pain and decreases potential further tissue damage. Splinting eases transportation from the field, minimizes blood loss, and aids in healing.12 In general, all fractures and dislocations should be splinted before transport unless the patient’s life is at immediate risk or the rescue scene is unsafe.13 Basic splint types include rigid, soft, anatomic, and traction. Splint choice is based on fracture type and available materials. In improvisational situations, splints can be made from just about any material. Examples include newspapers, pillows, umbrellas, and other supportive materials5 (Figure 19-2).

Spinal Immobilization Spinal cord injuries are rare, affecting 40 to 50 individuals per million annually in the United States. These injuries may result in long-term disability.22 The 5 million people each year who are placed in spinal immobilization after traffic collisions contribute

to the majority of spinal cord injuries. In one wilderness study, 3.6% of mountain trauma patients who were alive when rescued had spinal injuries.12 In an attempt to prevent further neurologic damage, prehospital spinal immobilization of urban trauma patients is the standard of care. This may not be practical in wilderness settings, but it should always be considered. Spinal stabilization is first accomplished by manual techniques, and then mechanical devices (e.g., backboards, collars, straps) are required. Indications, risks, benefits, and equipment descriptions are discussed later in this chapter.

INDICATIONS FOR SPINAL IMMOBILIZATION The most common scenario for prehospital spinal immobilization is an injury sustained during a motor vehicle collision. All-terrain vehicles, automobiles, snowmobiles, motorcycles, and other offroad vehicles are the most common causes of high-force spinal trauma in the wilderness setting. Falls and other high-force mechanisms are also concerning. Worrisome symptoms include spine pain or palpable tenderness, altered mental status, neurologic complaints, head injury, extremes of age, or an unreliable examination that involves a distracting injury, alcohol or drug use, or a communication barrier6 (Box 19-2).

For online-only figures, please go to www.expertconsult.com

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BOX 19-1  Principles of Splinting

BOX 19-2  Indications for Spinal Immobilization

Visualize the injured body part. Continually recheck the patient’s neurovascular status. Traction is indicated if the pulse is not palpable. Gentle traction involves less than 10 lbs of force. Cover open wounds with sterile dressings. Immobilize the joints above and below the injury. Padding prevents further tissue damage. Do not reset open or protruding fractures. Splint the extremity in the position in which it was found. Splint the patient before transport (if he or she is stable). Ice and elevate the injury after immobilization.

Spine pain or tenderness Traumatic mechanism of injury Altered mental status Distracting injury Unreliable examination (e.g., as a result of alcohol or drug use) Neurologic complaints Head injury Extremes of age

Modified from Bowman W, et al: Outdoor emergency care: Comprehensive prehospital care for nonurban settings, ed 4, 2003, Sudbery, Jones and Bartlett Publishers; and Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady.

Spinal immobilization is intended to prevent worsening of an existing spinal cord injury or the creation of a spinal cord injury in the case of a ligamentous disruption. The medical literature has multiple reports of worsening neurologic deficits after patients with spinal cord injuries are moved.6,34,35 Extreme settings mandate a different interpretation of “urban” recommendations to fit the survival wilderness scenario. Wilderness data are limited, so prehospital spinal immobilization is prudent when practical. Spinal immobilization is not performed without reservation. Backboards and collars may increase discomfort. Airway management may be restricted and evacuation times increased with spinal immobilization. However spinal immobilization remains the standard of care when practical in the wilderness setting.12 Further research is indicated to better classify appropriate indications and to further assess the risk-benefit ratio for spinal immobilization in the wilderness.

Modified from Brabson T, Greenfield M: Prehospital immobilization. In Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders.

CERVICAL SPINE IMMOBILIZATION High cervical spine (C-spine) injuries have great potential for morbidity and disability. The goals of C-spine immobilization are to minimize movement and maintain a “neutral” alignment. Standard C-spine immobilization is performed with a hard collar in conjunction with a backboard and lateral support devices. The modern standard cervical collar has five contact points and makes use of the head, C-spine, and thorax. The thorax contact points include the trapezius muscles (posterior), clavicle, and sternum (anterior). Hard collars alone do not adequately limit cervical motion. Backboards and lateral support devices are required in conjunction with a hard collar (Figures 19-3 and 19-4). The

FIGURE 19-3  Standard hard cervical collars. (Courtesy Laerdal Medical Corporation.)

A

B

FIGURE 19-2  Improvised cervical spine and ankle stabilization (pillow, towels, cardboard and tape) in Port au Prince, Haiti, 2010. (Courtesy Anil Menon, MD.)

376

C

D

FIGURE 19-4  A to C, Different lateral support devices. D, Complete spinal immobilization. (Courtesy Laerdal Medical Corporation.)

CERVICAL SPINE APPLICATION The application of a C-spine immobilization device depends on the position in which the patient is found and the device that is available. Universal application diagrams are generally helpful with regard to in-line stabilization, neutral neck alignment, chin positioning, and collar placement. Diagrams for application of C-spine collars on both upright and supine patients are easily referenced and generally intuitive (Figure 19-5). Diagrams for application of improvised C-spine collars or C-spine collars on patients who are found in sitting positions are also helpful (Figures 19-6 to 19-9; Figure 19-8, online).

SPECIAL CONSIDERATIONS Special populations require accurately sized equipment. This includes people with extra long or short necks for which a standard cervical hard collar is not effective. Children who are less than 8 years old are at risk for further injury when immobilized on a standard backboard because of a proportionately large head, which may cause increased flexion during a collision.36 Modifications to counter this anatomic feature include raising the shoulders to the level of the head by placing a pad underneath the shoulders (Figure 19-10). This should be considered for all children who are on backboards.28,29

IMPROVISATIONAL TECHNIQUES The key ingredients to an improvisational C-spine device include maximizing stability and fit while limiting airway compromise and allowing access for mouth opening, thus limiting aspiration risk.14 A “horse collar” technique involves a towel, blanket, or other available and malleable material rolled to the desired thickness and placed underneath the patient’s neck. The ends are then crossed over the patient’s chest and secured. As with the cervical hard collar, the patient’s C-spine is maintained in a neutral position during application and for as long as possible afterward by manual in-line stabilization2,6 (see Figure 19-6). A structural aluminum malleable (SAM) splint can also be molded into a C-spine collar. Studies have shown it to be as effective as a Philadelphia collar, with the advantage of being small, lightweight, versatile, and portable. These characteristics are advantageous in the wilderness setting26 (see Figure 19-7).

COMPLICATIONS OF CERVICAL SPINE STABILIZATION Studies have shown that C-spine collars cause increased intracranial pressure, which may be clinically significant for patients with head injuries. Therefore hard cervical collars should be removed immediately after exclusion of a C-spine injury, especially among patients with head injuries. C-spine collars may also be contraindicated in patients with penetrating neck injuries, because they may interfere with management of neck wounds or even conceal these wounds. Penetrating wounds to the spinal cord are rare. Cervical immobilization creates the real possibility of causing greater morbidity than protection.18,19

THORACOLUMBAR IMMOBILIZATION A full-length backboard best accomplishes immobilization of the thoracolumbar spine. In addition, a cervical collar, lateral neck stabilizers, and backboard straps are essential for full spinal immobilization. If the patient is already upright, standing, or lying supine, application of a full-body backboard is straightforward, as described later in this chapter. However, with the suspected cervical injury of a seated patient, an intermediate device is

required. There are many forms of this short board, such as a Kendrick Extrication Device (see Figure 19-9). Short boards are applied only after manual in-line stabilization and cervical collar placement. When the short board is in place, the patient can be safely transferred to a full backboard device.6 Strict contraindications for spinal immobilization are few but include emergency evacuation from an unsafe environment. Examples of such environments, with the risk of impending danger, include toxic spills, fire hazards, congested traffic areas, and other situations in which the application of an immobilization device would delay immediate evacuation to safety. In these dangerous situations, expedited removal with manual cervical stabilization is advised.21 When the patient is in a safe location, full spinal immobilization should be applied. Choices for full-body splints include hard backboards, scoop stretchers, and full-body vacuum splints (Figures 19-11 to 19-13). Full-body hard backboards are used for their ease of application, availability, and effectiveness. Unfortunately, their size and weight make them undesirable for backcountry use, so they are often improvised in the field. Secured straps minimize spinal movement during transport. These are especially important with vomiting patients, when the airway is potentially compromised and a quick change of position is required to allow for removal and drainage of emesis.6 Hard backboards are uncomfortable. Spinal pain that is induced by a backboard may be misinterpreted, and this can complicate and delay therapy.16 Vacuum splint devices offer certain advantages over rigid hard backboards. They can be applied more quickly, and are significantly more comfortable. They also offer a similar degree of spinal immobilization.20 During mountain rescue, vacuum splints are the preferred device for total spinal immobilization (see Figure 19-12).

FULL SPINE IMMOBILIZATION From a supine (lying) position and after the placement of a cervical collar, the patient is logrolled and placed onto a board or vacuum splint. Three people are required to transfer a patient onto a board. The first person is positioned at the head and applies in-line stabilization, the second is at chest level, and the third is at pelvis level. On the command of the person at the head, the patient is rolled onto his or her least-injured side. The board is then slid underneath the patient while the back is evaluated for injuries. Body straps and lateral neck stabilizers are then placed.6 Logrolling is not required with scoop stretchers, thereby minimizing spinal movement (see Figure 19-13). Full spinal immobilization can also be applied to a standing patient (see Figure 19-5). Complications of full spinal immobilization are listed in Box 19-3.

Upper-Extremity Splinting The most common upper-extremity injury scenario is bracing from a ground-level fall. Rigid and soft splints are used to stabilize upper-extremity injuries. It is always important to leave fingertips exposed to allow continuous assessment of neurovascular status.6 Common examples of upper-extremity splints include malleable, cardboard, air, vacuum, pillow, and sling and swathe splints. Specific splinting recommendations for upperextremity injuries are given in Table 19-1. When feasible, upperextremity injuries are splinted in a position of function (Table 19-2).

Lower-Extremity Splinting Although the principles of lower-extremity splinting are similar to those of upper-extremity splinting, the ramifications are not the same in terms of evacuation. Lower-extremity fractures are more likely to involve weight-bearing bones and thus to require rigid splinting. Specific recommendations, including positions of function, are found in Tables 19-2 and 19-3. One needs look no further than Joe Simpson’s 1985 epic selfrescue from the Peruvian Andes, which was described in Touching the Void, to appreciate the pain of an unsplinted weight-bearing fracture: 377

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patient’s neck requires manual stabilization in a neutral, in-line position until he or she is fully immobilized. Standard emergency medical services equipment includes lateral support devices (foam or plastic). In the wilderness setting, these devices can be improvised by rolling clothes, sheets, or blankets and placing them on both sides of head while securing everything in place with tape17 (see Figure 19-2).

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

D

G

B

C

E

F

H

FIGURE 19-5  Full spinal immobilization from a standing position. A, Step 1: Manual stabilization. B, Step 2: Apply a rigid collar. C, Step 3: Insert a long backboard. D, Step 4: Center the backboard. E and F, Step 5: Rescuers grasp the board with the use of a handle that is higher than the patient’s armpit. G, Step 6: Slowly lower the patient. H, Step 7: Fully immobilize the torso and then the head and neck. (From Elling R, Politis J: Backboarding the standing patient, JEMS 12:9, 1987. Used with permission.)

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FIGURE 19-6  Improvisational “horse collar.” (Courtesy Ferno-Washington, Inc.)

A

B

D

C

E

G

H

F

I

FIGURE 19-7  Improvised cervical spine collar from a SAM splint. A, Fold 36-inch splint 5 inches from the end. B, While bracing the thumbs on either side of the fold, pull the edges to create a V-shaped chin rest. C, Place the chin rest below the patient’s chin, and place the rest of the splint loosely around the patient’s neck. D, Bring the end forward and down in an oblique direction until it touches the chest. E, While supporting the chin, bring the chest portion of the splint around the chin to create a chin post. Squeeze to deepen the chin post. F, Insert the index fingers on either side of the splint and pull. G, Squeeze to create lateral posts to ensure a snug fit. H, Squeeze the back of the splint to create more stability. I, Fold up any excess splint and secure it with wrap or tape. (Courtesy SAM Medical Products.)

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A

C

B

D

FIGURE 19-9  A, Kendrick Extrication Device (KED). B, Manual in-line stabilization of the cervical spine with the KED slid behind the patient. C, Applied KED with cervical collar in place. D, Patient transferred to long board. (Courtesy Ferno-Washington, Inc.)

BOX 19-3  Complications of Spinal Immobilization Tight straps and a rigid board may cause discomfort or distress. Tight straps may cause vascular compromise. An immobilized position may interfere with normal respiratory function. Complications from emesis include aspiration. Loose straps may be inadequate for spinal immobilization From Brabson T, Greenfield M: Prehospital immobilization. In Clinical procedures in emergency medicine, ed 5, Philadelphia, 2007, Saunders; Campbell J: Extremity trauma. International trauma life support for prehospital care providers, ed 6, Upper Saddle River, NJ, 2008, Brady; Hamilton RS, Pons PT: The efficacy and comfort of full-body vacuum splints for cervical-spine immobilization, J Emerg Med 14:553, 1996; and Kwan I, Bunn F, Roberts I: Spinal immobilisation for trauma patients, Cochrane Database Syst Rev (2):CD002803, 2001.

380

The moment I jumped I knew I would fall…. I had lain face-down in the gravel, clenching my teeth, waiting for the pain to subside. It remained with me, burning my knee unbearably as it had never done before… I stood and fell, writhed where I fell, cried and swore, and felt sure in my heart that these were my last spastic efforts before I lay still for good.32

Rigid Splints Rigid splints can be improvised from materials such as cardboard, wood, and wire. Proprietary vacuum splints and air splints are commonly used in the field. Rigid splints are attached to the extremity with a variety of fasteners, including tape, straps, gauze, and Velcro. For all splints, ample padding is essential, especially over bony surfaces and swollen tissue to minimize pressure damage and pain.5

CHAPTER 19  Splints and Slings

A

B

C FIGURE 19-10  Backboard considerations and increased cervical flexion for children who are younger than 8 years old. A, A young child immobilized on a standard backboard. Note how the large head forces the neck into flexion. Backboards can be modified by B, an occiput cutout or C, a double mattress pad to raise the chest. The actual clinical consequences of this observation are unknown. (Modified from Herzenberg JE, Hensinger RN, Dedrick DK, et al: Emergency transport and positioning of young children who have an injury of the cervical spine, J Bone Joint Surg Am 71:15, 1989.)

Cardboard splints have the advantage of being lightweight, inexpensive, easy to apply, and radiolucent.6 They can be premade or improvised (Figures 19-2, 19-14 to 19-16; Figure 19-16, online). When improvising, it is important to cut the cardboard so that the corrugations run lengthwise to maintain the material’s intrinsic strength. Splints can be individually fitted

FIGURE 19-12  Example of a full-body vacuum splint used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department, Utah.)

using the unaffected extremity as a model and then placed on the affected extremity. They are usually secured with adhesive tape. Disadvantages include loss of integrity when wet and greater laxity as compared with other splinting options. The distorted and grossly swollen extremity is difficult to splint using this technique.12 Although they are initially malleable, vacuum splints are a type of rigid splint (Figure 19-17, online). These splints are made of many tiny plastic pellets in a closed, airtight bag. The bag is placed around the injured extremity, and then air is manually extracted via a hand pump to form a rigid “mold” of the injured extremity. The extremity is left in its position of injury to minimize pain (Figure 19-18). No external force is applied, thereby maximizing circulation.6 Unfortunately vacuum splints are expensive, moderately bulky, affected by changes in altitude, and penetrable. In addition, any perforation renders the splint nonfunctional.12 A lightweight, inexpensive, and popular rigid splint is the SAM splint (Figures 19-7, 19-8, and 19-19 to 19-33; Figure 19-8, online). Constructed of an aluminum center that is sandwiched between thin strips of foam, this splint is also malleable and versatile.6 It is very strong and pliable, and it can be used for

TABLE 19-1  Upper Extremity Splints Splint

Indication

Figure-8 splint Sling and swathe splint Sugar-tong splint   Proximal   Distal Posterior arm splint Volar splint

Medial clavicle fractures Shoulder and humeral injuries

Gutter splint Thumb spica splint Volar finger splint

FIGURE 19-11  Standard rigid splint. (Courtesy Laerdal Medical Corporation.)

Humeral fractures Wrist and distal forearm fractures Stable elbow and forearm injuries Wrist fractures and fractures of the second through fifth metacarpals Phalangeal and metacarpal fractures Scaphoid fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries Fractures of the distal phalanges and the interphalangeal joints

Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19:137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.

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TABLE 19-2  Splinting Guidelines: Positions

of Function

Splint

Position

Volar wrist splint

Neutral forearm (thumb up) with the wrist in 20 degrees of flexion Neutral forearm with the wrist in 20 degrees of extension; metacarpophalangeal joint in 50 degrees of flexion; proximal interphalangeal joint in slight flexion (e.g., 10 degrees); distal interphalangeal joint in extension Forearm neutral with the wrist in 20 degrees of extension and the thumb slightly flexed to allow for thumb–index finger opposition and alignment of the thumb and the forearm Finger in slight flexion Elbow at 90 degrees of flexion with a neutral position of the forearm and the wrist

Ulnar and radial gutter splints

A

Thumb spica splint Finger splint Sugar-tong and posterior arm splints Posterior leg splint

Ankle at 90 degrees

Modified from Abarbanell NR: Prehospital midthigh trauma and traction splint use: Recommendations for treatment protocols, Am J Emerg Med 19(2):137, 2001; Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, WB Saunders.

B

C Long backboard

Short backboard

Board splint

Ladder splint

D FIGURE 19-13  A, Scoop stretcher. B, Stretcher placed beside the patient. C, Stretcher slid under the patient. D, Stretcher locked in place with straps secured. (Courtesy Ferno-Washington, Inc.)

Padded board

Cardboard splint

Aluminum splint

Half ring

Air splint

FIGURE 19-14  Premade Washington, Inc.)

382

cardboard

splint.

(Courtesy

Ferno-

FIGURE 19-15  A variety of splints. (From Geiderman JM, Katz D: General principles of orthopedic injuries. In Marx J, Hockberger R, Walls R, editors: Rosen’s emergency medicine: Concepts and clinical practice, ed 7, Philadelphia, 2009, Saunders. Used with permission.)

Splint

Indication

Knee immobilizer splint Posterior ankle splint

Knee injuries Distal tibia and fibula injuries; ankle, tarsal, and metatarsal fractures Ankle fractures Toe fractures Femur fractures

Stirrup splint Buddy taping Traction splint

CHAPTER 19  Splints and Slings

TABLE 19-3  Lower-Extremity Splints

Modified from Boyd AS, Benjamin HJ, Asplund C: Splints and casts: Indications and methods, Am Fam Physician 80:491, 2009; Fitch MT, Nicks BA, Pariyadath M, et al: Videos in clinical medicine: Basic splinting techniques, N Engl J Med 359:e32, 2008; Garza D, Hendey G: Extremity trauma. In Mahadevan S, Garmel G: An introduction to clinical emergency medicine, Cambridge, UK, 2005, Cambridge University Press; and Chudnofsky CR, Byers SE: Splinting techniques. In Roberts J, Hedges J: Clinical procedures in emergency medicine, ed 5, Philadelphia, 2009, Saunders.

nearly all extremity requirements. Other malleable splints include ladder splints (i.e., pliable metal splints) and rolled-wire splints, both of which are readily available at most outdoor sporting goods stores5 (Figure 19-34). Given their weight, size, reliability, versatility, and cost, malleable splints have become a popular choice for the universal wilderness medical kit.12

Soft Splints A soft splint earns its name from the soft, padded material that is used to secure the injury. Soft splints include sling and swathe splints, pillow splints, and blanket-roll splints7 (see Figure 19-2). Soft splints allow for more laxity than rigid splints, but they can be combined with rigid splints for extra stability. Pillow splints are soft splints that are adapted for wrist and hand injuries. Their main advantages are ease of application and comfort.6 As with other soft splints, they allow for more movement at the fracture site, but are bulkier than other splints. Sling and swathe splinting can be used alone or in combination with other forms of splints. Shoulder, clavicle, upper arm, elbow, forearm, wrist, and even hand injuries are commonly stabilized with a sling and swathe. For a shoulder injury with which it is not possible to adduct the arm, a pillow (or similar material) can be used to bridge the empty space, with the sling supporting the arm and the swathe stabilizing it.6 This technique takes advantage of the chest wall to provide the splint foundation. Distal humeral injuries necessitate a sling and swathe splint in combination with rigid splints. Sling and swathe splinting is used alone for many clavicle, shoulder, and proximal humeral injuries. Advantages are its weight, portability, and improvisational versatility. Air splints are hybrid splints that are made from inflatable yet durable plastic. These splints are most often used for the elbow, knee, and ankle (Figure 19-35). They are placed around the injured extremity and inflated to the desired pressure and rigidity.5 They have the advantages of being lightweight and portable. Variable external pressures can be used to control hemorrhage. External pressure has the potential to limit distal perfusion. Air splints should be temporarily deflated (e.g., for 5 minutes every 90 minutes) to decrease the risk for ischemic damage.7 Air splint pressure varies with altitude and temperature. For these reasons, it is important to reevaluate neurovascular status during transport.12

FIGURE 19-18  Upper and lower body vacuum splints used for wilderness rescue. (Courtesy Sheri Trbovich and the Weber County Sheriff Department.)

A

B

“Click”

SAM Splints Malleable splints such as SAM splints37 no longer fall into the category of improvised splinting. These splints are commonly found in the standard wilderness medical kit. They are lightweight, reusable, versatile, and padded, and they are not affected by changes in pressure or temperature. They are also radiolucent to allow radiographs to be taken with the splint in place. The malleable SAM splint is pliable in its native form yet easily strengthened with creasing. The basic SAM splint adaptations are depicted in Figure 19-22. In addition, the SAM splint can be

C FIGURE 19-19  Application of the SAM pelvic sling. A, Remove all objects from the pockets. Place the sling under the patient’s hips.  B, Place the black strap through the buckle, and pull it completely through. C, Hold the orange strap with one hand, and then pull the black strap in the opposite direction under tension until a click is heard. Maintain tension, and place the black strap against the sling surface to secure. (Courtesy SAM Medical Products.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

D

C

E

FIGURE 19-20  The Slishman femur traction splint. A, Apply the ankle strap. B, Apply the groin strap. C, Extend the middle pole from the outer side of the leg, and lock it in place for coarse adjustment. D, Pull the cord to apply traction. E, Lock the splint in place. F, Splint the injured extremity. (Courtesy Sam Slishman, MD.)

F

A

A

B

B

C FIGURE 19-22  Basic SAM splint adaptations. A, C-curve. B, Reverse C-curve. C, T-curve (maximum strength). (Courtesy SAM Medical Products.)

FIGURE 19-23  Shoulder splint. A, Fold a 36-inch splint into three equal sections. Fold the outer sections along the longitudinal axis, and leave the middle section flat. Hook the outer ends together to make a triangle splint. B, Place the triangle splint under the patient’s axilla to support the abducted arm. The splint can then be held in place by the patient or secured with wrap. (Courtesy SAM Medical Products.)

SAM

SPLINT

®

CHAPTER 19  Splints and Slings

A

B

D

C

E

FIGURE 19-24  Humeral shaft splint. A, Fold one-third of a 36-inch splint on itself. B, Curve the double-layer portion into a fishhook shape, and secure it with tape or wrap. C, Form a C-curve along the shank of the fishhook to create strength, and then mold it to the arm. D, Apply the splint to the arm. Fold any excess splint back on itself. E, Secure the splint with wrap, and apply a sling and swath splint for additional support. (Courtesy SAM Medical Products.)

B

A

D

E

C

F

G FIGURE 19-25  Dislocated elbow splint. A. Use the unaffected arm as a model, and extend a 36-inch splint from under the patient’s armpit to the knuckles. B, Fold under the portion of the splint that extends past the knuckles. C, Form a C-curve along the entire length of splint. D, Use your own arm as a template, and shape the splint. E, You may reverse the C-curve bends on the edges for more strength. F and G, Apply and secure the splint to the patient with wrap or tape. (Courtesy SAM Medical Products.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

D

B

E

C

F

G

FIGURE 19-26  Sugar-tong splint. A, Fold a 36-inch splint in one-half. B, To determine the proper length, fold the splint around the patient’s elbow to the knuckles. C, Form a C-curve in each one-half of the splint, but no more than two thirds down each one-half. D, Shape the splint to fit, using your own arm as a template. E, Pad any bony prominences around the wrist and elbow. F and G, Fit and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

molded to form an adequate C-spine collar (see Figures 19-7 and 19-8, online).

lie in less effectiveness compared with commercial splinting devices.12

Improvised Extremity Splints

Pelvic Splinting

Improvised splints can be made from branches, boards, padded pack straps, or rolled-up newspapers or magazines. Anatomic splints involve an uninjured neighboring body part, primarily a digit. Slings can also be made from unused clothes.5 In these cases, one need not pack additional materials. Disadvantages

Pelvic fractures are potentially life-threatening injuries.24 Splinting is essential for pain and hemorrhage control. Pelvic fractures are often difficult to diagnose in the field, but must be suspected with a high-force mechanism in the face of pelvic pain or altered sensorium. A pelvic compression device should be applied.12

A

B

C

D

E

F

G FIGURE 19-27  Volar wrist splint. A. Roll the end of a 9-inch splint for children or an 18-inch splint for adults over to provide comfort for the patient’s fingers. B, Apply a C-curve. C, Mold the splint into a position of function, using your own wrist as a template. D, Create a generous curve for the base of the thumb. E, Fold up the ulnar side for additional strength. F and G, Apply and secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

386

B

C

D FIGURE 19-28  Ulnar gutter splint. A, Fold a 9-inch splint longitudinally. B, Mold the splint into a desired shape, using the ulnar aspect of your own wrist and hand as a template. C, Apply the splint to the patient. D, Make fine adjustments to the splint, and secure it with wrap or tape. (Courtesy SAM Medical Products.)

A

B

D

C

E

FIGURE 19-29  Thumb spica splint. A, Use a 9-inch splint. B, Use your hand and thumb to mold the splint to create a generous curve for the thumb. C, Add a reverse C-curve to strengthen the splint. D and E, Apply and secure splint with tape or wrap. (Courtesy SAM Medical Products.)

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A

Appropriate stabilization with such a splinting device slows hemorrhaging and stabilizes fracture fragments.6 “Open-book” fractures (i.e., diastasis of the pubic rami with posterior pelvic disruption) create a large surface area for potential hemorrhage. Circumferential compression of the pelvis is recommended for emergency stabilization.4 This can be accomplished by pelvic circumferential compression devices, a pneumatic antishock garment (PASG), or improvised techniques such as pelvic sheeting7 (see Figure 19-16, online). Optimal pelvic stabilization is achieved by applying a sling around both greater trochanters and the symphysis pubis.4 Pelvic circumferential devices are similar in function (see Figure 19-19). A pelvic compression device can be improvised in the wilderness. Sheets, jackets, and other long fabrics are readily available on most expeditions. The sheet or fabric is wrapped around the pelvis over the greater trochanters and the symphysis pubis and then pulled tight and secured to increase pressure at the wound and to decrease the potential space for hemorrhage. The PASG and the military antishock trouser, which were commonly used in the past, have generally fallen out of favor (Figure 19-36). Proponents of PASG and military antishock trouser use point to the position paper of the National Association of EMS Physicians for support. The paper states that the PASG is beneficial in the setting of a ruptured abdominal aortic aneurysm and that it is potentially beneficial in many other scenarios (e.g., hypotension from pelvic fractures, gynecologic bleeding, ruptured ectopic pregnancies, severe traumatic hypotension, and uncontrolled lower extremity hemorrhage).11 Postulated successful mechanisms for correcting hypotension include increasing peripheral vascular resistance, tamponade of local hemorrhage, and increasing blood return from the lower extremities.23 PASG disadvantages include prolonged scene time, pressure changes with altitude (e.g., potential compartment syndrome with air travel), and interference with normal pulmonary function.27 In addition, animal studies have demonstrated lactic acidosis after prolonged use. Rapid deflation may cause hypotension as a result of volume redistribution. Studies have not shown improvement in hospital duration, and others have actually shown increased mortality rates.9 PASGs are bulky and expensive. Absolute contraindications for PASG use include diaphragmatic rupture, penetrating thoracic injury, a splinted lower-extremity fracture, a gravid uterus, or abdominal evisceration.23 Thus the routine use of the PASG in the field is not recommended. In the case of isolated femur fracture, a PASG can be used, but other viable options are more readily available in the wilderness.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

FIGURE 19-30  Finger splint. A, Form a C-curve B, Place the affected finger into the curved splint, and then squeeze the tip to make a fingertip guard. C, Secure the splint with wrap or tape. (Courtesy SAM Medical Products.)

Hip and Femur Splinting Femur fractures result from high-force trauma. These fractures can be diagnosed clinically in the appropriate wilderness setting. Deformity, swelling, and tenderness along the thigh and in the face of significant trauma are highly suggestive of a femur fracture.15 Femur fractures produce significant hemorrhage; a closed femur fracture may bleed more than 1 L into the thigh.10 Femoral shaft fractures also have a high mortality rate that ranges from 20% to 54%.25 Traction splints minimize blood loss, pain, and other adverse sequelae while achieving realignment of bone fragments.6 Contraindications to traction splint placement are fractures that involve the knee, pelvis, or ankle, or that include damage

A

B

to the sciatic nerve.25 Unfortunately, such comorbidities are common with severe wilderness injuries, which makes it impossible or dangerous to anchor the traction splint.3 Controversy exists regarding whether a traction splint should be placed with an open femur fracture, but this is not a strict contraindication. An indication for traction splint placement is any suspected femur fracture in the nonambulatory patient.6 There are many femur traction splint devices, and all are based on the same principle: a rigid frame that anchors at the proximal pelvis and that extends traction beyond the distal heel. The proximal aspect is padded against the ischial tuberosity. Traction to the fractured femur is then applied with a heel strap that is anchored off of the distal frame. The thigh, knee, and leg are also secured with soft straps.12 Traction devices that have a halfring design (e.g., Thomas or Hare splints) can cause hip flexion (i.e., up to 30 degrees). This can cause incomplete fracture realignment unless the leg is elevated to match the angle.6 Traction splints that do not have a posterior half ring (e.g., Sager) do not compress the sciatic nerve and can be used with groin injuries. They can also be used for patients with pelvic fractures or for bilateral femur fractures by making use of two splints (i.e., one applied to each leg).31 Traction splint application is not always intuitive (Figures 19-20, 19-21, 19-37, and 19-38; Figure 19-21, online). Two rescuers are needed for proper placement.5 Manual traction should be applied to reduce the fracture until the splint can be placed.1 As with any splint placement, it is important to establish pain control, to check neurovascular status both before and after splint placement, and to fully explain the process to the conscious patient. After the proximal femur splint is in place, the thigh strap is fastened. The ankle harness is then placed just above the malleoli and attached to the distal splint. Traction (6.8 kg [15 lbs]) is applied, and the remaining straps are applied. After the traction splint is in place, the patient should be logrolled onto a backboard to minimize fracture fragment movement.5 Traction splint complications result from improper strap and splint placement and include sciatic or peroneal nerve injury, pressure wounds, hemorrhage and pain.7,12,25,31

Ankle Splinting C

D FIGURE 19-31  Thomas half-ring femur splint. A, The foot support is made by cutting an 8-inch section from the ski pole. Drill or puncture two holes that are 15 cm (6 inches) apart, with the entry hole being larger. Use duct tape, cord, and safety pins to secure. Create a half-ring support by placing two ski poles, handle facing handle, on the outer thirds of a 36-inch SAM splint. B, Roll the splint tightly around each handle, and secure with duct tape. Bend the splint so that the poles are now parallel and facing down. Firmly fit the pole ends through the foot support. C, Duct tape the thigh and calf supports, and reinforce them with cloth and elastic straps. An improvised ankle strap is required for traction. (Courtesy SAM Medical Products.)

388

Ankle sprains are common orthopedic injuries incurred during expeditions and the most common sprain.2 There are literally hundreds of examples of readily available over-the-counter ankle supports, braces, and splints. These include but are not limited to leather bracing, canvas bracing, air stirrups, air bladders, air casts and air boots, plastic splints with Velcro strapping, and malleable varieties, including wire ladder splints. On the basis of the high incidence of ankle sprains, it appears prudent to have a readily available lightweight ankle splint in one’s medical kit. The goal is to offer ankle support that will fit within the size constraints of the patient’s hiking boot. The time-tested alternative is athletic tape. The taped sprained ankle has talofibular ligament support (for a limited duration), and tape does not add significant weight to the medical kit. All wilderness health care providers should be adept at taping ankles.

Shoulder Dislocation Anterior shoulder dislocation is a common injury. The arm is most comfortable in an abducted position. This can be accomplished with a rolled blanket, a pillow, a jacket, or a SAM splint that has been fashioned into a triangle (Figure 19-23).

CHAPTER 19  Splints and Slings

SAM

SPLINT

NT

SA ® M LI

B

SP

SAM®

SPLIN T

SAM®

SPLIN T

A

C SAM

SAM

SAM

SA

M®

D

E F

G

FIGURE 19-32  Knee immobilizer splint. A, Fold a 36-inch splint in the center to create two equal lengths. Fan the halves so that the splint is twice as wide at one end as compared with the other. B, Apply tape to the top and middle of the splint to keep the fan shape. C, Create a second fan-shaped splint. D, Form a C-curve in each splint. E, The C-curves should appear as shown. F, Place the splints on each side of the knee. G, Secure the splint with tape. (Courtesy SAM Medical Products.)

Humeral Shaft Injury

Thumb Injuries

Humeral shaft fracture is often treated with a sling or with a sling and swathe splint alone. For pain control, a splint is often desirable (see Figure 19-24).

A thumb spica splint is used for suspected scaphoid (navicular) fractures, thumb dislocations and fractures, and ulnar collateral ligament injuries (see Figure 19-29).

Elbow Dislocation

Finger Injuries

A dislocated elbow can be reduced in the field with the appropriate analgesia and experience. The dislocated elbow can also be splinted in place and the patient transported for definitive care (see Figure 19-25).

Finger splints are used for finger fractures, fingertip injuries, and lacerations (see Figure 19-30).

Elbow Fracture A sugar-tong splint is useful for most elbow injuries. These most commonly include supracondylar, olecranon, and radial head fractures (see Figure 19-26).

A femur traction splint can be improvised in a variety of ways with a SAM splint. One practical wilderness example involves the use of ski poles and a SAM splint. An improvised version of a half-ring splint is made from two ski poles, a small piece of metal, and a 91.4-cm (36-inch) SAM splint (see Figure 19-31).

Wrist Fracture

Knee Injuries

The volar wrist splint is used for most wrist fractures, dislocations, sprains, lacerations, and other wrist injuries. A T-beam volar wrist splint (i.e., apply a T-curve to the folded SAM splint) can be used for greater support, when traveling over rough terrain, or when more support is desired (see Figure 19-27).

A knee immobilizer splint is used for knee injuries, patella tendon injuries, dislocations, and other severe ligamentous sprains when immobilization is required (see Figure 19-32).

Metatarsal Fractures

Long-leg splints are used for tibial and fibular fractures. Depending on the amount of stabilization needed, a single or double long-leg splint can be applied. The double long-leg splint offers more stabilization (see Figure 19-33).

Ulnar gutter splints are used for fourth and fifth metatarsal injuries and for corresponding digit injuries (see Figure 19-28).

Femur Fracture

Leg Fractures

389

PART 4  INJURIES AND MEDICAL INTERVENTIONS

B

A

SAM®

SPLINT

C

D

E

F

FIGURE 19-33  Single long-leg splint. A, Place padding around any bony prominences on both sides of the ankle. B, Make a C-curve out of 30 of the splint’s 36 inches, and leave the last 6 inches flat. C, Apply a reverse C-curve to the edges for extra strength. D, Place the splint against the outside of the leg, and fold the last 6 inches under the foot. E, Adjust the splint to fit the leg. F, Secure the splint with wrap or tape. (A double long-leg splint is made by repeating steps B to F so that the splints are on both sides of the leg.) (Courtesy SAM Medical Products.)

FIGURE 19-34  Pliable metal ladder splints. (Courtesy FernoWashington, Inc.)

FIGURE 19-36  Military antishock trouser/pneumatic garment. (Courtesy Common Cents EMS Supply.)

FIGURE 19-35  Lower-extremity air splint used for a wilderness rescue. (Courtesy Ed Gray.)

390

antishock

A

C

B

F

E

D

FIGURE 19-38  Applying the Sager traction splint. A, Position the splint between the patient’s legs, and rest the splint cushion against the ischial tuberosity. B, Fold down the number of comfort cushions needed to engage the ankle above the medial and lateral malleoli. C, Use the ankle straps to secure the splint snugly. D, Pull the control tabs to tightly engage the ankle harness against the crossbar. Grab the padded shaft of the splint with one hand and the traction handle with other, and then gently extend the inner shaft to obtain the desired traction. E, Adjust the thigh strap at the upper thigh securely. F, Firmly secure the elastic leg cravats. G, Apply the foot strap around the feet to prevent rotation. Check the patient for sensation and pulses. (Courtesy Minto Research and Development, Inc.)

CHAPTER 19  Splints and Slings

FIGURE 19-37  Ferno traction splint. A, Adjust the length of the splint to fit the patient. Use the patient’s uninjured leg to determine the desired length. B, One operator supports the injured leg and places the ankle wrap under the ankle. C, Center the foot, wrap the strap around the ankle, and secure it with the fastening strip. D, Support the leg, slide the splint under the injured leg until the pad rests against the lower pelvic bone, and then fasten the hip strap. E, Attach the S-hook to the D-ring, and apply traction. F, Reposition the splint, and then fasten the straps. (From Ferno-Washington Inc. Used with permission.)

B A

C

E

D

F

G 391

A

B

D

C

E

FIGURE 19-39  Ankle stirrup splint. A, Pad any bony prominences. B, Fold a 36-inch splint in half. C, Apply C-curves two thirds of the way down each half. Add reverse C-curves for strength. D, Fold the stirrup splint around the foot and ankle. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)

A

B

C

D

E

FIGURE 19-40  Figure-8 splint. A, Pad any bony prominences. B, Lay a 36-inch splint flat. Put the patient’s foot in middle, with the splint just in front of the heel. C, Conform one side of the splint around the ankle. D, Repeat with the other side of the splint around the opposite side of the ankle. Crimp to fit. E, Secure the splint with tape or wrap. (Courtesy SAM Medical Products.)

Ankle and Foot Injuries Ankle stirrup and figure-8 splints provide for the immobilization of ankle injuries. The ankle stirrup splint can also be used for fractures (Figures 19-39 and 19-40). The combination of an ankle stirrup splint and a figure-8 splint offers maximal support; this is done by first applying the figure-8 splint and then adding the ankle

stirrup splint last. The combination of the two splints provides greater stabilization and immobilization. This procedure could potentially be used for weight-bearing metatarsal fractures.30

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 20 

Emergency Airway Management SWAMINATHA V. MAHADEVAN Emergency airway management encompasses assessment, establishment, and protection of the airway in combination with effective oxygenation and ventilation. Timely and effective airway management can literally mean the difference between life and death, and it takes precedence over all other clinical considerations. Airway management in the wilderness must often be provided in austere or unusual environments under less-than-ideal circumstances. Many of the resources that are readily accessible in a hospital or emergency department setting are not available in the wilderness, so improvisation may prove invaluable. 392

Airway Anatomy Internally, the airway is composed of many structures and welldefined spaces. It originates in the nasal and oral cavities (Figure 20-1). The nasal cavity extends from the nostrils to the posterior nares or choanae. Because resistance to airflow through the nose is almost twice that of the mouth, patients who require high flow rates (e.g., during exercise) often breathe through their mouths. The nasopharynx extends from the end of the nasal cavity to the level of the soft palate. Tonsillar lymphoid structures are the primary impediments to airflow through the nasopharynx. The

For online-only figures, please go to www.expertconsult.com

Nasopharynx

Hyoid bone Thyroid membrane Thyroid notch Laryngeal prominence Thyroid cartilage Cricothyroid membrane Cricoid cartilage Tracheal rings

Oral cavity

Oropharynx Epiglottis

Thyroid gland

Vallecula Laryngeal inlet Laryngopharynx

Larynx Glottis

FIGURE 20-1  Lateral airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

oral cavity is bounded by the teeth anteriorly, hard and soft palates above, and the tongue below. The oropharynx, which communicates with the oral cavity and the nasopharynx, extends from the soft palate to the tip of the epiglottis. The tongue is the principal source of obstruction in the oropharynx. The oropharynx continues as the laryngopharynx (hypopharynx), which extends from the epiglottis to the upper border of the cricoid cartilage at the level of the C6 vertebral body. The larynx, which lies between the laryngopharynx and trachea, serves as an organ of phonation and a valve to protect the lower airway from aspiration. The larynx is made up of muscles, ligaments, and cartilages, including the thyroid, cricoid, arytenoids, corniculates, and epiglottis. The flexible epiglottis, which originates from the hyoid bone and base of the tongue, covers the glottis during swallowing and provides protection from aspiration. During laryngoscopy, the

FIGURE 20-2  External airway anatomy. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

epiglottis is an important landmark for airway identification and laryngoscopic positioning. The vallecula is the space at the base of the tongue that is formed posteriorly by the epiglottis and anteriorly by the anterior pharyngeal wall. The laryngeal inlet is the opening to the larynx that is bounded by the epiglottis, aryepiglottic folds, and arytenoid cartilages. The glottis is the vocal apparatus, which is made up of the true and false vocal cords and the glottic opening, which is a triangular fissure between the vocal cords and the narrowest segment of the adult larynx. Externally identifiable landmarks are also important to airway assessment and management (Figure 20-2). The mentum is the anterior aspect of the mandible that forms the tip of the chin. The hyoid bone forms the base of the floor of the mouth. The thyroid cartilage forms the laryngeal prominence (i.e., the “Adam’s apple”) and the thyroid notch. The cricoid cartilage, which lies inferior to the thyroid cartilage, forms a complete ring that provides structural support to the lower airway. The cricothyroid membrane lies between the thyroid and cricoid cartilages and serves as an important site for surgical airway management. Knowledge of the anatomic differences between adults and infants is integral to effective pediatric airway management. These important differences are summarized in Table 20-1 and Figure 20-3.

TABLE 20-1  Anatomic Airway Differences Between Children and Adults Anatomy

Clinical Significance

Large intraoral tongue that occupies a relatively large portion of the oral cavity High tracheal opening: C1 in infancy as compared with C3 or C4 at the age of 7 years and C4 or C5 in adulthood Large occiput that may cause flexion of the airway; large tongue that easily collapses against the posterior pharynx

High anterior airway position of the glottic opening as compared with that of an adult Straight blade preferred over curved blade to push distensible anatomy out of the way to visualize the larynx Sniffing position is preferred; the large occiput actually elevates the head into the sniffing position in most infants and children; a towel may be required under the shoulders to elevate the torso relative to the head in small infants Uncuffed tubes provide an adequate seal, because they fit snugly at the level of the cricoid ring; correct tube size is essential, because variable expansion cuffed tubes are not used <2 yr old, high anterior 2-8 yr old, transition >8 yr old, small adult Blind nasotracheal intubation not indicated for children; nasotracheal intubation failure

Cricoid ring is the narrowest portion of the trachea as compared with the vocal cords in adults Consistent anatomic variations with age, with fewer abnormal variations related to body habitus, arthritis, or chronic disease Large tonsils and adenoids may bleed; more acute angle between the epiglottis and the laryngeal opening results in nasotracheal intubation attempt failures Small cricothyroid membrane

Needle cricothyroidotomy difficult and surgical cricothyroidotomy impossible in infants and small children

Modified from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.

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CHAPTER 20  Emergency Airway Management

Nasal cavity

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Tongue

Vocal cords

Epiglottis

Cricoid membrane Cricoid ring

Junction of chin and neck Infant

Vocal cords

Tongue

Cricoid membrane

Epiglottis

Cricoid ring Junction of chin and neck

Adult FIGURE 20-3  Anatomic airway differences between infants and adults. The anatomic differences particular to infants include the following:  (1) a higher and more anterior position for the glottic opening (note the relationship of the vocal cords to the chin–neck junction); (2) a relatively larger tongue in the infant that lies between the mouth and the glottic opening; (3) a relatively larger and more floppy epiglottis in the infant; (4) the cricoid ring is the narrowest portion of the pediatric airway; in adults, the narrowest portion is the vocal cords; (5) the position and size of the cricothyroid membrane in the infant; (6) the sharper and more difficult angle for blind nasotracheal intubation; and (7) the larger relative size of the occiput in the infant. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

Assessment of the Airway and Recognition of Airway Compromise Assessment of the airway begins with an evaluation of airway patency and respiratory function. The goal is to determine whether the airway is patent and protected and whether breathing is present and adequate. This is accomplished by inspection, auscultation, and palpation, which is commonly known as the “look, listen, and feel” approach. Visual signs of airway compromise include agitation, obtundation, and cyanosis. Blue, gray, or ashen skin—especially around the eyes, lips, and nail beds—is a worrisome finding. Significant airway compromise may manifest without cyanosis; examples include an allergic reaction with upper airway edema and vasodilation (causing flushed red skin) and unconsciousness as a result of carbon monoxide poisoning. Bradypnea, tachypnea, and irregular respirations may be signs of impending respiratory compromise. Breathing that is shallow, 394

deep, or labored may indicate respiratory insufficiency. Respiratory muscle fatigue may result in recruitment of the accessory muscles of respiration; this is clinically manifested as suprasternal, supraclavicular, or intercostal retractions. Traumatic injury to the chest (e.g., flail chest) or an aspirated foreign body may result in paradoxic or discordant chest wall movement. In children, visual signs of airway compromise and respiratory distress include tachypnea, cyanosis, drooling, nasal flaring, and intercostal retractions. A child with severe upper airway obstruction may sit upright with the head tilted back (i.e., “sniffing” position) to straighten the airway and reduce occlusion. A child with severe lower airway obstruction may sit up and lean forward on outstretched arms (i.e., “tripod” position) to augment accessory muscle function. Under most circumstances, hearing the victim speak with a normal voice suggests that the airway is adequate at that moment. Unusual sounds or noisy respirations may be present with partial airway obstruction. Snoring indicates partial airway obstruction at the pharyngeal level; gurgling may be heard with blood or secretions in the airway; stridor may be associated with partial airway obstruction at the level of the larynx (inspiratory stridor) or at the level of the trachea (expiratory stridor); hoarseness suggests a laryngeal process. The central face and mandible should be assessed for structural integrity, because injuries to these structures may lead to airway distortion and compromise. The anterior neck should be carefully inspected for penetrating wounds, asymmetry, or swelling that may herald impending airway compromise. The palpation of subcutaneous air suggests direct airway injury. In the unconscious victim, feel for air movement at the mouth and nose. Open the mouth to inspect the upper airway, taking care not to extend or rotate the neck. Identify and remove any vomitus, blood, or other foreign bodies. Look for swelling, bleeding, or other abnormalities of the oropharynx. The gentle use of a tongue blade may facilitate this task. The victim’s ability to spontaneously swallow and handle secretions is an important indicator of intact airway protective mechanisms. In the unconscious victim, absence of a gag reflex has traditionally been linked with loss of protective airway reflexes. Auscultation of the lung fields should demonstrate clear and equal breath sounds. Diminished breath sounds may result from a pneumothorax, hemothorax, or pleural effusion. Wheezing and dyspnea are often associated with lower airway obstruction.

Opening the Airway Opening the airway and ensuring airway patency are essential for adequate oxygenation and ventilation; these are the first priorities of airway management. The conscious victim uses protective reflexes and the musculature of the upper airway to maintain a patent airway and to protect against aspiration of foreign substances, gastric contents, or secretions. In the severely ill, compromised, or unconscious victim, these protective airway mechanisms may be impaired or absent. Upper airway obstruction in the unconscious victim most commonly results from posterior displacement of the tongue and the epiglottis at the level of the pharynx and the larynx. Head positioning, manual airway techniques, and mechanical airway adjuncts may be employed to alleviate upper airway obstruction.

HEAD POSITIONING If the mechanism of injury or physical examination raises concern for cervical spine injury, the head and neck should be stabilized in the neutral position. Care should be taken to not flex, extend, or rotate the victim’s head. After cervical spine immobilization, the airway should be reevaluated for obstruction. The optimal head position for airway alignment and patency varies with age. A supine infant’s large occiput contributes to flexion of the head and neck and resultant airway obstruction; this may be alleviated by elevating the shoulders with a small towel (Figure 20-4). In children, slightly extending the head into the sniffing position helps to relieve airway obstruction. In adults,

Infant

Small child

CHAPTER 20  Emergency Airway Management

A

Older child/adult

B FIGURE 20-4  A, The clinical determination of optimal airway alignment with the use of a line passing through the external auditory canal and anterior to the shoulder. B, The application of the line to determine the optimal position. In this small child, the occiput obviates the need for head support, yet the occiput is not so large as to require support of the shoulders. Note that the line traversing the external auditory canal passes anterior to the shoulders. With only slight extension of the head on the atlanto-occipital joint, the sniffing position is achieved. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

placing a folded towel or article of clothing under the occiput, which flexes the neck at the torso, followed by gentle hype­r­ extension of the head at the atlanto-occipital joint, provides for the optimal alignment of the airway axes.

MANUAL AIRWAY TECHNIQUES Manual airway techniques are effective but often require con­ tinuous involvement of a single provider to maintain airway patency.

FIGURE 20-5  Head tilt with chin lift. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

An alternative to piercing the patient’s lower lip is to pass a string through the safety pins and then secure the end of the string to the victim’s shirt button or jacket zipper (Figure 20-8), thereby exerting traction on the tongue.

MECHANICAL AIRWAY ADJUNCTS Several airway adjuncts are available to maintain airway patency while freeing up the health care provider to perform other duties. Oropharyngeal Airway The oropharyngeal airway (OPA) is an S-shaped device that is designed to hold the tongue away from the posterior pharyngeal wall (Figure 20-9). When the OPA is properly placed, it prevents the tongue from obstructing the glottis, and also provides an air

Head Tilt With Chin Lift The head tilt with chin lift (Figure 20-5) is a simple and effective technique for opening the airway. The palm of one hand is placed on the victim’s forehead and applies firm backward pressure to tilt the head back. Simultaneously, the fingers of the other hand are placed under the bony part of the chin and lifted to bring the chin forward. These fingers support the jaw and maintain the head-tilt position. This maneuver extends the neck and should not be used if cervical spine injury is a concern. Jaw Thrust With Head Tilt If a cervical spine injury is not suspected, the jaw thrust with head tilt maneuver may be used to gain additional forward displacement of the mandible. Position yourself at the top of the victim’s head, and then grasp the angles of the mandible with both hands and lift to displace the jaw forward while tilting the head back. Jaw Thrust Without Head Tilt If a cervical spine injury is suspected or cannot be excluded, the jaw thrust without head tilt (Figure 20-6) can be performed while maintaining neutral cervical spine alignment. With this maneuver, the jaw thrust is performed without extending or rotating the neck. Tongue Traction If the patient is unconscious or in extremis, the airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins (Figure 20-7).

FIGURE 20-6  Jaw thrust without head tilt. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

395

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 20-7  Tongue traction. The airway may be opened temporarily by attaching the anterior aspect of the victim’s tongue to the lower lip with two safety pins.

channel and suction conduit through the mouth. These devices are most effective for unconscious and semiconscious victims who lack a gag reflex or cough. Use of an OPA in a victim with a gag reflex or cough is contraindicated, because the OPA may stimulate retching, vomiting, or laryngospasm. OPAs are made of disposable plastic, and come in varying sizes to accommodate children and adults. The size is based on the distance in millimeters from the flange to the distal tip. The proper OPA size is estimated by placing the OPA’s flange at the corner of the mouth so that the bite-block segment is parallel with the victim’s hard palate; the distal tip of the airway should reach the angle of the jaw. Two types of OPAs are commonly employed. The Guedel makes use of a tubular design, whereas the Berman is distinguished by having airway channels on each side. Technique for insertion: 1. Open the mouth and clear the pharynx of any secretions, blood, or vomitus. Remove dentures or partial dental plates, if present. 2. In an adult or older child, insert the OPA upside down or at a 90-degree angle to avoid pushing the tongue posteriorly during insertion. Slide it gently along the roof of the mouth. As the OPA is inserted past the uvula or the crest

FIGURE 20-8  Tongue traction. An alternative to piercing the lower lip is to pass a string through the safety pins and then exert traction on the tongue by securing the end of the string to the victim’s shirt button or jacket zipper.

396

FIGURE 20-9  Oropharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

of the tongue, rotate it so that the tip points down the victim’s throat. 3. In a child, grasp the tongue and gently pull it forward or use a tongue blade to displace it inferiorly and anteriorly. Insert the OPA with the tip pointing toward the tongue and throat (i.e., the intended position after placement). 4. The OPA flange should rest against the victim’s lips, and the distal portion should rest on the posterior pharyngeal wall. If the OPA is too short, it may displace the tongue into the hypopharynx and occlude the airway. If the OPA is too long, it may displace the epiglottis and thereby cause an airway obstruction. Nasopharyngeal Airway The nasopharyngeal airway (NPA) is an uncuffed trumpet-like tube that provides a conduit for airflow between the nares and the pharynx (Figure 20-10). The NPA is inserted through the nose rather than the mouth, and it has a flange at the outer end to prevent displacement or slippage beyond the nostril. These devices are better tolerated than are OPAs, and they are commonly used with intoxicated or semiconscious victims. They are also effective when trauma, trismus (i.e., clenched teeth), or other obstacles (e.g., wiring of the teeth) preclude OPA placement. NPAs are contraindicated in victims with basilar skull or facial fractures, because inadvertent intracranial placement may occur.

FIGURE 20-10  Nasopharyngeal airway. (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

Technique for insertion: 1. Lubricate the nasopharyngeal airway with a water-soluble lubricant to minimize resistance in the nasal cavity. Do not use petroleum jelly or a non–water-based lubricant. 2. If the NPA has a beveled (angled) edge, place the airway in the nostril with the bevel directed toward the nasal septum. 3. Gently insert the NPA straight back along the floor of the nasal passage (i.e., perpendicular to the coronal plane of the face). 4. If resistance is met, rotate the tube slightly, reattempt insertion through the other nostril, or try a smaller-diameter tube. Do not force insertion of the tube, because injury to the nasal mucosa can result in bleeding. 5. After insertion, the NPA flange should rest on the victim’s nostril, and the distal portion of the airway should rest in the posterior pharynx, behind the tongue. Any flexible tube of appropriate diameter and length can be used as an improvisational substitute for the NPA. Examples include a Foley catheter, radiator hose, solar shower hose, siphon tubing, or an inflation hose from a kayak flotation bag or sport pouch. An endotracheal tube (ETT) can be shortened and then softened in warm water to substitute for a commercial nasal trumpet. The flange can be improvised with the use of a safety pin through the nostril end of the tube (Figure 20-11). Although OPAs and NPAs help to establish artificial airways, they do not provide definitive airway protection from aspiration.

RECOVERY POSITION In the spontaneously breathing unconscious victim who is not at risk for cervical spine injury, the recovery position (Figure 20-12) allows for airway patency while reducing the risk of aspiration. In the recovery position, the tongue is less likely to fall back and occlude the airway, and vomitus is more likely to be expelled than inhaled. Even a diminutive rescuer can place a large person in the recovery position if the proper technique is employed.

Foreign-Body Airway Obstruction Foreign bodies—most commonly a piece of meat—may cause partial or complete airway obstruction. A victim with partial airway obstruction can usually phonate or produce a forceful

FIGURE 20-11  Improvised nasal trumpet.

CHAPTER 20  Emergency Airway Management

NPAs made of soft and pliable rubber or plastic come in varying sizes to accommodate children and adults. Sizes (as indicated by internal diameter) range from 12 to 36 Fr. Proper NPA length is determined by measuring the distance from the tip of the patient’s nose to the tragus of the patient’s ear.

FIGURE 20-12  Recovery position.

cough in an attempt to expel the foreign body. When encountering a victim with a partially obstructed airway, if air exchange is adequate, do not interfere with the person’s attempts to clear the airway. Encourage forceful coughing, and closely monitor the victim’s condition. If the obstruction persists or if air exchange worsens or becomes inadequate, the victim should be managed as if a complete airway obstruction exists. Worrisome findings that should prompt immediate aggressive airway management include a weak or ineffective cough, increased respiratory difficulty, decreased air movement, and cyanosis. A person with a complete airway obstruction cannot speak (aphonia), exchange air, or cough. The person will often grasp the neck (i.e., the universal distress signal for choking) and open the mouth widely. The unconscious victim with complete airway obstruction will not demonstrate any typical chest movements or other signs of adequate air exchange. Individuals with complete airway obstruction from a foreign body require immediate medical attention. Failure to rapidly relieve the obstruction can lead to cardiac arrest. A complete summary of the treatment for complete airway obstruction caused by foreign bodies in adults and children is provided in Table 20-2.

Suction All sick or injured victims are at risk for airway obstruction and pulmonary aspiration, typically of gastric contents or blood. Lifesaving interventions, such as bag-mask ventilation (BMV), may increase this risk. Suction is essential for removal of vomitus, secretions, blood, and foreign bodies that may occlude the airway or increase the risk for pulmonary aspiration. Portable suction devices, which are available from a number of manufacturers, are ideal for the wilderness setting. These portable units should provide enough vacuum flow for adequate pharyngeal suction. Portable devices may be powered by oxygen, air, or electricity, or they may be manually powered (Figure 20-13, online). Hand-operated units are popular because they are lightweight, compact, reliable, and inexpensive. All units should have large-bore, nonkinking suction tubing, an unbreakable collection container, and a sterile disposable suction catheter. Flexible (i.e., “French”) suction catheters are used to suction the nose, mouth, and oropharynx, whereas rigid suction catheters are used to suction the mouth and the oropharynx. These suction catheters should not be inserted beyond the base of the tongue. Adults should not be suctioned for more than 10 to 15 sec to prevent oxygen deprivation; children should be suctioned for less time. Care should be taken when using rigid suction catheters in children, because stimulation of the oropharynx may 397

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 20-2  Relief of Choking Adults and Children >1 Year Old

Children <1 Year Old

Signs

Rescuer Actions

Signs

Rescuer Actions

Mild airway obstruction

Good air exchange Responsive and can cough forcefully May wheeze between coughs

Good air exchange Responsive and can cough forcefully May wheeze between coughs

1. Do not interfere with the victim’s own attempts to expel the foreign body, but stay with the victim and monitor his or her condition. 2. If mild airway obstruction persists, activate EMS.

Severe airway obstruction

Poor or no air exchange Weak and ineffective cough or no cough at all High-pitched noise when inhaling or no noise at all Increased respiratory difficulty Possible cyanosis (turning blue) Unable to speak Clutching neck with thumb and fingers (universal choking sign) Unable to move air

1. As long as good air exchange continues, encourage the victim to continue spontaneous coughing and breathing efforts. 2. Do not interfere with the victim’s own attempts to expel the foreign body, but stay with the victim and monitor his or her condition. 3. If mild airway obstruction persists, activate EMS. 1. Ask the victim if he or she is choking. If the victim nods yes and cannot talk, severe airway obstruction is present, and you must activate EMS. 2. Perform abdominal thrusts (Heimlich maneuver). It may be necessary to repeat the thrusts several times to clear the airway. 3. Repeat until the object is expelled from the airway or the victim becomes unresponsive. 4. If the patient is pregnant or obese, perform chest thrusts instead.

Poor or no air exchange Weak and ineffective cough or no cough at all High-pitched noise when inhaling or no noise at all Increased respiratory difficulty Possible cyanosis (turning blue) Unable to cry Unable to move air

Choking in the unresponsive victim

Choking victims may be initially responsive and then become unresponsive. In this circumstance, you know that the choking has caused the victim’s symptoms.

Adults 1. Activate EMS. 2. Open the airway. 3. Remove the object if you see it. Children from 1 year old to puberty 1. Open the airway. 2. Remove the object if you see it. 3. Begin CPR. 4. After 2 min (or five cycles) of CPR, activate EMS.

Choking infants may be initially responsive and then become unresponsive. In this circumstance, you know that the choking has caused the victim’s symptoms.

1. If the victim cannot make any sounds or breathe, severe airway obstruction is present, and you must activate EMS. 2. Deliver five forceful back slaps between the victim’s shoulder blades with the use of the heel of your hand. 3. If the airway remains obstructed, perform five quick downward chest thrusts just below the nipple line at a rate of one per second. 4. Repeat the back slaps and chest thrusts until the object is removed or the victim becomes unresponsive. 1. Place the infant onto a flat surface. 2. Open the airway. 3. Remove the object if you see it. 4. Do not perform blind finger sweeps, because the foreign body may be pushed back into the airway, thus causing further obstruction or injury. 5. Begin CPR. 6. Each time you open the airway, look for the object, and remove it if you see it. 7. After 2 min (or five cycles) of CPR, activate EMS.

Modified from the American Heart Association: BLS for healthcare providers, Dallas, 2006, American Heart Association. CPR, Cardiopulmonary resuscitation; EMS, emergency medical services.

cause bradycardia. A bulb syringe may be used to suction the nose and mouth of infants up to 4 months old because they are obligate nose breathers. If time permits and supplies are available, a “mucus trap” suction device can be improvised from a jar with two holes poked in its lid and two tubes or straws duct taped into the holes (Figure 20-14). One straw goes to the rescuer, who provides suction, and the other is directed toward whatever has accumulated in the airway. The jar serves to trap the removed secretions, thereby preventing the rescuer from suctioning 398

bodily fluids or foreign substances (e.g., mud) directly into his or her mouth. In the absence of suction or in the presence of large pieces of foreign material, visible debris can be swept from the mouth of an unconscious victim with the use of a finger that is gloved or wrapped in cloth. When using this “finger-sweep” technique with infants and children, be sure to use your little finger. Never attempt to blindly sweep the mouth if you do not see debris. In addition, do not probe the mouth of a conscious victim, because this may precipitate gagging, vomiting, and aspiration. Victims

Tubing

Jar

FIGURE 20-14  Improvised mucus trap suction device.

without risk for cervical spine injury may be placed in the recovery position (i.e., with the head turned to the side) to facilitate clearing the mouth.

Supplemental Oxygen Supplemental oxygen therapy should be provided to all sick or injured people with cardiac disease, respiratory distress, shock, or trauma, even if their measured arterial oxygen tension is normal. Start with a high oxygen concentration and then titrate downward to maintain adequate oxygenation. Although oxygen should never be withheld from a hypoxic patient with respiratory distress, care should be exercised when administering oxygen to patients with chronic hypercarbia (e.g., patients with chronic obstructive pulmonary disease). Unmonitored treatment of such patients with high oxygen concentrations can result in respiratory depression from diminished hypoxic ventilatory drive. A variety of oxygen delivery techniques may be employed, depending on the desired oxygen concentration and clinical circumstances (see Chapter 76).

Ventilation Even with an open airway and supplemental oxygen, a person who is not adequately ventilating cannot conduct sufficient gas exchange. Adequate ventilation implies the inhalation of enough air to deliver oxygen to the alveoli and exhalation of enough air to facilitate the removal of carbon dioxide. The sequence of interventions for the inadequately ventilating victim is opening the airway and then providing positive-pressure ventilation (i.e., via mouth-to-mouth, mouth-to-nose, mouth-to-mask, or BMV). It is advisable to use barrier protection (e.g., a face shield) when performing mouth-to-mouth or mouth-to-nose ventilation. Face shields are clear plastic or silicone sheets that feature a centrally located one-way valve. They are placed over a victim’s face to allow rescue breathing while preventing direct contact with the victim. Face shields are compact, flexible, portable, and manufactured by a number of companies.

RESCUE BREATHING Rescue breathing techniques that make use of exhaled air from the rescuer will deliver approximately 16% to 17% inspired oxygen concentration to the victim, ideally producing an alveolar oxygen tension of 80 mm Hg. Mouth-to-Mouth Ventilation Mouth-to-mouth ventilation is an efficient approach to assisting ventilation. Failure to use a barrier device during mouth-to-mouth ventilation places the rescuer at risk for exposure to infectious bodily fluids. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected.

Mouth-to-Nose Ventilation Some people have conditions (e.g., injuries to the mouth or mandible, missing teeth or dentures) that make mouth-to-mouth ventilation ineffective. Under such circumstances, mouth-to-nose ventilation should be considered. The mouth-to-nose technique is similar to mouth-to-mouth ventilation, with a few specific differences. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected. 2. The victim’s nose is left open. 3. Maintain the head tilt with the heel of one hand placed on the victim’s forehead. 4. Support the victim’s chin with the other hand while sealing the victim’s lips (i.e., closing the mouth) with the thumb and forefinger. 5. Take a deep breath. 6. Place your mouth around the victim’s, nose and make a tight seal with your lips against the victim’s face. 7. Exhale slowly into the victim’s nose until you see the victim’s chest rise and feel resistance to the flow of your breath. 8. Break contact with the victim’s nose, and open the victim’s mouth to allow passive exhalation. Mouth-to-Mask Ventilation Mouth-to-mask ventilation is the safest and most effective technique for rescue breathing (Figure 20-15). The pocket face mask or a similar barrier device allows the rescuer to provide ventilation without making direct contact with the victim’s mouth and nose. The mask has a one-way valve in the stem to prevent exhaled gases and bodily fluids from reaching the health care provider. In addition, a disposable high-efficiency particulate air filter may be inserted into the pocket mask to trap infectious air droplets and secretions. The pocket face mask is made of a soft plastic material and can be folded and carried in a pocket. Some masks are available with an oxygen inlet to allow for supplemental oxygen administration. These devices are available in a number of sizes. Technique: 1. Open the airway using the head tilt with chin lift approach if cervical spine trauma is not suspected. 2. Connect the one-way valve to the mask. 3. If available, connect oxygen tubing to the inlet port, and set the flow rate at 15 L/min. 4. Position yourself at the head of the victim. 5. Clear the victim’s airway of vomitus, secretions, and foreign bodies, if necessary. 6. Insert an oral or nasopharyngeal airway. 7. Place the mask on the victim’s face. 8. Apply pressure to both sides of the mask with the thumb side of the palms to create an airtight seal. Apply upward pressure to the mandible (i.e., jaw thrust) using the index, middle, and ring fingers of both hands while maintaining a head tilt. 9. Take a deep breath and exhale into the port of the one-way valve, and observe for chest rise. 10. Allow the victim to passively exhale between breaths. 399

CHAPTER 20  Emergency Airway Management

Duct tape

2. If needed, clear the airway of vomitus, secretions, and foreign bodies. 3. Pinch the victim’s nostrils closed with the finger and thumb of one hand; the heel of that same hand may be placed on the forehead to maintain the head tilt. 4. Support the victim’s chin with the other hand, and hold the victim’s mouth slightly open. 5. Take a deep breath. 6. Place your mouth around the victim’s mouth, which should be open, and make a tight seal with your lips against the victim’s face. 7. Exhale slowly into the victim’s mouth until you see the victim’s chest rise and feel resistance to the flow of your breath. 8. Break contact with the victim’s mouth to allow passive exhalation.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

transferred by BMV is a clinical estimate that is based on patient weight.

Definitive Airway Management The presence of a definitive airway implies patency and protection. Provision of a definitive airway requires a tube in the trachea with the cuff inflated, secured in place, and attached to an oxygen-rich ventilation device. Whether in the wilderness or at the hospital, inability or failure to secure a timely and definitive airway can lead to disastrous or fatal consequences for the victim. Approaches to definitive airway management include immediate oral endotracheal intubation, awake oral intubation, rapid sequence oral intubation, nasotracheal intubation, and surgical airways (e.g., cricothyrotomy). Although the ultimate decision to endotracheally intubate a patient can be complicated and may depend on a variety of clinical factors, several clinical situations mandate definitive airway management: (1) failure of ventilation or oxygenation; (2) the patient’s inability to maintain or protect the airway; (3) the potential for deterioration on the basis of the patient’s clinical presentation; and (4) patient safety and protection. FIGURE 20-15  Rescuer using mouth-to-mask ventilation. The rescuer is providing rescue breathing with a face mask and supplemental oxygen during cardiopulmonary resuscitation. The rescuer is using the cephalic technique (i.e., the rescuer is positioned at the top of the victim’s head). Both of the rescuer’s hands are used to hold the mask securely in position while keeping the victim’s airway open. The rescuer’s thumbs and forefingers hold the mask in place while the third, fourth, and fifth fingers of each hand lift the jaw (i.e., jaw thrust) and maintain an open airway with the head tilted. Alternatively, the thumbs and a portion of the rescuer’s palms can anchor the mask, and the index and remaining fingers can lift the jaw and hold it against the mask. (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resus­citation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)

BAG-MASK VENTILATION The self-inflating ventilation bag with face mask (i.e., the BMV device) provides a means for emergency ventilation with high concentrations of oxygen. The device is equipped with several valves that allow coordinated airflow into and out of the victim. This includes a one-way valve that prevents exhaled air from reentering the victim’s lungs (Figure 20-16). When it is attached to a high-flow oxygen source (15 L/min), the BMV device can supply an oxygen concentration of nearly 100%. The adapter of the face mask is interchangeable with an ETT, so the same bag can be used after intubation. Competence with a BMV device is a vital emergency skill and prerequisite to the use of paralytic agents for endotracheal intubation. When using the single-hand mask hold technique, substantial proficiency is required to use only one hand to maintain an adequate mask seal, to position the victim’s head, and to ensure airway patency while using the other hand to ventilate with the proper tidal volume, neither underventilating or hyperventilating the patient. Although the mastery of solo BMV technique is imperative, recruitment of another individual allows one person to perform a jaw thrust and to ensure a good mask seal with both hands while the second individual squeezes the bag. Successful BMV depends on an adequate mask seal and a patent airway. Placement of an oral airway should always be considered before BMV. Slow and gentle ventilation minimizes the risk for gastric inflation and subsequent regurgitation. The efficacy of BMV can be determined by watching the chest rise and fall, feeling resistance in the bag, and monitoring the victim’s oxygen saturation. Smaller BMV devices are employed for infants and children to prevent overinflation and subsequent barotrauma. In the absence of a BMV device that precisely regulates the volume of air transferred by the device, the amount of air 400

A

B FIGURE 20-16  Detailed view of a bag-mask ventilation device. A, The rescuer provides ventilation with a bag and mask attached to an oxygen supply. The rescuer is using the E-C technique to hold the mask to the face by creating a “C” with the thumb and forefinger while lifting the jaw along the bony portion of the mandible with the last three fingers of the same hand; these fingers make the “E.” The second hand squeezes the bag while the rescuer watches the victim’s chest to ensure that the chest rises with each ventilation. The rescuer is keeping the victim’s airway open with both a head tilt and a jaw thrust.  B, Details of a bag-mask ventilation system with supplemental oxygen. The system consists of a self-refilling bag with an oxygen inlet; either a no pop-off valve or a pop-off valve (as shown) that can be disabled during resuscitation to ensure the delivery of adequate tidal volumes despite high pressures; and standard fittings (in this case, the bag is joined with a standard fitting to a mask). This system is capable of delivering high concentrations of oxygen, because it contains an oxygen reservoir. If additional gas is required during ventilation, it is drawn from the oxygen reservoir rather than from room air so that a high concentration of oxygen can be delivered during ventilation. (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)

Intubation

Time

Action

Zero minus 10 min Zero minus 5 min Zero minus 3 min —Time zero— Zero plus 20-30 sec Zero plus 45 sec Zero plus 45 sec Zero plus 1 min

Preparation Preoxygenation Pretreatment Paralysis with induction Protection and positioning Placement Proof Postintubation management

IMMEDIATE ORAL INTUBATION (CRASH INTUBATION) Individuals who present with respiratory arrest, agonal respirations, or deep unresponsiveness require immediate oral intu­ bation without the use of paralytic or sedative medications. Advantages of crash intubation are technical ease and rapidity. Disadvantages include the potential for increasing intracranial pressure from the stress of intubation and inducing vomiting and subsequent aspiration.

AWAKE ORAL INTUBATION Awake oral intubation is an approach that makes use of titrated intravenous sedation and liberal topical airway anesthesia before inspection of or intubation of an awake victim’s airway. This approach conveniently allows for preservation of the victim’s protective airway reflexes and spontaneous respirations while the laryngoscopist takes a gentle “awake” look at the glottis, vocal cords, and internal airway anatomy. The decision to intubate the victim immediately or to perform a controlled rapid sequence oral intubation depends on the potential for progression of airway difficulty or compromise. During the “awake” look, the clinician might elect to intubate a victim with an airway burn or anaphylaxis with progressive airway swelling, because that moment may be the most opportune time for airway management.

is limited, a patient may take eight vital capacity (i.e., largest possible) breaths in rapid succession from a 100% oxygen source to quickly preoxygenate. The time to desaturation after preoxygenation is determined by the duration of preoxygenation as well as by the type of victim. Young children, pregnant women, and obese adults tend to desaturate more rapidly than do normalsized adults. Pretreatment During RSI, the act of laryngoscopy as well as use of succinylcholine, which is a depolarizing neuromuscular blocking agent, can lead to a number of adverse effects, such as bronchospasm in patients with reactive airway disease, increased intracranial pressure, increased intraocular pressure, increased intragastric pressure, increased sympathetic discharge, and bradycardia (especially in children). Certain pretreatment medications may be administered before laryngoscopy to mitigate these adverse effects. These medications and their indications, mechanisms of actions, and doses are summarized in Table 20-5. Paralysis with Induction The next step in RSI is rapid intravenous administration of an induction agent to produce a complete loss of consciousness, which is followed immediately by administration of a neuro­ muscular blocking agent (NMBA) to induce complete motor paralysis. Induction agents.  All patients, with few exceptions, should receive an induction agent before neuromuscular blockade. Paralyzing a patient without providing adequate sedation can lead to detrimental physiologic and undesirable psychological sequelae. In addition induction agents that are administered in combination with NMBAs enhance muscle relaxation, thereby creating optimal intubating conditions.

TABLE 20-4  SOAP ME Mnemonic Suction Oxygen

RAPID SEQUENCE ORAL INTUBATION Rapid sequence intubation (RSI) is a coordinated series of procedures that allows for the rapid intubation of a victim without interposed BMV. Because victims who require emergent intubation may not have fasted, BMV can inadvertently lead to gastric distention, regurgitation, and aspiration. To perform RSI, the victim is first preoxygenated to allow for a period of apnea without interposed assisted ventilation. Sequential administration of an induction agent and a rapidly acting neuromuscular blocking agent induces a state of unconsciousness and paralysis, respectively. This allows the victim to be intubated without the need for BMV. The steps that make up RSI can be thought of as “the eight P’s” (Table 20-3).

Airway equipment

Preparation Before RSI, careful preparation is essential to achieve success. The mnemonic SOAP ME summarizes the necessary preparatory steps and essential equipment (Table 20-4). Preoxygenation During RSI, the process of direct laryngoscopy and ETT placement precludes oxygen delivery to the paralyzed apneic victim. This could potentially lead to rapid arterial oxygen desaturation (i.e., <90%). However, by preoxygenating the victim, an oxygen reservoir is established within the patient’s lungs and body tissues to allow for prolonged apnea without detrimental arterial oxygen desaturation. Preoxygenation effectively leads to “nitrogen washout” or replacement of any room air (i.e., about 80% nitrogen and 20% oxygen) within the lungs with near-100% oxygen. Administering 100% oxygen to a patient for 5 minutes before paralysis typically provides adequate preoxygenation. When time

Pharmacy

Monitoring Equipment

Suction should be tested and readily available at the bedside. A high-flow oxygen mask and a bag-valve ventilation device should be ready for use. At least two functioning laryngoscope handles and the appropriately sized and shaped laryngoscope blades should be obtained. The anticipated blade of choice should be clicked into position to ensure that the light functions properly. An endotracheal tube (ETT) should be chosen on the basis of the patient’s anatomy, and one of a smaller size should be prepared as well. The average adult male will require a 7.5- or 8.0-mm ETT, and the average adult female will need a size 7.0 or 7.5 mm. In children, the ETT size in mm may be estimated by the formula 4 + (age in years/4). The ETT cuff should be inflated to test for an air leak. A stylet should be inserted within the ETT to shape it into a configuration that will facilitate insertion into the airway. Care must be taken to ensure that the tip of the stylet does not protrude from the end of the ETT or through the small distal side port (i.e., Murphy’s eye). The patient should have at least one intravenous line placed, and patency of the line should be verified. The specific rapid sequence intubation medications, proper dosing, and sequence of administration should be determined, and the agents should be drawn up and labeled. Cardiac monitoring, blood pressure monitoring, and pulse oximetry are mandatory for all patients. If available, an end-tidal carbon dioxide monitor should be readied as well. In a wilderness setting, many of these hospitalbased amenities may not be available.

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CHAPTER 20  Emergency Airway Management

TABLE 20-3  The Eight P’s of Rapid Sequence

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 20-5  Pretreatment Medications Adult Dose (Intravenous)

Pediatric Dose (Intravenous)

Decreases intracranial response to intubation; mitigates bronchospasm with RAD Blunts sympathetic response to laryngoscopy

1.5 mg/kg

1.5 mg/kg

3-6 mcg/kg

1-3 mcg/kg

Mitigates bradycardic response to SCh

2.0 mg

0.02 mg/kg (minimum dose, 0.1 mg)

Drug

Indication

Mechanism

Lidocaine

Increased ICP and RAD

Opioid (fentanyl)

Increased ICP, ischemic heart disease, and aortic dissection Children <10 yr old; adults receiving a second dose of SCh

Atropine

Notes

Use with caution in young children

From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. ICP, Intracranial pressure; RAD, reactive airways disease; SCh, succinylcholine.

TABLE 20-6  Clinical Characteristics of Induction Agents Induction Agent

Induction Dose (Intravenous)

Onset of Action

Duration of Action

Methohexital

1-3 mg/kg

<30 sec

5-10 min

Midazolam

0.2-0.3 mg/kg

30-60 sec

15-30 min

Etomidate

0.3 mg/kg

15-45 sec

3-12 min

Ketamine

1-2 mg/kg

45-60 sec

10-20 min

Benefits

Precautions

Decreased ICP Short duration Reversible Amnestic Anticonvulsant Decreased ICP Rarely decreased BP

Decreased BP Laryngospasm, seizures Apnea No analgesia Variable dosing Myoclonic jerks Vomiting No analgesia Increased secretions Increased ICP Emergence phenomenon

Increased BP Bronchodilator Dissociative amnesia

From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. BP, Blood pressure; ICP, intracranial pressure.

There is no single induction agent of choice for RSI in the field or emergency department. The choice of an induction agent is based on the clinical circumstances and the agent’s attributes. The clinical characteristics of the most commonly used induction agents are summarized in Table 20-6. Neuromuscular blockade.  NMBAs are used to completely paralyze the patient to facilitate rapid endotracheal intubation. These agents do not provide analgesia, sedation, or amnesia. The ideal NMBA should have rapid onset action, short duration of action, and few adverse side effects. Succinylcholine (SCh), a depolarizing NMBA, comes closest to fulfilling these traits, and it is the most commonly used NMBA. At the neuromuscular junction, SCh binds tightly to acetylcholine receptors, causing depolarization of the motor endplate and the ensuing muscle contraction. Clinically this manifests as muscle fasciculations followed by complete paralysis. Intravenous administration of SCh results in muscle fasciculations in 10 to 15 seconds, and this is followed by complete paralysis after 45 to 60 seconds. Because of the short duration of action, patients may begin spontaneous breathing within 3 to 5 minutes. The dose of SCh is 1.5 mg/kg given via rapid intravenous push in adults; 2 mg/kg via rapid intravenous push in children less than 10 years old; and 3 mg/kg via rapid intravenous push in newborns. An insufficient dose of SCh can lead to inadequate paralysis and can adversely affect laryngoscopy and intubation. The main disadvantages of using SCh are its side effects, which include muscle fasciculations, bradycardia, hyperkalemia, prolonged neuromuscular blockade, malignant hyperthermia, and trismus (i.e., masseter muscle spasm). 402

Nondepolarizing NMBAs (e.g., rocuronium) cause paralysis by competing with acetylcholine for receptors at the neuromuscular junction. Although these agents are most commonly used for postintubation patient paralysis, they may also be used as the primary RSI paralytic agent for specific patient populations or for patients who have a contraindication to SCh. Although they possess fewer side effects than SCh, these agents are generally less effective for intubation because of their delayed time to paralysis, prolonged duration of action, or both. Specific attributes of both depolarizing and nondepolarizing NMBAs are listed in Table 20-7.

TABLE 20-7  Neuromuscular Blocking Agents Neuromuscular Blocking Agent Depolarizing Succinylcholine

Intubating Dose (Intravenous) 1.5 mg/kg (adult) 2 mg/kg (child) 3 mg/kg (infant)

Nondepolarizing Rocuronium 1.0 mg/kg Vecuronium 0.15 mg/kg Pancuronium 0.1 mg/kg

Onset

Duration

45-60 sec

6-12 min

50-70 sec 90-120 sec 100-150 sec

30-60 min 60-75 min 120-150 min

From Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press.

PA LA

FIGURE 20-17  Cricoid pressure (Sellick’s maneuver). (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department. Cambridge, UK, 2005, Cambridge University Press. Courtesy Chris Gralapp. http://www.biolumina.com.)

FIGURE 20-19  Head elevated on pad, neutral position. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

Positioning

Protection After sequential administration of the induction and paralytic agents, the patient will predictably lose consciousness and become apneic. Application of Sellick’s maneuver (i.e., approximately 10 lb of manual pressure to the cricoid cartilage) just as the patient is noted to lose consciousness will compress the esophagus, thereby preventing aspiration and passive regurgitation of gastric contents (Figure 20-17). Sellick’s maneuver should be maintained until the ETT has been inserted into the trachea, its position verified, and the cuff inflated. If Sellick’s maneuver is applied too early, the patient may find it uncomfortable or vomit. If the patient begins actively vomiting, Sellick’s maneuver should be discontinued, and the patient should be logrolled and suctioned. Cricoid pressure should also be applied when the victim requires positive-pressure ventilation before, during, or after intubation attempts. Positive-pressure ventilation, whether from rescue breathing or a BMV device, may lead to gastric distention, compromised diaphragmatic excursion, and an increased risk for emesis or gastric rupture. By employing Sellick’s maneuver during positive-pressure ventilation, air will be directed to the lungs rather than the stomach, thus avoiding these complications.

OA

The airway may be thought of as having three separate axes: oral, pharyngeal, and laryngeal. Proper positioning of the head before laryngoscopy can help to align these three axes, thereby improving visualization of the glottis and greatly increasing the likelihood of a successful intubation. In the neutral position, these axes are misaligned (Figure 20-18). Placing a small pillow or a similar-sized object under an adult’s occiput flexes the lower cervical spine relative to the torso and aligns the pharyngeal and laryngeal axes (Figure 20-19). Positioning the patient in the sniffing position with the extension of the head on the neck aligns all three axes (Figure 20-20). Patients with potential cervical spine injury should be maintained in the neutral position. Placement During RSI, administration of a paralytic agent will predictably lead to paralysis and apnea. With adequate preoxygenation, arterial oxygen saturations remain normal despite this apnea. Complete muscular paralysis can be confirmed by gently grasping the patient’s jaw and checking for flaccidity. Wait until the patient is completely relaxed before proceeding with intubation. With the laryngoscope in the left hand, gently open the mouth with the right hand. Insert the laryngoscope into the right side

OA PA

PA LA

LA FIGURE 20-18  Head on a bed, neutral position. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

FIGURE 20-20  Head elevated on a pad, head extended on neck. LA, Laryngeal axis; OA, oral axis; PA, pharyngeal axis. (Redrawn from Walls RM, Murphy MF, Luten RC, et al, editors: Manual of emergency airway management, ed 2, Philadelphia, 2004, Lippincott Williams & Wilkins.)

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CHAPTER 20  Emergency Airway Management

OA

PART 4  INJURIES AND MEDICAL INTERVENTIONS

of the patient’s mouth, and then sweep the tongue to the left. The curved (Macintosh) blade is slid into the vallecula; the straight (Miller) blade is positioned below the epiglottis. The handle is pushed along the axis of the handle at a 45-degree angle to the patient’s body. Care should be taken not to “crowbar” with the laryngoscope, because this may injure the patient’s teeth. If the glottic aperture is not readily visible, the intubator or an assistant may elect to perform the BURP maneuver: this involves placement of the right hand on the thyroid cartilage and is followed by application of backward, upward, rightward pressure to help to bring the glottis into view (Figure 20-21). The resulting displacement of the thyroid cartilage backward against the cervical vertebrae, upward or as superiorly as possible and laterally to the right, has been found to significantly improve the view of the glottis during laryngoscopy. When the glottis is clearly visible, use the right hand to gently insert the ETT until the cuff is about 2 to 3 cm past the vocal cords. For adult males, the 23-cm marker of the ETT should be located at the corner of the mouth; this should be 21 cm for adult women. When the ETT is in place, remove the stylet and inflate the cuff. An air leak should not be audible with a BMV. If the patient is adequately preoxygenated, the laryngoscopist may make multiple attempts at intubation before arterial oxygen desaturation occurs. If available, a dedicated team member should focus on the patient’s cardiac rhythm, blood pressure, and oxygen saturation, and he or she should alert the intubator to any abnormalities. After any unsuccessful intubation attempt, recheck the patient’s position, and make any necessary adjustments. It is important to “change something” (e.g., the size or type of laryngoscope blade) before taking a second look to ensure that the same mistake or problem is not encountered again. Proof (Confirmation of Endotracheal Tube Placement) Proper ETT positioning within the trachea needs to be confirmed after every intubation. Failure to recognize an inadvertent esophageal intubation can be disastrous for both the patient and physician. Sellick’s maneuver should not be released until after confirmation of correct ETT placement. Methods that are used to detect ETT placement include clinical assessment, pulse oximetry, end-tidal carbon dioxide (ETCO2)

FIGURE 20-21  The BURP maneuver (backward, upward, rightward pressure). (Redrawn from Mahadevan SV, Garmel GM, editors: An introduction to clinical emergency medicine: Guide for practitioners in the emergency department, Cambridge, UK, 2005, Cambridge University Press. Copyright Chris Gralapp. http://www.biolumina.com.)

404

detection, and aspiration techniques. Chest radiography assesses ETT position but does not confirm ETT placement within the trachea. Clinical Assessment Classic clinical observations that are used to confirm correct ETT placement include the following: (1) seeing the ETT passing through the vocal cords during intubation; (2) auscultation of clear and equal breath sounds over both lung fields; (3) absence of breath sounds when auscultating over the stomach; (4) observation of symmetric chest rise during ventilation; and (5) observation of “fogging” of the ETT during ventilation. All of these clinical findings are subject to failure and should not serve as the sole means for confirming ETT placement. Pulse Oximetry A drop in oxygen saturation after intubation should raise concern for an esophageal intubation; however, this drop may be delayed for several minutes if the patient was adequately preoxygenated. For certain patients (e.g., those with hypotension), oxygen saturation measurement may be unreliable or difficult to detect. Although pulse oximetry is important to assess after endotracheal intubation, it should not be the primary indicator of successful ETT placement. End-Tidal Carbon Dioxide Detection Detection of exhaled carbon dioxide is a highly reliable method for identifying proper placement of the ETT within the trachea. A colorimetric ETCO2 detector is a small disposable device that connects between the bag and the ETT. When this device detects ETCO2, its colorimetric indicator changes from purple to yellow; absence of this color change for six manual ventilations indicates that the tube is incorrectly placed in the esophagus. A falsepositive color change may occur if the tube is placed just above the glottis. A false-negative color change may occur (even with correct ETT placement) in some cases of cardiac arrest and profound circulatory collapse as carbon dioxide production and delivery to the lungs abruptly decline. Aspiration Devices Aspiration appliances (e.g., bulb and syringe aspiration devices) may also be used for confirmation of ETT placement. The bulb aspiration device is a round and compressible plastic globe (i.e., “turkey baster”) that is first compressed and deflated and then placed within the ETT and released. If the bulb reexpands rapidly, the ETT is likely in the trachea, whereas failure to reexpand or delayed reexpansion suggests that the ETT is in the esophagus. Syringe aspiration devices are large syringes (usually 30  mL [1  oz]) that are inserted into the ETT. The syringe plunger is then drawn back rapidly to allow for brisk aspiration of a large amount of air. The rapid and easy flow of air suggests tracheal intubation, whereas resistance suggests esophageal intubation. Postintubation Management After verification of correct ETT placement within the trachea, the tube should be secured (i.e., taped or tied) to prevent movement or migration. The patient’s blood pressure and other vital signs should be repeated. Bradycardia after intubation is worrisome for hypoxia and should prompt exclusion of an esophageal intubation. Hypertension after intubation suggests inadequate sedation. Hypotension after intubation may result from a tension pneumothorax, decreased venous return, the induction agent, or a cardiac cause. After intubation, consideration should be given to long-term sedation, analgesia, and paralysis. A benzodiazepine such as midazolam (0.1 to 0.2 mg/kg), diazepam (0.2 mg/kg), or lorazepam (0.05 to 0.1 mg/kg) may be given initially for sedation and repeated for any signs of awareness. An opioid agent such as fentanyl (3 to 5 mcg/kg) or morphine sulfate (0.1 mg/kg) may also be administered for additional patient comfort. Nondepolarizing NMBAs such as pancuronium (0.1 mg/kg) or vecuronium (0.1 mg/kg) may be used for long-term paralysis; a repeat dose that is one-third of the initial dose may be given after 45 to 60 minutes if any motor activity is detected.

There are certain clinical circumstances, such as the spontaneously breathing patient who presents with a difficult airway, in which RSI may not be advisable. In the patient with anatomic features that may pose a challenge to RSI and BMV, awake nasotracheal intubation (NTI) may provide a better alternative, because it can be performed while preserving the patient’s spontaneous respirations. Technique: 1. Prepare the mucosa to facilitate tube passage and to minimize the risk for epistaxis. Instill 2 to 3 drops of a topical vasoconstrictor agent such as phenylephrine hydrochloride (0.25%) or oxymetazoline (0.05%) in each naris. Anesthetize the nasal mucosa using a 4% cocaine pack or 2% lidocaine jelly. 2. Select a cuffed ETT that is sized 0.5 to 1.0 mm smaller than would be used for orotracheal intubation. The tube should be lubricated with a water-soluble lubricant to facilitate passage. 3. The patient may be seated or reclined while the clinician stands to the side of the patient. 4. The tube is inserted into the more patent of the two nares. The right side is preferable because the tube bevel will face the septum, thus avoiding Kiesselbach’s plexus. If going through the left nares, consider inserting the tube “upside down” and then rotating it so that the curve follows the posterior nasopharynx when the turbinates are passed. 5. Direct the tube straight back along the nasal floor toward the occiput, and rotate it 15 to 30 degrees with advancement. When the tube nears the glottis, listen for airflow within the tube with each breath. 6. When maximal airflow is heard, quickly and gently advance the tube. A cough will likely be heard with passage of the tube into the trachea. The tube should be advanced to 32 cm at the nares in the adult male and to 27 to 28 cm in the adult female. 7. Confirm the tube’s position with an ETCO2 detection device. Because the tube is placed blindly, it may also be misdirected into the esophagus, the piriform sinus, or the vallecula, although this is rare. When this occurs, withdraw the tube slightly, redirect it, and retry the procedure. If the tube FIGURE 20-22  Laryngeal mask airway (LMA). A, The LMA is an adjunctive airway that consists of a tube with a cuffed mask-like projection at the distal end. B, The LMA is introduced through the mouth into pharynx.  C, When the LMA is in position, a clear and secure airway is present. D, During insertion, the LMA is advanced until resistance is felt as the distal portion of tube locates in the hypopharynx. The cuff is then inflated. This seals the larynx and leaves the distal opening of the tube just above the glottis to provide a clear and secure airway (dotted line). (Redrawn from American Heart Association, International Liaison Committee on Resuscitation: Guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. Part 6: Advanced cardiovascular life support. Section 3: Adjuncts for oxygenation, ventilation and airway control, Circulation 102:I95, 2000.)

becomes caught on the vocal cords, rotate the tube slightly to realign the bevel with the cords. Occasionally, externally manipulating the larynx posteriorly or laterally with one’s nondominant hand will facilitate successful passage. NTI is absolutely contraindicated in the apneic patient, because air movement is essential to placement of the ETT. NTI is also contraindicated in patients with the possibility of cribriform plate injury, basilar skull fracture, or midface fracture out of concern that the tube may enter the cranial vault. Patients with bleeding disorders or coagulopathy may develop massive epistaxis from NTI. Other contraindications include combativeness; increased intracranial pressure; neck hematoma; upper airway obstruction or anatomic alteration from trauma, edema, or infection; and the need for immediate airway management. Blind nasotracheal intubation is not generally recommended for patients with neck trauma; it can be especially dangerous when there is a possibility of dislodging a clot. In addition, the distorted anatomy leads to a higher failure rate for blind nasotracheal intubation. Epistaxis and nasal turbinate injury from blind NTI can be greatly reduced by pretreatment with vasoconstrictor agents and proper technique. Long-term complications (e.g., sinusitis, turbinate destruction) are uncommon and result from multiple intubation attempts or prolonged intubation.

Alternative Airway Adjuncts and Techniques In certain wilderness conditions and settings, tracheal intubation may be difficult or impossible. Under such circumstances, alternative airway adjuncts or techniques may be employed to provide an airway. Alternative airways that require blind passage of the device into the airway may be simpler to master than passing an ETT under direct vision. To achieve good outcomes with these devices and techniques, health care providers must maintain a high level of knowledge and skills through frequent practice and field use.

LARYNGEAL MASK AIRWAY The laryngeal mask airway (LMA) is a modified ETT with an inflatable oval cuff (i.e., the laryngeal mask) at its base (Figure 20-22). The LMA is blindly inserted into the pharynx and advanced

A

B

C

D 405

CHAPTER 20  Emergency Airway Management

NASOTRACHEAL INTUBATION

COMBITUBE The Combitube is a double-lumen, dual-cuffed airway; one lumen functions as an esophageal airway, whereas the other performs as a tracheal airway (Figure 20-23). The Combitube is typically blindly inserted and advanced until the victim’s teeth lie between two guide marks that are printed on the tube. The distal end of the tube most commonly finds its way into the esophagus. The pharyngeal and distal balloons are then inflated, thus isolating the oropharynx above the upper balloon and the esophagus or trachea below the lower balloon. The location (i.e., esophagus or trachea) of the distal orifice is then ascertained, and the victim is ventilated through the appropriate opening. One lumen contains ventilating side holes at the hypopharyngeal level and is closed at the distal end; the other lumen has a distal open end with a cuff that is similar to that of a tracheal tube. Advantages of the Combitube over BMV include isolation of the airway, reduced aspiration risk, and more reliable ventilation. Because laryngoscopy and visualization of the vocal cords are not necessary for insertion, use of the Combitube is easier to teach, learn, and practice compared with tracheal tube placement. In addition, ventilation and oxygenation with the Combitube compare favorably with those achieved with the use of a tracheal tube. Fatal complications with the Combitube may result from incorrect identification of the position (trachea or esophagus) of the distal lumen. For this reason, an ETCO2 or esophageal detector device should be used in conjunction with the Combitube. Another possible complication is esophageal trauma.

KING LT The King LT airway is a single-lumen, dual-cuffed airway with ventilation outlets between the pharyngeal and esophageal cuffs. The King LT is inserted blindly, and a single pilot balloon inflates both cuffs simultaneously. Although it is similar to the Combitube, the King LT is shorter, easier to insert, and easier to inflate. Ventilation capability seems to be similar to that of the Combitube and the LMA. The device’s airway seal may be lost after insertion and require deflation of the balloons and repositioning. The King LT airway is available in newborn through adult sizes.

VIDEO LARYNGOSCOPY Video laryngoscopes, which consist of a micro video camera and a modified laryngoscope, transmit images of the glottis to an external monitor to allow for intubation while looking at the video screen. As compared with traditional laryngoscopy, video laryngoscopes such as the GlideScope provide superior glottic views and greater airway anatomic detail without requiring alignment of the airway axes. As a result, the GlideScope is associated with high intubation success rates and less cervical spine movement. Although rigorous trials to assess performance are limited, clinical experience (including that of the author) indicates that these devices are highly effective. The GlideScope Ranger is a rugged, portable, battery-operated unit that is designed for field use.

FIBER-OPTIC INTUBATION Fiber-optic techniques for endotracheal intubation have emerged as invaluable tools for difficult airway management and include fiber-optic intubating bronchoscopes and rigid fiber-optic laryngoscopes. These devices may allow for awake intubation in select victims for whom RSI or insertion of a laryngoscope blade may be disadvantageous. Use of fiber-optic devices may be difficult in the setting of uncontrolled secretions or active bleeding, because visualization is impaired.

LIGHTED-STYLET INTUBATION By transilluminating the soft tissues of the neck, a lighted-stylet apparatus can be used to facilitate blind ETT placement within the trachea. Devices such as the Rusch Trachlight take advantage of the anterior location of the trachea relative to the esophagus. When the ETT and the lighted stylet correctly enter the glottic opening, a well-defined and circumscribed glow can readily be seen in the anterior neck. If the tip of the tube is correctly

.2 No No.1

A

Insertion

B

Esophageal placement

2 No. No.1

2 No. No.1

PART 4  INJURIES AND MEDICAL INTERVENTIONS

until resistance is felt as the distal portion of the tube locates in the laryngopharynx. Inflation of the collar provides a seal around the laryngeal inlet to facilitate tracheal ventilation. Although the LMA does not provide a definitive airway or ensure absolute protection against aspiration, studies have shown that aspiration is uncommon and that regurgitation is less likely with an LMA as compared with a BMV device. The LMA provides ventilation equivalent to that with the tracheal tube. The LMA may have advantages over traditional endotracheal intubation when access to the victim is limited, when the possibility of unstable neck injury exists, or when appropriate victim positioning for tracheal intubation is impossible. However, studies have shown that a small proportion of patients cannot be ventilated, even when the LMA is successfully inserted. An updated version of the original LMA called the intubating ILMA facilitates blind endotracheal intubation by allowing for the passage of an ETT through the device and into the trachea with a high degree of success.

C

Tracheal placement

FIGURE 20-23  Esophageal–tracheal Combitube. (Redrawn from Skinner D, Swain A, Peyton R, et al, editors: Cambridge textbook of accident and emergency medicine, Cambridge, UK, 1997, Cambridge University Press.)

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RETROGRADE INTUBATION Retrograde intubation is an invasive technique that involves needle puncture of the cricothyroid membrane followed by threading a guidewire retrograde through the vocal cords and into the mouth or nose. The wire is then used to guide the ETT through the glottis. Kits are commercially available. Retrograde intubation may play a role in difficult airways as a result of anatomic abnormalities, upper airway trauma, and victims with limited neck mobility caused by cervical spine immobilization.

DIGITAL INTUBATION Digital or tactile intubation is a technique in which the index and long fingers of the nondominant hand are used to identify the epiglottis and then manually direct an ETT into the larynx. It may be useful when poor lighting, poor positioning, copious airway secretions, or equipment failure make laryngoscopy difficult or impossible. Digital intubation requires a profoundly unresponsive victim and is relatively contraindicated in the semiconscious victim with intact oropharyngeal reflexes. Other relative contraindications include caustic ingestions, thermal burns, and upper airway foreign bodies.

Surgical Airway Management Surgical airway management involves creation of an opening directly into the trachea by surgical means and includes both cricothyrotomy and needle cricothyrotomy with percutaneous transtracheal ventilation.

CRICOTHYROTOMY Cricothyrotomy is the creation of a surgical opening through the cricothyroid membrane to allow placement of an ETT or cuffed tracheostomy tube. The proximal ends of these tubes can be connected to a BMV device for oxygenation and ventilation. The primary indication for cricothyrotomy is need for a definitive airway in the victim in whom orotracheal or blind NTI has failed, is contraindicated, or is extremely difficult. Clinical scenarios include the victim with severe facial trauma for whom conventional airway management is extremely complicated or unfeasible, the victim with severe laryngeal edema, or the victim with upper-airway foreign-body obstruction that cannot be alleviated with the Heimlich maneuver or direct laryngoscopy. The primary contraindication to cricothyrotomy is young age. As a result of anatomic considerations, the procedure is extremely difficult for children who are less than 10 to 12 years old, and is generally avoided in this population. Other contraindications to cricothyrotomy include preexisting tracheal or laryngeal pathology, anatomic obliteration of the landmarks (e.g., hematoma), coagulopathy, and operator inexperience with the procedure. Complications of cricothyrotomy include incorrect airway placement, hemorrhage, tracheal or laryngeal injury, infection, pneumomediastinum, subglottic stenosis, and voice change. Standard Surgical Cricothyrotomy Technique (Figure 20-24): 1. Identify the thyroid cartilage; this is the only V-shaped structure encountered when palpating the anterior neck. The cricothyroid space is the gap immediately caudad to the thyroid cartilage. 2. Prepare the neck in sterile fashion. With the nondominant hand holding the thyroid cartilage, make a vertical midline incision with a No. 11 scalpel from the thyroid cartilage caudad about 3 to 4 cm (1.18 to 1.57 inches) (A).

3. Place a tracheal hook through the cricothyroid space, and hold cephalad traction with the nondominant hand (B, C, and D). 4. Make a transverse incision across the exposed cricothyroid membrane (E and F). If time permits, insert silk stay sutures in the trachea (G and H). Dilate the space using the Trousseau dilator while maintaining traction with the hook (I, J, and K). 5. Place a Shiley cuffed tracheostomy tube through the cricothyroid membrane, initially aiming posteriorly then redirecting caudad once through the membrane (L). The tracheal hook may be removed before insertion of the tube to avoid damaging the tube. Rapid Four-Step Cricothyrotomy Technique: 1. From a position at the head of the victim, palpate and identify the landmarks, especially the cricoid and thyroid cartilages and the cricothyroid membrane (Figure 20-25). 2. Incise the cricothyroid membrane and the overlying skin simultaneously with a single horizontal 1.5-cm (0.6-inch) incision using a No. 20 scalpel. While maintaining the blade within the airway, slide a tracheal hook along the caudal side of the blade into the wound. 3. Orient the hook caudally, and place gentle traction on the cricoid ring; this typically widens the incision. Then remove the blade from the airway. 4. The ETT is then placed through the incision into the airway and secured. Improvised Cricothyrotomy For circumstances in which formal cricothyrotomy equipment is not available, a knife and a hollow device (as a substitute for the tracheostomy tube) may be used. An improvised cricothyrotomy could be performed using a modified intravenous macro drip chamber or the cut barrel of 1- or 3-mL syringe (see Chapter 23). Any small hollow object (e.g., a ballpoint pen casing, a sports-bottle straw) may be employed as the cricothyrotomy tube; however, devices with an internal diameter of at least 3 mm (0.12 inch) provide the best gas exchange.

NEEDLE CRICOTHYROTOMY WITH PERCUTANEOUS TRANSTRACHEAL (TRANSLARYNGEAL) JET VENTILATION An alternative surgical airway procedure is needle cricothyrotomy with percutaneous transtracheal jet ventilation (TTJV). With this technique, a transtracheal catheter is inserted through the cricothyroid membrane into the trachea and connected to a jet ventilation system that includes high-pressure tubing, an oxygen source at 50 psi, and an in-line one-way valve for intermittent administration of oxygen. One hundred percent oxygen is then delivered at 12 to 20 bursts/min. The inspiratory phase should last 1 second, and the expiratory phase should last 2 to 4 seconds. Advantages of this technique include simplicity, safety, and speed. There is typically less bleeding as compared with cricothyrotomy, and age is not a contraindication, thereby making this the preferred surgical airway technique for children who are less than 12 years old. During TTJV, the upper airway must be free of obstruction to allow for complete exhalation; otherwise, the victim is at risk for barotrauma from air “stacking.” All victims who are receiving TTJV should have an oral and nasal airway placed. Unlike cricothyrotomy, TTJV does not provide complete airway protection; therefore it should be considered a temporizing measure until a definitive airway can be established. Technique: 1. Stand to one side of the victim at the level of the neck. Expose the neck, and identify the landmarks, especially the cricoid and thyroid cartilages and the cricothyroid membrane. 2. Prepare the neck with an antiseptic solution, and provide local anesthesia if time permits. 407

CHAPTER 20  Emergency Airway Management

placed in the esophagus, the light glow is diffuse and not readily seen. Lighted stylets may have a role in management of difficult airways as a result of anatomic difficulties (e.g., restricted mouth opening), severe facial trauma, and victims with limited neck mobility. Despite the absence of absolute contraindications to using the lighted stylet, this device should probably be avoided in any victim with an unknown cause of upper airway obstruction.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Cricoid cartilage

Cricothyroid membrane Cricoid cartilage Thyroid cartilage

Cricothyroid space

A

B

C

E

F

Left hand takes trachea hook from right hand L R

L

R

Right hand picks up scalpel

R

D

L R Right hand takes trachea hook from left hand

L

G

J

H

I

K

L

R

Left hand picks up trachea spreader

L

FIGURE 20-24  Standard surgical cricothyrotomy. (Redrawn from Walls RM: Cricothyrotomy. In Rosen P, Chan TC, Vilke GM, et al, editors: Atlas of emergency procedures, St Louis, 2001, Mosby.)

408

A

B

C

D

3. Immobilize the larynx between your thumb and middle finger while your index finger identifies the cricothyroid membrane. 4. Attach a large-bore (12- to 16-gauge) over-the-needle catheter to a 20-mL syringe. Hold the needle and syringe in the dominant hand. Direct the needle caudally through the cricothyroid membrane at a 30-degree angle to the skin while maintaining negative pressure on the syringe. As soon as the needle enters the trachea, the syringe should fill easily with air. 5. Advance the catheter to the hub while simultaneously removing the needle. Reconfirm catheter position within the trachea. 6. Connect the catheter to the jet ventilation system. Commercial kits with cannulas that have been designed for cricothyrotomy or percutaneous translaryngeal ventilation are available. Several of these employ the Seldinger technique for catheter placement, whereas others rely on direct percutaneous placement of the airway device. These kits include Nu-Trake, PCK-Portex, Pertrach, QuickTrach, and the Melker emergency cricothyrotomy catheter. In terms of expedition kit portability, three transtracheal puncture emergency airway devices deserve special mention. LifeStat manufactures a keychain emergency airway set that consists of a sharp-pointed metal trocar introducer that fits through a straight metal cannula that screws into a metal extension with a universal 15-mm (0.6 inch) male adaptor. Lightweight and less than 7.6 cm (3 inches) long, the three-component apparatus is attached to a separate and detachable keychain (Figure 20-26). Cook Critical Care offers a 6-Fr reinforced-catheter emergency transtracheal airway catheter (order number C-DTJV-6.0-7.5-BTT) with a molded Luer-Lok connection for jet ventilation or the added assembly of a 15-mm (0.6 inch) adaptor for standard modes of positivepressure ventilation. Cook Critical Care also offers the Wadhwa Emergency Airway Device (order number C-WEAD-100). This lightweight and impact-resistant assembly disassembles to yield a 12-Fr Teflon-coated cricothyrotomy catheter with a removable metal stylet, a molded plastic Luer-Lok connection for oxygen or jet ventilation, and a flexible nasopharyngeal airway adhered to a molded plastic flange (Figure 20-27). Both the cricothyrotomy catheter and the NPA screw into the Wadhwa case to provide a low-resistance extension and a 15-mm (0.6 inch) male connection for standard positive-pressure ventilation equipment.

CHAPTER 20  Emergency Airway Management

FIGURE 20-25  Rapid four-step cricothyrotomy. A, Step 1: Palpation (location of the cricoid membrane externally). B, Step 2: Incision (horizontal incision of the skin and soft tissues through the cricoid membrane). C, Step 3: Traction (application of caudal traction to the cricoid ring). D, Step 4: Intubation (passage of the tracheal tube). (Redrawn from Brofeldt BT, Panacek EA, Richards JR: An easy cricothyrotomy approach: The rapid four-step technique, Acad Emerg Med 3:1060, 1996.)

For circumstances in which a jet ventilator is not readily available, the clinician in the wilderness may improvise by using a self-inflating bag-valve device to ventilate the victim through the transtracheal catheter. The bag-valve device may be connected to a 3.0-mm-ID ETT adapter that is inserted directly into the transtracheal catheter or to a 7.5-mm-ID ETT adapter that is inserted into a 3-mL (0.1-oz) syringe barrel and then into the transtracheal catheter (Figure 20-28). Ventilation using such an apparatus is temporary at best, but it may have usefulness in children who are younger than 5 years old.

Airway Equipment for the Wilderness Although it is neither practical nor possible to bring every type of airway device to the wilderness, the airway equipment listed in Box 20-1 is worth considering. Emergency medical kits with basic or advanced airway equipment (e.g., the StatKit) are commercially available.

Universal adaptor

Cannula Trochar FIGURE 20-26  LifeStat emergency airway device. (Redrawn from LifeStat product information.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

15-mm adapter

Cricothyrotomy catheter

Nasopharyngeal airway catheter

Assembled airway device FIGURE 20-27  Wadhwa emergency airway device. (Redrawn from Cook Critical Care product information.)

Ventilation bag

BOX 20-1  Sample Contents of a Wilderness Airway

Management Kit

Standard endotracheal tube connector

Cricothyroid membrane

3-cc syringe barrel

14-gauge IV catheter-over-needle

Thyroid cartilage

Cricoid ring

FIGURE 20-28  A simple setup for translaryngeal ventilation with the use of standard equipment found in any emergency department. This setup is inadequate for adults. High-pressure (50-psi) ventilation systems are optimal. Even with the pressure relief valve on the bagvalve device turned off, only a suboptimal pressure can be developed. However this technique may be satisfactory for infants and small children. (Redrawn from Roberts JR, Hedges JR, editors: Clinical procedures in emergency medicine, ed 4, Philadelphia, 2004, Saunders.)

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Basic Airway Equipment Laerdal pocket mask CPR microshield barrier Nasal airway kit Oral airway kit Stethoscope Bulb suction device Advanced Airway Equipment Bag-mask ventilation device with pediatric and adult masks Manual suction device Endotracheal tubes with stylet Laryngoscope handles and blades Magill forceps Esophageal detector device Colorimetric end-tidal carbon dioxide detector Laryngeal mask airway, King LT, or Combitube Needle cricothyrotomy catheter or device Commercial cricothyrotomy kit Oxygen cylinder with toggle handle Nasal cannula, oxygen mask with strap, and nonrebreather bag Oxygen tubing Pulse oximeter

SUGGESTED READINGS Complete Suggested Readings used in this text are available online at www.expertconsult.com.

CHAPTER 21 

Wilderness Trauma and Surgical Emergencies* KIRBY R. GROSS, BRYAN R. COLLIER, WILLIAM P. RIORDAN, JR., AND JOHN A. MORRIS, JR.

Purpose This chapter is written to provide physicians and health care practitioners with a concise, pragmatic approach to the management of trauma and surgical emergencies encountered in a wilderness environment. Our focus is directed primarily at the health care professionals responsible for the well-being of expedition members. Wilderness expedition health care providers will have varied capabilities and experience, but it is the environment (location, time from medical facilities, and conditions) and available resources that will most influence patient outcome. Complex interventions in the field are frequently impractical. With ongoing debate concerning issues ranging from the value of field resuscitation for internal hemorrhage to the method (if any) of closure of animal bite wounds, it remains clear that simple things, such as identifying injuries, establishing an airway, keeping the patient warm, and making expedient evacuation plans, most strongly influence survival.21,26,74 The key to successful management of wilderness emergencies is preparedness. Knowledge of the Advanced Trauma Life Support (ATLS) protocols provides a scaffold for preparation for wilderness travel. The simple, concise principles contained in ATLS concepts are well suited to management of wilderness emergencies, where resources are scant and prompt response is essential to victim survival. Newer training programs, such as Advanced Wilderness Life Support (AWLS), provide additional wilderness-specific learning opportunities. In addition to knowledge and skill, physicians in the wilderness environment should prepare by understanding their role in the expedition. Lessons from teamwork management have application to the wilderness environment as well as the sophisticated medical environment. The basic tenets of teamwork are those of (1) team structure, (2) application of problem-solving strategies, (3) communication, (4) execution, and (5) improving team skills.79 The provider in an expedition should fully understand his or her role during preparation. Is the physician a team member because he or she has medical training and expertise that has application to the specific environment and potential risks? Is the provider serving in a capacity in which he or she has been directed to become the responsible physician if needed? Or, is the provider in the wilderness to escape from professional responsibilities and enjoy an avocation that can only be appreciated in the austere environment? The medical director of an expedition takes on a significant responsibility in preparation for the trip. He or she must provide input to the expedition leader regarding local health threats and also assess risk. Screening participants for durability and comorbidities is important. The medical director must be knowledgeable in wilderness medicine protocols. For longer expeditions, diagnostic capability such as handheld ultrasound and point-ofcare testing should be considered. Also, establishing contact with evacuation assets before commencing the trip is prudent. The medical director must have a plan for transfer of information to

*The views expressed in this chapter are those of the authors and do not reflect the official policy or position of the Department of the Army, the Department of Defense, or the U.S. Government.

the next level of care. It may be as simple as recording findings on a piece of tape applied to an uninjured location on the casualty. Paper is a poor way to transfer information. In the evacuation process, paper will often be lost because of helicopter rotor wash and jostling during travel. Standard time designations should be used. The casualty may be evacuated across different time zones. Any times recorded for findings or interventions should have the appropriate time zone clearly designated. In any austere environment, physicians will commonly and immediately be thrust into a position of authority. The time to clarify structure and roles is before the expedition. Understanding the expectations for each provider permits appropriate team preparation. The physician in a position of responsibility would be wise to brief team members about contingencies before entering the austere environment. The specifics of wilderness pre­paration, equipment, and medical supplies are presented in Chapter 91.

Wilderness Trauma Emergencies OVERVIEW All three classic mechanisms of trauma (penetrating, blunt, and thermal) may be seen in the wilderness. Particularly in the austere environment, blunt trauma presents pitfalls, because the patient is at risk due to blunt mechanisms. Delayed diagnoses in victims of blunt trauma occur in highly sophisticated medical environments. The possibility of delayed diagnoses in the wilderness is even greater due to lack of diagnostic resources.

BACKGROUND The medical literature is limited regarding the incidence of injury incurred during wilderness-related activities. It is estimated that greater than 10 million Americans participate in wilderness backpacking and camping activities annually. A study by Gentile and colleagues33 documented the injury and evacuation patterns recorded by the National Outdoor Leadership School over a 5-year period. Injuries occurred at a rate of 2.3 per 1000 persondays of exposure, with orthopedic and soft tissue injuries most frequent. Montalvo65 analyzed case incident report files from eight California National Park Service parks and found an injury incidence of 9.2 nonfatal events per 100,000 visits, with 78 fatalities reported in a 3-year period. In a prospective surveillance study evaluating 38,940 days of wilderness exposure on the Appalachian Trail,12 foot blisters and diarrhea were the most common reasons that hikes were prematurely ended. Leemon and Schimelpfenig52 showed that over 50% of evacuated participants in the National Outdoor Leadership School were able to return and finish their courses. These studies document a low risk for injury but highlight the possible morbidity resulting from wilderness injury or illness and the need for rapid, uniform intervention. A 2001 study from the University of Arizona36 highlighted wilderness mortalities over the past 13 years. Alcohol was the most common causative factor, involved in 40% of the 59 unintentional trauma deaths. In addition, 80% of these victims died immediately or before evacuation could be completed. This again emphasizes the importance of sound judgment and preparedness as keys to maximizing care to rescuers and expedition members. 411

PART 4  INJURIES AND MEDICAL INTERVENTIONS

ESTABLISHING PRIORITIES There are three immediate priorities in managing wilderness trauma: 1. Control oneself. It is normal to feel anxious when confronted with an injured victim. However, anxiety must not be transmitted to the victim or other members of the expedition team. One must be in control of oneself to take control of the situation. 2. Control the situation. The first priority in controlling the situation is ensuring the safety of uninjured members of the party. Expeditious evacuation of a victim requires that all expedition members function at maximal efficiency; even minor injuries to other members in the group can jeopardize physical strength, functional manpower, and success of the evacuation. Although the physician member of the team may not be the expedition leader, his or her position is automatically elevated during a medical crisis. However, this does not mean that the physician should dominate the evacuation process. Although the expedition leader must rely on the medical assessment provided by the physician, the leader is best prepared to plan the evacuation. 3. Obtain an overview of the situation. The victim’s general condition should be evaluated. Is the victim in immediate distress from a condition that requires relatively simple management, such as airway control? Is the victim in such a precarious environmental situation that he or she needs to be moved before resuscitation? Scene security may be integral to the safety of the injured and caregiver. Is the victim properly protected from the elements, including sun, wind, cold, and water? Hypothermia remains one of the most important contributors to trauma-related coagulopathies.91 In addition to these three priorities, McSwain and Kerstein62 have described the “golden principles” of prehospital trauma care. Although not intended for wilderness medicine, several key components are applicable: ensure scene and provider safety, use primary and secondary surveys, provide cervical spine immobilization, control external hemorrhage, keep the patient warm and use warm intravenous (IV) fluid resuscitation if possible, initiate early transport, and, above all, do no further harm. After the victim has been placed in the most stable and safe environment, the examining physician is ready to implement the ATLS-based five steps of wilderness trauma management:3 1. Primary survey 2. Resuscitation 3. Secondary survey 4. Definitive plan 5. Packaging and transfer preparation The purpose of the primary survey is to identify and begin initial management of life-threatening conditions by assessing the following (called the ABCDE’s of trauma care): • Airway maintenance and cervical spine stabilization • Breathing • Circulation, with control of significant external hemorrhage • Disability: neurologic status • Exposure/environmental control: completely undress the victim with careful attention to prevention of hypothermia After the primary survey is performed, resuscitation efforts are initiated. The level of resuscitation depends on the equipment and expertise available (see Chapters 23, 91, and 94). At a minimum, resuscitation consists of control of external hemorrhage and, when available, administration of oxygen and provision of warm IV fluids. The third step is the secondary survey, a head-to-toe evaluation of the trauma victim that uses inspection, percussion, and palpation techniques to evaluate each of the body’s five regions: head and face, thorax, abdomen, skeleton, and skin. A history should be taken at the same time as performance of the secondary survey. The specifics of the mechanism of injury, if unknown to the physician or caregiver, may be of vital importance. Loss of consciousness, head injury, the height of a fall, or the species of attacking animal may influence treatment and evacuation plans, as well as contribute to stability of the scene. The ATLS AMPLE method of rapid history taking is discussed later in detail 412

in the Secondary Survey section. After this survey, the examining physician should formulate a definitive plan. It is useful to document all observations if circumstances permit. Such data may prove of critical importance to field evacuation or hospital personnel. The first step in formulating a plan is to compile a list of the injuries. The next step is to determine if any injury warrants evacuation. A determination needs to be made as to the route of evacuation: air, land, or water. Aeromedical evacuation is expensive and, depending on the environment, may pose its own risk to both the victim and medical evacuation team. Aeromedical evacuation should be considered only for victims with potentially life- or limb-threatening injuries where the terrain and environment allow safe access, for the purpose of evacuation, to the patient. Packaging the victim for evacuation is the final step. The evacuation effort requires organization, coordination, and great effort on the part of the expedition team. Transfer protocols are discussed within the respective injury sections. Preparation for wilderness patient care should address the challenges associated with varying levels of personnel help, minimal medical resources, prolonged prehospital care, and difficult evacuation proceedings. However, with ATLS knowledge, improvisation, and an organized effort, the patient’s outcome can be maximized.

UNIVERSAL (BODY FLUIDS) PRECAUTIONS IN THE WILDERNESS A number of life-threatening viruses are transmitted through contact with bodily fluids. The Centers for Disease Control and Prevention (CDC) have established a set of standard precautions to be applied in all cases of contact with human body fluids: • Goggles • Gloves • Fluid-impervious gowns • Shoe covers and fluid-impervious leggings • Mask • Head covering Created in 1983 and revised in 1987, recommendations for universal precautions and use of the aforementioned equipment have undergone no additional changes over the past decade. Multiple types of body fluids (blood, semen, vaginal secretions, cerebrospinal, pleural, synovial, pericardial, peritoneal, and pericardial) can place a caregiver at risk. In the wilderness setting, the materials necessary for universal precautions are rarely available. However, every victim in the wilderness must be assumed to carry a communicable disease. Every effort should be made to approximate universal precautions, particularly covering the hands and eyes.

PRIMARY SURVEY Persons injured in the wilderness should be assessed and their treatment priorities established based on their mechanism of injury, vital signs, and specific injuries. The victim’s vital signs must be assessed quickly and efficiently, with restoration of lifepreserving vital functions. Airway The upper airway should be assessed for patency (see Chapter 20). This rapid assessment should include inspection for signs of airway obstruction, including foreign bodies and signs of facial or tracheal fractures that sometimes lead to airway obstruction. The chin lift or jaw thrust may be helpful in establishing an airway. If the victim can speak, the airway is likely not jeopardized, but this is not an absolute rule. Frequent repeated evaluation of the patient’s airway, breathing and circulatory status in the familiar ABC format is mandatory. In addition, a Glasgow Coma Scale (GCS) score of 8 or less indicates the possibility of a precarious airway and requires establishment of a definitive airway. Specific attention should be directed toward the possibility of cervical spine injury. The victim’s head or neck should never be

Breathing and Ventilation The victim’s chest should be exposed and chest wall movement observed. Because oxygenation and carbon dioxide elimination require adequate function of the diaphragm, chest and abdominal musculature, and ribs, any trauma sustained by these structures will alter normal pulmonary mechanics and increase the work of breathing. Establishment of an airway in the primary survey, although critical to patient survival, does not ensure adequate oxygenation or ventilation. All trauma victims must be continuously monitored for the signs and symptoms of hypoxemia and hypercarbia. Auscultation, observation, and palpation of the chest after establishment of the airway are integral parts of the primary survey. Absent breath sounds may indicate improper placement of an endotracheal tube. This can occur with inadvertent esophageal intubation or intubation of a single lung (right or left mainstem bronchial intubation). Diminished breath sounds or asymmetric chest wall movement can occur with pneumothorax (simple or tension), hemothorax, or tracheobronchial obstruction. Observation and palpation of the chest may identify thoracic injuries such as rib fractures, fractures with flail segments, or pneumothorax (by the presence of subcutaneous emphysema). Circulation Evaluation of circulation is divided into assessment of cardiac output and control of major external hemorrhage. Manometric blood pressure measurement is not easily performed in the field, although it may provide useful data. Important information regarding perfusion and oxygenation can be obtained rapidly by determining the victim’s level of consciousness, assessing peripheral and central pulses, looking at skin color, and evaluating capillary refill time. The pulse should be assessed first. Although the following are only general estimates and carry some inaccuracy, approximations of systolic blood pressure can be used if a palpable pulse is present: • Radial artery—80 mm Hg • Femoral artery—70 mm Hg • Carotid artery—60 mm Hg When circulating blood volume is reduced, cerebral perfusion pressure may be critically impaired, resulting in altered level of consciousness. Do not assume that altered level of consciousness is attributable to head injury. Altered levels of consciousness may be due to hypoperfusion of the brain. Peripheral perfusion can be assessed using skin color and capillary refill. Pressure applied to the thumbnail or hypothenar eminence causes underlying tissue to blanch. In a normovolemic person, color returns to the nail bed within 2 seconds. In a hypovolemic, poorly oxygenated person, capillary refill requires more than 2 seconds. There is no direct relation between blood pressure and capillary refill. Capillary refill reflects flow, which is more important than blood pressure. If hypovolemia is suspected on the basis of either absent pulses or prolonged capillary refill, the examiner should immediately assess the neck veins. Distended neck veins, although a nonspecific sign, may suggest tension pneumothorax or pericardial tamponade in the context of hypotension. Flat neck veins suggest hypovolemia and hemorrhagic shock. Major hemorrhage can occur in five anatomic areas: 1. Chest 2. Abdomen 3. Retroperitoneum 4. Thigh 5. External environment

Exsanguinating external hemorrhage should be identified and controlled during the primary survey. Blood loss should be controlled by direct pressure on the wound. Tourniquets should not be used to control external bleeding unless direct pressure fails to control the bleeding. Tourniquets may be considered in the situation where pressure cannot be applied as the patient is being transported. In this situation, a tourniquet may be applied temporarily. As soon as the operational situation permits, the tourniquet may be removed and direct pressure reapplied. The greatest challenge for extremity vascular injuries is hemorrhage, not ischemia. Recent military experience has demonstrated that tourniquets may be used with infrequent untoward consequences.50 Proper stabilization of long bone fractures (femur fractures specifically) minimizes blood loss into soft tissues. In the wilderness, little can be done about significant intrathoracic or intra-abdominal hemorrhage. In a modern trauma center, however, less than 5% of blunt trauma patients with intraabdominal or intrathoracic injuries require surgery to control bleeding. Consequently, even significant blunt injuries in the wilderness carry a real probability for survival if basic ATLS principles are followed. Rarely, large degloving injuries may be a source of significant blood loss. Hemostatic dressings have been developed to promote hemorrhage control in this type of wound. The hemostatic dressings require the benefit of pressure to be maximally effective. Several commercial products are available that promote clotting by different active agents. The hemostatic dressings are described in detail in Chapter 22. Disability and Neurologic Assessment The neurologic assessment of the injury victim conducted during the primary survey should be rapid and efficient. The victim’s level of consciousness should be established. In addition, pupillary size and reactivity should be assessed. Level of consciousness should be assessed using the GCS (Box 21-1). It is critical that the neurologic assessment be repeated hourly, particularly if evacuation is delayed. Deterioration in mental status portends a poor prognosis, although a variety of conditions other than intracranial injury can affect mental status. Hypoxia, hypovolemia, and hypothermia should be expeditiously corrected. Exposure and Environmental Control The victim should be fully undressed and exposed, if possible in a protected environment. Garments and gear should be removed if necessary by cutting them away, unless the garments can be dried and are essential for future protection from the environment. Wet clothing must be removed early to prevent BOX 21-1  Glasgow Coma Scale This scale evaluates the degree of coma by determining the best motor, verbal, and eye-opening responses to standardized stimuli. Eye Opening Spontaneous To voice To pain None

4 3 2 1

Verbal Response Oriented Confused Inappropriate words Incomprehensible words None

5 4 3 2 1

Motor Response Obeys command Localizes pain Withdraw (pain) Flexion (pain) Extension (pain) None Maximum Score

6 5 4 3 2 1 15

413

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

hyperextended, hyperflexed, or rotated to establish or maintain an airway. Approximately 10% of victims with head injuries or facial fractures have a concomitant cervical spine fracture. In one series of patients, 25% (29 of 116 patients) had unstable cervical fractures as defined by needing a halo or surgical intervention.23 Such a fracture should be assumed to exist in any person with a significant injury above the level of the clavicle. If a situation requires removal of immobilizing devices, in-line stabilization, not traction, must be maintained.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

hypothermia. It is mandatory to visualize the entire victim to document and assess injury. However, this step of the primary survey should be performed with caution. First, it is imperative to cover the victim immediately after removal of clothing. Hypothermia and its effects on mental status, cardiovascular function, and coagulation are among the most underappreciated entities in care of the trauma victim. The possibility of hypothermia should be entertained in all environments because it is most prevalent in the winter and summer months. Hypothermia reflects the inability of trauma victims to use available stored energy to carry on normal metabolic processes. A severely injured patient may become hypothermic in any ambient environment. Second, clothing and gear should not be removed from the victim unless complete immobilization of injuries can be achieved. Assessment of an area of injury should be performed, but clothing should be left to cover the patient to ensure body temperature is maintained. Expedition members may be wearing a variety of gear and clothing, including biking, skiing, or climbing helmets. Helmets should be removed with in-line stabilization of the cervical spine.

SHOCK The shock state has been defined in many ways. Essentially, shock describes the physiologic condition in which oxygen delivery to the tissues of the body is not adequate for the metabolic demands of those tissues. This results in cellular hypoxia, anaerobic metabolism, and, eventually, cell death. Shock was defined historically by John Collins Warren as “a momentary pause in the act of death.” Nowhere is this adage more applicable than in the wilderness setting. Any physician who cares for trauma victims has witnessed an apparently “stable” victim rapidly deteriorate and die. With only clinical acumen, the wilderness physician must be sufficiently astute to identify the subtle early signs of shock. The treatment for shock is resuscitation, which may be defined as any intervention that restores blood flow and cellular oxygenation. The power of the primary survey lies in the fact that it is essentially a form of resuscitation. Rapid identification and treatment of conditions leading to hypoperfusion facilitate their reversal. A key in resuscitation of the trauma victim is identification of and stopping ongoing hemorrhage.3 Rapid control of external hemorrhage is critical. External sources of hemorrhage can initially be managed with direct pressure. If direct pressure must be interrupted during extrication, other techniques may be used. Exsanguinating hemorrhage from the scalp can be managed with sutures. Tourniquets may be applied to extremities for temporary control.50 Although the majority of trauma victims exhibiting signs of shock in the wilderness have sustained acute blood loss, a nonhemorrhagic entity, such as a spinal cord injury or pneumothorax, may be responsible for shock. Hemorrhagic shock is classified according to the blood volume that has been lost. A central question in caring for victims of blood loss in the wilderness is the reliability of vital signs in quantifying degree of hemorrhage. Associated with each class of hemorrhage are clinical signs that allow a caregiver to quantify blood loss (Table 21-1). It is evident that assessing blood pressure alone is a poor way to predict impending deterioration. When hypotension is present, a normal individual has already lost 30% of his or her blood volume, and salvage may be impossible.

Resuscitation should be initiated at the first sign of shock, equating to class II hemorrhage, and evacuation planned accordingly.

VASCULAR ACCESS Vascular access must be obtained promptly. The standard method of obtaining access is by insertion of two large-bore (16-gauge or larger) catheters, preferably into peripheral veins of the upper extremity. Alternatives include using lower extremity veins and obtaining central venous access. If peripheral access cannot be secured, the femoral vein should be the next site attempted. Advantages of femoral vein access include ease of cannulation relative to jugular and subclavian access, and fewer complications.93 Depending on expertise, the internal jugular and subclavian veins may be accessed. Despite a higher incidence of complications compared with peripheral access, central access complication rates in trauma centers have been demonstrated to be less than 5% in most studies.93 If peripheral access is inadequate or unobtainable, it is clear that the next site attempted should be determined by the provider’s level of confidence and expertise. As a last resort, venous cutdown may be considered. Despite fewer complications than central access, cutdowns are experience and equipment dependent and not recommended in the wilderness environment. Intraosseous access is also to be considered in adults. Several commercially available products are available (Figure 21-1). The manubrium is the target for insertion of the FAST1 intraosseous device. The Bone Injection Gun (BIG) and EZ-IO can be used to access the bone in the proximal tibia and humerus. The FAST1 and BIG are impact-driven devices. The EZ-IO is a drill-based device. Skills to successfully place intraosseous venous access can be acquired with short training times.30 Children in the wilderness younger than 6 years of age in whom venous access cannot be obtained should undergo intraosseous resuscitation. This is accomplished by introducing a needle through the periosteum of the tibia just inferior to the tibial tuberosity. Needles that are 18- to 20-gauge are preferable, but any needle strong enough to penetrate the periosteum without bending can be used. Of the resuscitative therapies that potentially may be initiated in a well-prepared expedition, volume resuscitation deserves considerable attention. Fluid resuscitation in trauma has been a contentious topic, perhaps overly so, relative to fluid type and amounts used. A number of recent studies focusing on the prehospital administration of fluids in trauma victims not only rehashed the fluid composition debate but called into question the efficacy of prehospital resuscitation.74 Although further prospective trials are needed relative to fluid type and prehospital use, an impressive compilation of data has been amassed looking at resuscitative fluids in the trauma victim. Past studies have not only compared colloids with crystalloids89 but explored the use of blood and plasma substitutes and hypertonic saline. Detailed analyses of these studies is beyond the scope of this chapter, but a summary of fluid recommendations is in order. In small volumes, hypertonic saline has been shown to be an effective resuscitative fluid, and its efficacy in closed head injury is under evaluation. Currently, no improvement in survival has been demonstrated using hypertonic saline compared with

TABLE 21-1  Classes of Hemorrhagic Shock

Blood loss (mL) Blood loss (% blood volume) Pulse rate (beats/min) Blood pressure Pulse pressure (mm Hg) Respiratory rate (breaths/min) Urine output (mL/hr) CNS/mental status Fluid replacement (3 : 1 rule) CNS, Central nervous system.

414

Class I

Class II

Class III

Class IV

Up to 750 Up to 15 <100 Normal Normal or increased 14-20 >30 Slightly anxious Crystalloid

750-1500 15-30 >100 Normal Decreased 20-30 20-30 Mildly anxious Crystalloid

1500-2000 30-40 >120 Decreased Decreased 30-40 5-15 Anxious, confused Crystalloid and blood

>2000 >40 >140 Decreased Decreased >35 Negligible Confused, lethargic Crystalloid and blood

B

C

FIGURE 21-1  A, FAST1 intraosseous infusion system. B, Bone Injection Gun (BIG). C, EZ-IO.

crystalloid, and its use has been associated with hypokalemia, pulmonary edema, and dramatic increases in serum sodium and osmolarity.6 The significance of these reported complications in trained hands is questionable, and hypertonic fluids may have a future role in resuscitation. Further study is warranted on the use of hypertonic saline, but its use in the wilderness setting is not recommended at this time. Based on the current literature, it is clear that both colloids (including hetastarches and albumin) and crystalloids are efficient volume expanders.80 Larger volumes of crystalloids than of colloids are needed to achieve similar resuscitative end points, usually in a ratio of 3 to 1. However, no benefit in survival by using colloids has been demonstrated, and recent studies indicate that their use in critically ill patients may increase mortality.18,71 In addition, no proved detriment, including increased extravascular lung water, impaired wound healing, or decreased tissue oxygen diffusion, has been demonstrated with the use of large volumes of crystalloids. Crystalloids are safe, nonantigenic, easily stored and transported, effective, and inexpensive. Most experts in trauma care agree that crystalloid is preferable to colloid infusion in the prehospital, early resuscitative phase of trauma care. Accordingly, the resuscitative fluid recommended by ATLS protocol is normal saline. In expeditions in which weight and space are considerations, colloids may have an advantage. “Colloid fluids will achieve a given increment in plasma volume with only one-quarter to onethird the volume required of crystalloid fluids.”58 To restore circulating volume, colloids provide greater efficacy per weight/ volume trekked into the austere environment. For the expeditionist carrying resuscitation fluids in a backpack, 1 lb of colloid will provide about three times the volume expansion of 1 lb of crystalloid. Several animal studies and recent human clinical trials in trauma victims have found that treatment with IV fluids before control of hemorrhage resulted in increased mortality rates.8,60 Although these data are compelling, they have been accumulated in victims with penetrating injuries and short prehospital times, and the definition of prehospital resuscitation in these studies comprised widely varying volumes. Prehospital resuscitative protocols remain in evolution. However, application of these data to the wilderness setting at the current time is dangerous, for a number of reasons. First, the leading cause of death in wilderness trauma is head injury. Many multiple-trauma victims have a head injury, and it may be impossible to discern whether an intracranial lesion is present. Although under continued study, the current approach to management of head injury is aggressive maintenance of cerebral perfusion pressure to control intracranial pressure (ICP). Underresuscitation in the context of an intracranial injury could be catastrophic. Second, the multisystem-injured victim frequently presents with associated orthopedic injuries. A victim with closed extremity fractures with significant contained hemorrhage benefits from fluid resuscitation. Third, a victim with significant external hemorrhage that can be controlled before evacuation benefits from intravascular repletion.

In summary, resuscitation with IV fluids should be initiated in the field, particularly in victims with head injury and unquantified multiple trauma. Victims should have vascular access secured and resuscitative fluids given in the form of normal saline as dictated by severity of injuries and hemodynamics. In patients in whom urinary catheterization can be performed, a target of 30 mL/hr is a good target. In those patients in whom hourly urine output cannot be determined, other measures of perfusion, such as heart rate, blood pressure, and mental status, can determine the efficacy of resuscitation.

SECONDARY SURVEY The secondary survey is an extension of the primary survey and should not be undertaken until the primary survey is complete and the victim has been stabilized. In addition, resuscitative regimens, if available, should have been initiated. The secondary survey is a head-to-toe assessment of the victim, including history and physical examination. The face, neck, chest, abdomen, pelvis, extremities, and skin should be examined in sequence. A more detailed neurologic examination should be completed, including reassessment of the GCS. The neck should be examined independently of the thoracolumbar spinal cord. Examination of the pelvis should not include the traditional “rocking” to determine stability, because in the presence of pelvic fractures, this action may exacerbate existing comminution. The detailed secondary survey should not delay evacuation packaging. As in the nonwilderness setting, it is imperative to repeat the primary survey as the victim’s condition warrants. Specific examinations are discussed in the sections covering regional injuries. History The victim’s history should be assessed during the secondary survey. Knowledge of the mechanism of injury and any comorbid medical conditions or allergies may enhance understanding the victim’s physiologic state. The ATLS “AMPLE” history is a useful and rapid mnemonic for this purpose: Allergies Medications currently used Past medical history/Pregnancy Last meal Event or Environment related to the injury Adjuncts Resuscitation should be initiated simultaneously with the primary survey. The degree of resuscitation depends on available resources, experience of the rescuer(s), and environmental conditions. Under the best circumstances, initial management of the wilderness trauma victim provides for airway control, adequate oxygenation and ventilation, appropriate fluid resuscitation, and stabilization of cardiac function while continuing to monitor and reassess the patient’s vital signs. As adjuncts to the secondary survey, it also 415

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

A

PART 4  INJURIES AND MEDICAL INTERVENTIONS

includes placement of a urinary catheter and nasogastric (NG) tube. This degree of resuscitation will be almost universally unavailable in the wilderness setting. Here, resuscitation may be limited to oral administration of warm, high-calorie fluids and maintenance of victim comfort and body temperature. An NG tube and indwelling urinary (Foley) catheter should be placed if available and appropriate. Aspiration of gastric contents can be catastrophic in terms of patient survival after trauma. Gastric decompression with an NG tube may help prevent this type of adverse event in patients with a depressed level of consciousness. It should be remembered that children can exhibit significant hemodynamic consequences secondary to massive gastric distention. In this setting, decompression becomes critical. If possible, NG tubes should be placed in persons who are endotracheally intubated in the field. The tube can be aspirated sequentially with a syringe or left open to gravity drainage. Any suspicion of facial fracture should deter attempts to place an NG tube, and orogastric decompression should be chosen instead. A Foley catheter can assist in volume assessment and hemodynamic status determination in a critically injured victim. Hourly urine output typically does not decrease until the onset of class III hemorrhagic shock, with loss of 30% to 40% of blood volume. Contraindications to urinary catheter placement in the field are blood at the urethral meatus, high-riding prostate, scrotal hematoma, and personnel not experienced in placement. Injuries to the Head, Face, and Neck The secondary survey begins with examination of the entire head and scalp for evidence of skull or facial fractures, ocular trauma, lacerations, and contusions. The scalp is thoroughly palpated for tenderness, depressions, and lacerations. The bones of the face, including the zygomatic arch, maxilla, and mandible, are palpated for fractures. Elements of the GCS are repeated. The wilderness eye is discussed in detail in Chapter 28, but general examination principles are simple. Significant periorbital edema may preclude examination of the globe, so assessment should be carried out early. The globe should be evaluated for visual acuity, pupillary size, conjunctival hemorrhage, lens dislocation, and entrapment. Persons with significant facial trauma have a high incidence of associated ocular or orbital injuries.77 Recent studies of ocular injuries in trauma victims have emphasized underappreciation by many disciplines of ocular and periocular signs indicative of significant underlying injury.73

HEAD INJURIES Approximately 500,000 to 2 million cases of head injury occur in the United States yearly.34 Of these, approximately 10% result in the patient’s prehospital death.3 Long-term disability associated with head injury is significant, with more than 100,000 persons suffering varying degrees of permanent impairment. Because of the high-risk nature of traumatic brain injury (TBI) and the impact of initial management on disability and survival, clinical management objectives must address both immediate survival and longterm outcome. Management guidelines for head injuries in a wilderness do not exist, and a wide range of clinical approaches are used in hospital settings.34 However, the literature suggests that morbidity and mortality can be reduced by means of a protocol that includes early airway control with optimization of ventilation,40 prompt cardiopulmonary resuscitation, and rapid evacuation to a trauma care facility. Initial management of head injury in the wilderness should follow established ATLS protocols. Prompt attention must then be given to victim triage, evacuation strategies, and ongoing resuscitative needs to prevent or minimize secondary brain injury. Expeditious evacuation to a neurosurgery-capable trauma center is essential. Multiple clinical and experimental studies have demonstrated the detrimental effects of hypoxia on the injured brain. A definitive airway should be established if any degree of neurologic or respiratory compromise exists. Cervical spine injuries are common in patients with TBI. Therefore cervical spine immobilization is paramount in the prevention of further devastating neurologic injury. 416

After immobilization, attention is directed to the prevention of secondary brain injury. The purpose of the wilderness head injury protocol is to allow individuals with widely varying levels of experience and expertise to identify signs of significant head injury, begin proper resuscitation in the context of prevention of secondary brain injury through airway maintenance and hemodynamic support, and evacuate appropriately. Anatomy The scalp comprises five layers of tissue that cover the calvaria: skin, connective tissue, galea aponeurotica, loose areolar tissue, and periosteum of the skull. The galea is a fibrous tissue layer with important ramifications in closure of scalp wounds, discussed later in this chapter. Loose areolar tissue beneath the galea represents the site of accumulation of blood in scalp hematomas. A rich vascular network located between the dermis and the galea supplies the scalp. When lacerated, these vessels can be a significant source of hemorrhage, which may be important if evacuation is impossible or delayed. The skull is composed of two groups of bones that form the face and cranium. Cranial bones are divided into the calvaria and skull base. The calvaria is composed of frontal, ethmoid, sphenoid, parietal, and occipital bones. Within the skull, the brain is covered by three membranous layers that may be of pathophysiologic importance after injury. However, in the wilderness environment, these layers have little clinical relevance (except in terms of defining an open versus closed brain injury). Pathophysiology of Traumatic Brain Injury TBI can be divided into primary and secondary brain injuries. Primary injury consists of the physical or mechanical insult at the moment of impact, and the immediate and permanent damage to brain tissue. Little can be done in the wilderness setting relative to primary brain injury. Secondary brain injury is the biochemical and cellular response to the initial mechanical trauma and includes physiologic derangements that may exacerbate effects of the primary trauma. Such pathophysiologic alterations include hypoxia, hypotension, and hypothermia. Compounding these pathophysiologic alterations is elevation of ICP after TBI. Increased ICP increases cerebral ischemia and exacerbates secondary brain injury. Many forms of head injury result in elevated ICP, the duration of which is significantly correlated with poor outcome. The Monro-Kellie doctrine states that the volume of intracranial contents must remain constant because the cranium is a rigid container. The normal compensatory response to increased intracranial volume is to decrease venous blood and cerebrospinal fluid (CSF) volume within the brain. If this normal response is overwhelmed, small increases in intracranial volume result in exponential increases in ICP. A rigid bony cranium cannot expand to accommodate increases in brain volume and the resultant increase in ICP. Brain parenchyma becomes compressed and eventually displaced from its anatomic location. In the most devastating circumstances, the brain parenchyma herniates toward the brainstem through the largest cranial opening (the foramen magnum) and death rapidly follows. The volume– pressure curve in Figure 21-2 relates the small, but critical, time period between neurologic symptoms, hemodynamic decompensation, and brainstem herniation. Elevation in ICP directly correlates with secondary brain injury. Therefore the field provider must attempt to minimize ICP of head-injured patients to the greatest extent possible. The most important priority in minimizing secondary brain injury in the field is optimizing cerebral perfusion pressure (CPP). CPP is related to ICP and mean arterial pressure (MAP) as follows: CPP = MAP − ICP A CPP less than 70 mm Hg after head injury correlates with increased morbidity and mortality.3,39 Cerebral blood flow (CBF) should be maintained at approximately 50 mL/100 g brain tissue per minute.57 At 5 mL/100 g per minute, irreversible damage and potential cell death occur.3 Study data have shown a correlation between low CBF and poor outcome.57 At a MAP between 50 and 160 mm Hg, cerebral autoregulation maintains CBF at relatively constant levels. Not only is autoregulation disturbed in

Herniation

60 55 50 ICP (mm Hg)

45 40 35 30 25 20 15 10 5

Point of hemodynamic decompensation Volume of mass

FIGURE 21-2  Critical time period between decompensation and brainstem herniation after traumatic brain injury.

injured regions of the brain, but a precipitous fall in MAP can further impair autoregulatory function, decreasing CBF and exacerbating ischemia-induced secondary injury. The field provider is able to combat a rise in ICP by simply optimizing MAP through aggressive IV fluid resuscitation. Diagnosis The three useful descriptions of head injury that may be applied to field recognition are history, severity, and morphology. History includes mechanism of injury, timing of the event, and related circumstances. This knowledge assists in the decision-making process with regard to resuscitation and evacuation.3 Mechanism of injury is identified as blunt or penetrating trauma. The anatomic demarcation between blunt and penetrating injury is traditionally defined by violation of the outer covering of the brain (dura mater). Blunt injuries in the wilderness setting most often result from falls, falling objects, or assaults. Penetrating injuries are most commonly gunshot or other projectile wounds. Severity of injury can be estimated by quantifying the GCS and pupillary response. The generally accepted definition of coma is a GCS score less than or equal to 8; these patients often require endotracheal intubation. Although GCS score does not directly correlate with the need for intubation, it is essential that all head-injured patients be provided a stable, secure airway by the most appropriate means available. It is important to note the TBI victim’s best initial motor response because this is most predictive of long-term neurologic outcome. Any victim with a GCS score less than 15 who has sustained a head injury should be evacuated if possible. A low or declining GCS score suggests increasing ICP. Abnormal pupil size or asymmetric pupillary responses suggest increased ICP. These clinical deteriorations demand the rapid attention of rescue or evacuation personnel to optimize MAP and CPP, minimize secondary brain injury, and prevent brainstem herniation. Injury morphology may be difficult to assess in the wilderness setting and relies on level of suspicion and clinical signs and symptoms. After attention to the primary survey, including airway provision and spinal immobilization, the physical examination component of the secondary survey is imperative and can provide information about the presence of a TBI. Injury Classification Intracranial injuries range from concussion to massive subdural hematoma. Subdural hematomas are more common than are epidural hematomas, constituting 20% to 30% of mass lesions. “Subdurals” result from torn bridging veins between the cerebral cortex and draining venous sinuses. Their prognosis is worse than that of “epidurals,” although prompt recognition and drainage improve patient outcome. Epidural hematomas are most commonly located in the temporal region and result from injury to the middle meningeal artery, often associated with a fracture.

These patients may present with loss of consciousness, followed by a lucid interval and subsequent rapid neurologic deterioration. This sequence, however, is not frequently observed. Hemorrhagic contusion is also quite frequent, constituting 35% of traumatic injuries, and has the propensity to significantly increase ICP. Diffuse axonal injury (DAI) is the term used to describe prolonged post-traumatic coma not resulting from a mass lesion or ischemic insult. Similar to hemorrhagic contusion, diffuse axonal injury may result in elevated ICP. Physical Examination After the primary survey and initial attempts to resuscitate the victim, a more complete physical examination should be done. However, this examination should not delay patient evacuation. A hallmark of TBI is altered level of consciousness. Determination of the GCS score aids in recognition of TBI and should be regularly reassessed to provide a mechanism for quantifying neurologic deterioration. Physical signs that may denote underlying brain injury include significant scalp lacerations or hematomas, contusions, facial trauma, and signs of skull fracture. Findings specific for basilar skull fracture include ecchymosis behind the ears (Battle’s sign) and periorbital ecchymosis (raccoon eyes). Blood behind the tympanic membrane on otoscopic examination (hemotympanum), frank bleeding from the ears, and CSF rhinorrhea/otorrhea also suggest skull fracture and underlying TBI. The pupillary examination may provide valuable data in assessing underlying TBI. Herniation of the temporal lobe of the brain may be heralded by mild dilation of the ipsilateral pupil with sluggish response to light. Further dilation of the pupil followed by ptosis (drooping of the upper eyelid below its normal level), or paresis of the medial rectus or other ocular muscle, may indicate third cranial nerve compression by a mass lesion or herniation. Table 21-2 relates pupillary examinations to possible underlying brain lesions. Most dilated pupils (mydriasis) are on the ipsilateral side to the mass lesion. With direct globe injury, traumatic mydriasis may result, making evaluation of TBI more difficult. In addition, 5% to 10% of the population has congenital anisocoria (a normal difference in pupillary size between the eyes). Casual inspection may overlook a prosthetic eye, which is mistaken for a fixed pupil. Neither direct trauma nor congenital anisocoria should be assumed in a head-injured victim exhibiting mental status change in the wilderness. After quantification of GCS score, pupillary examination, and examination of the head and face for signs of external trauma, a concise neurologic examination should be performed. The goal of the field neurologic examination is to identify motor or sensory focal deficits suggestive of intracranial injury. Sensory deficits follow the general dermatome patterns shown in Figure 21-3. Unilateral hemiplegia may signify uncal herniation resulting from mass effect in the contralateral cortex because of compression of the corticospinal tract in the midbrain. Ipsilateral pupillary dilation associated with contralateral hemiplegia is a classic and ominous sign of tentorial herniation. Deep tendon reflex changes in the absence of altered mental status are not indicative of TBI. TABLE 21-2  Interpretation of Pupillary Findings in

Head-Injured Victims

Pupil Size

Light Response

Interpretation

Unilaterally dilated

Sluggish or fixed

Bilaterally dilated

Sluggish or fixed

Unilaterally dilated or equal Bilaterally constricted

Cross-reactive (Marcus Gunn) Difficult to determine; pontine lesion Preserved

Third nerve compression secondary to tentorial herniation Inadequate brain perfusion; bilateral third nerve palsy Optic nerve injury

Bilaterally constricted

Opiates Injured sympathetic pathway

417

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

VOLUME-PRESSURE CURVE

PART 4  INJURIES AND MEDICAL INTERVENTIONS

C2 C2 C3 C4 C5 T1 T2 T3 T4 T5

C6

Posterior cervical rami Posterior thoracic rami Supraclavicular (C3,4) Axillary (C5,6) Medial brachial cutaneous (C8–T1) Radial (C5,8) Anterior thoracic rami Lateral thoracic rami

T6 T7 T8 T9 T10 T11 T12 L1 L2 L3

L4

Musculocutaneous (C5,6) Medial antebrachial cutaneous (C8, T1) Iliohypogastric (L1) Posterior sacral rami Radial (C6–8) Ulnar (C8,T1)

S2 Ilioinguinal (L1)

Median (C5–8)

Lateral femoral cutaneous (L2,3) Obturator (L2,3,4) Anterior femoral cutaneous (L2,3)

C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3

L3 Posterior lumbar rami

S2 L1 L2

Posterior femoral cutaneous (S1,2,3)

L5

Common peroneal (L4,5,S1) Saphenous (L3,4)

S1 Superficial peroneal (L4,5,S1)

Sural (S1,2) Superficial peroneal (L4,5,S1) Deep peroneal (L4,5)

Dermatomes–anterior

CUTANEOUS NERVES

Dermatomes–posterior

FIGURE 21-3  Dermatome pattern, showing the skin area stimulated by spinal cord elements. Sensory deficits follow general dermatome patterns.

Detailed evaluation of brainstem function cannot be undertaken in the wilderness setting. Performance of gag and corneal reflex evaluations may provide some information helpful in triage and evacuation planning, but their presence would not automatically obviate the need for prompt evacuation. Resuscitation Resources and circumstances permitting, resuscitation should be initiated as an adjunct to the primary survey. The primary focus for the head-injured victim, similar to any traumatized victim, is the airway. During the primary survey and performance of the ABCDE sequence, IV access should be established. If IV resuscitation is impossible, it is not advisable to administer fluids orally to the victim with head injury because of the likelihood of vomiting, airway compromise, and aspiration. Individuals sustaining head trauma have a high incidence of concomitant injuries. Up to 32% of persons with severe head injury have a long bone or pelvic fracture, 20% to 25% a chest injury, and 10% an abdominal injury. A victim who does not have a palpable femoral pulse or presents with other signs of hypotension in the context of suspected head injury must not be assumed to have a neurogenic etiology of shock, so other etiologies must be thoroughly and aggressively investigated. Resuscitation is critical in the setting of head injury for multiple reasons. Management of a head injury should be secondary to other life-threatening injuries, which, if not addressed, may preclude survival. As previously discussed, maintenance of MAP (and thus CPP) is critical in preventing secondary brain injury. The type of resuscitative fluid administered to trauma victims continues to be controversial. Previously, recommendations warning of the dangers of overhydration in head injury led to 418

recommendations restricting fluids. Restriction of fluid has not been shown to reduce ICP or edema formation in laboratory models of TBI. Theories about limiting cortical free water content in TBI by using hypotonic IV solutions have not been borne out in animal studies.88 The need for resuscitation and intravascular volume support has been well established. Possible resuscitative fluids include isotonic crystalloids, hypertonic crystalloids, or colloid solutions. There is convincing evidence that hypotonic fluids are not appropriate in TBI secondary to an increase in whole-brain water content and subsequent elevation in ICP. Recent data from animal studies of TBI suggest that colloid solutions offer no advantage over isotonic crystalloids, such as lactated Ringer’s solution, in terms of augmenting CBF or preventing cerebral edema.97 As previously noted, no prospective trial has clearly documented an advantage of colloid over crystalloid administration in the victim with multiple systemic injuries. Evidence is accumulating that hypertonic solutions, particularly hypertonic saline, may be beneficial in TBI.90,94 However, an advantage has not been demonstrated in trauma victims overall, and expertise is necessary for their use. The recommended resuscitative fluid for the head-injured victim in the wilderness setting is isotonic crystalloid, with a target MAP of 85 to 95 mm Hg based on cuff blood pressure determinations or extrapolation from distal pulses evaluation. Further Management Numerous adjuncts exist in the management of the head-injured victim, few of which are applicable in the wilderness setting. Once the primary and secondary surveys are complete, the airway is secured, resuscitation has been initiated, and spine immobilization has been achieved, the victim should be placed

Skull Fracture Skull fracture in the wilderness mandates evacuation. Therapeutic options in the field are few, with intervention limited to identifying the injury and arranging rapid transport. Skull fractures may be open or closed, linear or stellate, and may occur in the vault or skull base. These fractures are associated with a high incidence of underlying intracranial injury. Skull fractures with depression greater than the thickness of the skull may require elevation. No attempt at elevation should be made in the field. Any exposed brain surface should quickly be covered with the most sterile covering available, preferably moistened with crystalloid solution. Loose bone or brain fragments should not be manipulated. If a broad-spectrum antibiotic is available, it should be administered. After attention to the wound and stabilization of associated injuries, the victim should be rapidly evacuated. Penetrating Head Injuries The majority of penetrating head injuries in the wilderness are gunshot wounds, although knives and arrows may penetrate the cranium. Such penetrating injuries are usually catastrophic. However, examples of survival exist with small-caliber, lowvelocity injuries and tangential wounds.59 As with closed head injury, management priorities consist of maintenance of airway, prevention of secondary brain injury, and rapid evacuation. If the cranium has been violated, the victim should receive antibiotics and tetanus immunization in the same manner as for open skull fracture. In the rare instance that the projectile is embedded

in the skull, no attempt at removal should be undertaken. If the length of the projectile makes immobilization or transport cumbersome, excess length may be removed, but only if this can be done without displacement of the intracranial segment. Evacuation Survival and outcome of head injury in the wilderness correlate directly with rapidity of evacuation. Certain situations dictate immediate evacuation. Any person with evidence of an open or closed skull fracture should be evacuated. The incidence of TBI associated with skull fracture is variable but significant throughout the literature. Recent data predict that 30% to 90% of persons with raccoon eyes or Battle’s sign will show abnormalities on computed tomography (CT) scan.11,17 Similarly, any person who sustains a penetrating injury should be evacuated. Decisions concerning evacuation of victims who have sustained closed head injuries can be simplified by dividing the victims into three groups based on probability of injury. A high-risk group, defined as patients with a GCS score of 13 or less, focal neurologic signs, or evidence of decreasing level of consciousness, requires evacuation. The low-risk group includes persons who have suffered a blow to the head but are asymptomatic, did not lose consciousness, and complain only of mild headache or dizziness. Data from recent studies suggest that persons who meet low-risk criteria (including a GCS of 15, no loss of consciousness, minimal symptomatology, and unlikely mechanism) have a minimal chance of having significant TBI and may be closely observed.11,17 This group includes patients who have suffered a concussion. The Quality Standards Subcommittee of the American Academy of Neurology78 defines concussion as a trauma-induced alteration in mental status that may or may not involve the loss of consciousness. The neurologic impairment is short-lived and resolves spontaneously without any structural injury to the brain. Close observation includes awakening the patient from sleep every 2 hours and avoidance of strenuous activity for at least 24 hours. The following signs indicate more advanced medical care is necessary: (1) inability to awaken the patient; (2) severe or worsening headaches; (3) somnolence or confusion; (4) restlessness, unsteadiness, or seizures; (5) difficulties with vision; (6) vomiting, fever, or stiff neck; (7) urinary or bowel incontinence; and (8) weakness or numbness involving any part of the body.51 No prospective validated guidelines for return to activity have been established. Generally, one should not return to an environment in which concussion is a risk (e.g., contact sports) until symptoms have been absent for 7 days. Patients with a predisposition to bleeding need a much more aggressive approach requiring evacuation and evaluation at a higher level of care. The group for which the evacuation decision is most difficult is the moderate-risk group. These persons have a history of brief loss of consciousness or change in consciousness at the time of injury, or a history of progressive headache, vomiting, or posttraumatic amnesia. If any of these signs is present in the face of concurrent systemic injury, the victim should be evacuated immediately. Studies associating clinical variables and abnormal results on CT scan have demonstrated the significance of decreased GCS score, symptoms, and loss of consciousness. If these signs are present in isolation and the evacuation can be completed in less than 12 hours, the evacuation should proceed. If the evacuation is impossible or will require longer than 12 hours, the victim should be closely observed for 4 to 6 hours. If the examination improves to normality during the observation period, it is reasonable to continue observation.

NECK INJURIES Blunt Neck Injuries Injuries to the neck may be classified as blunt or penetrating. Significant blunt injuries include cervical spine injuries and laryngotracheal injuries. Seventy-five percent of injuries to the trachea are confined to the cervical region.72 Fracture of the larynx and disruption of the trachea usually require surgical intervention unavailable in the wilderness. The sooner laryngeal repair is accomplished, the better the outcome with respect to phonation.20 Victims present with a history of a significant blow to the 419

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

in a 30-degree head-up position. This position assists in control of ICP, and thus CPP, through augmentation of venous outflow. This maneuver should not be attempted if the spine cannot be adequately immobilized. If endotracheal intubation is possible, ventilation should be optimized without hyperventilating the victim. Hyperventilation has been used aggressively in the past to promote hypocarbiainduced cerebral vasoconstriction, theoretically to decrease brain swelling. However, if the PaCO2 falls below 25 mm Hg, severe vasoconstriction ensues, effectively reducing CBF, promoting ischemia, and possibly augmenting secondary brain injury. Studies have demonstrated worse outcomes in victims with severe head injury who were hyperventilated.67 Inability to measure or titrate PaCO2 in the wilderness mandates that res­ piration be controlled to approximate near-normal minute ventilation. All bleeding from the scalp or face should be controlled with direct pressure. Scalp hematomas, regardless of size, should not be decompressed. Open wounds, particularly skull fractures, should be irrigated and covered with the most sterile dressing available. Fragments of displaced cranium overlying exposed brain tissue should not be replaced. If signs of skull fracture are present, broad-spectrum antibiotic prophylaxis and immunization against tetanus are recommended as soon as possible. Although diuretics have been widely used in the intensive care management of intracranial hypertension, no rationale exists for their use in the field. The wilderness trauma victim may have many injuries that are impossible to evaluate fully in the field. In this setting, particularly in the presence of hemorrhagic shock, attempts to induce osmotic diuresis to decrease ICP may be lifethreatening. Diuretics such as furosemide or mannitol may exacerbate hypotension, cause metabolic alkalosis, and induce renal complications in the absence of physiologic monitoring.2 Corticosteroids have no role in head injury in the field or intensive care unit. Studies have documented no beneficial impact on ICP or survival. Attempts at brain preservation by slowing metabolic rate and oxygen consumption have no role in the wilderness setting. Barbiturates have been used for elevated ICP refractory to other measures, but may induce hypotension, depress myocardial function, and confound the neurologic examination.2 Compared with minimizing ICP, these interventions offer no significant benefit.39 Approximately 15% of persons with severe head injury experience post-traumatic seizures. Phenytoin, if available, can be safely administered in the field, but only after a witnessed seizure. Prophylactic administration has not been shown to decrease long-term seizure activity.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

anterior neck. Physical examination findings include difficulty with phonation, subcutaneous emphysema that may extend as far inferiorly as the abdominal wall, stridor, odynophagia, and often acute respiratory distress. Treatment is focused on establishing and maintaining an airway until evacuation can occur. Frequently the airway is in jeopardy. Because of the propensity for injuries of this type to result in significant and progressive edema, endotracheal or nasotracheal intubation is often necessary. If these options are unavailable, airway maintenance techniques, as described in the Primary Survey section, should be used. In the event of intubation failure or lack of availability with impending hypoxic death, a surgical cricothyrotomy may be needed. A recent study of prehospital cricothyrotomy demonstrated that success rates were high regardless of medical specialty as long as previous training had been accomplished.53 For further descriptions of airway management, refer to Chapter 20. Background.  Vertebral column injury, with or without neurologic deficits, must be identified in any wilderness multipletrauma victim. Fifteen percent of victims sustaining an injury above the clavicles and 5% to 10% of persons with a significant head injury have a cervical spine injury. In addition, 55% of spinal injuries occur in the cervical region.59 In the wilderness setting, fractures or dislocations of the cervical spine are a result of falls from significant heights or of high-velocity ski or vehicular injuries. Twenty-eight percent of persons with cervical spine fractures have fractures elsewhere in the spine.10 Anatomy.  The cervical spine consists of seven vertebrae. The anteriorly placed vertebral bodies form the weight-bearing structure of the column. The bodies are separated by intervertebral disks and held in place anteriorly and posteriorly by longitudinal ligaments. The paraspinal muscles, facet joints, and interspinous ligaments contribute as a whole to the stability of the spine. The cervical spine, based on its anatomy, is more susceptible to injury than are the thoracic and lumbar spine. The cervical canal is wide from the foramen magnum to C2, with only 33% of the canal constituting the spinal cord itself. The clinically relevant tracts in the spinal cord include the corticospinal tract, spinothalamic tract, and posterior columns. Classification and Recognition.  Fractures of the cervical spine may result in neurologic deficit, with total loss of function below the level of injury.49 Spinal cord injuries should be classified according to level, severity of neurologic deficit, and spinal cord syndrome. Fractures of the C1-C2 complex generally result from axial loading (a C1 ring fracture, or Jefferson’s fracture) or an acute flexion injury (a C2 posterior element fracture, or hangman’s fracture). Approximately 40% of atlas (first cervical vertebra) fractures have an associated fracture of the axis (second cervical vertebra). The atlas fracture, if survived, is rarely associated with cord injury but is unstable and requires strict immobilization. Usually a complete neurologic injury at this level is unsurvivable owing to paralysis of respiratory muscle function. One-third of victims sustaining a severe upper cervical spine injury die at the scene. The severity of cervical spine fractures is a result of the neurologic compromise incurred. The most common mechanism of injury is flexion, and the most common level of injury is C5-C6.10 Fractures and dislocations may result in partial or complete neurologic injury distal to the fracture or in no neurologic injury at all. Partial injuries to the spinal cord result from typical patterns of injury. Because flexion injuries are the most common type of injury to the cervical spine, the anterior cord syndrome (see later) is the most commonly seen serious neurologic picture. A careful neurologic examination in the field to grade motor strength and document sensory response to light touch and pinprick yields important information that should be documented and reported to the treating physician at the definitive care facility. When appropriate resources are available, a rectal examination should be performed. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicate the presence of spinal cord injury. 420

When individuals with cervical spine fractures or dislocations are transported, the neck must be stabilized to prevent further injury to the spinal cord or nerve roots at the level of the fracture or dislocation. Approximately 28% of persons with cervical spine fractures have fractures elsewhere in the spine10; therefore the entire spine must be protected during transport. Occasionally a pure flexion event can result in dislocation of one or both of the posterior facets without fracture or neurologic injury. The victim may complain only of neck pain and limitation of motion. If so, the victim should be transported with the neck rigidly immobilized. With this injury, posterior instability is present (because the interspinous ligament is ruptured), and any further flexion stress could produce a spinal cord injury. Physical Examination.  A thorough neurologic examination should be performed. Initial documentation of deficits and frequent repeat examinations are critical to follow-up care. The classification of injury in the field begins with determination of the level of injury. Knowledge of sensory dermatomes (see Figure 21-3) and motor myotomes is invaluable. The sensory level is the lowest dermatome with normal sensation and may differ on each side of the body. C1 to C4 are variable in their cutaneous distribution, so assessment should begin at C5. The examiner should not be confused by the occasional innervation of the pectoral skin by C1 to C4, known as the “cervical cape.” Light touch and pinprick should be assessed. Motor function should be assessed by the myotomal distribution listed in Box 21-2. Each muscle should be graded on a sixpoint scale: 0—Total paralysis 1—Palpable or visible contraction 2—Full range of motion without gravity 3—Full range of motion against gravity 4—Full range of motion with decreased strength 5—Normal strength Each muscle must be tested bilaterally and documented. The reflexes alluded to in the classification section, as well as anal sphincter tone, must be tested. Syndromes.  There are three clinically useful spinal cord syndromes: Central cord syndrome is characterized by a disproportionate loss of motor power between the upper and lower extremities, with greater strength retained in the lower extremities. Sensory loss is variable. The mechanism of injury usually involves a forward fall with facial impact and hyperextension of the spine. Anterior cord syndrome is characterized by paraplegia and loss of pain and temperature sensation. It is the most common manifesting syndrome caused by cervical spine injury and carries a poor prognosis. Brown-Séquard syndrome results from hemisection of the cord. It consists of ipsilateral motor loss and position sense with contralateral sensory loss two levels below the level of injury. It is usually secondary to penetrating injury. Immobilization.  After identification of injury, the caregiver faces a critical decision with important ramifications—whether to immobilize.29 Victims who would as a matter of course be immobilized in an urban setting might not be appropriate candidates for immobilization in the wilderness. The decision to immobilize converts an otherwise ambulatory victim who can actively participate in his or her own evacuation to one requiring more involved evacuation procedures. The subsequent evacuation can be dangerous to the victim and rescuers and demands significant expense and resource utilization. Risk criteria for cervical spine injury and the need for immobilization have been defined.43,56 All criteria for the exclusion of immobilization must be satisfied. These include normal mental status without chemical influence; lack of distracting injury; normal neurologic examination; and a reliable neck examination without midline neck pain, deformity, or tenderness. Figure 21-4 presents an evidence-based algorithm for determining need for immobilization. Although the need for immobilization poses hazards for the evacuation process, if criteria are met, immobilization takes

Sensory C5: Area over deltoid C6: Thumb C7: Middle finger C8: Little finger T4: Nipple T8: Xiphisternum T10: Umbilicus T12: Symphysis pubis L3: Medial aspect of thigh L4: Medial aspect of leg L5: First toe web space S1: Lateral foot S4 and S5: Perianal skin FIGURE 21-5  Proper spine immobilization.

Motor C5: Deltoid C6: Wrist extensors C7: Elbow extensors C8: Finger flexors, middle finger T1: Small finger abductors L2: Hip flexors L3: Knee extensors L4: Ankle dorsiflexors L5: Great toe extensors S1: Plantar flexors

precedence over ease of evacuation.63 A difficult balance must be struck in the wilderness between the likelihood of true injury and the danger to the expedition members and rescuers that may ensue when the victim is immobilized. If a rigid litter is not available, the victim should be maintained on the flattest surface possible. A rigid cervical collar should be placed. All collars allow some degree of movement, particularly rotation. Soft collars offer the least immobilization.28 The Philadelphia collar has been shown to allow 44% of normal rotation and 66% of normal lateral bending.59 To achieve 95% immobilization, a halo and vest are necessary. Any number of materials may be used to improvise an immobilizing device (see Chapter 23). Restriction of flexion, extension, and rotation must be achieved to the greatest degree possible. Optimal immobilization consists of a long spine board or litter, rigid collar, bolsters to the sides of the head, and tape or straps restricting movement (Figure 21-5). Treatment.  The issue of pharmacotherapy for spinal cord injury is under continuous study. Currently, based on data accumulated by the National Acute Spinal Cord Injury Study Group,

documented blunt spinal cord injury should be treated with a bolus of 30 mg/kg of methylprednisolone within 8 hours of injury followed by a continuous infusion of 5.4 mg/kg/hr over the next 23 hours.14 Corticosteroids are not recommended in the field unless a victim clearly presents with a spinal cord injury in the absence of head injury. Because little definitive treatment for cervical spine injury can be accomplished in the field, survival and outcome depend on speed of transport and maintenance of airway. This is particularly true considering the association of cervical spine injury with head injury and major systemic trauma. Transport all victims with proven or suspected cervical spine injury to a definitive care facility. Penetrating Neck Injuries Similar to penetrating head injury, penetrating neck injury is usually due to gun or knife wounds. Most penetrating injuries do not confer bony instability; however, stability should not be assumed. Neurologic deficits, if present, can progress with further movement of an unstable spine. Projectiles should not be removed if embedded in the neck. Penetrating injuries to the neck may not directly injure the spine, but neurologic sequelae may result from blast effect. The same immobilization criteria should be implemented as when dealing with blunt injuries. Penetrating injuries to the neck are classified according to anatomic zones of injury (Figure 21-6). Zone I injuries extend from the clavicles to the cricoid cartilage. Zone II injuries occur between the cricoid cartilage and the angle of the mandible. Zone III injuries occur superior to the angle of the mandible. Historically, treatment has been based on penetration of the platysma muscle. In the wilderness setting, if the examiner is confident that platysmal penetration has not occurred, the victim may be observed and the wound considered a laceration. Much

Mechanism of injury suggestive of cervical spine injury? Yes/unknown Alert and oriented, no distracting injury, not intoxicated? Yes

III

II

Tenderness, pain spontaneously or with movement? No

I

Normal neurologic exam? Yes Immobilization unnecessary? FIGURE 21-4  Clinical assessment of cervical spine stability. Failure of any criterion suggests need for immobilization.

FIGURE 21-6  Zones in penetrating neck trauma (see text).

421

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

BOX 21-2  Sensory and Motor Deficit Assessment

PART 4  INJURIES AND MEDICAL INTERVENTIONS

debate has occurred over management of platysmal penetration within respective topographic zones, with treatment arms con­ sisting of surgical exploration versus radiographic evaluation. In the wilderness setting, such considerations remain relevant. A penetrating injury violating the platysma muscle indicates the possibility of significant neurovascular, esophageal, or tracheal injuries, so the victim should be evacuated with close attention to the airway.

INJURIES TO THE THORAX Background The mortality rate from thoracic trauma is approximately 10%. Approximately 25% of all trauma deaths in the United States are attributable to chest injury.3 However, only 15% of persons with penetrating thoracic trauma require thoracotomy. In the wilderness environment, blunt thoracic injuries usually result from falls or direct blows to the chest. Penetrating injuries result from gun, knife, or arrow wounds, or from impalement after a fall. Immediate, life-threatening thoracic injuries include airway obstruction, tension pneumothorax, flail chest, and cardiac tamponade. Pathophysiology Chest injuries often result in hypoxia, hypercarbia, and acidosis. The tissue hypoxia of thoracic trauma can be multifactorial. Inadequate delivery of oxygen can be from hemorrhagic shock, direct lung injury with ventilation–perfusion mismatch (pulmonary contusion, atelectasis, hematoma), or changes in normal intrathoracic pressure dynamics (tension or open pneumothorax). Hemodynamic instability and inadequate oxygen delivery may also result from cardiac tamponade or contusion. The expedition team member should report to any air crew the consideration of pneumothorax in the evacuated patient. Many wilderness expeditions involve travel to different altitudes. Flight medics are well trained in the impact of altitude on air in closed spaces. Flight medics may be better equipped and prepared to deal with chest injuries than is the expedition team. The air crew will also know the flight path and anticipated elevations to traverse to reach the next level of care. Physical Examination Thorough physical examination begins with visualization and inspection of the chest. Exposure of the chest should be completed in the primary survey. The airway is assessed for patency and air exchange, and the pattern of breathing is noted. In the immediate postinjury period, most trauma victims are tachypneic, partly from pain and anxiety. Dyspnea, cyanosis, the use of accessory muscles of respiration, and intercostal muscular retraction are abnormal and may give clues to the underlying injury. Chest wall movement during respiration should be symmetric. Paradoxical chest wall movement is associated with flail chest. The chest wall should be inspected for contusions and abrasions, which may herald underlying bony or visceral injury. Distention of the external neck veins in a person who has just suffered thoracic trauma and is hypotensive or tachycardic (heart rate greater than 130 beats/min) suggests impaired venous return to the heart. This finding may be seen in situations of increased intrathoracic or intrapericardial pressure and is associated with tension pneumothorax and pericardial tamponade. In tension pneumothorax, deviation of the trachea is in a direction opposite the lesion. One technique to identify the deviated trachea is to place the index finger in the suprasternal notch. Dyssymmetry of the space between the trachea and the lateral margins of the suprasternal notch facilitates identification of tracheal deviation. However, a recent review suggests the tracheal deviation should be de-emphasized as an indicator of tension pneumothorax because tracheal deviation was observed in less than 5% of two series of patients with pneumothorax.54 Significant sternal bruising may herald fracture or cardiac contusion. The thorax should be palpated systematically for bony tenderness, starting at the distal clavicles and working medially toward the sternum. The sternum is divided into the manubrium, 422

gladiolus (body), and xiphoid cartilage. The manubrium is joined to the gladiolus by fibrocartilage, but mobility at this joint is minimal. Each rib should be palpated individually. Ribs 1 to 7 are vertebrosternal; their costal cartilages join the sternum. Ribs 8 through 10 are vertebrochondral, with each costal cartilage commonly joining the cartilage of the rib above. Ribs 11 and 12 are vertebral ribs without attachment to the sternum. Point tenderness over a rib can be associated with contusion or fracture. Displaced fractures can be palpated; occasionally, bone grating can be palpated during respiration. Subcutaneous emphysema may extend up into the neck and down to the level of the inguinal ligaments. In the trauma situation, subcutaneous emphysema is invariably associated with pneumothorax. Vocal fremitus describes palpation of vibrations transmitted through the chest wall. During speech, the victim’s vocal cords emit vibrations in the bronchial air column that are conducted to the chest wall. Diminished vocal fremitus is associated with pneumothorax or hemothorax. To test for vocal fremitus, the examiner applies the palmar arch of the examining hand against the person’s anterior chest wall. The person is asked to repeat “one, two, three,” using the same pitch and intensity of voice with each repetition. If the vibrations are not well perceived, the patient is asked to lower the pitch of the voice. The chest should be symmetric, left to right. Percussion is used to detect changes in the normal density of an organ. Percussion of the chest is performed by placing the examining fingertips on the chest wall and sequentially striking the fingertips with the tip of the index or middle finger of the other hand. In the trauma victim, dullness replacing resonance in the lower lung suggests hemothorax. Hyperresonance or tympani replacing resonance occurs only with a large pneumothorax or tension pneumothorax. If a stethoscope is not available, primitive chest auscultation can be performed using a rolled piece of cardboard or paper. Any cylinder that can transmit sound through a column of air accentuates breath sounds when placed against the chest wall. The absence of sounds normally produced by the tracheobronchial air column indicates blockage in the airways or abnormal filtering of sound by fluid in the pleural cavity. In the trauma victim, this is invariably associated with pneumothorax or hemothorax. Ultrasound may be considered as an extension of the physical examination. Portable ultrasound systems are lightweight and durable. Ultrasound can be used to identify pneumothorax with greater sensitivity than physical examination. A pneumothorax can be identified by loss of the “comet tails” or pleural sliding. In a study using CT as the gold standard for identification of pneumothorax in 176 victims of blunt trauma, the sensitivity and specificity for ultrasound were 98.1% and 99.2%, respectively. This compared with the sensitivity and specificity for chest radiography of 75.5% and 100%, respectively.9 Six articles on the use of ultrasound to identify hemothorax concluded that ultrasound is a sensitive and specific method to identify hemothorax in trauma patients.61 Chapter 92 addresses the use of ultrasound and telemedicine in the wilderness. Blunt Chest Trauma Blunt chest trauma in the wilderness is most often associated with either a direct blow or a deceleration injury. The mechanism usually relates to a fall from a height. Compression of the chest wall by moving or falling debris may also contribute to intrathoracic injuries, as may be seen in traumatic asphyxia associated with burial in an avalanche or earthquake. Rib Fractures.  Rib fractures range in severity from an isolated nondisplaced single fracture, which causes minor discomfort, to a major flail segment, which can be associated with an underlying hemopneumothorax and pulmonary contusion. Rib fractures are characterized by painful respiration, most severe on inspiration. Victims often breathe in a characteristically rapid, shallow pattern. Point tenderness is palpated over the fracture, and displacement can occasionally be detected. Rib fractures are detected with a compression test, in which pressure is exerted on the sternum

Costochondral Separation.  It is difficult to distinguish between a rib fracture and costochondral separation. With the latter, pain is more likely to be predominantly anterior over the costochondral junction. Pain increases with inspiration and worsens with direct palpation. Costochondral separation also responds to intercostal nerve block and oral and IV analgesics. Sternal Fracture.  A sternal fracture is usually associated with a direct blow to the anterior chest wall. The injury is characterized by severe, constant chest pain that worsens with direct palpation. Sternal instability is unusual and can be associated with a significant underlying visceral injury, including pulmonary or myocardial contusion. If the sternum is unstable, the victim should immediately be evacuated by litter or helicopter. Pneumothorax.  Simple pneumothorax can occur from an injury that allows air to enter through the thoracic wall or, more frequently, from an injury to the lung that permits air to escape into the pleural space. Symptoms include tachypnea, dyspnea, resonant hemithorax, absence of breath sounds, and tactile fremitus. A person with chest pain after a blunt blow to the chest, particularly with accompanying rib fracture, should be suspected of having a pneumothorax. Treatment of pneumothorax involves decompression of the pleural space. In the wilderness environment, tube thoracostomy is rarely possible. Fortunately, although victims with isolated pneumothorax may complain of chest pain or dyspnea, they are not completely disabled. With analgesia to control pain, ambulation facilitates evacuation. It may be easier and more prudent to set a slow pace with frequent rest periods than to perform an unnecessary litter evacuation. If resources and expertise allow placement of a thoracostomy tube, it should be performed only when clinically indicated. Considering possible morbidity in a remote area, prophylactic decompression should never be undertaken. Suspicion of a pneumothorax alone on physical examination does not warrant a catheter or chest tube. When a high index of clinical suspicion is accompanied by incapacitating symptoms, such as shortness of breath, decompression should be considered. The key to saving a victim’s life is understanding that a condition exists that can rapidly progress from a nondisabling condition to a lifethreatening condition. Once the diagnosis of pneumothorax is entertained, vigilant observation and a high index of clinical suspicion are necessary in the event of progression to a tension pneumothorax. Symptoms should be closely monitored, and frequent repeat examinations should be performed. Tension Pneumothorax.  A tension pneumothorax develops when a one-way air leak follows lung rupture or chest wall penetration. Air is forced into the thoracic cavity with no means of escape, and pressure mounts within the hemithorax. With sufficient increases in intrathoracic pressure, the mediastinum is shifted to the contralateral side, which impedes venous return from both the superior and inferior venae cavae. Cardiac output is diminished, and the victim soon exhibits signs and symptoms

of shock. Victims with tension pneumothorax present with distended neck veins and tracheal deviation away from the side of the lesion. There is unilateral absence of breath sounds, and the hemithorax is hyperresonant or tympanitic. Respiratory distress, cyanosis, and frank cardiovascular collapse may occur. Tension pneumothorax is life threatening and frequently associated with additional serious injuries. It mandates rapid chest decompression, followed by evacuation to a medical facility. Decompression is performed by inserting a needle or catheter into the chest and converting the tension into an open pneumothorax. Ideally, a 14-gauge catheter is inserted percutaneously over the second rib in the midclavicular or over the fifth or sixth intercostal space along the anterior axillary line (Figure 21-7). Once the rib is identified with the tip of the needle, the needle is marched over the anterior superior surface of the rib and inserted through the intercostal muscles and pleura into the thoracic cavity. As the pressure within the hemithorax is released, a distinct rush of air is heard. The plastic catheter is advanced over the tip of the needle, the needle withdrawn, and the catheter left in place to ensure continued decompression. The needle should not be reintroduced into the catheter because it may damage or sever the catheter. Because tension pneumothorax is commonly associated with severe injury, the victim should be evacuated to a medical facility as rapidly as possible. A rubber glove or a finger cot can be attached to the external catheter opening to create a unidirectional flutter valve that allows egress of air from the pleural space. The Asherman chest seal (Figure 21-8) can be applied directly over the 14-gauge catheter and serves as a one-way valve to permit evacuation of pleural air. The Asherman chest seal can also be applied to sucking chest wounds to permit more normal chest dynamics (see Penetrating Chest Trauma). If resources are limited and treatment is needed, any number of devices can be used to decompress the chest. A sharp instrument and hollow tube sterilized as well as possible are all that is needed. Rapid cleansing of the skin surface is accomplished with antiseptic, alcohol, or water. A Heimlich valve kit is ideal for decompression and represents a valuable addition to the expedition first-aid arsenal. If resources permit placement of a thoracostomy tube, adequate anesthesia and expertise are required. The skin should be sterilized if possible, and local anesthetic should be infiltrated

Fifth rib Intercostal vessels and nerves Air escaping from pleural space

Lung

Sixth rib

Parietal pleura

Pleural space

Visceral pleura

FIGURE 21-7  Needle decompression of tension pneumothorax. This procedure is performed only for tension pneumothorax in patients with hemodynamic instability.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

while the victim lies supine. This will elicit pain over the fracture site. Most patients with rib fractures can be managed with oral analgesics and rest. Thoracic taping and splinting are contraindicated. Multiple rib fractures are significant because of the potential seriousness of associated injuries and increased pain. However, if extreme and compromising respirations, this pain responds well to an intercostal nerve block. Victims with multiple rib fractures need to be evacuated as conditions permit. After administration of an intercostal block, a person may regain the ability to hike out of the wilderness. The morbidity of rib fractures relates to decreased inspiratory tidal volume secondary to pain and splinting. In the wilderness setting, management must focus on pain control and pulmonary toilet. If oral analgesia is insufficient to control pain, an intercostal block is ideal. Depending on the anesthetic used, varying durations of analgesia can be attained, perhaps allowing transient ambulation for evacuation. Deep breathing should be encouraged at a rate of 10 times hourly to help prevent atelectasis.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

flail segment only to control unnecessary motion and pain may provide minimal relief from the discomfort.

FIGURE 21-8  Asherman chest seal.

into the skin and periosteum of the rib. Insertion is most effectively accomplished through the fifth intercostal space at the anterior axillary line. A small incision is made and the subcutaneous tissue bluntly separated with a finger or clamp. A blunt instrument, preferably a clamp, is forcefully inserted into the pleural space closely adhering to the superior surface of the rib to avoid the inferiorly located intercostal neurovascular bundle. Once the pleural space is entered, a tube (36F or greater in size) is inserted apically and posteriorly. The tube should then be secured with suture or tape and 10 to 20 cm H2O suction or underwater seal applied. A tube open to the atmosphere can accomplish decompression. The end of the tube can be covered with a rubber glove, finger cot, or plastic bag modified to permit unidirectional flow of air. One-way flow evacuating the chest is the goal. This procedure is not without morbidity and should be used only by trained personnel under optimal conditions. Antibiotics with grampositive coverage should be initiated if the pleural space is penetrated with an indwelling catheter or tube. Hemothorax.  Hemothorax is usually associated with multiple rib fractures resulting from a direct blow to the chest. The primary cause of a hemothorax is laceration of the lung, intercostal vessel, or internal mammary artery. The victim complains of chest pain, tenderness associated with rib fractures, inspiratory pain, and dyspnea. Vocal fremitus is absent, percussion may be flat or dull, and breath sounds are diminished or absent. A chest tube for hemothorax is rarely required in the wilderness setting but may be placed if proper equipment is available, the patient is symptomatic, and evacuation will be prolonged. Needle aspiration of a hemothorax is unnecessary in the immediate postinjury period and may precipitate a pneumothorax. Flail Chest.  When a series of three or more ribs is fractured in both the anterior and posterior planes, a portion of the chest wall may be mechanically unstable. As negative intrathoracic pressure develops during inspiration, the unstable segment paradoxically moves inward and inhibits ventilation. A flail segment indicates a severe direct blow to the chest wall with associated multiple rib fractures and decreased tidal volumes, often with associated underlying pulmonary contusion. The contusion can be expected to progressively impair ventilation and oxygenation over the succeeding 48 hours. Victims often tolerate a flail segment for the first 24 to 48 hours, after which they require mechanical ventilation. Any victim with a flail segment should be rapidly evacuated. Because the victim is usually incapable of participating in evacuation, a litter should be prepared or aeromedical evacuation considered. Intercostal nerve block may assist in short-term management of pain and pulmonary toilet. Restrictive (to chest wall expansion during inhalation) external chest wall supports, including taping or extensive stabilization with sandbags, are contraindicated. These measures hinder chest wall movement, decrease vital capacity, and are less effective than intercostal nerve block in pain control. However, focal stabilization or cushioning of the 424

Blunt Cardiac Injuries.  Blunt cardiac injuries leading to pericardial tamponade or cardiac contusion are rare. Pericardial tamponade is life threatening. The pericardial sac is fibrous and expands little. A small amount of intrapericardial blood can severely restrict diastolic function. Blunt injury resulting in tamponade is usually from chamber rupture and rarely survivable, particularly in a remote setting. The diagnosis of tamponade can be difficult, particularly in the wilderness. Beck’s triad, which consists of distended neck veins, hypotension, and muffled heart sounds, is present in less than 33% of cases of tamponade and is particularly difficult to ascertain under nonoptimal conditions. Pulsus paradoxus, an increase in the normal physiologic decrease in blood pressure with inspiration, may be indicative of tamponade. Kussmaul’s sign, or a rise in venous pressure with spontaneous inspiration, is possible to assess outdoors. Once pericardial tamponade is diagnosed, immediate evacuation is required. Treatment consists of median sternotomy in a hospital operating room. The only temporizing measure pending evacuation is pericardiocentesis. This procedure can be lifesaving, particularly if a cardiac injury with a slow leak exists. However, its application in the wilderness setting should occur only if there is a high index of suspicion, coupled with shock and impending death unresponsive to resuscitative efforts. A long (approximately 15 cm [6 inches]), 16- to 18-gauge needle with an overlying catheter is introduced through the skin 1 to 2 cm (0.5 to 0.75 inches) below and to the left of the xiphoid. The needle is advanced at a 45-degree angle with the tip directed at the tip of the left scapula. When the pericardial sac is entered, aspiration with a syringe follows. The catheter is left in place and secured for possible repeat aspirations as the victim’s condition warrants. Immediate evacuation should follow. Cardiac contusion is a rare condition resulting from a severe blow to the precordium. An overlying sternal contusion or fracture may be present. The diagnosis should be suspected in an isolated high-velocity blow to the precordium with unexplained evidence of increased venous pressure, arrhythmias, and hemodynamic instability. Chest pain is invariably present, usually resulting from musculoskeletal contusion. Morbidity results from ensuing arrhythmias. Diagnosis can be definitively made only at autopsy. Electrocardiographic abnormalities after injury have correlated with subsequent arrhythmias.55 In the wilderness setting, any person who is unstable or symptomatic from an arrhythmia should be evacuated. If evacuation is not possible, it is noteworthy that fatal arrhythmia potential decreases significantly after 24 hours. Traumatic Asphyxia.  Traumatic asphyxia is a rare syndrome of craniocervical cyanosis, facial edema, petechiae, subconjunctival hemorrhage, and occasional hypoxemia-related neurologic symptoms that results from severe thoracic crush injury. In the wilderness environment, it is associated with landslides or mud slides, avalanches, or falling debris. Any significant blunt compressive force to the thorax can result in the syndrome. Children are particularly susceptible because of high compliance of the chest wall.15 Traumatic asphyxia is associated with a high incidence of serious associated injuries,1,70 and the mortality rate in natural disasters is consequently high.32 A significant crush injury component may accompany traumatic asphyxia.32 Crush injuries and rhabdomyolysis are discussed later in the Extremity Trauma section of this chapter. The pathophysiology of traumatic asphyxia involves two elements. The crush injury results in acute increases in intrathoracic pressure and thus inferior and superior vena caval pressures. Venous flow is reversed in the veins of the head, which contain no valves. Venous hypertension leads to capillary rupture and the characteristic facial edema and petechiae. Recognition of the physical findings is imperative in diagnosing the syndrome and identifying concomitant injuries (Figure 21-9). Treatment consists of carefully extracting and, if necessary, immobilizing the victim. Rapid extrication is the single most important factor in improving survival. Establishment and

FIGURE 21-9  Typical clinical facial appearance of traumatic asphyxia.

maintenance of an airway is critical because significant facial and laryngeal edema may rapidly develop. Associated injuries should then be addressed in the primary survey. Subsequent care is supportive, consisting of airway control, administration of oxygen, head elevation of 30 degrees, treatment of associated injuries, and possible evacuation. The mortality rate is low in civilian environments but higher in wilderness disaster settings. Mortality is due to pulmonary dysfunction and associated injuries. Morbidity is secondary to neurologic damage; however, the majority of neurologic sequelae clear within 24 to 48 hours. If the victim survives, long-term sequelae are rare. Penetrating Chest Trauma Penetrating chest trauma above the nipple line is associated with hemopneumothorax and may also be associated with significant visceral injury. A victim with penetrating chest trauma below the nipple line often has intra-abdominal penetration in addition to possible thoracic injury. Such a victim requires immediate rapid evacuation. The open (“sucking”) chest wound produces profound intrathoracic physiologic alterations. Normal chest expansion creates negative intrathoracic pressure, which pulls air into the trachea and allows the lungs to expand. When the diaphragm and chest wall relax, positive pressure creates expiration. If the chest wall sustains an injury approximately two-thirds the tracheal diameter, negative intrathoracic pressure for inspiration is lost, the ipsilateral lung collapses, and loss of negative intrathoracic pressure affects the good lung. Consequently, it is important to rapidly reconstruct chest wall integrity. Initially this is most easily done by placing a hand over the sucking chest wound. Field treatment includes placing petrolatum gauze on top of the wound, covering it with a 4 × 4 gauze pad, and taping it on three sides (Figure 21-10). The untaped fourth side serves as a relief mechanism to prevent tension pneumothorax. Persons with sucking chest wounds should be rapidly evacuated to sophisticated medical care. Alternatively, an Asherman chest seal could be applied over the wound.

Anatomy.  For descriptive purposes, the abdomen may be divided into thoracic, true, and retroperitoneal compartments. The thoracic abdomen contains the liver, spleen, stomach, and diaphragm. The liver, spleen, and, more rarely, stomach may be injured by direct blows to the ribs or sternum. Twenty percent of persons with multiple left lower rib fractures have a ruptured spleen. A direct blow to the epigastrium may result in increased intra-abdominal pressure with subsequent rupture of the liver or diaphragm. The true abdomen contains the small bowel, large bowel, and bladder. Isolated bowel injuries are rare in the wilderness setting. Blunt bladder or rectal injury usually occurs in conjunction with severe pelvic fracture and carries high mortality. The retroperitoneal abdomen contains the kidneys, ureters, pancreas, and great vessels. It is notoriously difficult to evaluate by physical examination. Life-threatening hemorrhage can occur into the true abdomen or retroperitoneal space. Diagnosis.  The wilderness physician must have a high index of suspicion and perform a superlative history and physical examination. Physical Examination.  The physician should look for signs of early shock: tachycardia, tachypnea, delayed capillary refill, weak or thready pulse, and cool or clammy skin. Physical examination of the abdomen begins with visualization and inspection. Contusions and abrasions may be the only harbingers of occult visceral injury. Periumbilical ecchymosis associated with abdominal hemorrhage (Cullen’s sign) is virtually never present in a victim with acute abdominal trauma. Abdominal distention secondary to hemorrhage is a very late sign and never present before shock and cardiovascular collapse. Abdominal inspection should survey the flanks, lower chest, and back. Inspection of the back should follow palpation of the spine while the victim is supine. The victim should be very carefully logrolled if there is any suspicion of spinal injury. Looking for muscle guarding, the examiner gently palpates the abdomen in all four quadrants. Any persistent guarding or tenderness after wilderness trauma mandates rapid evacuation. Percussion tenderness is an indicator of peritoneal irritation, also mandating evacuation. The presence or absence of bowel sounds has little prognostic significance. Bowel sounds may be present in the face of significant intra-abdominal hemorrhage or, conversely, absent in victims when extra-abdominal injuries induce ileus. Referred pain to the left shoulder (Kehr’s sign) strongly suggests the presence of a ruptured spleen. This pain is often exaggerated by placing the victim in the Trendelenburg position,

INJURIES TO THE ABDOMEN Intra-abdominal injuries in the wilderness setting are difficult to recognize. However, if recognized, all intra-abdominal injuries require rapid resuscitation and immediate evacuation. The abdomen represents the most frequent site of life-threatening hemorrhagic shock; however, in the wilderness setting, few diagnostic and treatment options exist. Blunt Abdominal Trauma Blunt intra-abdominal injury is commonly associated with falls. Abdominal injuries are often associated with fractures or closed head injuries. Often the decision for evacuation is made on the basis of other injuries; however, the wilderness physician must

Petrolatum gauze and 4˝ x 4˝ gauzepad

FIGURE 21-10  Treatment of a sucking chest wound. Sealing the wound with a gel defibrillator pad works best because this pad adheres to wet or dry skin. Petrolatum gauze or plastic wrap also works well. Note that one side is not sealed to allow egress of air.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

be attuned to the potential for intra-abdominal hemorrhage as an occult injury.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

increasing the amount of left upper quadrant blood irritating the diaphragm. Pain from the retroperitoneal abdomen associated with injuries to the kidneys or pancreas may be referred to the back. However, referred pain is usually a late finding and not helpful in the evaluation of acute trauma. Gross hematuria that does not clear immediately or is coupled with an associated injury, such as pelvic fracture or abdominal or back pain, requires immediate evacuation. To minimize blood loss, the victim should be kept stationary and the evacuation team brought as close to the victim as possible. In a wilderness setting, rectal and vaginal examinations add little to the evacuation decision when evaluating for abdominal trauma. The unstable pelvic fracture associated with rectal and vaginal injuries is usually the determinant for evacuation. Diagnostic modalities in the austere environment are limited. Plain imaging, CT scans, and diagnostic peritoneal lavage have a very limited role. Ultrasound can be used to identify fluid in the peritoneum. Penetrating Abdominal Trauma Penetrating intra-abdominal injuries may result from gunshot, stab, or arrow wounds. The social context in which these injuries occur (accidental, intentional, or self-inflicted) makes little difference in the wilderness setting. Recrimination, guilt, and blame only interfere with the paramount goal of immediate evacuation. Gunshot Wounds.  Low-caliber gunshot injuries often manifest with small entrance and no exit wounds. High-caliber, highvelocity gunshot injuries may have relatively innocuous entrance wounds but may be associated with large, disfiguring exit wounds and extensive internal injuries. No matter what the caliber or trajectory and no matter where the entrance and exit, all gunshot wounds from the nipple line to the inguinal ligament should be presumed to have penetrated the abdominal cavity and created an intra-abdominal injury. These injuries mandate immediate surgical intervention. A victim of gunshot wounds to the head, neck, chest, abdomen, or groin should undergo immediate evacuation accompanied by the administration of a single-agent broad-spectrum antibiotic, such as an oral fluoroquinolone (e.g., ciprofloxacin, 750 mg orally [PO]). Hunting injuries are discussed in Chapter 24. Shotgun Injuries.  Shotgun injuries to the torso are managed in the same manner as gunshot wounds. Shotgun injuries have a potentially lower incidence of underlying visceral injury than gunshot wounds, but there is often extensive soft tissue damage requiring surgical debridement. The potential exists for delayed development of peritonitis from a single penetrating pellet to the viscera. Consequently, shotgun injuries should also be treated with emergency evacuation and a broad-spectrum antibiotic, as recommended previously for gunshot wounds. Occasionally, a close-range shotgun blast results in a soft tissue defect large enough for the injured bowel to extrude through the wound. The injured bowel should not be placed back into the abdomen. Injured bowel displaced from the abdominal cavity conceptually should be treated as though it were an enterocutaneous fistula. Because evacuation is often delayed in the wilderness, it is better to have fecal contents outside, rather than inside, the peritoneal cavity. The exteriorized bowel should be kept moist and covered at all times. Uncovered bowel outside the peritoneal cavity rapidly desiccates and becomes nonviable, mandating later surgical resection. Exposed bowel should be covered with an abdominal pack or cloth moistened with sterile saline at best, or at worst with potable water. The dressing should be checked and remoistened at least every 2 hours. Stab Wounds.  The penetrating object is usually a knife but may be as varied as a piton, ski pole, or tree limb. Any deep skin laceration from the nipple line to the groin should be considered to have damaged an intra-abdominal organ. Whereas the odds of an abdominal gunshot wound injuring a visceral organ exceed 85%, the odds of a stab wound injuring a visceral organ are less than 50%. 426

In certain urban hospitals, the high incidence of negative surgical explorations for stab wounds had led to a more selective approach toward patients with abdominal stab wounds.68 This approach uses local wound exploration and frequent physical examination. Although there are no data addressing the management of stab wounds in the wilderness environment, the following approach is practical and reasonable. If the wound extends into the subcutaneous tissue, the evacuation decision depends on local wound exploration. This procedure is simple to perform, even in the wilderness environment. The skin and subcutaneous tissue are infiltrated with local anesthetic, and the laceration is extended several centimeters to clearly visualize the underlying anterior fascia. It is helpful to use lidocaine (Xylocaine) 1% with epinephrine to minimize slight but annoying bleeding that can impair visualization. The wound should never be probed with any instruments, particularly if overlying the ribs. Wound exploration is confined to the area from the costal margin to the inguinal ligament. Local wound exploration is contraindicated in wounds that extend above the costal margin, because it is possible for such exploration to communicate with a small pneumothorax, potentially exacerbating respiratory distress. If thorough exploration of the wound shows no evidence of anterior fascial penetration, and if the victim demonstrates no evidence of peritoneal irritation, the wound can be closed with tape (Steri-Strips) or adhesive bandages, dressed, and the evacuation process delayed. Physical examination should be performed every few hours for the next 24 hours. If no peritoneal signs develop and the victim feels constitutionally strong, a remote expedition may resume with caution and an eye to evacuation should the victim become ill. In the wilderness environment, it is prudent to have a low threshold for evacuation because of technical difficulties in performing wound exploration, such as insufficient light and inadequate instruments. Persons who have been impaled by long objects, such as tree limbs or ski poles, should have the object left in place and carefully shortened, if possible, to facilitate transport.

PELVIC TRAUMA In the wilderness setting, fractures of the pelvis are generally associated with falls from significant heights, high-velocity ski accidents, or vehicular trauma. Pelvic fractures can be lethal. With opening of the pelvic ring, there may be hemorrhage from the posterior pelvic venous complex and occasionally from branches of the internal iliac artery. For hemodynamically unstable victims with severe pelvic fractures, resuscitative efforts should be instituted. In addition, simple techniques to reduce increased pelvic volume through the application of sheets or slings may slow bleeding. Several pelvic binders are available commercially and all provide circumferential pressure to minimize the pelvic volume (e.g., T POD [www. pyng.com], SAM Pelvic Sling II [www.sammedical.com]). The key factor in initial management of pelvic fractures is identification of posterior injury to the pelvic ring. Posterior ring fractures or dislocations are associated with a greater incidence of significant hemorrhage, neurologic injury, and mortality than are other pelvic fractures. The diagnosis of a posterior ring fracture is based on instability of the pelvis associated with posterior pain, swelling, ecchymosis, and motion at the sacroiliac joints with application of manual pressure at the anterior superior iliac spines. Persons with posterior ring fractures must be immediately evacuated on backboards, with care taken to minimize leg and torso motion. The flank, scrotum, and perianal areas should be inspected for blood at the urethral meatus, swelling or bruising, or a laceration in the perineum, vagina, rectum, or buttocks suggestive of an open pelvic fracture. The pelvis should be examined carefully once, without any aggressive rocking motion. The first indication of mechanical disruption is leg length discrepancy or rotational deformity in the absence of an obvious leg fracture or hip location. For more information on pelvic fracture, see Chapter 27.

BOX 21-3  Vascular “Hard Signs”

The majority of wilderness-related extremity injuries involve fractures and sprains, which are discussed in Chapter 27. This section focuses on the general field management of significant extremity vascular injury, traumatic amputation, and recognition and treatment of rhabdomyolysis.

Pulsatile bleeding Palpable thrill Audible bruit Expanding hematoma Six “P’s” of regional ischemia Pain Pulselessness Pallor Paralysis Paresthesia Poikilothermia

Vascular Injuries Injury to the major vessels supplying the limbs can occur with penetrating or blunt trauma. Fractures can produce injury to the vessels by direct laceration (rarely) or by stretching, which produces intimal flaps. Penetrating injuries can be devastating if transection of a vessel occurs. Significant vascular injuries, from both penetrating and blunt causes, can result in multiple vessel injury subtypes, each of which may be limb-threatening. Injury subtypes include laceration, transection, contusion with spasm, thrombosis, or aneurysm formation (true and false), external compression, and arteriovenous fistula. An accurate history, expeditious physical examination, and prompt evacuation are the keys to life and limb salvage. Significant vascular injuries result in one of two clinical presentations—hemorrhage or ischemia. The greatest priority is cessation of hemorrhage. The victim of trauma may die in short order from a major vascular injury. Stop the bleeding. Ideally, control of hemorrhage can be accomplished without resultant ischemia of the distal extremity. The vast majority of times, hemorrhage from an extremity wound can be controlled with pressure dressings and direct pressure. These measures permit circulation to and from the extremity outside the area of pressure application. In the very rare circumstance, a tourniquet may be required. History.  A complete history of the time and mechanism of injury is invaluable in planning further management. Although no absolute ischemia time has been established, a goal of less than 6 hours to reperfusion is prudent.28 The amount of blood present at the scene should be quantified. A history of bright pulsatile blood that abates suggests arterial injury. Thirty-three percent of victims with arterial injuries have intact distal pulses. Physical Examination.  Vascular examination in the field can be highly variable. Hypovolemia, hypothermia, and hostile conditions make accurate examination challenging. Skin color and extremity warmth should be first assessed. Distal pallor and asymmetric hypothermia suggest vascular injury. Pulses should be palpated. In the upper extremity, the axillary, brachial, radial, and ulnar pulses should be assessed. In the lower extremity, the femoral, popliteal, posterior tibial, and dorsalis pedis pulses should be assessed. Location and direction of the wound, amount of hemorrhage, and presence of hematomas or palpable thrill should be noted. A neurologic examination that quantifies motor and sensory deficits is critical. Because of the high metabolic demands of peripheral nerves, disruption of oxygen delivery makes neuronal cells highly susceptible to ischemic death. Conversely, skeletal muscle is relatively resistant to ischemia. Loss of sensation or limb paralysis is an alarming sign of impending anoxic necrosis. Treatment of Vascular Injuries.  All external hemorrhage should be identified during the primary survey and controlled with direct pressure at the site of injury. Tourniquets should be applied only when direct pressure fails to control bleeding or when direct pressure cannot be applied (such as while a casualty is being evacuated by hoist to an aircraft). In the civilian experience, the need for tourniquets should be uncommon, because direct pressure is the preferred technique. Tourniquets should be released every 5 to 10 minutes to attempt to limit ischemia, unless severe hemorrhage continues when the tourniquet is loosened. In this case, it should be left tightened. Efforts to control bleeding with pressure should be undertaken. Direct pressure permits collateral flow to provide some perfusion to the distal extremity. Hematomas should never be explored or manually expressed without surgical capability readily available. Attempts to clamp or ligate vessels are not recommended. Frequent repeat neurovascular examinations are mandatory.

Once bleeding is controlled and the wound is covered with a sterile but nonconstrictive dressing, completion of the primary survey, identification and stabilization of associated injuries, and appropriate resuscitation with normal saline should follow. After hemostasis is achieved, a nonconstrictive dressing will obviate the chance for unintended venous outflow obstruction. The extremity should be splinted to prevent movement. The need for evacuation depends directly on the results of the physical examination. Examination results can be grouped into “hard signs,” indicative of ischemia or continued hemorrhage, and “soft signs” that are suggestive but not indicative of ischemia (Boxes 21-3 and 21-4). All victims with hard signs should be evacuated emergently. Based on current data, an isolated soft sign may warrant observation alone, depending on the remoteness of the expedition and the risks of evacuation. The data for observation of soft signs have emerged from hospital settings and must be applied with great caution in the wilderness. If soft signs are present, clinical suspicion is high, and evacuation can be accomplished safely, the victim should be transported and observed in a medical facility. Traumatic Amputation In the wilderness environment, amputation victims require immediate evacuation. Hemorrhage is controlled during the primary survey with direct pressure, and resuscitation is instituted. Tourniquets are rarely required. The victim should be kept warm and calm. Reassurance and analgesics should be administered. Amputations should be completed only if minimal tissue bridges exist and it is clear that the neurovascular supply has been interrupted. Amputation of a mangled extremity, defined as an extremity with high-grade open fracture and soft tissue injury, should not be carried out in the wilderness except to free a trapped victim to avoid further severe injury or even death, or in the case of uncontrollable hemorrhage threatening the life of the victim, and then only by experienced surgical personnel. All other severely injured extremities should be wrapped in available sterile materials, splinted, and kept moist. Amputated extremities should be cooled if possible, optimally in a plastic bag in ice or ice water. Avoid placing the extremity in direct contact with ice. Without cooling, the amputated extremity remains viable for only 4 to 6 hours; with cooling, viability may extend to 18 hours. The amputated extremity should accompany the victim throughout the course of the evacuation. Crush Injuries and Rhabdomyolysis Rhabdomyolysis is a potentially fatal syndrome that results from lysis of skeletal muscle cells. In its fulminant form, BOX 21-4  Vascular “Soft Signs” Injury in proximity to major vessel Diminished but palpable pulses Isolated peripheral nerve deficit History of minimal hemorrhage

427

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

EXTREMITY TRAUMA

PART 4  INJURIES AND MEDICAL INTERVENTIONS

rhabdomyolysis can affect multiple organ systems. Compartment syndrome, renal failure, and cardiac arrest represent the major complications. Any condition resulting in significant acute or subacute striated muscle damage can precipitate rhabdomyolysis. Crush injuries of the extremities and pelvis, revascularization of ischemic tissue, ischemic extremities, animal bite and snakebite,16,22 frostbite, and traumatic asphyxia32 can all result in rhabdomyolysis in a wilderness setting. Crush injuries are frequently results of avalanches, falls from heights, or rock slides. The pathophysiology of rhabdomyolysis remains controversial. The exact mechanism of muscle injury appears not to be simple direct force or isolated ischemia and is probably multifactorial.32 The common cellular derangement is interference of the normal function of muscle cell membrane sodium-potassium adenosine triphosphatase (ATPase) with intracellular calcium influx and cell death.76 After cell death, multiple intracellular constituents, including myoglobin, creatine kinase, potassium, calcium, and phosphate, are released into the systemic circulation. The metabolic derangements of rhabdomyolysis depend directly on release of intracellular muscle constituents. Myoglobinemia, hypercalcemia, hyperphosphatemia, hyperkalemia, hyperuricemia, metabolic acidosis, coagulation defects, and contracted intravascular volume result. The clinical presentation of rhabdomyolysis may include muscle weakness, malaise, fever, tachycardia, abdominal pain, nausea and vomiting, or encephalopathy. Symptoms may mimic those of persons with spinal cord injury.7 The danger of the syndrome lies in the cardiovascular effects of electrolyte disturbances and renal failure69 secondary to changes in renal perfusion and direct toxicity of myoglobin to tubular cells. Successful treatment relies on prompt diagnosis based on clinical signs and urinalysis, aggressive hydration, and forced diuresis. Myoglobin turns urine tea-colored, which is an important indicator of significant muscle death and need for aggressive treatment. Normal saline should be administered IV at 1 to 2 L/hr to achieve a urine output of 100 to 300 mL/hr. Signs for fluid overload should be monitored. Victims who are trapped in rubble should have resuscitation initiated before extrication, if possible. The addition of agents to alkalinize the urine and promote diuresis has been shown to improve clearance of myoglobin but not to alter survival. In addition, diuretics may be detrimental in multisystem trauma victims who are hypovolemic. All victims demonstrating myoglobinuria should be evacuated.

Wilderness Surgical Emergencies THE ACUTE ABDOMEN In the wilderness, the critical distinction between the surgical and nonsurgical abdomen determines whether the victim should be evacuated. A myriad of nonsurgical conditions mimic a surgical abdomen. It has been extensively reported that the bite of the black widow spider, Latrodectus mactans, can induce abdominal pain indistinguishable from a surgical acute abdomen,48 and mushroom ingestion can cause severe gastroenteritis.83 Pain, anorexia, nausea, vomiting, and fever are characteristic manifestations of an acute abdominal disorder. Tenderness and guarding are the hallmarks of peritoneal irritation and suggest that surgery is indicated. The approach to someone with abdominal pain begins with a detailed history that includes age, gender, systemic symptoms, and past medical history. This information provides a framework for more detailed questioning about the character of the pain, its mode and time of onset, severity, and precipitating and palliating factors. In persons 15 to 40 years of age, women are more likely to have abdominal pain, but men have a higher incidence of surgical disease. Common genitourinary causes for abdominal pain in men include epididymitis, renal colic, urinary retention, and testicular torsion. Common causes in women include pelvic inflammatory disease (PID), urinary tract infection (UTI), dysmenorrhea, ruptured ovarian cyst, and ectopic pregnancy. Pain is the hallmark of a surgical abdomen (Table 21-3). It can be characterized by nature of onset, severity, location, and precipitating factors. The onset of abdominal pain can be explosive, rapid, or gradual. The person who is suddenly seized with explosive, agonizing pain is most likely to have rupture of a hollow viscus into the free peritoneal cavity. Colic of renal or biliary origin may also be sudden in onset, but seldom causes pain severe enough to prostrate the victim. If someone has rapid onset of pain that quickly worsens, acute pancreatitis, mesenteric thrombosis, or small bowel strangulation should be suspected. The person with gradual onset of pain is likely to have peritoneal inflammation, such as that accompanying appendicitis or diverticulitis. Severity of the pain may be characterized as excruciating, severe, dull, or colicky. Excruciating pain unresponsive to narcotics suggests an acute vascular lesion, such as rupture of an abdominal aneurysm or intestinal infarction. Both conditions are

TABLE 21-3  Differential Diagnostic Features of Abdominal Pain Disease Acute appendicitis Intestinal obstruction Perforated duodenal ulcer Diverticulitis Acute cholecystitis Renal colic Acute pancreatitis Acute salpingitis

Ectopic pregnancy

428

Location of Pain and Prior Attacks

Mode of Onset and Type of Pain

Associated Gastrointestinal Problems

Periumbilical or localized generally to right lower abdominal quadrant Diffuse

Insidious to acute and persistent

Anorexia common; nausea and vomiting in some

Sudden; crampy

Vomiting common

Abrupt; steady

Anorexia; nausea and vomiting Diarrhea common

Epigastric; history of ulcer in many Left lower quadrant; history of previous attacks

Gradual; steady or crampy

Epigastric or right upper quadrant; may be referred to right shoulder Costovertebral or along course of ureter Epigastric penetrating to back Bilateral adnexal; later, may be generalized

Insidious to acute

Anorexia; nausea and vomiting

Sudden; severe and sharp Acute; persistent, dull, severe Gradually becomes worse

Frequently nausea and vomiting Anorexia; nausea and vomiting common Nausea and vomiting may be present

Unilateral early; may have shoulder pain after rupture

Sudden or intermittently vague to sharp

Frequently none

Physical Examination Low-grade fever; epigastric tenderness initially; later, right lower quadrant Abdominal distention; high-pitched rushes Epigastric tenderness; involuntary guarding Fever common; mass and tenderness in left lower quadrant Right upper quadrant pain Flank tenderness Epigastric tenderness Cervical motion elicits tenderness; mass if tubo-ovarian abscess is present Adnexal mass; tenderness

General Field Treatment Principles When evaluating someone with a possible emergent surgical condition in the wilderness, correctly identifying the etiology of a given condition is less important than identifying peritoneal inflammation and the need for operation. When dealing with a surgical abdomen or other condition requiring evacuation, adjuncts to definitive hospital treatment can be initiated in the field. Dehydration and intravascular volume depletion accompany many surgical conditions, particularly when the disease process has progressed and evacuation is delayed. Crystalloid resuscitation in the field is beneficial for patients who have developed or have the potential to develop septic or hypovolemic shock. Dehydration is common in the wilderness, and frank hypovolemia can result from vomiting associated with gastroenteritis, appendicitis, renal colic, and small bowel obstruction. Perforated viscus, pancreatitis, cholecystitis, small bowel obstruction, PID, and necrotizing soft tissue infections all may feature volume depletion. The goal in the wilderness setting is to recognize the signs of hypovolemia and initiate resuscitation to decrease perioperative morbidity. Nasogastric tube decompression of the stomach may help alleviate emesis secondary to abdominal pain or obstruction. Large-bore (i.e., 18F) catheters are best and can be easily aspirated with a syringe. Placement should be confirmed by aspiration of gastric contents or auscultation of gastric air on insufflation of the stomach. Foley catheters are becoming increasingly more available in wilderness first-aid kits (Figure 21-11). Recording urine output provides an effective estimate of intravascular volume status. Foley catheter placement should never hinder the possibility of ambulatory evacuation. Radiographic imaging techniques will not be available. Some expeditions will have the availability of portable ultrasound and the professional expertise to use this modality. A team of three emergency medicine physicians described their application of ultrasound in the austere environment following mud slides in Guatemala. In a series of 99 patients, ultrasound was used to identify an emergent problem in 6% of patients and rule out an emergent problem in 42% of patients.19 Appendicitis Acute appendicitis is the most common cause of a surgical abdomen in persons younger than 30 years of age. Acute appendicitis is more than a single disease entity. In terms of physical signs and symptoms, appendicitis proceeds from inflammation to obstruction to ischemia to perforation, all within approximately 36 hours. Symptoms reflect the stage of the disease. Unfortunately, the time frame for the progression of clinical events is highly variable.

The differential diagnosis of appendicitis includes gastroenteritis and mesenteric adenitis, the most common inflammatory disorders in adults. The first symptom of gastroenteritis is typically vomiting, which precedes the onset of pain and is often associated with diarrhea; it is rarely associated with localizing signs or muscular spasm. Bowel sounds are usually hyperactive. A rectal examination rarely shows abnormalities in gastroenteritis but frequently does in adults with appendicitis. Mesenteric adenitis is often preceded by an upper respiratory infection and is associated with vague abdominal discomfort that often begins in the right lower quadrant. Abdominal examination reveals only mild right lower quadrant tenderness that is often poorly localized. The incidence of PID in young women with abdominal pain confounds the diagnosis of appendicitis. Some clinicians have documented a connection between menses and onset of pain. If abdominal pain occurs within 7 days of menses, the incidence of PID is twice that of appendicitis. If onset of pain occurs greater than 8 days from menses, appendicitis is twice as likely as PID. This history with a pelvic examination may enable the examiner to differentiate between the two entities. Acute appendicitis mandates evacuation, because untreated perforation is associated with significant mortality. Recent literature has supported nonoperative management of acute appendicitis.5,41,92 However, in these series, patients who do not improve promptly with antibiotics proceed to appendectomy. The prudent medical director of an expedition would seek to evacuate the patient with presumed appendicitis to ensure surgical capability is available. Broad-spectrum antibiotics (if IV capability, cefotetan [Cefotan] 2 g IV every 12 hours, or as an alternative, piperacillin/ tazobactam [Zosyn] 3.375 g IV every 6 hours; if only oral antibiotic capabilities, a fluoroquinolone, such as ciprofloxacin [Cipro] 750 mg PO twice a day) should be initiated, attempting coverage against gram-negative and anaerobic organisms. IV crystalloid resuscitation should be initiated, particularly if the victim is older or perforation is suspected, and the victim should be placed on bowel rest. Acute Cholecystitis and Biliary Colic Biliary colic refers to pain induced by obstruction of the cystic duct, usually by gallstones. The label of this condition as “colic” is a misnomer because the pain is usually constant. The condition is rarely seen before adulthood and is several times more common in women than in men. A sufferer often relates a past history of gallstones and previous episodes of similar pain, which is described as constant right upper quadrant or epigastric pain, radiating to the right scapula and back. Onset ranges from insidious to acute and frequently follows a meal. The episode usually lasts 15 minutes to 1 hour and then abates.66 If pain is severe, nausea and vomiting may be present (60% to 70%). Acute cholecystitis is an infection of the gallbladder secondary to cystic duct obstruction, usually from gallstones. In the wilderness setting, it is useful to think of these interrelated conditions as a continuum of one unified disease process. Both biliary colic and cholecystitis manifest with right upper quadrant pain; however, biliary colic has the potential to be self-limited and may not require evacuation. Not all persons with biliary colic develop cholecystitis, and signs of infection should be excluded. Cholecystitis symptoms typically escalate in severity. Pain that persists for more than 1 to 2 hours is suspect for cholecystitis, particularly when accompanied by fever, more significant nausea and vomiting, and right upper quadrant tenderness. Studies have shown that fever may be an unreliable predictor of severity of infection.38 Acute cholecystitis mandates hospitalization, and evacuation plans should be instituted. The disease can progress to gangrenous changes in the gallbladder wall, leading to perforation and death if untreated. The definitive treatment of cholecystitis is cholecystectomy. In the field, IV antibiotics (ampicillin/sulbactam [Unasyn] 3 g IV every 6 hours) or an oral alternative (ciprofloxacin 750 mg PO twice a day) should be given, directed at common biliary organisms, including Escherichia coli and Klebsiella, Bacteroides, Enterobacter, Streptococcus, and Proteus species. Oral antibiotics with optimal bioavailability should be initiated in the absence of parenteral forms, ensuring the broadest spectrum of coverage 429

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

unusual in the wilderness environment. Severe pain readily controlled by medication is characteristic of peritonitis from a ruptured viscus or acute pancreatitis. Dull, vague, and poorly localized pain suggests an inflammatory process and is a common initial presentation of appendicitis. Colicky pain characterized as cramps and rushes is suggestive of gastroenteritis. The pain from mechanical small bowel obstruction is also colicky but has a rhythmic pattern, with pain-free intervals alternating with severe colic. The peristaltic rushes associated with gastroenteritis are not necessarily coordinated with colicky pain. Physical examination of the abdomen is initiated by inspection. Valuable clues to the underlying condition that may be obtained in this manner include stigmata of cirrhosis, distention, hyperperistalsis, or incarcerated hernia. The victim may not be able lie still, which is indicative of renal or biliary colic. Persons lying perfectly still frequently have peritoneal inflammation. Auscultation is helpful if the classic “rushes and tinkles” of small bowel obstruction are present. Palpation in the wilderness setting is most helpful in documenting the presence or absence of peritoneal signs. Shake or percussive tenderness, particularly in the context of fever, nausea, and/or vomiting, indicates a need for evacuation. Rectal and vaginal examinations should be performed as dictated by the clinical presentation and setting.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

available. As with most abdominal infections, IV hydration should be started in the field. If significant nausea and vomiting are present, NG decompression may improve comfort and prevent aspiration. Peptic Ulcer Disease The incidence of peptic ulcer disease (PUD) is decreasing in the United States. With the advent of treatment of Helicobacter pylori infections and the variety of acid-reducing agents available, PUD is now rarely seen by surgeons. The exception is perforation of a gastric or duodenal ulcer, which should be considered in the differential diagnosis of acute abdomen in the wilderness. Victims frequently relate a history of PUD and need for medication. This history, in combination with acute onset of unrelenting epigastric pain radiating to the back, is suspect for perforation of an ulcer. The physical examination greatly assists in differentiation between simple ulcer disease symptoms and perforation. Pain may be severe. Gastric secretions are caustic to the peritoneum and, as a result, the abdomen frequently displays a rigid, boardlike character with associated diffuse peritoneal signs. History and examination consistent with gastric or duodenal perforation mandate evacuation. Dehydration may be significant. IV resuscitation should be started and the victim placed on bowel rest. Diverticulitis Diverticulitis is localized infection of a colonic diverticulum. Impacted material in the diverticulum, usually feces, leads to a localized inflammatory process that can lead to abscess formation and perforation. Diverticulitis manifests over a wide range of severity, from mild, localized infection to an intra-abdominal catastrophe. It is more common in middle age; one-third of the population older than 45 years of age has diverticula, 20% of whom will develop diverticulitis.81 Victims often relate a history of previous attacks. Pain is typically described as gradual in onset and localized in the left lower quadrant of the abdomen, although right-sided diverticulitis can occur. Diarrhea and fever are frequently associated complaints. Examination findings range from mild left lower quadrant abdominal tenderness to frank peritonitis, depending on the severity of the underlying infection. Treatment in the wilderness setting consists of hydration, bowel rest, antibiotics, and evacuation. If evacuation is impossible or significantly delayed, oral broad-spectrum antibiotics may be effective. Mild cases of diverticulitis are frequently treated on an outpatient basis with broad-spectrum oral antibiotics,81 such as ciprofloxacin 750 mg PO twice a day. Antibiotic therapy is directed primarily at gram-negative aerobic and anaerobic bacteria, and single-agent therapy covering these organisms has been demonstrated to be as effective as multiple-agent regimens.47 Because of unpredictability of response to antibiotic treatment, evacuation is indicated. Mechanical Small Bowel Obstruction Small bowel obstruction is a true emergency in the wilderness. When the obstruction is complete, expedient surgery is the only treatment. Small bowel obstruction in the United States is almost invariably the result of adhesions from previous laparotomy or incarceration of abdominal hernias. Victims complain of sudden onset of diffuse, crampy abdominal pain associated with vomiting and obstipation. With progression of the process to strangulation and infarction of bowel, fever and tachycardia develop. Late physical examination findings reveal a distended, tympanitic abdomen. Although variable, high-pitched tinkling bowel sounds suggest obstruction. A thorough inspection for hernias should be performed. Progression of examination findings to frank peritonitis is alarming and suggests ischemic bowel. The adage, “Don’t let the sun set on a small bowel obstruction,” is sound advice in the wilderness setting. All persons suspected of having a small bowel obstruction should be evacuated immediately. In the interim, the stomach should be decompressed with an NG tube to relieve vomiting and abdominal distention, and aggressive IV hydration should be started. 430

Incarcerated Abdominal Wall Hernias Abdominal wall hernias are common. Hernias can become incarcerated or strangulated, which constitutes a surgical emergency. Seventy-five percent of hernias occur in the groin84; the majority of incarcerated hernias manifesting in the wilderness setting are inguinal hernias. Other common hernias with the capacity for incarceration are incisional and umbilical hernias. Many people live with bulging asymptomatic hernias. Others manually reduce symptomatic hernias. New painful hernias or known hernias that can no longer be reduced are concerning. The pain of inguinal hernias is usually intermittent. A description of constant pain is suspect for incarceration. Associated symptoms of fever, tachycardia, nausea, and vomiting are indicative of possible incarceration or strangulation. On physical examination, a mass should be sought along the course of the spermatic cord. Masses may manifest from the external inguinal ring to the scrotum. The differential diagnosis for painful inguinal or scrotal masses includes lymphadenopathy, testicular torsion, and epididymitis. Associated tenderness of the spermatic cord may be present. A painful mass at the umbilicus, a previous incision site, or below the inguinal ring could represent an incarcerated umbilical, incisional, or femoral hernia, respectively. Bowel within an incarcerated hernia sac can become gangrenous in as little as 4 to 5 hours64; therefore it is important to determine the time of incarceration. The decision to evacuate is influenced by the presence of contraindications to manual reduction (see later), which are essentially physical signs that suggest progression to strangulation. Femoral hernias should not be reduced. The danger is en masse reduction of compromised or gangrenous bowel. Contraindications to reduction include associated signs of toxicity, such as fever, tachycardia, or evidence of bowel obstruction in association with a painful, irreducible mass. If the hernia itself is exquisitely tender to palpation and the overlying skin is erythematous and warm, the hernia should not be reduced. Victims with incarcerated hernias with signs of systemic or local toxicity should be evacuated. Similarly, victims with irreducible hernias—which require emergent surgery—should be evacuated. A newly incarcerated hernia without contraindications to reduction may be reduced by personnel experienced in such techniques. Gentle pressure is exerted on the hernia mass toward the inguinal ring, optimally with the victim flat and hips elevated. Analgesia and sedation may aid in reduction. Gangrenous bowel can rarely be reduced by this method.64 If successful, the victim should be closely observed for signs of recurrence or abdominal pain.

UROLOGIC EMERGENCIES Renal colic describes a symptom complex resulting from acute obstruction of the urinary tract secondary to calculus formation. The goal of the wilderness physician is to recognize the symptom complex and institute treatment. After obstruction of the urinary tract, the pain crescendo of renal colic begins in the flank. The pain progresses anteriorly over the abdomen and radiates to the groin and testes in men and the labia in women. Because the autonomic nervous system transmits visceral pain, many abdominal complaints may manifest. Nausea and vomiting are common. With severe colic, the victim writhes in pain and is unable to find a comfortable position. Physical findings are less revealing than is the review of systems. Tenderness to deep palpation of the region of obstruction or to percussion of the flank is present. Diagnosis in the wilderness is assisted by the presence of gross hematuria. Management of ureteral colic is pain control. Although almost universally deployed, forced diuresis may reduce ureteral peristalsis. Thus, forced oral fluids or aggressive IV hydration are of questionable benefit.96 The majority of calculi pass spontaneously in 4 to 6 hours. The goal of management is to control pain until passage of the stone has occurred. A number of pharmacologic approaches may be used. Nonsteroidal antiinflammatory drugs, such as ibuprofen and ketorolac, have been shown to be effective in the management of renal colic.96 For symptoms

Urinary Retention Urinary retention is a painful experience that requires immediate medical, and often surgical, intervention.13 The etiology of urinary retention ranges from prostatism45 in men to atonic bladder in women. In general, causes have been broadly divided into four groups: obstructive, neurologic, pharmacologic, and psychogenic.95 Twenty-five percent of men reaching 80 years of age will experience acute retention,13 which has been shown to increase prostate surgery perioperative mortality rates.75 Acute urinary retention can lead to incapacitating symptoms in the wilderness; prompt recognition and intervention are necessary. Principal symptoms are bladder distention and pain that may mimic acute abdomen, overflow incontinence, dribbling, and hesitancy. Physical examination findings include prostatic enlargement in men and lower midline abdominal tenderness and distention. If painful distention of the bladder is present, decompression should be undertaken. Medical therapy may be considered before complete obstruction to urinary flow. Tamsulosin (Flomax CR) is a third-generation α-blocker that may provide some relief. The α-blockers promote bladder neck and prostatic urethral relaxation.35 Bladder decompression should be initially attempted with a standard Foley catheter. In men with prostatic hypertrophy, passage of the catheter may be challenging, and a large catheter or coudé catheter should be used if a standard Foley catheter cannot be passed. Instrumentation of the urethra with hemostats or dilators is dangerous and should not be attempted in the field. The OPTION-vf (female) (see Figure 21-11, A) and OPTIONvm (male) (see Figure 21-11, B) are valved urinary catheters

A

B FIGURE 21-11  A, OPTION-vf (female) catheter. B, OPTION-vm (male) catheter. (Courtesy Opticon Medical, Dublin, Ohio.)

that eliminate the need for urine drainage bags and connecting tubes normally required with Foley catheters. These catheters incorporate a manually activated valve at the end of the catheter that allows the patient to store urine in the bladder and to mimic normal voiding behavior. The catheters may be used with a continuous drainage adapter when appropriate, so that a bag may be placed and urination rate and volume assessed. If multiple attempts are unsuccessful and symptoms are severe, needle decompression is indicated. The skin of the suprapubic region should be anesthetized, if possible. The distended bladder is palpated to guide aspiration. A 22-gauge needle attached to a syringe is introduced through the skin of the lower abdomen two finger breadths above the pubic symphysis and directed at the anus. The needle is advanced with simultaneous aspiration of the syringe until free-flowing urine is visualized. Palpation of the bladder in combination with adherence to this technique should lead to successful decompression. Complications related to decompression can occur.82 Drainage of greater than 300 mL/hr can induce mucosal hemorrhage. In addition, 10% of victims develop postobstructive diuresis that may lead to dehydration, in which case aggressive oral hydration or crystalloid repletion should be undertaken. Finally, surgical decompression is temporizing, and retention will recur. Treatment may need to be continued or repeated. Drainage of the bladder acutely relieves symptoms and may allow ambulatory evacuation, but the underlying etiology must be addressed in a medical facility. The Acute Scrotum Acute onset of scrotal pain and swelling requires immediate attention. Etiologies are multiple, but incarcerated hernia and testicular torsion are the most clinically significant in the field. Although any one aspect of the history and physical examination may not be diagnostic, when taken as a whole, they frequently suggest the etiology of the scrotal pathology.46 Testicular torsion can occur at any age, but it is more likely near puberty. The likelihood of testicular salvage is inversely proportional to elapsed time from torsion; this is a true surgical emergency. Acute onset of severe testicular pain is the hallmark. Mild to moderate pain is more suggestive of torsion of a testicular appendage or epididymitis. It has been stated that victims who can ambulate with minimal pain are less likely to have testicular torsion. In addition, nausea and vomiting may accompany torsion, whereas fever, dysuria, and frequency are associated with epididymitis. Physical examination reveals a patient in extreme discomfort with a swollen scrotum and a tender testicle; the affected testicle may be higher than normal and have a horizontal lie.46 Scrotal skin may be edematous and discolored. Unilateral scrotal swelling without skin changes is more indicative of a hernia or hydrocele. In testicular torsion, the affected testis is often larger than the unaffected testis. Testicular torsion can be somewhat differentiated from acute epididymitis by Prehn’s sign,86 which is relief of pain accomplished by elevation of the testicle. Because torsion twists the spermatic cord and elevates the testicle, pain is not relieved by elevation (negative Prehn’s sign). Conversely, pain is relieved in epididymitis with elevation (positive Prehn’s sign). This maneuver has low sensitivity in distinguishing the two conditions, but may be helpful in conjunction with other findings.86 Treatment consists of surgical detorsion, which should be accomplished within 12 hours of torsion.46 Manual detorsion is not the treatment of choice; however, remoteness of the wilderness environment may mandate manual attempts. Studies of manual detorsion are scant and the cohorts small.42 If manual detorsion is necessitated, the victim should be placed supine. Because testicular torsion typically occurs in the medial direction, detorsion is initially attempted with outward rotation of the testis (toward the ipsilateral thigh). Simultaneous rotation in the caudal to cranial direction may be necessary to release the cremasteric muscle.31 The surgical treatment of testicular torsion includes pexing the testis to prevent recurrent torsion. Thus, although detorsion may temporize an acute situation in the field, all victims must be evacuated for definitive treatment. 431

CHAPTER 21  Wilderness Trauma and Surgical Emergencies

uncontrolled by antiinflammatory agents, narcotics may be added. Narcotic analgesics are most effective given parenterally; however, agents such as meperidine (Demerol), codeine, and hydromorphone (Dilaudid) may be given orally. Antiinflammatory agents and analgesics can be combined. An antiemetic may be added to relieve nausea. When administering pain medication in the field, particular attention should be given to airway maintenance and induced nausea and vomiting. Any person whose symptom complex cannot be controlled must be evacuated. Additional indications for evacuation include calculus anuria and evidence of obstruction-induced infection.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Prostatitis A number of forms of prostatitis have been defined, including viral, bacterial, nonbacterial, and chronic forms. The acute bacterial form may potentially lead to severe infection. Bacterial prostatitis is an infection of the prostate caused primarily by gram-negative bacteria, with 80% attributable to E. coli. It is an acute, febrile illness characterized by perineal pain radiating to the low back, chills, malaise, and voiding symptoms, such as urgency, frequency, and dysuria. Urinary retention is common, and cystitis frequently accompanies the infection. On rectal examination, the prostate gland is usually boggy, warm, and tender and enlargement is variable. In an ideal situation, treatment is individualized to the cause, which may be difficult to discern in the wilderness. The infection may respond to an oral antibiotic such as ciprofloxacin (750 mg PO twice a day), ampicillin (500 mg PO 4 times a day), or tri­ methoprim (160 mg with sulfamethoxazole 800 mg PO twice a day). Penetration of prostatic secretions has been shown to be best achieved by trimethoprim/sulfamethoxazole (TMP/SMX). The chosen antibiotic should be administered for 30 days. If retention is present, catheterization or suprapubic aspiration should be undertaken. Acute bacterial prostatitis can escalate in severity to systemic toxicity. Persons with evidence of systemic toxicity unresponsive to a trial of oral or parenteral antibiotic therapy should be evacuated. Urinary Tract Infection UTIs are extremely common and include episodes of acute cystitis and pyelonephritis occurring in otherwise healthy individuals. These infections predominate in women; approximately 25% to 35% of women 20 to 40 years of age report having had a UTI.44 Conversely, men between the ages of 15 and 50 years rarely develop a UTI. Despite the striking difference in prevalence, symptoms are similar between men and women. The symptoms may represent urethritis, cystitis, or an upper UTI; the distinction is often difficult. Common symptoms include frequency, urgency, dysuria, suprapubic pain, flank pain, and hematuria. Flank pain with tenderness to percussion suggests pyelonephritis. On urinalysis, pyuria is nearly invariably present, and hematuria may assist in the diagnosis. Definitive diagnosis is based on significant bacteriuria. The leukocyte esterase test has a screening sensitivity of 75% to 96% and a specificity of 94% to 98% in detecting greater than 10 leukocytes per high-power field.44 Treatment in the wilderness setting for both men and women should be directed at the most common causative agents, although 50% to 70% of cases resolve spontaneously if untreated. Causative bacteria include E. coli (70% to 95%); Staphylococcus species (5% to 20%); and, less frequently, Klebsiella, Proteus, and Enterococcus. Fortunately, oral antibiotics are highly effective. Although resistant E. coli strains are being reported, trimethoprim/ sulfamethoxazole (Bactrim DS) is an excellent first-line drug. Alternative regimens include nitrofurantoin, a fluoroquinolone, or a third-generation cephalosporin. A 3-day course of therapy has been shown to be more effective than single-dose therapy.44 For pyelonephritis, a similar antibiotic in a 10- to 14-day course is an acceptable initial treatment. Evacuation should be reserved for systemic toxicity unresponsive to oral antibiotics.

SKIN AND SOFT TISSUE INFECTIONS Poor hygiene, superficial skin wounds, blisters, dermatologically significant plants, and insect bites contribute to disruption of the skin barrier. Most often seen are superficial pyodermas that do not extend beyond the level of the skin. These include erysipelas, impetigo, folliculitis, furunculosis, and carbunculosis. The majority of superficial skin infections are self-limited. However, with less than optimal hygiene and limited resources, skin infections may progress to deep soft tissue infections. Cellulitis Cellulitis is acute infection of the skin involving subcutaneous tissue. The superficial form of cellulitis, erysipelas, is identified 432

by well-demarcated, warm, and erythematous plaques with raised borders. The face, scalp, hands, and lower extremities are most often affected. Cellulitis is frequently preceded by a superficial wound. In the wilderness setting, there are ongoing infection risk factors. Members of expeditions may be physically stressed and nutritionally depleted. High altitude is associated with immunosuppression. Clostridium species and other pathogens are ubiquitous in the soil, and proper initial wound care may be suboptimal. Under such conditions, cellulitis can progress to abscess formation and tissue necrosis, leading to septicemia. Wounds that develop erythematous, warm, and boggy margins should be treated with antibiotics and closely observed. The margins of erythema should be marked to gauge progression. Treatment consists of proper wound hygiene and antibiotic therapy. Local wound measures include elevation, application of moist heat every 4 to 6 hours, and immobilization. Antibiotic therapy is directed at common causative pathogens. Group A streptococci and Staphylococcus aureus are most commonly implicated. If complications occur and the cellulitis appears to be progressing, a mixed infection is likely. Because Gram’s stain and culture-directed therapy are not possible, the most broad-spectrum antibiotic available should be administered. Parenteral antibiotics are indicated for serious or mixed infections. Penicillin G (1 to 2 million units every 4 to 6 hours) is recommended, with first-generation cephalosporins as an alternative. Because oral antibiotics may be the only available therapy, they should be initiated early in the field. Suggested agents include erythromycin (for the penicillin-allergic victim); cephalexin; a macrolide, such as clarithromycin; or a fluoro­ quinolone, such as ciprofloxacin or levofloxacin. Methicillinresistant S. aureus is present in wilderness settings. If infection with this organism is suspected, appropriate antibiotics should be used. Lymphangitis Acute lymphangitis is an infectious process involving subcutaneous lymphatic channels. Its recognition in the wilderness setting is important relative to its propensity to follow puncture wounds, hand wounds, infected blisters, and animal bite wounds. Clinical presentation involves linear erythematous streaks that originate in the lymphatic drainage basin of the wound and “point” to the draining nodal group. Causative agents are similar to those common for cellulitis, with the addition of Pasteurella multocida from animal bite wounds. Treatment consists of antibiotics; warm, moist soaks every 4 to 6 hours; and immobilization and elevation of the extremity. Optimal treatment consists of parenteral antibiotics, but as with cellulitis, oral agents should be initiated if parenteral drugs are not available. Broad-spectrum agents with good oral bioavailability and gram-positive coverage are recommended.85 Abscess Formation When untreated, many superficial skin infections convert to abscesses. Development of a raised, fluctuant mass with overlying warmth and erythema should raise suspicion that surgical drainage is necessary. Frequently, the lesion will “point” when purulent fluid has amassed below the dermis and rupture is impending. Warm soaks and observation are recommended by some clinicians, particularly if the presence of drainable pus is uncertain. However, the definitive treatment is drainage. Antibiotics are recommended if significant associated cellulitis is present, but penetration may be poor. Local anesthesia should be administered before incision. The lesion should be incised in line with tissue planes over the point of maximum fluctuance. The value of cruciate incisions over linear incisions is debatable; the important feature is assurance of adequate drainage to prevent recurrence. If drainage is undertaken, the incision must be large enough to adequately drain the cavity. All purulent material should be evacuated and the cavity copiously irrigated with saline or water. Packing is unnecessary if continued drainage is ensured. The wound should be covered with a sterile dressing, changed two to three times per day with concurrent irrigation, and closely observed for reaccumulation of purulence.

Necrotizing skin and soft tissue infections are life-threatening conditions caused by virulent, toxin-producing bacteria. Depth of tissue involvement is variable and may involve skin, fascia, or muscle. The etiology of necrotizing infections is related to breaks in normal cutaneous defenses associated with some form of injury. Although rare, such infections are of importance to the wilderness physician because of the array of documented inciting injuries and the reduction in mortality possible if diagnosis and treatment are rapid.27 Necrotizing infections have developed after innocuous-appearing injuries, including simple scratches, insect bites, ankle sprains, and sore throats.37 The incidence of necrotizing soft tissue infections is unknown, and there is no age or gender predilection. They most commonly occur on the extremities, abdominal wall, and perineum, within 1 week of the inciting event. Common pathogens include Streptococcus species, Staphylococcus, Vibrio species, Clostridium, Pseudomonas, Aeromonas, Enterobacter, and fungi. Many infections become polymicrobial. The clinical manifestations can be subtle. An area of cellulitis is commonly the first indication of infection. Pain is often excruciating, and fever is usually present. The infection then progresses to spreading erythema, induration, blue-black discoloration, and blister formation. Necrosis of skin, subcutaneous fat, muscle, or fascia follows, depending on the organism involved. Necrotic tissue exudes a foul-smelling, watery “dishwater” fluid. Subcutaneous emphysema may be present, particularly with clostridial infections, although enteric organisms may also produce air in tissues. Unfortunately, treatment is limited in the wilderness environment. Debridement of infected tissue should be carried out to the greatest degree humanely possible, but further debridement in a hospital setting is invariably necessary. The extent of debridement necessary is often striking. After debridement, parenteral antibiotics are necessary. Vancomycin and gentamicin are appropriate first-line agents. The most broad-spectrum oral antibiotic available should be initiated, and the victim expeditiously evacuated. Time is of the essence because the infection can be halted only by aggressive surgical intervention.

FIELD OPERATING ENVIRONMENT On a rare occasion, surgical procedures must be performed in the austere environment. By definition, the austere environment is not the ideal situation in which to conduct any invasive procedure. Site security is a consideration. The circumstances responsible for the injury must not continue to exist. Otherwise, the caregivers may be at risk for suffering the same fate as the casualty. The medical expeditionist will need to select a location that provides optimal illumination, yet protection from the elements. Sterility in the Austere Environment One of the major disadvantages of operative procedures in the austere environment is the inability to establish a sterile field. The goal will be to decrease the risk for bacterial contamination to as little as possible. Antiseptics are agents that are used to decontaminate the skin. Chlorhexidine is an antiseptic with excellent antimicrobial activity and prolonged length of activity. In many health care facilities, chlorhexidine has replaced iodophors as the antiseptic of choice. Isopropyl alcohol may be used if no other antiseptics are available. Isopropyl alcohol is commonly available, but it is particularly ineffective on dirty skin and it has little persistent activity. If nothing is available, soap and water may be of benefit. Soaps

will remove the bacteria on the surface of the skin that are not attached, but will do nothing for adherent bacteria. Sterile irrigation may not be available for wound irrigation. If no sterile fluid is available, potable water may be used. Water could be boiled before irrigation, but boiling does not rid the water of spores. If water is to be treated by boiling, the boiling should be at a rolling boil for 20 minutes to be effective. Any irrigation that is used should be removed from the wound as best possible. Wounds should be managed to ensure that no devitalized tissue or foreign bodies remain to minimize the chance of infection. Should an expedition make preparations for the possibility of surgical procedures, instruments taken into the field should be packed sterile in durable containers. Paper wrappers can become perforated, permitting contamination. The term disinfectant means an agent to decontaminate inanimate objects. If surgical instruments are not sterile, disinfectants can be used to decrease the bacterial count on the surface. Of course, all instruments should be clean of debris. Unfortunately, many of the disinfectants used in health care facilities are not practical for the austere environment. Ortho-phthalaldehyde (Cidex OPA), peracetic (Nu-Cidex, Perasafe), and glutaraldehyde (Cidex) are agents that are effective disinfectants, but hazardous for personnel and the environment and impractical in the field environment.24 The antiseptic chosen for skin preparation may be applied to the instruments in the absence of a disinfectant. Placing the instruments into boiling water will decrease the bacterial count, but will not completely eliminate bacterial spores. Applying flame to the instruments may kill bacteria but may leave products of combustion on the instruments that are then left in the wound as foreign material. The U.S. Army has developed a field sterilization system that is lightweight and does not require an external energy source. The system is the size of a suitcase and has the capacity to accommodate a surgical tray. A mixture of water and dry reagents controllably generates chlorine dioxide. The chlorine dioxide kills all vegetative cells and bacterial spores within one-half hour.24 Anesthesia Local and regional anesthesia will be the techniques of choice to provide comfort during minor operative procedures. General anesthesia should not be considered without a full complement of trained personnel and equipment. Procedural sedation and analgesia may be used with the availability of adequate monitoring, and the capability to establish a definitive airway should be immediately available. Common agents to supplement local or regional anesthesia are opioids and benzodiazepines. Should these agents be used, reversal agents of naloxone and flumazenil should be available. Another consideration would be the use of ketamine to provide dissociative sedation.4 Chapter 17 discusses pain management more specifically. Any operative interventions performed in the wilderness should keep in mind “damage control” principles. The general concept of damage control is to manage immediately lifethreatening problems, such as hemorrhage and gross contamination. Definitive management is delayed. Resuscitation continues during this period of time.87 Damage control principles should be kept in mind before considering any procedure in the austere environment. Generally, the approach in the wilderness should be temporizing with resuscitation or lifesaving or limb-saving procedures before contemplating definitive management.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 21  Wilderness Trauma and Surgical Emergencies

Necrotizing Infections

CHAPTER 22 

Wound Management RAMIN JAMSHIDI

Management of wounds sustained in remote and wilderness environments requires special preparation and knowledge. The basic elements of wound care can be outlined so that a provider in a remote, austere, or wilderness environment can safely manage the immediate wound and thereby limit secondary injury. In the care of acute injuries, attention is frequently focused on wound closure. In truth, most traumatic wounds would fare well if left open to heal by secondary intention.17 However, open wounds incur prolonged time to complete healing, discomfort of wound care, vulnerability to further injury, and larger scars. The critical goals of immediate wound care are to stop hemorrhage and limit morbidity related to infection. Secondary goals are to promote rapid healing and optimize cosmetic outcome.44

Types of Wounds and Definitions Abrasions result from tangential (shearing) forces. Although abrasions are most commonly superficial, they can be extensive and involve deep tissues. Superficial abrasions pose no threat to the patient but may require use of analgesics. Deep abrasions that have completely obliterated skin and denuded underlying fascia are at increased risk for infection and must be kept clean. By virtue of the mechanism of injury, abrasions involve more surface area than they do depth. As a consequence, they are not amenable to suture closure. Abrasions are treated by extensive irrigation to remove all debris (often dirt or gravel) and application of nonadherent dressings. Topical antiseptic solutions are not necessary but are useful adjuncts in preventing gauze dressings from adhering to raw tissue. Such dressings should be changed once daily or more frequently as needed for soiling or adherence (“drying out”). Abrasions do not form abscesses because they have no deep spaces to contain infection. They may become superinfected and develop cellulitis; although this is generally rare, the possibility is more real in the exposed wilderness environment. Diagnosis and management of cellulitis are discussed later in this chapter. Burns (see Chapter 13) may result from thermal or chemical insults. These injuries span a spectrum from trivial sunburn to deep tissue necrosis. The first principle of management is to limit further injury by extinguishing the source, seeking shade, washing out chemicals, and so on. For chemical exposures, voluminous irrigation is the key to limiting further injury. This should be done with clean (not necessarily sterile) water, and the run-off irrigant should be prevented from injuring more skin.7,15,34 Chemical quenchers (i.e., alkaline solution for an acid burn) should never be used because the resulting exothermic reaction will cause secondary injury. Once the burning process is arrested, burn care must focus on antisepsis because infection poses the single most important immediate threat. Burn wounds should be fastidiously cleaned to remove all foreign material and devitalized skin. Depth was formerly described as first, second, or third degree, but modern description relies on the descriptors partial thickness and full thickness (Figure 22-1). Blisters should be left intact unless they interfere with function. There is some debate about the management of blisters, but in a wilderness environment, the “biologic bandage” provided by an intact blister supersedes any academic debate about the presence of inflammatory mediators in the blister fluid. Blisters over the palms or joints are exceptions to this rule, because their presence will significantly limit motion and potentially engender contraction or decrement in function. One school of thought is that these blisters should be unroofed and gently scrubbed away with a moistened gauze or trimmed with scissors. 434

Once cleaned, burns should be dressed and kept clean. Topical antiseptic agents should be applied to burns with invasion deep enough to result in blistering or erosion through the skin to white tissue or burned muscle underneath. Silver sulfadiazine is an excellent agent, and can be reapplied once or twice daily to prevent the wound from desiccating. In the absence of silver sulfadiazine (and for burns <1% of body surface area), antibiotic or antiseptic ointment (e.g., bacitracin), can be employed. Lacerations can be deep or superficial, simple or irregular (Figure 22-2). Generally, lacerations are amenable to primary repair (i.e., closure at the time of injury). Closure simplifies wound care and optimizes cosmetic outcome. Much of the following discussion is dedicated to management of lacerations. Punctures are lacerations with very small entry site injury, but extended depth. Generally these injuries should not be closed because they cannot be adequately cleansed. There is little cosmetic benefit to closure, whereas there is significant risk for trapping infectious agents deep within them because of the inherent difficulty of properly irrigating the tract.

Clinical Presentation Immediate evaluation of traumatic wounds should include determination of the type of injury. Focused assessment includes determination of surface area and apparent depth. Distal sensation and passive and active range of motion must be assessed to elucidate any associated nerve injury, tendon disruption, or fracture. Nerve and tendon injuries will not affect acute management but are important as a baseline examination. Fractures require immobilization, which is discussed in Chapter 27. Distal perfusion must be assessed to determine likelihood of vascular injury. If there is suspicion of vascular injury based on examination, depth of the wound, or blood at the scene, the wound should not be probed (nor blood clots dislodged) until one is prepared to place direct pressure to control hemorrhage and potentially ligate or suture the injured vessel. Time since injury is very important when considering wound closure. Within several hours of injury, traumatic wounds become colonized with bacteria. Even without frank infection, heavy colonization impedes proper wound healing.17,23,45 A bacterialaden wound that has its edges approximated will generally not heal and has increased risk for developing an abscess. Various investigators have tried to establish a firm time limit beyond which traumatic wounds should not be closed, but results are inconsistent.3,28,49 With copious irrigation and removal of foreign bodies, most wounds that are otherwise suitable for closure (see earlier discussion) can be closed if this is accomplished within 6 hours of injury.21 This deadline may be extended in the hospital setting, where thorough sharp debridement can be undertaken and the environment controlled. In some circumstances, wounds may even be closed days or even weeks after initially generated, but this involves sophisticated surgical care.29 This situation should not be confused with an acute wound in the wilderness, which in all circumstances should be thoroughly irrigated, foreign bodies removed, and dressings applied. Acute wounds in the wilderness should be closed only if they are clean, suitable materials and instruments are at hand, and less than 6 hours have passed since the injury.

Treatment Personal protective equipment should be donned before interrogating, preparing, possibly closing, and dressing a wound. Eye

For online-only figures, please go to www.expertconsult.com

CHAPTER 22  Wound Management

FIGURE 22-1  Campfire burns, mostly partial thickness with both intact and ruptured blisters. The distal forearm is pale white without capillary refill, representing full-thickness injury. (Courtesy Ramin Jamshidi, MD.)

FIGURE 22-2  A deep and irregular laceration that is suitable for irrigation and multi-layer closure with interrupted mattress sutures (see text). (Courtesy Ramin Jamshidi, MD.)

shields and gloves are considered mandatory equipment. Eye shields are particularly important in preventing exposure of mucous membranes to bodily fluids. Gloves are essential and should be made of a nonlatex material and contain no talcum or other lubricant. Talcum, calcium carbonate, and cornstarch are common glove lubricants, and all have been shown to cause wound granulomas, foreign body reactions, adhesions, and chronic sinuses. Sterile gloves are less cumbersome to work with but are not required because they do not reduce the incidence of infection in an austere setting.37 Use of a mask has also not been demonstrated to reduce rates of acute wound infection but certainly provides a protective barrier for the care provider. Hair coverings are not necessary, because studies have failed to demonstrate reduction in wound infection rates.

possible, an antiseptic ointment can be used to paste the hair down away from the wound. Water should be used to clean the wound. There is no demonstrated benefit to use of saline solutions, and there is no absolute need for the irrigant to be sterile.7,15,34 Although some persons mention use of dilute (1%) povidone-iodine as an irrigant, this is not proved to be more efficacious. Whatever method is available to generate potable water (e.g., iodine tablets, mechanical filter, irradiation, boiling) is sufficient to generate irrigation fluid for wound care. Hydrogen peroxide is injurious to deep tissues and should not be used as an irrigant. The greatest impact on wound cleanliness is gained from volume of irrigant and simple mechanical debridement. Debridement is achieved by removal of obvious foreign material (as with forceps) and also by pulsing irrigant at the wound (the fluid agitation is an effective debrider) (Figure 22-3).30 The available volume should be used in successive bursts rather than a single “gush,” because dilution of wound contaminants is far superior with small serial volumes. Although the matter has not been systematically researched, a guideline that is often used is a minimum of 100 mL per centimeter of wound length. Optimal stream pressure has been determined to be 5 to 10 psi, but in a remote setting, use of pressure gauges or regulators is unnecessarily cumbersome; it is sufficient to realize that excessive pressures are not required.43,49 A large (20 to 60 mL) syringe attached to a 19- or 20-gauge needle or catheter is an effective instrument for this purpose. Alternatively, holes can be punched into the cap of a squeezable water bottle to generate the same effect. A splash shield at the tip of the

Cleansing Techniques Cleansing involves removing devitalized tissue, clearing debris, and copiously irrigating the area.21 This may involve vigorous manipulation of painful and sensitive tissues, so if oral analgesics are available, they should be used. Constricting jewelry and equipment should be removed from the affected area (e.g., rings, piercings). Ideally, hair around the wound is trimmed because the roots harbor bacteria. Hair should be trimmed to a few millimeters in height because shaving at the surface increases wound infection rates by causing superficial skin trauma.2 Eyebrow hair is an important exception, because trimming or shaving can result in permanent abnormal hair growth. If hair trimming is not

A

B

C

FIGURE 22-3  A, Irrigation of a deep inguinal wound to remove debris. B, Placement of an interrupted vertical mattress suture to approximate the deep tissue defect with eversion of the edge and relief of tension. C, Completed interrupted closure. (Courtesy Ramin Jamshidi, MD.)

435

PART 4  INJURIES AND MEDICAL INTERVENTIONS

instrument decreases personal exposure risk. If not available as a specific commercial product for this purpose, one can easily be fashioned from a paper or plastic plate, or base of a disposable water bottle or drinking cup. Preparing for the actual wound closure, the skin edges may be prepared with an iodine, povidone-iodine, chlorhexidine, hydrogen peroxide, or isopropyl alcohol solution, but these antiseptic agents should not be used within the wound itself because of potential toxicity. If concentrated ethyl alcohol (i.e., liquor) is available, it may be effective in reducing wound contamination, but this has not been systematically evaluated. These agents should be used to cleanse the skin surrounding the wound, using a gauze soaked with the liquid to paint an overlapping spiral from the wound outward to a distance of approximately 5 cm. The cleansed skin must be allowed to dry to achieve full effect; this takes 3 to 5 minutes at 20° C (68° F). Honey instilled into a wound has demonstrated certain antimicrobial properties, but conflicting research exists on this topic. Although it is recommended by some as an improvisational technique, it cannot be recommended as a routine adjunct at this time.

Vascular Injuries Evaluation of hemorrhage is a major component of acute wound management; even if bleeding has stopped, there may be a risk for delayed rebleeding. The wound should be irrigated vigorously so that if bleeding is to occur, it happens while the wound is being interrogated and one is poised to address it. Inadequate hemostasis during initial treatment engenders avoidable delayed blood loss. Bleeding from wounds can almost always be controlled with direct pressure. The most common reason for failure of direct pressure to control bleeding is too short a compression time. Initial pressure should be applied for 5 minutes (checked with a timepiece to ensure accurate timing). If bleeding persists, either pressure should be reapplied for 10 minutes, or pressure should be applied at both the wound and a proximal inflow point (e.g., popliteal, femoral, or brachial artery).24 The second most common reason for failure of direct pressure is that pressure is not applied in a focused manner over the site of bleeding. A broadly applied towel over a large wound will not be as effective at controlling bleeding as will finger-point pressure applied over the actual site of greatest bleeding. In the face of profuse diffuse bleeding (as from a large raw wound), topical adjuncts are available to promote thrombosis.4 QuikClot is a granular coagulant that was originally designed to be poured onto wounds to stop diffuse bleeding. The mechanism of action of the original product is adsorption of water onto zeolites, which activates factor XII and catalyzes platelet aggregation. However, the granule form of this material is difficult to use for two reasons: the poured material is unwieldy and difficult to control in windy situations; and the reaction is exothermic, causing pain and risking burn injury. QuikClot has now been modified and integrated into a gauze dressing (also marketed as Combat Gauze). The active element is now kaolin, an alumina silicate that activates and accelerates the enzymatic clotting cascade. The solid consistency of Combat Gauze is more manageable and generates no heat on application. Celox gauze is based on chitosan, a natural product derived from shellfish. Initial versions of this product were granules to be poured into a wound, but it is now embedded into an actual gauze dressing and also has no exothermic properties. HemCon bandages are also chitosan based and not exothermic. These agents are all designed to be applied directly to bleeding wounds and compressed with direct pressure. Before wound closure, these dressings must be removed and bulky gelatinous deposits in the wound irrigated out (although mild residual coatings are reportedly safe to leave in place). All of these agents are supported by anecdotal reports of success and are clearly superior to simple gauze dressings, reducing bleeding by nearly an order of magnitude. However, head-to-head studies published to date have been underpowered and are difficult to interpret. Ongoing development of these products and comparative evaluation are the most active areas of acute wound care research and development. 436

FIGURE 22-4  Severe complex crush injuries of both legs. These wounds mandate immediate evacuation, but profound hemorrhage may require tourniquet placement to prevent exsanguination until advanced surgical care is available. (Courtesy Ramin Jamshidi, MD.)

In contrast to the above products, which are designed to control gross hemorrhage, there are adjuncts intended to assist with lower volume bleeding within the wound. Surgicel products are procoagulant materials composed of a scaffold of cellulose polymer. They have been in clinical use for more than 60 years and are manufactured in fibrillar consistency as well as woven sheets. The major benefit of these agents is that they are totally absorbable, so they can be left on or within the wound, even suturing the wound closed over them. Gelitacel is a procoagulant dressing that is similar to Surgicel. It is a knitted sheet of resorbable cellulose that boasts complete dissolution in as short as 96 hours (more rapidly than Surgicel, thus theoretically less likely to result in an encapsulated collection within the wound). Tourniquets may be considered as a last resort to stop lifethreatening hemorrhage. Great debate exists over the use of tourniquets and who should be allowed to apply them (laypersons, emergency first responders, midlevel health care providers, physicians, or even specialty-specific physicians). The more proximal a tourniquet is applied, the greater the risk for devastating tissue/limb loss. The best potential use of a tourniquet may be for a traumatic amputation in which there is copious diffuse bleeding at the open end. In this case, a tourniquet can be firmly applied just proximal to the open wound so that little distal ischemic tissue is created (Figure 22-4). Commercial tourniquets such as the Combat Action Tourniquet are available, but a blood pressure cuff is often an effective instrument. Whatever device is employed, it should be applied and intensified until pressure exceeds arterial pressure and then increased at least another 20 mm Hg or until bleeding stops. If transport to advanced surgical care is expected to be prolonged (more than 1 hour), the tourniquet should be slowly released every 45 to 60 minutes and allowed to gently bleed (i.e., so long as bleeding is not torrential) for 3 to 5 minutes. This allows intermittent perfusion of tissue and can gradually induce ischemic conditioning of the affected tissue to lessen the effects of ischemia and reperfusion. However, this is controversial, and some authorities do not advocate intermittent loosening to avoid dangerous hemorrhage. When a tourniquet is released, it should be done slowly over a minute or two, because recirculation of stagnant, acidic, and hyperkalemic blood from the nonperfused distal limb can lead to hemodynamic instability. If dysrhythmia is noted, the tourniquet should not be released further until the patient stabilizes. Hypotension and even cardiac arrest may result when a tourniquet is released; these dangers are frequently overlooked and can cause tragic outcomes. Although profuse external hemorrhage is easy to localize, ischemic complications of vascular injuries are more subtle and sometimes overlooked. Examination findings are classically divided into “soft” and “hard” signs of vascular trauma, indicating the relative likelihood of a significant vascular injury (Table 22-1).24 Presence of a hard sign is more than 90% predictive of need for vascular intervention. Only about one-third of patients with a single soft sign have an abnormality on arteriography, and

“Hard Signs”

“Soft Signs”

Active or pulsatile hemorrhage Pulsatile or expanding hematoma New thrill or bruit Limb ischemia/compartment syndrome Diminished/absent distal pulse

Hypotension/shock Neurologic deficit immediately following injury Stable, small, nonpulsatile hematoma Proximity of wound to major vessels

few of these require emergent intervention. Any patient with a hard sign of vascular injury requires immediate evaluation by a surgeon.

Anesthesia Manipulation of traumatic wounds can be painful and anxiety provoking. Studies have demonstrated that music can reduce procedural anxiety.32,42 For most patients, explaining the steps involved can improve tolerance by guiding expectations.54 If vigorous debridement or suture closure is to be attempted, infiltration of local anesthetic can provide tremendous comfort for the patient and thus facilitate technically superior closure. Anesthetic solutions can be applied locally within tissue, as topical agents, or as regional nerve blocks. Direct intradermal or subcutaneous injection is the most common technique of local anesthetic use. These agents are synthesized in two related chemical classes: aminoamides (lidocaine, bupivacaine, dibucaine, etidocaine, mepivacaine, prilocaine, and ropivacaine) and aminoesters (chloroprocaine, procaine, tetracaine, and cocaine ). Characteristics of the most commonly used local agents are listed in Table 22-2. Inclusion of epinephrine in the solution effects local vasoconstriction by α1-adrenoceptor agonism and nearly doubles the duration of the local effect of the medication. By slowing systemic absorption of the anesthetic, it also increases the maximum allowable total dose. Inclusion of epinephrine in the anesthetic solution is believed by some to improve local hemostasis, but this is a minor contribution relative to the effect of increased tissue turgor from infiltration of the solution. Conventional teaching is that epinephrine-containing local anesthetic solutions should not be used in TABLE 22-2  Properties of Select Local Anesthetics Name* Amide Class Lidocaine   with epi Bupivacaine   with epi Ester Class Chloroprocaine   with epi

Maximum Dose

Weight-Based Dose

30-60 min 60-120 min 90-240 min 180-360 min

300 mg 500 mg 175 mg 225 mg

5 mg/kg 7.5 mg/kg 2 mg/kg 3 mg/kg

15-30 min 30-60 min

800 mg 1000 mg

Duration

7 mg/kg 10 mg/kg

*With epi, epinephrine 1 : 200,000 (5 mcg/mL).

end-vascular beds such as the nose, fingers, toes, and penis because of concern for ischemia. However, there is literature to support safe use of these solutions for digital blocks.46,51 Using anesthetics without epinephrine allows maximum flexibility in terms of allowable location of use. Pain of injection for any local anesthetic can be attenuated by mixing 1 mEq of sodium bicarbonate with each 9 mL of anesthetic to buffer the solution. It should be noted that this delays the onset of action by approximately 5 minutes. The most common reasons for apparently ineffective local anesthetic effect are use of an insufficient dose and inadequate time allowed for onset of effect. Time to onset depends on the agent’s ability to cross cell membranes, which is determined by the compound’s intrinsic pKa. In general, a minimum of 3 minutes is required for onset of effect (as with lidocaine), but sometimes as much as 15 minutes is required (as with bupivacaine). This chemistry explains the delayed onset of action when the anesthetic is mixed with bicarbonate. For all agents, intravascular administration or overdose will first cause agitation, tremor, and tinnitus, then seizures, and finally, cardiac arrest through aberrant conduction.19 These risks are particularly important to consider in children, in whom toxicity occurs at lower doses. Table 22-2 lists maximum doses of commonly employed local anesthetics, along with weight-based guidelines for children. Although ample anesthetic should be administered, caution must be exercised to ensure that no intravascular administration occurs and to avoid nearing the maximum dose. This principle is complicated by the fact that maximum doses are ill defined and are set at different levels in different nations.38 Of note, patients with liver disease and those taking medications (such as systemic antifungals) interfering with cytochrome P-450 metabolism will have decreased capacity to metabolize aminoesters. In patients with renal failure, the metabolism of bupivacaine is altered, which requires a dose reduction of 15% to 20%. Concern frequently arises over administration of epinephrine-containing local anesthetics to patients with heart disease. However, these dilute local/regional doses do not cause significant systemic hemodynamic effects. Local anesthetics can be applied topically as well and have demonstrated efficacy in numbing the skin, although 20 to 30 minutes is required for onset. Topical anesthetics are particularly useful for superficial wounds over a large surface, such as burns and abrasions.26 A variety of formulations are available: TAC (0.5% tetracaine, 0.027 epinephrine, 11.8% cocaine), LET (4% lidocaine, 0.1% epinephrine, 0.5% tetracaine), and EMLA (2.5% lidocaine, 2.5% prilocaine in a eutectic mixture containing a thickener, emulsifier, and distilled water buffered to pH 9.4), and 5% lidocaine jelly. Characteristics of these agents are summarized in Table 22-3. Care must be taken to avoid application near mucous membranes because of the potential for systemic absorption and toxicity. Compared with TAC, LET has less potential for toxicity, is not a controlled substance, and is less expensive.1 LET should be stored in a light-resistant container and is stable for 6 months refrigerated and 4 weeks at room temperature. It should be discarded if the solution becomes discolored. Near mucous membranes, 3 mL of LET solution can be combined with 150 mg methylcellulose (4000 cps) by stirring for a few minutes, to create a gel preparation that should be used immediately. This lessens the likelihood of having the topical preparation run onto the mucous membranes.

TABLE 22-3  Properties of Topical Anesthetics

TAC LET EMLA LMX 4 or 5

Composition

Time to Onset

Notes

0.5% tetracaine 0.057 epinephrine 11.8% cocaine 0.5% tetracaine 0.14 epinephrine 4% lidocaine 2.5% lidocaine 25% prilocaine 4 or 5% liposomal lidocaine

30 min

Seizures and cardiac arrest reported; controlled substance; avoid mucosal surfaces

15-30 min

Inactivated by extensive light exposure

30-120 min

Longer duration; requires occlusive dressing; methemoglobinemia reported; do not place over open wound

15-40 min

437

CHAPTER 22  Wound Management

TABLE 22-1  Relative Indicators of Vascular Injury

PART 4  INJURIES AND MEDICAL INTERVENTIONS

True IgE-mediated allergic reactions to local anesthetics are very rare, particularly with aminoamide anesthetics.12,19,38 Typically these reactions are actually caused by preservatives such as methylparaben in multidose vials. One alternative is to use an aminoester anesthetic such as chloroprocaine. However, the principal metabolite of the aminoesters is para-aminobenzoic acid, which is chemically similar to methylparaben and can induce the same reactions. A reasonable approach to a reported allergy to a particular anesthetic is to use a preservative-free anesthetic of the other class. Use of diphenhydramine has been described as an alternative to traditional local anesthetics.36 At 1% concentration, it can be injected subcutaneously or subdermally but causes more pain from injection than do the classic anesthetics, and this pain is not diminished by dilution or mixing with bicarbonate.39 More importantly, diphenhydramine injection can result in vesicle formation and tissue necrosis.18 Because of these characteristics, it is not recommended as a local anesthetic. In the absence of any pharmacologic anesthetics, ice may be applied around the wound edges for 5 minutes to diminish sensation. Regional anesthetic techniques can be very useful for dealing with extremity wounds or fractures. This involves infiltrating the anesthetic around the nerve(s) innervating the affected region.52 These techniques rely on specific anatomic landmarks and are beyond the scope of this chapter.

Wound Closure Techniques The first determinant of whether or not to close a wound is the type of trauma sustained. The next is the degree of contamination and time since injury. If the wound clearly has foreign material that cannot be removed or devitalized tissue that cannot be completely debrided, then the wound should be left open to heal by secondary intention. Critical factors are the experience of the health care provider and availability of instruments. Wound closure is almost never so necessary that an untrained provider should attempt it. A variety of materials and approaches may be taken to close wounds. Sutures are generally required to approximate deep tissues, but the superficial aspects of wounds can be addressed with adhesive strips, sutures, glues, staples, or some combination thereof.22 Small superficial lacerations in areas with modest skin tension may be amenable to reapproximation with dressing strips such as Steri-Strips, Leukostrips, or Episeal. This can also be achieved with clean, semiporous medical paper tape. These strips of tape are laid perpendicular to the direction of the wound while holding the edges together. Small gaps should be left between strips to ensure ventilation. Different manufacturers boast superior adhesiveness, but the greatest impact on tape adherence is the use of liquid adhesive on the skin before applying the tape. Tincture of benzoin and Mastisol are equally effective for this purpose as long as they are allowed to dry for a minute before applying the strips. Modern genesis of these products was application of plastic medical tape to approximate wounds in remote locations when providers found the skin too thin or delicate to retain sutures. Modern adhesive strips can still be used for this purpose, or even in a hybrid fashion; strips can be placed along wound edges to reinforce the skin and help it “hold” suture. This practice actually dates back to the 16th century, when Ambroise Paré pasted linen strips to wound edges to reinforce suture closure. Modern cyanoacrylate skin glues are effective, affordable, and more versatile than adhesive strips.8,22,40 They boast the added benefit of sealing the incision, which may be particularly useful in a wilderness setting involving exposure to the elements. Cyanoacrylate glues are popular. These include Dermabond, Indermil, and SurgiSeal. Each of these differs slightly in time to drying, maximum tensile strength, and viscosity, but the clinical variability is minor; selection should be based on availability and cost. Although many are stable at lower than 30° C (86° F), it should be noted that storage of Indermil for longer than 4 weeks requires refrigeration. Another technique to close a wound if only tape, needle, and thread are available is accomplished as follows. Cut two strips of adhesive tape 2.5 cm (1 inch) longer than the wound. Fold 438

FIGURE 22-5  Folding a longitudinal piece of tape to prepare for a suture anchor strip.

one-quarter of each strip of tape over lengthwise (sticky to sticky) to create a long nonsticky edge on each piece (Figure 22-5). Attach one strip of the tape on each side of the wound, 0.6 to 1.3 cm (0.25 to 0.5 inch) from the wound, with the folded (nonsticky) edge toward the wound. Using a needle and thread, sew the folded edges together, cinching them tightly enough to bring the wound edges together properly (Figure 22-6). The tape will stick much better if you first apply a thin layer of benzoin to the skin.5 Sutures are the workhorse of wound closure because of durability and versatility; summary characteristics of the most versatile sutures for acute traumatic wounds are listed in Table 22-4.13,16,41 When suturing deep tissue, intermediate-durability absorbable materials such as polyglactin (e.g., Vicryl) or copolymeric glycolic and lactic acids (e.g., Polysorb) should be used. At 2 weeks, these materials retain approximately three-quarters of their original strength.11,14 Nondyed varieties are preferred within 5 mm (0.2 inch) of the skin surface to avoid wound tattooing. For mucosal lesions (such as within the mouth), rapid-absorbing gut suture is the most suitable.9 In all these cases, a tapered-tip needle should be used so that deep tissue is not lacerated. Ideally, skin suturing should be done with monofilament nonabsorbable material attached to a cutting needle. Nylon (e.g., Ethilon, Dermalon) and polypropylene (e.g., Prolene) are typical nonabsorbable sutures. Polypropylene is blue but does not tattoo skin as noted above for absorbable sutures. If proper materials are not available, nondyed absorbable suture with a tapered needle can be used on the skin, but nonabsorbable suture should not be buried within the wound; in this case, deep mattress sutures should be placed so that deep tissue is approximated but the suture can still be removed once healing is complete. Size selection is based on visibility and the degree of tension expected on the wound. For skin approximation, recommended sizes are: 5-0 or 6-0 for the face/neck/ears; 5-0 or 4-0 for fingers/hand; 4-0 or 3-0 for scalp/arm/leg/feet/chest/abdomen; and 3-0 or 2-0 on the back or over a major joint. Deeper layers (below the skin) generally require suture one size larger than or the same as is being used for the skin (e.g., deep upper arm laceration receives 4-0 absorbable suture to approximate deep layer, followed by 4-0 for skin). The goals of deep tissue closure are to take tension off the skin closure and to obliterate the gap in deep tissue so that seroma or abscess is less likely to form.13,16,41 Muscle sheaths (i.e., fascia) should be reattached, and subcutaneous tissues should be

FIGURE 22-6  Sewing the tape suture strips together to close the wound.

Name

Material

Structure

Tensile Strength

Absorption

Uses

Chromic gut

Bovine intestinal serosa and chromium acid Glycolide and dioxanone Polyglactic acid

Monofilament

0% at 2 wk

21 days

Mucosal repair

Monofilament

90-110 days

Skin

55-70 days

Glycolic and lactic acid copolymer Polypropylene

Braided

75% 40% 75% 50% 80% 30%

Monofilament

Long-term hydrolysis

55-70 days complete absorption Not absorbed

Deep tissue, including ligation of small bleeding vessels Deep tissue, including ligation of small bleeding vessels

Nylon

Monofilament

Long-term hydrolysis

Not absorbed

Nylon

Braided

Long-term hydrolysis

Not absorbed

Silk

Braided

Poorly defined

Permanent

Biosyn Vicryl Polysorb Prolene, Surgipro, Surgilene Ethilon, Dermalon, Monosof Nurolon, Surgilon Sofsilk

Braided

sutured together in interrupted fashion. A deep wound may require multiple layers of suture before skin closure, but usually one or two suffice. Each “layer” of suture is indicated not by the absolute depth of tissue, but by the presence of distinct anatomic “planes” (e.g., separate fascial sheaths) that must be approximated. If significant muscle, tendon, or nerve injuries are recognized, suture repair should not be attempted in the acute setting, but written notes should be recorded for long-term follow-up (Figure 22-7). If required later, these repairs are performed in an elective setting after healing has occurred and functional deficits are delineated. Traumatic wounds are typically irregular in shape and thus lend themselves to closure by interrupted technique. Running closure may be employed if there is a truly linear laceration. A straight or smoothly curved incision may be closed with a running suture to save time. An irregularly shaped wound should be closed with interrupted sutures to achieve optimal alignment (Figure 22-8, A; see Figure 22-3, B and C). Mattress techniques can be applied in deep wounds, thin skin, or those under tension.41,55 Vertical mattress sutures approximate the wound at two depths and evert wound edges for optimal healing (Figure 22-8, B). Horizontal mattress sutures close a single depth, evert wound edges, and distribute tension along the length of the incision (Figure 22-8, C ). More complex wounds can benefit from application of advanced techniques, such as local rotational or advancement flaps.48,50 Mechanical clips can be applied more rapidly than can sutures. Ancient Hindus used ant mandibles to pinch skin edges together, then twisted off their bodies.53 Modern skin staplers are made by various manufacturers and are useful for rapid closure of wounds

A

B

2 3 2 3 2 3

wk wk wk wk wk wk

Skin or full-thickness wound; major vessel ligation/repair Skin or full-thickness wound Skin or full-thickness wound (holds knots better than monofilament nylon) Can be used to ligate vessels, but falling out of use because of high tissue reactivity

on thick skin such as the scalp or back. They can be particularly effective for rapidly achieving hemostasis in the scalp, which is richly perfused and frequently rebleeds after direct pressure is released. Wounds of the abdomen and chest have the potential to involve the viscera. If air is felt, heard, or seen emanating from

FIGURE 22-7  Deep laceration over the wrist that is likely to involve nerve, tendon, and vascular injury. There is no role for attempting tendon or nerve repair in the field; care should focus on irrigation, control of hemorrhage, and aseptic aftercare. (Courtesy Ramin Jamshidi, MD.)

C

FIGURE 22-8  A, Interrupted simple sutures. B, Interrupted vertical mattress sutures. C, Interrupted horizontal mattress sutures.

439

CHAPTER 22  Wound Management

TABLE 22-4  Properties of Select Sutures

PART 4  INJURIES AND MEDICAL INTERVENTIONS

a chest wound, or if the patient is complaining of shortness of breath, some form of pneumothorax must be present. The wound should not be closed tightly, but rather covered with a nonocclusive dressing. This will minimize contamination while allowing outflow of air so that tension pneumothorax does not develop. If intestine or omentum protrudes from an abdominal wound, there is considerable likelihood of visceral injury (Figure 22-9). Such a wound should be covered with a moist, secure dressing and not be sutured. Both of these conditions require prompt evaluation by a surgeon. Scalp wounds occur frequently, can be very bloody, and have unique management options. The scalp is richly perfused, so even superficial lacerations can bleed profusely. Initial care should include firm direct pressure for several minutes. If bleeding does not abate, then secure scalp closure is necessary to assist in local pressure and minimize the potential space for hematoma formation. If the galea aponeurotica is lacerated and suture is available, it should be primarily repaired to further limit the space available for hematoma expansion. For skin closure, staplers are excellent in this circumstance because staples are rapidly applied and effective, and the scars are less noticeable on the scalp. Sutures may be used but are not necessary. If a scalp wound is bleeding and needs to be closed but no instruments are available, a hair tie may be performed. Hair is parted along the incision and twisted into cords on either side of the incision. Cords opposing one another across the laceration are then tied together to approximate the wound edges5,25 (Figure 22-10). Timing of skin suture and staple removal depends on the individual wound. Healing and wound remodeling are gradual processes—at 1 week after injury, a typical wound has just 5% to 10% of the original tensile strength. The majority of healing takes place over the first 6 weeks, at which point tensile strength reaches 70% of baseline.17,44 Leaving skin closure material in place longer keeps tension off the wound but increases the likelihood of visible scar from the suture or staple itself. Therefore timing of removal varies based on durability and visibility of the affected area. On the face/neck, sutures are removed at 3 to 5 days, fingers/hand at 5 to 7 days, scalp/leg/chest/abdomen at 7 to 10 days, back/arm/feet at 10 to 14 days, and 14 days across any major joint. For each site, sutures should be left in place longer if scar integrity seems poor, malnutrition has been involved, or if the orientation of the wound subjects it to excessive tension. Sutures are removed with scissors, and staples are removed with a staple remover or by laterally spreading a hemostat between skin and staple. Once the sutures or staples are removed, the healing wound may be reinforced with adhesive strips or skin glue (as described earlier) to minimize tension while healing continues, especially in a wilderness environment where vigorous activity may strain the wound. Visibility of the resulting scar is minimized by keeping it out of direct sunlight, particularly for the first 3 months following injury.

FIGURE 22-9  Abdominal laceration with omentum emanating from the wound. This signifies the possibility of serious visceral injury and mandates immediate surgical evaluation. (Courtesy Ramin Jamshidi, MD.)

440

FIGURE 22-10  String and hair-tying method for closing a scalp wound.

Dressings and Aftercare Wounds should be kept as clean as possible. Any wounds addressed in austere environments are at increased risk for infection and should be carefully monitored for cellulitis or abscess (see Complications). Incidence of infection obviously depends on the specific wound characteristics, anatomic location, and context of injury. Although up to 25% of acute wounds reveal Streptococcus, Staphylococcus, or Escherichia when cultured, most studies have revealed just a 5% rate of infection. Weighing this against the risk for adverse reactions and effect of selecting resistant species, antibiotics are not prescribed for all traumatic wounds.33 The decision to administer prophylactic or empiric antibiotics must be individualized to each situation. Patient factors that should encourage consideration of antibiotics include poorly controlled diabetes mellitus, malnutrition, recent chemotherapy, prosthetic valve or organ transplant recipient, peripheral vascular disease, renal failure, chronic liver disease, chronic corticosteroid use, or other immunocompromising condition. Wound factors include delay (more than 10 hours) to cleansing and repair, extensive devitalized tissue, heavy contamination or retained debris, bites, oral lacerations, foot wounds, open fractures, or injury to poorly perfused tissue (bone, joint, tendon).3,28,33 Tetanus is caused by Clostridium tetani, an organism found in soil and the excrement of humans and animals. The often fatal disease can be prevented by immunization, but 40% of Americans age 60 years or older lack seropositivity.31 Tetanus immunization status must be evaluated for all patients with traumatic wounds, and a booster dose of toxoid and/or immune globulin administered if the patient is at risk for infection (Table 22-5). The formulation of tetanus toxoid booster depends on the age of the patient and vaccination history (Table 22-6).10,27 Dressings serve a few limited purposes: protect the wound from the elements and contamination, absorb fluid from the wound and thereby protect surrounding skin, and provide an environment conducive to healing. Generally these goals can be achieved by dry gauze secured with a bit of tape. Gauze dressings should be changed once daily or more frequently as needed when soiled. For wounds left open to heal by secondary intention, episodic dressing changes are required to provide gradual debridement

Complications

History of Immunization (Doses of Adsorbed Tetanus Toxoid Previously Received)

Cellulitis is diagnosed by the presence of blanching erythema around and spreading away from the edges of a wound and may demonstrate proximal streaking along lymphovascular channels. It is important to distinguish this from the hyperemia that commonly surrounds the edges of a healing wound. Erythema associated with normal wound healing is not as bright red as is cellulitis, has less dramatic blanching with pressure, is symmetric around the edges of the wound, and extends not more than a centimeter from the wound edges. If erythema is not limited by these characteristics, or it progresses in size, wound infection is present. The treatment for cellulitis is a systemic antibiotic. The chosen antibiotic (first-generation cephalosporin or antistaphylococcal penicillin) should cover typical skin flora but also take into consideration any particular exposures (e.g., open water injury, animal bite, soil contamination) that may be associated with the trauma and dictate coverage of different microbes.6 Cellulitis without abscess does not require suture removal. If cellulitis persists or progresses after 36 hours of the above treatments, the antibiotic spectrum should be broadened and the wound reevaluated to ensure that there is not an underlying abscess. Abscess is a suppurative soft tissue infection. Pus is a mixture of dead organisms, leukocytes, and debris contained within a deep tissue space. An abscess will continue to expand, causing progressive pain, surrounding cellulitis, and potential systemic illness until drained (Figure 22-11, online). Antibiotics may stunt the growth or spread of associated cellulitis, but abscesses require drainage. This is accomplished by removing any sutures, staples, or tape keeping the wound closed. The abscess cavity is then copiously irrigated, and a soft probe is used to ensure that any loculated collections are properly drained. An excellent probe is a cotton-tipped swab dipped in antiseptic ointment to prevent deposition of cotton threads. Necrotizing soft tissue infections are true emergencies and require surgical intervention. These can take the form of superficial infections or deep fasciitis. The superficial variety can be easily recognized by the foul-smelling gray (“dirty dishwater”) drainage, but necrotizing fasciitis can develop surreptitiously because skin findings are often subtle and mistaken for simple cellulitis. The signs of deep infection include pain on passive motion, woody induration, and rapid spread.20 Antibiotics may stall the pace of progression, but these conditions are uniformly fatal if not addressed by a general surgeon. The definitive treatment is wide incision and drainage along with fluid resuscitation and intensive supportive care. This typically results in large, disfiguring wounds. Compartment syndrome results from elevated pressures within a contained compartment; as pressure rises, it exceeds venous pressure, then eventually arterial pressure, resulting in tissue ischemia. In the wilderness setting, this is most likely to occur from blunt trauma, particularly with crush injury or a closed fracture. The classic evidence of increased compartment pressures are pulselessness, pallor, pain on passive motion, poikilothermia, and paresthesia.47 Pain on passive motion is the most sensitive and earliest sign to develop, but all are relatively late signs of compartment syndrome. Immediate surgical evaluation is needed because the definitive intervention is incision and release of the involved compartment. If signs of compartment syndrome develop from a penetrating injury, it suggests that there was an occult vascular injury and an expanding hematoma is trapped beneath the closure. The closure should be opened, blood/hematoma evacuated, and a fresh attempt made to control bleeding. If compartment syndrome is not addressed, irreversible tissue necrosis begins by 6 hours. Persistent bleeding is a common concern of wilderness medical providers. Typically this indicates a missed injury or inadequate direct pressure. If a wound continues to bleed through a dressing, the bandage should be removed to allow direct inspection. Consider that a discrete vascular injury may have been missed, and an exposed vein or artery requires direct pressure or ligation.24 If a prolonged period of direct pressure does not stop hemorrhage, one may need to use hemostatic adjuncts or tourniquet application as discussed earlier.

Unknown/less than series of three doses Three or more   Last within 5 yr   Last within 10 yr   Last over 10 yr

Clean and Minor Wound †,‡,§

All Other Wounds*

Toxoid

Toxoid and TIG‡,§,॥

No prophylaxis No prophylaxis Toxoid

No prophylaxis Toxoid Toxoid and TIG‡,§,॥

TIG, Tetanus immune globulin. *Such as contaminated with dirt, soil, saliva, or feces. Includes punctures, avulsions, missile injuries, crush, burns, and frostbite. † Tetanus toxoid formulation depends on the age of the patient (see Table 22-6). ‡ No toxoid should be administered to infants younger than 6 weeks of age. § Patients with acquired immunodeficiency syndrome (AIDS) should receive TIG regardless of immunization history. ॥ TIG 250 units intramuscularly (for both adults and children). Toxoid should not be administered at the same site.

and prevent desiccation. The simplest and most traditional approach is to apply gauze moistened with water, normal saline, or lactated Ringer’s solution directly onto the wound and covered by a layer of dry gauze. These dressings should be changed 3 times daily as the outer dry gauze wicks fluid away from the wound surface. In the absence of infection, this process can be simplified by use of hydrogels that do not evaporate as quickly as do crystalloid solutions. Tegagel and Curafil are two of the most widely used hydrogels available in an amorphous form (gel in a squeezable tube). This is a more effective formulation for a wilderness provider (as opposed to prepackaged individual gauze and hydrogel dressings). If hydrogels are used, moist-todry gauze dressings can be changed just once a day. The last few years have witnessed a proliferation of wound care products intended to accelerate healing and increase simplicity of care. One of the most notable and applicable to wilderness care is Mepilex. This is a silicone foam dressing designed to wick exudates away from wounds while keeping them hydrated to allow healing. This versatile adjunct self-adheres to the skin surrounding the wound and can be left in place for up to 5 consecutive days to manage open or weeping wounds. The foam should be trimmed to cover the wound and overlap onto surrounding skin by about 2 cm (0.8 inch). It should be stored in dry conditions at a temperature under 35° C (95° F); sunlight will discolor the material but not alter its function. Antiseptic ointment is produced in a variety of formulations by many manufacturers. These greasy or gelatinous materials contain povidone-iodine, bacitracin, polymyxin B, or a combination of topical antimicrobials; no substantive evidence exists for the superiority of one formulation over another. However, one must be sure that the patient is not allergic to any of the agents in the ointment. Antiseptic ointments are useful topical agents for injured areas that do not penetrate the skin but are predisposed to desiccation (e.g., superficial abrasions or burns). The viscosity of these ointments make them particularly effective in areas that are difficult to dress and are in constant motion (such as the face or hands). TABLE 22-6  Recommended Tetanus Toxoid Types Age

Tetanus Toxoid Formulation

<6 wk >6 wk and <7 yr 7-10 yr 11-64 yr

No toxoid DTaP Td Td if previously received Tdap or if pregnant Tdap if never received Tdap Td

65 yr or older

DTaP, Pediatric diphtheria and tetanus toxoids and acellular pertussis; Td, tetanus and diphtheria toxoids; Tdap, tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis.

441

CHAPTER 22  Wound Management

TABLE 22-5  Postinjury Tetanus Prophylaxis

TABLE 22-7  Wound Care First-Aid Kit

Personal protection

Instruments

Wound preparation

Closure materials

Dressings

Medications

Core Items

Optional Items

Gloves (nonlatex) Eye shield Mask Headlamp Needle driver (15.2 cm [6 inches]) Scissors (iris tip) Toothed forceps (Adson type) Nontoothed forceps (DeBakey type) 60-mL syringe 18-guage needle or blunt cannula 21-guage needle Water filtration system Povidone-iodine swab packets 2-0 nylon (cutting needle) 4-0 nylon (cutting needle) 3-0 Vicryl (tapered needle) Skin stapler Dermabond skin glue vials Adhesive strips (1.3 cm [0.5 inch]) Gauze (10 × 10 cm [4 × 4 inches]) Porous paper tape (1.3 cm [0.5 inch]) Gauze roll (11.4 cm × 3.7 m [4.5 inches × 4 yards]) Flexible, reusable splint 0.25% bupivacaine (10-mL vials) Antiseptic ointment (30 g [1 oz]) Cephalexin (500 mg) Ciprofloxacin (500 mg)

Sterile gloves (nonlatex, nonpowdered) Surgical cap

Many wounds can be managed in a backcountry environment without interrupting the activities. However, some injuries mandate evacuation. These include open fractures, compartment syndrome, persistent bleeding, tourniquet use, progressive loss of sensation or motor function, progressive infection, and fullthickness burns that are circumferential or involve more than 5% of body surface area. Many wilderness-acquired wounds that do not necessitate evacuation still require formal medical evaluation upon return to civilization.35 These include any persistent detriment in motor function or sensation, ongoing drainage from the wound, persistent open wound, burns over the face or genitals, and burns over joints.

Hemostats (curved)

Splash shield Chlorhexidine surgical scrub brush

5-0 nylon (cutting needle) 6-0 nylon (cutting needle) 4-0 Vicryl (tapered needle) Mastisol (15 mL) Elastic roll (7.6 cm × 4.6 m [3 inches × 5 yards]) Mepilex (10 × 20.3 cm [4 × 8 inches]) Surgicel Nu-Knit (2.5 × 8.9 cm [1 inch × 3.5 inches]) QuikClot (10 × 10 cm [4 × 4 inches]) Silver sulfadiazine 1% cream (50 g [1.8 oz]) 5% lidocaine jelly (35 g [1.2 oz])

Wound Care Kit Many adjuncts are available to facilitate wilderness wound care, but a kit with core supplies will suffice in the majority of circumstances. Table 22-7 lists suggested components of such a kit.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 23 

Improvised Medicine in the Wilderness KENNETH V. ISERSON AND HOWARD J. DONNER

At the heart of wilderness medicine is improvisation, a cre­ ative amalgam of formal medical science and commonsense problem solving. Medical emergencies can arise at any time in wilderness settings; clinicians in these environments often encounter situations requiring their interventions with little or no medical equipment at hand. Even when they have supplies, as they might if they are the designated providers for a wilderness group or part of a search and rescue team, clinicians venturing into a wilderness environment will soon discover that some improvisation may still be nece­ ssary. When improvising medical equipment, consider whether it (1) will accomplish the purpose for which it is intended, 442

(2) is practical, or (3) may worsen the situation.23 Improvisa­ tion encompasses many variations, is governed by few abso­ lute rights and wrongs, and is limited more often by imagination than by personnel or equipment. As Louis Pasteur reportedly said, “Chance favors the prepared mind.” This chapter is in no way exhaustive but suggests the types of improvisations that may be possible in wilderness or remote settings. Of note is that all these methods have been tested, with many appearing in peer-reviewed literature. Although some of the improvisations, such as transportation methods, border on first aid, they are an integral part of the complexities of remote medical care.

For online-only figures, please go to www.expertconsult.com

HEIGHT To measure an ambulatory patient’s height, use marks in 0.5-cm (or 0.5-inch) increments on any rigid, vertical surface, such as a wall or the side of a doorway. For infants and bedridden patients, put similar marks along the sides of stretchers or beds. Height approximations can be made with marks 0.25 m (or one foot) apart. To estimate a sitting adult’s height, measure the distance (in centimeters) from midsternum to the extended middle finger. Patient’s height = [ 0.73 × (2 × half arm span )] + 43 cm. 79 Alternatively, doubling the longest measurement from mid­ sternum to the tip of the patient’s third finger produces a very accurate height estimate.45

WEIGHT

FIGURE 23-2  Blood pressure cuff on forearm.

A relatively accurate way to obtain an adult patient’s weight is to use weight estimates by experienced health care workers. Esti­ mates by paramedics, for example, have been shown to correlate well with the patients’ actual weights in adult cardiac arrest victims.49 Weight estimates of children can be more difficult. Parents can estimate their child’s weight (ages 1- to 11-years-old) within 10% of the measured weight only 78% of the time. This is better, however, than what is estimated by the Broselow tape, which is within 10% of the measured weight only 61% of the time and is less accurate as children get older. In less-developed coun­ tries, the Broselow tape underestimates children’s weights.4,8,35,48 All other forms of guessing a child’s weight, including the Argall, the Advanced Pediatric Life Support, and the Best Guess methods, perform poorly.43 If the parents are not around, use the following formula: (2 × age in years ) + 8 = weight in kilograms.

PULSES IN INFANTS The typical method of deciding whether an infant has a pulse requires providers to palpate the pulse. This means knowing where and how to locate it, even if it is barely (or not) palpable. Palpating an infant’s pulse, especially when the child is critically ill and a decision must be made immediately about whether to begin resuscitation, can be very difficult. However, determining infant cardiac activity is quickly and easily done by simply placing one’s ear against the infant’s chest wall and listening for heart sounds (Figure 23-1).38

RADIAL PULSE AND TRAUMA PROGNOSIS Tachycardia is a much more reliable sign of hypovolemia than is blood pressure (BP). In trauma patients who are 18 to 50 years old without a head injury, a weak radial pulse indicates a

FIGURE 23-1  Direct precordial auscultation.

markedly increased mortality (29%) compared with only 3% of patients with a normal pulse, as well as a high likelihood that the victim will require intubation and intensive care unit admis­ sion. Patients with no radial pulse are usually moribund.51

BLOOD PRESSURE Research has shown that the “ability to obtain a blood pressure measurement in an austere environment is often limited by time constraints, equipment availability, and noisy conditions.”51 Blood Pressure Without a Cuff Pulse characteristics are an unreliable sign—and “should be used only as a last resort.”51 Originally, the advanced trauma life support (ATLS) course taught that systolic blood pressure can be estimated from whether radial (>80 mm Hg), femoral (70 to 80 mm Hg), or carotid (60 to 70 mm Hg) pulses are pal­ pable. This tends to overestimate the patient’s blood pressure. Although the radial pulse always disappears before the femoral, which always disappears before the carotid, most patients’ actual BP is lower than that predicted by these guidelines. But that, by itself, is useful information in a crisis.15 Although an exact BP measurement cannot be obtained, patients with cool extremities compared with those of other patients have hypoperfusion. This can be localized to one extremity, but if it is located in multiple extremities—especially in both an arm and a leg—checking palpable temperature is an effective diagnostic technique. These patients have lower cardiac indexes, lower pH, lower bicarbonate levels, lower mixed venous oxygen saturation, and higher lactate levels.42 A cold or dusky sole of a neonate’s foot can indicate one or all of the following: hypothermia, hypoxemia, or hypotension.14 Blood Pressure Without a Stethoscope Because it may be hard to auscultate BP when transporting patients by air or in a noisy ambulance, palpate the systolic pres­ sure. If done carefully, this method is as accurate as using a stethoscope. Alternatively, use a pulse oximeter by obtaining a good waveform on a finger, inflating the sphygmomanometer until the waveform disappears, and then slowly deflating the cuff until the waveform reappears. The cuff measurement that reap­ pears is the systolic pressure.50 Wrist and Calf Blood Pressure Measurements To be accurate, a BP cuff must be the correct size for the arm. It should cover two-thirds of the length of the upper arm. A BP cuff that is too small causes an abnormally high BP reading; one that is too large results in an abnormally low reading. If you do not have a cuff that fits the arm correctly, move it to a location where it fits properly. Place a BP cuff on the patient’s forearm (Figure 23-2) or ankle (Figure 23-3) to obtain better access during patient transport (1) with very obese patients on whom the standard adult cuff is too small, (2) for adults when only a child’s-size cuff is available, (3) to avoid periodically occluding an arteriovenous fistula (e.g., 443

CHAPTER 23  Improvised Medicine in the Wilderness

Vital Signs

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 23-3  Blood pressure cuff on calf above ankle.

TABLE 23-1  Clinical Measurements Using Body

Parts*

Approximate Length 1.3 cm (0.5 inch) 2.5 cm (1 inch)

3.8 cm (1.5 inch)

Measurement Site(s) Finger width: greatest width of the distal phalanx of the small finger Phalanx: length of the middle phalanx of the small finger (Figure 23-4) Thumb: width of thumb at the interphalangeal joint (Figure 23-5) Span: when opening the hand and spreading the fingers widely, from the tip of the thumb to the tip of the index finger (Figure 23-6) Grasp: the greatest diameter of the circle formed with the thumb and index finger (Figure 23-7)

*Some of these measurements were suggested by White J, editor: Handbook of Indians of Canada, published as an appendix to the Tenth Report of the Geographic Board of Canada, Ottawa, 1913, pp 280-281. http:// faculty.marianopolis.edu/c.belanger/quebechistory/encyclopedia/ MeansofMeasurementbyIndians.htm. Adapted from Iserson KV: Improvised Medicine: Professional Treatment with Scarce Resources. McGraw-Hill (in press).

FIGURE 23-5  Thumb (2.54 cm [1 inch]).

MEASURING LENGTH, AREA, AND VOLUME A way to most accurately estimate the sizes of wounds is to measure them against the clinician’s own body parts. Table 23-1 gives approximate lengths and areas for upper extremity body parts to use with measurements corresponding most closely with adult white men. Because body sizes vary greatly, especially between men and women, practitioners should measure these sites on their own bodies before using them to measure patient lesions. Standard measurements, in centimeters or in inches, can be made on personal medical equipment, such as the metal ear­ pieces of a stethoscope (Figure 23-8), a reflex hammer handle, penlights, and scissors.

dialysis patients) or intravenous (IV) line, (4) or to avoid com­ pressing an area with traumatic injuries. BP cuffs at these sites produce the same or nearly the same mean and diastolic pressure readings, but the systolic pressures vary. Use the mean BP with a forearm or calf BP cuff. (Calculate this by multiplying the diastolic pressure by 2 and adding the systolic pressure. Then divide the result by 3. Alternatively, take one-third of the difference between the systolic and the diastolic pressures, and add this number to the diastolic pressure.)40

Volume Measurement Volume measurements are used to determine the outputs of urine, blood, and other secretions, and to measure fluids and medications. To obtain an accurate volume measurement, use kitchen measuring devices or food containers that have their volume indicated on the label. Generally, they only need to be cleaned of food or whatever else they previously contained. Sterilize the measuring container only if the specimen also has to go to the laboratory or will be used to measure injectable medications. Measuring containers for items that will be taken orally need to be “potable clean,” meaning that one could safely drink from them.

FIGURE 23-4  Phalanx (2.54 cm [1 inch]).

FIGURE 23-6  Span (15.24 cm [6 inches]).

444

Rubber tubing

Funnel

FIGURE 23-9  Improvised stethoscope.

Precordial Stethoscope

Ear to Patient If no other option is available, use the method that was common before Laennec invented the stethoscope: put one ear directly against the chest, heart, or abdomen. The sound quality will not be as good as through a stethoscope, but one can get a general idea of cardiac rhythm, abnormal chest sounds, and bowel sounds. Putting one’s ear on an infant’s chest is the fastest and most accurate method for assessing the presence of cardiac activity.

5

Improvised Standard Stethoscopes Laennec-type stethoscopes can easily be fashioned by using rolled paper or, even better, a hollow wooden tube, such as bamboo. The cardboard tube from toilet paper or paper towels also works well. When one end is placed on a patient’s chest and the clinician’s ear is at the other end, one can hear the heartbeat clearly. This, of course, depends on ambient noise and the patient’s body habitus. Use any hollow tube, including short lengths of garden hose, ivory or wood tubes, and metal pipes, as a monaural stethoscope. A simple way to construct a slightly more sophisticated stetho­ scope is to attach a funnel to two pieces of tubing as shown in Figure 23-9. The juncture of IV tubing works well as a T-tube connector. Put the tube ends directly in your ears, or fashion earpieces as described in Stethoscope Earpiece, later.

20

STETHOSCOPES

15

Improvised Diagnostic Equipment/ Supplies

10

FIGURE 23-7  Grasp (3.81 cm [1.5 inches]).

One very useful monitor during patient transport or procedural sedation is a precordial stethoscope. Taped to the patient’s chest, a precordial stethoscope provides the clinician with continuous assessment of the patient’s audible heart rate and rhythm and breath sounds. Only one earpiece is normally used so that the caregiver can also monitor everything around him or her. In adults, place the stethoscope over the midsternum, in the supra­ sternal notch, in the perilaryngeal area, or in the axilla. In infants, place the stethoscope to the left chest so that both the heartbeat and breath sounds can be heard. Several improvised methods will produce a workable precordial stethoscope. The quickest way to make a precordial stethoscope is to attach a piece of rubber tubing (that goes in the clinician’s ear) to the top of a screw-top plastic bottle that has a narrow, tapered opening, such as a ketchup/mayonnaise dispenser. Alternatively, cut off the tapered end of a rubber bulb suction syringe or stethoscope head, if one is available.16,77 A slightly more complex method is to make a precordial stethoscope from a 20-mL syringe, a 3-way stopcock, IV tubing, and an earpiece (Figure 23-10). Cut the 20-mL syringe 2.5  cm

A

B

C

D FIGURE 23-8  Stethoscope marked to measure lengths.

E FIGURE 23-10  Improvised precordial stethoscope.

445

CHAPTER 23  Improvised Medicine in the Wilderness

T-tube

PART 4  INJURIES AND MEDICAL INTERVENTIONS

(1 inch) from the infusion end (see Figure 23-10, A). Then, smooth the edges with a file, and place adhesive tape around the cut end of the syringe. Remove the plunger’s rubber sealer (see Figure 23-10, B), cut a large hole in its center (see Figure 23-10, C), and insert the rubber piece into the small piece cut off the syringe barrel (see Figure 23-10, D). After connecting this to a three-way stopcock, connect the stopcock to IV tubing (or other tubing) and then to an earpiece (see Figure 23-10, E).32 Esophageal Stethoscope Another way to simultaneously monitor respirations and cardiac rhythm in austere situations and during transport is to use an esophageal stethoscope. Make an esophageal stethoscope from a rubber glove, a nasogastric (NG) tube, suture, and a regular stethoscope. Cut a finger off of the glove, and tie the finger over the end of the NG tube (Figure 23-11). Remove the bell from the stethoscope. Pass the NG tube approximately halfway down the esophagus, and connect the proximal end to the end of the stethoscope. The NG tube can also be passed through the nose.17

A

Hearing Aid When necessary, substitute a stethoscope for a patient’s hearing aid during an examination. Put the earpieces in the patient’s ears and talk into the diaphragm. Unfortunately, this only works, as do hearing aids, for patients with specific types of hearing loss. Stethoscope Earpiece To replace a stethoscope earpiece, use the nipple from a baby bottle or pacifier, or the rubber bulb from a medicine or an eye dropper (Figure 23-12). Make the normal pinhole opening in the nipple slightly larger, and tie the nipple in place on the stetho­ scope. Cut the nipple so that only the distal 1 to 2 cm (0.4 to 0.8 inch) of the rubber piece is used.40

B FIGURE 23-12  Earpieces for a stethoscope.

Improvised Treatment Equipment/Supplies GOWNS, GLOVES, MASKS, BOOTIES, AND GOGGLES Standard Precautions In an austere environment the basic protective gear used for standard or universal precautions often must be made rather than purchased. Gowns A plastic garbage bag with head and arm holes cut out is the simplest waterproof gown, and can be enhanced with arm pieces cut from another bag and stapled or taped in place. Although not waterproof, a sheet cut like a poncho will also work. Fold a flat sheet so that one-third is doubled over to form the arms. In the center of the folded edge, cut out a hole large enough for the head to pass through. The sleeve is fashioned by cutting slits on both sides of the sheet, midway down the folded section. The slits should extend to the approximate sites of the axillae (Figures 23-13 and 23-14). Once the patient dons the gown, the arms can be secured with safety pins, staples, or tape (Figure 23-15). The large pieces are wrapped around the back under the arms, and the flap on the back makes a tie for the gown. (Depending on the person’s girth, the tie may also need to be pinned.)55,40

A

B FIGURE 23-11  Making an esophageal stethoscope.

446

Caps and Masks Masks are useful to protect both the examiner and patients against particulate matter, virulent organisms, and nauseating smells (tincture of benzoin on one’s mask covers up most bad smells). Caps protect patients’ wounds from the examiner’s hair. The most basic masks are towels or a cloth held to the mouth and nose, either with one’s hand or tied in place. Make an improvised surgical mask and cap from a piece of cloth about 46 × 31 cm (18 × 12 inches). Cut a 10-cm (4-inch) narrow oval to fit over the eyes, about 12.5 cm (5 inches) from one end. The cloth should allow a person to breathe through it

B FIGURE 23-16  Improvised cap-mask.

Eye Protection Put tape around the edges of standard eyeglasses to help to protect the eyes from splattered blood and fluids. An alternative is to wear ski or woodworking goggles—separately or over eyeglasses. FIGURE 23-13  Improvised surgical/patient gown, Step 1.

Booties Make waterproof booties from a large plastic bag. Cut it open so that it lays flat. From that piece, for a standard-sized foot, cut out a portion that is as long as the distance from the foot to the knee and as wide as three lengths of the foot. Make them larger if longer booties are needed, such as in a bloody procedure or when caring for a victim of trauma. Secure them on the foot (not too tight) with duct tape. Clear plastic bags can also work. Cut open as many as needed and tape them to cover the shoes. When using either type of plastic bootie, but especially those made from clear plastic bags, use tape on the bottom to prevent slipping.40

DRESSINGS AND BANDAGES FIGURE 23-14  Improvised surgical/patient gown, Step 2.

as easily as is done through a normal surgical mask. Attach a long piece of tape, extending over the edges of the material, at both sides of the slit. Also attach a long piece of tape to the bottom of the short end. Adjust the slit over the eyes, flip the long piece of material over the head for a cap, and then tie both pieces of the tape behind the neck (Figure 26-16). Cover your head with a long cloth or towel (Figure 23-17) and pin or tape it to the nape of your neck to make a simple cap.56,40

Dressings go directly on wounds and can be adherent or non­ adherent, wet or dry, and absorbent or not. Dressings are often sterile. Bandages cover dressings, can hold them in place, and place pressure on the wound. Although most clean fabrics can be used as dressings or as bandages, do not use paper products because they disintegrate when wet and leave fibers in the wound. Dressings Most clean, closed wounds do not need a dressing. Wounds without dressings permit easier inspection for infection or dehis­ cence, eliminate a moist, possibly anaerobic, space over the wound, and make it much easier to keep the wound clean. Have the patient clean the wound with soap and water. Dressing Material.  If a dressing is being used to help absorb serosanguineous drainage, to keep the wound moist after small

FIGURE 23-15  Improvised surgical/patient gown, completed.

FIGURE 23-17  Improvised cap.

447

CHAPTER 23  Improvised Medicine in the Wilderness

A

PART 4  INJURIES AND MEDICAL INTERVENTIONS

plastic closures, or to keep air off an open wound to lessen pain, any absorbent material may be used. A menstrual pad works well to absorb exudates, and more absorbent cotton fabrics can also be useful. If nothing else is available, use moss, especially sphag­ num (peat) moss, a traditional absorbent dressing. Make nonad­ herent dressings from sheer synthetic materials, such as parachute cloth or nylon stockings. Use any clean piece of plastic sheeting, such as a plastic bag, to fashion an occlusive dressing for openchest wounds. Using clean, rather than sterile, dressings will rarely affect the incidence of infection. Bandages Bandages hold dressings in place. If there is a dressing, there is no need for a bandage. The most expedient bandages are torn from expendable pieces of cloth—often clothing. If no cloth bandage is available, use duct tape to secure a dressing after first shaving the area to help the dressing adhere and reduce pain on removal. Poke holes in the tape (especially thick adhesives, such as duct tape) to reduce moisture and allow fluids and sweat to escape. Clean the skin with soap and water or alcohol to remove oils. To make an adhesive dressing, cover a small square of dressing with a piece of tape. If you need to see the wound but still want it covered, make a transparent bandage from clear plastic wrap (e.g., Saran Wrap) or a piece of clear plastic bag with its edges affixed to the skin with tape or cyanoacrylate glue.40 A pressure bandage over dressings, used when there is sig­ nificant seepage or concern about hematoma development, is most easily constructed from an elastic bandage, a bungee cord (use only over fabric stiff enough to distribute the cord’s force), or the elastic from a piece of clothing or equipment.

SYRINGES, NEEDLES, AND INTRAVENOUS EQUIPMENT Venipuncture Tourniquet A rubber glove (sterile or unsterile, but “stretchy”) works well as a venous tourniquet when starting IV lines or drawing blood. Even better, cut the wrist portion off of a surgical glove and slip it over the arm (or an infant’s head).60 Needles When necessary, use needles for injection as IV needles. Note, however, that they may be more difficult to thread into a vein, because injection needles tend to puncture the vessel wall rather than slide in as does the plastic-coated needle on a catheter. Take care when securing an injection needle, using an arm board or generous bandaging so that the needle does not perforate the vessel. Saline Locks To quickly make a saline lock, slip the rubber end of the plunger from a 2- or 3-mL disposable syringe over the end of an IV catheter (Figure 23-18). This also works on a straight needle if it needs to be used as an IV catheter. Simply fill the catheter with saline (or heparin) as would normally be done.40

FIGURE 23-18  Improvised saline lock.

the end of the suture appears, hold it in place and break off the hub by repeatedly bending it (Figure 23-19). Then pull the suture through the needle so that only a small amount remains within the needle. Finally, crimp the “hub” end of the needle to fix the suture in place.31 Do this either at the patient’s bedside or prepare several in advance, wrapping the sutures around a piece of cardboard and autoclaving them en masse.75 Newer safety needles may make this process difficult.

SCALPELS When necessary use any clean, preferably sterile, sharp object to perform surgical procedures. Nearly any piece of metal can be sharpened sufficiently to serve as a scalpel. Honing the entire length of a blade to surgical sharpness takes special metal, tools, and expertise. One option is to start with a straight razor or a cutting knife and sharpen it as well as possible before steriliz­ ing it. Make a scalpel from a common multi-blade disposable razor by first carefully separating a blade from its plastic holder. Use pliers or a similar tool to bend one end; the blades pop out (Figure 23-20, online). Then put a few drops of cyanoacrylate glue on both the blade and the utensil/holder; the blade can be affixed along the metal blade of a butter knife, the handle of a spoon, or similar items that can be easily held and manipulated during a procedure. The blade should extend over the side of the handle

Intravenous Tubing One way to adjust IV flow rates is to wrap a small piece of mal­ leable metal (e.g., heavy aluminum foil) around the tubing. Tighten it to the tubing to achieve the desired flow rate. Pressure for Intravenous Fluids/Blood Bags Apply external pressure to IV bags so that, especially when patients must be transported, the pressurized IV bag can simply lie on or next to the patient. Ways to increase the IV or blood bags’ external pressure include inflating a blood pressure cuff around them, and wrapping them with an elastic bandage, a belt (“stretchy” if possible), nylon stockings, a rope, or similar materi­ als. The IV bag can also be placed under an adult patient; body pressure keeps the IV flowing. Suture Needles To make a “swaged” suture needle from a hypodermic needle, first pass the suture through the needle from the sharp end. When 448

FIGURE 23-19  Improvised swaged suture.

When trying to guide health care professionals in their reuse of single-use devices, many major governing bodies cannot agree on their recommendations. The United States, however, has a consistent policy among several agencies. According to the U.S. government’s report, equipment and supplies “will be rationed and used in ways consistent with achieving the ultimate goal of saving the most lives (e.g., disposable supplies may be reused).”34 Other federal agencies concur, noting that whether medical equipment should be reused depends on the type of equipment and the disinfection method used. 47,12,46

A

B FIGURE 23-21  Improvised skin hooks.

and be parallel to the other side for better control of the scalpel. Wait about 10 minutes for the cyanoacrylate glue to dry.

SKIN HOOKS The best way to handle wound tissue with the least amount of trauma is to use skin hooks. To improvise a skin hook, grasp the tip of a small-gauge needle with a utility tool and bend it into a U-shaped curve (Figure 23-21). Then attach it to a 1- to 10-cc syringe, which serves as a handle. Alternatively, unbend a safety pin so that the two “limbs” on each side of the spring form a straight line. Then bend the sharp end into a U-shape. Sterilize them before use.24

RETRACTORS Self-retaining retractors make procedures easier when working alone or with inexperienced assistants. To make these retractors, bend stiff metal rods into the form shown in Figure 23-22. Use 3-mm rods for minor surgery and heavier rods for major wounds.37 If made from lighter material, such as paper clips, they can be used on more delicate tissues.

TWEEZERS Fashion tweezers to remove foreign bodies or for surgical proce­ dures from pieces of thin metal strips, such as the metal straps that secure boxes for shipping. If folded with a slight bulge in the end they are less likely to break at the fold after repeated use (Figure 23-23). Use a file to make as fine of an end as you need.

Cleaning and Reusing Medical Supplies and Equipment Much modern medical equipment is labeled as “disposable.” When resources are scarce, this is a luxury that cannot be sus­ tained. On the other hand, is it safe to reuse this equipment? Caregivers do not want to put patients at risk by introducing infections from previously used equipment or by using malfunc­ tioning equipment.

FIGURE 23-22  Lightweight self-retaining retractor.

RISK STRATIFICATION The infection risk that medical equipment poses to patients differs and can be stratified according to the equipment’s use, as follows:67 • High-risk items (sterilization required) that come into close contact with breaks in the skin or mucous membranes or are introduced into a normally sterile body area. These include surgical instruments, needles, and urinary or other catheters. • Intermediate-risk items (disinfection required) that come into close contact with mucous membranes or are items contaminated with particularly virulent or readily transmis­ sible organisms. Examples are respiratory equipment (including laryngoscope blades), endotracheal and trache­ ostomy tubes, and oropharyngeal and nasal airways. • Low-risk items (cleaning required) that only come into contact with normal, intact skin. These include stetho­ scopes, stretchers and wheelchairs, other physical examination equipment, and electrocardiography and elec­ troencephalography leads.

CLEANING Cleaning must be done so that equipment can be properly disin­ fected or sterilized. Cleaning removes visible dirt or secretions, including dust, soil, large numbers of microorganisms, and organic matter (e.g., blood, vomit) on which microorganisms grow.67 Immediately after use, clean equipment by washing it thoroughly with warm water without soap. Then brush it thoroughly with warm water and soap, rinse with water, and dry completely. Clean surgical instruments with a small brush, such as a soft toothbrush. Leave scissors and forceps open during drying.40

DISINFECTION Disinfection reduces the number of microorganisms to a level that is not harmful to health, although the process does not necessarily kill or remove all microorganisms or bacterial spores.67 The CDC recognizes three levels of disinfection: high, intermedi­ ate, and low.12 • High-level disinfection using a chemical germicide, includ­ ing bleach and ethyl alcohol, kills all organisms, except when there are high levels of bacterial spores. • Intermediate-level disinfection kills mycobacteria, most viruses, and bacteria with a chemical germicide registered as a “tuberculocide” by the U.S. Environmental Protection Agency. • Low-level disinfection kills some viruses and bacteria with a chemical germicide, such as soap. Boiling The best way to disinfect equipment in austere environments is to boil it (100° C [212° F] for 10 to 30 minutes at sea level) in clean water, with or without soap. The time starts when the water has come to a full boil. The temperature at which water boils decreases 449

CHAPTER 23  Improvised Medicine in the Wilderness

FIGURE 23-23  Surgical “pickups.”

PART 4  INJURIES AND MEDICAL INTERVENTIONS

at higher altitudes, so a longer boiling time will be required. In theory, the time should be increased by 5 minutes for each 300-m (1,000-foot) rise in altitude. For example, at 4000 m (approxi­ mately 12,000 feet) above sea level, water boils at 86° C (187° F), so boiling for 60 minutes or longer is required for disinfection. A way to increase the disinfectant effect of boiling is to use “double boiling.” Boil the instruments for 30 to 40 minutes. Let them cool, and then boil for another 30 to 40 minutes.36 This process kills all organisms except for certain bacterial spores. Alcohols Alcohols (e.g., methanol, ethanol, and isopropanol) have good activity against bacteria and viruses so long as the equipment first has been cleaned—or, at least, after all the visible surface dirt has been removed from the area to be disinfected. Use 70% or greater concentrations, and have the equipment in contact with the alcohol for 10 minutes or longer; the longer the contact time the better. To prepare a 70% ethanol solution, add 8 parts 90% ethanol to 2 parts water. To prepare a 70% isopropanol solution, add 7 parts standard isopropanol to 3 parts water.71 Povidone-Iodine Povidone-iodine (PVD-I; Betadine) may be used for disinfecting instruments. Although exact information about this is sketchy, studies seem to support its use. Use 1 part 10% povidone-iodine solution to 3 parts water for 15 minutes.71

DISINFECTING SPECIFIC ITEMS “Sterile” Dressings Clean and disinfect cloth for dressings by boiling it in water for 15 minutes or saturating it in alcohol. Syringes and Needles It is not possible to clean the interior of disposable syringes and needles well enough to use them safely on another patient. Although syringe reuse is a common practice throughout the world, it is so dangerous that it negates any good that medical treatment produces. Only when no other option exists should cleaning and reusing syringes be considered. If that is the case, the best option is one that the U.S. governmental agencies rec­ ommend for needles and syringes potentially contaminated with human immunodeficiency virus. That is, they should be thor­ oughly cleaned and then immersed in full-strength bleach (5.25% sodium hypochlorite).64 Single-Use Needle on Same Patient With proper precautions, single-use needles can be used multiple times on the same patient. For example, diabetics routinely reuse the same syringe for up to a week. They do this by keeping the needle clean, storing it in a clean container, and ensuring that no one else uses it.

FIGURE 23-24  Rescue/recovery position.

POSITIONING FOR SAFE AIRWAY Preventing aspiration may be all that is necessary in many patients to maintain an airway, especially in the presence of copious secretions or vomiting. Use the “rescue” or “recovery” position—with the patient on his or her side with face aimed down (Figure 23-24). If possible, elevate the patient’s feet so that he or she is in the head-down position.

OPENING THE AIRWAY Chin Lift/Jaw Thrust Elevating the chin is often the easiest method of maintaining an open airway (Figure 23-25). For many patients with diminished consciousness, this is often all that is needed to keep the airway patent. If a cervical spine injury is suspected, the alternative is to push the jaw forward from the mandibular angles. Head Turn When cervical spine injury is not a concern, turning the patient’s head to one side is a simple but rarely used procedure to open an airway. In patients with significant amounts of redundant tissue in the pharynx and hypopharynx this procedure usually improves airflow. Positioning the Tongue If a suspected cervical spine injury prevents head repositioning or the patient’s tongue still blocks the airway after positioning the head, grasp the tongue with gauze and pull it forward. If this opens the airway (it usually does), put a heavy (approximately 2-0) suture vertically through the tip of the tongue in the midline (Figure 23-26), or use a wire fishing line (or similar material), or safety pin (Figure 23-27). This placement avoids significant bleeding. Initially, have someone hold the suture; if needed longterm, pass it through the skin of the lower lip and tie it. Do not use a clamp or forceps that “may in the excitement of the

Surgical Instruments Use alcohol or, if the equipment does not contain plastic or polymers, acetone to chemically sterilize sharp or delicate instru­ ments. Following this soak, rinse them in hot, sterile water and let them dry.66 Surgical instruments without a fine tolerance or sharp edges, such as mosquito clamps, towel clips, and large needle holders, may be disinfected in boiling water.66 If you do not mind that sharp instruments will lose their edge, metal can be sterilized by holding it over a flame or, even better, by placing the instrument in a pot with a small amount of isopropyl alcohol (enough to create a small pool on the bottom of the pot). Ignite the alcohol, and allow it to burn out, which takes about 5 to 10 minutes. The alcohol burns without leaving significant carbon residue. These techniques may be used when sterilization is really needed or when available resources or time do not allow for disinfection by boiling or soaking in alcohol.40

Improvised Airway Management Because establishing or maintaining a patient’s airway is the most fundamental lifesaving skill, clinicians must be able to do this despite limited or unusual equipment. 450

FIGURE 23-25  Chin lift.

When placing a nasal airway, lubricate it well, and pass it along the floor of the nose (straight back, not cephalad).40

MOUTH-TO-MOUTH RESCUE BREATHING BARRIER A glove can be modified and used as a barrier shield for perform­ ing rescue breathing. Cut the middle finger of the glove at its halfway point and insert it into the victim’s mouth. Stretch the glove across the victim’s mouth and nose, and blow into the glove as if inflating a balloon. After each breath, remove the part of the glove covering the nose to allow the victim to exhale. The slit creates a one-way valve, preventing backflow of the victim’s saliva (Figure 23-29).

FIGURE 23-26  Suture used to hold the tongue out.

moment be so firmly applied as to nip a piece out of the tongue.”25 Physicians, surgeons, and anesthetists have used these methods since at least the 19th century without complication.40 Nasal Airways One of the most useful pieces of airway equipment, a nasal airway, or “trumpet,” is easy to improvise. Put a safety pin through the end of any soft piece of rubber tubing (e.g., Foley catheter, uncuffed endotracheal tube, radiator hose, solar shower hose, siphon tubing, or inflation hose from a kayak flotation bag or sport pouch) that is the appropriate size for the patient’s nose (Figure 23-28). In adults, the tube’s length beyond the safety pin equals the length from their nares to the meatus of their ears (11 to 13 cm [4.5 to 5 inches]).10 This “Goldman’s airway” can be made to fit any nose. Consider using nasal airways bilaterally.

Surgical Airway (Cricothyrotomy) Cricothyrotomy—the establishment of an opening in the crico­ thyroid membrane—is indicated to relieve life-threatening upper airway obstruction when a victim cannot be ventilated effectively from the mouth or nose and endotracheal intubation is not fea­ sible. This may occur in a victim with severe laryngeal edema or with trauma to the face and upper larynx. Cricothyrotomy may also be useful when a person’s upper airway is obstructed by a foreign body that cannot be extracted by abdominal thrusts or direct laryngoscopy. To perform a cricothyrotomy, cut a hole in the thin cricothy­ roid membrane and place an endotracheal tube or, in austere circumstances, a suitable hollow object into the trachea to allow ventilation (Box 23-1). Locate the cricothyroid membrane by palpating the victim’s neck, beginning at the top. The first and largest prominence felt is the thyroid cartilage (“Adam’s apple”); the second prominence (below the thyroid cartilage) is the cricoid cartilage. The small space between these two, noted by a depression, is the cricothyroid membrane (Figure 23-30). With the victim lying on his or her back, cleanse the neck around the cricothyroid membrane with an antiseptic if one is readily avail­ able. Put on protective gloves. Make a vertical 2.5-cm (1-inch) incision with a knife through the skin over the membrane (go a little bit above and below the membrane) while using the fingers of your other hand to pry the skin edges apart. Anticipate bleed­ ing from the wound. After the skin is incised and spread, punc­ ture the exposed membrane by stabbing it with a knife or other sharp, penetrating object (Figure 23-31, A). Stabilize the larynx between the fingers of one hand and insert the improvised cri­ cothyrotomy tube through the membrane with the other hand (Figure 23-31, B). Secure the object in place with tape. BOX 23-1  Improvised Cricothyrotomy Tubes

FIGURE 23-27  Safety pin holding the tongue out.

Intravenous (IV) administration set drip chamber: Cut the plastic drip chamber of a macro drip (15 drops/mL) IV administration set at its halfway point with a knife or scissors. Remove the end protector from the piercing spike and insert the spike through the cricothyroid membrane. The plastic drip chamber is nearly the same size as a 15-mm endotracheal tube adapter and fits snugly in the valve fitting of a bag-valve device (Figure 23-32). Syringe barrel: Cut the barrel of a 2- or 3-mL syringe with the plunger removed at a 45-degree angle at its midpoint to create an improvised cricothyroid airway device. The proximal flange of the syringe barrel helps secure the device to the neck and prevents it from being aspirated (Figure 23-33). Any small hollow object: Examples include a small flashlight or penlight casing, some pen casings, or small hollow tube. The key question is whether sufficient air can pass through the tube for effective ventilation.

451

CHAPTER 23  Improvised Medicine in the Wilderness

FIGURE 23-28  Goldman’s nasopharyngeal airway.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 23-29  An improvised cardiopulmonary resuscitation (CPR) barrier is created using a latex or nitrile glove.

Adam’s apple (thyroid cartilage) Adam’s apple

Cricothyroid membrane

Cricothyroid membrane

A

FIGURE 23-30  The cricothyroid membrane is found in the depression between the Adam’s apple (thyroid cartilage) and the cricoid cartilage.

Complications associated with this procedure include hemor­ rhage at the insertion site, subcutaneous or mediastinal emphy­ sema resulting from faulty placement of the tube into the subcutaneous tissues rather than into the trachea, and perforation through the posterior wall of the trachea with placement of the tube into the esophagus.

Improvised Wound Management The same principles that govern wound management in the emergency department apply in the wilderness setting. The main problem faced in the wilderness is access to adequate supplies. In deciding whether to close a wound or pack it open, take into account the mechanism of injury, degree of contamination, patient’s age, site of the wound, and ability to effectively clean the wound. 452

B FIGURE 23-31  Cricothyrotomy. A, Locate the cricothyroid membrane and make a vertical 1-inch incision through the skin. B, Insert the pointed end of an improvised cricothyrotomy tube through the membrane.

WOUND IRRIGATION The primary determinants of infection are bacterial counts and amount of devitalized tissue remaining in the wound.21 Ridding a wound of bacteria and other particulate matter requires more than soaking and gentle washing with a disinfectant.44 Irrigating the wound with a forceful stream is the most effective method

Wound Irrigation

A

B

1. Fill a sandwich or garbage bag with disinfected water. 2. Disinfect the water with iodine tablets, iodine solution, or povidone-iodine, or by boiling it. 3. Normal saline can be made by adding 9 g (2 teaspoons) of table salt per liter of water. 4. Seal the bag. 5. Puncture the bottom of the bag with an 18-gauge needle, safety pin, fork prong, or knife tip. 6. Squeeze the top of the bag forcefully while holding it just above the wound and directing the stream into it. 7. Use caution to ensure that none of the irrigation fluid splashes into your eyes.

of reducing bacterial counts and removing debris and contami­ nants.68 The cleansing capacity of the stream depends on the hydraulic pressure under which the fluid is delivered.20 Irrigation is best accomplished by attaching an 18- or 19-gauge catheter to a 35-mL syringe, or a 22-gauge needle to a 12-mL syringe. This creates hydraulic pressure in the range of 0.49 to 0.56 kg/cm2 and 0.91 kg/cm2 (7 to 8 psi and 13 psi), respectively.63 The solu­ tion is directed into the wound from a distance of 1 to 2 inches (2.5 to 5 cm) at an angle perpendicular to the wound surface. The amount of irrigation fluid varies with the size and contamina­ tion of the wound but should average no less than 250 mL.20 Remember: “The solution to pollution is dilution.” Tap water (and presumably boiled/cooled water) has been found to be as effective as sterile saline for irrigating wounds. In one study, the infection rate was significantly lower after irriga­ tion with tap water, and no infections resulted from the bacteria cultured from the tap water.3 Improvised wound irrigation requires only a container that can be punctured to hold the water, such as a sandwich or garbage bag, and a safety pin or 18-gauge needle (Box 23-2).

WOUND CLOSURE

C FIGURE 23-32  Improvised cricothyrotomy tube. A, Cut the plastic drip chamber at its halfway point. B, Insert the spike from the drip chamber through the cricothyroid membrane. C, A bag-valve device will fit over the chamber for ventilation.

Before a wound is closed, remove all foreign material and grossly devitalized tissue. Debridement can be accomplished using scis­ sors, a knife, or any sharp object, and wounds can be closed with sutures, staples, tape, pins, or glue. Although suturing is still the most widely used technique, stapling and gluing are ideal methods for closing wounds in the wilderness.

ADHESIVES Cyanoacrylate adhesive is the improviser’s best tool. Duct tape is a close second. One can always use sutures to hold vital equip­ ment in place. This includes putting a suture through the anteriorinferior part of the nasal septum and using the ends to tie NG tubes. A heavy suture or orthopedic/dental wire can be tied around an anterior tooth and then used to secure an endotracheal tube. Another method of securely fixing tapes and leads is to use tincture of benzoin. Absent that, the same effect can be achieved by saturating alcohol gauze with povidone-iodine. As the alcohol evaporates, the remaining residue is similar to that from tincture of benzoin. This method is convenient and readily applied without using extra 4 × 4’s.61 Alternatives to tape (for IV lines, equipment, bandaging) include cellophane tape, duct tape, electrician’s or other very sticky tape, and sutures.

WOUND GLUES

FIGURE 23-33  An improvised cricothyroid airway device can be created by cutting the barrel of a syringe at a 45-degree angle at its midway point.

Tissue glue is ideal for backcountry use because it precludes the need for topical anesthesia, is easy to use, reduces the risk for needlestick injury, and takes up much less room than a conven­ tional suture kit. When applied to the skin surface, tissue glue provides strong tissue support and peels off in 4 to 5 days 453

CHAPTER 23  Improvised Medicine in the Wilderness

BOX 23-2  Recommended Technique for

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 23-3  Technique for Gluing Lacerations

Staples

1. Irrigate the wound with copious amounts of disinfected water. 2. Control any bleeding with direct pressure. Place a gauze pad moistened with oxymetazoline (Afrin) nasal spray into the wound to help control bleeding. 3. Once hemostasis is obtained, approximate the wound edges using fingers or forceps. 4. Paint the tissue glue over the apposed wound edges using a very light brushing motion of the applicator tip. Avoid excess pressure of the applicator on the tissue because this could separate the skin edges, forcing glue into the wound. Apply multiple thin layers (at least three), allowing the glue to dry between each application (about 2 minutes). 5. Glue can be removed from non-tissue surfaces with acetone, or loosened from skin with petroleum jelly.

Although staples are a great way to quickly close wounds, they cannot be improvised. The best suggestion, if you know that you will be in an austere medical situation, is to carry a staple gun and the staples with you. They are lightweight and relatively inexpensive.

without leaving evidence of its presence.63 It provides a faster and less painful method for closing lacerations than does suturing and has yielded similar cosmetic results in children with facial lacerations (Box 23-3).62 Tissue glue evokes a mild acute inflam­ matory reaction with no tissue necrosis.74 Availability Cyanoacrylate (e.g., superglue), which bonds surfaces almost instantly, is available in a wide variety of commercial brands for medical and nonmedical use. Although nonmedical cyanoacry­ late is not approved for medical use, it has been used to treat patients for decades without complications. Although carrying medical grade (expensive) cyanoacrylate may be feasible, nonmedical superglues effectively close wounds in a similar manner to medical tissue adhesives. Although they are not sterile, they are unlikely to negatively affect the patient. Two benefits of medical grade cyanoacrylate (2-octyl cyanoacry­ late) are that its bond is about four times stronger than those of nonmedical brands and its more viscous gel form is better con­ trolled when applied to wounds. Nonmedical cyanoacrylate is often used to treat superficial painful fissures of the fingertips (“polar hands”), which commonly occur in cold climates and at high elevations.40 Advantages/Disadvantages In austere circumstances, cyanoacrylate’s advantages are that (1) it is readily available, (2) it can be applied rapidly, (3) it requires little technical knowledge, (4) a small tube can be used for many patients, and (5) it can be used on many parts of the body (e.g., skin, intraoral, intraabdominal). Its primary disadvantages are more frequent wound dehiscence because of its lower tensile strength compared with sutures, and contamination of other body parts. Also, using petroleum-based ointments and salves, includ­ ing antiseptic ointments, on wounds closed with cyanoacrylate can weaken the polymerized film and cause wound dehiscence. One can lessen the incidence of dehiscence by (1) not using cyanoacrylate on wounds over areas under tension, such as joints, and (2) using it only when a 5-0 or smaller suture would be appropriate to close a wound.22 Other common glues can also be used for wound closure. These include wood glue, panel adhesive, hobby cement, and various native substances. Be aware, however, that these common glues may irritate the tissues, the incidence of dehiscence is higher, and they may contain toxins. Contamination of Other Areas If cyanoacrylate spreads onto the eyelids or lips during wound closure on the face, it can seal them shut for hours. Avoid this by positioning the patient so that any extra cement runs away from, rather than toward, the eyes or mouth. This may require the patient to turn his or her head away from the wound, lie on his or her side, sit up, or, if the wound is above the eye, lie in Trendelenburg’s position. If cyanoacrylate does stick to an unwanted area, use a petroleum-based product such as ophthal­ mic bacitracin, erythromycin ointment, or mineral oil to remove it. Or, simply wait (usually less than a day) and the lids will open without treatment. 454

BINDING/TAPING Skin tapes are useful for shallow, nongaping wounds and have several advantages over suturing, including reduced need for anesthesia, ease of application, decreased incidence of wound infection, and availability. Nearly any tape can be used to close a wound. There is no magical quality to medical tapes. Other than cleaning and debriding a wound, using tape requires no technical expertise and is fast, painless, and virtually cost-free. Duct tape or any adhesive tape can be used to close a wound. Cut it lengthwise into strips, and allow gaps during placement if it is necessary to have part of the wound visible (Box 23-4). Puncturing holes in the tape before application helps prevent exudate from building up under the tape. Tapes do not stick well on areas that are hairy (therefore shave, if necessary), wet, or prone to perspiring, or are under tension, such as joints. As with medical tape, use benzoin, cyanoacrylate, or another adhesive to help the strips stick. Alter­ natively, wrap a bandage around the closed wound or use addi­ tional tape. Many materials can be used as sutures. Nylon fishing line, for example, provides results comparable to commercial nylon suture,30 and is used routinely around the world. Others must be improvised from available materials. Natural Materials Hair Tying (With Glue) for Scalp Wound Closure.  If a patient with a scalp laceration less than 10 cm (3.9 inches) long has hair over the area that is longer than 3 cm (1.2 inches), use the hair to close the wound. To do this, twist a few strands of hair together on each side of the laceration. Tie them and immediately place benzoin or a similar adhesive on the knot to hold it in place. Cut these knots out after the wound heals. Alternatively, pull several strands of hair across the laceration to the opposite sides and twist them around each other one time. Place a drop of cyanoacrylate at the juncture (Figure 23-34). These “sutures” do not have to be removed; the cyanoacrylate gradually wears off.40 Tell the patient not to wash his or her hair or put petroleum hair products near the wound for 48 hours.54,57 Chicken Egg Membrane.  Use a fresh chicken egg membrane (the thin layer just inside the shell) to close wounds and reduce bleeding. The membrane contains types I, V, and X collagen; retains albumen; and prevents penetration of bacteria. It has been BOX 23-4  Wound-Taping Technique 1. Obtain hemostasis and dry the wound edges. 2. Apply benzoin or cyanoacrylate glue to the skin adjacent to the wound. Benzoin should be allowed to dry long enough for it to become tacky, but tape should be applied to the glue while the glue is still wet. 3. Tape should be cut to 6- to 13-mm (0.25- to 0.5-inch) widths, depending on the size of the laceration, and to a length that allows for 2 to 2.5 cm (0.75 to 1 inch) of overlap on each side of the wound. 4. Secure one-half of the tape to one side of the wound. Appose the opposite wound edge using a finger while the tape is secured to the other side. 5. Wound tapes should have gaps of 1.5 to 3 mm (0.06 to 0.12 inches) between them to allow for serous drainage. 6. Cross-stays of tape can be placed perpendicular over the tape ends to prevent them from peeling off. 7. Additional glue can be applied to the tape edges every 24 hours to reinforce adhesion.

High-level disinfection of most alternative suture materials is more practical in austere situations than is sterilization. Boil the material in water or soak it in alcohol (medicinal, drinking), hydrogen peroxide, bleach, surgical or regular soapy water, or lemon juice. Note that some of the substances used to disinfect the suture (e.g., alcohol, bleach, lemon juice) may be painful; use local anesthetic if possible. If sterilizing the suture material is desired, wrap it in foil and put it in or near the coals from a fire. How well this works without destroying the suture material varies depending on the type of material used.

Blister Management FIGURE 23-34  Wound closure with hair and cyanoacrylate.

used as a skin graft donor-site dressing and, in one patient, used to close a full-thickness lip laceration. It stopped the bleeding and, when removed after 3 days, produced a well-healed wound.81 Horsehair Sutures.  Hairs from the tail of a horse can also serve as effective sutures. First wash the hairs with soap and water, followed by alcohol. Sterilize them before use in boiling water or steam. They are not as strong as silk, but they are able to resist all the tension which any suture ought to have.26 Silk and Cactus (Agave) Fibers.  Threads of natural silk or linen/flax are excellent for sutures and ligatures. These may be soaked in sterile water before use or waxed for better flexibility.37 Similarly, to use fiber “threads” from agave plants, pull on the point of the agave plant with your teeth and the thread comes out. Other Non-Traditional Materials5 Dental Floss.  Although dental floss is often cited as a good suture alternative, most dental floss is about the size of a 0 or 00 suture. This is far too big for most wounds. Additionally, floss is produced from many different fibers (e.g., silk, nylon, or Teflon), which may make it difficult to know how tissues will react.18 Cotton Thread.  Cotton and linen threads, long used as the standard surgical suture, are good, non-irritating substitutes for standard suture materials. They should be disinfected in boiling water; any colored thread should be boiled long enough to extract as much of the dye as possible.27 In austere circumstances, a guideline for use is to use ordinary sewing cotton, No. 30, white, for the heavier work on the abdominal wall, and No. 40 or No. 50, black, for finer work on intestine or delicate tissues.59

A

B

To dress blisters without moleskin, use Molefoam, or improvise another commercial blister dressing by using a piece of duct tape. Duct tape’s smooth outer surface provides protection from fric­ tion, while its adhesive side adheres strongly to skin. Duct tape is ideal for preventing blisters when “hot spots” are present. Avoid applying duct tape directly to formed blister surfaces. Cover the blister with a nonadhesive dressing, such as a plastic sandwich bag, and use the duct tape or glue to hold it in place. Cut the corner of the sandwich bag and apply a lubricant between the two surfaces (Figure 23-35).

Ring Removal Rings should always be removed soon after injury to fingers and trauma to the hands because progressive swelling may cause rings to act as tourniquets. If a ring cannot be removed with soap or lubricating jelly, the string wrap technique can be used. Pass a 51-cm (20-inch) length of fine string, dental floss, umbilical tape, or thick suture between the ring and the finger. Pull the string so that most of it is on the distal side of the digit. Then wrap it around the swollen finger from proximal to distal, beginning next to the ring and continuing past the proximal interphalangeal joint. Place successive loops of the wrap close enough together to prevent any swollen skin from bulging between the strands. Remove the ring by unwinding the proximal end of the string and forcing the ring over the distal string. If the string is not long enough, the technique may require repeated wraps (Figure 23-36).

Trauma TENSION PNEUMOTHORAX In dyspneic patients, signs and symptoms that suggest a tension pneumothorax include distended neck veins, tracheal deviation away from the side of the pneumothorax, unilateral absent breath sounds, hyperresonant hemithorax to percussion, subcu­ taneous emphysema, cyanosis, and cardiovascular collapse. In the wilderness, treat these patients as if they have a tension

C

FIGURE 23-35  A to C, Blister dressing improvised with plastic sandwich bag.

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CHAPTER 23  Improvised Medicine in the Wilderness

Disinfecting Rather than Sterilizing Alternative Suture Materials

Super Glue

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Glove finger

A

B

C

FIGURE 23-37  A, Finger of (or, even better, the entire) glove is attached to needle or catheter to create flutter valve. B, Flutter valve allows air to escape. C, Flutter valve collapses to prevent air entry.

FIGURE 23-36  String technique for removing a ring from a swollen finger (see text).

pneumothorax—with rapid pleural decompression; it may save their lives. Possible complications of pleural decompression include infection; profound bleeding from puncture of the heart, lungs, or a major blood vessel; or laceration of the liver or spleen. Improvised Pleural Decompression Technique Swab the entire chest with povidone-iodine or another antiseptic. If sterile gloves are available, put them on after washing your hands. If local anesthesia is available, infiltrate the puncture site down to the rib and over its upper border. Insert a large-bore IV catheter, needle, or any pointed sharp object that is available into the chest just above the third rib in the mid-clavicular line (midway between the top of the shoulder and the nipple in a line with the nipple approximates this loca­ tion) (Box 23-5). If you hit the rib, move the needle or knife upward slightly until it passes over the top of the rib, thus avoid­ ing the intercostal blood vessels that course along the lower edge of every rib. The chest wall is 4 to 6 cm (1.6 to 2.4 inches) thick, depending on the individual’s muscularity and amount of fat present. A gush of air signals that one has entered the pleural space; do not push the penetrating object any further. Releasing the tension converts the tension pneumothorax into an open pneumothorax. BOX 23-5  Improvised Pleural Decompression Devices • Large-bore (12- or 14-gauge) intravenous catheter or needle • Endotracheal tube (instead of a chest tube) • Section of a tent pole • Hose from a hydration pouch

456

Leave the needle or catheter in place (it often comes out of the pleural space with respiration, so continue monitoring it), and use a rubber glove to make a flutter valve (Figure 23-37). Use the entire glove and push a needle through one finger (best) or cut the finger from a rubber glove, making a tiny slit cut at the tip. Place this over the external opening to create a unidirec­ tional flutter valve that allows continuous egress of air from the pleural space. To create a one-way flutter valve, cut one finger portion of a latex glove off at the proximal end of the finger and insert the needle or catheter into the open end of the glove finger, through the tip as shown (see Figure 23-37, A). The cutout finger portion of the glove creates a unidirectional flutter valve that allows egress of air from the pleural space during expiration, but collapses to prevent air entry on inspiration (see Figure 23-37, B and C). Note that this is a tenuous device that can easily slip out of place. If symptoms redevelop, insert another one. Also note that although an endotracheal tube and other semi-rigid devices work well as makeshift chest tubes, Foley catheters only work well in infants; they collapse because of pressure from the chest wall in older children and adults.40

OPEN (“SUCKING”) CHEST WOUND Penetrating trauma to the chest can produce a chest wound that allows air to be sucked into the pleura on inspiration. Place a piece of plastic food wrap or aluminum foil or one side of a plastic sandwich bag on top of the wound, and tape it on three sides. The untaped fourth side serves as a relief valve to prevent formation of a tension pneumothorax.

DRAINAGE SYSTEM (BOTTLES/BAGS) The fundamental idea of a chest tube drainage system is for air to leave the thorax (chest) without any air being able to re-enter the chest via the system. An example of a two-bottle chest tube drainage system was constructed from an empty 1-L plastic sterile water bottle, a 1-L IV bag, two IV tubing sets, and a 24F chest tube.76 This system collects and measures fluid that drains out of the tube. To reproduce this system, empty a plastic sterile water bottle and put two holes in the bottle, one in the cap and one

FIGURE 23-38  Sterile water bottle, IV tubing, and IV bag can serve as a chest tube drain. (From Vinson ED: Improvised chest tube drain for decom pression of an acute tension pneumothorax, Mil Med 169:403, 2004.)

in the bottle’s neck, each of which allow just enough room for passage of the IV tubing (Figure 23-38). Cut the patient end (IV catheter attachment) off one (the “first”) IV tubing set and insert this cut end into the hole in the top of the empty saline bottle. The other end (IV bag-spike) should fit into the end of the 24F chest tube. Now take the other (the “second“) IV tubing set and cut off the spike end between the filter and the reservoir. Posi­ tion the fluid-filled IV bag with ports up and the saline bag down, and insert the cut-off spike from the second IV tubing set into one port in the IV bag. This is now the system’s air vent. Open the other port (cut or remove the rubber cap) and insert the cut end of the second IV tubing so that it is well beneath the level of the saline in the bag. The other end of the second IV line should then be placed through the hole in the neck of the empty saline bottle. Use duct tape, cyanoacrylate, or any other cement to seal the tubes in position. Keep the IV bag inverted to provide a water seal for the system. To dispose of any accumulated fluid, clamp the chest tube and unscrew the cap from the water bottle and empty it out. Then screw the cap back on and unclamp the chest tube.40

Orthopedic Injury—Improvised Treatment GENERAL GUIDELINES When working with improvised systems, if time allows, test them on a noninjured person (“work out the bugs”) before applying them to the patient, and continually reevaluate them while in use. Creativity is needed when searching for improvisational materials, although it helps to carry materials that lend themselves to improvisation, as described later. The victim’s gear can also provide needed items, such as foam pads and the straps and internal stays from backpacks. Especially in patients with dimin­ ished consciousness, be observant for pressure points and friction potential, because these devices are not ergonomically efficient. When in doubt, add extra padding.

SPINAL TRAUMA Because of its mobility, the cervical spine is the spinal column area most commonly injured in trauma. Any obvious or suspected cervical spine injury demands full spinal immobilization using both a rigid or semirigid cervical collar and long-board immobi­ lization. Historically dogma about cervical spine injuries has specified a “splint ‘em as they lie” approach. Transporting a victim who is not in anatomic position is arduous in the

Improvised Cervical Collars Cervical collars are always adjuncts to full spinal immobilization; they should rarely be used alone. The improvised cervical collar is used in conjunction with manual cervical spine stabilization followed by complete immobilization of the victim on a spine board. A properly applied and fitted collar is a primary defense against axial loading of the cervical spine, particularly in an evacuation that involves tilting the victim’s body uphill or down­ hill. Improvised cervical collars have had a bad reputation, and textbooks continue to depict them made from a simple cravat wrapped around the neck. This type of system is no more effec­ tive than are the soft cervical collars often used by urban plaintiffs trying to impress a jury (i.e., not effective at all). An improvised cervical collar works effectively only if it has the following features: • It is rigid or semi-rigid. • It fits properly (many improvised designs are too small). • It does not constrict or choke the victim. • It allows the victim’s mouth to remain open if vomiting occurs. Improvisational approaches to cervical collars are outlined below. Closed-Cell Foam System.  The best closed-cell foam systems incorporate a full-size or three-quarter–length pad folded longi­ tudinally into thirds that is centered over the back of the victim’s neck and wrapped forward. The pad is crossed under the chin, contoured underneath opposite axillae, and secured. If the pad is not long enough, tape or tie on extensions. This system also works well with blankets, beach towels, or even a rolled plastic tarp. Avoid small flexible cervical collars that do not optimally extend the chin-to-chest distance. Padded Hip Belt.  A padded hip belt or fanny pack removed from a large internal- or external-frame backpack can sometimes be modified to work perfectly. Wider is usually better. Take up excess circumference by overlapping the belt, and secure the excess material with duct tape (Figure 23-39).

Hip belt of inverted backpack Cervical stabilizer Fanny pack as cervical collar

FIGURE 23-39  Inverted pack used as spine board. The backpack waist belt can be seen encircling the head.

457

CHAPTER 23  Improvised Medicine in the Wilderness

backcountry. It is uncomfortable for the victim, difficult for the rescuers, and increases the risk for further injury. In general, gentle axial traction back to anatomic position is indicated unless (1) return to anatomic position significantly increases pain or focal neurologic deficit or (2) movement of the head and neck results in any noticeable mechanical resistance.39 All cervical spine injuries (or suspected injuries) warrant full long-board immobilization. Movement of the pelvis and hips laterally is potentially more dangerous than anterior–posterior movement; therefore it is appropriate during extended transport to allow gentle flexion at the hip with immobilization in that position if the victim is more comfortable. Soft pads behind the knees and small of the back also add to the victim’s comfort during a long transport.9

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

C

B

D

FIGURE 23-40  Padded aluminum splint cervical collar. A, Place a vertical bend in the malleable aluminum splint approximately 6 inches from one end to form a vertical pillar. Then, add bilateral flares to make the splint comfortable for the victim where it rests against the lower mandible. B, Place the anterior pillar securely beneath the victim’s chin and wrap the remaining length of the splint around the victim’s neck. C, Side view of cervical collar fashioned from a SAM Splint. Note the formation of lateral, and if possible, posterior pillars. D, Frontal view. The end is angled inferiorly to provide an adequate chin-to-chest distance. Note the formation of the anterior pillar.

Clothing.  Bulky clothing, such as a fiber pile or fleece jacket, can be rolled and then wrapped around the victim’s neck to make a cervical collar. The extended sleeves can be used to secure the collar. Prewrapping a wide elasticized (Ace) wrap around the jacket compresses the material and makes it more rigid and supportive. Malleable Aluminum Splint.  Well-padded aluminum splints (e.g., SAM Splint) can be molded into various configurations to splint extremity injuries. They are built from a thin core of alu­ minum and sandwiched between two layers of closed-cell foam. SAM splints can be adjusted to fit almost any size neck. One common mistake made when applying padded aluminum splint cervical collars is to inadequately construct the anterior portion of the device. Simply wrapping a SAM Splint in a circumferential manner provides an adequate chin-to-chest distance, thus allow­ ing excessive neck flexion. It is possible, by overlapping the splint inferiorly, to extend the anterior portion as needed. Note the adequate chin-to-chest distance created by moving the final portion inferiorly (Figure 23-40). Improvised Spinal Immobilization As noted, the improvised cervical collar is only an adjunct to full spinal immobilization. Two acceptable immobilization systems are (1) short-board immobilization, used for difficult or shortduration transport (that is, getting the victim out of immediate danger) or when used in conjunction with a long-board, and (2) long-board immobilization, used for definitive immobilization during extensive transport. Use either of these systems in conjunction with a rigid or semi-rigid cervical collar, as described previously. Improvised lateral “towel rolls” are often added to these systems for addi­ tional head and neck support. These rolls can be constructed from small sections of closed-cell foam sleeping pads. Alterna­ tively, a U-shaped head support, or “horse collar,” can be made from any rolled garment, blanket, tarp, or tent fly; this is placed over the victim’s head in an inverted U and used with the impro­ vised cervical collar and spine board. Hiking socks or stuff bags 458

filled with dirt, sand, or gravel also work well for this purpose. The patient’s boots, filled with rocks, sand, or other heavy materi­ als can provide extra stabilization. Rapid immobilization can often be achieved by quickly wrapping duct tape around the patient’s head and spine board. Stuff bags filled with snow for support should never be used because the snow can melt during transport, which may result in excessive head and/or neck motion. However, snow-filled stuff bags can act as temporary support while more definitive systems are being constructed. Short-Board Immobilization Internal-Frame Pack and Snow Shovel System.  Some internal-frame backpacks can be easily modified by inserting a snow shovel through the centerline attachment points (the shovel handgrip may need to be removed first). The victim’s head is taped to the lightly padded shovel (Figure 23-41); in this context, the shovel blade serves as a head bed. This system incorporates the remainder of the pack suspension as designed (i.e., shoulder and sternum straps with hip belt) and works well with other

FIGURE 23-41  Head immobilized on a padded shovel.

to conform to the victim’s width. Tie a small loop at the foot end of the rope, and place a tarp on the rope loops. A large poncho, tent fly, space blanket, or similar item may be sub­ stituted if necessary. If the tarp is short, angle it so that the victim is positioned diagonally (i.e., along the hypotenuse). In cold or wet conditions, the tarp should be placed so that extra material can be folded up over the victim’s feet before wrap­ ping (i.e., hypothermia or “burrito wrap”). On top of the tarp, lay foam pads over the full length of the system (the pads can be overlapped to add length). Then lay stiffeners on top of the pads on the same axis as the victim (Figure 23-42, B). Add additional foam pads on top of the stiffeners, followed optionally with a sleeping bag (Figure 23-42, C). Place the victim on the pads. To form the daisy chain, bring a single loop through the pretied loop, pulling the loops to the center, feeding them through the loops brought up from the opposite side. It is important to continuously take up the rope slack. When the victim’s armpits are reached, bring a loop over each shoulder and tie it off or clip it off with a carabiner (Figure 23-42, D). One excellent modification involves adding an inverted internal-frame backpack. This can be incorporated with the padding and secured with the head end of the rope. The pack adds rigidity and padding, and the padded hip belt serves as an efficient head and neck immobilizer (see Figure 23-38). If the victim vomits during transport, the entire unit can be turned on its side or even partially inverted.

Inverted Pack System.  An efficient short-board can be made using an inverted internal- or external-frame backpack. The padded hip belt provides a head bed, and the frame is used as a short-board in conjunction with a rigid or semi-rigid cervical collar. Turn the pack upside down, and lash the victim’s shoulders and torso to the pack. Fasten the waist belt around the victim’s head, as in the top section of a Kendrick extrication device. The hip belt is typically too large, but excess circumference can be eliminated with bilateral closed-cell foam rolls and by overlap­ ping the excess material with duct tape. Unlike the snow shovel system, this system requires that the victim be lashed to the splint. Remember that the integral pack straps and buckles can often be reconfigured to conform to the application (i.e., pack straps can be crisscrossed or simply tied with knots to fit your needs). Snowshoe/Snowboard System.  A snowshoe or inverted snow­ board can be made into a fairly reliable short spine board. Pad the device, and rig it for attachment to the victim.20 Long-Board Immobilization Continuous Loop System (Also Known as the Daisy Chain, Cocoon Wrap, or Mummy Litter).  This quick and efficient improvised system provides adequate immobilization for potentially spine-injured patients. It is especially useful when pre-existing planks, tables, or boards are not available (i.e., mountaineering extreme wilderness environments). It may be used for both short- and long-distance transports. To construct the continuous loop system, the following items are needed: • Long climbing or rescue rope • Large tarp (or tent fly) • Sleeping pads • Stiffeners (e.g., skis, poles, snowshoes, canoe paddles, or tree branches) Lay the rope out, making even U-shaped loops as shown in Figure 23-42, A. The midsection should be slightly wider

Backpack Frame Litters.  Functional litters can be constructed from external-frame backpacks. Traditionally, two frames are used, but three or four frames (Figure 23-43) make for a larger, more stable litter. Cable ties or fiberglass strapping tape simplifies this fabrication. These litters can be reinforced with ice axes or ski poles. Kayak System.  Properly modified, a kayak makes an ideal rigid long-board improvised litter. First, remove the seat along with sections of the upper deck if necessary. A serrated river knife (or camp saw) makes this improvisation much easier. Open deck canoes can be used almost as is once the flotation material has been removed.

A

C

B

D

FIGURE 23-42  Continuous loop, or “mummy,” litter made with a climbing rope. A, Rope is laid out with even U-shaped loops. B, Stiffeners such as skis and poles are placed underneath the victim to add structural rigidity. It is important to pad between the stiffeners and the victim. C, A sleeping bag may be used in addition to the foam pads. D, Loop of rope is brought over each shoulder and tied off (see text).

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CHAPTER 23  Improvised Medicine in the Wilderness

long-board designs, such as the continuous loop system (see Continuous Loop System, later). Always assess the amount of cervical spine flexion or extension the system will cause; if it is unacceptable, the system must be modified appropriately.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 23-44  Improvised head rest.

head of an injured victim (Figure 23-44). Tape this head bed to a commercial or improvised backboard.

EXTREMITY FRACTURES/DISLOCATIONS— PHYSICAL EXAMINATION FIGURE 23-43  Backpack frame litter.

Canoe System.  Many rivers have railroad tracks that run parallel to the river canyon. The tracks can be used to slide a canoe by placing the boat perpendicular to the tracks and pulling on both bow and stern lines. Improvised Head Bed.  A padded aluminum splint can be formed to create a head bed to assist in securing the immobilized

Lacking radiographs or other imaging capability, clinicians need to rely on physical signs and symptoms to diagnose fractures and dislocations. Table 23-2 lists the common signs and symptoms of fractures, ranking them according to their diagnostic usefulness. Fracture Versus Dislocation When using clinical findings, it may sometimes be difficult to differentiate between a fracture and a dislocation. In general, fractures, once reduced, do not remain in place without fixation, whereas the reverse is generally true of dislocations: “As a rule, after reduction in the latter case, displacement will not again occur.”33

TABLE 23-2  Usefulness of Clinical Information for Diagnosing Fractures (10 = Most Useful; 1 = Least Useful) Open fracture with observable bone fragments (10) False point of motion (10) Palpable discontinuity in bone (9) Deformity (8)

Crepitus (8)

Shortening (7)

Loss of function (4)

Pain and tenderness (1) Swelling (1) Ecchymosis (1) Altered percussion (1)

When bone fragments or fat that contains blood extrude from a wound, the question is not whether a fracture exists, but rather its extent and how best to treat it. This is definitive proof of a disruption in the bone and, after acute trauma, indicates a fracture. Its absence does not indicate anything. Testing for this is detailed below.* This is an excellent indicator of bony discontinuity, especially in the patella, long bones, and diastasis of the symphysis pubis. Soft tissue defects, edema, and hematomas may limit palpation of or simulate this defect. Presume diagnosis of fracture or dislocation if deformity can be discerned. This is more likely seen if the patient presents before there is significant edema or several days later when edema has resolved, and if the fracture is away from the joints, is angular, is not a partial (e.g., stress, torus) fracture, and is not a compression fracture. Old fractures and some chronic bone deformities, such as rickets, may appear to be a fracture but generally will not have the acute pain and skin tenting often seen after trauma. Crepitus or a grating sound, caused by contact of the broken surfaces with each other, is highly suggestive of a fracture. Crepitus is generally a rough, grating sensation. In fractures with many spicules, the sensation is often that of a click. Fractures that are badly comminuted, impacted, and days or weeks old may have no crepitus. Occasionally, chronic joint disease or blood clots near a suspected fracture may produce crepitus, so the sign is not perfect. Test for crepitus in the same way as for false motion.* This is a very convincing sign of a long-bone fracture. Both extremities should be measured using easily identified landmarks (e.g., anterior iliac spine and medial malleolus). The difference may be an inch or more. Dislocations or prior injuries on either side may also cause shortening, but other signs can often differentiate between these. Measurements can also be used to determine if adequate traction has been applied. Note that the measurements must be taken accurately. Many injuries can limit the ability or willingness to use the extremity. There is often inability to lift the limb owing to pain or separation of the bony lever on which the muscles act; but this inability does not extend to all fractures, and especially does not exist in all partial or impacted fractures. Mild, nonsedating analgesics may help make the diagnosis by allowing a patient to better test his or her use of an extremity. Unreliable sign. Often present, even severe, with only soft tissue injury; may be minimal or absent with a fracture. Unreliable acutely. Swelling is such a common sign that it loses its diagnostic significance. If the swelling is out of proportion to the soft tissue injury or persists longer than such apparent damage would warrant, it may indicate a fracture. If deep swelling persists after the skin edema resolves, it often indicates a displaced bone or callus. Although ecchymosis is more common in fractures than in dislocations, even if it occurs acutely, it has minimal diagnostic value. If it persists over several days, it probably indicates ongoing bleeding from a deep (probably bony) vessel. Although highly touted, listening for changes of tone across fractures produced either by percussion or a tuning fork is grossly unreliable. False-positive and false-negative results are the rule, rather than the exception.

Adapted from Iserson KV: Improvised medicine: Professional treatment with scarce resources, McGraw-Hill (in press). *Testing for abnormal (“false point of”) motion in an extremity, a pathognomonic sign of a fracture. To test for a false point of motion, grasp the bones firmly above and below the suspected fracture site. Gently manipulate the area to see if it moves (1) in an anteroposterior direction, (2) laterally, (3) so that one broken end slides over the other, (4) laterally, and (5) rotationally. The keys are to firmly grasp the bones and to use gentle manipulation.

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Tuning Fork/Percussion Diagnoses One of the most persistent myths that still appears in the medical literature is that fractures can be diagnosed using a tuning fork or percussion and a stethoscope.72,58,13,11 This has long been shown to be nonsense. Stimson, for example, wrote in 1910 that even under the best circumstances, it added nothing to the diag­ nosis: “Auscultatory percussion,” he wrote, “the stethoscope being moved from one fragment to the other while percussion is made upon the first, will sometimes give a marked change in the sound as the line of fracture is crossed; but it is rarely sig­ nificant, except in cases in which the diagnosis can be made by other means.”69 Shoulder Dislocation Diagnosis Without Radiographs To diagnose a shoulder dislocation, feel for the “hole” made by the now-empty joint at the glenoid (Figure 23-45). If there is any doubt, feel the other side. Also observe flattening of the shoulder, inability to bring the elbow to the side of the body, and the head of the humerus in an abnormal position, usually below the cora­ coid process. Finally, if the arm is measured from the tip of the acromion to the external condyle, the dislocated arm will be shorter than the other, especially when the arm is abducted.28

EXTREMITY FRACTURES/ DISLOCATIONS—TREATMENT Reduction Treatment Without Radiographs There are three goals of fracture treatment: 1. Reposition bone fragments to eliminate any bone angula­ tion and to restore limb length. This is particularly impor­ tant if pulses are absent below the site of the injury or when the limb’s position will interfere with patient trans­ port. Whenever possible, undertake a dislocation reduction immediately after the injury, that is, when muscle spasm and resistance are minimal. Try to minimize pain during this process by using local or regional anesthesia, hypnosis, or sedation.40 2. Immobilize the fragments by using splints and, if necessary, traction to keep the limb at length. 3. Restore function when possible. Evaluate the limb’s neu­ rovascular status before and after any manipulation. Remeasure.  Measure the affected and opposite extremities before any manipulation. Repeat the process after manipulating any fracture where there has been shortening of the extremity. Generally, if the shortening continues to be greater than 0.05 inch, reduction is unsatisfactory, either because the fragments did not return to their normal position, or the muscles were distracted again once the reduction had occurred. In either case, attempt another reduction; if that fails, splint the limb.29 Shoulder Dislocation Reduction Clinicians need to know several methods to reduce shoulder dislocations, because they occur so often and no single method

FIGURE 23-45  Digital diagnosis of shoulder dislocation.

FIGURE 23-46  “Snowbird” traction for anterior shoulder dislocation.

has proved successful. In wilderness settings, it’s best to use non-sedating methods so that the patient can continue to func­ tion. When sedation is needed, consider using hypnosis or intra-articular injection, both of which work well for joint reductions.41,52 An easy method that is not well known is the Snowbird trac­ tion technique. Have the patient sit facing the back of a chair (or on a rock or stool), with his or her affected arm draped over the chair’s back or a low-lying tree limb. After placing padding under the axilla, flex the elbow to 90 degrees and drape a stocki­ net or other cloth loop over the proximal forearm, letting it hang to the ground. Using the chair back or tree limb as countertraction, the clinician should place his or her foot in the loop and apply firm, steady downward pressure. This way, the clini­ cian’s hands are free to apply pressure or to rotate the arm as needed (Figure 23-46). The success rate is reported as 97%; more than 90% can be done without sedation or narcotic analgesia.78

Splinting and Traction Methods NONRIGID SPLINTS Sling (Arm) A sling, the most basic upper extremity support, can be impro­ vised by putting the patient’s wrist inside his or her shirt and buttoning the buttons around it (Figure 23-47). For more support, use a long-sleeved shirt and pin the sleeve containing the affected arm to the opposite shoulder area of the shirt. Alternatively, the bottom of a short-sleeve shirt or a t-shirt can be doubled up over the forearm and pinned to both shoulder areas. More formal slings can be made from any available material (Figure 23-48). If a strip of material is pinned with a loop around the wrist and around the neck, it becomes a “collar-cuff” sling, which allows movement of the shoulder and is ideal to avoid a frozen shoulder. Although most splints are designed to immobilize an injured extremity completely, in the backcountry a splint may need to allow for a limited range of motion so that the victim can facilitate his or her own rescue. Many functional splints can be improvised quickly using nothing more than a closed-cell foam sleeping pad and some tape or elastic wrap. With the advent of inflatable sleeping pads, foam pads are not as ubiquitous as they once were in the backcountry. However, many of these splints can be made using a partially inflated sleeping pad. Once applied, these pads can be inflated to provide the necessary support, fit, and comfort (Figure 23-49). 461

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

FIGURE 23-47  Techniques for pinning the arm to the shirt as an improvised sling. A, With a long-sleeved shirt or jacket, the sleeved arm is simply pinned to the chest portion of the garment. B, With a short-sleeved shirt, the bottom of the shirt is folded up over the injured arm and secured to the sleeve and upper shirt.

Shoulder Immobilizer (Shoulder Spica Wrap) After reducing a dislocated shoulder, immobilize it with a func­ tional system made with a 15-cm (6-inch) elastic wrap around the torso. This method allows the victim limited function to facilitate his or her own evacuation (e.g., ski poling or kayak paddling) but prevents complete abduction of the arm (Figure 23-50). Buddy Taping One of the simplest effective methods of splinting an injured finger or toe is to tape it to the adjacent digit. The keys to success are to put absorbent cloth or gauze between the digits before taping and to change the material at least 3 times a day, or any time it gets wet, to avoid macerating the tissues. Keep the buddy tape in place until the injured digit feels better without the tape than with it. A field-expedient method of stabilizing long bone fractures in a lower extremity is to buddy tape the legs together, preferably with some padding between them. This may be more comfortable than a rigid splint. Buddy taping can also be used

FIGURE 23-49  Functional knee and lower leg immobilizer. Wrap a sleeping pad around the lower leg from the mid thigh to the foot. Fold the pad so that the top of the leg is not included in the splint. This provides better visualization of the extremity and leaves room for swelling. A full-length pad forms a very bulky splint and may need to be trimmed before rolling. Because of the conical shape of the lower extremity and the effects of gravity, foam-pad lower extremity splints tend to work their way inferiorly when the victim ambulates. A simple solution is to use duct tape “suspenders” to keep the splint from migrating downward.

for humerus fractures in infants. Bandage the arm to the torso and it will quickly heal. “Pillow” Splints Make “pillow” splints for joint fractures, dislocations, or other injuries. These can be made from pillows, blankets, sleeping bags, sleeping pads, or similar items (Figure 23-51). Wrap a pillow or multiple layers of other materials around the injured part. Secure it tightly with bandaging material. It is often a more comfortable method of splinting than using traditional materials. Sandbag Splints Use a garbage bag, fanny pack, or similar soft-sided container filled with sand or dirt to effectively splint extremities. Mold the bag to the extremity, and tape or bandage it in place. Because these splints are heavy, the patient tends to move the extremity less than with a pillow splint.

RIGID SPLINTS

FIGURE 23-48  Webbing sling. A 2.5 m (8-foot) length of 2.5-cm (1-inch) tubular or flat webbing is used to form a functional arm sling. A Crazy Creek Chair can be used to improvise both upper and lower extremity splints. Its inherent integral strapping system precludes the need for additional straps or tape.

462

Splint all fractures, either after reduction or if no field reduction can or will be done. In general, make sure the splint incorporates the joints above and below the fracture. If possible, the splint should be fashioned on the uninjured extremity, and then trans­ ferred to the injured one. Numerous items can be used as splints. On ski trips, skis and poles can be used as improvised splints. On white-water rafting trips, canoe and kayak paddles can be used in a similar manner. Airbags used as flotation for kayaks and canoes can be converted into pneumatic splints for arm and ankle injuries. The mini-cell

CHAPTER 23  Improvised Medicine in the Wilderness

A

B

C

D FIGURE 23-50  A to D, Shoulder spica wrap.

pillars found in most kayaks can be removed and carved into pieces to provide upper- and lower-extremity splints. A life jacket can be molded into a cylinder splint for knee immobilization or into a pillow splint for the ankle. The flexible aluminum stays found in internal-frame packs can be molded into upper extremity splints. Other improvised splint­ ing material includes sticks or tree limbs, rolled-up magazines, books or newspapers, ice axes, tent poles, and dirt-filled garbage bags or fanny packs. Ideally, a splint should immobilize the fractured bone in a functional position. In general, “functional position” means that the legs should be straight or slightly bent at the knees, the ankle and elbow bent at 90 degrees, the wrists straight, and the fingers flexed in a curve as if the person were attempting to hold a can of soda or a baseball. Splints can be secured in place with strips of clothing, belts, pieces of rope or webbing, pack straps, gauze bandages, or elastic bandage wraps. When molded into any of several “struc­ tural curves,” SAM Splints become much more rigid and can be used to immobilize most fractured or injured extremities. If pro­ longed use is anticipated (more than a few hours), place absor­ bent material, such as cotton cloth, between the splint and the skin to prevent skin irritation. Also, to prevent uncomfortable pressure points during prolonged use, place soft padding, such

as gauze pads, around all bony prominences (Figures 23-52 to 23-57).

PELVIC FRACTURES Compressing the iliac crests reduces morbidity and mortality in patients with unstable pelvic fractures by effectively controlling venous hemorrhage.9 Clothes, sheets, a sleeping bag, pads, an air mattress, tent, or tent fly can be used to improvise a very effective pelvic sling in the backcountry. The object should be wide enough so that it does not cut into the victim when tightened. Applying an Improvised Pelvic Sling 1. Ensure that objects have been removed from the patient’s pockets and that any belt has been removed so that the pressure of the sheet or object does not cause additional pain by pressing items against the pelvis. 2. Gently slide the improvised sling under the patient’s but­ tocks, and center it under the bony prominences at the outer part of the upper thigh or hips (greater trochanters/ symphysis pubis) (Figure 23-58). Cross the object over the front of the pelvis and tighten the sling by pulling both ends; secure it with a knot, clamp, or duct tape. Another tightening technique is to wrap the sling snugly around the 463

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

FIGURE 23-51  Pillow splints on ankle (A), elbow (B), and knee (C).

FIGURE 23-53  Humerus splint. Used in conjunction with a sling and swath, this splint adds extra support and protection for a fractured humerus.

FIGURE 23-52  Padded aluminum thumb spica.

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CHAPTER 23  Improvised Medicine in the Wilderness

A A

B FIGURE 23-54  Forearm splint. These splints are used for treatment of wrist or forearm fractures. The sugar-tong splint (A) prevents pronation and supination and has the advantage of greater security and pro­ tection than the volar splint (B) because of its anterior–posterior construction. Tape is shown for purposes of illustration; elastic wrap  or self-adherent wrap (3M Coban) or something similar is more comfortable and efficient.

A

B

B FIGURE 23-55  A, River dry bag used to create a simple proximal support with a kayak paddle. B, Here a paddle is pushed up against the proximal support strap. It is taped for security but the forces are pushing against the strap, not the tape.

C

D

FIGURE 23-56  Knee immobilizer using two padded aluminum splints. The splints are folded in one-half (A), then fanned out (wider at the top for the thigh) and taped (B). Tape is applied to maintain the fan shape. The splint is then applied bilaterally and secured (C and D).

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 23-59  Pelvic sling improvised with inflatable sleeping pad and duct tape.

FEMORAL FRACTURES

FIGURE 23-57  Lower leg or ankle splint. A sugar-tong splint can be used to immobilize fractures of the tibia, fibula, or ankle. When used on an adult, two splints should be used. A third splint may be placed posteriorly for additional support.

pelvis, and tie an overhand knot. Place tent poles, a stick, or similar object on the knot and tie another overhand knot. Twist the poles or stick until the sling becomes tight. The sling should be tightened so that it is snug and the pelvis is returned to its normal anatomic position. 3. Theoretically, if a Therm-a-Rest pad or other inflatable sleeping pad is available, it could be folded in one-half so that it approximates the size of the pelvis. Gently slide the pad under the patient’s buttocks and center it under the greater trochanters and symphysis pubis. Secure the pad with duct tape, and then inflate the pad as you would normally until it produces a snug fit and the pelvis is reduced (Figure 23-59). This method has not yet been used on a pelvic fracture patient. 4. Place padding between the legs and gently tie the legs together to further stabilize the fracture in a position that is most comfortable for the victim.

FIGURE 23-58  Pelvic sling improvised with jacket.

466

In the backcountry environment, traction for femoral fractures may limit blood loss in the thigh and sometimes reduce pain. Traction devices may, however, make extrication from the wil­ derness more difficult. Many reasonable splint designs become so bulky and awkward that litter transport, technical rescue, or helicopter evacuation is impossible. General Principles of Femoral Traction The potential variety of traction designs is unlimited, but five key design principles should be considered when evaluating any femoral traction system: 1. Does the splint provide inline traction? Or does it incor­ rectly pull the leg off to the side or needlessly plantar flex the foot? 2. Is the splint comfortable? Be sure to ask the patient. 3. Does the splint compromise neurologic or vascular func­ tion? Constantly check distal neurovascular function. 4. Is the splint durable, or will it break when subjected to backcountry stresses? Try improvised traction devices on an uninjured person, stressing it to determine its strength. 5. Is the splint cumbersome? Will it hinder evacuation? Femoral Traction System Every femoral traction system has six components: 1. Ankle hitch 2. Rigid support that is longer than the leg 3. Traction mechanism 4. Proximal anchor 5. Method for securing the splint to the leg 6. Additional padding Ankle Hitch.  Various techniques are used to anchor the distal extremity to the splint. Many work well, but some are impossible to recall in an emergency. Choose an easy-to-remember tech­ nique, and practice it. It is best to leave the shoe on the victim’s foot, and apply the hitch over it. Cut out the toe section of the shoe to periodically check circulation. Single Runner System.  Loop a long piece of webbing, shoe­ lace, belt, or rope over itself, bringing one end through the middle to create a stirrup. After rotating it away from the patient by 180 degrees, slip the hitch over the shoe and ankle. Double Runner System.  In this straightforward technique, lay two short webbing loops (“runners”) over and under the ankle (Figure 23-60, A). Pass the long loop sides through the short loop on both sides (Figure 23-60, B) and adjust as needed (Figure 23-60, C). One advantage of this system is that it is infinitely adjustable, enabling the rescuer to center the pull from any direc­ tion. As always, proper padding is essential, especially for long transports. The victim’s boot can distribute pressure over the foot

B

C

FIGURE 23-60  Double runner ankle hitch. A and B, Two webbing loops (runners) are laid over and under the ankle. C, Completed double runner ankle hitch. The traction can be easily centered from any angle, ensuring in-line traction.

and ankle but will obscure visualization and palpation of the foot. A reasonable compromise is to leave the boot on and cut out the toe section for observation. Victim’s Boot System.  Another efficient system uses the vic­ tim’s own boot as the hitch. Cut two holes into the side walls of the boot just above the midsole and in line with the ankle joint. Thread a piece of nylon webbing or cravat through the holes to complete the ankle hitch (Figure 23-61). Cutting away the toe may be necessary for neurovascular assessment. Buck’s Traction.  For extended transport, Buck’s traction can be improvised using a closed-cell foam pad (Figure 23-62). Wrap the pad around the lower leg as shown, and loop a stirrup below the foot from the medial calf to the lateral calf. Fasten this assem­ bly with a second cravat wrapped circumferentially around the calf over the closed-cell foam (duct tape or nylon webbing can be used instead of cravats). This system increases the surface area over which the stirrup is applied and thus decreases the potential for neurovascular complications and dermal ischemia. In addition, improvised Buck’s traction has been used to manage backcountry hip fractures. However, it has been suggested that this technique may have little benefit.2 If Buck’s traction is used for a hip injury, use smaller amounts of traction (roughly 2.5 kg [5 lb]).

FIGURE 23-61  Traction using cut boot and cravat.

Rigid Support.  The rigid support can be fabricated as a unilat­ eral support, similar to the Sager traction splint or Kendrick traction device, or as a bilateral support, such as the Thomas half-ring or Hare traction splint. Unilateral supports tend to be easier to apply than bilateral supports. The following are some ideas for rigid support. Double Ski Pole or Canoe Paddle System.  This is fashioned like a Thomas half-ring splint, with the interlocked pole straps slipped under the proximal thigh to form the ischial support. Some mountain guides carry a prefabricated, drilled ski-pole section or an aluminum bar that can be used to stabilize the distal end of this system. Single Ski Pole or Canoe-Kayak Paddle.  Use a single ski pole or paddle either between the legs, which is ideal for bilateral femur fractures, or lateral to the injured leg. The ultimate rigid support is an adjustable telescoping ski pole used laterally. Adjust the pole to the appropriate length for each victim, making the splint compact for litter work or helicopter evacuation (Figure 23-63). Tent Poles.  This system uses conventional sectioned tent poles. Fit the poles together to create the ideal length for rigid support. Because of their flexibility, tent poles must be secured well to the leg to prevent them from flexing out of position. Place a blanket pin or a bent tent stake in the end of the pole to provide an anchor for the traction system. Alternatively, use a Prusik knot (Figure 23-64) to secure the system to the end of the tent pole.

FIGURE 23-62  Buck’s traction. Duct tape stirrups are added to a small foam pad that is wrapped around the leg. The entire unit is wrapped with an Ace bandage. This system helps distribute the force of the traction over a large surface area.

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CHAPTER 23  Improvised Medicine in the Wilderness

A

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 23-63  Single ski pole system. An adjustable telescoping ski pole is used as the rigid support. A stirrup is attached to a carabiner placed over the end of the pole. Traction is applied by elongating the ski pole, while another rescuer provides manual traction on the victim’s leg. Additional padding and securing follow (not shown).

Miscellaneous.  Any suitable object, such as a canoe or kayak paddle, two ice axes taped together at the handles, or a straight branch, can be used to make a rigid support. Although skis immediately come to mind as suitable rigid components, they are too cumbersome to work effectively. Because of their length, skis may extend far beyond the victim’s feet or require placement into the axillae, which is unnecessary and inhibits mobility (e.g., sitting up during transport). Premanufactured canvas pockets, available from the National Ski Patrol System, provide a ski tip and tail attachment grommet for use with the ski system. Traction Mechanism.  The amount of traction required may be difficult to estimate. A general rule is to use 10% of body weight or about 4.5 kg (10 lb) to a maximum of 7 kg (15 lb) of traction force for the average victim.1 Consider practicing with a com­ mercial system, such as a Sager Traction Device (Minto Research and Development, Inc., Redding, California), ahead of time to get a feeling for what these forces look and feel like. Check the opposite extremity to compare lengths. After the traction is applied, always recheck distal neurovascular function (circula­ tion, sensation, and movement). Some sources advise applying traction to maximize patient comfort.6 However, patients with these injuries are often in extremis, and relative “comfort” is hard to assess. Lacking other indicators, applying traction to approxi­ mate the opposite leg’s length is a reasonable goal. Cam Lock or Fastex-Like Slider.  This simple, effective system uses straps that have a Fastex-like slider (ITW Fastex, Des Plaines, Illinois). Such straps are often used as waist belts or to attach items to packs. Alternatively, a cam lock with nylon webbing can be used. Attach the belt to the distal portion of the rigid support and then to the ankle hitch. Traction is easily applied by cinching the nylon webbing (Figure 23-65).

1

2

3

FIGURE 23-64  A Prusik knot made from a small-diameter cord is used as an adjustable distal traction anchor. Although two wraps are shown in the illustration for simplicity, an additional one to two wraps are usually necessary to add further security when applied to a smooth surface, such as a kayak paddle.

468

FIGURE 23-65  A Fastex-type or cam-lock utility strap makes a very efficient traction device and can be adapted for most systems.

Trucker’s Hitch.  A windlass can be easily fashioned using small-diameter line (parachute cord) and a standard trucker’s hitch for additional mechanical advantage. Prusik Knot.  Almost any system can be rigged with a Prusik knot (see Figure 23-64). Prusiks are ideal for providing traction from rigid supports with few tie-on points (such as a canoe paddle shaft or a tent pole). The Prusik knot can be used to apply the traction (by sliding the knot distally) or simply as an attachment point for one of the traction mechanisms already mentioned. Spanish Windlass.   The first popularized modern improvised traction mechanism was the Spanish windlass. These systems can be awkward to apply and are often not durable. The windlass can unwind if it is inadvertently jarred, and can apply rotational forces to the leg. Litter Traction.  If no rigid support is available and a rigid litter, such as a Stokes, is being used, apply traction from the rigid bar at the foot end of the litter. If this system is used, ensure that the patient is immobilized on the litter with adequate counter-traction, such as inguinal straps. Proximal Anchor.  The simplest proximal anchor uses a single proximal thigh strap, which can be made from a piece of climb­ ing webbing or a prefabricated strap, belt, or cam lock (Figure 23-66). A cloth cravat can be used in a pinch. On the river, a life jacket can be used (Figure 23-67). When climbing, a climbing harness is ideal. Securing and Padding.  Check all potential pressure points to ensure that they are adequately padded. An excellent padding system can be made by first covering the upper and lower leg with a folded length of Ensolite (Figure 23-68). This is preferred over a circumferential wrap because the folded system allows one to see the extremity. The victim is more comfortable if femoral traction is applied with the knee in slight flexion (padding placed beneath the knee during transport). Secure the splint firmly to the leg. Almost any strap-like object will work, but a 10- to 15-cm (4- to 6-inch) elasticized bandage wrapped circumferentially provides a comfortable and secure union. Finally, strap or tie the ankles or feet together with adequate padding between the legs to give the system additional stability. Tying the ankles together also prevents the injured leg from excessive external rotation during transport, which greatly improves patient comfort.

CHAPTER 23  Improvised Medicine in the Wilderness

A

B

C

FIGURE 23-66  A, Proximal anchor using cam lock belt. The belt is applied as shown. The strap is adjusted loosely to allow the belt to ride up to the point of the hip. If the strap is improperly tightened, it can create pressure over the fracture, and it moves the traction point to a less optimal distal position. Padding is helpful, but not always necessary if the victim is wearing pants and the strap is properly adjusted. B and C, The end of the ski pole is pushed into the strap (1) and then taped in place (2). Note that forces are applied to the strap, not the duct tape.

Eye, Ear, Nose, and Throat Improvisation EPISTAXIS Epistaxis is a common problem among travelers. Reduced humid­ ity in airplanes, cold climates, and high-altitude environments can produce drying and erosion of the nasal mucosa. Other etio­ logic factors include facial trauma, infections, and inflammatory rhinitis. Although most cases of epistaxis are minor, some present life-threatening emergencies.80 Anterior epistaxis from one side of the nasal cavity occurs in 90% of cases. If pinching the nostrils against the septum for a full 10 minutes does not control the bleeding, nasal packing may be needed. Soak a piece of cotton or gauze with a vasoconstric­ tor, such as oxymetazoline nasal spray, insert it into the nose,

and leave it in place for 5 to 10 minutes. Petroleum jelly– impregnated gauze or strips of a nonadherent dressing can then be packed into the nose so that both ends of the gauze remain outside the nasal cavity (Figure 23-69). This prevents the victim from inadvertently aspirating the nasal packing.80

A

B FIGURE 23-67  Life jacket proximal anchor. An inverted life jacket worn like a diaper forms a well-padded proximal anchor. A kayak paddle is rigged to the life jacket’s side adjustment strap.

FIGURE 23-68  Lower extremity Sam Splint. A, Note the reverse bends at the edge to add structural rigidity. B, Lower leg/ankle splint with reverse bends.

469

PART 4  INJURIES AND MEDICAL INTERVENTIONS

IMPROVISED EYEGLASSES Exposure of unprotected eyes to ultraviolet radiation at high altitudes may produce photokeratitis (snowblindness). Symptoms are delayed, and the victim is often unaware that an eye injury is developing. When sunglasses are lost at 4267 m (14,000 feet) in the snow, photokeratitis can develop in 20 minutes. One can improvise sunglasses from duct tape, cardboard, or any lightimpermeable material that can be cut. Cardboard “glasses” with narrow eye slits can be taped over the eyes for protection. Slits can also be cut into a piece of duct tape that has been folded over on itself with the sticky sides opposing. After a tri­ angular wedge is removed for the nose, apply another piece of tape to secure the glasses to the head. If a sunglass lens is broken or lost, the above technique can be used over the existing frame (Figure 23-71). Pinhole tape glasses can improve vision in a myopic person whose corrective lenses have been lost. With myopia, parallel light rays from distant objects focus in front of the retina. The pinhole directs entering light to the center of the cornea, where refraction (bending of the light) is unnecessary. Light remains in focus regardless of the refractive error of the eye (Figure 23-72). Pinhole glasses decrease both illumination and field of vision, so puncture a piece of duct tape or cardboard repeatedly with a safety pin, needle, fork, or other sharp object until enough light FIGURE 23-69  Anterior epistaxis from one side of the nasal cavity can be treated using nasal packing soaked in a vasoconstrictor. Petroleum jelly–impregnated gauze or strips of nonadherent dressing can be packed in the nose so that both ends of the gauze remain outside the nasal cavity.

Complete packing of the nasal cavity of an adult victim requires a minimum of 1 m (3.3 feet) of packing to fill the nasal cavity and tamponade the bleeding site. Although commercial packing is available, a tampon or the balloon tip from a Foley catheter is more likely to be available, and both work well as improvised packing.80 Anterior nasal packing blocks sinus drainage and predisposes to sinusitis. Prophylactic antibiotics are usually recommended until the pack is removed after 48 hours.80 If the bleeding site is located posteriorly, use a 14F to 16F Foley catheter with a 30-mL balloon to tamponade the site (Figure 23-70). Prelubricate the catheter with either petroleum jelly (Vaseline) or a water-based lubricant, then insert it through the nasal cavity into the posterior pharynx. Inflate the balloon with 10 to 15 mL of water, and gently withdraw it back into the posterior nasopharynx until resistance is met. Secure the catheter firmly to the victim’s forehead with several strips of tape. Pack the anterior nose in front of the catheter balloon as described earlier.

ESOPHAGEAL FOREIGN BODIES Esophageal foreign bodies may cause significant morbidity. Respiratory compromise caused by tracheal compression or by aspiration of secretions may occur. Mediastinitis, pleural effusion, pneumothorax, and abscess may be seen with perforations of the esophagus from sharp objects or pressure necrosis caused by large objects. Foley balloon-tipped catheters can be used safely to remove blunt esophageal foreign bodies, either by using them to push or pull the object.19 Success rates of 98% have been cited.7 Asso­ ciated complications include laryngospasm, epistaxis, pain, esophageal perforation, and tracheal aspiration of the dislodged foreign body.53 Sharp, ragged foreign bodies or an uncooperative victim preclude use of this technique.70 Lubricate a 12F to 16F Foley catheter, and place it orally into the esophagus while the victim is seated. After placing the victim in Trendelenburg’s position, pass the catheter beyond the foreign body, and inflate the balloon with water. Withdraw the catheter with steady traction until the foreign body can be removed from the hypopharynx or is expelled by coughing. Take care to avoid lodging the foreign body in the nasopharynx. Terminate the attempt if there is any significant impedance to withdrawal. 470

FIGURE 23-70  Packing the back of the nose. Insert a Foley catheter into the nose and gently pass it back until it enters the back of the throat. After the tip of the catheter is in the victim’s throat, carefully inflate the balloon with 10 to 12 mL of air or water from a syringe. Inflation should be done slowly and should be stopped if painful. After the balloon is inflated, gently pull the catheter back out until resistance is met.

CHAPTER 23  Improvised Medicine in the Wilderness

FIGURE 23-73  Pinholes improve vision in person with myopia.

FIGURE 23-71  Improvised lens for sunglasses (see text).

enters to focus on distant objects. Secure the device to the face (Figure 23-73).

some persons may be sensitive to the adhesive. Fiberglass strap­ ping tape has greater tensile strength and is ideal for joining rigid components, such as taping two ice axes together. However, it is less sticky than duct tape and not as useful for patching torn items. Extra tape can be carried by wrapping lengths of it around pieces of gear.

PLASTIC CABLE TIES

Useful Tools and Equipment to Carry KNIFE The knife can be a fairly simple model, but it should have an awl for drilling holes into skis, poles, sticks, and so on. The awl on a Swiss Army knife works quite well for this purpose, allow­ ing creation of well-fitted components during improvisation (e.g., a drilled crossbar attached to ski tips for an improvised rescue toboggan).

TAPE Carry some form of strong, sticky tape. All duct tape is not created equal. Look for an exterior grade weatherproof product. This item cannot be improvised. Use either cloth adhesive tape (already in the medical kit) or duct tape. Duct tape is ideal for nearly all tasks, even on skin when needed (e.g., to close wounds, treat blisters, or tape an ankle). Note, however, that

Lightweight cable ties can be used to bind almost anything together (e.g., to bind pack frames together for improvised litters or ski poles together for improvised carriers). They are also perfect for repairing many items in the backcountry.

PARACHUTE CORD Parachute cord has hundreds of uses in the backcountry. It can be used for trucker’s hitch traction and for tying complex splints together. Parachute cord is light; carry a good supply.

SAFETY PINS Box 23-6 lists various uses for safety pins.

WIRE Braided picture-hanging wire works well because it is supple and ties like line. Its strength makes it superior for repairing and improvising components under an extreme load, (i.e., fabricating improvised rescue sleds or repairing broken or detached ski bindings).

BOLTS AND WING NUTS Bolts and wing nuts make the job of constructing an improvised rescue sled much easier (see Improvised Rescue Sled or Tobog­ gan, later). Bolts are useful only if holes can be created to put them through. Therefore a knife with an awl is needed for drill­ ing holes through skis, poles, or other improvised items.

PREFABRICATED CROSSBAR

FIGURE 23-72  Pinholes in duct tape to improve vision in person with myopia.

A prefabricated crossbar can be used to construct double ski pole traction splint systems. A crossbar is easily fabricated from a branch or short section of a ski pole, but carrying a prefabricated device, such as a 15-cm (6-inch) predrilled ski pole section, saves time (see Figure 23-65). 471

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 23-6  How to Use a Safety Pin • To hold the tongue out to maintain an airway, place a pin vertically through the anterior midline of the tongue (see Figure 23-27). • To replace the lost screw in a pair of eyeglasses, which prevents the lens from falling out. • To make pinhole eyeglasses. • To perform neurosensory skin testing. • To puncture plastic bags for irrigation of wounds. • To remove embedded foreign bodies from the skin. • To drain an abscess or blister. • To relieve a subungual hematoma. • As a fishhook. • As a finger splint (for mallet finger). • As a sewing needle, using dental floss as thread. • To hold gaping wounds together. • To replace a broken zipper on clothing. • To hold gloves or mittens to a coat sleeve. • To unclog jets in a camping stove. • To pin triage notes to victims’ clothing. • To remove a corneal foreign body (with ophthalmic anesthetic). • To secure a sling and swath for shoulder or arm injuries. • To fix a ski binding. • To extract the clot from a thrombosed hemorrhoid. • To pin a strap or shirt tightly around the chest for rib fracture support. • To remove ticks.

CLOSED-CELL FOAM PADS Since the introduction of Therm-a-Rest types of inflatable pads, closed-cell foam has become increasingly scarce; however, closed-cell foam is still the ultimate padding for almost any improvised splint or rescue device. The uses for closed-cell foam are virtually unlimited. Even die-hard Therm-a-Rest fans should carry a small amount of closed-cell foam, which is lightweight and doubles as a comfortable seat cushion. Further­ more, unlike inflatable pads, closed-cell foam will not puncture and deflate. Inflatable pads also have their place, and are useful padding for long-bone splints and immobilizers (e.g., an improvised uni­ versal knee immobilizer). An inflatable pad can also be used to cushion pelvic fractures. First, wrap the deflated pad around the pelvis. Then secure the pad with tape and inflate it. It helps to wrap duct tape circumferentially around the pad at the level of the pelvis.

Improvised Transport CARRIES Three-Person Wheelbarrow Carry (Figure 23-74) This system is extremely efficient and can be used for prolonged periods on relatively rough terrain. The victim places his or her arms over the shoulders of two rescuers standing side by side. The victim’s legs are then placed over a third rescuer’s shoulders. This system equalizes the weight of the victim very efficiently. Two-Hand Seat Two carriers stand side by side. Each carrier grasps the other carrier’s wrists with his or her opposite hand (e.g., right hand to left). The victim sits on the rescuers’ joined forearms. The carriers might maintain one free hand to place behind the back of the victim for support (support hands can be joined). This system places great stress on the carriers’ forearms and wrists. Four-Hand Seat Two carriers stand side by side. Each carrier grasps his or her own right forearm with the left hand, palms facing down. Each carrier then grasps the forearm of the other with his or her free hand to form a square “forearm” seat. With the forearm seat, the victim must support himself or herself with a hand around the rescuers’ backs. Ski Pole or Ice Ax Carry Two carriers with backpacks stand side by side with two to four ski poles or joined ice ax shafts resting between them and the base of the pack straps (Figure 23-75). The ski poles or ice ax shafts can be joined with cable ties, adhesive tape, duct tape, wire, or cord. Because the rescuers must walk side by side, this technique requires wide-open, gentle terrain. The victim sits on the padded poles or shaft with his or her arms over the carriers’ shoulders. Split-Coil Seat The split-coil seat (“Tragsitz”) transport method uses a coiled climbing rope to join the rescuer and victim together in a pig­ gyback fashion (Figure 23-76). The victim must be able to support himself or herself to avoid falling back, or must be tied in. Two-Rescuer Split-Coil Seat The two-rescuer split-coil seat is essentially the same as the splitcoil Tragsitz transport, except that two rescuers split the coil over their shoulders. The victim sits on the low point of the rope between the rescuers (Figure 23-77). Each rescuer maintains a free hand to help support the victim.

FLUORESCENT SURVEYOR’S TAPE Surveyor’s tape can be used, much like Hansel and Gretel’s breadcrumbs, to help locate a route into or out of a rescue scene. It is also ideal for marking shelters in deep snow and can serve as a wind sock during helicopter operations on improvised landing zones. Surveyor’s tape is not biodegradable, so it should always be removed from the site after the rescue is completed.

SPACE BLANKET OR LIGHTWEIGHT TARP For improvising hasty shelters in times of emergency, some form of tarp is essential. In the snow, a slit-trench shelter can be built in a matter of minutes using a tarp. Otherwise, the complex and time-consuming construction of improvised structures, such as snow caves, igloos, or tree branch shelters, might be necessary. Typically, little time or help is available for this task during emergencies. In addition, tarps are essential for “hypothermia wraps” when managing injured persons in cold or wet condi­ tions. The only advantage of a space blanket over other tarps is its small size, which means there is a good chance it is packed for the trip. 472

FIGURE 23-74  Three-Person Wheelbarrow Carry. The victim places his or her arms over two rescuers’ shoulders (the rescuers stand side by side). The victim’s legs are then placed over a third rescuer’s shoulders.

CHAPTER 23  Improvised Medicine in the Wilderness

A

FIGURE 23-77  Two-rescuer split-coil seat. Balance could be improved by using a longer coil to carry the victim lower.

Backpack Carry

B FIGURE 23-75  Ski pole seat. A, Ski poles are anchored by the packs. B, The victim is supported by the rescuers.

A large backpack can be modified by cutting leg holes at the base. The victim sits in it as a child would in a baby carrier. Some large internal frame packs incorporate a sleeping bag compartment in the lower portion of the pack that includes a compression panel. With this style of pack, the victim can sit on the suspended panel and place his or her legs through the unzipped lower section without damaging the pack, or the victim can simply sit on the internal sleeping bag compression panel without the need to cut holes. Nylon Webbing Carry Nylon webbing can be used to attach the victim to the rescuer like a backpack (Figure 23-78). At least 4.6 to 6.1 m (15 to 20 feet) of nylon webbing is needed to construct this transport. The

A

B

C

FIGURE 23-76  Split-coil seat. A, Rope coil is split. B, Victim climbs through rope. C, Rescuer hoists the sitting victim.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

should be taped first to prevent them from tearing through the parkas. Internal-Frame Pack Litter The internal-frame pack litter is constructed from two to three full-size internal-frame backpacks that must have lateral compres­ sion straps (day packs are suboptimal). Slide poles or skis through the compression straps; the packs then act as a supportive surface for the victim. Life Jacket Litter Life jackets can be placed over paddles or oars to create a make­ shift nonrigid litter.

FIGURE 23-78  Webbing carry. Webbing crisscrosses in front of the victim’s chest before passing over the shoulders of the rescuer.

center of the webbing is placed behind the victim and brought forward under the armpits. The webbing is then crossed and brought over the rescuer’s shoulders, then down around the victim’s thighs. Finally, the webbing is brought forward and tied around the rescuer’s waist. Additional padding is needed for this system, especially around the posterior thighs of the victim.

NONRIGID LITTERS Many nonrigid litter systems have been developed over the years. These systems are best suited for transporting non–critically injured victims over moderate terrain. They should never be used for trauma victims with potential spine injuries. Blanket Litter A simple nonrigid litter can be fabricated from two rigid poles, branches, or skis and a large blanket or tarp. The blanket or tarp is wrapped around the skis or poles as many times as possible and the poles are carried. The blanket or tarp should not be simply draped over the poles, but securely fastened. For easier carrying, the poles can be rigged to the bases of backpacks. Large external-frame packs work best, but internal-frame packs can be rigged to do the job. Alternatively, a padded harness to support the litter can be made from a single piece of webbing, in a design similar to a nylon webbing carry. Tree Pole Litter The tree pole litter is similar to the blanket litter. However, in the tree pole litter, instead of a blanket or a tarp, the side poles are laced together with webbing or rope and then padded. Again, the poles may be fitted through pack frames to aid carrying. To give this litter more stability and to add tension to the lacing, the rescuer should fabricate a rectangle with rigid crossbars at both ends of the poles before lacing. Parka Litter Two or more parkas can be used to form a litter (Figure 23-79). Skis or branches are slipped through the sleeves of heavy parkas, and the parkas are zipped shut with the sleeves inside. Ski edges 474

Rope Litter On mountaineering trips, the classic rope litter can be used, but this system offers little back support and should never be used for victims with suspected spine injuries. The rope is uncoiled and staked onto the ground with sixteen 180-degree bends (8 on each side of the rope’s center). The rope bends should approximate the size of the finished litter. The free rope ends are then used to clove-hitch off each bend (leaving 5 cm [2 inches] of bend to the outside of each clove hitch). The leftover rope is threaded through the loops at the outside of each clove hitch. This gives the rescuers a continuous handhold and protects the bends from slipping through the clove hitches. The rope ends are then tied off. The litter is padded with packs, Therm-a-Rest pads, or foam pads. This improvised litter is somewhat ungainly and requires six or more rescuers for an evacuation of any dis­ tance. A rope litter can be tied to poles or skis to add lateral stability if needed.

IMPROVISED RESCUE SLED OR TOBOGGAN A sled or toboggan can be constructed from one or more pairs of skis and poles that are lashed, wired, or screwed together. Many designs are possible. Improvised rescue sleds may be clumsy and often bog down hopelessly in deep snow. Nonethe­ less, they can be useful for transporting a victim over short distances to a more sheltered camp or to a more appropriate landing zone. They have sometimes been used for more exten­ sive transports, but they do not perform as well as commercial rescue sleds. To build an improvised rescue sled or toboggan, the rescuer needs a pair of skis (preferably the victim’s) and two pairs of ski poles; three 61-cm (2-foot)-long sticks (or ski pole sections); 24.4 m (80 feet) of nylon cord; and extra lengths of rope for sled hauling. The skis are placed 0.6 m (2 feet) apart. The first stick is used as the front crossbar and is lashed to the ski tips. Alternatively, holes can be drilled into the stick and ski tips with an awl, and bolts can be used to fasten them together. The middle stick is lashed to the bindings. One pair of ski poles is placed over the crossbars (baskets over the ski tips) and lashed down. The second set of poles is lashed to the middle stick with baskets facing back toward the tails. A third rear stick is placed on the tails of the skis and lashed to the poles. The lashings are not wrapped around the skis; the crossbar simply sits on the tails of the skis under the weight of the victim. Nylon cord is then woven back and forth across the horizontal ski poles. The hauling ropes are passed through the baskets on the front of the sled. The ropes are then brought around the middle crossbar, and back to the front crossbar. This rigging system reverses the direction of

FIGURE 23-79  Parka litter. On the right, the sleeves are zipped inside to reinforce the litter.

pull on the front crossbar, making it less likely to slip off the ski tips.73 Another sled design uses a predrilled snow shovel incorporated into the front of the sled. A rigid backpack frame can also be used to reinforce the sled. This requires drilling holes into the ski tips and carrying a predrilled shovel. This system holds the skis in a wedge position and may offer slightly greater durability.65

Conclusion This chapter is not, by any means, exhaustive. Rather, it provides some ideas about how to improvise medical equipment or do medical procedures when the clinician is not in his or her normal setting and may have limited tools with which to work. The key

is to do what is necessary to optimally treat the patient, and keep in mind that the methods used may not be ideal. It is always important to balance medical treatment with patient safety. The time necessary to get the patient to standardized care, the patient’s condition, and the situation all play roles in deter­ mining how far “outside of the box” the clinician should operate. With that in mind, an experienced clinician’s skill and knowledge married to onsite improvisation can easily save lives.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 24 

Hunting and Fishing Injuries EDWARD J. OTTEN Even as Nimrod the mighty hunter before the Lord. GENESIS

Hunting is a popular pastime in the United States, and injuries are quite common. The instruments used to kill game are inherently dangerous, and hunters often place themselves in dangerous situations, such as tree stands, to improve their success. Understanding wound ballistics, types of firearms, arrows, and traps can aid the clinician in caring for the various wounds produced by these instruments. Fishing has specific injuries as a result of hooks and spears, and the clinician should know various techniques for their removal. Anthropologists have many theories concerning the origins and importance of hunting in the evolution of the human species. The physical attributes of bipedal locomotion, binocular vision, and an opposable thumb all make humans more efficient hunters. Whether these exist because humans have an innate compulsion to hunt or whether humans are hunters because of these traits is debatable. There is no debate, however, that human social evolution, language, the use of tools, and domestication of animals are directly related to more efficient hunting. In a survival situation, and in some ways with regard to evolution, hunter–gatherer animals have a distinct advantage over strictly vegetarian animals because of the relative food value of meat over plants. Hunters tend to be males. Approximately three-fourths of all calories in modern hunter–gatherer groups are derived from plants, and this portion of the food is usually supplied by the women in the group. Even in Inuit tribes where plants make up little of the diet, women do most of the fishing while the men hunt. Hominids were at a disadvantage, even in groups, when hunting large animals or driving off other predators from their kills until they began using stones, long bones, and sticks to enhance their relatively weak teeth and claws. Implements for hunting and skinning animals were the earliest tools found by anthropologists. Human cultural evolution followed closely the technologic changes in weapons, although sports, business, and war had replaced the need for hunting in most cultures, even by the time Nimrod walked the earth. Bows and arrows, slings, spear throwers, nets, harpoons, traps, and firearms were designed to extend the reach and increase the lethality of the human hand. Unfortunately, humans discovered that they could kill each other with these weapons. Since the discovery of gunpowder, the development of weapons technology has surpassed all other forms of human endeavor, including medicine and transportation.4,5,14

10:9

Only a few cultures still depend on hunting as their primary food-gathering method. Examples are the Mbuti tribe of the Ituri Forest in Zaire, Andaman Islanders in the Bay of Bengal, and the Inuit. Many cultures use hunting to supplement agriculture, plant gathering, or raising livestock. Most hunting in the United States is done for sport or pleasure, although in some areas of the country, hunting and trapping are still the primary source of income for a few people.

Hunting in the United States The total number of hunters and trappers is unknown. Some participate illegally and are not licensed. In 2006, throughout the United States, 12.5 million individuals purchased hunting licenses, and hunting expenditures totaled $22.9 billion. Although hunting seasons are regulated and relatively short, hunters spent 16 million visitor-days in the national forests and 220 million days total. Fishing numbers for 2006 show 30 million anglers and $42.2 billion in expenditures. The North American Association of Hunter Safety Coordinators (NAAHSC), a division of the New York State Office of Wildlife Management, reported 860 fatal hunting injuries in the United States during the 4-year period between 1983 and 1986, with a total of 6992 injuries from firearms.44 Interestingly, 34% of the total injuries and 89% of the handgun injuries were self-inflicted. Shotguns accounted for 106 of the fatalities and 906 of the total injuries, whereas rifles accounted for 79 fatalities and 465 injuries. The New York State Department of Environmental Conservation reported that the average number of hunting injuries decreased from an average of 137 per year in the decade of the 1960s to only 48 in 2001 and 37 in 2002.8 They credit the institution of hunter safety programs in 1960. In 2001 Colorado reported 9 injuries and 1 death per 500,000 licensed hunters.11 Michigan reported 2 deaths per 2,665,952 hunters in 2003, giving hunting one of the lowest injury and fatality rates of any recreational activity.57 The type of hunting also influences the rate of injury. Smith and colleagues51 reviewed 1345 hunting injuries in Pennsylvania from 1987 to 1999. They showed that turkey hunters had the highest rate of injury (7.5 per 100,000 hunters) and grouse hunters the lowest (1.9 per 100,000 hunters). This was attributed to turkey hunters not wearing orange hunter clothing. Deer

For online-only figures, please go to www.expertconsult.com

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

hunters had the highest case-fatality ratio at 10.3%, and pheasant hunters the lowest at 1.3%. This higher fatality rate was largely because most deer-hunting injuries were due to wounds caused by rifle bullets. They also noted that younger hunters suffered the highest rate of injuries, and the largest percentage of incidents occurred on opening day. Hunting-related shootings represent a very small portion of the total number of accidental firearm deaths in the United States. In Colorado, from 1997 to 2005, there were four deaths during hunting, all attributed to cardiac causes, and none in hunters from firearms, falls, or penetrating injuries. The most common traumatic injuries were lacerations; 75% of lacerations were from knife injuries while field dressing the animals. Of 131 unintentional firearm deaths in California from 1977 to 1983, only 8 were the result of hunting accidents.* Hunting injury data may be inaccurate for a number of reasons. Many minor nonfatal injuries may go unreported, and most states do not differentiate accidental firearm hunting deaths from deaths that occur during any other activity. Also, automobile and all-terrain vehicle accidents that occur while hunting, or gunshot wounds inflicted while “cleaning a gun” at home, may be classified as hunting or nonhunting injuries.

TYPES OF INJURIES ENCOUNTERED Most injuries to hunters are the same types of injuries seen in backpackers, fishermen, and climbers. Frostbite, sprains, burns, and fractures occur with the same frequency in hunters as in others who visit wilderness areas. Prolonged extraction times may increase the risks of hypothermia, wound infection, dehydration, missed medications, and other time-dependent secondary complications. Injuries that are unique to hunters are those caused by their weapons. Most hunting is done with firearms. Shotguns and rifles are more commonly used, although handguns are increasing in popularity. Use of bows and crossbows in hunting is also rapidly increasing. Hunters using these weapons frequently are permitted an extended hunting season that does not overlap with periods for rifle and shotgun hunting. Hunters who use bows and crossbows pose far less danger to people in the hunting area at long range compared with those using rifles and shotguns. Bow hunting requires more skill, use of camouflage, and stealth because of the short effective ranges of arrows and bolts. These factors place bow hunters at greater risk for being mistaken for a game animal at long ranges, which is why rifle and shotgun seasons rarely run concurrently with bow-hunting activity. Other weapons used for hunting are less likely to be encountered. For example, spears, harpoons, and nets are used by some hunters in the Arctic, Australia, and Africa. Spear injuries from gas-powered spearguns or rubber band–powered Hawaiian slings have been associated with fatal injuries, especially when occurring in ocean or lake environments where secondary drowning or shark attack may be an additional hazard. Harpoon and fishing spearheads may separate from the shaft and, depending on the force used, may penetrate the skull or a body cavity. Slingshots are rubber band–powered devices that use the energy in a stretched piece of rubber to hurl a projectile, often a small rock or ball bearing, at 61 to 91 m/sec (200 to 300 ft/sec). Although this is considered a low-velocity and thus low-energy projectile, injuries to the head and face, especially the eyes, have been reported. Blowguns, although mainly used by aboriginal hunters, have become popular with some recreational hunters of birds and small game. The blowgun varies in length, and a variety of darts can be projected 6 to 15 m (19.7 to 49.2 feet) by the exhaled breath. The darts have low energy and do not penetrate very deeply. Modern blowguns rarely cause serious injury unless striking the eye or possibly a blood vessel. To effectively kill small game, the darts generally must carry an immobilizing or poisonous toxin. Darts used by some tribes contain toxins derived from both animal and plant sources. These toxins can cause paralysis and death in humans who have been punctured by the dart either *References 6, 10, 11, 34, 42, 44, 48, 51, 57, 58, 62.

476

accidently during transport or purposefully during tribal war. Animal toxins are primarily neuromuscular toxins and many have been developed for medical use. South American tribes have used Dendrobates frog toxins, which are steroidal alkaloid compounds known as batrachotoxins and homobatrachotoxins. These toxins act at voltage-gated sodium channels and cause irreversible depolarization of nerves and muscles. Several other toxins, including gephyrotoxin, pumiliotoxins, histrionicotoxins, and epibatidine, have been isolated from poison dart frogs. The last toxin is the most potent nicotinic agonist known and is a powerful nonopiate analgesic. Interestingly, these frogs lose their ability to produce toxins in captivity, leading to the finding that the frog’s diet of Melyridae beetles actually is the source of the toxins. Plant-derived toxins include strychnine, curare, and a number of cardiac glycosides from Africa, South America, and Asia, where dart and arrow poisons are still used by indigenous people. All of these toxins, especially the cardenolides from the Maquira, Naucleopsis and other Moraceae species, have been studied for possible medicinal value.46,49 Veterinarians commonly use air-powered darts fired from rifles or blowguns to subdue large animals. These darts contain pharmacoactive agents, such as succinylcholine, phencyclidine, ketamine, and xylazine, in concentrations great enough to bring down an elephant, lion, or rhinoceros. The darts are 3-mL plastic syringes with 16-gauge needles delivered using a 1.8-m (5.9-foot) blowgun or rifle. Accidental human injection can be rapidly fatal if reversing agents or advanced life support is not available. Homemade blowguns are frequently used for sport and usually consist of a needle or pin attached to a wooden shaft and a cotton ball or piece of yarn for a feather. Although these darts do not contain any toxins, they are still capable of causing injuries, especially to the eye. There have been reported cases of aspiration of darts.27,29,59 Trap injuries may be included in the definition of hunting injuries. Most traps are designed to catch and hold small game. Injuries usually occur when a trapper triggers a spring-loaded trap prematurely. Crush injuries and puncture wounds to the hands are most common. Hikers occasionally tread on unmarked traps, and domestic animals such as dogs are accidentally caught in poachers’ traps. Another problem with traps occurs when an animal (wild or domestic) is caught in a trap and attacks the trapper while being released. Many knife lacerations occur when hunters clean game. Lack of familiarity with the process or techniques for field dressing and cleaning game is the likely cause. Failing to wear protective gloves; using the wrong type of knife; working with bloody, slippery material; and having cold hands all contribute to accidents. Tree Stand Injuries A frequent preventable cause of serious injury and death among hunters is not associated with firearms at all. It is the tree stand injury. Tree stands are small platforms designed to hold hunters high above the ground so they can more easily spot and kill large game while remaining undetected. Whether homemade or of commercial design, the platforms generally are small, portable devices that the hunter attaches to the trunk of a tree near game trails or water holes. The stands may have attached ropes or ladders for access, or the hunter may free-climb the tree for placement of the stand or fasten small climbing steps on the tree (Figures 24-1 and 24-2). Hunters may fall asleep on the platforms and fall off or fall while climbing up or down trees. At least one-half of these injuries could be prevented if all hunters wore tree stand safety harnesses (Figure 24-3). Although most of the injuries are similar to those seen with any type of fall, occasionally a hunter drops a firearm, which discharges, or falls on an arrow or rifle, causing an additional weapons injury. Over 10 years, injuries of this type in Georgia accounted for 36% of reported hunting injuries and 20% of hunting fatalities.7 A study from the University of Rochester, New York, looked at tree stand injuries from 1996 to 2001.47 The authors noted that 51 injuries occurred, all in men, with a mean age of 42. Alcohol was present in 10% of patients and 2 of 3 deaths. Spinal fractures were the most common injuries (51%), followed by extremity (41%), head (24%), and lung injuries (22%). Only two patients had been using

CHAPTER 24  Hunting and Fishing Injuries

FIGURE 24-1  The wrong way to use a tree stand. This hunter is not wearing a safety harness, is drinking alcohol, and is pulling his firearm into the tree stand with the muzzle pointing upward.

FIGURE 24-3  The correct way to bring a firearm or quiver into the tree stand, with the muzzle or arrowheads pointing down and the hunter wearing a safety harness at all times.

a safety belt (4%). Sixteen spinal cord injuries were reported between 1987 and 1999 in Oklahoma; the mean height of fall was 16 feet, and 18% were related to alcohol ingestion. Ninety percent resulted in paraplegia/paraparesis, and 12.5% were fatal.*

FIGURE 24-2  A commercially produced tree stand can be used to climb the tree and obviates the need for a ladder or steps, which are the cause of many falls.

Arrow Injuries Modern arrows are usually made from aluminum, graphite, or fiberglass, although many beginners still use inexpensive wooden arrows. A number of types of arrowhead are in use, such as field points and target points, but most injuries are due to specially designed hunting arrowheads called broadheads. These razorsharp metal points come in a variety of sizes and shapes and are designed to kill game by lacerating tissue and blood vessels, causing bleeding and shock. Unlike hunting firearms projectiles, which are designed to kill quickly through massive tissue damage and rapid incapacitating hemorrhage, arrows usually kill more slowly with less tissue damage (Figure 24-4).3,22,23,25Arrows are propelled by a conventional bow, which may be straight, recurved, or compound, or by a crossbow. Crossbow projectiles may be called arrows or bolts and generally are shorter and heavier than arrows fired from a bow. The force used to propel the arrow is usually measured in draw weight, which is the number of foot-pounds necessary to draw a 71.1-cm (28-inch) arrow to its full length. The higher the pound draw, the more powerful the bow and the deeper the penetration acheived by the same type of arrow. Arrows have a much shorter range than do bullets, and arrows must be more accurately placed to kill the animal quickly; therefore most shots taken are under 50 m (164 feet). Because brush and tree branches can easily deflect an arrow, most shots are taken with a clear field of view. For these reasons, bow hunters rarely mistakenly shoot another hunter they presumed was a game animal. Most arrow injuries occur when hunters fire illegally at night in heavy brush and are not sure of their target. Another common injury occurs when a hunter runs after a wounded animal and falls on an arrow that was to be used for *References 9, 20, 40, 50, 53, 56.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

safety precautions are not used.21,31 Paintball guns, although not designed or generally used for hunting, are commonly used in outdoor activities that mimic tactical games. Most injuries occur in children who are not wearing eye protection, but there are also reported cases of vascular injuries. Paintballs are 14-mm (0.6-inch) gelatin capsules that are filled with water-soluble paint of various colors. Because of their small size, they can bypass the bony orbital protection of the eye. Paintballs propelled by carbon dioxide can travel over 91.4 m/sec (300 ft/sec). At this velocity, the globe, cornea, and retina can be disrupted with a direct hit. The American Society for Testing and Materials has standards for eye protection for paintball sports. These include a helmet with integral eye, face, and ear protection (Figure 24-5). Unfortunately, many children either do not wear the recommended protection or remove it during play because of fogging or discomfort.12,24,28,30,38 FIGURE 24-4  Types of arrows. Top, Aluminum shaft arrow with hunting broadhead. Middle left to right, Small game blunt hunting head with spring claws to prevent arrow loss from burrowing into the ground, two types of hunting broadheads, four field points of varying weights. Bottom, Fiberglass shaft for interchangeable heads.

a second shot or falls out of a tree stand onto an arrow. A loaded crossbow is similar to a loaded gun. Hunters have been accidentally shot when dropping the weapon or snagging the trigger on a branch or fence. Hunting arrowheads are quite sharp; selfinflicted injuries may occur when a hunter is sharpening the blades of the broadhead or returning an arrow to the quiver. Injuries From Firearms Nonpowder Firearms.  Although the word firearms technically defines guns that fire projectiles by ignition and burning of a propellant, similar designs referred to as “nonpowder” firearms using springs, compressed air, or compressed gas cartridges are in widespread use among sportsmen and children and will be considered as firearms in practical use. Whereas traditional firearms discharge a projectile by the contained expanding gases generated in the gun barrel by modern fast-burning powders or old-fashioned black powder, nonpowder firearms use a spring, compressed air, or carbon dioxide cartridge to accelerate the projectile out of the barrel. Although air guns are quite accurate at short distances and can develop muzzle velocities in excess of 365.8 m/sec (1200 ft/sec), the small lightweight projectiles usually cannot penetrate skin at distances greater than 100 m (328 feet). Nonpowder firearms are commonly used by children, who cannot legally obtain or use other types of firearms. Uninformed parents buy them as toys, erroneously believing them to be harmless by design. Without supervision and proper training in gun safety, severe injury and death can result. The wounds they cause can be lethal, especially from high-powered air rifles, which can send out pointed projectiles at sufficiently high velocities to penetrate the skull and body cavities. In a recent technical report, Laraque and colleagues estimated 21,840 injuries during the year 2000 from nonpowder firearms, with a 4% hospitalization rate. There were 39 resultant deaths between 1990 and 2000. Care must be taken not to trivialize these injuries, especially in the pediatric patient, where softer, thinner bone may lead to deep penetration by even lightweight projectiles.* Less than lethal (LTL) rounds are used by police and military to subdue individuals without causing serious injury. These rounds may be rubber, wooden, synthetic sponge, or soft wax. Although designed to disperse a crowd or incapacitate a person until he or she can be subdued, they can cause significant injury. This usually occurs when the person is struck in the head or in some cases the abdomen or thorax. These rounds are not designed for hunting but may be encountered if used by the uninitiated. Rounds such as airsoft are used in many police and military training facilities to add realism to the training scenario. These rounds may cause eye injuries if *References 32, 35, 36, 39, 43, 55, 61.

478

Powder Firearms.  In older style weapons (black powder weapons), gunpowder is loaded directly into the barrel. In modern weapons, gunpowder is contained in a cartridge. Black powder weapons use a centuries-old slow-burning propellant that is ignited with a spark from flint striking steel or a percussion cap. The firearms are usually single shot and loaded from the muzzle by pouring a measured amount of black powder down the barrel and then inserting the projectile and tamping it down onto the powder charge. When ignited, the propellant is converted to a gas that expands and pushes the projectile out of the barrel of the weapon. With modern design and manufacturing techniques, these weapons are sufficiently accurate to hunt large game, such as deer and elk. The injuries from black powder weapons are similar to those from modern weapons and are discussed later. The same precautions should be used when hunting with or shooting any type of firearm, whether the propellant is air or gunpowder.1,2,13,45 The term cartridge is used to refer to the intact, unfired assembly of projectile and propellant loaded into the gun for firing. Rifle and pistol cartridges consist of a metal case that contains the gunpowder propellant and into which the bullet is seated and held by compressing the case around the bullet base at the time of manufacture. The base of the case contains a small metal primer filled with a small amount of high explosive that serves to ignite the fast-burning propellant when it is struck by the firing pin of the gun. The primer is in the center of the base of the case (center-fire ammunition) in all cartridges except in small-caliber .22 cartridges, where it is incorporated into the entire circumference of the cartridge base rim (known as rimfire ammunition). Rifle and pistol cartridges generally contain a single bullet, although some may be loaded with very small shot to increase the probability of hitting small objects at short distances. Shotgun cartridges consist of a center-fire metal base combined with a paper or plastic shell in the form of a closed-end tube. Within this tube is placed the propellant and then the projectile(s),

FIGURE 24-5  American Society for Testing and Materials–approved helmet designed for paintball activities with integral eye, face, and ear protection.

Slug

Case Wad Shot

Powder charge

Wad Powder charge

Case

Brass head Primer Primer FIGURE 24-6  Cutaway diagram of shotgun shell.

along with associated plastic, cotton, or paper materials collectively referred to as wadding (Figure 24-6). Shotgun projectiles consist of shot ranging in size from 1 to 10 mm (0.04 to 0.4 inch) (Figure 24-7) or a single solid projectile known as a slug. Shot pellets used to be made of lead. Because of high lead levels in ducks and geese that ingested spent shot while feeding, lead shot for bird hunting was banned in 1991. Approved shot may be made of steel, tin, or various mixtures of tin, bismuth, and up to 15% iron. Steel shot can be identified on radiographs because it retains a perfect round shape, whereas lead and tin shot deforms inside the barrel during firing, resulting in nonspherical shapes. Determining the shot type can help clinicians decide about the safety and usefulness of magnetic resonance imaging scans in the setting of steel projectiles, or the risk for lead toxicity. FIGURE 24-7  Standard shot size number and letter system (with corresponding metric measurements) of hunting shotgun shell projectiles. The smaller the shot size, the more pellets loaded in a single shotgun shell. Larger pellets are heavier, lose less velocity per unit of flight time, and penetrate more deeply than do smaller pellets. (From Shotgunworld.com. Used with permission.)

Lead shot sizes:

Pellet diameter (inches) (mm)

The wadding is commonly a single plastic cup with a thickened expandable base designed to contain the shot and serve as a seal inside the barrel to contain the expanding gases behind the shot cup for maximal muzzle velocity. Slugs also have a type of wadding known as a sabot, which surrounds the slug inside the barrel of the shotgun. In all cases, the wadding is fired from the gun and immediately peels away from the slug or shot. Wadding is commonly found inside close-range wound channels but generally is not involved in wounds at firing distances of more than 5 to 7 m (16 to 23 feet). Beside the wadding and projectile(s), hot gas and unburned powder also exit the muzzle. In cases of close-proximity wounds, usually under 1.1 m (3.5 feet), powder stippling may appear on clothing or skin. The presence of powder stippling or wadding in a wound may have important forensic applications and should always be noted. With contact wounds, where the muzzle is pressed into the skin at the time of firing, escaping hot gases may enter the wound channel and expand inside the victim, causing burns, organ damage, burst skin, and/or a stellate laceration around the point of entrance. Figures 24-8 to 24-10 show examples of gunshot wounds. Hundreds of types of cartridges are available for firearms. They may be factory loaded or hand loaded, which adds the variables of propellant amount and type. Rifle and pistol cartridges are initially classified according to caliber, or diameter, of the bullet. For example, .22 caliber means the diameter of the bullet is 0.22 inch (5.6 mm); .45 caliber is 0.45 inch (11.4 mm); and so forth. The caliber may be expressed in metric measurement; for example, a 9-mm bullet is 9 mm in diameter, which is 0.35 inch. However, bullet diameter alone is insufficient to name a cartridge, because bullet length can vary, as do cartridge length and width. The U.S. Army M-16 service rifle fires a .22 caliber bullet weighing 4 g (62 grains) at 945 m/sec (3100 ft/sec) initial velocity. The common .22 rimfire rifle used by generations of young shooters fires a .22-caliber bullet weighing 2.6 g (40 grains) at 335.3 m/sec (1100 ft/sec) initial velocity. Obviously the wounding potential of these two projectiles is vastly different. Nomenclature for a particular cartridge is made more specific by including a measurement of cartridge length, name of the

12

.05 1.27

9

8

81/2

.080 2.30

71/2

.085 .090 .095 2.16 2.29 2.41

Buck shot sizes: No. 4

No. 3

No. 2

Pellet diameter (inches) (mm)

.25 6.35

.27 6.86

Steel shot sizes:

Pellet diameter (inches) (mm)

.24 6.10

6

5

6

4

3

.110 2.79

No. 1

.30 7.62

2

1

5

4

.120 3.05

.130 3.30

No. 0

.32 8.13 Air Rifle

2

BB

.150 .180 3.81 4.57

No. 00 No. 000

.33 8.38

BB BBB

.36 9.14

T

F

.11 .12 .13 .14 .15 .16 .177 .18 .19 .20 .22 2.79 3.05 3.30 3.56 3.81 4.06 4.49 4.57 4.83 5.08 5.59

Note: the size of shot, whether lead or steel, is based on American Standard shot sizes. Thus, a steel No. 4 pellet and a lead No. 4 pellet are both .13 inches (3.3 mm) in diameter.

479

CHAPTER 24  Hunting and Fishing Injuries

Shot

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 24-8  Gunshot wound to the face and mandible showing extensive bone and soft tissue injury. Patient was initially able to protect his airway, but later required endotracheal intubation because of edema and bleeding.

inventor or inventing company, amount of powder in the case, length of the entire cartridge, or the year the cartridge was invented. For instance, the M-16 round is generally referred to as a 5.56 mm (metric) or a .223 cartridge (English system of measurement), with the third digit differentiating it from the common low-power .22 rimfire cartridge. Other common hunting cartridge names illustrating these variations are .45/70 (70 grains of powder), .30-06 (adopted in 1906), and .35 Whelen (the man who developed the round). Magnum refers more to the type and amount of powder than to the size of the bullet used. Magnum cartridges are designed to give hunters the ability to successfully hunt large game with

FIGURE 24-9  Shotgun wound to the upper arm. Initially the wound looked benign. Both entrance and exit can be seen.

FIGURE 24-10  Radiograph of the same shotgun wound to the upper arm as seen in Figure 24-9. Extensive bone and soft tissue injury, as well as vascular and nerve damage, can be seen.

480

FIGURE 24-11  Examples of hunting bullets. Left to right, .50 caliber black powder lead bullet, .22 caliber long rifle lead bullet, .22 magnum caliber copper jacketed bullet, .44 magnum semijacketed hollow-point bullet, .44 magnum shotshell, .223 caliber (5.56 mm) full metal jacket bullet, .30/30 caliber soft point flat nose bullet, .30-06 caliber round nose soft point bullet, and .270 caliber pointed soft nose bullet.

pistols by improving terminal ballistic performance of the bullet. Figure 24-11 shows some examples of different bullets. Shotgun terminology is a little less complicated, based on the number of lead balls, the diameter of the barrel, and how many lead balls it takes to make a pound. For example, a 12-gauge shotgun has a barrel that is the same diameter as a lead ball that weighs 0.08 lb (37.6 g); a 20-gauge, 0.05 lb (22.7 g). The higher the gauge number, the smaller the barrel and the smaller the projectile. The only exception is the .410 shotgun, which is caliber .410, or 0.410 inch (1 cm) in diameter. Figure 24-12 shows some examples of shotgun rounds and the shot and wadding within them. The type and severity of wounds inflicted by a firearm depend on several factors. The most often quoted factor, but the least important, is the amount of energy the bullet (projectile) has when leaving the firearm. The kinetic energy formula, Ek = 1 2 MV2, can be applied to any moving object and can be used to calculate the muzzle energy for a particular type of firearm. Energy increases much more as a function of the velocity of the bullet than as a function of the mass. For this reason, most firearms are classified according to muzzle velocity. The higher the velocity of the bullet, the greater the energy and the greater the potential for injury. Firearms with muzzle velocities greater than 762 m/sec (2500 ft/sec) are considered high velocity, 457.2 to 762 m/sec (1500 to 2500 ft/sec) are medium velocity, and less than 457.2 m/sec (1500 ft/sec) are low velocity (Table 24-1). Bullets cause damage to tissue by crushing. The energy of a bullet may be transmitted to the tissue in part or in total depending on the surface area the bullet presents to the tissue. Bullets that yaw, expand, or fragment present more surface area than do bullets that stay in one axis and maintain one shape. By international agreement codified in the articles of the Hague Convention IV of 1907, military bullets are not to be designed in a manner to produce “superfluous” wounding effects by features that would encourage the bullets to flatten or expand on impact with tissue. They are typically completely encased in a copper jacket to prevent deformation of the soft lead core. Such rounds

FIGURE 24-12  Examples of shotgun rounds. Left to right, 12-gauge slug round, empty 12-gauge plastic round, plastic 12-gauge wadding, and No. 6 shotgun pellets.

Velocity, and Muzzle Energy

Caliber

Weight in Grams (Grains)

.22 .223 .44 magnum .30/60

2.6 3.6 11.7 9.7

(40) (55) (180) (150)

Muzzle Velocity Feet/sec

M/sec

Muzzle Energy in Foot-Pounds

1080 3250 1600 2750

329 991 488 838

90 1280 1045 2500

generally pass through an individual, leaving a permanent wound tract similar in diameter to that of the bullet. The ammunition is designed to wound a soldier and put him or her out of combat, but not to kill the soldier. In contrast, hunting ammunition is designed to expand on impact up to two or three times its diameter, resulting in a much larger wound channel, greater tissue damage, and rapid incapacitation and death (Figure 24-13). This feature of planned deformation also promotes retention of the bullet within the target and reduces the risk for injury to unseen individuals downrange from the game animal. In fact, many states require the use of expanding ammunition for hunting large game. This may increase the wound severity of hunting injuries compared with military and criminal shootings. In addition to direct tissue destruction by the deforming bullet, fragmentation may occur when a bullet strikes bone and sends bone and bullet fragments in several directions. These secondary missiles cause injuries within the body similar to those from bullet fragments and may even exit the body to injure bystanders. A second injury mechanism of terminal ballistic bullet behavior is temporary cavitation, which occurs at all velocities to some degree but becomes a significant wounding mechanism factor only at high velocities. The temporary cavity is created by radial dispersion of tissue by the bullet surface as a result of acceleration of tissue away from its path. A permanent cavity

FIGURE 24-13  The .30-caliber Nosler 180 g AccuBond Polymer Tip bullet fired into calibrated 10% ordnance gelatin is typical of the .30caliber hunting bullets used for .30-06, .308, .300 Win Mag, and other cartridges. This photo shows this bullet fired from a .308 rifle with an 45.8 cm- (18-inch) long barrel. Muzzle velocity was 762 m/sec (2499 ft/ sec). Penetration depth exceeded 50.8 cm (20 inches). Temporary cavity maximum width was 11.4 cm (4.7 inches) at a depth between 7.1 cm (2.8 inches) and 22.1 cm (8.7 inches). Diameter of the recovered bullet at the front surface was 1.4 cm (0.6 inches). Weight of the recovered bullet was 149.5 g (5.3 oz); 17% of the bullet turned into fragments. Terminal performance of this type is suitable for all medium to heavy game encountered in the lower 48 U.S. states, including moose, elk, black bear, pigs, and deer. Ten-cent coin (dime) is shown for comparison. (Courtesy Gary K. Roberts, DDS.)

Permanent cavity

.22 Cal (5.6 mm) FMC Detached muscles Wt.-55gr (3.6 g) Vel-3094 f/s 943 m/s Final wt-35gr (2.3 g) 36% Fragmentation

Temporary cavity

Bullet fragments 5

10

15

20

25

30

36

FIGURE 24-14  Wound profile of a .223 rifle bullet in 10% ballistic gelatin showing the permanent and temporary cavities and the effects of tumbling and fragmentation.

occurs when a bullet or fragment crushes tissue. In high-velocity bullet wounds, the temporary cavity may be many times larger than the permanent cavity. This wave is well tolerated by most elastic tissue, such as muscle, bowel, and lung; however, inelastic tissues, such as liver or brain, do not tolerate it and may be severely damaged by the temporary cavity. Bullet motion in flight is described by rotation, yaw, and pitch. The rifle grooves cut into the inside of the barrel cause the bullet to spin around its long axis, just like a football thrown in a tight spiral. Yaw and pitch describe bullet motion left or right, or up and down relative to the long axis of the bullet. In wound ballistics, yaw is used to describe both axes of motion. A rifle bullet will usually yaw after striking any object outside the body, such as a tree branch, belt, or clothing, and when striking skin and other tissue within the body. Yaw can result in complete endover-end rotation of the bullet within tissue, causing the bullet to increase the area that is crushed as the entire side profile of the bullet passes through the tissue. Bullets with round ends, for example the .45 automatic Colt pistol bullet or round musket balls, routinely do not yaw, and produce wound channels equal to their caliber or expanded caliber. Yaw causes maximum damage at 90 degrees of rotation, when the entire side profile of the bullet crushes tissue. This factor, combined with any bullet expansion, can cause the exiting bullet to produce a much larger wound than when it entered. To allow laboratory comparison of projectile designs and to study the effect of velocity and expansion, experimental wounding profiles have been described using ballistic gelatin, which accurately simulates human muscle tissue. These wounding profiles show the various aspects of potential ballistic injury, including cavitation, yaw, and fragmentation (Figures 24-14 and 24-15).19 The total effect of high energy, fragmentation, expansion, yaw, and temporary cavity formation results in tissue injury. Although the kinetic energy formula yields the total energy available to cause injury, the physical behavior of the projectile(s) and the transited tissues are the actual determinants of the complete injury pattern. The type of tissue struck is the most important factor. As can be seen from Table 24-1, the .22-caliber long rifle

FIGURE 24-15  The path of a test bullet through ballistic gelatin suggests the amount of tissue damage that a hunting bullet can do inside the human body, even if entrance and exit wounds are small. The data for this bullet are given with Figure 24-13. (Courtesy Gary K. Roberts, DDS.)

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CHAPTER 24  Hunting and Fishing Injuries

TABLE 24-1  Comparison of Bullet Caliber, Weight,

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

D

E FIGURE 24-16  A, A leghold trap set. B and C, A leghold trap sprung. D and E, To release a trap that has been sprung, stand on each end of the trap and compress the spring.

rimfire bullet has a low mass and velocity and thus a low muzzle energy, yet more fatalities have occurred from this round than from any other. It is very inexpensive, can be fired from a number of rifles and handguns, is commonly used to hunt game, and is not thought of as particularly dangerous by inexperienced hunters. For these reasons, more people are shot by this cartridge than by any other single bullet type. The bullet is highly lethal when striking the brain, heart, or a major blood vessel.* Rubber or plastic bullets, although generally not used for hunting, may be encountered. These bullets travel at about 61 m/sec (200 feet/ sec) and will not usually penetrate skin, although at short ranges (under 15.2 m [50 feet]) they can cause fractures, eye trauma, and other blunt injuries.19 Other rare problems associated with firearms are explosions that occur within the firearm itself. These can cause burns or fragment types of injuries. When firearms are loaded with excessive amounts of powder or when the wrong powder is used in reloading bullets, the resultant detonation may cause the frame or cylinder of the firearm to explode. The burning powder or fragments of metal can cause injuries to the shooter. These injuries usually occur to the face and hands; penetrating eye injuries are also common. Obstruction of the barrel of the firearm by snow, mud, or other foreign material may cause a similar explosion. *References 1, 2, 13, 15-19, 37, 54.

482

Trap Injuries Traps are designed either to kill animals or to capture them alive and uninjured. The latter type poses no risk to humans unless they should happen upon a trap and attempt to free the animal or otherwise approach the trap. The trapped animal often will bite or claw anyone within range. Leghold traps designed to kill or injure an animal may occasionally cause problems for unwary hikers or campers. These traps have a spring-loaded jaw that closes when triggered by something touching the trigger plate, usually involving only 0.5 to 1 kg (1 to 2 lb) of pressure. Most injuries involve the foot, but any area of the body that can fit between the jaws potentially can be injured. The jaws can be released by compressing the spring controlling the jaws (Figure 24-16). Very large traps used to trap poachers or to catch large animals, such as tigers or bears, cannot easily be released without help. These traps may also be attached to large weights, such as logs or concrete blocks, to prevent escape. Fortunately, most of these large traps are now collector’s items and not used in the field. Many injuries occur when the person setting the trap inadvertently causes the trap to spring before being set in the ground. This often causes hand and finger injuries, especially with amateur trappers unfamiliar with the type of trap (Figure 24-17). Unconventional traps, such as snares, deadfalls, and pit traps, may rarely be encountered, but the mechanisms and types of

injuries are quite variable. Trap guns are illegal in most areas of the world; injuries are similar to gunshot wounds.

TREATMENT OF HUNTING INJURIES Treatment of hunting injuries involves standard principles and priorities of trauma care. Airway, breathing, circulation, bleeding control, immobilization of the spine and fractured extremities, wound care, and stabilization of the victim for transport should be performed in an expedient manner. The victim should always be disarmed to prevent accidental injury to the rescuer or further injury to the victim. Removing the firearm or arrow from the vicinity of patient care is usually sufficient, but ideally the firearm should be made safe by removal of the ammunition and opening the firing chamber. Arrows should be placed in a quiver, or the points may be wrapped in cloth to prevent injury. Management of common traumatic injuries and illnesses, such as hypothermia and mountain sickness, is no different than normal except for one important point: always disarm the victim. A victim with a charged weapon and a head injury or change in mental status for any reason presents immediate danger to a well-meaning rescuer. If the person attempting to offer aid to an injured hunter is not familiar with weapons, it is usually best to move the weapon several feet from the victim and point it in a direction where accidental discharge will do the least harm. Arrow Injuries Lacerations from razor-sharp hunting points are not unusual and can be treated like any similar laceration. The wound should be irrigated, any foreign material removed, and the laceration closed primarily. Victims pierced by an arrow should be stabilized, and the arrow should be left in place during transport, if possible. Attempts to remove the arrow by pulling it out or pushing it through the wound may cause significantly more injury and should be avoided. It is acceptable to cut off the shaft of the arrow and leave 8 to 10 cm (3 to 4 inches) protruding from the wound to make transport easier if this can be accomplished with a minimum of arrow movement. A large pair of paramedic-type shears can usually cut through an arrow shaft if it is stabilized during cutting. The portion of the arrow that remains in the wound should be fixed with gauze pads or cloth and tape. A similar approach should be used for spears and knives. The victim should be transferred as quickly as possible to an operating room, where the arrow can be removed under controlled conditions. Radiographs are helpful to identify associated anatomic structures before removal is attempted in the operating room (Figure 24-18). Gunshot Wounds Myths About Gunshot Wounds.  Many myths associated with the management of gunshot wounds should be repudiated.

Emergency Department Care.  Emergency department care of the gunshot wound victim includes securing the airway, placing two intravenous lines in unaffected extremities, performing cardiac monitoring, and providing oxygen therapy. The patient with a neck wound and expanding hematoma should be endotracheally intubated as soon as possible. If endotracheal intubation is not possible, a needle cricothyrotomy followed by a surgical cricothyrotomy should be performed. Relief of tension pneumothorax with a needle or tube thoracostomy or occlusion of a sucking chest wound should be done immediately. Any external bleeding should be controlled by direct pressure. In a wilderness situation, a tourniquet may be necessary to control significant bleeding. A radiograph should be obtained of the involved area, and where there is a presumed entrance wound without an exit wound, multiple radiographic studies may be needed to find the location of the bullet. On rare occasion, bullets have been observed to embolize from the chest area via the aorta to the

FIGURE 24-18  Arrow wound to the left side of the neck near the mandible. The shape of the wound resembles the blades of the broadhead as shown in Figure 24-4.

483

CHAPTER 24  Hunting and Fishing Injuries

FIGURE 24-17  Spring traps must be set carefully to avoid injury to the person setting the trap.

Myth 1: The size or caliber of the bullet can be determined by the size of the wound. In truth, skin is quite elastic and has high tensile strength. Although a knife or arrow can cut the skin, a blunt bullet must crush the tissue by stretching. This stretching occurs until the bullet passes through and then retracts, causing the wound in the skin to be smaller than the caliber of the bullet. Myth 2: The size of the wound determines whether it is an exit or entrance wound. Actually, the bullet usually tumbles or yaws after striking the skin and soft tissue; if the bullet exits while still tumbling, the exit wound may be larger than the entrance. This commonly occurs when a missile strikes an arm or leg where the bullet is in midtumble at 90 degrees when exiting. Often the bullet fragments and only a small portion of the bullet exit, making the exit wound much smaller than the entrance. In addition, pieces of bone or tooth may exit, causing an odd-size wound. Myth 3: The path of the bullet can be determined by connecting the entrance and exit wounds. This myth may lead to inappropriate intervention in gunshot wounds. For example, a gunshot wound victim had two wounds about 15 cm (5.9 inches) apart on his upper thigh, and they were initially thought to be an entrance and exit wound. The patient developed abdominal pain, and on chest radiograph it was noted that there were two bullets in the left chest. Subsequent surgical intervention revealed injury to the colon, spleen, bowel, stomach, diaphragm, lungs, and subclavian vessels. So, what appeared to be entrance and exit wounds were actually two gunshot wounds sustained while the patient was lying supine. The outcome of most gunshot and blast wounds depends primarily on the body part that has been injured and secondarily on the environment in which the injury occurred and the quality and timeliness of medical intervention. Although knowing the type of weapon and the physics of ballistics and blast can help predict the extent of physical damage, there is no substitute for attention to detail when examining the patient.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

lower extremity arteries or to the heart via the vena cava. A type and crossmatch and basic trauma laboratory tests should be performed. Tetanus toxoid and immunoglobulin should be administered as indicated by the victim’s history. Broad-spectrum antibiotics should be administered to cover the wide range of pathogens associated with gunshot wounds, especially with complex wounds to the abdomen and extremities. The bacteriology of gunshot and blast injury wounds is quite complex. There are a number of environmental pathogens, including soil and water bacteria, such as Clostridium, Aeromonas, Staphylococcus, Streptococcus, Bacteroides, and Bacillus. These bacteria and associated bacteria on the victim’s clothing and skin account for the majority of infections in soft tissue. Wounds penetrating the abdomen increase the presence of Pseudomonas, Proteus, Escherichia coli, and other coliforms. Systemic antibiotics should be started as soon as possible and continued for at least 24 hours. Although there is no specific antibiotic that will cover all organisms, selection of antibiotic should be on the basis of probable type of infection. Cellulitis and necrotizing soft tissue infections can be treated with ceftriaxone plus metronid­azole plus gentamicin. Intra-abdominal infections can be treated with the same regimen or cefotetan, and ampicillin–sulbactam can be substituted for ceftriaxone, clindamycin for metronidazole, and ciprofloxacin for gentamicin. There is no substitute for drainage of abscesses and empyemas, excision of devitalized tissue, and removal of foreign debris. Topical antibiotics have not been shown to be useful. Surgical debridement and systemic antibiotics are the mainstays of prevention and treatment of wound infection. Victims in shock should be taken to the operating room immediately to control bleeding. If this is not possible, type O-negative or type-specific blood should be transfused. Autotransfusion, when available, can be an ideal way to replace lost blood in the victim in shock. Starch or other blood substitutes may raise the blood pressure temporarily, but large amounts of crystalloid fluids may cause increased bleeding. Hypotensive resuscitation, which allows the patient to remain relatively hypotensive as long as organ perfusion is adequate, may be the best intervention if an operating room is not readily available. A systolic blood pressure of 80 mm Hg may not be “normal,” but it may be sufficient for a supine patient. Increasing the blood pressure to 110 mm Hg may seem “normal,” but it may also cause rebleeding and irreversible shock. Hypotensive resuscitation should be the standard unless the patient loses his or her pulse or level of consciousness. At that time, blood products are the fluids of choice, followed by a starch such as hetastarch (Hextend). Level of consciousness and return of pulse should be the clinical goals. Once the bleeding is controlled, fluid resuscitation based on physiologic criteria, such as blood pressure, hematocrit, oxygenation, and acid-base status, can be used. Military antishock trousers or pneumatic antishock garments have not been shown to be beneficial in the treatment of shock secondary to penetrating trauma. Emergency thoracotomy is indicated for victims who have lost vital signs shortly before reaching the emergency department or while in the emergency department. Injuries to the heart or great vessels can be occluded with Foley catheter balloons, pericardial tamponade can be relieved, and the aorta can be cross-clamped. Hypothermia is commonly unrecognized in the trauma victim and may lead to coagulopathy, cardiac arrhythmias, or electrolyte disturbances. Rectal temperatures should be obtained and only warmed fluids and blood given to the victim.13,26,33,60 Wounds from high-velocity bullets are similar to other types of wounds, and standard rules of debridement should be followed. Wide debridement of normal-appearing tissue is unnecessary and should not be done. In general, victims of gunshot wounds should be evacuated quickly and stabilized if possible. Most victims (80%) of gunshot wounds to the chest who survive the first 30 minutes can be treated with a thoracostomy tube and observation.33 The amount of blood that is drained from the thoracostomy tube determines whether operative intervention is necessary. Draining more than 1500 mL of blood immediately or more than 200 mL/ hr for over 4 hours is an indication for thoracotomy. Signs of pericardial tamponade are an indication for immediate pericardiocentesis and operative repair. All gunshot wounds to the abdomen should be explored in the operating room. These include all penetrating injuries below the nipples and above the symphysis pubis. 484

Radiographs should be used to identify bullets, bullet fragments, and bony injuries. Extremity wounds can be treated conservatively unless signs of vascular injury are present. Signs of arterial injury include pulsatile bleeding, expanding hematoma, absent pulses, presence of a thrill or bruit, or an ischemic limb. Experience in combat has shown that vascular injuries do best when identified and treated immediately. However, life takes priority over limb, and a tourniquet may be needed to control vascular bleeding that may ultimately lead to loss of the limb. Obviously, major bony injuries and nerve injuries eventually need operative therapy, but immediate intervention is rarely necessary. Most important, the underlying injury cannot be determined by examination of the external wound. Vascular injuries may not be identified during the initial examination; therefore noninvasive, portable, Doppler ultrasound studies can be extremely valuable in the emergency department. Contrast angiography should be performed on any victim with a suspected vascular injury. The removal of the bullet or bullet fragment is not necessary unless the bullet is intravascular, intraarticular, or in contact with nervous tissue, such as the spinal cord or a peripheral nerve. Bullets found during exploratory laparotomy or wound debridement should be removed, but it is unnecessary to explore soft tissue, such as muscle or fat, solely to remove a bullet. Shotgun pellets that have minimal penetration can be removed from the skin with a forceps. Plastic or cloth wadding found in superficial shotgun wounds should be removed. Shotgun blasts may produce large soft tissue defects that need extensive debridement and either skin grafting or surgical flap rotation to maximize coverage. Patients with powder burns should have as much of the powder residue removed as possible with a brush under local anesthesia. The powder will tattoo the skin if it is not removed, and the deep burns may need dermabrasion or surgical debridement (Figure 24-19).13,60,61,63 Retained lead bullets and shotgun pellets for the most part are not hazardous; however, when they are within joint spaces or the gastrointestinal tract, significant amounts of lead can be absorbed and toxicity can occur. Infection of gunshot wounds is common, especially with large tissue injuries, injuries to the bowel and wounds that are highly contaminated with clothing or other debris. Despite myths to the contrary, bullets are not sterile. Certainly, clothing, skin, and other substances that the bullet may acquire during flight are not sterile.52

PREVENTION OF HUNTING INJURIES Most state fish and wildlife agencies have recognized that hunters are at risk for injuries and have tried to develop programs to minimize morbidity and mortality. National organizations such as the Boy Scouts of America and the National Rifle Association have been teaching firearm and hunting safety for decades. The Hunter Education Association and the IHEA have attempted to identify high-risk groups and situations by collecting data on both fatal and nonfatal hunting-related injuries. IHEA-approved hunter safety programs are available in every state, and all states except Alaska, Massachusetts, and South Carolina require the course before issuing a license to hunt. These courses are roughly 12 hours long and cover hunter responsibility, firearms and ammunition, bow hunting, personal safety, game care, and wildlife identification. They stress respect for the wilderness and a rational approach to game management. All hunters, potential hunters, and persons going into hunting areas should take one of these courses. Approximately 650,000 hunters complete a hunter safety course annually. Since the first course given in Kentucky in 1946, more than 18 million hunters have been certified. Most injuries could probably be prevented by following a few simple rules. Nonhunters should be aware of hunting seasons and designated hunting areas and wear international orange clothing while in hunting areas (Figure 24-20). Hunters should always be sure of their target before shooting, use safety harnesses in tree stands, and use appropriate technique and tools for cleaning game. Tree stands should be well constructed. Hunters should never consume alcohol or mind-altering drugs that might interfere with their judgment. Eye protection in the form of safety glasses should be worn while hunting or target shooting to prevent injuries from ricocheting fragments and

A

Fishing Injuries

B FIGURE 24-19  A, Close-range 12-gauge shotgun wound to the right side of the upper chest. The large central wound was caused by the plastic wadding, and the pellets have struck at an angle toward the shoulder. The patient was turning to the right when shot. The external appearance of the wound indicates a massive injury to the chest.  B, Chest radiograph of the patient in A. No pellets have penetrated the chest, and there was no pneumothorax, pulmonary contusion, or vascular injury. The injury was totally superficial, and the patient was admitted for observation and local wound care.

FIGURE 24-20  Hunter wearing bright orange clothing, which is essential to distinguish a human from the background and avoid an accidental shooting. Many accidental shootings have occurred when one hunter’s movement was mistaken by another hunter for the movement of an animal.

Sport fishing is associated with a large number of relatively minor injuries compared with hunting. The usual problems associated with outdoor recreation are common among fishermen: sunburn, frostbite, hypothermia, near drowning, sprains, fractures, motion sickness, and heat illness. Lacerations are relatively more common because of the use of knives to cut bait and fishing lines and to clean fish. These lacerations are often contaminated with a variety of marine and freshwater pathogens that may increase the incidence of wound infection. Thorough debridement of the wound and copious irrigation with sterile saline solution are the best initial methods to prevent infection. If sterile saline in not available, then the cleanest water available should be used. Chlorhexidine scrub incorporated into a brush makes an excellent wilderness cleansing device.

FISHHOOK INJURIES Fishhooks are designed to penetrate the skin of fish easily and to hold fast while the fish is played and landed. To perform this dual role, they are extremely sharp at the tip, have a barb just proximal to the tip, and are curved so that the more force applied to the hook, the deeper it penetrates. Fishhooks may be single or in clusters of two, three, or four to increase the chance of catching the fish. Some state fishing laws limit the number of hooks allowed on a single line when fishing for certain game fish, to make fishing more sporting. The greater the number of hooks on a lure or line, the greater the chance of catching a fisherman. The most common fishhook punctures occur when fish are removed from hooks. The combination of sharp hook, slippery fish, and inexperienced fisherman leads to puncture wounds or embedded fishhooks. Many fishermen use commercial fishhook removers or large Kelly forceps to remove hooks. Some fishing guides simply cut the hook with a side-cutting pliers; they believe the remaining segment of hook will eventually oxidize in the fish and disintegrate. Often, a fishhook is stepped on with a bare foot or a fisherman catches himself or another person on the backcast. Fishhooks can penetrate skin, muscle, and bone, and they may pierce the eye or the penis. Care must be taken in removing a fishhook so that further damage to underlying structures is avoided. The first step is to remove the portion of the hook that is embedded from any attached lines, fish, bait, or lure. This is best done with a sharp side-cutting pliers. A bolt cutter may be needed for large, hardened hooks such as used in shark or swordfish fishing. Treble hooks, with three separate hooks attached at a single eye, are designed to improve the chance of catching a fish going after a live or artificial bait (Figure 24-21). They are also used in “snagging” fish, in which the line with one or more treble hooks is pulled through the water in an attempt to snag a fish on any part of its body. They may be found on many types of fishing lures, some with three or more treble hooks on a single lure (Figure 24-22, online). When this type of hook is embedded, often more than one of the hooks is involved. Cutting the embedded hooks off the lure or the treble hook will prevent further injury before removal. Most fishermen carry a multitool or needle-nose pliers for removing hooks and lures from fish. These same tools can be used in the field to remove or stabilize embedded hooks. 485

CHAPTER 24  Hunting and Fishing Injuries

shotgun pellets. High-frequency hearing loss is common in hunters because of the loud report of the firearm. Although earplugs and headsets can protect the hunter, they are impractical for most hunting and are used mainly for target shooting. Some hunters use a single ear plug for the ear closest to the muzzle of the firearm. This protects the ear most likely to be injured but still allows the hunter to hear approaching game and other hunters. Bow hunters should always use wrist and finger protection to prevent injuries from the arrow fletching and the bowstring. All arrows should be carried in a quiver until ready for use. The broadhead arrow should always be pointed away from the hunter. These few steps would probably eliminate most hunting injuries.45,47

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 24-21  Typical treble hook attached to a fishing lure.

A number of techniques are used for removing embedded fishhooks, but all involve a certain amount of movement of the hook, which causes increased pain. A local anesthetic should be infiltrated around the puncture site to minimize pain and movement of the patient. The following method can be used if the hook is not deeply embedded (Figure 24-23, E ). Pressure is applied along the curve of the hook while the hook is pulled with a snapping motion away from the point. Because the barb is on the inside of the curve of the hook, this enlarges the entrance hole enough to allow the barb and point to pass through. Sometimes a string looped through the curve of the hook facilitates the process. If the hook is deeply embedded, pressure can be applied along the curve of the hook to advance it further into the tissue until the point and barb penetrate the skin at another place on the surface, and then the barb can be cut off and the remainder (shaft) of the hook backed out (Figure 24-23, A to D). Most fishhook injuries are not significant. However, penetrating eye injuries can lead to loss of vision in one or both eyes. These type of injuries can occur when the angler has snagged the fishing lure on a rock or other object and in order to attempt to free the lure, gives a pull that displaces the lure and strikes the angler in the eye. This can also occur when attempting to land a fish, when the lure pulls out of the fish’s mouth and strikes the angler in the eye. Many anglers also hook other anglers stationed behind them in a boat or on shore with their backcast. Fishhooks embedded in the eye should be left in place; the eye covered with a noncompressing metal patch, goggles, glasses, or cup; and the victim referred to an ophthalmologist for further care. Local anesthetic can be used to anesthetize the eye before applying the protection. If possible, the body of the fishing lure should be separated from the hook if it can be done without causing further harm. A wire cutter or multipurpose tool can be used for this (Figure 24-24). A plastic cup can be cut to size, or safety glasses or goggles can be used as an expedient eye shield. A pressure patch should not be applied, because this may lead to more serous injury. The cup, glasses, or goggles should be taped in place to prevent the victim from touching the eye and to prevent displacement during evacuation. It is not necessary to patch both eyes (Figures 24-25

A

B

D

to 24-27). All persons with penetrating eye injuries should be given oral antibiotics as soon as possible to prevent visionthreatening endophthalmitis. Rarely hooks become embedded in bone or cartilage; this victim must be taken to the operating room to have the hook removed via a surgical incision.

FISHING SPEAR INJURIES Fishing spears, like fishhooks, are designed to penetrate and hold fish. They may be jabbed, thrown, or propelled by rubber straps or carbon dioxide cartridges. The more force used to propel the spear, the deeper the penetration into tissue. Although arrows are designed to cause bleeding and bullets to cause crushing, fishing spears are designed to hold the fish until it drowns or is otherwise

FIGURE 24-25  Improvised eye shield using a plastic cup cut to fit over the eye without touching it.

C

E

FIGURE 24-23  A to D, Removal of a fishhook that has deeply penetrated a fingertip. E, “Press-and-yank” method of fishhook removal.

486

FIGURE 24-24  Cutting off the body of a fishing lure before applying an eye shield.

FIGURE 24-26  Improvised eye shield using a pair of glasses.

CHAPTER 24  Hunting and Fishing Injuries

A FIGURE 24-27  Improvised eye shield using a pair of goggles.

dispatched. Spears may penetrate the human chest or abdominal cavity, skull, or any other anatomic area. Some bleeding may occur, especially if major blood vessels are struck. The victim should be removed from the water as soon as possible and immediate attention given to airway, breathing, and bleeding control. The spear should be stabilized in place, and the victim immediately transported to a medical facility. Penetrating neck and chest injuries may require endotracheal intubation and tube thoracostomy. If a spear is embedded in the victim’s cheek and interferes with his or her airway, cutting the spear off with a bolt cutter and removing it through the mouth is permitted. Spears in all other locations should be left in place, although they may be cut off to facilitate transportation or improve the victim’s comfort (Figure 24-28).41

OTHER FISHING INJURIES Although spears and hooks cause the majority of penetrating injuries, fishing weights or sinkers can also be hazardous. Fishing sinkers are usually composed of lead and range in size from a few grams to 85 to 113 g (3 to 4 oz). When propelled by the action of a rod, they may act as projectiles with quite a bit of kinetic energy. Ancient hunters and warriors used lead and stone projectiles propelled by slings to hunt game or in battle to inflict serious injuries. The energy stored in a 2.1-m (7-foot) fiberglass fishing rod is potentially more than that delivered by a standard sling, so it is not surprising that an injury such as the one shown in Figure 24-29 is possible.

B FIGURE 24-28  A, Male patient with a multipronged fishing spear through the foot. He said he saw something move, and he speared it. B, Same patient with the spear being cut off in the emergency department with a bolt cutter. The patient was taken to the operating room to have the remainder of the spear removed.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

FIGURE 24-29  Intracranial fishing line sinker, A, Eye sinker wound. B, Skull sinker radiograph. (From Seitelman E, Premo J, Cardoza S, et al: Young man with fishing injury: Intracranial fishing line sinker, Ann Emerg Med 54:854, 2009.)

A

B 487

CHAPTER 25 

Tactical Medicine* LAWRENCE E. HEISKELL, BOHDAN T. OLESNICKY, AND SYDNEY J. VAIL

Tactical medicine can be defined as both emergency and nonemergency care provided to victims of illness or injury related to law enforcement or military operations, often in a hostile environment.54 Tactical medicine in the early years was often referred to as tactical emergency medical support (TEMS). The emergency medical services (EMS) and prehospital community called it tactical EMS, and the U.S. military coined the phrase combat casualty care. Numerous law enforcement agencies now have tactical medical teams composed of physicians and prehospital care providers. Because many law enforcement agencies throughout the United States and branches of the U.S. military have embraced this concept, it is now commonly known as tactical medicine. Before 2001 there was a perception of professional separation between physicians in traditional medical practice and the tactical medicine physicians involved in law enforcement. This was probably related to what might be seen as competing priorities for physicians when dealing with sick or injured patients who are suspects in a law enforcement investigation. No other subspecialty in emergency medicine has experienced the growth rate of tactical medicine. In the past 20 years, more than 200 publications addressing tactical medicine issues have been written. Tactical medicine educational programs have trained thousands of emergency medical technicians (EMTs), paramedics, and physicians, who have responded to the call to provide on-scene emergency medical care to members of the law enforcement community or active duty military50 (Figure 25-1). Tactical medicine is very similar for both military and civilian tactical providers. Techniques, strategies, protocols, and equipment are all virtually identical, with few differences. The military tactical medical provider must deal with long deployment times, therefore incurring a significant preventive medicine requirement. Although routine medical care and performance enhancement (e.g., conditioning, nutrition, and rest) are important for both civilian and military tactical teams, they take on a longerterm function for the military tactical medicine provider. A civilian tactical operation typically takes hours to days. (The Waco and Ruby Ridge incidents were exceptions, more in concert with a military-style length of engagement.) A typical tactical military operation may take days to months, and other aspects—such as disease and nonbattle injury—have become as important as the tactical medical care (Table 25-1). Tactical medicine has been a mainstay of military operations since the beginning of modern warfare. The hospital corpsman, or combat medic, was deployed on the front lines with the warriors to provide basic medical care. This care was often provided under fire, sometimes in the harsh environments of the jungle, desert, ocean, high mountains, and other austere conditions. As the science of medicine improved, the need to deliver higher levels of care further toward the forward edge of the battle area was recognized. During Operation Iraqi Freedom, shock trauma platoons, composed of emergency physicians and support staff, were sent to the front lines to provide advanced resuscitative support. These units could be fully operational and caring for patients in less than 30 minutes. Mobile surgical teams and forward resuscitative surgical teams developed the technology to put trauma surgical teams within minutes of the location of a combat casualty. These teams have evolved to become fully mobile and able to set up or dismantle in 30 minutes, use tent *See also Chapter 26.

488

shelters or shelters of opportunity within which to perform operations, and provide lifesaving damage-control surgery to multiple patients under the extreme conditions of modern warfare. During civilian law enforcement tactical operations, the tactical medic can be deployed within seconds to care for an injured officer (Figure 25-2). Tactical medics are trained to resuscitate, treat, and transport patients in extreme hot or cold temperatures, over rough terrain and hostile territory, while protecting the patient from further injury. The capabilities are such that a critical patient can be pharmacologically paralyzed and intubated, while wounds are still open and attempts are made to prevent the hypothermia, dehydration, and coagulopathy inherent in postsurgical patients (Figure 25-3). Tactical medicine has advanced to anticipate and react to changes in combat strategy, which translates directly to law enforcement. For instance, during Operation Iraqi Freedom, the most serious injury patterns were primarily high-velocity penetrating wounds—that is, mostly gunshot wounds (Figure 25-4 and Table 25-2).29 As the war against terrorism has progressed, the weapon of choice of the insurgents has become the improvised explosive device (IED).77 This weapon produces significantly more trauma, including shrapnel, blast, and thermal injuries. It has also required a change in protective body armor because the injury patterns have changed to include more devastating extremity and head-and-neck wounds than torso wounds (Figure 25-5).28 The IED has also continued to cause problems with torso injuries, because the blast patterns cause shrapnel to angle up under traditional body armor and through arm openings. This has promoted development of armor that better helps protect these areas. Suspects may also sustain penetrating injuries during tactical operations (Figure 25-6). The terrorist attacks of September 11, 2001, and events such as the 1999 Columbine High School shootings, heightened our nation’s awareness of the real threats of terrorism and violence on U.S. soil and diminished some of the resistance to medical providers being actively and closely involved in law enforcement special operations. Today, hundreds of fire and EMS agencies provide tactical emergency medical support to federal, state, and local law enforcement special operations teams. Law enforcement special operations, often referred to as SWAT (special weapons and tactics) teams, are intended to deal with a wide range of high-risk criminal problems and threats.67 These include, but are not limited to, hostage rescues, terrorist acts, barricaded suspects, violent and suicidal suspects, take-over bank robberies, high-risk warrant services, and active shooter situations. Tactical medics must train and prepare for these types of difficult situations17,43,44 (Figure 25-7, A). Patient advocacy, with priorities of ensuring the best possible quality of care and patient confidentiality, can be at crosspurposes with a law enforcement officer trying to gather important facts in an investigation to ensure public safety and justice. Tactical medicine providers must respect both patient rights and mission goals. Medics during tactical operations must have a constant awareness of evidence preservation while operating in the tactical environment (Figure 25-7, B). SWAT teams are found in most midsize and larger law enforcement departments throughout the United States. In some areas, a number of small departments have banded together to form multijurisdictional or regional SWAT teams.15 Harsh environ­ mental conditions, including what many regard as wilderness

CHAPTER 25  Tactical Medicine

FIGURE 25-1  Police tactical medic administers intravenous fluids to a downed officer. (Courtesy International School of Tactical Medicine.)

FIGURE 25-2  Forward resuscitative surgical team tactical medics evaluate an injured tactical team member. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

FIGURE 25-4  A high-velocity gunshot wound to the left arm. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.) FIGURE 25-3  Injured tactical officer being extracted from the hot zone. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.) TABLE 25-1  Nonbattle Conditions Encountered by

TABLE 25-2  Battle Conditions Encountered by

Primary ICD-9 Disease Category

Mechanism of Injury

n

% of Total

Gunshot wound Shrapnel/fragmentation RPG (handheld antitank grenade-launcher)/ grenade Motor vehicle accident Fall Explosion Unknown/not recorded Land mine Mechanical/machinery Blast Other Multiple (NOS [not otherwise specified]) Blunt Debris Total

76 65 39

24.1 20.6 12.4

28 17 16 16 14 13 11 10 4 3 3 315

8.9 5.4 5.1 5.1 4.4 4.1 3.5 3.2 1.3 1.0 1.0 100.0

Tactical Medical Personnel (Spring 2003)*

Digestive Symptoms ill defined Mental disorders Musculoskeletal Genitourinary Nervous system sense organs Skin Supplemental Infectious and parasitic Circulatory Endocrine, nutritional Neoplasms Respiratory Pregnancy Congenital Total

n

% of Total

44 38 29 29 21 17 15 15 10 10 8 6 5 3 3 253

17.4 15.0 11.5 11.5 8.3 6.7 5.9 5.9 4.0 4.0 3.2 2.4 2.0 1.2 1.2 100.0

ICD, International Classification of Diseases. *Navy/Marines Operation Iraqi Freedom from March 21 to May 15, 2003.

Tactical Medical Personnel (Spring 2003)*

*Navy/Marines Operation Iraqi Freedom from March 21 to May 15, 2003; wounded in action.

489

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Naval Health Research Center Sponsored by The Office of Naval Research Marine Corps Systems Command and Marine Corps Warfighting Lab

Anatomical Location of Injury US Navy, Marine Corps and Army - WIA only Sample from April - February 2005

Total patients 610 / Total injuries 1088

Neck

01 Jun 05

Head

Eye

Injuries 110 Percent of patients 18.0%

Injuries 46 Percent of patients 7.5%

Ear Injuries 60 Percent of patients 9.8%

Injuries 52 Percent of patients 8.5%

Face

Chest

Injuries 103 Percent of patients 16.9%

Injuries 56 Percent of patients 9.2%

Back Injuries 36 Percent of patients 5.9%

Upper extremity Injuries 270 Percent of patients 44.3%

Abdomen Injuries 41 Percent of patients 6.7%

Buttock Injuries 18 Percent of patients 3.0%

Pelvis Injuries 23 Percent of patients 3.8%

Lower extremity Injuries 267 Percent of patients 43.8%

Genitalia

Percentage of patients by anatomical location

Injuries 6 Percent of patients 1.0%

Upper extremity Lower extremity Head Face Ear Neck Chest

44.3% 43.8% 18.0% 16.9% 9.8% 8.5% 9.2%

Eye Abdomen Back Pelvis Buttock Genitalia

7.5% 6.7% 5.9% 3.8% 3.0% 1.0%

FIGURE 25-5  Anatomic location of injury (wounded in action [WIA] only). (Courtesy Naval Health Research Center.)

situations, will increasingly provide a backdrop for incidents requiring tactical efforts and the ongoing need for field medical support. Regardless of the scale of the program, tactical medicine has grown into a multifaceted specialty.

History of Tactical Medicine Much of the training and tactics of civilian SWAT teams is based on the experience of military special operations teams. Such military teams have their origins in the U.S. Office of Strategic Services and the British Special Air Service during World War II. Some of the earliest military special operations teams incorporated tactical medical components. German Fallschirmjäger (paratroopers) incorporated a wellorganized medical support team with physicians. Dr. Heinrich Neumann jumped with the unit during the invasion of the island of Crete in 1942.36 During the Normandy invasion of June 6, 1944, at Pegasus Bridge on the Orne River, the British, led by Major R. J. Howard, landed with medical support, accompanied by a

A

B FIGURE 25-6  Suspect sustained a self-inflicted gunshot wound to the chest moments before a dynamic entry. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

490

FIGURE 25-7  A, Tactical medics train for active shooter situations. B, Preservation of evidence is a critical component of tactical medicine. (Courtesy International School of Tactical Medicine.)

25% KIA – Surgically uncorrectable torso trauma

10% KIA – Surgically correctable torso injury 9% KIA – Exanguination from extremity wounds

31% KIA – CNS injury

12% DOW – Largely from infections and complications of shock 5% KIA – Tension pneumothorax

A

7% KIA – Blast mutilating trauma

1% KIA – Airway obstruction

B FIGURE 25-8  A, How people die in ground combat. CNS, Central nervous system; DOW, died of wounds; KIA, killed in action. B, Tactical medics establish an airway during a training exercise. (Courtesy International School of Tactical Medicine; A courtesy Colonel Ron Bellamy; B courtesy Lawrence E. Heiskell, MD.)

regular civilian EMS providers staged at a safe location removed from the area of operation, or they simply dialed 9-1-1. Although this took advantage of an established prehospital care system, care for injured officers could be significantly delayed.98 Other agencies trained full-time SWAT officers as EMTs or paramedics. This concept of getting medical care “close to the fight” was also realized in the Gulf War, and the military put this new concept in place during Operation Iraqi Freedom. Information obtained from interviews with military emergency physicians who served in Iraq has suggested success of the new model of battlefield care.

Shared Principles of Military Tactical Combat Casualty Care and Civilian Tactical Medicine Tactical combat casualty care (TCCC) varies from ATLS in several distinct ways, primarily because in a TCCC situation, the victim and medical provider are not in a safe environment. In addition, medical care of the victim may not be the highest priority, and the team may be operating in the open under extreme environmental conditions, hours from higher levels of care. The premise of TCCC is to do the right things at the right times. Underlying this basic statement is the suggestion that good 491

CHAPTER 25  Tactical Medicine

physician, Captain J. Vaughan of the Royal Army Medical Corps.2 The U.S. Armed Forces during World War II also incorporated physicians in their assault on fortressed Europe. Dr. Robert Franco and Dr. Daniel B. McIlvoy both parachuted into Sicily with the 82nd Airborne Division in April 1943 and jumped into Normandy in June 1944.25 During the 1950s, the Army Special Forces (77th Special Forces Group) was formed. As U.S. Special Operations teams evolved, other specialized teams, such as DELTA, America’s elite counter-terrorist force, were formed.35 Each of these special operations units has a plan for tactical medical support. The growth of terrorism in the 1970s resulted in the formation of other special operations groups worldwide. The Germans established a special unit within their border police, later presented to the world as the GSG9 (Grenzschutzgruppe-9).96 This unit emerged after the 1972 tragedy at the Olympic Village in Munich, Germany. The French formed the Groupe d’Intervention de la Gendarmerie Nationale in 1974, and many other countries have since developed similar units. Medical providers in the combat environment were traditionally taught to perform with the principles of the traditional hospital-based Advanced Trauma Life Support (ATLS). Although this training was instrumental in decreasing morbidity and mortality of trauma victims in the noncombat scenario, it fell short of providing appropriate care for the patient and the combatant team members on the field of battle. Numerous reviews of past and recent conflicts have noted inadequacies of this approach to battlefield medical care.6,8,14,99 Ninety percent of battle deaths occur in the field, before any medical intervention. Bellamy did a landmark review of wounds and death in battle.7,71 In this study,7 he noted that 31% of battlefield deaths resulted from penetrating head injury, 25% from surgically uncorrectable torso trauma, 10% from potentially correctable torso trauma, 9% from exsanguinating extremity wounds, 7% from mutilating blast trauma, 5% from tension pneumothorax, 1% from airway obstruction, and 12% from various wounds (sepsis and shock off the battlefield) (Figure 25-8). Potentially preventable battlefield causes of deaths include bleeding to death from extremity wounds, tension pneumothorax, and airway obstruction.53 These statistics have proved true in today’s conflicts in the global war on terrorism and in most tactical medical scenarios. They gave rise to questions about the pure application of the basic advanced life support precepts of airway, breathing, and circulation (ABC) for battlefield and tactical situations. In 1993, led by the Naval Special Warfare Command, a multiagency working group (Committee on Tactical Combat Casualty Care), including special operations physicians, medics, corpsmen, and operators, began a 2-year study of this issue. This led to the guidelines titled Tactical Combat Casualty Care in Special Operations.14 The committee meets regularly and reviews new equipment, practices, and current operations for lessons learned and then revises the guidelines as appropriate. These guidelines, which evolved from the special operations community, are currently being evaluated and implemented in most combatant units of the U.S. military and of many other countries.13 The need for civilian SWAT teams in the United States evolved from high-profile criminal acts that resulted in shocking losses of human life. The seminal incident involved a sniper at the University of Texas at Austin. On August 1, 1966, Charles Whitman shot and killed 16 people and wounded 31 others.68 In the midst of this tragedy, it became apparent that the law enforcement agencies called out were ill equipped to deal with the threat, hampered by inadequate weaponry and not trained to respond in a timely and optimal fashion. After this incident, many law enforcement agencies began developing specially trained and equipped tactical units to respond rapidly to such threats to public safety.30 The Los Angeles Police Department and the Los Angeles County Sheriff’s Department were among the first law enforcement agencies in the United States to organize and develop full-time tactical units specifically trained to handle highrisk incidents. Before 1989, there existed great diversity in the ways emergency medical care was provided during law enforcement tactical operations. Early on, most law enforcement agencies relied on

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 25-9  CATSSOF (combat application tourniquet system). (Courtesy International School of Tactical Medicine and Tactical Medical Solutions, Inc, Lawrence E. Heiskell, MD.)

hospital-based medicine is often not good battlefield medicine,13 as logically follows from these three statements: 1. Good medicine can be bad tactics. 2. Bad tactics can get everyone killed. 3. Bad tactics can cause the mission to fail. The ultimate goals of TCCC are the following: 1. Treat the casualty. 2. Prevent additional casualties. 3. Complete the mission. TCCC is divided into three main stages of care:13 care under fire, tactical field care, and combat casualty evacuation care. These are defined in the following paragraphs.

CARE UNDER FIRE Sometimes care is rendered by the medic or corpsman at the scene of the injury while still under effective hostile fire. Medical equipment is limited to what the individual operator or the corpsman or medic can carry in the medical pack. The most effective medical care during this stage of TCCC is fire superiority—that is, winning the battle, or at least keeping enemy heads down and reducing hostile incoming fire. The medical provider (and the casualty if able) must work to suppress hostile fire and eliminate the threat as directed by the mission commander, and, if possible, to protect the injured fighter from further harm. For many reasons, this is undoubtedly the most difficult phase of TCCC. First, the traditional provider, trained to be a “medic first,” may find it hard to direct attention to the threat and not maneuver to respond to the casualty. Second, this phase usually occurs in the most exposed environment, where the provider cannot use normal assessment tools. For example, during nighttime the provider cannot use a light, because it could draw fire, and listening for lung sounds with a stethoscope in an explosionrocked firefight is useless. In earlier conflicts, it was noted that many medics and corpsmen who responded to casualties, instead of suppressing gunfire were wounded or killed, and that a significant number of the victims that they were trying to rescue

FIGURE 25-10  Mechanical advantage tourniquet. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

492

FIGURE 25-11  Chitosan QuikClot Combat Gauze Vacuum Packed and Z-Folded hemostatic dressing. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

were already dead. The priorities for the provider during this phase of care therefore are as follows:13 1. Return fire as directed or required. 2. Try to keep yourself from getting shot. 3. Try to keep the casualty from sustaining additional wounds. 4. Stop any life-threatening external hemorrhage with a tourniquet. 5. Take the casualty with you when you leave. Airway and breathing problems are not addressed during this phase. The key action is to stop exsanguinating hemorrhage. A tourniquet is the primary means to stop the bleeding on an extremity (Figures 25-9 to 25-12). The tourniquet can be applied and left in place by the injured operator or medic, who can then return fire in support of the team. If a tourniquet cannot be placed because of the location of the wound, then direct pressure and a hemostatic dressing are recommended as the appropriate actions. As soon as possible, the casualty is moved to a safer location, and the next phase of TCCC is instituted. This movement is performed with techniques dictated by the tactical situation. It can be done by, for example, vehicles, buddy lifts, or dragging. Another departure from traditional ATLS teaching is that cervical spine protection is not routinely provided in this phase of care. Studies of penetrating neck injuries in Vietnam demonstrated that only 1.4% of patients with penetrating injuries would have benefited from cervical spine immobilization.4 Although not all combat-related injuries are penetrating, the complexities of moving a patient in an environment where the patient and

FIGURE 25-12  Emergency bandage. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

TACTICAL FIELD CARE The tactical field care phase consists of care rendered once the medic and the casualty are no longer under effective hostile fire. It also applies to situations in which an injury has occurred on a mission but there has been no hostile fire. Available medical equipment is still limited to that carried into the field by mission personnel. Time before evacuation to a medical treatment facility may vary considerably. In this phase, the medic has a short time to evaluate and treat the wounded. The medic assesses injuries, performs medical care as able (equipment still limited to what was carried onto the battlefield), and then informs the mission commander of the findings. The mission commander then determines what action will be taken (evacuate, abort, continue). This again may be a major departure from nontactical medical care, in that the medical provider is not the ultimate authority on patient disposition. The mission commander decides how much time is taken to care for the casualty in any phase of the operation, if and when medevac will occur, and what assets will be allocated from the primary mission toward care of the injured. Step 1: During this phase, the provider must assume not only that hostile fire may occur at any time but also that any injured team member with altered mental status may become a threat. The provider must therefore disarm the team member, an action that most warriors resist. Step 2: Address airway compromise. Airway actions are usually rendered as follows: if the victim is unconscious without obstruction, use a nasopharyngeal airway (better tolerated and less likely to become dislodged with movement)1 and a rescue position if able. If airway obstruction is present and cannot be alleviated with these maneuvers, the next recommended treatment is to move directly to a surgical cricothyrotomy. Endotracheal intubation is not recommended at this level of care for several reasons: (1) It requires the medic to carry onto the battlefield equipment that has no other purpose; (2) the medic must practice regularly to maintain his or her skills; (3) success rates under austere conditions are believed to be significantly less than those done in a controlled or semicontrolled setting; and (4) the laryngoscope light may compromise team safety on the field.81,93,94 Emergency cricothyrotomy is the best option in this phase of TCCC. Because of distorted anatomy, it is the best way to protect the airway of a patient with maxillofacial wounds. Blood and tissue in the airway preclude visualization of the cords and make endotracheal intubation difficult or impossible.13,89 Step 3: Treat breathing difficulties. Any severe progressive respiratory distress is assumed to be due to a tension pneumothorax (the number-two cause of preventable battlefield deaths). One cannot wait for the classic signs (which are unreliable at best and most often impossible to ascertain on the battlefield) of diminished breath sounds, hyperresonance, and tracheal deviation to make this diagnosis.74 Therefore, faced with victims in increasing respiratory distress and with unilateral penetrating chest trauma, the medic will go directly to a needle thoracostomy. This is the definitive procedure in this phase. A chest tube is not usually needed, it is difficult to perform on the battlefield, and it would only further complicate patient care, transportation, and mission completion.13 Step 4: Readdress bleeding. The medic rapidly locates uncontrolled hemorrhage and any wounds where a tourniquet has been placed. If possible, a hemostatic dressing is placed; the tourniquet may be discontinued if the wound and tactical scenario permit. Even if the bleeding appears controlled, further “rough” evacuation may necessitate keeping a tourniquet in place to prevent rebleeding. Each action that the medic takes is designed to save life with minimal further care by the medic. For example, a medic who is holding pressure on a bleeding wound cannot return fire, take care of other casualties, or perform other procedures on this

patient. The patient is not optimally prepared for transportation, which may consist of being thrown over someone’s back and carried out. Thus a tourniquet that would be a last-ditch effort in a noncombat environment becomes the method of choice in the tactical combat situation. Each operator in the field carries, and knows how to use, at least one tourniquet that can be self-applied. This allows the operator to self-administer lifesaving bleeding control and then continue with the fight until treatment by the medic is possible. Step 5: The medic should determine whether an intravenous (IV) line or a saline lock is beneficial. The advantages would be that the patient could receive fluid resuscitation and IV antibiotics. Disadvantages include a probable delay in transportation, the additional equipment required (and the bulky apparatus that could become dislodged or tangled during evacuation), and difficulty in placing a line under austere tactical conditions. If an IV is deemed necessary but cannot be expeditiously placed, the intraosseous route is used. Several devices can be used to achieve this, including largebore hypodermic needles, traditional intraosseous needles, and devices such as the FAST1 Intraosseous Infusion System and BIG (Bone Injection Gun), which quickly and accurately place the needle in the sternum or in another appropriate location. Step 6: Determine whether fluid resuscitation is required. In general, if the patient is not in shock (the best indicators of shock in the field are altered mental status in the absence of head injury, and weak or absent pulses), then no IV fluids are necessary. If the patient is conscious, oral rehydration is permissible and preferred in many tactical scenarios. If the patient is in shock, the medic can give Hextend65 as a 500-mL bolus and reassess after 30 minutes. If the victim is still in shock, the Hextend is repeated once. Usually no more than 1000 mL of Hextend is given, and further efforts at resuscitation are determined by the tactical scenario. If the patient has a traumatic brain injury and is unconscious and pulseless, fluid resuscitation is given to restore the pulse. This protocol maximizes survivability of the patient and limits the amount of equipment necessary to be carried onto the battlefield. Step 7: Inspect and dress known wounds. The medic locates and appropriately treats wounds already identified but not yet treated because of tactical considerations and then proceeds with a quick but thorough head-to-toe assessment for additional wounds. This is analogous to the secondary survey of ATLS, with a couple of notable exceptions. First, the patient is not exposed. This is because the patient may have to be moved quickly if the tactical situation changes and because the patient must be kept warm and protected from further injury for a much longer time than in an urban setting. The medic often does this examination by feel to avoid using white light, to keep the victim’s body armor as intact as possible, and to avoid cutting off protective clothing that may be required during evacuation. Step 8: Assess for pain control. Analgesia is administered in this phase of care with the following considerations. If the victim is able to fight, non-narcotic preparations are used. These do not affect mental status, allowing the victim to remain armed and responsive. If the victim is unable to fight, morphine and promethazine, IV or intramuscular (IM), are given as needed. Step 9: If not already done, fractures are splinted and neurovascular status is rechecked. Step 10: Consider early administration of antibiotics for open combat wounds, which significantly reduces the rate of infection.11 Oral medication is preferred if the patient is conscious. Gatifloxacin has been shown to be highly effective with minimal risks. Gatifloxacin is a broad-spectrum fluoroquinolone that is active against gram-positive and gram-negative microbes, aerobes, anaerobes, and freshwater and saltwater pathogens; is a once-a-day drug; and has a long shelf life. If the victim is unable to take oral medication or has significant abdominal trauma, IV/IM antibiotics are used, with cefotetan being the current drug of choice. 493

CHAPTER 25  Tactical Medicine

provider are under fire often preclude even rudimentary cervical spine immobilization.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

In many units, the operators are given a “wound pack,” consisting of an antiinflammatory, acetaminophen, and gatifloxacin, and instructed to take the entire pack as soon as possible after being wounded. Step 11: Continue to communicate with the victim, giving encouragement, explaining the care given, and giving updates on the tactical scenario if appropriate. Traumatic cardiac arrest is treated on the battlefield just as it is in the civilian setting. If the victim is pulseless, apneic, and has no sign of life, resuscitation is not attempted. After these measures have been taken, or if medical evacuation is now available, the last phase of TCCC, combat casualty evacuation care, is entered.

COMBAT CASUALTY EVACUATION CARE This phase of care is rendered once the casualty (and usually the rest of the mission personnel) has been picked up by an aircraft, land vehicle, or boat. Additional medical personnel and equipment that have been prestaged in these assets should be available at this stage of casualty management. The management plan aligns closely with that of the tactical field care phase, with the addition of more equipment and perhaps higher levels of medical providers. This phase is also the phase most similar to ATLS, although it may occur in the back of a moving conveyance and is still somewhat limited by available equipment and the tactical scenario. The basic medical plan for combat casualty evacuation care is as follows: 1. Airway management: Same as for tactical field care, with the addition of laryngeal mask airway/Combitube/endotracheal intubation for definitive airway management before cricothyrotomy if the operators are trained and the patient can be endotracheally intubated (e.g., has no midface injuries). Spinal immobilization is still not deemed necessary for casualties with penetrating trauma for the reasons stated earlier. 2. Breathing: Same initial considerations as for tactical field care. A chest tube can be placed if needle thoracostomy has produced no improvement in breathing, or if long transport is anticipated. Most combat casualties do not require oxygen, but its administration may be of benefit in the following situations: low oxygen saturation by pulse oximetry, injuries associated with impaired oxygenation, unconscious patient, and traumatic brain injury (to maintain oxygen saturation >90%). Sucking chest wounds should be treated with petroleum gauze applied during expiration, covering it with tape or a field dressing, placing the victim in the sitting position, and monitoring for development of a tension pneumothorax. Asherman seals are also ideal for quickly securing chest tubes and for sucking chest wounds. 3. Bleeding: Same as for tactical field care. 4. IV line: Same as for tactical field care. 5. Fluid resuscitation: Same as for tactical field care, with blood and/or lactated Ringer’s solution possibly available. 6. Monitoring, wound care, reinspection for additional wounds, analgesia, reassessment of fractures, antibiotics: All the same as for tactical field care. A main precept of TCCC is to move medical care from being the sole responsibility of the combat medic, to involve each operator and each level of leadership. Each fighter carries a tourniquet that can be self-placed. Each fighter is trained in basic combat lifesaving skills so that the effects of wounds can be minimized (within defined limits) and fire can be returned until the medic can arrive and perform the appropriate advanced medical care. Each leader, from the squad level up, is trained to evaluate medical concerns as an integral part of the mission execution and is able to decide when to abort the mission, when to continue, and when to alter the plan, based on the mission objective and the issues that the injured team member or members bring to the fight.

Principles of Tactical Medicine The tactical environment presents unique challenges to law enforcement officers, and the same is true for personnel 494

FIGURE 25-13  Tactical medics discuss placing a suspect under arrest during a tactical operation operational preplan during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

providing EMS medical support in that environment. Tactical medical care providers must have an understanding of and consideration for law enforcement tactics and mission-specific objectives when planning and providing medical support (Figure 25-13).52 Most comprehensive law enforcement tactical medicine programs require medical providers to attend some formal law enforcement training. Before deployment, further training in SWAT school will most likely also be required to familiarize the tactical medic with basic and advanced tactics. This extensive training may result in reserve police officer status for the medical provider if there is a reserve program in existence at the law enforcement agency where the program is based. The operator then enters a true hybrid role between medicine and law enforcement. Traditional EMS doctrine maintains that rescuer and scene safety are first priorities, and that patient care is a secondary concern.76 The nature of tactical operations requires that law enforcement officers and tactical medical personnel operate in unsecured environments and situations with significant potential for violence and injury (Figure 25-14).72 Tactical scenes are rarely safe from the civilian standpoint, but tactical medical personnel are trained to conduct concise and limited medical evaluations and interventions in potentially threatening areas.82 What sets tactical EMS apart from standard EMS is the ability to render immediate care in an environment that may not be completely secured from threats (Figure 25-15). When a SWAT

FIGURE 25-14  At the International School of Tactical Medicine, law enforcement tactical medics train for high-risk vehicle assault situation treating a tactical officer with massive blood loss during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

team relies on traditional EMS to provide medical care and an operator or civilian is acutely injured during the mission, the EMS unit must either wait until the victim is brought out to the safe (“cold”) zone (Figure 25-16) or wait for the entire scene to be secured by law enforcement before evaluating and moving the victim. The Columbine School shooting illustrated how victims will die if medical aid is not rendered in a timely manner. When a tactical medical unit is present, care can generally be rendered to the victim swiftly, and when the injuries involve acute airway issues or life-threatening hemorrhage, lives may be saved by faster access to care. Other differences between tactical EMS and conventional EMS include limitations in medical equipment at hand, performing in adverse or austere environments (e.g., while maintaining light or sound discipline), and performing patient assessment from remote locations.87 “Medicine across the barricade” involves remote evaluation and management of patients, such as when a hostage has become ill or injured and the provider attempts to assist the victim by using the eyes, ears, and hands of someone closer to the situation.34 The tactical medical provider must use skills not unlike those of an EMS dispatcher handling an

Hot zone • Highest threat of gunfire, Level of care injury, etc. • Limited to stopping major hemorrhage and extricating the victim to a safer location

Cold zone • Secured area, safe for civilian EMS responders

Warm zone • Lower risk of gunfire or injury, but not secured Level of care • Standard care available in the prehospital environment using any equipment available on an ambulance or medical helicopter

Level of care • Limited to that which can be rendered with the equipment carried by the tactical medical provider (largely focused on the ABC’s)

FIGURE 25-16  The zones-of-care concept of tactical emergency medical services. ABC, Airway, breathing, and circulation; EMS, emergency medical services. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

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CHAPTER 25  Tactical Medicine

FIGURE 25-15  Tactical medics perform advanced airway management in a tactical training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

emergency over the radio. In addition, standard EMS medical care performed in specific clinical scenarios may require a different approach when the same situation is encountered under tactical conditions.33 Tactical medicine can be provided by EMTs, paramedics, registered nurses, midlevel providers (physician assistants, nurse practitioners), or physicians who serve on law enforcement tactical teams.47 Midlevel providers and physicians traditionally have training in advanced surgical and medical procedures beyond what is normally allowed for traditional EMS personnel.22 The primary goal of tactical medicine is to assist a tactical team in accomplishing its mission. This is achieved through a comprehensive program outlined first by the California Commission on Peace Officer Standards and Training (POST) and the California Emergency Medical Services Authority (EMSA). State Regulation 1084 established operational programs and standardized training recommendations for tactical medicine programs in California. This produced the first tactical medicine operational and standardized training recommendations set forth by a state regulatory body in the United States. Its seven elements are medical oversight, medical contingency planning, operational support, quality improvement, team health management, training and education, and medical equipment acquisition and maintenance. A tactical medicine program cannot be effective with only the operational component in place. It must include other elements, such as team health management—keeping the tactical team members healthy before, during, and after special operationss.20,59 A full tactical medicine program encompasses provision of preventive and acute medical and dental care and for some teams, even canine support veterinary care.49 Ready access to such care has a positive effect on team morale (Figure 25-17). One of the most important roles of the provider is to create a formal medical threat assessment for each training and operational deployment. This includes consideration of issues such as environmental conditions (heat, cold, wind), low-light conditions (Figure 25-18, A),41,42 operator fatigue (and the possible need for rotating operators), nutritional issues,21 plant and animal threats, and a plan for extrication and transport of patients.10 When operational, this medical plan should include any medical intelligence that can be gathered before or during the mission, including issues such as who is involved, ages of persons involved, medical history and background, preexisting medical conditions, geographic location, and weather19 (Figure 25-18, B). Predetermining evacuation routes to ensure timely transport to the

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Medical equipment acquisition and maintenance

Medical oversight Medical contingency planning

Tactical medicine Training and education

Team health management

Operational support (TEMS)

Quality improvement

FIGURE 25-17  California tactical medicine diagram.

appropriate medical facility is also part of the medical threat assessment. This should include both ground and air evacuation plans, or water transportation where necessary. Aeromedical evacuation planning includes predetermined landing zone coordinates that are cleared for approach before the start of the mission if possible. Day and night landing zone requirements

differ, so both need to be considered, depending on the time of day. SWAT teams and their tactical medical teams are important community resources not only for responding to major emergencies but also in planning for the community response. Tactical medical operators, in conjunction with local medical control, EMS, and public health officials, should take a leadership role to ensure that aggressive, proactive planning for future threats is completed before resources are needed.16,100 Although no one doubts that some terrorists, outlaw states, and organized criminals have the capability to produce or access chemical and biologic agents, the question is whether they will use them.38 The use of explosive devices is on the rise worldwide. The potential for terrorist acts against the United States is immeasurable. As a result, domestic preparedness and proper training for blast injuries are essential.26,31,37,73,95 Any terrorist incident is a large crime scene by definition. Initially it is unsecured, and additional threats, such as bombers, gunmen, or secondary devices, may present themselves. Tactical medics are trained to deal with such a situation. Knowing how not to disturb evidence, take care of a patient, and provide security are a combination of skills needed at any terrorist incident. It is advantageous to have more than one provider as part of a tactical team, particularly in the event of a serious injury or when multiple casualties are involved (e.g., in a school shooting or an act of community violence).46,60 Team medical personnel can lessen the agency’s liability exposure with adequate written, photographic, diagrammatic, or video documentation of the injuries.64 Another benefit of having multiple providers is the ability to send a provider to the hospital with an officer who becomes ill or injured during a mission. This provider can serve as a concerned advocate for the officer and as a liaison with hospital personnel. This provides significant reassurance to the entire tactical team.40,45,69

A

B

C

D

FIGURE 25-18  A, Tactical medic trainees for low-light situations. B, Tactical medic trainees discuss their operation plan with an instructor at the International School of Tactical Medicine. C, Tactical medic trainees apply a tourniquet to an injured officer who is suffering from massive blood loss. D, Tactical medics must prepare for the unexpected, including evaluating and treating pediatric patients injured during tactical operations. (Courtesy International School of Tactical Medicine.)

496

Tactical medical providers ensure that everyone on the team is healthy and optimally fit for duty.48 The team’s medical officer is responsible for the team’s physical fitness, diet, exercise, sleep, stress management, and preventive medicine. The tactical unit can be viewed as a group of elite operators who are “occupational athletes.” Strength training for many tactical operators consists of traditional bodybuilding exercises. However, this type of physical conditioning does not duplicate the actions needed to perform as a tactical operator. Tactical operators, like professional athletes, need a broad-based program of training and physical conditioning tailored to the specific actions they will perform. The team’s medical officer should stress regular physical conditioning. A comprehensive plan of proper nutrition and exercise must be established and maintained. This should include a balance of aerobic and anaerobic exercises and stretching. Cardiovascular fitness workouts, such as running or swimming, are excellent for the tactical team. Full-body or resistance circuit weight training is excellent for strength training, but it must be a total body workout. Training some parts of the body but ignoring others can lead to costly injuries and a lower level of fitness.90 Flexibility training is one of the best ways to prevent injuries in the field. Unfortunately, it is frequently ignored. Regular stretching or yoga has been long recognized as beneficial in athletic physical conditioning. In this respect, the tactical unit is no different from any other group of athletes. When the physical conditioning program encompasses all these points, the team operates at its peak potential with fewer injuries. A sound diet should be stressed and maintained, but diet is often a controversial topic. In response to the obesity problem in the United States, the Food and Drug Administration (FDA) and many other researchers have looked at diets worldwide and their effects on the human body. Randomized clinical trials studying the risks and benefits of various individual diets are recent.9,27,80,97 The FDA studied the traditional food pyramid (which is based on four food groups and is now no longer considered a valid nutritional program).70 Many other diets have been extensively studied.24 Based on these and other studies, the FDA revised the food pyramid to a more balanced program designed for variations in age, gender, and level of physical activity. It now contains five food groups: grains, vegetables, fruits, milk, and meat and beans. Fats, sugars, sodium, and total caloric intake are restricted. The FDA has an interactive website for the new food pyramid (http://www.foodpyramid.gov). Although our knowledge of diet and exercise has improved, data continue to be gathered, and the perfect dietary program for the tactical operator is not yet known. Nonetheless, fast foods and simple sugars should be deemphasized or eliminated from the tactical operator’s diet. Smart nutrition, coupled with physical training, are the keys to the fitness level necessary to perform at the expected level for a SWAT operator. Preventive medicine should be stressed with regular physical examinations, weight loss programs, and treatment where appropriate. Smoking cessation, alcohol and drug counseling, and stress management are the responsibilities of every team medical officer.

OPERATIONAL CASUALTY CARE Education from military medical operations has helped civilian law enforcement medical providers recognize injury patterns coupled with appropriate treatments, as well as identify equipment that can be used during SWAT operations. The typical ABCs cannot be directly extrapolated to a hostile environment. Extrication to a place where appropriate medical care can be provided is a priority that may be unfamiliar to normal urban EMS. Hemorrhage control is paramount; saving as much of the victim’s own blood as possible has more value than trying to replace blood volume with IV fluid. Tourniquets are a first-line treatment modality in tactical medical support, whereas they may be seen as a last resort in routine EMS (Figure 25-18, C ). Tactical medical personnel are aware that tactics come first, followed by appropriate medical care. When the two entities are

blurred or reversed, a poor outcome is more likely. Each tactical medical provider must be knowledgeable in the tactics of his or her team and trained to the satisfaction of the team leader in order not to jeopardize a team’s mission or increase the chances of an injury being mistreated. The medical providers must constantly reassess as much of the dynamic component of the operation as possible. Contingency planning and the ability to adapt to the fluid nature of these situations is required to be successful as a member of the SWAT team (Figure 25-18, D). The public safety agency developing a tactical medicine operational program should conduct a needs assessment to determine the level of emergency care required by the SWAT team to support its mission and operations. The operational program must consider the needs for medical oversight and coordination with the local EMS agency; medical direction; use of EMTs, paramedics, and other advanced life support personnel; and minimum training and equipment standards. The agency should develop policies and procedures for medical support during tactical operations. Approved tactical medicine training programs, which provide initial and refresher or update tactical medicine training to personnel, should adhere to the minimum training guidelines established by California POST and EMSA and the standards outlined in the guidelines. The goal of the guidelines manual is to describe minimum core competencies and to define the written and skills testing necessary to achieve the standards prescribed by California POST and EMSA. The guidelines that have been approved are available at the POST website at http://www.post.ca.gov/ Training/Tactical_Medicine/default.asp.

TACTICAL MEDICAL EQUIPMENT In general, tactical EMS medical equipment comes from other areas of emergency medicine and law enforcement and is combined into field-expedient, multifunction toolkits. Looking at the gear as a whole, a modular approach may be most helpful (Figure 25-19, A). The gear differs depending on the roles of the providers and the tactical unit.32 Basic equipment for the operator includes essential items. Typically an operator has a duty uniform consisting of a battle dress uniform.92 The uniform may undergo appropriate modifications depending on weather conditions. As with other areas of outdoor activity, it is wise to use a system of layers that can be easily adjusted to changing weather conditions. Waterproof and breathable outer layers may be a consideration, as are wicking underlayers. In addition to the standard duty uniform, a Nomex balaclava and gloves are worn on many entries to protect from exposure to pyrotechnic devices. Because this is an environment where gunfire may be encountered, ballistic protection in the form of body armor is needed. For the tactical medical provider, levels I and II-A are not advised. Level II is the bare minimum if the body armor is concealed under a shirt or uniform, but levels III-A to IV are better (Table 25-3 and Figure 25-19, B). These levels of protection have a good balance of bullet stopping power and ability to absorb blunt trauma. Many tactical operators combine body armor with ballistic plates made of metal or ceramic, which stop high-velocity rifle bullets. Body armor is chosen by the agency from a vast array of different types and styles. Some tactical medical providers also carry a Kevlar blanket or ballistic shield, which can be used to cover a patient in harm’s way or can be used as a mobile source of cover when providing care or extracting a downed victim. These blankets, although effective, are extremely heavy and bulky. Despite the best ballistic protection, limbs are very susceptible to ballistic trauma. As a result, uniforms with integrated tourniquets have become available. This simplifies the application of lifesaving tourniquets because they are already in place. The weight and bulk of all nonmedical tactical equipment hinders the ability to carry large amounts of additional material. The medic needs to decide how much can be carried and whether to wear a backpack or a load-bearing vest, or neither. In general, the tactical medical provider must be able to effectively carry equipment and operate in a tactical situation without hindering the rest of the team. Of the two general sets of medical equipment, one is carried for immediate care, typically worn in 497

CHAPTER 25  Tactical Medicine

TEAM HEALTH MANAGEMENT

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Radios with microphones and headsets are fairly standard for most tactical units. Radios should be set to secure channels. Some communications may even be encrypted. Simple communication during the operation between members may involve standard or specialized sign language (Figure 25-19, C ).

ENTRY AND BREACHING TOOLS

A

Specialized entry tools are used to gain access to barricaded subjects or closed doors. Typical items, familiar to firefighters and EMS personnel, include pry bars, battering rams, sledge hammers, hooks on chains or rope, stop blocks, and halligan tools (Figure 25-20). Ladders may be needed to gain access to an elevated or depressed point. In extreme cases, explosive devices are available to trained explosive experts in the tactical unit to gain entry to an area.

WEAPONS SYSTEMS

B

Whether a team medic should be a sworn law enforcement officer or an armed civilian has been a subject of much debate. Regardless, a provider must be familiar with the unit’s weapons systems. Weapons systems are constantly encountered in the tactical arena. A provider who is a sworn officer has a primary role as an operator on the unit and a secondary role as a medical provider.75,78 However, a provider who is first a medical officer would still have to protect himself or herself in a hostile situation and therefore would be armed defensively. In another scenario, the provider may be unarmed but may have to take charge of an officer’s weapon in a medical or tactical situation. An armed officer who is disoriented may become a danger to the team, so the provider would need to take charge of all of the officer’s weapons and render them safe. In the worst case, the provider may have to defend a downed officer using the officer’s weapon. Weapons system familiarity is paramount for the tactical medicine provider. A provider should be familiar with every handgun, shotgun, rifle, submachine gun, assault rifle, and smoke or chemical agent gun used by the team. All tactical team members, whether providers or not, should be able to use and render safe any weapon carried by a team member.88 The provider should not be exempt from this requirement (Figures 25-21 and 25-22). Weapons systems use a variety of ammunition (see Chapter 24) Typically there is a duty handgun, which shoots low-velocity handgun ammunition. This same ammunition may be used by a submachine gun, such as the Heckler and Koch (HK) MP5 UMP 40, or UMP 45. Calibers of the handgun and submachine gun should be matched to avoid the wrong caliber ammunition going into the wrong weapon, causing malfunction in a crisis situation. Law enforcement and military weapons such as the Colt M4, fire

C FIGURE 25-19  A, Blackhawk Products Group special operations medical backpack in use by tactical medics. B, Tactical heavy body armor ballistic vest, level III-A, showing trauma plate worn for law enforcement tactical operations. C, Communication with the entry team is critical for the tactical medic. This medic is equipped with headset, microphone, and encrypted radio. He is also staged behind the SWAT armored vehicle for hard cover. (B courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD; C courtesy International School of Tactical Medicine.)

a small backpack or load-bearing vest, and the second is carried in a larger backpack or duffel bag in the support vehicle. The latter is used for more extensive treatment, multiple casualties, and prolonged transports.57

COMMUNICATION Communication between team members and tactical medical providers outside the area of the operation is often essential. 498

FIGURE 25-20  Special tools and equipment are used to gain rapid entry by SWAT teams. (Courtesy International School of Tactical Medicine.)

Test Variables

Armor Type I

Test Round 1 2

II-A

1 2

II

1 2

III-A

1 2

III

—

IV

—

Special requirement

—

Test Ammunition 38 Special RN Lead 22 LRHV Lead 357 Magnum JSP 9 mm FMJ 357 Magnum JSP 9 mm FMJ 44 Magnum Lead SWC Gas Checked 9mm FMJ 7.62mm (308 Winchester) FMJ 30–06 AP *

Nominal Bullet Mass

Performance Requirements Minimum Required Bullet Velocity

Required Fair Hits per Armor Part at 0° Angle of Incidence

Maximum Depth of Deformation

Required Fair Hits per Armor Part at 30° Angle of Incidence

44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches) 44 mm (1.73 inches)

2

44 mm (1.73 inches) 44 mm (1.73 inches)

2

44 mm (1.73 inches) 44mm (1.73 inches)

0

10.2 g 158 gr 2.6 g 40 gr 10.2 g 158 gr 8.0 g 124 gr 10.2 g 158 gr 8.0 g 124 gr 15.55 g 240 gr

259 m/sec (850 ft/sec) 320 m/sec (1050 ft/sec) 381 m/sec (1250 ft/sec) 332 m/sec (1090 ft/sec) 425 m/sec (1395 ft/sec) 358 m/sec (1175 ft/sec) 426 m/sec (1400 ft/sec)

4

8.0 g 124 gr 9.7 g 150 gr

426 m/sec (1400 ft/sec) 838 m/sec (2750 ft/sec)

4

10.8 g 166 gr *

868 m/sec (2850 ft/sec) *

1

4 4 4 4 4 4

6

*

2 2 2 2 2 2

0

*

From U.S. Department of Justice National Institute of Justice: Ballistic resistance of police body armor, NIJ Standard 0101.03; 5.2.1, April 1987. *See section 2.2.7 of reference. g, Grams; gr, grains.

.223-caliber high-velocity cartridges. The provider may be exposed to shotgun ammunition, typically 00 buckshot. The team sniper deploys with a .308 high-velocity rifle that is bolt action. The flight characteristics and ballistics of shotgun, rifle, and handgun ammunition vary depending on the weight, shape, and velocity of the ammunition. The provider should be familiar with

A

the characteristics of gunshot wounds in order to treat field wounds appropriately. In addition to traditional ammunition, the provider may be faced with distraction devices, chemical munitions, and less lethal munitions. Chemical munitions deliver a chemical agent to an intended target to disorient or incapacitate and facilitate capture or surrender without loss of life. Typical chemical agents used in tactical operations are tear gas or a derivative of pepper spray. Less lethal munitions are used to incapacitate and facilitate capture. Unfortunately, with this use of force, injury is common, so the provider should be familiar with the injuries and their treatments. These munitions are low-velocity projectiles of wood, hard rubber, foam rubber, plastic, or beanbags. They have enough force to cause pain and usually make an assailant stop aggressive action on contact. They usually cause minor blunt trauma, but they may achieve enough force and velocity to penetrate into body cavities (Figure 25-23). Tasers are another example of less lethal devices. A Taser delivers an electrical charge to incapacitate the attacker, but below the level that causes cardiac arrhythmias. The assailant experiences intense muscular contraction throughout his or her

B FIGURE 25-21  Law enforcement tactical medics receive training with the tactical pistol (A) and HK MP5 submachine gun (B). (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

FIGURE 25-22  Tactical medics receive training and familiarization with the 40-mm less-lethal munitions launcher. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

499

CHAPTER 25  Tactical Medicine

TABLE 25-3  U.S. Department of Justice Rating of Body Armor

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 25-23  Victim of a 40-mm round to the head with lethal consequences. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

body and loss of muscular control. The resultant injury patterns are typically a result of the subsequent fall to the ground. Clearance for booking should include an electrocardiogram, local wound care, removal of the electrodes from the skin, and an update of tetanus immunization if needed (Figure 25-24). Explosive breeching techniques and distraction devices are often deployed during tactical operations. The small explosives used to gain entry into an area can create injuries.66 For example, a distraction device that is hand thrown into an area to deliberately disorient a suspect and divert attention toward the device and away from the entry team. These devices usually have a nonexploding canister and a small explosive charge. The device is activated and thrown much like a military hand grenade. It creates a brilliant flash of light (6 to 8 million candlepower) and a thunderous noise of approximately 175 decibels. This is accomplished by venting explosive gases through multiple holes in the canister. Physical effects of distraction devices and explosive entries include major and minor burns, smoke-induced bronchospasm, vestibular dysfunction, transient visual disorientation, and emotional upset and anxiety. In general use, the distraction device has not been reported to cause ear drum rupture. Explosive breaching is the role of the team’s explosives expert, with whom

FIGURE 25-24  Tasered suspect. The darts are intact in the left lower back area. (Courtesy International School of Tactical Medicine.)

500

FIGURE 25-25  Tactical team training for explosive breeching. (Courtesy International School of Tactical Medicine.)

the medic should consult, as part of the medical threat assessment, about the types of explosives planned and the blast forces that may be encountered (Figure 25-25).

VISION Covert operations and low-light situations dictate the use of visual adjuncts. Binoculars, tactical mirrors, spotlights, periscopes, strobe lights, chemical lights, and headlamps are often deployed in a low-light tactical environment (Figure 25-26). Proper training and discipline are required for use of these devices in the tactical environment, because they may give away one’s position and alert a hostile opponent to the team’s position. Similarly, electronic night vision equipment, which operates outside of the range of visible light, is also extensively used.

MEDICAL THREAT ASSESSMENT Any mission planning must include a medical threat assessment (MTA). The SWAT commander uses information from many sources to create a tactical plan before execution of a mission, including available personnel, building layouts, street layouts, necessary support equipment, nature of the mission, available weaponry, and various sources of intelligence.63 An MTA is an important component of the intelligence the commander needs to properly execute the mission. It is the responsibility of the tactical medic to provide a concise and accurate medical briefing to the commander. MTA forms should be used on every mission to ensure systematic planning, because scenarios and problems may be unique. Only a systematic approach ensures complete assessment of the situation. The tactical medical team and its MTA are key factors in dealing with apocalyptic terrorist events, such as the Columbine

FIGURE 25-26  A SureFire headlamp setup can use white light or LED light in low-light tactical situations. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

Location Type of operation

Hostage #

Suspect #

Warrant #

Protection #

Open terrain search #

Terrorist #

Other teams

Tactical

EMS/medics

K9

Patrol

Detective

FBI/other

school shootings and the school hostage crisis in Beslan, Russia.84 Other venues, such as protection details and the war on drugs, rely heavily on a team’s internal capacity for medical care, as evidenced by the U.S. Marshals Service judicial protection training program.85 A complete threat assessment should include these elements: 1. Location of the operation, with a brief description of the goals of the mission and the other teams involved, with their needs and resources (Table 25-4). 2. Locations of all surrounding hospitals and medical care facilities, such as designated burn and trauma centers, with telephone numbers to facilitate communication. Local EMS numbers should be listed. 3. Helicopter flight plan. Before the mission, it should be ascertained that a helicopter is available and that there is an acceptable landing zone (LZ) for day or night conditions. This should include the exact Global Positioning System (GPS) coordinates of the LZ. Obstructions and debris should be cleared before the mission (Table 25-5 and Figure 25-27). 4. Weather. Factors to be evaluated include temperature, rain, wind, humidity, wet bulb temperature (TW), and windchill. Sunrise and sunset times should be recorded and logged. The TW is the lowest temperature to which air can be cooled by the evaporation of water into the air at a constant pressure, so it reflects the limit to which a person can shed heat through sweating in a hot environment. The TW is used to determine fluid requirements and the need for work–rest cycles. The weather-related components of the MTA are used to determine the appropriate uniform and shelter required to prevent overheating or hypothermia (Table 25-6). Water sources should be recorded before the mission as part of the MTA. 5. Plant and animal threats. Plant exposures, especially to poison ivy and poison oak, are common to snipers. Snakebites are common to team members working with police dogs. Anticipated animal threats should be recorded, along with telephone numbers for the police veterinarian, animal control, and poison control, including sources of antivenom (Table 25-7).

Without a medical record, there is no proof that appropriate medical care was given.

Medical Personal Protective Equipment Standard precautions against infectious diseases must be deployed; tactical medicine is no different from any other venue in this respect. Medical personal protective equipment includes masks, eye protection, gloves, and perhaps gowns. In remote locations, surgical treatment may be provided before transport to a tertiary care center. The basics for protection should be carried on the provider’s person in a readily accessible location. Some tactical medics don surgical gloves underneath their shooting gloves before an operation so they will be ready if the need arises. Although not sterile, they provide protection from blood and body fluid–borne pathogens.

PERSONAL SUPPLY MODULE To reduce the amount of equipment carried by the medic and to help team members help themselves, each member of the tactical unit should carry a personal supply module (PSM), or “self-help kit,” with medical supplies. A team member can thus provide self-help or aid another member, and the medic may not have to be summoned until the scene is more secure. A typical PSM should be vacuum sealed and contain supplies for basic trauma care and for IV access (Table 25-8). Vacuum sealing these contents provides protection from the elements and makes them last longer. It also cuts down greatly on bulk but adds some weight. Each medical provider should carry a casualty response kit. This kit should be small, lightweight, and contain the necessary components to specifically treat gunshot wounds, hemorrhage, tension pneumothorax, sucking chest wounds, eye injuries,

FORMS AND DOCUMENTATION Medical records should be kept for the team and for anyone treated or evaluated as a TEMS patient. Records should be stored for a minimum of 10 years and have proved to be indispensable as defense documents in several antipolice liability lawsuits. TABLE 25-5  Sample Form for Helicopter

Information

Helicopter

Obstructions?

LZ coordinates

LZ cleared before mission start? Landing zone (LZ)

Address:

Latitude

Longitude FIGURE 25-27  Air ambulance helicopter preparing for tactical casualty evacuation. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

501

CHAPTER 25  Tactical Medicine

TABLE 25-4  Sample Form to Provide Operational Information

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 25-6  Sample Form for Weather-Related Information Temp high

Wet bulb temp °C (°F)

<15.6 (60)

15.6-25.6 (60-78)

25.6-27.8 (78-82)

27.8-29.4 (82-85)

29.4-31.1 (85-88)

31.1-32.2 (88-90)

>32.2(90)

Sunrise:

AM

Temp low

H2O qt/hr

0.5

0.5

0.5

0.5-1.0

1.0

1.0-1.5

2.0

Sunset:

PM

Rain %

Rest Min/Hr

0

0

0

10

15

30

40

Wind: mph

Cold casualties

Y/N

Work cycles

Heat casualties

Y/N

Yes/No

Uniform adjustments

Y/N

Shelter: Y/N

Humidity %

Night ops: Duration: Location:

TABLE 25-7  Animal and Plant Threats Animal Threats Yes/No

Animals present?

Yes/No

Police dog?

Types of animals

Number:

Do you anticipate wild animals?

Poisonous snake exposure:

Yes/No

# Yes/No

Veterinarian's address:

What type? Vet phone:

Yes/No Animal Control:

Poison Control:

973-470-2242

800-222-1222

Plant Threats Yes/No

Exposure to poisonous plants likely?

Yes

Type No

Tecnu or Ivy Block available?

Yes No

Uniform adjustments needed?

Yes

Recommendations:

No

burns, and lacerations. The drop leg configuration is often used by tactical medics because it is readily accessible (Figures 25-28 and 25-29).

BASIC MEDICAL MODULE In addition to a PSM, a basic medical module (BMM) should be carried by team medics. Because every team member in a tactical unit should have at least basic EMT certification, a BMM could be used by any team member to provide initial care to a victim. The BMM should have basic splinting material and dressing material (Table 25-9). Basic airway tools, such as nasal airways and pocket mask, should be included. A bag-valve-mask or a more compact alternative is advisable in the tactical environment. A simple bagvalve-mask alternative device (BVMAD) can be constructed out of respiratory supplies from a one-way valve, flexible tubing, and TABLE 25-8  Sample Contents of Personal Supply

Module

Trauma dressing IV start kit Minor dressings Saline bullets Medicines

Other wound items IV, Intravenous.

502

Bandages such as the Israeli bandage can be easily self-administered by the victim on most extremity wounds 100 mL IV fluid, an alcohol wipe, tourniquet, IV catheter (3), IV tubing, tape, flush and saline lock Adhesive bandages should be carried by all team members Foreign bodies in the eyes are very common on entries, and a bottle of eye drops (saline bullets) may allow an operator to continue on a mission Pain: acetaminophen, ibuprofen, narcotic analgesics Antibiotics: ciprofloxacin, metronidazole, cephalexin Surgical staples or liquid tissue adhesive

a mouthpiece (Figure 25-30).5 This is the preferred ventilatory device in the tactical environment, because it allows a rescuer to provide ventilation without unnecessary bulk. If the tubing is long enough, the person providing ventilation can work handsfree if the patient is intubated. The additional length leaves the rescuer’s hands free to carry the patient, perform other medical tasks, or to even defend the patient with a weapon. Oxygen is rarely useful in the immediate tactical environment, so oxygen cylinders are left in the support vehicle with a regular bag-valve-mask and retrieved when necessary. An automated external defibrillator (AED) should be carried in the support vehicle.3 A small collapsible litter for extrication of a downed person should be a part of every BMM.

INTERMEDIATE MEDICAL MODULE An intermediate medical module (IMM) is intended for use by paramedics and registered nurses. Unlike the BMM, it contains equipment and supplies suitable for advanced life support (ALS). Under standing orders from a team physician, ALS providers may provide advanced cardiac life support to a victim. An IMM is much more extensive than a BMM. It contains medications, IV

FIGURE 25-28  Saline bullets remove the most common injury: foreign bodies in the eyes. Personal medical kit typically carried by SWAT officers. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

FIGURE 25-29  Casualty response kit for tactical medics. It can be carried on the belt or MOLLE (modular lightweight load-carrying equipment) system or in the drop-leg configuration. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

tubing, IV fluids, endotracheal tube, Combitube, laryngoscope, light wand, and, if protocol allows, cricothyrotomy kit (Table 25-10 and Figure 25-31). These facilitate placement of a definitive airway before transport, which, when used with a BVMAD, permits hands-free ventilation of a patient, allowing extrication by one or two team members. Proficiency with the airway toolkit is of high priority.

ADVANCED MEDICAL MODULE The most complex module is the advanced medical module (AMM), intended for independent practitioners, such as nurse practitioners, physician assistants, and physicians. These practitioners can perform advanced surgical procedures and medical interventions that can make the difference between life and death on a long transport. Transport to definitive care should not be delayed unless medically necessary. However, if advanced care in the field is indicated, it can be provided by an independent practitioner with an AMM.

MAJOR TRAUMA MODULE Lengthy surgical interventions in the field are not advised and have extremely poor prognoses. Although rapid transport to a TABLE 25-9  Sample Contents of Basic Medical

Module

Splints Airway Litter Wound care Other

Two SAM splints Pocket mask, bag-valve-mask (BVM) or BVM alternative device (BVMAD), oral and nasal airways Fold-up stretcher Various trauma dressings Elastic (Ace) wraps and cravats

FIGURE 25-31  A well-stocked and functional tactical intermediate medical module (IMM) airway kit, containing a laryngoscope, a bagvalve-mask alternative device (BVMAD), oral airways, bougie, stylette, endotracheal tubes, tape, and surgical airway kit. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

trauma center should not be delayed, some surgical procedures may be of benefit when performed in the field: laceration repair to stop bleeding or facilitate evacuation, cricothyrotomy, and, in critical situations, chest tube insertion. These types of procedures can usually be performed using only the essential equipment found in a vacuum-sealed minor-surgery tray (Figure 25-32), which can be one component of the major trauma module (MTM) for advanced providers (Table 25-11). Many users include hemostatic dressings in trauma kits, but their use is not yet well studied.58,83 The efficacy versus the potential harm of hemostatic dressings is a subject of debate. Direct pressure with a sterile dressing is the initial approach to hemorrhage control. The traditional and time-tested approaches of pressure-point compression and tourniquets are useful adjuncts to any bleeding problem, so these materials should be included in the MTM. A set of combine dressings, gauze, petrolatum gauze, and Israeli dressings should also be carried.

SUPPORT VEHICLE MODULE Additional supplies and equipment are kept in the support vehicle module (SVM). Consumable items should be kept in the SVM so that other modules can be restocked from it (Table 25-12). The SVM contains equipment such as oxygen cylinders, an AED, airway adjunct devices, fiberoptic scopes, nebulizers, surgical trays, chest tubes, cervical collars, backboards, peroxide, TABLE 25-10  Sample Contents of Intermediate

Medical Module

Airway Medications

Endotracheal tubes, laryngoscope, stylette, bougie, bag-valve-mask alternative device (BVMAD) Intravenous setup and tubing, pain medication, rapid sequence intubation medications, antibiotics

503

CHAPTER 25  Tactical Medicine

FIGURE 25-30  The bag-valve-mask alternative device (BVMAD) as it is stored, with the mouthpiece (red arrow) over the exhaust port. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 25-32  A vacuum-sealed minor-surgery tray. Many procedures in the tactical environment can be accomplished with a minimum  of equipment. (Courtesy International School of Tactical Medicine, Bohdan T. Olesnicky, MD.)

povidone-iodine, liter bags of crystalloid IV fluid, replacement filters for gas masks, and fiberglass splinting material. Field care is limited only by the equipment that can be transported and the training of the providers. Items carried by advanced providers include the following: • Central line • Cricothyrotomy/tracheotomy set • Retrograde intubation set • Laryngeal mask airway • Chest tube set • Fiberoptic intubation set • Blood products or blood substitutes

CHEMICAL, BIOLOGIC, RADIOLOGIC, OR NUCLEAR SPECIALTY MODULES Depending on the role of the tactical unit, chemical, biologic, radiologic, or nuclear (CBRN) threats may be encountered. These incidents require tactical emergency medical care because they involve large crime scenes with casualties. Individuals trained in tactical emergency medicine are much more familiar with evidence

collection and preservation, and they usually already have necessary security clearance to enter such an area. Until the scene is cleared, the tactical physician may be the only one who can provide medical care to victims. Chemical and biologic environments are specialized depending on the agent released. Various civilian and military protective gear and respirators or supplied air sources may need to be worn. Operating in CBRN protective gear requires extensive training in addition to regular tactical training. Antibiotic prophylaxis with ciprofloxacin, as well as agent detection equipment, may be carried by the medic. Several biologic and chemical diagnostic kits and meters are available but costly. Radiologic incidents potentially involve dispersal of a radiologic agent with conventional explosives, the combination often referred to as a dirty bomb. Nuclear detonations refer to splitting of a radioisotope and the resultant massive energy release from a nuclear bomb. Geiger counters are available for radiologic and nuclear situations. These situations require a great deal of additional training, but they are not beyond the realm of tactical emergency medicine. Hazardous material (hazmat) situations are frequently seen in civilian law enforcement raids on clandestine drug laboratories. Level A, B, or C protective suits with gas masks or supplied air may be required in these situations as well. Hazmat and CBRN situations are highly specialized in their nature and require extensive training, beyond the scope of this text.

The Tactical Mission Each mission has a number of phases:52,91 1. Warning order (issued when the tactical team is first requested and establishes the situation and chain of command) 2. Gathering of intelligence a. Building intelligence (includes location and surrounding areas, avenues of approach, escape routes, and rally points, as well as natural and man-made obstacles, fields of fire, opportunities for cover and concealment) b. Suspect or hostage intelligence (as detailed as possible) c. Medical threat assessment (complete) TABLE 25-12  Sample Contents of Support Vehicle

Module (SVM)

TABLE 25-11  Sample Contents of Major

Biohazard container Saline eye flush

Israeli dressing

Elastic wraps Splinting material

Trauma Module

Combine dressings Gauze pads Antibiotic packs Tourniquet Wound closures Minor-surgery tray Elastic wraps Splinting material IV fluids

Supplies Other IV, Intravenous.

504

May be self-administered by the patient with one hand; combines an elastic wrap, combine dressing, and tourniquet in one device To control heavy bleeding or cover eviscerated bowel and open fractures Multiple uses Pre-prepared medication packs for major trauma, containing pain medication and antibiotics Several excellent devices are available for tactical use Sutures, staples, and wound adhesives For performing surgical procedures that cannot wait for extrication or transport Strains, sprains, and fractures are common SAM splint or a short sealed roll of fiberglass casting material. Bullet wounds frequently fracture long bones For infusion of medication and management of shock as needed. Also used for wound irrigation and eye irrigation. Several IV start kits should also be on hand Gloves, tape, trauma shears, tweezers, adhesive bandages, roll gauze, cravats, nasal airways, 60-mL syringes, headlamp Duct tape, biohazard bags, medical record sheets, and trauma tags for multiple casualties

Intravenous (IV) fluids Ice packs

Wound dressings Advanced airway tools Spare uniforms Oxygen cylinders Bag-valve-mask (BVM) Automated external defibrillator (AED)

Disposal container for used sharps and medical waste Foreign bodies in the eyes are common on entries Strains, sprains, and fractures are common Fairly bulky and difficult to carry in the medical pack. Cervical collars are frequently kept here and may be retrieved when needed For prolonged transport or massive hemorrhage, more IV fluid should be kept in the SVM and not carried on entries. Multiple IV start packs for use when necessary Ice packs are commonly used, because ice is not always available in the field. If the location has a freezer, bags should be kept to use existing ice Additional adhesive bandages, Israeli dressings, combine dressings, ABD pads, and burn dressings Difficult-airway tools may be needed in the cold zone before transport to secure a definitive airway If decontamination is needed, the victim will need to be reclothed in a clean, dry uniform, particularly in cold or wet environments Best left in the support vehicle because of their weight Replaces the BVM alternative device when hooked up to oxygen in the cold zone The AED is proved to save lives but is too bulky to carry on entry

Reserve Programs The methods in which a tactical medical team is used by a law enforcement agency can differ widely, especially between the East Coast and the West Coast. For example, in the western United States, especially California, Arizona, Nevada, Washington, Utah, and Oregon, there are many reserve programs in the police and sheriff’s departments.61 In these programs, the tactical medical provider has additional, formal law enforcement training, such as found in the POST program in California. This program allows the provider to be a sworn peace officer (carry firearms and have powers of arrest), bringing about an enhanced comfort level for the department and potentially mitigating some issues of civil liability. On the East Coast, reserve opportunities are less common, and medical providers typically serve as auxiliary units borrowed from traditional fire and EMS agencies. The liability issues and expenses in this type of relationship are often resolved via a written “memorandum of understanding” between the participating agencies.79 Selecting appropriate providers must be accomplished through interviews, psychological testing, background investigations, and physical fitness testing. The tactical team leaders should use a careful approach in the selection process for each candidate, just as they do for other members of the team.56

Military Combat Field Units Field units vary significantly with the mission, service, and threat (Figure 25-33). Most often, medical care is provided in the open or in as secure a location as possible. It is done on the ground,

on a table, in the back of a Humvee, or on an aircraft or a watercraft. Specific types of shelter and equipment are available, most often in the far-forward care under fire and the tactical field care phases, but generally the equipment is as noted earlier. When CBRN threats or high explosives are added to the scenario, the forward elements are the same, with the exception of the appropriate protective clothing. Once evacuation occurs, the injured team member is taken to a standard unit with the capability for decontamination and treatment, much as is done in the civilian setting. Most larger military transport planes have the capability to accept a critical care air transport team, which has a physician trained in critical care (emergency medicine, anesthesiology, internal medicine), critical care nurse, and respiratory technician. Most larger Navy ships are equipped with fully functioning operating rooms and intensive care units, or they can expand to provide this service quickly. All the services have basic medical units, from the self-aid or buddy-aid, to an aid station (with a physician), to forward resuscitative systems (surgical and nonsurgical), to surgical companies, combat surgical hospitals, and their equivalents. All services also have teams that are available to move far forward to provide surgical capabilities quickly should the need arise. These units can operate on any semiflat surface, do resuscitative surgery, and package the patient for expeditious transport for further care.12

UNIFORMS AND PERSONAL PROTECTIVE GEAR The standard law enforcement tactical operator carries between 40 and 60 lb of equipment. For longer missions, gear is heavier. Clearly, the operator needs to be in excellent physical condition, and the mission commander must proactively manage nutrition, hydration, and exertion levels. From anecdotal reports, the military has seen a significant decrease in truncal injuries because body armor has improved. The medical personnel noted that the insurgent combatants in Operation Iraqi Freedom changed their IEDs to target the head, neck, and extremities more than the whole body. Continued development is under way to produce body armor that will protect against higher-energy weapons, protect extremities, and be sufficiently lightweight and flexible to allow fieldwork. Because protective clothing is not removed in the field, the medic must work under and around it. Vigilance is required to check all body areas for hidden wounds. This is clearly more difficult in the field, in the dark, with sound and light restrictions, and with clothing in place than when the patient is undressed on the trauma table. Because the medic carries all the usual combat equipment, medical equipment is additional. Stethoscopes are usually left behind, because the medic cannot use the earpieces under the helmet, the environment is not conducive to being able to hear anything, and the victim is usually wearing body armor. Advanced medical gear is usually found on the medevac vehicle, or farther to the rear where it is safe enough to remove protective equipment and further evaluate and treat the patient.

Education and Training Programs

FIGURE 25-33  Law enforcement tactical medical team during a training exercise. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

Tremendous advancement in tactical medicine education over the last decade has resulted in numerous training programs, many providing formal continuing medical education credits. These courses focus on the core issues of tactical medicine. A unique aspect of tactical medicine is application of ALS in an austere environment. The traditional approach to providing EMS is often not feasible in a tactical situation.86 Cost-effective tactical medicine training and education is available and should be afforded to all involved medical personnel, including prehospital care providers and physicians. All team medical personnel should be trained to the highest level possible. Such training provides emergency medical personnel with an understanding of tactical procedures and an appreciation for why some routine prehospital care techniques may not be appropriate in the tactical environment.51,55 Tactical medicine training should be as realistic as possible with live teaching scenarios in full tactical gear. This allows the medical 505

CHAPTER 25  Tactical Medicine

3. Operation order 4. Briefing phase a. Detailed planning b. Detailed briefing c. Equipment selection d. Move to staging 5. Execution phase a. Entry b. Secondary search c. Transfer to arrest team and investigation team d. End of mission 6. Debriefing phase a. All persons, weapons, equipment, injuries, shots fired, and ammunition must be accounted for. b. Any problems must be discussed. Medical personnel should have the opportunity to discuss the mission from their perspective. In general, a tactical mission follows this order, although it may differ somewhat between agencies and missions. Proper handling of each point is required for a mission to flow seamlessly. Without proper intelligence, a mission becomes hazardous.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 25-13  Sample Curriculum for Basic Tactical

TABLE 25-14  Sample Curriculum for Advanced

Day 1

Day 1

Medicine Training

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Introduction to Tactical Medicine Tactical Medical Equipment Tactical Equipment Team Concepts and Planning Slow and Deliberate Team Movement Introduction to Tactical Pistol Medical Aspects of Chemical Agents and Distraction Devices Forced Entry Techniques Dynamic Clearing Techniques Operational Casualty Care Wound Ballistics Hemostatic Techniques and Dressings Team Health Management Medical Aspects of Clandestine Drug Labs Tactical Medical Scenarios Introduction to MP5 Submachine Gun Special Operations Aeromedical Evacuation Medical Management of K-9 Emergencies Disguised Weapons and Street Survival Medical Threat Assessment Written Exam Safety Briefing Tactical Medical Scenarios

Tactical Medicine Training

Day 2

Day 3

Day 4

Day 5

Administration and Introduction Pediatric Trauma Management Trauma Anesthesia Building Clearing Techniques Review Tactical Medical Scenarios Range Advanced Pistol–MP5 Advanced Airway Management Advanced Airway Management Skills Stations Environmental Injuries WMD Biological Weapons Part 1 WMD Biological Weapons Part 2 Medical Issues of Less-Lethal Weapons Low Light Tactics and Team Movement Tactical Medical Scenarios Pistol–MP5 Field Courses Explosive Entry Demonstrations Medical Management of Blast Injuries WMD Chemical Weapons WMD Nuclear and Radiation Injuries Written Exam Safety Briefing Tactical Medical Scenarios

From International School of Tactical Medicine, copyright 1996-2005. http://www.tacticalmedicine.com. WMD, Weapons of mass destruction.

From International School of Tactical Medicine, copyright 1996-2005. http://www.tacticalmedicine.com.

providers to more fully understand the unique aspects of law enforcement tactical operations and the roles and responsibilities of each team member, along with the integration and application of EMS. With an established body of knowledge and skills, graduates of such training programs are better prepared to effectively perform as safe tactical medical providers (Figure 25-34).62 The International School of Tactical Medicine (http://www. tacticalmedicine.com), a law enforcement agency program, is based at the Palm Springs Police Department Training Center in Palm Springs, California. This school offers a comprehensive 2-week, 80-hour program. The training and educational courses are designed for law enforcement agencies and military special operations teams to enhance their provision of medical care in the austere tactical environment. The program is approved by POST, EMSA, and the United States Department of Homeland Security. The curriculum for each course can be seen in Tables 25-13 and 25-14.

FIGURE 25-34  Tactical medics must be able to provide medical support under any and all operative conditions. (Courtesy International School of Tactical Medicine, Lawrence E. Heiskell, MD.)

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The Tactical EMS School of Columbia, Missouri, offers a 70 hour Essentials of Tactical EMS course (http://www. tactical-specialties.com). The Counter Narcotics and Terrorism Operational Medical Support (CONTOMS) program offers a 56 hour TEMS program (http://www.casualtycareresearchcenter.org).

The Future of Tactical Medicine Tactical medicine will continue to grow as a medical discipline. Emergency medicine and wilderness medicine are the ideal specialties to collaborate on its development. Since the fall of 2002, under the leadership of the International Tactical EMS Association (ITEMS), a multidisciplinary group of subject matter experts has been working to achieve consensus on development of a standardized national curriculum for tactical medicine training.18 Emergency physicians and wilderness medicine physicians should have an understanding of tactical medicine, because they may well have the opportunity to treat an injured operator or victim of violence associated with a tactical law enforcement action.23,39 Tactical medicine is wilderness medicine taking place in both the urban environment and some of the most remote places on Earth. There is a need for research into the unique aspects of tactical medicine, such as injury prevention during operations, methods of ensuring optimal mental and physical preparedness for tactical operators, and evaluation of various standard EMS therapies for their feasibility and efficacy in tactical scenarios. In these times, when the threat of violence to civilians in our society is at an all-time high, we rely on law enforcement professionals and the military to do all they can to keep us safe and protected. It is the role of tactical medics, providing medical care under any and all operative conditions, to give back to these professionals by ensuring that someone is there to care for them if they are injured in the course of doing their duty. Because it is no longer a matter of “if” a law enforcement officer will be injured in the line of duty, it is a matter of “when,” it is no longer a matter of “if” the wilderness medicine physician will encounter medical care related to armed conflict, it is also a matter of “when.”

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 26 



Combat and Casualty Care MICHAEL E. FRANCO, EDWARD J. OTTEN, THOMAS F. DITZLER, SHON COMPTON, AND PATRICIA R. HASTINGS It is difficult to emphasize sufficiently the importance of initial treatment on the battlefield. What the wounded soldier does in his own behalf, or what his infantry colleagues do for him; and what the company aidman does for a traumatic amputation or gaping wound of the chest, in the thick of battle, in dust and heat or in blowing snow—on these simple procedures depend life and death. … A slight improvement in the skill and judgment of the company aidman will save … more human lives than will the attainment of 100 percent perfection in the surgical hospital. COLONEL (DR.) DOUGLAS LINDSEY, U.S. ARMY,

1951

It is not commonly recognized that many of the most significant advances in medical science have been made by medical officers in the armed services … working under the stimulus of wartime exigency. PROFESSOR JOHN FULTON, CIRCA

1953

Wilderness Medicine is Combat Medicine with the exception of heavy artillery and aerial bombardment. Both are charged with the delivery of medicine/lifesaving interventions in less than optimal environments, with minimal equipment, and varying evacuation times. MAJOR (PA-C) MICHAEL E. FRANCO,

The Beginnings of Military/ Operational Medicine Wilderness medicine practitioners and disaster, humanitarian, and nongovernmental organization workers venture into environments that are complex, often with unique geography, political/ governmental systems (or lack thereof), and unfamiliar cultures; economic and resource situations may be constrained or desperate. These areas may be involved in conflict, so it is beneficial to have an understanding of the nature of combat casualty care. The first “operational wilderness medicine” courses and training were created centuries ago by military forces. Operational and wilderness medicine requirements have shared a long and symbiotic relationship with exchange of information, lessons learned, and equipment between the military and those physicians and responders willing and able to work in austere environments. Much of the knowledge, both remotely and recently, has benefited emergency care in general and wilderness medicine in particular. Much of the equipment and expertise now used by the military have resulted from improvements and refinement of wilderness medicine professionals. One of the first wilderness medicine experts to document wilderness medicine knowledge was Ibn Al Jazzar (circa AD 895-979) a physician from the Medical School of Kairouan in what is now Tunisia, once known as Carthage, the home of Hannibal (circa 200 BC). He wrote the then landmark wilderness medicine manuscript, Zad El Mousa Fir-Wa Qaout El Hadhir (Provisions for a Voyager Traveling Afar and for the Day’s Subsistence).56 The word for healer in ancient Greek was iatros, meaning remover of arrows. Whether removing arrows in ancient Greece or shrapnel in the 21st century, the unfortunate reality of conflict as part of the human condition requires health care providers to be involved in operational and military medicine. Since the beginning of recorded history, advice for medical response to be applied during conflict has come from those often noted for medical progress unrelated to conflict. Hippocrates (460-370 BC) is known as the Father of Medicine and for the concept, “First, do no harm.” He also gave the advice that “He who would become a surgeon should join the army and follow it.”

2011

Early accounts of medicine in war came from the classic literature, such as Homer’s The Iliad and Virgil’s The Aeneid. The Romans learned from these wars and trained medics (medici vulnerarii); each soldier carried his own bandages, which is similar to the Improved First Aid Kit (IFAK) carried today by soldiers and wilderness trekkers. In these accounts, medicine was rudimentary. Medical intervention concentrated on basic issues of bleeding, infection, and injury. These were the leading early killers in war though the ages and remain so to this day.

Introduction In ancient times any significant injury was likely to result in death. In the Revolutionary War, lethality of combat injury was 42%. In the Civil War, the combat mortality rate was 33% for persons wounded; this decrease was due to improvements made in evacuation from the field with an ambulance corps and surgical care closer to the field. Even with the horrors of chemical munitions and trench warfare, World War I showed a decrease in war injury deaths to 21%. Great strides were made in World War II, including antibiotics and blood/plasma replacement; however, the combat mortality rate remained high at 30%. Korea moved Mobile Army Surgical Hospitals to the front and was the first conflict to routinely use air transport to get injured soldiers to the surgeons. The Korean conflict mortality fell to 25%. Vietnam further emphasized quick evacuation to combat hospitals, but the mortality rate remained steady at 24%.56 In Vietnam, fewer than 3% died after arrival at a combat hospital, attributed to meaningful medical interventions being made earlier.28,29,34 Most deaths were due to hemorrhage and airway/breathing compromise. Desert Storm in 1991, with a short but very intense combat phase, recorded 159 deaths from 626 total traumatic injuries, for a mortality rate of 25%. Military medical leadership studied previous lessons and created a better medical field response. The rates of mortality in the current conflicts of Operation Iraqi Freedom and Operation Enduring Freedom are the lowest seen in the history of conflict. Combat lifesavers (first responders) and then combat medics are at the scene immediately and buy time for injured soldiers. The likelihood of coming home is over 90%24,28,29,34,40 (Table 26-1).

For online-only figures, please go to www.expertconsult.com

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

who have advanced medicine on every front and in many cases have forged a path for others to follow.

TABLE 26-1  Lethality of War Wounds

War

Killed in Action (KIA)

Wounded or KIA

Lethality (%)

Revolutionary War (1775-1783) Civil War (1861-1865) World War I (1917-1918) World War II (1941-1945) Korean conflict (1950-1953) Vietnam War (1961-1973) Persian Gulf War (1990-1991) OIF/OEF (2001-2004) OIF/OEF (2001-present)

4,435 140,414 53,402 963,403 33,741 47,424 147 1,004 4,720

10,623 422,295 257,404 291,557 137,025 200,727 614 10,369 49,337

42 33 21 30 25 24 24 10 9.5

Data from Department of Defense: Operation Enduring Freedom (OEF) U.S. casualty status: Fatalities as of Nov 18, 2010, 10 am EST. http://www.defense. gov/news/casualty.pdf; and Department of Defense: Operation Iraqi Freedom (OIF) U.S. casualty status: Fatalities as of Nov 18, 2010, 10 am EST. http://www.defense.gov/news/casualty.pdf. OEF, Operation Enduring Freedom; OIF, Operation Iraqi Freedom.

In addition, disease, nonbattle injury (DNBI) has been a constant concern for the field surgeon and medic. The outcome of many conflicts has been determined by DNBI. Athens fell to Sparta in 430 BC as a result of an unknown communicable disease. DNBI affecting the outcome of conflict played out again in the trench warfare of World War I, and DNBI was deadly even in the same region of Gallipoli where the British and Australians lost many soldiers to dysentery and other nonbattle injuries.33 In the U.S. Civil War, for every death due to trauma, there were three deaths due to DNBI and starvation. In the Russian-Afghan war over the course of 10 years, the war’s outcome was influenced greatly by disease; some contend that Russia was “beaten by the bugs.”37 Combat by its very nature is a chaotic, dynamic, and unpredictable environment in which military medicine must function well to save lives. The methods and technologic advances used to kill and maim have increased the numbers of injured and the seriousness of the injuries. The nature of war has become less focused on armed conflict between sovereign nations fought by professional militaries and become an undertaking of insurgents, child soldiers, and terrorists. Battlefields often have “no front lines,” and conflict is more dangerous for soldiers, as well as deliberately targeted noncombatant civilians; military medical providers are using new skills to care for these patients. Forward military medicine, performed before reaching combat support hospitals (CSHs), shares attributes with wilderness medicine. These include minimal equipment, harsh climates, remote and austere settings, and sometimes primal conditions. In militaries of the past, operational and wilderness medicine were taught after initial training as “on-the-job training.” Today they are primary medical training and education. Austere conditions typically connote an image of uncivilized remoteness, but they are also found in large populated areas where medical conditions may be impacted by armed conflict, supply shortages, bad weather, and impassable evacuation routes. For persons who deliver prehospital care on the battlefield, in disaster or humanitarian situations, whether urban or rural, working in the “wilderness” is the norm, not the exception. Regardless of environment, combat units within a battle space require medical capability. This capability is also used for injured civilians and forces that have laid down their arms. As strong as military medicine is as a force multiplier, it is also often used as a national engagement tool to shorten conflict, because medicine’s center of gravity and power is science and humanity, not geography, religion, or politics. When used in this manner, medicine may enhance progress toward peace.60 This chapter reviews a few lessons learned from military medicine, with the battlefield as the construct. The intent is to provide operational civilian health care providers an understanding of unique military medical capabilities, the continuum of care, and unique battlefield injuries, as well as describe some of the medical treatments and evacuation issues from the point of wounding to definitive medical care. We thank the hard work and sacrifice of military medical providers throughout history 508

Combat Medicine Compared With Standard Civilian Prehospital Care In conflict environments, completion of the mission and preserving one’s own forces take precedence. Medicine has a place in the tactical environment but is relegated to a secondary role at certain points. Mission-focused combat care is divided into three distinct classifications designed to support the mission: decrease loss of life using principles of triage, take care of immediate life threats with simple interventions of proved benefit, and save as many lives as possible through rapid evacuation. These phases of care do not normally rely on a complete assessment, physical examination or evaluation of past medical history, as might be expected in a secure location in a routine field emergency situation.17,18 The first phase of care, also known as care under fire, can be thought of as any event in which one is called on to render aid in an uncovered, unsecure, or potentially life-threatening situation. One cannot and should not “treat in the street” in a hostile environment. The first action will be to return fire and take cover (or take cover and return fire if more appropriate). There are many reflexive and simultaneous actions that will take place in this phase if the soldiers have been trained and drilled to an adequate degree of fine muscle memory. If one is able to provide care in this phase, the clinical intervention is likely to be only the most basic, such as moving the patient to a covered area to avoid further injury or placing a tourniquet. The usual protocols for ABCs (airway, breathing, circulation) may be reordered to CAB in order to focus on the interventions most likely to have the greatest impact on outcome in the working time frame.63 Care under fire may simply determine whether or not a person is still alive. Mortal wounds or conditions such as an unresponsive patient without a carotid pulse are circumstances in which cardiopulmonary resuscitation would not be performed. After this phase is over, it is important to not forget security issues. These are easily overlooked because of euphoria that may result from the relief of surviving, or the need to begin to care for one’s comrades.18,63 Field medics have long noted that one of their most critical first actions is to provide a confident demeanor. If the casualty is alert and responsive, the medic asks, “Where are you hurt?” and uses words and body language to let the victim know, “I’ve got you, and we’re going to get you out of here.” This is important because the casualty will be trying to determine his or her survivability and prognosis from the medic’s reaction. Major Shon Compton (U.S. Army physician assistant) teaches, “If the mind quits or doubts its chances; the body soon follows …” Tactical field care is rendered after the situation is secure and allows care to proceed. Depending on how quickly the patient is extracted, tactical field care may be the first care provided. The next phase of care is casualty tactical evacuation, in which the patient is stabilized and transported to a more definitive level of care. Evacuation platforms most often are “nonstandard” and nonmedical vehicles that are quickly drafted into use for critical casualty evacuation (CASEVAC).

Scopes of Practice for Combat Lifesaver, Combat Medic Injured soldiers are unlikely to see a physician at the point of wounding. The Army has taken the civilian trauma system lessons of the “golden hour” to the next stage in what it calls the “platinum 10 minutes,” using combat lifesavers and combat medics to provide initial response on the battlefield. Many military emergency physicians note that in that first few minutes, there should be no qualitative difference in the response to traumatic injury between the medic and the physician. Given the same aid bag, the same set of circumstances, and the same patient, the expectation is that the same immediate lifesaving interventions will be made.63

airway skills include use of an adjunct such as a Combitube or King LT device and surgical cricothyrotomy (see Figure 26-1). The 68W is also taught the skills of needle chest decompression and chest tube placement. The 68W has the ability, with special training, to place an IV or intraosseous line and in certain cases administer blood products. The 68W has additional training in management of shock, including resuscitation from hypotension and prevention of hypothermia. Because closed head injury, burns, and stress reactions are prevalent wounds of the Iraq and Afghanistan conflicts, combat medics are entrusted with the initial evaluations of these problems. If the patient cannot be evacuated in a timely fashion, the combat medic may initiate protracted care, to include the placement of a nasogastric tube and urinary catheter. Combat medics also have the capacity to perform limited primary care, using protocols for minor sick call problems, and assist with monitoring for DNBI. They are given training in international humanitarian law (Geneva Law) focused on

Core skill requirements

CLS

68W

RN

PA/MD

Airway: cervical spine immobilization Airway: clear an upper airway obstruction Airway: insert an oral/nasopharyngeal airway Airway: insert Combitube Airway: insert laryngeal mask airway (LMA) Airway: perform endotracheal intubation Airway: perform rapid sequence intubation Airway: perform a needle cricothyroidotomy Airway: perform a surgical cricothyroidotomy Airway: perform endotracheal suctioning Breathing: perform needle chest decompression Breathing: place chest tube for hemo/pneumothorax Breathing: ventilate a patient with bag-valve-mask Breathing: ventilate patient using Impact 754 ventilator Circulation: control bleeding using pressure dressings Circulation: apply tourniquet to control bleeding Circulation: recognize signs/symptoms of shock Circulation: obtain vital signs and recognize changes Circulation: place peripheral intravenous line Circulation: place central line Circulation: perform venous cutdown Circulation: perform intraosseous line placement Circulation: initiate intravenous crystalloid infusion Circulation: administer blood/blood products Circulation: administer volume with Level 1 infuser Circulation: perform pericardiocentesis Circulation: apply a dressing to an open chest wound Circulation: apply a dressing to an open abd wound Circulation: apply a dressing to an open head wound Disability: recognize signs/symptoms of increased intracranial pressure Disability: splint a suspected fracture Exposure: prevent hypothermia Exposure: recognize and treat hypothermia FIGURE 26-1  Core skill requirements. ACLS, Advanced Cardiac Life Support; CLS, combat lifesaver; ECG, electrocardiogram; MD, physician; Continued PA, physician assistant; RN, registered nurse.

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CHAPTER 26  Combat and Casualty Care

Combat lifesavers are first responders that are sometimes called the “battle buddy” of the medic. They buy time for the patient after the initial trauma. Their primary military occupational specialty may be that of infantry, aviation, maintenance, or other military nonmedical specialty, but after the situation is secured, they offer an extra set of hands for the medic. In addition to basic first aid, they are able to provide such skills as to deploy nasopharyngeal airways, apply tourniquets, or perform needle chest decompression for breathing difficulty after a penetrating wound to the chest (Figure 26-1).5 They do not, however, initiate intravenous (IV) lines or perform certain other advanced skills. The combat medic is also known by the designation 68W (68 Whiskey). The scope of practice of the combat medic is most analogous to an EMT-Intermediate, with some special skills training in combat operational medicine based on the security, sick call, and unit issues with which the medic must deal. Additional

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Core skill requirements

CLS

68W

RN

PA/MD

Exposure: protect yourself from heat, cold, biting insects, and diarrhea and dysentery Adjuncts: place and monitor pulse oximeter Adjuncts: monitor ECG rhythm strip Adjuncts: perform hemodynamic monitoring Adjuncts: perform diagnostic peritoneal aspiration/lavage Adjuncts: insert naso/orogastric tube Adjuncts: perform arterial line placement Adjuncts: manage arterial line Adjuncts: insert urinary catheter Management: apply traction splint for extremity fracture Management: apply pelvic sheet/binder for pelvic fracture Management: ligate/clamp bleeding in traumatic amputation Management: provide initial treatment for burns Management: perform regional anesthetic techniques Management: administer first aid to a chemical agent casualty Management: manage combat stress reaction (battle fatigue) Disposition: request medical evacuation Disposition: perform initial triage of casualties ACLS: recognize cardiac arrest and dysrhythmias ACLS: use defibrillator to treat cardiac dysrhythmias ACLS: treat dysrhythmias pharmacologically ACLS: manage hemodynamic alterations pharmacologically FIGURE 26-1, cont’d.

the rights, duties, and responsibilities of combat medics in areas of armed conflict, as well as caring for detainees.

Levels of Care and Capabilities MILITARY HEALTH SYSTEM ECHELONS OF CARE The continuum of care in the military extends from the point of wounding to a battalion aid station (BAS), usually staffed by a physician assistant and/or physician, to the forward surgical team (FST) to the CSH (Figure 26-2).26 At each point of care, the level of surgical and holding capability increases. Military medical planning includes support at each of these levels.3,27,31,54 Level I The first medical care a soldier receives occurs at Level I, which may begin at the point of wounding. Initially, these first responder actions are provided by soldiers with combat lifesaver training, and later with assistance from the combat medic. If the service member is transported to a BAS, care is augmented by a senior medic or physician assistant. Level I initiates triage, patient collection, resuscitative care, and medical evacuation to higher levels of care. If the injuries or illness are minor, treatment is given and the disposition is “return to duty.” If the care required is more than minor, the patient is evacuated to a Level II or Level III facility. The decision is made based on the security situation, 510

distance, and nature of the injuries. The civilian equivalent is similar to a first responder ambulance squad with advanced skills. Level II Level II is broken down into Levels IIA and IIB. Level IIA is an expanded care hub for the BAS, called an area support medical battalion (ASMB); this is similar to an urgent care clinic. This level of care duplicates Level I and augments services, with limited dental, laboratory, optometry, preventive medicine, health service logistics, mental health services, and patient-holding capabilities. The ASMB can further evaluate a casualty to determine if evacuation to a CSH (Level III) is warranted. In remote locations, Level II facilities are often teamed with an FST, also designated as Level IIB, to provide initial damage control surgery. The FST has an orthopedic surgeon, two or three general surgeons, two anesthetists, and critical care nursing capability. It is configured to be able to complete 10 major surgeries per day. Level IIB is similar to an emergency department with emergency surgical services. Level III Level III may be a CSH, a hospital ship, or Air Force facility. These facilities are in the combat zone and are analogous to regional trauma centers, with a full complement of medical and surgical services. There are intensive care and patient wards. These facilities are modular and can expand from 44 to 248 beds. If the patient requiring rehabilitation or extended treatment can

En route care capability

CHAPTER 26  Combat and Casualty Care

Definitive capability

Full range of acute, convalescent, restorative, and rehabilitative care

Theater hospitalization capability Forward resuscitative capability First responder capability Prevention and protection capability Policy and resource acquisition capability

Full range of acute, convalescent, restorative, and rehabilitative care Forward advance emergency medical treatment performed Medical care rendered at the point of initial injury or illness Promotion and improvement of mental and physical well-being Policy formulation, planning, programming, budgeting, and disbursing resources

FIGURE 26-2  Taxonomy continuum of health care capabilities. (From Defense Medical Readiness Training Institute: Joint operations medical managers course guide, San Antonio, Tex, 2009.)

be evacuated in less than 48 hours, or will have a prolonged recovery time, he or she is evacuated out of the theater. Local national civilian patients are not evacuated out of the theater, and civilian care may require extended hospitalization and rehabilitation that was not initially planned. Level IV The backstop of theater military care is the regional trauma medical center. This facility is within the theater, but on the evacuation pathway out of the combat zone. Definitive care, rehabilitation, and medical specialty services are available. The average stay is short for patients not expected to return to duty. These patients are further stabilized and evacuated out of theater for continued care at a Level V facility. Level V Definitive care describes Level V (primarily continental United States/CONUS) care. The Department of Defense and U.S. Department of Veterans Affairs hospitals provide this care. There are mechanisms to increase bed space using civilian hospitals in the National Disaster Medical System if this is vital to the effort. Medical planning considerations loom large in the military because of the effects of practicing in an area of armed conflict often exacerbated by austerity of the environment itself. At one time an afterthought, military medical planning is now routinely considered at mission planning events. As for any wilderness medicine expedition, the specific characteristics of military health service support are determined by the mission, the threat, intelligence, anticipated number of patients, duration of the operation, the theater patient movement policy, available lift, and hospitalization and movement requirements. Military medical planners are expected to have an understanding of all the areas below: • Threats/medical intelligence considers opposing force actions; occupational, environmental, geographic, and meteorological; endemic diseases and psychological stressors; and weapons of mass destruction. • Patient movement and all this entails from planning, equipping, and patient care perspectives often have the greatest impact on the structure of the health service support design. Delays in transport will require holding capability and more assets for care . As for any expedition, weather, terrain and distance contribute greatly to decisions. • Preventive medicine and health surveillance

• Prevention of stress casualties—The medical system is responsible for care related to mental health issues; however, a great deal can be done to prevent problems through establishment of a collaborative relationship with unit leadership. • Veterinary service—The working dogs, civilian livestock in humanitarian situations, and any local animal issues such as rabies or disease reservoirs need to be considered in planning. Working dogs, in particular, are critical to many missions, such as security. These animals are considered soldiers in every sense of the word and may need full trauma resuscitation, including blood transfusions. • Dental readiness needs should be addressed before deployment. Dental pain is a frequent reason for movement to the rear in unprepared soldiers. • Medical care for prisoners of war and detained personnel— The care for this population may be more labor intensive than anticipated due to previous lack of medical care and significant traumatic injuries. • Mass casualty situations preparation

Theater Trauma System Much of the improvement in survival rates in the Afghanistan and Iraq conflicts is directly attributable to implementation of a trauma system. In both military and civilian populations, large numbers of patient requiring treatment for trauma or illness are best served through a “system approach.” The best systems have a designated trauma system director who is responsible for data acquisition, critical review of collected records, development of medical policy and practice guidelines, and ongoing evaluation of medical resources utilization, including staffing.37

JOINT THEATER TRAUMA REGISTRY The Joint Theater Trauma Registry (Figure 26-3) is a key component of the Joint Theater Trauma System and was implemented in November 2004. As would any civilian trauma system, it collects the usual demographic and mechanism of injury data points. In addition, it collects information on unique transportation solutions, protective gear, service affiliation of the injured, and some unique aspects of conflict injuries (e.g., chemical, nuclear). 511

Unique Aspects of Military Triage and Other Considerations As in civilian mass casualty situations, triage attempts to provide the greatest good for the greatest number of victims. In most cases, military triage categories mirror those for civilians: immediate, delayed, minimal, expectant. In military triage situations, the security situation is often grim, transportation may be delayed, and the triage category of wounded soldiers, who in a less dire situation might have a survivable injury, becomes “expectant.” In addition, the military trains for scenarios involving chemical, nuclear, and radiologic incidents to practice continued combat effectiveness. Triage and treatment may be delayed because of mission requirements. The apportionment of resources may be based on the need for mission success. An interesting illustration of the need for continued combat effectiveness was described in World War II, where penicillin was first used extensively for wound infections. Penicillin was very effective in the treatment of sexually transmitted diseases (STDs), also seen in the military population. Because of its limited availability, penicillin was rationed and at times used first for those soldiers with sexually transmitted diseases rather than for the badly wounded, to keep the fighting forces at the front.53 Military triage has a component related to international humanitarian law. Soldiers who have laid down their weapons are offered the same opportunity in triage for care and treatment of their combat-related injuries. Triage for persons experiencing an emotional stress reaction, with or without wounding, require disarming before care can proceed.

Trauma Record

Trauma Record

For use of this form, see DoD Memeo Subject: Trauma Record, dtd 1 APR 04; the proponent agency is OTSG AUTHORITY: PURPOSE: ROUTINE USES: DISCLOSURE:

DISCHARGE SUMMARY

AR 40-66 To provide a standard means of documenting all trauma care at echelons 1-3 The “Blanket Routine Uses” set forth at the beginning of the Army compilation of systems of records notice apply. This is protected health information. HIPAA laws apply.

MTF DESIGNATION: Number

CASUALTY NAME: FIRST

TYPE

Arrive Date-Time Group (DTG):

Rank

Non-MED GND ARRIVAL METHOD: SHIP EVAC WALKED GND AMB CARRIED AIR AMB Non-MED AIR OTHER ____________________________

Nation

Gender Male

Service

US Host Nation Enemy( Coalition(

MECHANISM OF INJURY: GSW/BULLET BLUNT TRAUMA SINGLE FRAGMENT MULTI FRAGMENT

Penetrate

Struck

UNK

HELMET

REGION

Female

SOF NGO( Other

Head & Neck (incl C-spine) Chest (incl T-spine)

3

8

12

15

CERAMIC PLATE UNC

EYE PROTECTION

STUPOR

LETHARGY

Abdomen (incl L-spine)

ALERT

TIME

OTHER: BURN (thermal, flash) CRUSH FALL SMOKE Inhalation

HEAT COLD BITE/STING OTHER _______ __________________

Pulse Temp

Pelvis

B/P Resp SpO2

UPPER/LOWER Extremities

TX & PROCEDURES: SEDATED

L

L

R

L

R

L

R

CHEM PARALYZED INTUBATED CRIC NEEDLE DECOMP Chest Tube IO line COLLOID CRYSTALLOID TOURNIQUET

Skin L

R

DISPOSITION

air/blood ml

LR/NS/HTS ml Time on Time off

OXYGEN

OR Start DTG: Stop DTG: PROVIDER:

BL Bleeding B Burn X Fracture

D F S

Deformity Foreign Body Stab Wnd

H Hematoma L Laceration G Gunsh Wnd

Units Units

CRYO

Units

Pits

Packs

ICU in DTG:

Fresh Whole Bld

Out DTG:

rFVlla

SPECIALTY:

Liters/min.

FFP

Off DTG:

EXT Fix/splint

EVAC to ___________________________ RTD DECEASED (see below)

Units mcg/kg

ANATOMIC: Airway Head Other PHYSIOLOGIC: Breathing CNS

Neck

Chest

Hemorrhage

COMMENTS:

Extremity

FIGURE 26-3  Joint theater trauma registry.

512

Hypothermic (<34°C)?

Evacuation Priority ROUTINE PRIORITY URGENT Y/N

Coagulopathy?

Cause of Death at DTG

RBC

Vent On DTG:

DTG:

Damage Control Procedures? Y / N

Collar/C-spine Back board HEMOSTATIC DEVICE

AM Amputation AV Avulsion P Puncture

DIAGNOSIS, PROCEDURES, and COMPLICATIONS

)

GLASCOW COMA SCALE (circle one)

INJURY Description (Location, nature and size in cm)

R

PMH:

Face

TRIAGE CATEGORY: IMMEDIATE DELAYED MINIMAL EXPECTANT

FLAK VEST

KNIFE/EDGE BLAST CRASH (a/c, veh, ped) Chem/Rad/Nucl

XRAYS:

Allergies: Unit

USA USN USMC USAF

Civilian Combantant Contractor

) )

Worn

WOUNDED BY: US/COALITION (Nation _______________) ENEMY NonENEMY CIVILIAN (Nation ____________________) TRAINING SELF ACCIDENT SELF NON-ACCIDENT SPORTS-RECREATION OTHER

LABS:

LAST Date of Birth

PROTECTION:

Wound DTG:

MEDICATIONS:

CASUALTY SSN:

Not Worn

PART 4  INJURIES AND MEDICAL INTERVENTIONS

This information has been analyzed extensively to develop and improve clinical practice guidelines, protective measures, medical and nonmedical training and best practices for patient care from the prehospital resuscitation, to damage control surgery, through rehabilitative care. The data have a very high fidelity in the fixed facilities but are less complete directly from the field.20,15,16,30 Field collection of information is more difficult to obtain due to communications problems, the chaotic and insecure environments inherent in combat operations, and initial care and evacuation by nonmedical responders. The military recognizes field collection of data as a critical link in combat care and is exploring many areas for improvement, if not full resolution of field data collection issues. The preliminary findings are the same as those found in civilian trauma systems; the solution needs to be simple, lightweight, fast, and easy to append to patient records. The military has experimented with the Battlefield Medical Information System–Tactical (BMIST), an electronic data collection system. It is still the goal to use an electronic patient care recorder. Though relatively lightweight, the BMIST weighs 11.1 to 14.1  oz; every item in a combat medic’s aid bag increases difficulty in mobility and decreases treatment items. Currently, as a fail-safe method, a simple tactical combat casualty care (TCCC; also referred to as TC3 in other venues) card (Form DA 7656) is used and carried in the soldier’s IFAK. If the soldier is injured, this card is completed as best possible and moves with the patient to the treatment facility, where it is able to be scanned into the record. It is a better method of recording trauma data than was the previous field medical card (Figure 26-4).

Abdomen

Pelvis

Total Body Disruption

Extremity (Upper/Lower)

Sepsis

Multi-organ failure

SURGEON: (printed name)

Y/N

Name/ID: DTG: Friendly

ALLERGIES: Unknown NBC

A:

Intact

B:

Chest Seal NeedleD Chest Tube

Adjunct

Cric

Intubated

C: TQ Hemostatic Packed Pressure Dx IV IO

TQ TIME

FLUIDS:

NS/LR

500

1000

1500

Hextend 500 1000 Other: DRUGS (Type/Dose/Route): PAIN ABX OTHER GSW BLAST MVA Other

TIME AVPU PULSE RESP BP Medic’s Name

Clinical Applications of Lessons Learned SOLDIER MEDICAL FIRST AID KITS (Figures 26-5 to 26-7) AND WARRIOR AID AND LITTER KIT Improved survival rates in the current conflicts have been evaluated to search for further improvements. The reasons given for the 90% survival, even with increased lethality of wounding agents, are improved personal protective equipment, adherence to TCCC precepts, faster evacuation, and better-trained medics. The IFAK (see Figure 26-5) was developed based on the continuous review of injuries and is carried by every deployed soldier. It contains the essential items to address the major causes of preventable combat death: compressible hemorrhage, airway compromise, and tension pneumothorax. The IFAK contains a combat application tourniquet (CAT), kaolin-impregnated rolled gauze (Combat Gauze) that promotes hemorrhage control, 15.2-cm (6-inch) compression dressing (Israeli Trauma Bandage), nasopharyngeal airway, and 8.9-cm (3.5-inch) 14-gauge IV catheter for needle chest decompression. Hemorrhage is the leading cause of combat death. Interestingly, combat injuries have

MOLLE IFAK pouch and insert

Coiled retaining lanyard Nasopharyngeal airway (NPA) Examination gloves (4)

Combat application tourniquet (CAT) stored

2-inch tape Kerlix Emergency bandage

FIGURE 26-5  Improved First Aid Kit (IFAK) components. MOLLE, Modular lightweight load-carrying equipment. (From Army Medical Department Center and School: Briefing on Combat Equipment, 2007.)

• Canvas pouch • 12 gauze bandages/adhesive surgical plaster/ carton medium safety pins • 3 triangular bandages/8 small first-aid bandages • 1 flask with cup/1 small glass bottle • 1 metal container with 6 iodine swabs • 1 bandage scissors/double-blunt scissors/1 forceps • 2 litter carrying straps, to help support weight of litter and patient • 20 emergency medical tags (Form 52b)/1 pencil FIGURE 26-6  World War II aid bag. (From Army Medical Department Center and School: Briefing on Combat Equipment, 2007.)

513

CHAPTER 26  Combat and Casualty Care

FIGURE 26-4  Form DA 7656.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Tourniquets are the number 1 instrument that a medic can employ to lower the KIA (killed in action) numbers. COMMITTEE ON TACTICAL COMBAT CASUALTY CARE

• IV bottle/IV set up • Compressed bandages/gauze rolls/elastic bandages/ triangular bandages/stomach bandage/2-inch gauze pads/ paper and adhesive tape/Q-tips • Wire splints • Aspirin with and without codeine • Cough medicine with and without codeine • Burn ointment/Neosporin/eye ointment • pHisoHex soap/peroxide/mercurochrome/alcohol • Epinephrine syringe and needle/Benadryl/Ornade/ Darvon • Morphine was carried by the medic; never in the aid bags FIGURE 26-7  M5 Vietnam aid bag. IV, Intravenous. (From Army Medical Department Center and School: Briefing on Combat Equipment, 2007.)

remained relatively similar in distribution since the Civil War; extremity injuries are the most common. A Warrior Aid and Litter Kit (Figure 26-8) is carried on vehicles, although it can also be easily dismounted and carried via shoulder straps to the point of wounding. The additional equipment increases a unit’s capabilities to provide self-aid/buddy-aid for multiple casualties and interventions for the three leading causes of death on the battlefield. Furthermore, it provides a military squad the ability to evacuate a nonambulatory casualty (folding litter) and increases survivability during dispersed operations (i.e., improvised explosive device [IED]/rocket-propelled grenade [RPG] attack on convoy).

HEMOSTATIC AGENTS AND TOURNIQUETS I am afeard there are few die well that die in a battle; for how can they charitably dispose of anything when blood is their argument? WILLIAM SHAKESPEARE, THE LIFE OF KING HENRY THE FIFTH

WALK

514

6545–01–532–4962

The U.S. Army Institute of Surgical Research in San Antonio, Texas, finds that one-half of those injured in combat suffer “potentially survivable” wounds. Eighty percent of these are hemorrhage. In these bleeding events, 30% are in the extremities and “compressible,” where a tourniquet can be used to stop bleeding; 20% are in the neck, groin, axillae, or areas where a tourniquet cannot be used, but pressure can be applied to stop bleeding; and thorax or abdominal account for the remaining 50%, where surgical intervention is necessary.8,20,23 Jean Louis Petit, a French surgeon, developed a screw device in 1718. He coined the term tourniquet from tourner (to turn).64 The earliest known usage of a tourniquet dates back to 199 BC. Tourniquets were used by the Romans to control bleeding, especially during amputations. These tourniquets were narrow straps made of bronze covered with leather (Figure 26-9). These look remarkably similar to the CAT (Figure 26-10) used today. The CAT was selected after extensive testing and research. Other methods, such as a triangular bandage and sticks, can be used if a CAT is unavailable. The imperative is to occlude the distal pulse. It may take multiple tourniquets to accomplish obliteration of the pulse. Do not remove previously applied tourniquets if bleeding continues; tighten the tourniquet further if possible, or apply another tourniquet proximal to the first.63 TCCC teaches to attempt to control all sources of bleeding and consider and assess for any bleeding not immediately detectable. The TCCC protocol for life-threatening compressible external hemorrhage or amputation is tourniquet application. The tourniquet is placed on the skin 5.1 to 7.6 cm (2 to 3 inches) above the wound. For neck, groin, and axilla hemorrhage, Combat Gauze is used. It is packed in the wound, and direct pressure is applied for at least 3 minutes. Then, a pressure dressing is placed over the wound site if possible. For anatomic reasons, a pressure dressing may have to be innovative. It is impossible to circle the neck with a pressure dressing because the blood supply to the brain and airway will be disrupted. All tourniquet sites should be exposed and clearly marked using an indelible marker with the time of tourniquet application. A “T” drawn on the patient’s forehead is a common designation. A bandage that stops bleeding has been sought for centuries. Combat Gauze, which is a kaolin-impregnated Kerlix gauze, is the best hemostatic dressing at this time. Other agents have been reviewed and/or used but had drawbacks. Factor concentrators, such as QuikClot, that removed water from blood, created a significant exothermic reaction, were difficult to use in some environments, and were difficult to wash out of wounds. WoundStat used concentrated clotting factors without a significant

FIGURE 26-8  Warrior Aid and Litter Kit (WALK). (From Army Medical Department Center and School: Briefing on Combat Equipment, 2007.)

The Airway in Combat

FIGURE 26-9  Roman tourniquet. (Courtesy Science Museum, London. http://www.sciencemuseum.org.uk/broughttolife/objects/display. aspx?id=4304.)

increase in temperature, but caused some tissue damage and embolic episodes. Mucoadhesive vehicles, such as HemCon, Chitoflex, TraumaStat, and Celox, were made of shrimp exoskeletons. Although tissue damage was not seen, the hemostatic properties were not as robust as those seen with Combat Gauze. Combat Gauze is a procoagulant supplement that uses gauze impregnated with Kaolin (active agent is aluminum silicate) and is the hemostatic dressing issued to the U.S. military for combat use. In the future, fibrin dressings and spray-on sealants may become available.1,13,22,44-46 Combat Gauze may be used after the initial application of a tourniquet has stopped bleeding or if a tourniquet is not essential on inspection of the wound after the care under fire phase. It is vital to continually monitor bleeding if a tourniquet is placed or if other techniques are used, because these may become dislodged or the patient may start to bleed after fluids are replenished or the patient is warmed. Hypotensive resuscitation to avoid normalization of blood pressure and “blowing the clot” until surgical control is achieved is a key principle. Before releasing any tourniquet on a casualty who has been resuscitated for hemorrhagic shock, to ensure a positive response to resuscitation efforts, one should have applied a pressure dressing and be ready to reapply the tourniquet. Tourniquets cause ischemia in the treated extremity. Release of a well-placed and functioning tourniquet after several hours releases lactic acid and potassium generated by anaerobic metabolism and cell injury. Before removal of a tourniquet that has been in place for any significant period of time, make sure the patient is well hydrated and as fully resuscitated as is reasonably possible, and consider adding 50 mEq of sodium bicarbonate to a liter of IV fluid for administration. Release the tourniquet slowly. If cardiac arrhythmias occur, reapply the tourniquet and wait to remove it until after further fluid resuscitation and sodium bicarbonate is administered. If the limb is “dead,” the overriding tenet is “life over limb.” Consider a fasciotomy (four compartment) in any lower extremity with extensive tourniquet time (over 2 hours).10 Control of bleeding is paramount in combat care. Adequate bleeding control may turn an “immediate” category patient into

FIGURE 26-10  Combat application tourniquet (CAT).

The protective equipment worn by the military is working well to decrease injuries to the thorax. However, the face remains relatively exposed, with the result that 10% to 15% of combat casualties sustain maxillofacial trauma. Penetrating facial/airway trauma often presents a frightening picture but is often manageable if taken one step at a time. In emergency medicine, clinicians are always taught to control cervical spine (c-spine) movement by using a hard collar and immobilizing the patient on a spine board. However, this approach may cause further airway complications in a patient with significant penetrating facial trauma. Blunt forces cause c-spine injury in 2% to 6% of patients in civilian studies and may be up to 10% in patients with extensive blunt facial trauma. Unstable cervical spine trauma is uncommon in neurologically intact patients with penetrating (as opposed to blunt) force injuries.12,48,51 In many cases, simple positioning or use of a nasopharyngeal airway will allow an adequate airway until definitive treatment is available. If the patient is able and wants to sit up, it is preferable to allow this rather than suffer an airway loss. The contraindications for combat nasopharyngeal airway placement are severe head or facial injuries, evidence of a basilar skull fracture (e.g., Battle’s sign, raccoon eyes, cerebrospinal fluid/blood from ears), or known coagulopathy. Loss of a marginal airway can occur quickly if medications with sedating properties are used, so it is best to defer these until medical personnel are ready to manage the airway. If pain medications are used, be prepared to take over the airway.10 The usual interventions are IV access, monitoring, suction, and supplemental oxygen. Before taking over definitive airway management for the patient, everyone should be ready to perform it and those with the most expertise should be in attendance. If sedation is required, IV ketamine in titrated doses allows the patient to maintain breathing and some protective reflexes. Difficulties arise from inadequate suction and bleeding into the field of vision. If oral endotracheal intubation is impossible, cricothyrotomy is performed. Alternatively, video intubation scopes are small, lightweight, and very portable and are a useful adjunct, although visualization is still difficult in situations with brisk bleeding or in the absence of suction. In environments where use of a laryngoscope could garner unwanted attention from the enemy, a cricothyrotomy might be necessary even if oral intubation is an option. In mass casualty situations, the threshold for cricothyrotomy is decreased due to time and resource constraints.

Hypothermia Hemorrhage and trauma can be precipitating events for hypothermia. The combination of hypothermia (defined as core body temperature under 35° C [95° F]), acidosis, and coagulopathy put trauma patients at greater risk for multisystem organ failure and death. This triad was first described in 1982 as the “bloody vicious cycle.” Hypothermia itself inhibits coagulation. Under 32.2° C (90° F), hypothermia is life threatening by affecting cardiac and respiratory function. Hypothermia is seen commonly in trauma patients, even in environments where heat injury might seem more likely. The Joint Theater Trauma System noted that patients evacuated to the combat support hospitals were hypothermic, and the system developed a hypothermia clinical practice guideline, which is emphasized by the Committee on Tactical Combat Casualty Care and its training recommendations.3,7,39 Prevention measures are protection from the environment, removal of wet clothing (blood or other fluids), keeping the patient covered, and using adjuncts such as the Hypothermia Prevention Management Kit (HPMK). The latter is especially 515

CHAPTER 26  Combat and Casualty Care

a “delayed” category patient, able to wait for secure transport. Tourniquets and hemostatic agents (QuikClot Combat Gauze) are the current best methods of bleeding control. Blind attempts at clamping vessels in bleeding wounds cause more damage than good and should be avoided. Bandages should be inspected frequently because they can hide continued bleeding.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

useful during the CASEVAC phase, where prevention of hypothermia may be difficult due to altitude, flying with open doors, and the injury. The HPMK has a self-heating, four-cell shell liner that is able to sustain continuous dry heat, and a skull cap to keep the patient warm.63 Also, if portable fluid-warming devices, such as the Thermal Angel Blood Warmer, are available, they should be used on all IV fluid sites. If adjuncts are unavailable, one uses whatever is at hand, such as dry blankets and sleeping bags. Wool blankets alone are not particularly good at keeping the patient warm, but a “hot pocket” has shown good results to prevent passive heat loss. This method puts the patient in a body bag, covered in two wool blankets and a space blanket, with an opening for an endotracheal tube.2,10

Damage Control Surgery The goal of damage control surgery is to prevent the physiologic derangements caused by trauma and severe hemorrhage. The surgery does not reestablish normal anatomy but is rather a planned series of surgeries to normalize function. Damage control is a planned management of the patient with three defined phases: 1. Abbreviated operation to control hemorrhage and contamination, as well as determine the extent of injury; defer definitive repair. Abdominal surgeries are not initially closed to avoid compartment syndrome. Retroperitoneal bleeding is packed to avoid magnifying life-threatening bleeding. 2. Intensive care unit resuscitation, consisting of rewarming, stabilization of vital signs, and correction of coagulopathy and acidosis. 3. Return to surgery, either definitive or before evacuation for definitive care. This care continues as the patient is moved through the evacuation process to definitive care.3,10,57

Blood The U.S. Army clinical practice guideline for damage control resuscitation (with massive transfusion defined as >10 units of red blood cells [RBCs] in under 24 hours) was instituted in March 2006. It endorsed a 1 : 1 fresh frozen plasma (FFP) to RBC transfusion ratio with less emphasis on crystalloid use.49,59,62 In most cases blood component therapy is used. However, in austere circumstances use of fresh whole blood (FWB) may be a way to augment the blood bank with “fresh” donors, especially if FFP and platelets are in limited supply or nonexistent. There is some indication that FWB may blunt the inflammatory response and organ failure seen in hemorrhagic shock states. In addition, oxygen-carrying capacity and decreased hemolysis (associated with hyperkalemia) are seen with FWB.

Factor VIIa Factor VII initiates the process of coagulation in conjunction with tissue factor, which is found on the outside of blood vessels and therefore is normally not exposed to the bloodstream. Upon vessel injury, tissue factor is exposed to the blood and circulating factor VII. Factor VII is activated to factor VIIa. Factor VIIa is a procoagulant that was first used in uncontrollable bleeding seen in hemophilia patients with factor VIII or IX deficiency and inhibitors against replacement coagulation factor. Factor VIIa was first reported used for trauma in 1999 for an Israeli soldier in extremis due to a high-velocity gunshot wound with disruption of the inferior vena cava.43 In the U.S. military, factor VIIa is used in uncontrollable hemorrhage with significant coagulopathy as an addition to FFP and packed red blood cells in a 1 : 1 ratio. Platelets are given if massive transfusion is necessary. Factor VIIA requires adequate platelets for optimal results. Acidosis must be corrected in order for it to work. There is a theoretic risk for deep vein thrombosis, pulmonary embolism, and myocardial infarction. However, prospective randomized trials and retrospective trials on combat wounded have not shown any increase in thromboembolic events. 516

Wounds Combat wounds range from minor to devastating. All require meticulous care and can initially be deceiving as to extent. For the initial combat wound, the soldier takes antibiotics that are supplied in the combat pill packs. The usual antibiotic is moxifloxacin 400 mg orally (PO) once a day. If the soldier is unable to take oral medications, then cefotetan 2 g IV or intramuscularly (IM) every 12 hours (or ertapenem 1 g IV or IM) once a day is administered. Even though most soldiers have current immunizations, one must consider tetanus immunization status in all wounds. This is especially true in nonmilitary personnel. Antibiotic prophylaxis is included for any penetrating wounds to the eyes/globe.* Wounds from blast injury include burns, tissue loss, and/or extensive maceration. These injuries should all be treated as though there is underlying structural injury until proved otherwise; these patients are often candidates for damage control resuscitation and surgery. Initially bleeding may be unimpressive, but it can increase with improvement in blood pressure, warming, and manipulation during exploration, debridement, and irrigation. Primary closure of wounds is rarely considered.10,50 After debridement, the wound should be packed with rolled gauze. If necessary, the skin is sutured over the packing for tamponade of bleeding. This is a temporary measure for life-threatening bleeding until damage control resuscitation is under control.3,10 Injuries to large arteries and veins need to be controlled and may require a tourniquet, pressure dressing, vascular shunt, or ligation. In initial damage control surgery, a nasogastric tube or IV tubing can be used as a temporary vascular shunt, and the aorta can be shunted with a small pediatric chest tube. If a shunt is performed and the patient is to be transferred, a tourniquet should be placed loosely (i.e., not tightened) proximal to the shunt for transport in case of shunt dislodgment. Similarly a nontightened tourniquet should be placed before evacuation after amputation to be prepared for bleeding.10 Unique aspects of blast injuries are the extensive damage and the path the blast may follow up the bone in an extremity. Although physicians are taught to spare as much tissue as possible during debridement, in blast/land-mine injuries a common problem is underestimation of the depth of the injury.

Wound Vacuum-Assisted Closure (VAC) Wound VACs are critical tools that have changed the face of wound care … seriously. No CSH should deploy without them. COLONEL (DR.) THOMAS G. CRABTREE, 2006 Wound care has been a defining characteristic of military medical care through the ages. The principles are cleansing, debridement, and elimination of effects harmful to the wound (such as wound cautery used in the Middle Ages and early Renaissance). In today’s battlefield, more soldiers survive blasts, high-velocity missile strikes, and other combat injuries because of better protective gear, highly trained combat medics, and faster evacuation to surgical care. These survivors have complex wounds with high probability of infection that are unable to be closed primarily. They require not only adherence to the basics, but new modalities and a team approach to care that involves physical and emotional care.3,10,50,54 Wound VAC devices are used extensively with good results for massive wounds with tissue loss seen in combat injuries. Other circumstances that benefit from this therapy are pressure ulcers, partial-thickness burns, orthopedic injuries with tissue loss, skin grafts, and abdominal wounds that are left open after damage control surgery. This therapy can decrease healing time and reduce risk for infection and other complications. Commercial devices consist of a dressing that is fitted with a tube and attached to the wound VAC device. *References 3, 10, 35, 41, 54, 63.

Burns Prehospital burn care is the same as that for civilians with a few additional considerations. The burn patient in a combat zone must be considered for additional injuries, wounds, hemorrhage, and possibly blast injury. If this is the situation, Hextend is used as per the shock protocols along with crystalloid (lactated Ringer’s) burn resuscitation. The amount of Hextend used should not exceed 1000 mL. The U.S. Army Institute of Surgical Research Burn Center, which serves as the U.S. Department of Defense burn center, developed a new fluid resuscitation “rule of 10” used for burns greater than 20%. It is based on current research regarding burn resuscitation.10,21

TO USE THE “RULE OF 10” 1. Calculate and round the affected body surface area (BSA) to the nearest 10%. Use a burn calculation sheet if possible. 2. Calculate the fluid resuscitation protocol: a. Initial IV/intraosseous (IO) fluid rate is calculated as percent BSA × 10 mL/hr for adults weighing 40 to 80 kg (88.2 to 176.4 lb). For every 10 kg (22 lb) over 80 kg (176.4 lb), increase the initial rate by 100 mL/hr. 3. Monitor urine output to achieve 30 to 50 mL/hr. Example: Casualty weighing 100 kg (220.5 lb) with 50% BSA affected:

The military is performing ongoing research into pain relief on the battlefield. The challenges are distance, security situations that may delay transport, provider inexperience, and severity of the injuries.9,38 Causalgia (reflex sympathetic dystrophy) was a common diagnosis seen after the Civil War, and chronic pain states are still seen today in patients without adequate pain management. Current studies indicate that the cause or exacerbation of post-traumatic stress disorder (PTSD) is related to poorly or untreated, unrelenting pain.38 The standard is that all casualties with pain are given analgesia. The determinants of type and route of medication are as follows: (1) is the casualty conscious? (2) is the casualty able to fight? and (3) is there IV access? At the point of wounding for severe pain, the combat medic (68W) is able to give morphine 5 mg in titrated doses IV (preferred), IO, or via IM injection. Oral transmucosal fentanyl citrate 400 to 800 mcg6,32 is an alternative to morphine for use before arrival at a combat support hospital. Naloxone is available for respiratory depression. Promethazine 25 mg (IV/IM/IO) every 6 hours as needed has been added to the prehospital pain medication regimen to treat the nausea that is common with injury and often seen with narcotic administration. If the patient is treated with these medications, his or her weapon is secured and the patient is no longer able to fight. Splinting, positioning, and emotional support are provided as the patient is prepared for evacuation. Military members in combat carry a combat pill pack, which is taken as soon as possible after injury or wounding. These are oral medications: meloxicam 15 mg (a cyclooxygenase-2inhibitor selective nonsteroidal antiinflammatory drug) once a day and acetaminophen 650 mg (bilayer caplet) two pills every 8 hours. These medications were chosen for the ability to relieve moderate pain without causing platelet dysfunction or decrease in mental alertness. The soldier is still able to carry a weapon and able to fight if necessary. An antibiotic is carried in the combat pill pack and used for all open combat wounds. Currently the antibiotic of choice is moxifloxacin 400 mg PO once a day.63 After arrival at a BAS, FST, or CSH, other medications and modalities are available. Low-dose ketamine is an excellent analgesic. In the future, intranasal ketamine may be an option10 Clonidine may be used in stable patients.9,38 Peripheral nerve blocks and regional blocks (if trained personnel are available) offer excellent relief. A fascia iliaca block is useful for pain relief of injuries involving the hip, anterior thigh, and knee. This block is useful for fractures of the hip and proximal femur, especially before prolonged transport. Intercostal blocks are beneficial for chest wall pain after trauma, especially in the presence of rib fractures.

50 × 10 mL = 500 mL/hr + 200 mL = total fluid rate of 700 mL/hr

Telemedicine

Abdominal compartment syndrome is a complication of massive crystalloid resuscitation and carries a high mortality. An intraperitoneal drain may allow for enough intraperitoneal fluid removal to avoid a decompressive laparotomy.

Telemedicine has been used successfully to diagnose dermatologic conditions, send radiologic studies for interpretation, and give reports on patients being evacuated to higher levels of care. Combat medics in remote sites have used e-mail contact with their unit physician assistant or physician to make determinations of evacuation or therapy for ill or injured soldiers. The U.S. Army Medical Research and Materiel Command and the Telemedicine and Advanced Technology Research Center have worked on surgical robots and mentoring programs to assist in surgery. Colonel Bruce Adams has successfully experimented with camera observation and advice to combat medics for assistance in performance of surgical cricothyrotomy on manikins. Although telemedicine currently has limitations because of bandwidth, privacy issues, and urgency of trauma patient consultations, it holds promise for the future.47

Pain Management Homer’s The Iliad has some of the first descriptions of war wounds and their treatment; pain relief was recognized as a principal tenet of combat medicine. The need remains the same today. There Patroclus made him [Eurypylus] lie at length, and with a knife cut from his thigh the sharp-piercing arrow, and from the wound washed the black blood with warm water, and upon it cast a bitter root, when he had rubbed it between his hands, a root that slayeth pain, which stayed all his pangs; and the wound waxed dry, and the blood ceased. (Figure 26-11, online) Pain is a common manifesting symptom in injuries directly related to combat. In the deployed environment, there are also other more ordinary causes of pain, such as motor vehicle accidents, long periods in confined spaces, heavy personal protective equipment, and lifting and training accidents.9,38

Casualty Evacuation (CASEVAC) Wilderness medicine providers operating in conjunction with the military should be aware that evacuation platforms, both ground and air, are tremendously different when compared with the civilian evacuation system. Civilian evacuation platforms (ground and air) are generally equipped to provide en route care (oxygen, diagnostics, medications, communication with medical control) 517

CHAPTER 26  Combat and Casualty Care

Before use of the device, the wound is meticulously debrided, irrigated, and cleansed. A sterile sponge (or reticulated open-cell foam) is cut to fit inside the wound, the wound is sealed with a film to prevent leaks, and a suction tube is placed in the sponge. The opening of the tube through the skin is also sealed and connected to a wound VAC device. The suction pressures are usually 50 mm Hg to 200 mm Hg (average 125 mm Hg). The device is turned off for dressing changes. For drainage, a wound VAC can be highly beneficial. The interval between dressing changes can be extended because the VAC drains fluids from the wound and leaves less media for bacteria. In cases that may compromise circulation because of edema, a wound VAC improves blood flow to the wound and surgical area. Vacuum wound closure systems and their benefits as an important adjunct to modern combat wound care are discussed in the U.S. Department of Defense’s Emergency War Surgery,3 First to Cut: Trauma Lessons Learned in the Combat Zone,10 and War Surgery in Iraq and Afghanistan: A Series of Case Studies, 2003-2007.54 These also describe field-expedient methods to produce a wound VAC system with available equipment.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

and are staffed with paramedics with advanced training. Military evacuation platforms are essentially patient transport platforms with very little en route patient care. The military places greater emphasis on casualty stabilization before evacuation because of this configuration. The military evacuation system is designed for speed of transport into and out of combat areas with active small arms fire. Hence, the ability of a lightweight, agile, fast, and rugged platform (ground and air) to enter and exit an active skirmish, while providing a modicum of safety to the patient and medical attendants, is vital. The speed and effectiveness of the military medical patient transport system are often overlooked; however, the success of the system is reflected in the less than 10% dead on arrival (DOA) rate seen in current conflicts. At the point of wounding, the evacuation platform is more often going to be a tactical vehicle than any sort of ambulance. Due to increased use of IEDs and RPGs, most vehicles are armored or hardened. The space is very limited, so to the greatest extent possible, any control of bleeding, placement of tourniquets, and other medical procedures are accomplished before transport. It is also important to work with equipment such as litters to make sure they will fit in the vehicles. During transport, it is critical to ensure medical interventions, such as control of bleeding, remain intact. For the badly injured casualty, evacuation from the time and point of wounding to the closest and most appropriate initial care at an FST or CSH averages about 1 hour. If the determination is that there is a lesser injury, the patient can be taken to a BAS for a determination of injury and evacuated to a higher level later if required.54 Casualty evacuation is a multifaceted transport system designed to enhance patient evacuation based on proximity of stage evacuation assets, not based on injuries. Regardless of the type of injury, a triage category and then an evacuation category will be assigned. During casualty evacuation planning, all platforms and locations are plotted to facilitate entry into the evacuation system. Helicopters are used extensively for casualty transport. In combat situations, a white light, such as that in a laryngoscope, in the helicopter compartment may be forbidden. Because the doors are often left open for security reasons, protection of the patient from the wind and hypothermia becomes more critical. If the patient is in a helicopter and the time to a CSH is not significantly greater than the FST, the decision may be made to go directly to the CSH. Although the FST has a great deal of surgical capability, its roles are lifesaving interventions and limited surgery to stabilize the patient to allow evacuation to the CSH. Transportation after initial advanced-level care often involves an intubated (and possibly ventilated) patient. Sedation and analgesia are essential for these transfers. In addition, no paralytic agent should ever be given without a potent sedative. Some evidence suggests that the administration of sedation and pain relief may decrease the probability of later PTSD. Absent hypovolemia, a sign of inadequate pain and sedation may be persistent tachycardia. The airway and patient should be adequately prepared because loss of the airway during combat evacuation is a major life threat. Reestablishment in a limited space with inability to hear breath sounds may necessitate a surgical airway. The attendant in transfer must have sufficient medications and doses to keep the patient comfortable and sedated and be able to provide an airway if the patient is extubated. For the most critical airways, the endotracheal tube may be wired onto the teeth.10 For any ground or air transport, including longer transports such as aeromedical (Air Force flying hospital; C-17) transfer out of the combat zone, a pretransport check to ensure necessary medical items (e.g., oxygen, tourniquets, sedation, analgesia, antibiotics, IV fluids, decompression needles, urinal) is important because the transferring facility is responsible for the patient’s medical equipment needs during movement. A patient with a minimal pneumothorax or on positive pressure ventilation is susceptible to a tension pneumothorax during transport, so the attendant must be able to address this. Other possible causes, such as a kinked tube or mucus or blood clot in the tube, need to be quickly ruled out. It is difficult to evaluate a patient in a helicopter; if there is any question as to which side is under tension treatment, a 3.25-inch 14-gauge needle is inserted into the second intercostal spaces bilaterally. If there is a question of 518

FIGURE 26-12  Example of the Fallen Soldier Battle Cross and the memorial service.

pneumothorax before transport, a chest tube should be placed before transport. Any patient who has had a tourniquet placed in the field, is a postoperative amputee, or has had a vascular repair is at risk for hemorrhage. As the patient becomes normotensive or coagulopathic, the area can rebleed when a tourniquet or suture is dislodged with movement. The same can happen with a vascular repair or vascular shunt. During transport, at least two tourniquets for each injured/operated extremity is judicious. The tourniquet can be preplaced on the injured extremity, to be tightened if there is the onset of exsanguinating hemorrhage.

Death In the midst of the savagery of war, it is critical to maintain the tether to humanity. Care of the deceased is an important service, not only for the soldier’s family, but for the unit’s morale and well-being. Although the care of remains is under the direction of the Quartermaster Corps, it is usual that no matter where the death occurs, the unit will bring the body to the medical personnel in the area. The body is cooled if at all possible. As in any medical examiner’s case in the United States, all medical procedure items are placed in the body bag with the deceased. Clothing and operational gear are transported with the remains. Any records of the incident are preserved and sent with the remains. A full autopsy is completed by the military to determine the cause of death and enter the data into the trauma registry. In response to the loss, the unit holds a memorial service, where the deceased soldier is represented by the Fallen Soldier Battle Cross. The cross consists of the soldier’s rifle with bayonet attached and stuck into the ground; the helmet is placed on top, accompanied by dog tags that hang from the rifle with the boots of the fallen soldier in front of it (Figure 26-12). Its purpose is to show honor and respect for the fallen at the battle site. The ceremony for the lost comrade is formal and used as a ritualized means to collectively acknowledge the commitment and sacrifice of the soldier and to mourn his or her loss. Commanders are cognizant of the distress brought by the death of a unit member, especially if the unit has suffered multiple losses. Commanders use this ceremony to reaffirm with unit members the sense of unity, cohesion, and commitment to each other as they pursue their shared sense of mission.

Veterinary Issues Dogs in conflict areas are ubiquitous. Despite education and warnings, soldiers often voluntarily interact with local dogs. U.S. military working dogs are vaccinated against rabies; the likelihood of rabies in local animals may be considerable. Dog bite treatment is similar to that in any emergency department, except

Unexploded Ordnance* Unexploded ordnance (UXO) may include aerial bombs, rockets, artillery and mortar shells, grenades, and mines. Any location where a war has been fought within the past century has potential for retaining these items. Crews excavating streets in urban areas of England, France, and Germany often uncover UXO from World War I or World War II. Many areas of the United States that have been used for bombing or artillery ranges are adjacent to wilderness regions. Although they are usually well marked as impact areas, they still may pose a risk for the unwary traveler. Many areas of the shallow ocean accessible to scuba divers contain sunken munitions transports and warships that contain massive amounts of unexploded bombs, shells, and torpedoes. Another problem that has arisen is the use of mines and booby traps to protect marijuana and opium fields and illegal drug laboratories. Currently, unexploded land mines represent a significant health problem in Southeast Asia, the Balkans, Central America, Egypt, Iran, and Afghanistan. The International Red Cross estimates that someone is killed or injured by a land mine every 22 minutes. The average number of mines deployed per square mile in Bosnia is 152; in Iran, 142; in Croatia, 92; and in Egypt, 59. There are a total of 23 million mines in Egypt alone.10 Land mines may be commercially manufactured or produced locally from available materials (Figure 26-13). Commercial land mines currently produced in the United States have a limited active life and self-destruct after their active life has expired. Unfortunately, this is not true of older types of mines or mines produced by other countries. Locally produced mines have no standard size, shape, or detonation pattern and may be very difficult to detect and defuse. These types of land mines are used extensively in El Salvador, Malaysia, and Guatemala. Land mines have two primary functions, the first of which is to cause casualties—the so-called antipersonnel mines. These may be blast or fragmentation type. Fragments may be accelerated at 4,500 ft/sec (3068 mph), or double the speed of a highvelocity rifle. The fragmentation type may be either directional or nondirectional (Figure 26-14). Antipersonnel mines may cause lethal or nonlethal injuries in several persons. Wounded soldiers require more care than do killed soldiers, and the tactical effect may be the same. The second primary function is to destroy vehicles, such as tanks, so mines intended for this purpose are usually much larger. All mines have three basic components: (1) triggering device, (2) detonator, and (3) main explosive charge. The triggering device differs depending on the type of mine. Blast mines usually involve a pressure type of trigger and occasionally are command detonated, especially for antitank purposes. Many antitank mines will not explode unless a pressure of 136 to 181 kg (300 to 400 lb) is applied. The M14 blast antipersonnel mine needs only 9 to 14 kg (20 to 30 lb) of pressure to trigger detonation. Fragmentation mines are usually triggered by trip wires or similar “touch” devices. The M18A1 fragmentation mine, or claymore mine, can also be command detonated by an electronic trigger. *Reference 63.

Main charge

Fire assembly adapter plug Soft metal plate

Wire

Striker Retaining wall Detonator Detonator adapter plug

Delay-arming mechanism

FIGURE 26-13  An example of an antipersonnel mine manufactured by the Soviet Union.

Booby traps other than land mines may be mechanical, chemical, or explosive. During the Vietnam War, venomous snakes were used, as well as the notorious sharpened bamboo spikes known as punji or tiger traps. The distribution of mines usually entails spreading them on the surface of the ground; by air along roads, railways, and defensive positions; or hiding them by burying or camouflage along trails or suspected routes of approach. The energy transmitted from blasts may cause extensive damage. When a detonation occurs, a solid or liquid is converted into a gas under pressure with extreme energy release. Detonation of a high-speed chemical reaction also causes high temperatures and pressures. Factors influencing the blast wave are the Mach stem, reflection, absorption, flow of the pressure wave, and the medium in which the blast occurs (e.g., air, water, soil). Injuries from land mines depend on several factors: type of mine (blast versus

A

B FIGURE 26-14  A, An improvised mine, or booby trap, manufactured from a hand grenade and materials at hand. B, A directional type of mine used against unarmored vehicles or personnel.

519

CHAPTER 26  Combat and Casualty Care

that the ability to catch and monitor the animal is decreased, so watchful waiting to determine vaccination status of an animal is not an acceptable approach. Therefore postexposure rabies immunization is started.10 The lessons learned have been consideration of preexposure rabies vaccination for personnel with high exposure to local dogs; this requires that adequate supplies of rabies vaccine are reasonably available. It is better to have the rabies vaccine on hand than have to transfer the service member to another location for treatment; this is especially true if the environment is not secure. Working dogs may be seen as patients in emergency treatment areas of the hospital, especially if a veterinarian is not immediately available. Care of working dogs is described in First to Cut: Trauma Lessons Learned in the Combat Zone.10 Basic damage control principles are used for resuscitation and surgery.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

fragmentation), position on the ground, method of detonation, whether it explodes above the ground, position of the victim, environment, and type of soil. Four general patterns of injuries occur with land mines. Pattern A injuries occur with small blast mines, such as the U.S. M14 and the Chinese Type 72. These injuries usually involve only the leg below the knee. Complete or partial foot amputations are most common, and trunk or head injuries are rare. Pattern B injuries are caused by larger blast mines, such as the Russian PMN. These mines contain four to six times as much highexplosive material, and the cone of explosion is much larger. The injuries seen with this type of land mine usually involve massive soft tissue injuries to both legs below and above the knee and also commonly the pelvis, abdomen, and chest. Pattern C injuries are generally caused by Russian PFM-1, or “butterfly,” mines. These mines are usually distributed by air, and the wings are designed to help spread the mines. They are triggered by pressure applied to the wings; handling the mine commonly does this. Most of the injuries involve amputation of the hand at the wrist; often the head, neck, and chest are also injured. Unfortunately, loss of one or both eyes is not uncommon with this mine. Pattern D injuries are caused by fragmentation mines. These may be bounding mines, such as the U.S. M16 or the Russian OZM, or directional mines, such as the U.S. M18A1 or the Russian MON. They are designed to spread metallic fragments over a wide area at the height of a person’s waist. The fragments lose their energy much faster than a bullet projectile but at close range can be devastating. The lethal range is usually 25 to 50 m (82 to 164 feet), with casualties occurring out to 200 m (656 feet). The injuries are quite similar to gunshot wounds and are often multiple. Large, unexploded artillery shells or bombs may cause a combination of blast and fragment injuries but on a larger scale, sometimes involving scores of victims. Many military and civilian casualties are caused by IEDs, which may be conventional explosives; improvised from fertilizer, propane, or other unconventional explosives; artillery, mortar, or other ordnance; or explosive charges removed from such ordnance. IEDs are commonly used by terrorist groups, which may detonate the devices either by timing mechanisms or by command, sometimes in suicidal attacks. These devices are usually detonated in crowded areas or near important political or military targets to create the greatest impact. Examples are attacks on Oklahoma City’s Alfred P. Murrah Federal Building, the Beirut Marine barracks, and multiple incidents in Iraq. Injuries from explosives can include any combination of blunt, penetrating, burn, or blast wave/pressure injury. Injury patterns are usually worse with closer proximity. These injuries can also involve cavitation, crush, embolism, fractures, lacerations, and perforations of organs. The primary blast injury is due to the pressure wave and the direct effects of the pressure pulses, both overpressure and negative pressures. Significant blast winds can be produced because of the detonation. Injury is most often associated with the gas-filled organs, middle ear, lungs, and intestines. Lung injuries cause the greatest morbidity and mortality. Rapid acceleration of shrapnel to 50 ft/sec (34.1 mph) lacerates tissue, and at 400 ft/sec (272.7 mph) shrapnel is able to penetrate body cavities. Because the wounds are deceptive, the need for amputation may first be recognized later. Tetanus prophylaxis must be rendered. The tertiary injuries involve the victim being accelerated by the blast and thereby impacting other objects when thrown any distance. The median lethal dose (LD50) of being thrown is about 26 ft/sec (17.7 mph), and the limit of human tolerance is about 10 ft/sec (6.8 mph). The other injuries that commonly may occur are burns, crush (from building collapse), and chemical exposures. A very important aspect of the care for any patient with an explosive munition mechanism of injury is the possible lack of any initial overt manifestation of injury. There must be a high index of suspicion because many victims will not manifest for several hours. The first sign of respiratory failure is usually increased respiratory rate. Acute respiratory distress syndrome may not manifest for 24 hours. Treatment of these injuries can be very complex and involves vascular, orthopedic, soft tissue, abdominal, and craniofacial procedures. In most of these injuries, massive debridement is necessary. Rarely, UXO may be 520

embedded in soft tissues and body cavities and must be removed in the operating room, possibly endangering the lives of medical personnel. Initial treatment involves airway control, treating tension pneumothorax, and controlling hemorrhage. Tourniquets are often necessary to control the bleeding from amputated limbs. Splinting the injured extremity and covering the wound to prevent further contamination is necessary. Initial debridement must be done carefully; removal of fragments may cause bleeding to recur. Penetrating injuries of the pelvis and abdomen usually require laparotomy, and soft tissue injuries may require multiple reconstructive procedures. The wounds are usually highly contaminated with soil, clothing, and fragments that may be driven deeply into tissue proximal to the obvious injuries.39 Broad-spectrum antibiotics and tetanus prophylaxis are appropriate in all cases, and fluid resuscitation is usually indicated with extremity injuries. Postsurgical infection of mine injuries is common and greatly increases morbidity and mor­tality. Most victims who survive never completely regain normal function, especially if the initial treatment was delayed or inadequate. Air-filled organs are most susceptible to damage. The tympanic membrane can rupture at a pressure of approximately 150 kPA (kilopascal) or 5 to 7 psi over atmospheric pressure. Blast injuries without fragmentation may cause tympanic membrane rupture, blast lung resulting from alveolar rupture, and intestinal rupture, although the latter is more common with underwater mine explosions. Pulmonary blast injury may manifest as contusions and hemoptysis. The victim may have subcutaneous emphysema, respiratory distress, and tachypnea. Arterial air embolism may occur with cardiac and neurologic manifestations. The mechanism is production of an overpressure wave that travels through tissue of various densities and causes tearing injuries at membrane interfaces. These injuries must be suspected in any victim involved in a blast, whether from a land mine or other explosive device. Solid organs, although more protected from overpressure, are very susceptible to missiles. Neurologic and head injuries are commonly associated with blast injury. Blast winds can cause extremity injury as severe as traumatic amputation. Scuba divers and swimmers who are involved in underwater explosions may have more serious injuries because of the increased speed of sound in a liquid medium. This can cause more severe tearing of membranes at the fluid–air interface and additional trauma secondary to a “water hammer” effect and spalling. The position of the victim and the number of shock waves caused by reflection of the blast wave off walls and ground may increase the amount of damage. Victims in contact with solid objects, such as the hull of a ship or vehicle, may have increased injuries because of increased velocity of the blast wave through solids. Burns and translational injuries, whereby the victim is thrown by the blast and has injuries similar to a fall or motor vehicle crash, also occur. Traumatic brain injury (TBI) is common in blast injuries and is referred to as the “hallmark injury” of the current Iraqi and Afghani conflicts. Symptoms can range from coma to mild cognitive dysfunction, depression, and behavioral changes. PTSD is often associated with TBI. Generally speaking, the closer the victim is to the blast, the greater the injury. The tympanic membrane will rupture at overpressures of 5 to 7 psi. This causes acute hearing loss, pain, and tinnitus. Blast lung is caused by the overpressure wave passing through the chest wall and may involve one or both lungs. Chest pain, dyspnea, and hemoptysis may manifest immediately or be delayed up to 48 hours. Chest radiograph may show patchy or diffuse infiltrates, pneumothorax, subcutaneous air, and hemothorax. Implosion of air into the vascular system may cause air embolism and sudden death. Abdominal injuries in air blast are uncommon, but in water blast may manifest as abdominal pain, nausea, vomiting, and tenesmus. Sigmoid and transverse colon injuries are most often seen, followed by small bowel and solid organ (such as liver and spleen) injuries from the water hammer effect. Abdominal injuries may have a delayed (up to several days) presentation. The key to therapy is to be suspicious of occult injuries in any victim of a blast, whatever the cause. Most injuries will manifest within the first hour; however, because injuries may be delayed in presentation, observation and close

succinctly—“The closer you are and the uglier it is, because the longer it lasts, the worse you’re going to feel.”

DEALING WITH RETAINED UNEXPLODED ORDNANCE

SOURCES OF PERSONAL TRAUMA

Any patient that has retained UXO requires extremely delicate handling. If it is possible to limit transportation and perform surgical removal, that is the best plan. There should be an explosive ordnance disposal specialist available to advise on UXO type and triggers. The surgical team should be limited to critical members only. Every member of the team wears complete protective gear, including protective eyewear and sandbags or other material to deflect any blast. This gear is also placed around the patient. Radiographs may be necessary to determine the extent of implantation and the best way to remove the ordnance. One should never use ultrasound or electrocautery on the patient, because these may set off the UXO. Similarly, avoid contact with the UXO with metal surgical instruments. Inhalational anesthesia is contraindicated due to explosive concerns, and patient monitoring will be limited. IV anesthesia is used; the patient should be well anesthetized and paralyzed to avoid movement.

Traumatic Emotional Stress in Austere Environments: The Continuum of Effects Traumatic emotional stress is a common and serious problem that is especially relevant to the field of austere medicine. The military has found that all military members, including enlisted soldiers and officers, can benefit from an overview of the causes and signs and symptoms that define the continuum of traumatic stress. This section reviews basic precepts, describes the general concept of traumatic stress, and cites some of the management strategies that have demonstrated their utility in the field. If the patient is armed, a safety issue that needs to be addressed is disarming the patient and ensuring safety of the team and the injured individual. Frederick M. Burkle, MD, stated, “Current studies support that no single pattern of psychological consequences to disasters exists. However, human generated disasters appear to result in more severe, intrusive, and long term psychological consequences than natural disasters.” 14 This certainly pertains to military personnel in areas of armed conflict and also holds true for other responders and aid workers.

CLINICAL ASPECTS OF PSYCHOLOGICAL TRAUMA It has been suggested that the two principal determinants of the severity of psychological trauma are the gradient of exposure and the magnitude of personal loss. The gradient of exposure describes how close one is to the event(s). Questions might include the following: Did you hear about it? Read about it in print media? See photographs? View it on television? Witness it personally? How much of it were/are you exposed to, and how many times? Did it happen to someone you know? To a loved one? To you? In general, the closer or more directly affected an individual is by the event, the greater the likelihood of significant psychological distress. The magnitude of personal loss describes the “comprehensiveness” of the event. Does the event produce meaningful physical or psychological pain or limit abilities because of injuries? Do losses affect areas such as physical mobility or capacity/ employment/future personal or professional opportunities? Were feelings of terror, horror, or helplessness involved? Informally the gradient of exposure and magnitude of personal loss might be reduced to the phrase “how close and how big?” Taken together, these are highly predictive of the degree of psychological distress—or, as it can be expressed *References 4, 15, 18, 24, 26, 30, 34, 53, 61, 63, 64.

We define our world with our senses. Armed conflict is, at its core, an assault on our senses. Our senses provide the sights, sounds, smells, and sometimes physical pain that create the psychological imagery of the indelible memories, intrusive thoughts, and disturbed feelings that are the cardinal features of psychological trauma.

HOW ARE MILITARY STRESS REACTIONS CHARACTERIZED? In general, the military recognizes three types of stress reactions. In ascending order of severity, these are combat and operational stress reaction (COSR), acute stress disorder (ASD), and PTSD. Although the military focuses principally on combat-related issues, the general template applies well to nonmilitary stress responses. Because the civilian sector does not use the term combat, one might substitute the word initial in its place for COSR. All three reactions may have a combination of common physical, emotional, and behavioral signs. The following is a list of the signs most commonly reported. Combat and Operational Stress Reaction It is not unusual for combat exposure or other circumstance of interpersonal violence or imminent danger to create physical and emotional problems. Such reactions may occur as the result of combat-like conditions that are present throughout the entire spectrum of military operations, which include training, traditional offensive and defensive operations, stability operations, and civil support activities. In the authors’ experience, civilian humanitarian workers involved in peace operations, disaster response, humanitarian support, and related missions may have experiences and responses that are similar to those of combat troops. Outward signs and symptoms of COSR often include a combination of physical, emotional, behavioral, and cognitive disturbances. Common physical complaints associated with COSR may include fatigue, exaggerated startle response, sweating, sleep disturbance, rapid heartbeat, dizziness, frequent urination, dry mouth, and persistent muscular tension. Emotional distress may include grief, distractibility, self-doubt, anger/agitation, loss of confidence in self or unit, and rumination about distressing events. Common behavioral representations of these emotions often include indecisiveness, irritability, distractibility, inattention, hypervigilance or withdrawal, decreased arousal/initiative, tearfulness, and inability to relax. The patient may also initiate or increase the use of mind-altering substances, from common substances (caffeine, nicotine, alcohol) to more powerful prescription or street drugs. Acute Stress Disorder ASD is a diagnostic category developed in 1994 to describe reactions to trauma that are time limited. ASD describes the behavioral disturbances that develop within a month of exposure to extreme psychological trauma. Such extreme events could include rape or other severe physical assault, near-death experiences during accidents, witnessing personal violence, and combat. In some cases, ASD can also result from actions taken or not taken by an individual that leave the person with meaningful feelings of guilt or shame. In addition to the COSR symptoms noted above, ASD may also include derealization, depersonalization, reduction in awareness of vicinity, psychological numbing, and dissociative amnesia. Derealization is a change in an individual’s experience of the environment, where the world around him or her feels unreal and unfamiliar. Depersonalization is a change in an individual’s self-awareness, such that they feel detached from their own experience, with the self, body, and mind seeming alien. Dissociation is also characterized by a sense of the world as a dreamlike or unreal place and may be accompanied by poor memory of the specific events, which in severe form is known as dissociative amnesia. The symptom of dissociation, which 521

CHAPTER 26  Combat and Casualty Care

follow-up are critical. Treatment is generally supportive for ear and lung injuries and operative for abdominal injuries.*

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 26-2  Difference Between ASD and PTSD ASD

PTSD

The diagnosis of ASD can be given only within the first month following a traumatic event.

If post-traumatic symptoms persist beyond a month, the clinician should assess for the presence of PTSD. The PTSD diagnosis does not include a dissociative symptom cluster.

It includes a greater emphasis on dissociative symptoms. An ASD diagnosis requires that a person experience three symptoms of dissociation (e.g., numbing, reduced awareness, depersonalization, derealization, or amnesia).

ASD, Acute stress disorder; PTSD, post-traumatic stress disorder.

reflects a perceived detachment of the mind from the emotional state or even the body, is a critical feature. Other features of ASD include symptoms of generalized anxiety and hyperarousal, avoidance of certain situations or stimuli that elicit memories of the trauma, and persistent, intrusive recollections of certain events via reexperiencing (“flashbacks”), dreams, or recurrent thoughts or visual images. Although ASD is not an “early” form of PTSD as such, it may proceed to PTSD if the individual does not receive appropriate care. Post-Traumatic Stress Disorder If the symptoms and behavioral disturbances of the ASD persist for more than a month, and if these features are associated with functional impairment or significant distress to the sufferer, the diagnosis is changed to PTSD. These terms describe the outward manifestations of trauma-induced anxiety. Essentially, the individual’s adaptive responses to an unstable environment have been internalized as a general mode of responding to all environments. In the words of one patient, “I know that I’m not in theatre (combat zone) now, but I still can’t stand being in a department store or any other crowd of people.” The symptoms of ASD and PTSD are very similar (Table 26-2). The proper diagnosis revolves around two issues that can be framed as questions: How long have the problems lasted, and are the problems getting better, worse, or remaining the same?

WHICH TREATMENTS WORK? In general, treatment focuses on helping people process their experiences in ways that decrease or eliminate their combat arousal state. Treatment strategies that have demonstrated usefulness include prolonged exposure therapy, eye movement desensitization and reprocessing, pharmacologic treatment, couple/ family counseling, and spiritual support. In addition, adjunct pharmacologic management for problems of mood or anxiety may also be indicated. There may be a role for medication in the prevention of PTSD. Recent research by Holbrook and colleagues suggests that administration of morphine during early resuscitation and trauma care at or near the point of injury is associated with a lower risk for PTSD following injury.38 One of the greatest historical barriers to care has been the stigma associated with the need for behavioral health support. U.S. Army Vice Chief of Staff, General Peter Chiarelli, is an outspoken advocate for the identification and treatment of PTSD and the often-related issue of TBI (http://www.neuroskills.com/ mtbi.shtml). He has been especially vocal in speaking about the terrible toll of stigma: The “signature wounds” of this war are post traumatic stress disorder and traumatic brain injury … I want to change the stigma linked to these wounds … They are in fact real … these are not phantom issues made up by weak Soldiers. They are as real as if you fell and broke your leg or lost an arm.” Leaders need to be careful on the tone they use with this issue. It affects how their subordinates view these conditions and if you believe anxiety and depression are signs of weakness, so will they. 522

To paraphrase General Chiarelli in a related comment, “Is your brain more important or less important than your leg … or hand?”

Mild Traumatic Brain Injury Mild traumatic brain injury (MTBI) is commonly known as concussion; it is rarely life threatening (Figure 26-15). Gioia and Collins stated the following: Concussion (MTBI) is a complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head. Disturbance of brain function is related to neurometabolic dysfunction, rather than structural injury, and is typically associated with normal structural neuroimaging findings (i.e., CT scan, MRI). Concussion may or may not involve a loss of consciousness (LOC). Concussion results in a constellation of physical, cognitive, emotional, and sleeprelated symptoms. Symptoms may last from several minutes to days, weeks, months or even longer in some cases.36 Further, the American Congress of Rehabilitation Medicine52 characterizes MTBI as “a traumatically induced physiologic disruption of brain function which involves at least one of the following: 1) any period of loss of consciousness; 2) any loss of memory for events immediately before or after the accident; 3) any alteration in mental state at the time of accident (e.g. feeling dazed, disoriented, or confused); 4) focal neurologic deficit(s) that may or may not be transient.” Specific causes of MTBI commonly include a blow to the head or violent shaking often caused by motor vehicle accidents, falls, and sports injury; among military personnel, the most common source is overpressure wave blast caused by explosion. Although not life threatening, the symptoms of MTBI can be serious and a meaningful threat to quality of life.

SIGNS AND SYMPTOMS In patients presenting with possible head injury, initial medical response focuses on identification and management of the most serious injuries, so the diagnosis of MTBI may be delayed. The signs and symptom of MTBI are highly variable in both type and time. Headaches, for example, often have rapid onset, whereas many of the cognitive and affective behavioral symptoms may begin subtly and not become problematic for days or weeks. Disturbances in executive function, including decision making, foresight, insight, judgment, and planning, are frequently present. Most people with MTBI recover completely, but the process can sometimes take considerable time. This is especially the case for sufferers who are older, have a history of previous head injury, or who are taking psychiatric medications. Although patients recover, different symptoms may resolve at different rates, making the course of recovery highly variable.19 In the immediate postconcussive phase, patients may experience brief unconsciousness. Even without unconsciousness, patients most commonly report feeling dazed or confused or

2000-2010 Penetrating 3304 Severe 1986 Moderate 31,974 Mild 144,453 Not classifiable 6553 Total – All severity 188,270

FIGURE 26-15  2000-2010: Traumatic brain injury categories. (From Defense and Veterans Brain Injury Center: Military Acute Concussion Evaluation. http://www.pdhealth.mil/downloads/MACE.pdf.)

“seeing stars.” In addition, patients may experience amnesia for the injury or event that caused the problem. Common motor and sensory symptoms include dizziness, fatigue, sleep disturbances, and sensory deficits involving vestibular and visual systems, muscle strength, and/or coordination. One of the most common pain symptoms of MTBI is headache that typically begins within the first 14 days. The patient may complain of a dull, aching pain that is typical of tension headache, but MTBI can also trigger migraine headaches in persons with a genetic disposition. Headaches often originate from structures external to the brain and skull, such as muscles and connective tissue of the skull, spine, and shoulder.52,58 Behavioral symptoms of MTBI can be especially problematic and may include a range of disturbances in affect, cognition, and behavior. The patient may become irritable, agitated, disruptive, or overtly aggressive and may demonstrate marked emotional lability, disinhibition, or impaired impulse control. Cognitive symptoms often include slowed thinking, impaired judgment, distractibility, and impaired cognitive focus. Patients may use terms such as feeling foggy or other terms representing a vague sense of being out of touch with their senses. Over time some persons may develop depression, substance abuse problems, or alterations in their baseline personality characteristics. These concerns must be referred to the appropriate health care provider for proper assessment and management.

IDENTIFICATION AND MANAGEMENT OF MILD TRAUMATIC BRAIN INJURY IN AN AUSTERE ENVIRONMENT (Table 26-3) The following comments describe techniques that have demonstrated their utility in caring for military personnel deployed to austere environments or those involving combat action. The response to mild-to-moderate TBI has four components: assess, inform, monitor, and evacuate. Assess.  Austere environments do not typically lend themselves to thorough assessment of TBI; this is especially true in complex emergencies or other situations where security limitations preclude administration of a more comprehensive evaluation.42 In response, the military and Department of Veterans Affairs have developed tools to screen, assess, and longitudinally track and treat MTBI as a subset of TBI. For first responders, the Military Acute Concussion Evaluation (MACE) screening tool has demonstrated its usefulness. The MACE tool includes the Standard Assessment of Concussion, a four-part cognitive screening in the domains of orientation, immediate recall, concentration, and

TABLE 26-3  Severity of Traumatic Brain Injury

Rating Scale

Severity

GCS*

LOC

Mild Moderate Severe

13-15 9-12 3-8

<30 min 30 min to 24 hr >24 hr

AOC† (hr) 24 >24 >24

PTA <24 hr 24 hr to <7 days >7 days

Data from the Severity Ratings Scale for TBI, Defense and Veteran's Brain Injury Center. http://www.dvbic.org. AOC, Alteration of consciousness; GCS, Glasgow Coma Scale; LOC, loss of consciousness, PTA, post-traumatic amnesia. *Although not used in severity classification by the Department of Defense, GCS is frequently used in assessing traumatic brain injury severity. † AOC includes being dazed or confused or seeing stars.

memory recall.42 It may be downloaded from http://www. pdhealth.mil/downloads/MACE.pdf. The MACE is essentially a modified Mini-Mental State Examination (MMSE) that includes a review of historic events, mechanism of injury, and symptoms. During assessment, it is also important to note current medications, especially psychiatric medications for mood, attention deficit hyperactivity disorder, and so forth. Inform.  Provide the patient with information about the most common and serious symptoms, and reinforce the fact that most people recover completely. Make it clear that if problems persist, treatment is available. Respond directly to any patient questions, and be clear that someone is monitoring the patient’s condition. Monitor and Evacuate.  As much as possible, keep the patient at rest. Appearance of more severe symptoms (e.g., pupillary abnormalities, vomiting, blurred vision, sleepiness, drowsiness, slurred speech) warrants immediate evacuation. Chronic sleep deprivation is a pervasive problem and may hinder apportionment of symptoms caused by acute injury. Patients who are desynchronous may exhibit headaches or illusory phenomena irrespective of a closed head injury; if such symptoms are preexisting, they may be exacerbated by concussive injury.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 27 



Wilderness Orthopedics JULIE A. SWITZER AND RALPH S. BOVARD Life is sweeter nearer to the bone. HENRY DAVID THOREAU

The textbook discussion of orthopedic trauma in wilderness medicine has traditionally focused on discrete musculoskeletal injury to individuals or small groups in the mountain, sea, or desert setting. The scope of wilderness medicine today has widened significantly to include terrorism, military engagement, and the forces of nature. Recent disasters, such as the Great Indian Ocean tsunami of 2004, Hurricane Katrina in August 2005, and the Haitian and Chilean earthquakes of 2010, serve as powerful examples of situations in which orthopedic injuries were myriad and the provision of care limited in significant part by the remoteness of setting or inaccessibility of resources.

The wilderness practitioner needs to approach trauma outside the normal clinic or hospital setting with a sense of anticipation and improvisation. One needs to be prepared for a scenario of chaos, inadequate medical supplies or support, sepsis, and limited or delayed evacuation potential. The tidy fractures of individual sport injury or accidental trauma in civilized society share little in common with massive crush injuries, limb mangling with segmental loss, and severed limbs of natural or terroristic disasters. Issues of triage and prioritization become paramount. The successful organization of resources and effective mobilization of personnel skills often determine the outcome of the

For online-only figures, please go to www.expertconsult.com

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different in the wilderness. Once a victim’s airway is secured and his or her breathing is deemed adequate, evaluation of obvious musculoskeletal injuries can commence. Small portable pulse oximeters, comparable in size with a 35-mm film canister, are now available for less than $100 (Figure 27-2, online). These can be especially helpful if one is engaging in outdoor activities at high altitudes. These devices provide pulse rate and arterial oxygen saturation (SaO2), vital measures in any hypoxic or hemodynamically unstable patient. Vascular Function Penetrating or blunt trauma can injure major vessels that supply the limbs. Fractures can produce vessel injury by stretching, which can produce intimal flap tears, or by direct laceration. Intimal injuries can occlude distal flow or lead to platelet aggregation and delayed occlusion. Thus, examination of vascular function should be performed and repeated at regular intervals before the victim’s arrival at the definitive care center. Color and warmth of the skin or distal extremity should be assessed; pallor and asymmetric regional hypothermia may indicate vascular injury. In the upper extremity, the brachial, radial, and ulnar arteries should be palpated. In the lower extremity, the femoral, popliteal, posterior tibial, and deep peroneal arteries should be palpated. If blood loss, hypothermia, or obesity makes these pulses difficult to assess, temperature and color must be relied on to determine vascular integrity. Any suspected major arterial injury mandates immediate evacuation after appropriate splinting.

FIGURE 27-1  Improvised traction following the 2010 earthquake in Haiti. (Courtesy Sam Slishman.)

operation. Improvisation in splinting to stabilize or immobilize shattered limbs can minimize neurovascular compromise and reduce morbidity and mortality (Figure 27-1). Although most of us will hopefully not experience such large-scale tragedy, readiness and focus are required of the modern wilderness caregiver!

Problem Scope Musculoskeletal injuries account for 70% to 80% of injuries that occur in a wilderness setting.11,18 Presumably as a result of the use of flak jackets and core protective gear that shield axial and central anatomic structures, bone and soft tissue injuries have also accounted for 70% of injuries in the Iraq and Afghanistan wars.16 In the initial management of a musculoskeletal injury that occurs in a wilderness or nondeveloped setting, the following must be considered: etiology and time of the injury, direction of the causative force in relation to the individual or limb, and environment where the accident occurred. These factors may indicate the severity of the injury and help determine examination and treatment priorities that can affect outcome. Stabilization of a victim’s cardiovascular and pulmonary status is critical. Once this has been accomplished, examination of the musculoskeletal system should be undertaken in a systematic manner. Careful initial attention should be devoted to the spine. After the cervical, thoracic, and lumbar spine are evaluated and stabilized, the focus is brought to bear on the pelvis and extremities.

PHYSICAL EXAMINATION The physical examination should address respiratory, circulatory, nerve, skeletal, and joint function. Respiratory Function Basic resuscitation efforts in any setting begin with evaluation of an individual’s airway and breathing. This prioritization is no 524

Nerve Function Nerve function may be impossible to assess in an unconscious or uncooperative person. In the conscious person, the results of light touch and pinprick tests should be carefully documented. For spinal and pelvic injuries, dermatomal distribution of spinal nerves is assessed, and muscle function is evaluated by observing active function and by grading the strength of each muscle group against resistance (Figure 27-3). If possible, once the victim’s condition has been stabilized, nerve function to the distal extremities is established. These initial findings should be compared periodically with repeat examinations during transport. Any change and, in particular, any deterioration in condition should be noted. Skeletal Function The long bones of the lower extremity serve as the major structural supports for locomotion, whereas those of the upper extremity stabilize the soft tissues and allow functional use of the arm and hand for manual dexterity. A visible angular deformity suggests a fracture; palpable crepitus confirms the diagnosis. The health care provider in the field should perform appropriate splinting after aligning the limb using gentle axial traction. After noting the degree and orientation of the limb’s position when the victim is found, there should be no delay in aligning and splinting fractures. The risk-benefit of fracture reduction and realignment in the wilderness to protect neurovascular status and reduce pain typically outweighs the medical center imperative to image before manipulation. Distinguishing joint injuries and intra-articular or very proximal or distal fractures must wait for the definitive care facility, where radiologic studies can be done. Similarly, distinguishing a wrist or ankle ligamentous injury from a fracture is not required for initial treatment. Joint Function Muscle forces act across joints to optimize the positions of the lower limbs for ambulation and the upper extremities and hands for manual dexterity. Each joint has a normal range of motion and limits to ensure stability. Making the diagnosis of a joint injury in the field allows appropriate splinting and prevents further damage during transport. Diagnosis is usually made by palpation of the limb and fracture. If a tuning fork is available, it can be used in the following manner: the tuning fork is struck and then placed on one end of a limb in question. If the vibration cannot be auscultated at the other end of the bone, or if the vibration is significantly diminished when compared with the other limb, a discontinuity (fracture) may exist. Portable

C2 C3 C4 C5

C7 C8

T1 T2 T3 T4 T5 T6 T7 T8 T9 T10

C6

C6 T1 C5

C8

C7

T11

C6

T12

C8

L1

C7

C7

C8

CHAPTER 27  Wilderness Orthopedics

Schematic demarcation of dermatomes (according to Keegan and Garrett) shown as distinct segments. There is actually considerable overlap between any two adjacent dermatomes. An alternative dermatome map is that provided by Foerster (see References).

C2 C3 C4 C5 C6 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2

S3 S4

S2, 3 L2

S1

S5

L3

S2

L5 L4

L1 L2 L3

L5

S1 S2

L4 S1

L5

L5 L4

Levels of principal dermatomes C5 C5, 6, 7 C8, T1 C6 C6, 7, 8 C8 T4

S1

Clavicles Lateral parts of upper limbs Medial sides of upper limbs Thumb Hand Ring and little fingers Level of nipples

L4

T10 Level of umbilicus L1 Inguinal or groin regions L1, 2, 3, 4 Anterior and inner surfaces of lower limbs L4, 5, S1 Foot L4 Medial side of great toe S1, 2, L5 Posterior and outer surfaces of lower limbs S1 Lateral margin of foot and little toe S2, 3, 4 Perineum

FIGURE 27-3  Sensory dermatomes. (Netter illustration from http://www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

ultrasound can also be employed if it is available and if doubt remains regarding the existence and location of a fracture. The palpation of long bones begins distally and proceeds across all joints. A splint should be applied if there is palpable crepitus, swelling, deformity, or a block to motion. If the victim can cooperate, each joint is taken through an active range of motion to quickly locate any injury. When this is not possible, passive motion of each joint is evaluated after palpation for crepitus and swelling. Any dislocations are carefully reduced after completing the neurovascular examination. This generally relieves the victim’s discomfort considerably. Once relocation has occurred, stability is evaluated by careful, controlled motion. Joints with associated fractures or interposed soft tissues may still be unstable after reduction. Great care is required in applying splints to prevent redislocation or further soft tissue injury. A report of details of the reduction or relocation maneuver, including orientation of the pull, amount of force involved, amount of sedation, and residual instability of the joint, should be provided to the

definitive care physician (see Reduction and Relocation Maneuvers, later).

Potentially Life-Threatening Musculoskeletal Injuries SPINAL INJURIES Cervical Spine In the wilderness, cervical spine fractures or dislocations can be the result of a fall from a height, a high-velocity ski crash, in a combat setting, or a diving accident. Because head and cervical spine injuries are highly associated, a victim with a significant head injury should be considered to have a cervical spine injury, especially if the individual is unconscious. Ideally, a person with a suspected cervical spine injury is placed on a backboard with neck immobilization to prevent further injury and promptly evacuated. Approximately 28% of persons with cervical spine 525

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 27-4  C1 ring, Jefferson’s fracture.

fractures also have other spinal fractures.3 Therefore the person providing care must protect the entire spine. When a cervical spine injury is suspected, the field examination involves grading motor strength, documenting sensory response to light touch and pinprick, and noting the presence or absence of the Babinski reflex (see Figure 27-3). When appropriate supplies are available, a rectal examination should be done. Complete lack of tone and failure of the sphincter muscles to contract when pulling on the penis or clitoris (the bulbocavernosus reflex) indicates spinal cord injury. Neurologic deficit often results from cervical spine fracture. Complete neurologic injury from the occiput to the C4 level is usually fatal because of paralysis of the phrenic nerve, diaphragm, and respiratory muscles. The corollary to this is that surviving victims generally have partial deficits or are neurologically intact. Axial cervical spine fractures may result from flexion forces (most common), extension forces, rotational forces, or a combination of these. Cervical spine fractures most commonly occur at C5-6.3 Fracture of the C1-2 complex results from axial loading (a C1 ring fracture, or Jefferson’s fracture) (Figure 27-4) or from an acute flexion injury (a C2 posterior element fracture, or hangman’s fracture) (Figure 27-5). A pure flexion event may dislocate one or both posterior facets, producing neck pain and limitation of motion. Because the interspinous ligament is ruptured and this fracture dislocation is highly unstable, victim transport must be done with the neck rigidly immobilized to reduce the risk for posterior motion. Fractures and dislocations may result in neurologic insult distal to the bony injury. Because flexion injuries are the most common cervical spine injuries, the neurologic deficit is generally an anterior cord syndrome. In this setting, the victim suffers

FIGURE 27-5  C2 hangman’s fracture.

526

FIGURE 27-6  Wedge compression fracture from axial or flexion loading at the thoracolumbar junction.

complete motor loss and partial sensory loss but retains proprioception. Thoracolumbar Spine Thoracolumbar spine fractures occur most frequently at the T12-L1 junction. Because the thoracic spine is well splinted by the thoracic cage, when an axial or flexion load is applied, the ribs diminish forces on the thoracic vertebral bodies and transmit the force to the upper lumbar levels. In the wilderness, falls from significant heights or a high-velocity sporting vehicle crash may produce these fractures (Figure 27-6). Thoracolumbar spine fracture may also be associated with other fractures that occur with axial loading, such as femoral neck fractures (Figure 27-7) and calcaneus fractures (Figure 27-8). These injuries commonly occur when there is an axial force, such as a fall onto the lower limbs from a height. Therefore an individual who sustains a presumed hip fracture or calcaneus fracture as the result of a fall from a height generally should be transported under spinal precautions.

FIGURE 27-7  High-energy basicervical femoral neck fracture with greater trochanter fracture after a 40-foot fall while rock climbing.

CHAPTER 27  Wilderness Orthopedics

FIGURE 27-8  Calcaneus fracture.

A study of mortality in the wilderness setting in Pima County, Arizona, between 1980 and 1992 demonstrated that most deaths occurred as a result of falling or drowning.12 Pelvic fractures generally occur with a fall from significant height, high-velocity ski accident, or vehicle crash. The Young and Burgess classification of pelvic fractures is based on the mechanism of injury. Pelvic fractures are categorized as anteroposterior compression injuries, lateral compression injuries, and vertical shear injuries.5 These fracture patterns have been shown to correlate with blood loss, associated injuries, multisystem morbidities, and

mortality.5,7,31 Anteroposterior compression injuries can result in rotational instability if there is greater than 2.5 cm (1 inch) of pubis symphysis separation (Figure 27-9). Furthermore, if the posterior pelvic ring is disrupted, this can lead to both rotational and vertical instability. These fractures, which may include acetabular fractures, are often accompanied by hemorrhagic, neurologic, urologic, gynecologic, and gastrointestinal injuries (Figures 27-10 and 27-11). Because the posterior pelvic ring accounts for about 60% of pelvic stability, in a suspected pelvic fracture, it should be determined whether there is an injury to the posterior pelvis. Posterior pelvic fractures are identified by instability of the pelvis associated with posterior pain, swelling, and ecchymosis. This victim should be immediately evacuated on a backboard, taking care to minimize leg and torso motion. Hemodynamic instability may occur with pelvic fractures, especially if the injury is the result of translational or shear forces or if the posterior pelvic structures are primarily involved. Bleeding associated with a pelvis injury is usually from cancellous bone at fracture sites, a retroperitoneal lumbar venous plexus injury, or, rarely, pelvic arterial injuries. Medical antishock trousers, the portable SAM sling, or even a bedsheet wrapped around the pelvis of an individual with a suspected unstable pelvic fracture may provide stability and accomplish adequate tamponade of bleeding from the fracture22 (Figure 27-12). Other similar devices are available or may be improvised. The applied sling belt (pelvic

FIGURE 27-9  Pelvic injury after being thrown from a horse. Pubic symphysis widening of greater than 2.5 cm (1 inch) is generally considered to be unstable.

FIGURE 27-10  Highly unstable pelvic ring injury with pubic rami fractures and displaced iliac wing fracture. This patient also had a severe bladder injury.

When a thoracolumbar spine fracture is suspected, a careful neurologic examination should be performed as part of the secondary survey, and close attention should be paid to the dermatomal response to light touch and pinprick, motor function, and the presence or absence of cord level reflexes. Because significant fluctuations in sympathetic tone may occur, the rescuer should monitor blood pressure and body temperature, taking appropriate steps to cool or warm the victim. If evacuation cannot be performed immediately, hemodynamic and neurologic function should continue to be noted and documented. The victim should be logrolled, maintaining perfect spinal alignment, and carefully placed on a backboard. The scoop stretcher may be used in this situation (see Chapter 19).

Pelvic Injuries

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

Acetabulum

Femoral head

FIGURE 27-11  Right hip dislocation with acetabular and femoral head fractures.

FIGURE 27-14  Prone patient with an unstable pelvic fracture and a large degloving (Morel-Lavallée) flank lesion.

generally appreciated as areas of tenderness without instability. Lateral compression injuries are usually stable, with impaction of the posterior structures.

Extremity Injuries—General Considerations SPLINTING TECHNIQUES

FIGURE 27-12  SAM sling.

binder) or similar contrivance should be left in place until definitive care is available (Figure 27-13). Degloving injuries can also be seen in high-energy pelvis injuries (Figure 27-14). In addition to these high-energy injuries, simple, nondisplaced inferior or superior ramus fractures and avulsion fractures can occur. On clinical examination, these pelvic fractures are

Splinting in the wilderness is performed so that alignment is maintained and further soft tissue injury is minimized. A victim with suspected cervical or thoracolumbar spine trauma should be transported on a hard surface. Backboards or scoop stretchers (see Chapter 19) are most effective, but improvisation with hard pieces of wood, fiberglass, or straight tree limbs lashed together may be needed. If cervical spine injury is suspected, a roll of clothes or a water bottle can be placed as high as the victim’s midface on either side of the head to prevent rotational movement. Tape applied from the supporting stretcher across the objects and the victim’s forehead adds stability. A child with a suspected spine injury should be transported on a backboard with the child’s body slightly elevated relative to his or her head (Figure 27-15). Any victim with a suspected major pelvic injury is transported in a similar fashion, stabilizing the pelvis with a circumferential sheet or piece of clothing or special belt and holding the lower extremities as immobile as possible, with the knees slightly flexed (see Figure 27-12). Many different extremity splints are available for use in the wilderness setting. These splints are lightweight, compact, and easy to use. They are, of course, more elaborate than a hiking pole or branch that is more readily available. These more intricate devices have considerable advantages for larger-scale evacuations in the setting of natural disasters. They are designed to provide traction through the injured extremity while using the

Backboard FIGURE 27-13  Appropriate application of a sheet for an unstable pelvic fracture (centered at the greater trochanters, as opposed to the iliac wings).

528

Blanket to elevate body

FIGURE 27-15  Child with suspected spine injury should be transported on a backboard with the child’s body slightly elevated relative to his or her head.

FIGURE 27-16  Lower extremity splints.

intrinsic properties of the splint and the injured limb to apply the traction. With proper splint application, the injured limb can be immobilized securely in a functional position until definitive care is reached (Figure 27-16). Air splints may be of some benefit, but they are generally manufactured in one shape. Especially in the setting of injured tissues and in environments that might include wide temperature variability, these splints can cause compressive damage to an already injured extremity. Therefore, in more extreme conditions, an air splint is used only if it has an automatic adjustment valve to account for atmospheric variability. Also, these splints should be stored in a minimally inflated state when the temperature is below freezing, to prevent ice from causing splint dysfunction. Beaded vacuum splints can also be used. However, temperature and altitude considerations can make adequate and consistent inflation less reliable. When beaded vacuum splints and air splints are used, vigilance is required to ensure that no excessive pressure is applied to already injured soft tissues. Upper extremity splints may also be made from plaster or fiberglass, which can be applied over a soft cotton roll. Lightweight fiberglass splints, such as Ortho-Glass and FareTec, are easy to use and effective in the initial management of these injuries (Figure 27-17). These splints are prepadded and can be applied with either cold or warm water. The warmer the water, the faster the fiberglass sets and the greater the exothermic reaction. Hot water should be avoided because it may generate an excessively exothermic reaction and possibly burn the skin. The fiberglass is immersed in water, excess water is gently squeezed out, and the splint is applied. An elasticized bandage helps hold the splint where desired until the fiberglass is hard. Air splints,

when inflated, can adequately splint the upper extremity in a stable position. Wooden or metal splints, custom made or improvised, also can be used to stabilize an injured extremity. New thermoplastic casts and braces may be used in a wet outdoor environment and immersed in water without compromising function or stability (Figure 27-18). Hand splints are applied with the metacarpophalangeal (MCP) joints flexed to 70 to 90 degrees and the interphalangeal (IP) joints extended. This position places the collateral ligaments at maximal length and prevents joint contracture (Figure 27-19). Wrist or forearm splints are applied with the wrist in a neutral position; excessive wrist flexion or extension might detrimentally affect median or ulnar nerve function in an already compromised limb. The elbow is positioned in a splint or sling at 90 degrees, if possible. For shoulder fractures or dislocations, a commercially available sling or improvised triangular bandage should be used to take the weight of the arm off the injured structures. Although it may be difficult to place an injured elbow in 90 degrees of flexion and neutral rotation, the upper extremity should be splinted in the position of comfort and function whenever possible. For the lower leg, air splints provide adequate immobilization of tibia or fibula fractures and of ankle fractures and dislocations. Splints made from plaster or fiberglass may be applied over cotton padding and held in position with elasticized bandages. The SAM Splint, an excellent first-aid item that may be molded to immobilize a wide variety of injuries, provides stability and strength through its aluminum and foam core (Figures 27-20 and

FIGURE 27-19  Hand and wrist in position of function.

FIGURE 27-17  Water-activated FareTec splint for distal radius fracture, with wrist and hand in position of function.

FIGURE 27-20  SAM Splint.

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CHAPTER 27  Wilderness Orthopedics

FIGURE 27-18  Swimmer in Exos fracture brace.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

1

2

FIGURE 27-21  Versatile splint for upper or lower extremity.

3

4

FIGURE 27-24  Improvisation of an ankle wrap to be used for traction.

walking stick placed between them. If possible, the victim is transported on a backboard. FIGURE 27-22  Slishman splint applied for femur fracture following the 2010 earthquake in Haiti. (Courtesy Sam Slishman.)

27-21). The aluminum structure can be bent into three configurations to provide different degrees of stability, flexibility, and immobilization. The ankle is held in neutral position and the splint applied firmly. For transport, the lower extremity is positioned with the hip and knee extended and the ankle in neutral position. Victims with unstable lower extremity fractures or dislocations are transported in the recumbent position with the afflicted limb elevated. For hip or femur fractures or dislocations, traction is applied whenever possible, improvising as necessary. For suspected hip, femur, or knee injury, one of multiple splints can be used. The basic principle guiding application of these is to provide traction of the lower extremity using a lightweight device (Figures 27-22 and 27-23). The ischium and/or pubis are proximal structures against which the splint is set. The ankle is usually the structure through which traction is applied (Figure 27-24). Lightweight splints that may be of use in the wilderness setting include those known either by their manufacturer or developer, such as Donway, Thomas, Kendrick, Slishman, Reel, FareTec, Sager, CT-6, and Hare (see Chapter 19). It behooves a backcountry health care provider to be familiar with whichever splinting device he is carrying. If commercial splints are unavailable, the injured leg is strapped to the noninjured leg, with a tree limb or

FIGURE 27-23  Lower extremity splint.

530

REDUCTION AND RELOCATION MANEUVERS Even in the wilderness, the four principles of fracture reduction should be followed: • Traction: in-line or longitudinal force application • Fracture fragment disengagement; included in this step is recreation of the forces that created the fracture • Reapposition of fracture ends • Counteraction of forces that lead to deformity Steady traction and patience are the mainstays of fracture and dislocation reduction maneuvers.4 For distal radius fractures, the usual dorsiflexion deformity is reproduced and a flexion force is applied through the fracture. Steady traction can also assist with reduction of these fractures (Figures 27-25 to 27-27 ). For ankle fractures, traction is applied. Most fractures are the result of an eversion, external rotation force. Therefore reduction is undertaken and a splint applied so that the ankle is in inversion and internal rotation, known as the Quigley maneuver. Care must be taken in the absence of diagnostic imaging so that excessive force on a limb, which has already sustained significant vascular or nerve injury, is not exerted (Figure 27-28).

TRACTION PINS Skeletal traction is applied in the setting of pelvis or acetabular fracture or lower extremity fractures, such as femur or tibia fracture. This mode of stabilization can be used for temporary or more definitive treatment. This technique can be used in a setting such as a natural disaster (see Figure 27-1). Distal femoral traction pins are inserted from medial to lateral. The knee is flexed during insertion to facilitate access to the medial aspect of the distal femur and to allow for flexion of the knee once the pin has been placed; if the pin is placed with the knee in extension, the iliotibial band might be tethered and thereby prevent knee flexion. The pin is placed approximately two finger breadths proximal to the adductor tubercle. If the pin is placed too distally, it can enter the intercondylar notch of the

CHAPTER 27  Wilderness Orthopedics

Reduction of Colles’ fracture by manipulation method under local (infiltration) anesthesia: 1: Hyperextension and traction to break up impaction combined with direct thumb pressure; countertraction and fixation of forearm by assistant

2: With continued traction, countertraction, ulnar deviation of the hand, and thumb pressure, the ends of the fragments are brought into apposition; the operator’s index fingers press on the proximal fragment while the thumbs press on the distal one

3. The hand is now quickly flexed at the wrist, maintaining traction and pressure on the fragments to bring them into alignment FIGURE 27-25  Reduction maneuver for the most common distal radius fracture (dorsally angulated). (Netter illustration from http://www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

knee. If the pin is placed too proximally, it can injure the superficial femoral artery near its exit from the adductor hiatus, or one of the branches of the superficial femoral artery, near the knee. Proximal tibial traction pins are inserted from lateral to medial. The pin is placed approximately two finger breadths distal to the tibial tubercle and two finger breadths posterior to the anterior tibial crest. These pins should not be placed in children, if possible; proximity of the tibial tubercle physis puts this important structure at risk during insertion of a proximal tibial traction pin (Figure 27-29). A calcaneal pin can also be used for applying lower extremity traction. This type of traction pin may be of particular benefit in the setting of ipsilateral femur and tibia injuries. It is usually placed medial to lateral, with care taken to avoid the posterior tibial neurovascular bundle. The pin is driven through the calcaneus and exits laterally (Figure 27-30). If possible, balanced traction should be maintained. This helps to counteract deforming forces and to allow for relatively comfortable movement in bed. There are no hard-and-fast rules for the amount of weight to apply. If balanced traction is employed, the

rule of thumb is for enough traction to be applied that the ipsilateral buttock is elevated just barely off the bed. When radiography is available, traction is applied until the fracture fragments are well aligned and nearly out to length. For an average-sized adult, this likely will be between 6.8 and 13.6 kg (15 and 30 lb).

OPEN FRACTURES Recognizing an open fracture is imperative; without prompt surgical treatment, the incidence of osteomyelitis in this setting is high.14 In an open fracture, the fractured bone communicates with a break in the skin. With subcutaneous bones (e.g., tibia), open fractures are easily identified, but with other bones that have more surrounding soft tissue (e.g., humerus, femur, pelvis), identification is more difficult because the fractured bone end usually retracts once it punctures the skin and is then covered by soft tissue. A laceration near a fracture may be an indication of an open fracture. Most open fractures persistently ooze blood or fat globules from the laceration, which may facilitate diagnosis (Figure 27-31). Clothes should be split and skin examined. 531

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 27-28  Quigley maneuver for ankle fracture reduction. Anterior and inversion forces on the foot and ankle created by hanging leg by the great toe, held medial to midline of the body (or hung with stockinette as depicted.)

Distal femoral traction pin

FIGURE 27-26  Distal radius fracture with distal radioulnar joint dislocation sustained after a fall on an outstretched hand.

Proximal tibial traction pin

FIGURE 27-29  Proper positioning of distal femoral and proximal tibial traction pins.

FIGURE 27-27  Reduced fracture dislocation.

532

FIGURE 27-30  Calcaneal traction pin placement—slightly more anterior than is usually desired—in the setting of subtalar dislocation.

SIGNIFICANT SOFT TISSUE INJURIES FIGURE 27-31  Type IIIB open tibia-fibula fracture that occurred as a result of a fall while the individual was holding a chainsaw.

Familiarity with the Gustilo-Anderson open fracture classification system is useful. This open fracture classification assigns musculoskeletal trauma to one of three major categories (types I to III) depending on the mechanism of injury, extent of soft tissue damage, and degree of skeletal involvement. Type I • Wound is less than 1 cm (0.4 inch) with minimal soft tissue injury. • Wound bed is clean. • Fracture is usually a simple transverse, short oblique fracture, with minimal comminution. Type II • Wound is greater than 1 cm with moderate soft tissue injury. • Wound bed may be moderately contaminated. • Fracture is usually a simple transverse, short oblique fracture, with minimal to moderate comminution. Type III Type III fractures involve extensive damage to the soft tissues, including muscle, skin, and neurovascular structures. They are often the result of a high-velocity injury or a severe crushing component. The following special patterns are classified as type III: • Open segmental fracture, irrespective of the size of the wound • Gunshot wounds—high-velocity and short-range shotgun injuries • Open fracture with neurovascular injury • Farm injuries, or highly contaminated wounds, irrespective of size • Traumatic amputations • Open fractures over 8 hours old • Mass casualties (e.g., war and tornado victims) Subtype IIIA The wound is less than 10 cm (3.9 inches) with crushed tissue and contamination, or it is the result of high-energy trauma, irrespective of the size of the wound. This includes segmental fractures or severely comminuted fractures. Adequate soft tissue coverage is usually possible despite soft tissue laceration or flaps. Subtype IIIB There is extensive soft tissue loss (greater than 10 cm [3.9 inches]) with periosteal stripping and bony exposure. This is usually associated with massive contamination and typically will require regional or free-flap reconstruction. Subtype IIIC Subtype IIIC is a fracture in which there is a major arterial injury requiring repair for limb salvage. Mangled Extremity Severity Score can provide prognostic considerations for limb salvage versus amputation.15

Degloving injuries (sometimes referred to as Morel-Lavallée lesions) and/or crush injuries can occur in the wilderness (see Figure 27-14). Although they are seen more commonly in highenergy, urban accidents, they can also occur as the result of a significant fall or crush beneath a boulder, for example. Natural disasters and warfare can also result in a mangled or crushed limb. Splinting, monitoring for compartment syndrome, and expeditious evacuation are imperative.

TOURNIQUETS Although the use of tourniquets outside of a medical facility historically has been anathema, there has been a resurgence in their use in the field by the military. In fact, in the Iraq and Afghan theaters, soldiers are trained in the application of tourniquets on themselves and others, and tourniquet use in the setting of a mangled or badly injured extremity is high. Evacuation as soon as possible after tourniquet application is crucial. Exsanguination remains a major cause of death in military conflicts. Reduction of blood loss volume is seen as an important way to reduce mortality in war casualties. Sacrificing a limb to save the soldier is a difficult but clear decision.19

AMPUTATION In the wilderness, the amputation victim requires immediate evacuation. Control hemorrhage using direct pressure, or employ a tourniquet. Without cooling, an amputated part remains viable for only 4 to 6 hours. Cleanse the amputated part with saline or water, wrap it in a moistened sterile gauze or towel, place it in a plastic bag, and transport the bag in an ice-water mixture. Do BOX 27-1  Antibiotic Options Intravenous Cefazolin (Ancef ) 1 g q 6 hr and gentamicin (5 mg/kg) q 24 hr or piperacillin with tazobactam (Zosyn) 3.375 g q 6 hr Intramuscular Ceftriaxone (Rocephin) 1 g q 24 hr Oral ciprofloxacin 750 mg bid and cephalexin (Keflex) 500 mg qid Water Exposure Ciprofloxacin 400 mg IV or 750 mg PO bid; or a sulfonamide and trimethoprim combination (Bactrim DS: 800 mg sulfamethoxazole and 160 mg trimethoprim) with either cefazolin (Ancef) 1 g IV   q 8 hr or cephalexin (Keflex) 500 mg PO q 6 hr Dirt or Barnyard Add penicillin 20 million units IV daily or 500 mg PO q 6 hr If Penicillin Allergy Use clindamycin 900 mg IV q 8 hr or 450 mg PO q 6 hr in place of penicillins and cephalexin (Keflex) Alternatives Erythromycin 500 mg q 6 hr or amoxicillin with clavulanic acid 875 mg bid Bid, Twice a day; IV, intravenously; PO, orally; qid, 4 times a day.

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CHAPTER 27  Wilderness Orthopedics

General care of an open fracture outdoors depends on evacuation time. Open fractures require prompt operative irrigation, debridement, and stabilization. If evacuation can be completed within 8 hours, realign the fracture, administer a broad-spectrum antibiotic, and splint the extremity. If bone ends extrude through the skin, cover the exposed bone with a dilute povidone-iodine solution–soaked gauze sponge, splint the extremity, and arrange for prompt evacuation. If evacuation time exceeds 8 hours, in addition to antibiotic administration and splinting, irrigation and debridement in the field may be attempted. If available, and tetanus vaccine is not known to have been given in the past 7 years, this should also be provided. Antibiotic options are listed in Box 27-1.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 27-32  Thumb amputation/avulsion as a result of a rider’s thumb getting caught in a horse’s reins before he fell from the horse.

not use dry ice. Keep the amputated part with the victim throughout the evacuation (Figures 27-32 and 27-33).

COMPARTMENT SYNDROME A compartment syndrome begins when locally increased tissue pressure reduces capillary blood flow to a muscle compartment. When local blood flow is unable to meet metabolic demands of the tissue, ischemia ensues. In the wilderness, a compartment syndrome most frequently occurs in association with a fracture, crush injury, or severe contusion. It can also occur when the victim has been lying for some time across an extremity so that the body weight occludes the arterial supply. Elevated local tissue pressure (compartment pressure within 10 to 20 mm Hg of diastolic arterial blood pressure) can also occur with acute hemorrhage or after revascularization of an ischemic extremity. Because perfusion pressure is the most important variable in development of compartment syndrome, hypotension can increase the risk for a compartment syndrome. Compartment syndrome can occur in the thigh, hand, foot, and gluteal regions. It is more common, however, in the lower

FIGURE 27-34  Developing compartment syndrome in the setting of a tibia-fibula fracture, 6 hours following a crush injury.

leg and forearm, because of the tight fascia in these regions. The conscious victim complains of severe pain out of proportion to the injury. The muscle compartment feels extremely tight, and applied pressure increases the pain. There may be deceased sensation to light touch and pinprick stimuli in the areas supplied by the nerves traversing the compartment. Stretching muscles within the compartment produces severe pain. The most reliable signs of a compartment syndrome are pain, tight compartments, hypesthesia, and pain on passive stretch. Pulselessness, pallor, and slow capillary refill may not be observed, even with a severe compartment syndrome (Figure 27-34). Emergency evacuation is required when compartment syndrome is suspected. The victim must be definitively treated in the first 6 to 8 hours after onset to optimize return of function to the involved limb. Emergency fasciotomy, the treatment of choice, relieves the pressure. If a compartment syndrome develops and evacuation cannot occur within 8 hours, it must be decided whether the treating individual possesses the skill to perform a fasciotomy and whether it can be performed in an aseptic manner. Fasciotomies can convert a closed fracture into an open fracture and can provide a conduit for limb- or life-threatening infection: the function of a limb with nonfunctioning nerves and muscles as a result of compartment syndrome months after the compartment syndrome can be salvaged with tendon transfers, whereas a limb that becomes infected after providing fasciotomies in the wilderness could easily result in an amputation. If a fasciotomy is to be done, antibiotics should be administered. In the forearm, the procedure usually involves making volar and dorsal incisions and splitting the underlying fascia. In the lower leg, the procedure usually involves making two long incisions, one on the medial aspect and the other on the lateral aspect of the leg, and splitting, in a vertical fashion, the compartmental fascia in each of the four lower leg compartments. Fasciotomies for compartment syndrome that cannot be done within 12 hours of the syndrome’s development should not be undertaken. A retrospective analysis of individuals who underwent late release for compartment syndrome (more than 35 hours after the injury) demonstrated significant complication and amputation rates. Therefore, even in an urban trauma hospital, delayed compartment release for compartment syndrome is not recommended.10

RICE PRINCIPLE

FIGURE 27-33  Traumatic near amputation of a foot that occurred in a boating accident. Patient was treated with below-knee amputation.

534

The general principle in the acute management of extremity injuries is rest, ice, compression, and elevation (RICE). For unstable fractures, immobilization is also indicated. Avoid heat for the first 72 hours after injury. Chemical cold packs work well, but cold packs made from ice or snow will suffice. If cold packs are unavailable, the extremity can be immersed intermittently in a cold mountain stream. If ice is used, mix some water in a bag with the ice to more evenly distribute the cold. The cold pack

CHAPTER 27  Wilderness Orthopedics

to the injured area may be held in place with an elasticized bandage. A piece of fabric is placed between the cold pack and the victim’s skin to prevent frostbite. The ice is applied to the elevated extremity (above the level of the heart) for 30 to 45 minutes every 2 hours. A compressive dressing also helps decrease swelling but should not be used if development of a compartment syndrome is possible. In this situation, keep the limb at the level of the heart and avoid compressive dressings.

Upper Extremity Injuries In the wilderness, without benefit of radiographic images and high-dose analgesics, determination of the exact anatomic structures affected by an injury can be a challenge. The following sections have therefore been divided in a manner that is based on the location of general pathology.

SHOULDER GIRDLE Clavicle Fracture Fracture of the clavicle usually occurs in the middle or lateral one-third of the bone and is associated with a direct blow or with a fall onto the lateral shoulder (Figure 27-35). Clavicle fractures are common in snow skiing and mountain biking accidents. The victim complains of shoulder pain, which may be poorly localized. Arm or shoulder motion exacerbates the pain. To localize the problem, gently palpate the clavicle to identify the area of maximal tenderness. The presence of crepitus at the clavicle confirms the diagnosis. Although rare, a pneumothorax can be associated with a clavicle fracture if the cupola of the lung is punctured; therefore auscultate the chest for breath sounds. Shortness of breath and deep pain on inspiration increase suspicion for a pneumothorax. Clavicle fracture may also be accompanied by injury to the brachial plexus, axillary artery, or subclavian vessels. In an individual with a fractured clavicle, a thorough neurovascular examination of the affected extremity is performed, and the skin is examined carefully. Approximately 3% to 5% of clavicle fractures may be open because of the bone’s subcutaneous location. The victim should be evacuated if there is a significant open wound, suspected pneumothorax, or nerve or vascular injury. Field treatment for a clavicle fracture consists of a sling or figure-8 bandage and judicious use of analgesics.

FIGURE 27-36  Three-dimensional computed tomography view of scapula fracture. Complete disassociation of glenoid from scapular body is present.

conjunction with thorax injuries, such as rib fracture or pneumothorax. Palpation and auscultation for breath sounds assist in making these associated diagnoses. Symptomatic, nonoperative treatment for a scapula fracture is usually indicated.

Scapula Fracture These injuries to the “wing-bone” are uncommon in the wilderness but may result from a fall on the back or a direct blow. Confirmation of the exact injury often requires radiographic or computed tomography evaluation (Figure 27-36). Scapula fractures can be seen in isolation or, in higher-energy injuries, in

Sternoclavicular Joint Dislocation Traumatic dislocation of the sternoclavicular joint generally requires tremendous force, either direct or indirect, applied to the shoulder. Consequently, it is rare. Anterior dislocation is most common, with the medial head of the clavicle going anterior to the manubrium of the sternum (Figure 27-37). The victim complains of pain around the sternum and frequently has difficulty taking a deep breath. When the dislocation is posterior, significant pressure may be placed on the esophagus and superior vena cava. The victim may complain of difficulty swallowing and have engorgement of the veins of the face and upper extremities, representing superior vena cava obstruction syndrome. A step-off between the sternum and the medial head of the clavicle (compared with the uninjured side) confirms this diagnosis. Unreduced anterior dislocation does not produce neurocirculatory compromise and is treated with a sling. Reduction of a posterior sternoclavicular dislocation should be attempted as soon

FIGURE 27-35  Midshaft clavicle fracture sustained by a 13-year-old snowboarder, riding in the backcountry with his friends. Proximal humerus demonstrates physis normal growth plate, often mistaken for a fracture. Comparison view of the opposite shoulder may be obtained if proximal humerus fracture is suspected.

FIGURE 27-37  Anterior sternoclavicular dislocation.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

Sand bag between shoulders

A

B B

C

FIGURE 27-39  Acromioclavicular joint injury. A, Normal anatomy. B, Grade 2 injury. C, Grade 3 injury.

Acromioclavicular Joint Dislocation

C FIGURE 27-38  Technique for closed reduction of the sternoclavicular joint. A, The patient is positioned supine with a sandbag placed between the shoulders. Traction is then applied to the arm against countertraction in an abducted and slightly extended position. For anterior dislocation, direct pressure over the medial end of the clavicle may reduce the joint. B, For posterior dislocation, in addition to the traction, it may be necessary to manipulate the medial end of the clavicle with the fingers to dislodge the clavicle from behind the manubrium. C, For a stubborn posterior dislocation, it may be necessary to sterilely prepare the medial end of the clavicle and use a towel clip to grasp around the medial clavicle and lift it back into position. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)

as possible if any neurocirculatory compromise is present. The victim is placed supine with a large roll of clothing or other firm object between the scapulae. Traction is applied to the arm against countertraction in an abducted and slightly extended position. The medial end of the clavicle may need to be manually manipulated to dislodge the clavicle from behind the manubrium (Figure 27-38). If this fails, sharp, firm pressure is applied posteriorly to both shoulders. This maneuver is repeated several times, with a larger object placed between the scapulae if reduction attempts are initially unsuccessful. Alternatively, with the victim seated and the caregiver’s knee against the back between the shoulders, both shoulders are pulled back. Although it might seem macabre, if the victim remains in extremis, the medial end of the clavicle is grasped with a towel clip or pliers and forcefully pulled out of the thoracic cavity. Once reduced, the injury is usually stable. The posterior sternoclavicular dislocation requires evacuation. 536

These injuries to the acromioclavicular joint are commonly known as shoulder “separations,” to be distinguished from a true shoulder glenohumeral (GH) dislocation. Acromioclavicular separations are typically classified as grade I, II, or III (Figure 27-39). These injuries are painful, but surgery rarely improves clinical outcome. The acromioclavicular joint is usually injured by a blow or fall onto the shoulder (Figure 27-40). Because using the hand increases pain, the arm on the affected side is placed in a sling. As long as the individual can tolerate the discomfort associated with such an injury, evacuation is not necessary. Glenohumeral Joint Dislocation Dislocations of the GH joint are the most common dislocation in the human. Ninety-five percent of GH dislocations occur in an anterior/inferior direction (Figure 27-41). The usual mechanism of injury is a blow to the arm in the abducted and externally rotated position. This frequently occurs in skiing as the individual crosses the ski tips or goes forward on a mogul and lands face down with the arm(s) akimbo. When a posterior GH dislocation occurs in the wilderness, it is often in the setting of seizure or lightning strike. Usually, external rotation is completely lost. On palpation of the shoulder, posterior fullness that is not found on the uninjured side can usually be detected. Recurrent dislocations and dislocations in younger patients may be easier to reduce than first-time dislocations in older

FIGURE 27-40  Grade III acromioclavicular separation of the left shoulder after a fall from a mountain bike.

CHAPTER 27  Wilderness Orthopedics

Coracoid

Clavicle

AC joint Hill sachs legion

Glenoid Acromium

FIGURE 27-41  Axillary lateral radiograph demonstrating anterior glenohumeral dislocation that resulted following a fall while backcountry skiing.

patients. A thorough motor, sensory, and circulatory examination of the involved extremity is performed. Axillary and musculocutaneous nerves are the nerves most commonly injured with an anterior dislocation and therefore must be assessed carefully. Serial examinations of distal pulses, capillary refill, and forearm compartments are performed. The treatment of shoulder dislocations still requires, as it did several thousand years ago, the laying on of hands and manual reduction. Today, as in the past, there are no surefire or infallible ways to reduce a shoulder dislocation. Anyone who has treated a significant number of dislocations knows that it can be, on occasion, a very simple, quick procedure and at other times an ordeal that leaves the practitioner sweating, exhausted, and cursing and the patient on the way to the operating room for anesthetic relaxation. Beginning with the Hippocratic technique described in approximately 400 BC, many techniques have been touted for manipulation and relocation of the shoulder. Although we have never seen a physician put a patient’s dislocated arm through a ladder for levered reduction on the rung (a diagrammed technique!), we have seen doctors’ feet in armpits, patients groaning on a gurney with weights taped to their wrists, various leverage techniques and maneuvers, wrestling holds (similar in appearance to the Verne Gagne “sleeper hold”), bedsheets and straps, and struggles, wherein the poor victim’s arm looked like a rope in a tug-of-war contest with a doctor on each end. The fact that so many methods continue to exist suggests that most of them are effective, although none is perfect. Common techniques include Kocher, Milch, Stimson, Spaso, Legg, scapular manipulation, and the Snowbird maneuver2,8,9,20,29 (Figures 27-42 to 27-48). Self-reduction has been proposed by some but is

FIGURE 27-42  Traction and countertraction for dislocated shoulder reduction.

FIGURE 27-43  Repositioning a dislocated shoulder. Attached to the victim’s forearm with a strap, rope, or sheet, the rescuer uses his body weight to apply traction, leaving his hands free to manipulate the victim’s arm. A second rescuer applies countertraction, or the victim can be held motionless by fixing the chest sheet to a tree or ground stake. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 4, Guilford, Conn, 2003, Lyons Press.)

arguably a challenging procedure. The technique favored by the authors uses sustained, gentle traction–countertraction to overcome muscle spasm, minimizes rotational maneuvers, and avoids leveraging (Figure 27-49). Of interest to the wilderness caregiver is the “Eskimo technique” used by natives of Greenland, in which the patient is lifted from the ground by the affected arm (while lying on the unaffected side) so that the patient’s body weight serves as a countertraction.23 Mel Gibson, in his Lethal Weapon films, demonstrates a body-slam technique that may be performed, in the absence of an assistant or physician, against any solid stationary object. The recurrence rate is evidently high with this maneuver. Greater tuberosity or glenoid fractures may accompany acute GH dislocations. Transient musculocutaneous and/or axillary nerve neuropraxia occurs in approximately 20% of shoulder dislocations.27 Dislocation of the GH joint remains an injury of potential long-term consequence for the patient. It is especially important

FIGURE 27-44  Milch technique of closed reduction of anterior glenohumeral dislocation with the patient prone. The arm can be manipulated in the same manner with the patient supine. (Redrawn from Lacey T II, Crawford HB: Reduction of anterior dislocations of the shoulder by means of the Milch abduction technique, J Bone Joint Surg 34A:108, 1952. In Browner BD, Jupiter JB, Levine AM, et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1998, Saunders.)

537

PART 4  INJURIES AND MEDICAL INTERVENTIONS FIGURE 27-45  Scapular manipulation technique for closed reduction of anterior glenohumeral dislocation. (Redrawn from Anderson D, Zvirbulis R, Ciullo J: Scapular manipulation for reduction of anterior shoulder dislocation, Clin Orthop Relat Res 164:181, 1982. In Browner BD, Jupiter JB, Levine AM, et al: Skeletal trauma, vol 2, ed 2, Philadephia, 1998, Saunders.)

for the younger individual, whose risk for redislocation may exceed 50%, to visit an orthopedic surgeon.27 Arthroscopic or open repairs of the damaged anterior capsule and labrum may be appropriate in some cases after the first injury, and recurrent dislocations of the GH joint warrant surgical intervention to lessen the risk for further shoulder instability and progressive arthritic change. Individuals over 40 years of age have a significant risk for associated rotator cuff injury in the setting of GH dislocation and should be evaluated for this injury if, after a week or two, active forward elevation or abduction is impaired. If the reduction maneuver is successful, the arm is placed in a sling until definitive care is reached. If possible, a posterior dislocation is held in neutral or slight external rotation. Because of the significant incidence of fractures with these injuries,

FIGURE 27-47  Stimson technique. (Redrawn from Rockwood CA, Green CP, editors: Fractures in adults, vol 1, Philadelphia, JB Lippincott, 1984. In Browner BD, Jupiter JB, Levine AM, et al: Skeletal trauma, vol 2, ed 2, Philadelphia, 1998, Saunders.)

radiologic examination is required to make the diagnosis, and evacuation is mandated. If the reduction maneuver is not successful, the injured extremity is placed in a sling and evacuation is arranged as soon as possible.

ARM AND ELBOW Proximal Humerus Fracture In the wilderness, fracture of the proximal humerus can be difficult to differentiate from shoulder dislocation. The mechanism often is a high-velocity fall onto an abducted, externally rotated arm, or a direct blow to the anterior shoulder. The victim complains of severe pain around the shoulder with palpation or with any arm motion. Palpable crepitus confirms the diagnosis. Although the inclination to attempt an emergent reduction may be compelling (this injury may be mistaken for a shoulder dislocation), it does

A

FIGURE 27-46  Pulling on the hanging arm to relocate a dislocated humerus. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 4, Guilford, Conn, 2003, Lyons Press.)

538

B

FIGURE 27-48  A, Pushing the lower edge of the scapula toward the spine while an assistant pulls downward on the handing arm to assist in the relocation of a dislocated humerus. B, The downward pull on the arm may be slightly forward to help put the humerus back in the glenoid. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 4, Guilford, Conn, 2003, Lyons Press.)

CHAPTER 27  Wilderness Orthopedics

G HH S

A

HH

G

S

FIGURE 27-49  Reducing an anterior shoulder dislocation with steady traction. Dr. Steve Paul demonstrates a proper controlled tractioncountertraction technique for reduction of a glenohumeral shoulder dislocation.

not routinely require acute reduction; application of an arm sling is appropriate field management (Figure 27-50). Fracture-dislocation of the proximal humerus can also occur. Although most dislocations with fracture are anterior, some can be posterior (Figure 27-51). Anterior or posterior fullness with crepitus on the injured side compared with the uninjured side suggests the diagnosis. This is a more severe injury than a simple shoulder dislocation, so a very careful neurovascular examination

R 69

FIGURE 27-50  Proximal humerus fracture sustained in a 75-year-old hiker following a fall.

B FIGURE 27-51  Bilateral proximal humerus fractures and posterior dislocations that occurred when an ultramarathoner suffered a seizure during a race. Computed tomography scan of right and left shoulders demonstrating posteriorly dislocated humeral heads, perched on respective glenoids. G, Glenoid; HH, humeral head; S, scapula.

should be performed. Any significant nerve or vascular injury should prompt evacuation to a definitive care center. Humerus Fracture Fracture of the shaft of the humerus may result from a direct blow or torsional force on the arm. This fracture frequently occurs with a fall, rope accident, or skiing accident. Fractures of the midshaft and junction of the middle and distal third of the humeral shaft can violate the spiral groove, the path of the radial nerve (Figure 27-52). If there is arm pain with deformity and crepitus, the arm is stabilized and the sensory and motor function of the radial nerve is carefully checked as part of the overall neurovascular examination (Figure 27-53). Radial nerve function is evaluated by checking sensation in the dorsal thumb web space and documenting active wrist extension. When fracture of the humeral shaft is suspected, an appropriate coaptation splint made of plaster, fiberglass, or wood is firmly applied with an elastic bandage on the medial and lateral sides of the humerus. A sling is useful for comfort. Acute reduction of the fracture is not routinely required. Fracture Around the Elbow (Distal Humerus, Olecranon, Radial Neck or Head) Elbow pain, crepitus, deformity, and swelling after a fall could represent a distal humerus, olecranon, or radial head or neck fracture. A neurovascular examination is performed, and then a splint is applied with the elbow at 45 or 90 degrees of flexion, depending on the victim’s comfort. Reduction should not be attempted without radiographic confirmation, unless deformity is gross, because crepitus is more often associated with a fracture than with a dislocation. Evacuation should be performed promptly if there is an open fracture or neurocirculatory deficit. 539

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

FIGURE 27-54  A, AP view, B, Lateral view of intra-articular distal humerus fracture dislocation sustained in a fall from an all-terrain vehicle.

FIGURE 27-52  Path of the radial nerve in the arm.

FIGURE 27-53  Midshaft humerus fracture in a 45-year-old man who fell while ice climbing. He presented with radial nerve palsy.

540

Fracture of the distal humerus is frequently extra-articular in children and intra-articular in adults (Figure 27-54). Children generally sustain supracondylar fractures after falls from heights. Extension types of injuries are much more common than the flexion type, and they usually occur in children ages 4 to 8 years. Deformity, swelling, pain, and crepitus are present, and the diagnosis of fracture is fairly obvious. A careful neurovascular examination should be performed, focusing on motor examination of flexion of the thumb and distal IP joint of the index finger, because injury to the anterior interosseus nerve, which supplies innervation to these muscles, is frequently associated with these fractures. If the radial pulse is absent, an attempt should be made to flex or extend the elbow while palpating the radial pulse. If the pulse improves, the limb is splinted in that position for transport. If the pulse does not improve and definitive care is more than an hour away, a reduction is performed. After available sedation is given, the supinated forearm is extended with gentle longitudinal traction. The fracture is reduced by flexing the elbow while maintaining longitudinal traction, and the elbow is splinted in 90 degrees of flexion. Evacuation should be performed promptly. Fracture of the proximal ulna (olecranon) results from a fall onto the posterior elbow, or from violent asymmetric contraction of the triceps muscle. The victim may be unable to extend the elbow actively against gravity if the triceps is dissociated from the forearm with a complete olecranon fracture. On initial examination, the victim has pain, significant swelling, and a palpable gap in the olecranon. With severe trauma, an olecranon fracture may be associated with an elbow dislocation or an intra-articular fracture of the distal humerus, which can only be diagnosed radiographically (Figure 27-55). A complete distal neurovascular examination should be performed. The shoulder and wrist should be examined, and a splint should be applied in the position of function and comfort. An open fracture, absent pulse, severe swelling, or neurologic deficit should prompt immediate evacuation. Fractures of the radial head and/or neck generally occur in young to middle-age adults who fall onto outstretched hands. The victim complains of pain about the elbow, with loss of full extension, and pain at the radial head on the lateral side of the elbow with direct gentle pressure and rotation of the forearm. Fracture of the radial head or neck frequently produces elbow hemarthrosis, which is identifiable by fullness posterior to the radial head and anterior to the tip of the olecranon (Figure 27-56). The elbow is gently moved through a range of motion and then placed in a posterior splint in 90 degrees of flexion with the forearm supinated. On a prolonged expedition when definitive care cannot be reached, the splint is removed after 3 to 5 days so that the victim can perform intermittent range-of-motion exercises (both flexion–extension and pronation–supination). With

more comminuted radial head fractures, attempts at motion produce pain and crepitus, and motion remains restricted. These injuries require operative treatment. Although most individuals lose some extension and pronation–supination, early motion may prevent permanent loss of motion when the radial head fracture is nondisplaced or minimally displaced. The arm is splinted in supination to prevent contracture of the intraosseous ligament and loss of supination. Subluxation of the radial head in children (nursemaid’s elbow) occurs when a longitudinal pull is applied to the upper extremity (Figure 27-57). The orbicular ligament partially tears, allowing a portion of it to slip over the radial head. An audible snap may be heard at the time of the injury. The initial pain from the injury subsides rapidly, and the child does not seem distressed but refuses to use the extremity. Any attempt to supinate the forearm brings a cry of pain and distress. If a definitive care center is nearby, the injury is splinted and evacuation is arranged. Otherwise, if the history and examination are consistent with the diagnosis, a reduction can be attempted. First the slightly flexed forearm is supinated; if this fails to produce the characteristic snapping sensation of reduction, the elbow is gently, maximally flexed in supination until the snapping sensation occurs (Figure 27-58). If the reduction is successful, the child is usually content and playing within 5 to 10 minutes, and no immobilization of the joint is indicated. If the reduction is unsuccessful, the child continues to avoid using the involved arm and should be evacuated for definitive care.

FIGURE 27-56  Fracture of the neck of the radius, sustained in a fall. Pain on palpation at the lateral aspect of the elbow, in the region of the radial neck and head, would be anticipated.

FIGURE 27-57  Nursemaid’s elbow most commonly occurs when a longitudinal pull is applied to the upper extremity. Usually the forearm is pronated on presentation. There is a partial tear in the orbicular ligament, allowing it to subluxate into the radiocapitellar joint. (From Rockwood CA Jr, Wilkins KE, King RE, editors: Fractures in children, ed 3, Philadelphia, 1991, JB Lippincott.)

Elbow Dislocation Dislocation of the elbow occurs with hyperextension or axial loading from a fall onto an outstretched hand. The direction of dislocation is generally posterior and lateral. The diagnosis is clear, with posterior deformity at the elbow and foreshortening of the forearm. After carefully assessing distal sensory, motor, and vascular status, reduction is performed. With countertraction on the upper arm, linear traction is applied with the elbow slightly flexed and the forearm in the original degree of pronation and supination. Downward pressure on the proximal forearm to disengage the coronoid from the olecranon fossa may be helpful. Hyperextension should be avoided. Adequate analgesia can be extremely helpful. An alternative method (Parvin’s method) is to place the patient prone over a log or makeshift platform and apply gentle downward traction on the wrist for a few minutes. As the olecranon begins to slip distally, the arm is lifted up gently. No assistant is needed, and if the maneuver is done gently, no anesthesia is required (Figure 27-59). A modification of this maneuver (Meyn and Quigley’s method) is to hang only the forearm over the platform while applying gentle downward traction via the wrist and guiding the reduction of the olecranon

FIGURE 27-58  Reduction of nursemaid’s elbow injury. Left, The forearm is supinated. Right, The elbow is then hyperflexed. The rescuer’s thumb is placed laterally over the radial head to feel the characteristic snapping as the ligament is reduced. (From Rockwood CA Jr, Wilkins KE, King RE, editors: Fractures in children, ed 3, Philadelphia, 1991, JB Lippincott.)

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CHAPTER 27  Wilderness Orthopedics

FIGURE 27-55  Closed, displaced olecranon fracture dislocation. A sling or posterior splinting is appropriate for this injury until definitive care can be provided.

PART 4  INJURIES AND MEDICAL INTERVENTIONS FIGURE 27-59  Parvin’s method of closed reduction of an elbow dislocation. The patient lies prone on a stretcher, and the physician applies gentle downward traction on the wrist for a few minutes. As the olecranon begins to slip distally, the physician lifts up gently on the arm. No assistant is required, and if the maneuver is done gently, no anesthesia is required. (Redrawn from Parvin RW: Closed reduction of common shoulder and elbow dislocations without anesthesia, Arch Surg 75:972, 1957. In Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)

FIGURE 27-61  Both-bone forearm fracture following fall while snowboarding.

FOREARM, WRIST, AND HAND Radius Fracture

with the opposite hand (Figure 27-60). Reduction provides nearly complete relief of pain and restoration of normal surface anatomy. A posterior splint is applied with the elbow in 90 degrees of flexion and the forearm in neutral position. Collateral elbow ligament injuries and possible interposed bone or cartilage fragments are often a consequence of elbow dislocations. Follow-up evaluation and monitored therapy for range of motion are essential to avoid chronic instability or a possible arthrofibrosis. A sling is provided for comfort. If reduction is not successful after three attempts, or if a nerve injury is suspected, a splint is applied to the arm as it lies and evacuation is initiated.

FIGURE 27-60  In Meyn and Quigley’s method of reduction, only the forearm hangs from the side of the stretcher. As gentle downward traction is applied on the wrist, the physician guides reduction of the olecranon with the opposite hand. (Redrawn from Meyn MA, Quigley TB: Reduction of posterior dislocation of the elbow by traction on the dangling arm, Clin Orthop Relat Res 103:106, 1974. In Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)

542

Radial shaft fracture occurs with a fall involving angular or axial loading of the forearm. A radial shaft fracture may be associated with dislocation of the distal radioulnar joint (Galeazzi fracture) (see Figure 27-26). Therefore, in the setting of known or suspected radial shaft fracture, the wrist should be examined for tenderness, swelling, and deformity. The victim generally complains of pain. Deformity and crepitus are noted over the radial shaft after a fall or direct blow. Any arm motion exacerbates the pain. When both the radius and ulna are fractured, forearm instability is marked (Figure 27-61). The joint above (elbow) and the joint below (wrist) should always be examined for tenderness, crepitus, and deformity. Once a fracture of the radius or both bones of the forearm is identified, the wrist, forearm, and elbow are splinted in the position of function. Fracture of the distal metaphyseal radius is generally associated with the fall of an older osteoporotic individual onto the outstretched hand (FOOSH injury) (Figure 27-62). Ulnar styloid fracture often accompanies intra-articular fracture of the distal radius. Pain, deformity, and crepitus are obvious. When this injury is suspected, a distal neurovascular examination is performed, focusing on sensory function of the median nerve. Median nerve injury or compression at this level of injury would manifest primarily as decreased sensation in the volar palm and fingers (the thumb, index finger, middle finger, and the radial half of the ring finger). Weakness in the opponens and abductor pollicis muscles might also be noted. If there is neurovascular compromise and definitive care is more than 2 hours away, a gentle reduction is performed. One hand is placed on the forearm to provide countertraction and the other around the wrist of the involved extremity. The wrist is dorsiflexed, and longitudinal traction is applied as the wrist is returned to a neutral position. A splint is applied to immobilize the wrist and elbow. Distal radius and ulna fractures occur commonly in children. They are seen most frequently in girls ages 11 to 13 and in boys ages 13 to 15. A familiarity with the Salter-Harris fracture classification system is important to understanding injuries in the child or adolescent (Figure 27-63). These fractures are not usually comminuted but can be difficult to reduce (Figure 27-64). In cases involving an open fracture, a significant distal neurologic deficit, or an abnormal circulatory examination, splinting and

CHAPTER 27  Wilderness Orthopedics

A

B

FIGURE 27-62  Distal radius fracture after fall.

C FIGURE 27-64  Technique for reduction of a distal radius fracture. A, Initial fracture position. B, Hyperextend fracture to 100 degrees to disengage the fracture ends. C, Push with the thumb on the distal fragment to achieve reduction. (From Green N, Swiontkowski MF: Skeletal trauma in children, vol 3, ed 2, Philadelphia, 1998, Saunders.)

Diaphysis (shaft of bone) Metaphysis

Epiphyseal disk (growth plate)

evacuation should be prompt. The limb should be kept elevated above the heart during transport.

Epiphysis Normal

Type I A complete physeal fracture with or without displacement

Type II

Type III

A physeal fracture that extends through the metaphysis, producing a chip fracture of the metaphysis, which may be very small

A physeal fracture that extends through the epiphysis

Type IV

Type V

A physeal fracture plus epiphyseal and metaphyseal fractures

A compression fracture of the growth plate

FIGURE 27-63  Salter-Harris pediatric fracture classification.

Ulna Fracture Ulna shaft fracture is most often associated with fracture of the radial shaft at the same level. When isolated, it usually occurs as a result of a direct blow, the so-called nightstick fracture (Figure 27-65). Fracture of the ulnar shaft can be associated with dislocation of the radial head (Monteggia lesion), so elbow function is carefully assessed. In the wilderness, the most frequent mechanism of injury is bracing a fall or collision with the forearm. Pain, localized swelling, and crepitus are present. A long-arm splint is applied in the position of function. An open fracture is an indication for prompt evacuation. Wrist/Carpus Fracture Wrist fractures occur with significant rotational forces or high axial loading forces, as occur in falls onto the hand. The victim first complains of pain and later of wrist swelling. Hand use or forearm rotation produces significant pain. Many carpal bone fractures are associated with wrist dislocation. Carpal bone fractures cannot be accurately diagnosed without radiographs. Scaphoid (navicular) fracture is the most common fracture and is suspected when the patient’s area of maximal tenderness is in the “anatomic snuffbox” (Figures 27-66 and 27-67). If appropriate splinting materials are available, a thumb spica splint is applied, immobilizing both the radius and the entire thumb. With fracture of the hook of the hamate bone, the victim complains of pain at the base of the hypothenar eminence (Figure 27-68). This injury occurs when the hand is used to apply significant force to an object with a handle on it, such as an ax or hammer, and great resistance is met. A short-arm splint suffices for this injury, and for other suspected carpal injuries, until definitive treatment is obtained. With open fractures or those accompanied by median nerve dysfunction, the victim should be promptly evacuated. 543

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 27-67  Scaphoid fracture with scapholunate widening.

FIGURE 27-65  “Nightstick” ulna fracture.

Metacarpal Fracture Fracture of the metacarpal base or shaft occurs with crush injuries or with axial loads, such as when rocks or other immovable objects are struck. Fractures at the bases of the metacarpals are suspected when tenderness, crepitus, and occasionally deformity (“sunken knuckle” sign) are present (Figure 27-69). These should be managed with a short-arm splint or an ulnar gutter splint. Fractures of the metacarpal necks also occur by the same mechanism and usually involve the fifth and fourth metacarpals. These fractures can be associated with significant flexion deformity. Up to 40 degrees of flexion in the fifth and fourth digits can be accepted without compromising hand function, so these fractures seldom require surgical reduction and fixation. Rotational deformity of the metacarpal is poorly tolerated, however, and should be anticipated with suspected metacarpal fractures. With the MCP and the IP joints flexed 90 degrees, the fingernails should

Extensor pollicis longus

H

FIGURE 27-68  Hook of hamate fracture.

Scaphoid

Extensor pollicis brevis Abductor pollicis longus FIGURE 27-66  The scaphoid (navicular) bone sits in the “anatomic snuffbox” of the radial aspect of the wrist.

544

FIGURE 27-69  “Sunken knuckle” sign, fourth metacarpal.

FIGURE 27-70  Fracture of base of the first metacarpal.

be parallel to one another and perpendicular to the orientation of the palm. The terminal portions of the digit should point to the scaphoid tubercle in an anatomic “cascade.” If this is not noted, a rotational deformity should be strongly suspected. When malalignment or significant shortening with a suspected shaft fracture is noted, the fracture is reduced with longitudinal traction on the involved digit. A fractured metacarpal shaft or neck is immobilized by applying an aluminum splint (or stick) to the volar surface of the finger and palm and taping the involved digit to the adjacent digit, with the MCP joint at 70 to 90 degrees. This position provides optimal length of the collateral ligaments. Immobilizing the joint in this position prevents contractures that can lead to subsequent loss of motion. Fracture of the base of the thumb metacarpal often occurs with an axial force directed against a partially flexed thumb metacarpal (Figure 27-70). If the fracture extends into the joint, it often requires operative fixation. If this fracture is suspected, the thumb and wrist are immobilized in a thumb spica splint. An open metacarpal fracture needs cleansing, debridement, and presumptive antibiotic therapy for 48 hours or until definitive care is obtained. Metacarpophalangeal Joint Dislocation MCP joint dislocation is rare and may be produced by a crush injury or when the hand is caught in a rope. This dislocation may be dorsal or volar, with dorsal dislocation more common. Clinically, the joint is hyperextended and the phalanx shortened. Most dorsal dislocations are easily reduced. First, the proximal phalanx is hyperextended 90 degrees on the metacarpal, then the base of the proximal phalanx is pushed into flexion, maintaining contact at all times with the metacarpal head to prevent entrapment of the volar plate in the joint (Figures 27-71 and 27-72). Straight longitudinal traction is avoided because it may turn a simple dislocation into a complex dislocation. The wrist and IP joints are flexed to relax the flexor tendons. The joint usually reduces easily with a palpable and audible clunk. A dorsal–volar splint is applied with the joint held at 90 degrees of flexion. Irreducible or complex dislocations occur when the volar plate is interposed in the joint. Clinically the joint is only slightly hyperextended, and the volar skin is puckered over the joint. These dislocations are most common in the index finger, thumb, and small finger. A single attempt at reduction using the

technique just described is indicated, but these dislocations usually require open reduction. If reduction of an MCP joint dislocation is unsuccessful, the joint should be splinted in the position of comfort and definitive treatment obtained as soon as possible. The thumb MCP joint is most commonly injured. Dislocations are reduced as already described. Injury to the ulnar collateral ligament of this joint (skier’s or gamekeeper’s thumb) results from a valgus stress, as may occur when an individual falls holding an object in the first web space. The victim complains of tenderness over the ulnar aspect of the MCP joint. There may be instability to radial stress with the joint held in 30 degrees of flexion, an indication for surgical repair. Often the adductor aponeurosis becomes interposed between the ligament and its bony attachment, resulting in a Stener lesion (Figure 27-73). In the field, a thumb spica splint is applied and definitive care sought within 10 days. If splinting material is not available, the thumb is taped until definitive care can be obtained (Figure 27-74).

FIGURE 27-72  Dislocation of the right thumb; first metacarpophalangeal joint.

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CHAPTER 27  Wilderness Orthopedics

Fracture

FIGURE 27-71  The single most important element preventing reduction in a complex metacarpophalangeal dislocation is interposition of the volar plate within the joint space. It must be extricated surgically. (From Rockwood CA Jr, Green DP, Bucholz RW, editors: Rockwood and Green’s fractures in adults, ed 3, Philadelphia, 1991, JB Lippincott.)

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

D

FIGURE 27-73  Diagram of the displacement of the ulnar collateral ligament of the thumb metacarpophalangeal joint. A, Normal relationship, with the ulnar ligament covered by the adductor aponeurosis.  B, With slight radial angulation, the proximal margin of the aponeurosis slides distally and leaves a portion of the ligament uncovered.  C, With major radial angulation, the ulnar ligament ruptures at its distal insertion. In this degree of angulation, the aponeurosis has displaced distal to the rupture and permitted the ligament to escape from beneath it. D, As the joint is realigned, the proximal edge of the adductor aponeurosis sweeps the free end of the ligament proximally and farther away from its insertion. This is the Stener lesion. Unless surgically restored, the ulnar ligament will not heal properly and will be unstable to lateral stress. (Redrawn from Stener B: Skeletal injuries associated with rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb: A clinical and anatomical study, Acta Chir Scan 125:583, 1963.)

FIGURE 27-75  Ring finger proximal interphalangeal joint dislocation that occurred while diving.

Phalanges Fractures of the digital phalanges occur with crush injuries or when the digits are caught in ropes or in equipment being used to haul objects. Angular or rotational deformity and crepitus make these fractures obvious. Without radiographs, an intraarticular fracture with subluxation or dislocation is difficult to differentiate from an IP joint dislocation (Figure 27-75). Angular deformities in these fractures can be reduced using a pencil or thin stick placed in the web space as a fulcrum to assist in reduction. A fracture of the shaft of a phalanx is reduced by applying traction and correcting the deformity. The fractures are immobilized by taping the injured digit to the neighboring uninjured digit or to a volar splint. Nail-bed fractures or crushes are cleansed with soap, a sterile dressing is applied, and a protective volar splint is applied to prevent further injury. Interphalangeal joint dislocations are relatively common and can typically be reduced with gentle axial traction on the digit (Figures 27-76 and 27-77). Reduction is typically accompanied by an audible pop and improved ability to flex and extend through the IP joint. After reduction, the finger should be buddy taped to the adjacent digit.

A

finger

proximal

interphalangeal

joint

B

FIGURE 27-74  Taping the thumb for immobilization. A, The buddytaping method. B, A thumb-lock. If possible, padding should be placed between the thumb and forefinger. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 4, Guilford, Conn, 2003, Lyons Press.)

546

FIGURE 27-76  Middle dislocation.

FIGURE 27-77  Radiograph demonstrating dorsal displacement of base of the middle phalanx.

CHAPTER 27  Wilderness Orthopedics

FIGURE 27-78  Extended posture of ring and small fingers that strongly suggests traumatic flexor tendon lacerations.

Prolonged immobilization of the digit in a rigid splint (more than 3 days) should be avoided to prevent finger stiffness. Dorsal IP dislocations can cause a rent in the skin volar to the joint. Although this skin tear may appear benign, the wound should be cleaned as well as possible, because contamination of the adjacent flexor tendon sheath can result in severe hand infections. Soft Tissue Injuries Injuries to the volar or dorsal aspect of the hand or wrist can result in nerve and tendon injuries. A deep laceration over the volar palm or digits often cuts the digital flexor tendons and nerves (Figure 27-78). Loss of sensation or inability to flex the digit should prompt medical evaluation, because these structures will not heal without surgical intervention. Any wounds should be carefully cleaned and bandaged and the fingers splinted in flexion to prevent further retraction of the lacerated tendons and nerves. Lacerations on the dorsum of the hand may disrupt digital extensor tendons, although the functional loss may be less apparent due to interconnections with adjacent intact tendons.

Hip and Leg Injury FEMUR FRACTURE In general, healthy, active individuals sustain fractures of the proximal femur only in falls from significant heights or from high-velocity injuries sustained, for example, in motorized vehicle accidents (all-terrain vehicles, snowmobiles, four-wheelers) or snow skiing. These fractures occur in the femoral neck, intertrochanteric, or subtrochanteric region (Figure 27-79; see Figure 27-7). The victim complains of severe pain within the proximal thigh. There may be generalized swelling or deformity around the hip region to aid in diagnosis. Any movement of the affected limb, noticeably shortened and externally rotated, produces significant pain. After a careful sensory, motor, and circulatory examination, the limb is realigned and, if available, a splint is applied. An improvised traction splint can be fabricated. If none is available, the victim is transported on a backboard, with the limbs strapped together or tied to a board with a tree limb placed between them. Fracture of the femoral neck is associated with a significant risk for post-traumatic femoral head necrosis (see Figure 27-7). Without a radiograph, this fracture is impossible to distinguish from a subtrochanteric or an intertrochanteric hip fracture. Because there is evidence that emergency treatment of a fracture of the femoral neck in a young person decreases the risk for post-traumatic avascular necrosis,24,26 rapid evacuation should be arranged for any victim in whom this injury is suspected.17

FIGURE 27-79  Comminuted femoral shaft fracture in a 30-year-old who rolled his all-terrain vehicle and hit a tree. Subcutaneous pieces of bone laterally suggest how close this injury was to being an open fracture.

Fracture of the femoral shaft occurs by similar mechanisms (see Figure 27-79). Crepitus and maximal deformity are noted in the midportion of the thigh. After neurovascular examination, the limb is placed in traction or protected, as noted previously. Any gross deformity of the shaft is corrected with gentle traction, and the neurovascular examination is repeated. This fracture may be an open injury, so the victim’s pants should be split to complete the examination. Discovery of an open wound should prompt rapid evacuation.

HIP DISLOCATION Posterior hip dislocation is produced by axial loading of the femur with the hip flexed and adducted14 (Figure 27-80). It generally occurs in a motor vehicle crash but can follow a fall or a sledding or skiing accident. With posterior dislocation, the victim

FIGURE 27-80  Right hip dislocation with femoral head fracture.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

complains of severe pain about the hip, and the affected limb appears shortened, flexed, internally rotated, and adducted. Any hip motion increases the pain. It is not clinically possible to determine if there is an associated acetabular or femoral neck fracture. With the rare anterior dislocation, the limb is externally rotated, slightly flexed, and abducted. This type of dislocation is generally produced by wide abduction of the hip caused by significant force. The victim is placed in the supine position for a complete survey of all organ systems. The distal limb is carefully examined for associated fractures, and a thorough sensory and motor examination is performed. The peroneal division of the sciatic nerve is most susceptible to injury with a posterior hip dislocation. Hip dislocations are an orthopedic emergency, because time to reduction is directly linked to the incidence of avascular necrosis of the femoral head.6 Immediate transfer to a definitive care center is desirable because hip radiographs may reveal an associated femoral neck fracture that could become displaced if closed reduction is attempted. However, if it will be more than 6 hours before the victim can be evacuated to a definitive care center, closed reduction should be attempted. To perform the Allis technique (Figure 27-81), the victim is positioned supine on the ground or a stretcher. If available, analgesic medication is administered. The caregiver stands above the victim and applies in-line traction on the extremity while an assistant applies countertraction to the iliac wings. Posterior dislocations are reduced FIGURE 27-82  Patella fracture as a result of a direct blow to the anterior knee.

by flexing the hip 60 to 90 degrees. Internal rotation and adduction of the hip facilitate the relocation. With anterior dislocation, traction is applied with the leg slightly abducted and externally rotated and the hip gently extended. Successful reduction is usually indicated by an audible “clunk” and restoration of limb alignment. As with any reduction or relocation maneuver, adequate analgesia and a slow, progressive increase in traction force are helpful. This is not a technique that involves a sudden “jerk”; gradual fatiguing of the muscles that, in spasm, may be maintaining the hip in a dislocated position remains the most likely means of achieving relocation.

KNEE AND LOWER LEG INJURIES

A

B

Distal Femur or Patella Fracture Fracture of the distal femur is frequently intra-articular and occurs with high-velocity loading when the knee is flexed. With axial loading on the femur, the patella becomes the driving wedge and the femoral condyles suffer direct impact, producing either a patella fracture or a fracture of the femoral condyles or distal femoral metaphysis (Figure 27-82 and 27-83). Occasionally, in high-energy trauma, a distal femur fracture and an ipsilateral proximal tibia fracture can occur concurrently. With a patella fracture, the injury may be obvious on deep palpation. This is often an open injury because there is very little soft tissue overlying this sesamoid bone (Figure 27-84). After initial neurovascular examination, the limb is realigned. A posterior splint is applied to the realigned limb for transportation. As with all fractures, open wounds in the region of the fracture or an abnormal nerve or vascular examination should prompt immediate evacuation.

C

FIGURE 27-81  A combination of Allis’s and reverse Bigelow’s maneuvers for reduction of a hip dislocation. A, The healthe care provider’s position must provide a mechanical advantage for the application of traction. In-line traction with hip flexed. B, Internal and external rotations are gently alternated, perhaps with lateral traction by an  assistant on the proximal thigh. C, Adduction is often a helpful adjunct to in-line traction. (Redrawn from Rockwood and Green: Fractures in adults, vol 2, ed 3, Philadelphia, 1991, JB Lippincott.)

548

Knee Dislocation A knee dislocation (tibia–femur dislocation) is a high-energy injury. Knee dislocation is usually obvious because of the amount of deformity (Figure 27-85). The most common dislocation directions are anterior and posterior. A knee dislocation represents a true emergency because 5% to 40% of these injuries have associated vascular injuries.1,25,30 In a large series, Green and Allen13 reported an above-knee amputation rate of 86% for vascular injuries associated with knee dislocations that were not repaired within 8 hours of injury. The vascular injury occurs

CHAPTER 27  Wilderness Orthopedics FIGURE 27-85  Anterior knee dislocation. Significant attention should be devoted to relocation, if possible, and to assessment of the neurovascular structures that run posterior to the knee joint, such as the popliteal artery and the tibial and common peroneal nerves. FIGURE 27-83  70-year-old woman with a total knee arthroplasty sustained a periprosthetic distal femur fracture when she fell while hiking.

because of tethering of the popliteal vessels by the soleus fascia along the posterior border of the tibia. When this injury is suspected, a careful screening neurovascular examination must be performed. Intact distal pulses do not definitively rule out an arterial injury. Intimal flap tears can produce delayed thromboses of the popliteal artery. In addition, injury to the peroneal nerve can occur. Many knee dislocations spontaneously reduce and may lead the examiner to underestimate the seriousness of the injury. Instability in extension to either varus or valgus stress indicates disruption of at least one of the cruciate ligaments and signifies the potential for a knee dislocation. After the initial examination, the persistent dislocation should be reduced. Anterior dislocation is reduced with traction on the leg and gentle elevation of the distal femur. Posterior dislocation is reduced with traction in extension and anterior elevation of the tibia. Posterolateral rotatory dislocation (which occurs when the medial femoral condyle buttonholes through the medial

FIGURE 27-84  Open patella fracture wound with typical stellate appearance.

capsule) can be very difficult to reduce and usually requires open reduction. A transverse furrow on the medial aspect of the knee is pathognomonic for this injury. For transport, a posterior splint is applied to the limb, and the victim is moved on a backboard. The possibility of an arterial lesion or emerging compartment syndrome requires vigilance. Emergency evacuation is advised because of the risk for amputation related to vascular injury. The patellofemoral joint is more commonly dislocated than is the tibia–femoral joint. Generalized ligamentous laxity may predispose to this problem. Patellofemoral dislocations, especially recurrent patellofemoral dislocations, are more common in females than males and may be associated with an accentuated Q angle. Dislocation of the patella may result from a twisting injury or an asymmetric quadriceps contraction during a fall. These mechanisms can occur with hiking, climbing, and skiing accidents. The patella usually dislocates to a position lateral to the articular surface of the distal femur. Although neurovascular injuries rarely occur in association with a dislocated patella, a screening examination should be conducted. The patella can often be reduced by simply straightening the knee. If this is not successful, gentle pressure is applied to the patella to push it back up into the distal femoral articular groove. A knee splint is applied with the joint in extension; weight bearing is allowed. The knee is kept in extension until definitive care can be obtained. A radiograph is ultimately required to rule out osteochondral fractures, which can be associated with this injury. Tibia and Fibula Fractures The tibial plateau is the broad articular surface and metaphysis of the upper tibia that articulates with the distal femur. This area can be fractured in a fall or leap from a height. A valgus moment of force produces a fracture of the lateral tibial plateau, whereas a varus moment of force produces a medial plateau fracture (Figure 27-86). Pain, swelling, and deformity are obvious on initial examination. With a tibial plateau fracture, significant hemarthrosis develops quickly. Because of anatomic tethering of the popliteal artery by fascia of the soleus complex, arterial injury may result from this fracture, especially when it is associated with a knee dislocation. Distal pulses and capillary refill should be assessed at 1-hour intervals. After initial examination, the limb is carefully realigned, and a posterior splint is applied for transportation. 549

PART 4  INJURIES AND MEDICAL INTERVENTIONS

ANKLE AND FOOT INJURIES Ankle and Foot Fractures The articular distal tibia (pilon), medial malleolus, and distal fibula, or any combination of these may be involved in an ankle fracture, which is generally produced by torsional moments of force about a fixed foot (Figure 27-88). With the pilon tibia fracture, axial loading from a fall or jump may also be involved. Any significant pain and swelling should be noted as the shoe is removed. Palpation along the medial and lateral malleoli confirms the clinical suspicion. After the shoe is removed to inspect the skin for open wounds, a neurovascular examination is performed. If there is a rotational deformity in the ankle, the ankle is realigned with gentle traction before applying a posterior splint with the ankle in neutral position. During transport, the limb is elevated above the level of the heart. Ankle Dislocation or Sprain

FIGURE 27-86  Tibial plateau fracture sustained in fall from a height.

Tibial shaft fractures may or may not be associated with fibula fractures. These fractures result from high-impact trauma. Before the development of modern, higher, anatomically conforming ski boots, improved binding-release systems, and shorter parabolic skis that reduced the lever arm of the old long skis, these fractures were the most common ski injuries. The injury was sustained when the body rotated around a fixed foot (a ski caught against a rock, tree stump, or the slope), which produced a torsional, spiral fracture of the tibia and fibula. Tibial shaft fracture is the most common type of open fracture in the wilderness setting (Figure 27-87) When this injury is suspected, the entire limb should be inspected for distal sensory, motor, and vascular function before realignment. A posterior splint is applied for transport. Because this is the most common anatomic location for this problem, the limb is serially examined for the possibility of a compartment syndrome.

FIGURE 27-87  Tibia fracture sustained in a snowmobile accident.

550

Ankle dislocations are almost always accompanied by fractures of one or more malleoli. These dislocations generally occur with falls onto uneven surfaces or with twisting injuries of moderate velocity. The area about the ankle is carefully examined for open injuries, and a neurovascular examination is conducted to obtain a baseline status. Then the ankle joint is aligned by grasping the posterior heel, applying traction with the knee bent (to relax the gastrocnemius–soleus complex), and bringing the foot into alignment with the distal tibia. Again, as with all reduction maneuvers, sustained gentle traction to fatigue the spasming muscles is most effective. After this maneuver, the foot is reexamined, any wounds are dressed, and a posterior splint is applied. During transport, the limb is elevated above the level of the heart. The most common musculoskeletal injury occurring in the wilderness setting is an ankle sprain. Inversion injuries to the ankle usually damage the lateral ligament structures, most commonly the anterior talofibular ligament. The calcaneal fibular ligament and posterior talofibular ligaments are less commonly injured but are consistent with more significant lateral ankle injury. The less common eversion injuries to the medial ankle may strain the large medial deltoid ligament (Figures 27-89 and 27-91).

FIGURE 27-88  Distal tibia-fibula fracture in a young Enduro rider— Salter Harris II fracture.

CHAPTER 27  Wilderness Orthopedics

FIGURE 27-89  Ligaments of the anterior ankle.

Tibialis anterior

Interosseous membrane

Medial malleolus

Anterior inferior tibiofibular ligament

Dorsal ligament Anterior talofibular ligament Interosseous talocalcaneal ligament Calcaneocuboid ligament

Dorsal talonavicular ligament Navicular bone

Cuboid bone

Dorsal calcaneonavicular ligament?

3rd cuneiform bone

1st cuneiform bone Dorsal tarsometatarsal ligament 1st metatarsal bone

Dorsal metatarsal ligaments

Ankle sprains are often considered minor injuries—“just an ankle sprain.” However, if a sprain is improperly rehabilitated or if someone returns to activity too soon, it may result in a chronically unstable joint. Ligament sprain, or tearing of the fibers, is differentiated (or categorized) into three grades. Grade 1 injury is partial disruption of some of the ligament fibers. Grade 2 injury is significant disruption of a portion of the ligament fibers. The main substance of the ligament remains intact, and the injury is characterized by moderate hemorrhage. Grade 3 injury is complete disruption of the ligament fibers, which can result in instability of the ankle joint. The amount of discoloration and swelling of the ankle and foot usually is consistent with the degree of injury. Even grade Tibia

Lateral malleolus Calcaneofibular ligament

Anterior inferior tibiofibular ligament Talus Anterior talofibular ligament Dorsal talonavicular ligament Navicular

Calcaneus

Dorsal Lateral calcaneocuboid talocalcanean Interosseous ligament ligament talocalcanean ligament

Cuboid

FIGURE 27-90  Ligaments of the lateral ankle.

3 injuries usually heal without surgery if treated appropriately. Use of an ankle stirrup for 3 to 6 weeks may be adequate for grade 1 injuries; a walking boot or cast is often indicated for grade 2 to 3 injuries, with protected motion for 6 to 8 weeks. Ligament injuries, depending on degree of injury, typically require at least 6 and often 12 weeks for complete healing. When an ankle sprain is suspected, the shoe and sock are removed, and a screening neurovascular examination is conducted. Ankle ligaments and bone are palpated to help distinguish between an ankle fracture and an ankle sprain. The ankle is evaluated for instability with the anterior drawer test. This test is performed by stabilizing the tibia with one hand and grasping the posterior heel to pull the foot forward with the

Groove for tibialis posterior Neck of talus Tibionavicular fibers Dorsal talonavicular ligament 1st cuneiform bone Navicular bone

Medial malleolus

Achilles tendon

Tibial posterior Posterior Medial tendon Tibiocalcaneal tibiotalar tubercle fibers fibers of talus Sustentaculum tali

Plantar calcaneonavicular ligament and associated fibers

FIGURE 27-91  Ligaments of the medial ankle.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

FIGURE 27-92  Taping sprained ankle. Strips of adhesive tape are placed perpendicular to each other (A) to lock the ankle with a tight weave (B). The edges are covered to prevent peeling (C). (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 4, Guilford, Conn, 2003, Lyons Press.)

other hand. If the talus slides forward within the ankle mortise (using the uninjured side as a comparison), the injury represents a grade 3 injury. The foot and ankle are placed into a posterior splint or air splint. If possible, the victim is kept from bearing weight on the limb. If this examination does not reveal instability and is thus indicative of a grade 1 or 2 sprain, an elasticized bandage is applied or the ankle is taped. All injuries should be acutely treated using the RICE principles. Commercially available stirrup air splints also aid in ambulatory management of these injuries. In the field, the ankle is taped both to decrease pain and to limit swelling (Figure 27-92). During taping, the victim’s ankle is kept perpendicular to the tibial shaft. This makes walking easier, because the ankle is not plantar flexed, and helps prevent development of an Achilles tendon contracture. If available, an Aircast ankle brace provides additional ankle support and can be used with a shoe or boot. A fracture of the lateral process of the talus, which is a fairly common lower extremity fracture in snowboarders, may be confused with a lateral ankle sprain, so radiographs are generally needed to rule out this injury.7 Inversion injuries are also infrequently associated with fractures at the insertion of the peroneus brevis tendon. This injury can be identified by the point tenderness at the base of the fifth metatarsal, but a radiograph is required for definitive diagnosis. Early management is the same as for an ankle sprain. The eponym Jones fracture is used to describe the more worrisome transverse fracture to the metaphyseal portion of the fifth metatarsal; nonunion is a concern with these injuries (Figure 27-93). Hindfoot Dislocation The subtalar joint may infrequently be dislocated in a significant fall or jump when an individual lands off balance or on an uneven surface. The calcaneus may be dislocated medially or, more commonly, laterally relative to the talus (Figure 27-94). The position of the heel relative to the ankle is assessed. With either dislocation, a reduction is attempted if it will be more than 3 hours until the victim will reach a definitive care center. Medial dislocation is reduced more easily than is lateral dislocation, in which the posterior tibial tendon frequently becomes displaced onto the lateral neck of the talus, blocking the reduction. The maneuver is the same for both: the heel is grasped with the knee flexed (relaxing the gastrocnemius– soleus complex), the deformity is accentuated, linear traction is applied, and the heel is brought over to the ankle joint. This maneuver is generally successful for medial dislocation, but lateral dislocation, especially when associated with open wounds, often requires open treatment. After reduction is attempted, a posterior splint is applied, and the limb is elevated above the heart. Even if the reduction is successful, the victim must not be allowed to bear weight until definitive care is obtained. Midfoot Dislocation Midfoot fracture dislocation (Lisfranc injury) is described in the metatarsal fracture section (Figure 27-95). 552

FIGURE 27-93  Base of fifth metatarsal fracture—technically not a Jones fracture because it is in the metaphyseal, not the metadiaphyseal region.

Tarsal Fracture The calcaneus and talus can be fractured when the victim lands on his or her feet following falls or jumps from significant heights (see Figure 27-8). With a calcaneus fracture, significant heel pain, deformity, and crepitus are immediately evident after the boot is removed. Talus fracture usually occurs when the foot is forced into maximal dorsiflexion. A talus fracture may be impossible to differentiate from an ankle fracture on clinical grounds. One rule of thumb is that an ankle fracture is tender at the malleolus level, whereas a talus fracture distal to the malleoli. Knowing the point of the foot’s impact with the ground is also helpful in differentiating a talus fracture from an ankle fracture. Talus fracture may be associated with subtalar or ankle joint dislocation (Figure 27-96). Emergency evacuation should be arranged when this injury is suspected because these injuries are very difficult to reduce closed, and pressure on the skin from the displaced talar body can produce significant skin slough.

FIGURE 27-94  Subtalar fracture dislocation.

FIGURE 27-95  Lisfranc midfoot fracture dislocation.

Metatarsal Fracture Fractures at the base of the metatarsals often accompany midfoot dislocation, a so-called Lisfranc injury. The mechanism usually occurs with axial loading of the foot in maximal dorsal f lexion as a result of a motor vehicle crash, most frequently snowmobiling (see Figure 27-95). The victim complains of midfoot pain and swelling. On removing the shoe, crepitus and tenderness are noted at the bases of the metatarsals (especially the first, second, and fifth metatarsals), and plantar ecchymosis may be present. Overall foot alignment is maintained, but stressing the midfoot by stabilizing the heel and placing force across the forefoot in the varus and valgus directions reveals instability. The foot is placed in a well-padded posterior splint and elevated whenever possible. The patient is not allowed to ambulate. Swelling associated with Lisfranc dislocation can produce a foot compartment syndrome. Metatarsal shaft fracture occurs with a crush injury or a fall or jump from moderate height. Midshaft metatarsal fractures also occur as “fatigue” (or “march”) fractures. These classic overload injuries may result from prolonged hiking or running with poor preconditioning. Pain and localized tenderness are the hallmarks of this diagnosis. The dull pain at the midshaft of a metatarsal (often the second or fifth) may be converted to more severe pain with associated crepitus by a jump from a log or a rock. These fractures can be temporarily managed with a stiff-soled boot or orthotic insert. If there is fracture instability or extreme pain, a short-leg splint is applied, and no further weight bearing is allowed until more definitive evaluation and treatment can be accessed. Phalanx Fracture Toe phalanges are usually fractured by a crush mechanism that can be prevented by use of steel-toed or hard-toed boots. A great toe phalanx fracture can be a significant problem because force is placed on this digit during the toe-off phase of gait (Figure 27-97). Phalanx fractures are managed by buddy taping the toe to an adjacent uninjured digit with cotton placed between

A

B FIGURE 27-96  Fracture-dislocation of left ankle that occurred during a fall while bouldering. A, Anterior view with lateral displacement of foot at subtalar joint. B, Medial aspect of lateral subtalar dislocation.

FIGURE 27-97  Great toe proximal phalanx fracture.

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CHAPTER 27  Wilderness Orthopedics

Fractures of the other tarsal bones are exceedingly rare but can be defined by localizing the tenderness to a specific site. A short-leg splint with extra padding is applied, and the limb is elevated during transportation.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

ACL

FIGURE 27-98  Gustilo type II open great toe dislocation occurred during a fall while hiking in sandals.

the toes. Displaced intra-articular fracture of the proximal phalanx of the great toe may need operative fixation. Stiff-soled boots minimize discomfort during weight bearing. Metatarsophalangeal and Interphalangeal Joint Dislocations MTP joint dislocations of the toes are relatively uncommon but can occur when a moderate axial force is directed at the great toe. Crush injuries and rock-climbing accidents while the victim is wearing flexible-sole shoes can produce this injury; wearing boots with reinforced toe boxes of adequate depth generally prevents it. Injuries of this type at the great toe may be associated with fractures of the metatarsal joint or phalanx. The dislocation is generally dorsal. Because these may be open injuries, the foot must be inspected carefully. The joint is reduced in a manner similar to that used for dorsal proximal IP joint dislocation of the hand. MTP dislocation of the great toe can occasionally require open reduction if the head of the metatarsal buttonholes through the sesamoid–short flexor complex. The lesser MTP joints are generally dislocated laterally or medially. The most common mechanism for this injury is striking unshod toes on immovable objects. The toes are relocated by applying linear traction with the victim supine and using the weight of the foot as countertraction. Similar mechanisms produce dislocations of the IP joints, which are also reduced by applying linear traction with gentle manipulation (Figure 27-98). Once reduced, the injured toe is taped to the adjacent toe for 1 to 3 weeks, and the victim wears a protective boot with a stiff sole and deep toe box.

FIGURE 27-99  Anterior cruciate ligament (ACL) tear.

always, the knee becomes swollen secondary to hemarthrosis. A sense of instability is common. On examination, there may be marked laxity to anterior stress on the tibia relative to the femur (Lachman test). Although it may be easy to produce anterior tibial translation in extension, ACL injuries do not necessarily require immobilization. Grading of sprains is based on laxity or translation anteriorly of the tibia on the femur: grade 1, less than 5  mm (0.2 inch); grade 2, 5 to 10  mm (0.2 to 0.4 inch); and grade 3 (complete tear), greater than 10  mm (0.4 inch). If the mechanism of a knee injury suggests that it is more likely to be ligamentous than bony, weight bearing as tolerated and range of motion as tolerated are safe recommendations. Nonsteroidal antiinflammatory drugs (NSAIDs), compression dressing, and ice, if it is available, are palliative methods that may enhance the victim’s ability to leave the wilderness setting under his or her own power. The collateral ligaments stabilize the knee in the lateral and medial directions (Figure 27-100). The medial collateral ligament (MCL) is more commonly injured than is the lateral collateral ligament (LCL), because collisions to the knee usually occur on the outer aspect or lateral side, which causes the medial joint to “book” open. The opposite leg usually protects the knee from

Other Soft Tissue and Musculoskeletal Injuries INTRA-ARTICULAR KNEE DISRUPTION Sprains or tears of ligaments about the knee are common occurrences in sporting events and in vigorous activities. They often involve a sudden fall or a twisting mechanism. The anterior cruciate ligament (ACL) restrains the tibia from forward displacement relative to the end of the femur. The posterior cruciate ligament (PCL) restrains the tibia from posterior displacement relative to the femur. ACL injuries are most common in pivot-twisting sports such as basketball, soccer, and alpine skiing but can occur with simple falls or work injuries (Figure 27-99). PCL trauma is often seen in “dashboard” injuries in which the anterior knee is suddenly pushed backward. ACL injuries are more commonly seen than are PCL injuries, and the incidence is higher in female than in male athletes. Biomechanical issues in jumping and landing are thought to be largely involved and more relevant than are hormonal or intrinsic knee anatomy (“notch” size). The individual who sustains this injury often sustains concomitant knee injuries, such as a meniscus tear or an injury to another ligament in the knee. Tearing of the ACL may be accompanied by the sound of a pop in the knee. Usually, but not 554

MCL

LCC

FIGURE 27-100  Medial collateral ligament (MCL) tear with lateral condyle contusion (LCC).

Treatment Most isolated LCL sprains, like MCL sprains, heal with conservative management. The typical time frame of 6 to 12 weeks may be anticipated for return to full unrestricted activity. A hinged knee brace that protects the knee from valgus stress is indicated. When associated with a multiligament injury, especially a cruciate ligament disruption and posterior lateral instability, surgical repair may be necessary to restore function. Individuals and athletes who wish to return to competitive sports typically will have ACL injuries “fixed”; PCL tears are treated on a case-by-case basis because many individuals can compensate for this injury without surgery. An ACL deficient knee will often result in ongoing instability (a “trick” knee), even in nonathletic individuals, and the risk for tearing the meniscus or causing other damage to the knee is high. Rehabilitation from this injury is usually a minimum of 6 months. Meniscal tears in the setting of a ligamentous injury are common (Figure 27-101). Some tears—so called bucket-handle tears— can become caught in the joint. These can result in a “locked knee.” Manipulative procedures have been described for liberating an incarcerated meniscal fragment. However, unless evacuation is substantially hindered by the locked knee, it is generally better to get the injured individual as quickly as possible to a facility where further analysis and diagnostic imaging may be obtained. Sometimes, surgery is the sole solution for this problem.

ACHILLES TENDON RUPTURE Achilles tendon ruptures occur most commonly in the 35- to 55-year-old age group. This injury usually happens as an individual applies an eccentric (lengthening while contracting) load to the calf and Achilles tendon. The affected individual often feels as though he or she has been struck by a baseball bat at the posterior aspect of the ankle. Active plantar flexion is impossible. In the Thompson squeeze test, the injured person kneels on an elevated surface without sitting on the haunches and allows the feet to hang over the edge of the surface. Squeezing the calf does not result in an involuntary plantar flexion on the injured side. If a short leg splint can be applied as a temporizing measure, this should be done. The affected individual may bear weight as tolerated. This injury may be treated with or without surgery.

HAMSTRING PULL OR TEAR A hamstring pull or tear can occur when there is a hyperflexion mechanism applied to the hip simultaneously with a hyperextension mechanism to the leg (eccentric load). A hamstring tear or

Medial meniscus tear

FIGURE 27-101  Medial meniscus tear.

strain can also occur as an overuse injury. Generally the best way to treat this injury is to apply ice, stretch gently, and bear weight, as tolerated. Most hamstring tears heal with conservative management. If a complete tear or significant avulsion from the ischial tuberosity occurs, surgical repair may be indicated. There are no evidence-based recommendations for repair. However, in active people with greater than 2 cm (0.8 inch) of retraction from the ischium, repair can result in decreased pain and improved function over time.

EFFUSIONS Joint or bursal effusions occur when there is excess production of synovial fluid. Effusions may result from trauma (for example, hemarthrosis as a result of an ACL tear, or lipohemarthrosis as the result of a tibial plateau fracture). Because it is rarely possible to perform aspiration under sterile conditions in the wilderness, the effusion should be treated with NSAIDs, compression dressing, and application of cold. A painful effusion without trauma in a person over the age of 40 years is more likely gout or pseudogout than infection. If there is strong suspicion that the effusion may be infected (in the setting of fever, chills, and lack of trauma), antibiotics can be administered.

Overuse Syndromes and Special Considerations Overuse syndromes that affect the musculoskeletal system are very common in the wilderness.

PLANTAR FASCIITIS Plantar fasciitis is inflammation of the fascia (tough connective tissue) on the sole of the foot. An individual with plantar fasciitis complains of insidious onset of pain at the origin of the plantar fascia, which is located at the most anterior medial aspect of the heel pad. Any activities that stretch the plantar fascia elicit pain. The pain is worst when first getting up in the morning or after resting and is accentuated when the ankle and great toe are dorsiflexed (e.g., during push-off). Conservative treatment consists of (1) heel cord stretching, (2) NSAIDs, (3) taping, and (4) wearing an orthotic that cups the heel, has a soft spot under the tender area, and supports the arch. It may take several weeks for symptoms to improve, but conservative therapy is successful in 90% of cases. An ankle–foot splint worn at night may help 555

CHAPTER 27  Wilderness Orthopedics

being struck medially so that the LCL of the contralateral knee is often spared. Collateral ligament injuries are graded as 1, 2, or 3. A strain causing pain, but less than 5 mm (0.2 inch) of discernable joint space opening compared with the uninjured knee, is consistent with a grade 1 injury. A joint space opening of 5 to 10 mm (0.2 to 0.4 inch) is consistent with a grade 2 injury. Greater than 10 mm (0.4 inch) or the absence of an endpoint with valgus stress applied to the knee is consistent with a grade 3 injury. The MCL is attached to the medial meniscus, so injuries to the medial knee may also cause injury to the medial compartment cartilage. If symptoms do not improve in a timely fashion, further evaluation to rule out a meniscal tear is appropriate. MCL injuries are typically treated with conservative management. A hinged knee brace that stabilizes the knee from varus and valgus stress is indicated. Isolated injuries to the LCL are less common than are those of the MCL. They typically will occur when the outstretched leg is struck from the medial or inner aspect, producing a varus stress to the knee. The LCL can then be strained or torn. The LCL may often be injured in association with a cruciate ligament injury. Complex injuries to the posterior lateral corner of the knee may involve the popliteus tendon as well and can be disabling injuries in terms of knee stability. The LCL connects from the lateral femoral condyle to the lateral tibial plateau but has no direct attachment to the lateral meniscus (as does the MCL with the medial meniscus).

PART 4  INJURIES AND MEDICAL INTERVENTIONS

because it holds the foot in a neutral position, keeping the plantar fascia slightly stretched. The orthosis also provides significant pain relief if used while walking.

CARPAL TUNNEL SYNDROME Carpal tunnel syndrome (CTS) occurs when the median nerve is compressed within the carpal tunnel (Figure 27-102). The carpal tunnel, located on the palmar side of the wrist, is formed by the transverse carpal ligament volarly and the carpal bones dorsally. The flexor digitorum profundus and superficialis tendons to the second through fifth digits, the long thumb flexor, and the median nerve pass through this canal. Individuals with “compressive median neuropathy” (CTS) complain of pain and paresthesias along the palmar aspects of the radial digits. They also complain of frequently dropping objects. Symptoms are worse at night and aggravated with prolonged wrist extension or flexion. The Phalen sign, which is numbness and tingling in the median nerve distribution after sustained wrist flexion, is suggestive of CTS. Thenar muscle atrophy is seen only in severe cases. Etiology of CTS includes pregnancy, endocrine disorders (diabetes or hypothyroidism), and acute or chronic trauma. Treatment consists of wrist splinting in slight extension, activity modification, and NSAIDs.

STRESS FRACTURES Stress fractures can occur in individuals who suddenly increase their activity. Although tibia and metatarsal fractures are most common, any bone can sustain a stress fracture (Figure 27-103). Victims complain of pain with weight bearing, swelling, tenderness to palpation, and increased warmth at the fracture site.

FIGURE 27-103  53-year-old woman who sustained a fibular stress fracture after a several-week hike along the Pacific Crest Trail. FIGURE 27-102  Anatomic basis of carpal tunnel syndrome. A, General view of the relationship between the median nerve and the flexor retinaculum. B, Cross section of the distal carpal row, showing the structures in the carpal tunnel. (Redrawing based on an illustration by Li-Guo Liang, in Yu Hi, Chase RA, Strauch B: Atlas of hand anatomy and clinical implications, Philadelphia, 2004, Mosby, p 513.)

Hypothenar muscles

Thenar muscles

Median nerve Transverse carpal ligament

A Median nerve Tubercle of the trapezium Tendon of the flexor carpi radialis

Tendon of the flexor pollicis longus

Superficial branches of the ulnar vein, artery, and nerve Transverse carpal ligament

Palmar carpal ligament Tendons of the flexor digitorum superficialis Deep branches of the ulnar vein, artery, and nerve Hook of the hamate Tendons of the flexor digitorum profundus

B 556

CHAPTER 27  Wilderness Orthopedics

Treatment consists of activity reduction, protective weight bearing, and avoidance of activities that produce pain. As the pain subsides, the activity level can be increased. Resolution of symptoms may require 2 to 3 months.

BURSITIS, INFLAMMATION, AND IRRITATION The iliotibial band travels along the lateral thigh, from its origin at the iliac crest to it insertion at Gerdy’s tubercle on the proximal, lateral tibia. Irritation and inflammation occur along the path of the iliotibial band at the bony prominences over which it runs— proximally at the greater trochanter and distally at the lateral femoral epicondyle. Treatment for these conditions in the wilderness involves NSAIDs, ice, and, insofar as it is possible, decreased activity. Stretching can also be of benefit for these conditions, especially as a preventive measure or as treatment over the long term. Olecranon bursitis and prepatellar bursitis can also occur in the wilderness setting. If either condition arises and is painful, the antiinflammatory interventions mentioned above can be of benefit.

Spinal Disorders Back strain/pain episodes may occur during an outing and dampen the enthusiasm of even the most dedicated outdoor purist. Most often, these events represent low back strain or musculoskeletal spasm. These conditions can occur in the setting of heavy lifting, bending, or twisting activities. Treatment involves low-impact exercise, such as walking on a level surface, ice, and NSAIDs. Occasionally, however, symptomatic disk herniation, protrusion, or extrusion may occur. Typically this will be painful and may manifest with or without focal radicular symptoms. In an individual with severe, intractable pain, loss of motor strength, or loss of bowel or bladder function, evacuation and emergent consultation may be necessary. As is well known, it is important to treat patients rather than diagnostic images. Individuals with significant scoliosis, spinal angulation, spondylolysis, spondylolisthesis, or arthritis on radiographs (or other imaging studies) may still function normally in the wild. The 56-year-old woman in Figure 27-104 has significant scoliosis yet remains vigorously active in yoga and carries a full backpack down into the Grand Canyon on an annual pilgrimage (Figure 27-105).

FIGURE 27-105  This 56-year-old woman does not let her scoliosis slow her down. She is performing a yoga pose in the Grand Canyon.

Returning to the Wilderness After Total Joint Replacement Increasing numbers of outdoor enthusiasts have had total joint replacement surgeries, primarily of the knee and hip, and have returned to their previous activities. New technologies, such as hip resurfacing, have been developed to possibly improve the longevity of arthroplasty for young active individuals (Figure 27-106). Given appropriate physical therapy and rehabilitation, many individuals can regain near-normal function. Although the possibility of reinjury, prosthesis damage, or periprosthetic fractures remains a concern, many individuals are more than willing to take such risk to enjoy the pursuit of wilderness passions (Figure 27-107). It was barely 50 years ago that Sir John Charnley implanted the first total hip in England. He would certainly be amazed to see a 61-year-old patient who had previously suffered from advanced hip arthritis trekking in the Himalayas and climbing 6,000-m peaks after staged cementless, bilateral hip arthoplasties.21 There were no signs of prosthesis loosening or abnormal

FIGURE 27-106  Right hip resurfacing for osteoarthritis in an active FIGURE 27-104  Lumbar spine radiograph of active individual that demonstrates significant scoliosis.

58-year-old man. Resurfacing arthroplasty provides a surgical option for osteoarthritis treatment that requires less bone resection than do more traditional total hip arthroplasty techniques.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

C

FIGURE 27-107  A and B, A 70-year-old woman with a total knee arthroplasty sustained a periprosthetic distal femur fracture when she fell while hiking. C, One year following open reduction and internal fixation of her fractures, she hiked the same trail.

wear of the bearing materials in the mountaineer in Figure 27-108 at age 69, 16 years after the first procedure and 8 years following the second. Most individuals temper activities following total joint replacement. Current recommendations regarding return to activity following total joint replacement are variable. However, a rule of thumb is to not engage in vigorous new activities after joint replacement; an experienced athlete can usually return to a sport in which he or she is skilled following total joint arthroplasty, given reasonable limits (Table 27-1). Despite such recommendations, patients continue to “push the envelope” in returning to aggressive sporting activities. Examples of highly successful returns to play after total hip or total knee replacement abound: • Bo Jackson returned to professional baseball in 1993 after his total hip arthroplasty (THA) in 1992. • Golfer George Archer had a right hip replacement in 1996 and won the Senior PGA tour in 1998.

FIGURE 27-108  Bilateral total hip arthroplasties in a patient who, following her second surgery, climbed to the summit of Mt Rainer.

558

• Golfing great Jack Nicklaus had a THA in 1999 and returned to high-level play. • Figure skater Rudy Galindo had bilateral ceramic-onceramic THAs in 2003 and was landing triple jumps with Champions on Ice in 2004. • A 69-year-old mountaineer, after bilateral THAs in 1987 and 1995, climbed two peaks over 6000 m in the Andes. • Floyd Landis had a hip resurfacing in 2006, was riding a stationary bike 5 days after surgery, and has returned to competitive cycling since then.

TABLE 27-1  Return to Activity After Total Knee

and Total Hip Replacement*

Generally Safe

Greater Risk

Risky Activities

Swimming Stationary bike/cycling Low-resistance rowing Walking Hiking with poles, even terrain Low-resistance lifting Canoeing Bowling Croquet Golf Tennis: doubles Table tennis Ballroom dance Classic cross country skiing Horseshoes Shooting Shuffleboard

Ice skating Cross country skiing Roller blading Horseback riding Softball Volleyball Hunting, uneven terrain Fencing Nordic track

Downhill skiing High-impact aerobics Basketball Football Hockey Soccer Gymnastics Power lifting Rock climbing Parachuting Hang gliding Rodeo Distance running Hardball Lacrosse/rugby Tennis: singles

*There is no absolute consensus regarding return to activity after joint replacement. These suggestions are a synthesis of survey results from the knee society and the hip society. Virtually all agree, however, that it is important to limit impact loading and rotational/levering forces on the artificial joint. Failure to control these forces increases the possibility of prosthetic dislocation, biomechanical failure, or periprosthetic fracture.

CHAPTER 27  Wilderness Orthopedics

In general, however, a cautionary and commonsense approach is advised. Although one may attempt to return to a “skill” sport in which one has participated in the past, it is not recommended that one attempt to learn a “new” sport that requires advanced proprioceptive skills and/or significant impact loading as categorized in Table 27-1. Sports and fitness regimens will vary significantly with the competence, confidence, and risk tolerance of the individual. The necessity for revision arthroplasty has a markedly increased cost and rate of complications relative to primary joint replacement.

Prosthetics in the Wilderness Orthotics and limb replacement devices have given individuals who have sustained amputations, whether from trauma, congenital disorder, or cancer, the chance to participate in wildernessbased adventures that in the past may have been unavailable to them. Computer-assisted and computer-guided prosthetics now enable amputees’ prostheses and therefore provide the opportunity to participate in outdoor activities with other “able-bodied” individuals, often on an equal basis. Some persons have claimed that the new prostheses, in certain instances, offer an enhanced level of performance, as in the case of the South African runner, Oscar Pistorius, with his bilateral graphite-carbon “feet.” In the wilderness setting, there may be significant benefits in not worrying about frostbite or getting one’s foot back into a cold boot at dawn (Figure 27-109). However, additional concerns, including limb swelling, skin breakdown in a limb stub, inability to change a sock liner on a regular basis, or the possibility of prosthesis damage, remain. Intrepid mountaineers, such as Tom Whittaker, who became the first below-the-knee amputee to summit Mt Everest in 1998, testify to the capabilities of a motivated athlete despite limb loss28 (Figure 27-110). Whittaker founded and has worked for years from Prescott, Arizona, with the Cooperative Wilderness Handicapped Outdoor Group (C.W. HOG) in Pocatello, Idaho. Many members of this organization suffer from spinal cord injuries, cerebral palsy, amputations, or other neuromuscular problems. In spite of this, they have participated in diverse activities and mountaineering (Figure 27-111).

FIGURE 27-110  Tom Whittaker on Aconcagua’s Argentine Andes. Note carbon flex prosthesis on right lower extremity. (Copyright Tom Whittaker Collection.)

New Technologies Plaster of Paris and fiberglass casting tape have provided stabilization for extremity injuries for many years. The Flemish army surgeon Mathijsen first introduced muslin rubbed with calcium that formed a hard shell and provided the first plaster of Paris casts in 1852. Synthetic fiberglass became popular in the 1980s and has become the dominant material used in casting and splinting in the United States. Plaster remains desirable in some situations because it molds easily and is inexpensive. Both plaster

FIGURE 27-109  Tom Whittaker marked his tent at Mt Everest base camp with a spare prosthesis so that his 70-year-old father who hiked to 18,000 feet after a total hip replacement could find the correct tent. (Copyright Tom Whittaker Collection.)

FIGURE 27-111  Tom Whittaker assists fellow Cooperative Wilderness Handicapped Outdoor Group (C.W. HOG) member, Carl Brinker, with rappeling down an 80-foot basalt cliff. (Copyright Tom Whittaker Collection.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 27-112  New dry heat–formable thermoplastic technologies, such as this Exos fracture brace, are durable, waterproof, and lightweight, allowing earlier return to outdoor activities.

of Paris and fiberglass are removed using a cast saw. Plaster of Paris will become sodden, heavy, and lose stability when wet. Waterproof linings, such as Gortex, may allow the fiberglass cast or splint to be used in a wet environment. Other materials, such as Aquaplast and Orthoplast, may be softened in a hot water hydrocollator and have specific indications in appropriate patients. New prefabricated casting and bracing materials have evolved from ski-boot technologies. These use dry heat–formable polymers laminated with closed-cell foam and antiabrasive fabrics to provide custom-fitted musculoskeletal support devices. These materials are waterproof, lighter than fiberglass, durable, remoldable, and use adjustable closure systems. Such products offer improved patient comfort and allow early return to hiking, skiing, or water sports (Figure 27-112).

Evacuation Decision The decision to evacuate an orthopedically injured individual depends on the goals of the expedition or mission and available support. Criteria for evacuation of an injured person in a family

FIGURE 27-114  A wilderness expedition rests for the night.

BOX 27-2  Indications for Emergent Evacuation • Suspected spine injury • Suspected pelvic injury • Open fracture • Suspected compartment syndrome • Hip or knee dislocation • Vascular compromise to an extremity • Laceration with tendon or nerve injury • Uncertainty of severity of injury

of four spending a week hiking in the Rockies differ from those of a military campaign or group of 25 climbers in the Himalayas with physician support and a field hospital at base camp. In all cases, party leaders should have a plan for contacting evacuation support teams if a serious injury occurs (Figure 27-113). Musculoskeletal injuries that warrant immediate evacuation to a definitive care center are listed in Box 27-2. These include any suspected cervical, thoracic, or lumbar spine injury. A victim who has a suspected pelvic injury with posterior instability, possibly significant blood loss, or injury to the sacral plexus should be emergently evacuated on a backboard. Any open fracture requires definitive debridement and care within 8 hours to prevent deep infection. Victims with suspected compartment syndromes must be evacuated on an emergency basis. Joint dislocations involving the hip or knee warrant immediate evacuation because of the associated risk for vascular injury or post-traumatic avascular necrosis of the femoral head. Lacerations involving a tendon or nerve warrant urgent evacuation to a center where an extremity surgeon is available. In all but the most serious wilderness expeditions, arrangements should be made to evacuate the victim when the treating individuals are not reasonably sure of the injury with which they are dealing or with its appropriate management (Figure 27-114).

REFERENCES FIGURE 27-113  Prompt evacuation in certain scenarios is crucial.

560

Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 28 

The Eye in the Wilderness FRANK K. BUTLER, JR.

This chapter considers several commonly encountered types of eye disorders: periocular trauma; chemical injury to the eye; sudden vision loss in a white, quiet eye; acute orbital and periorbital inflammation; and the acute red eye. A diagnostic and therapeutic approach to these disorders that is suitable for the wilderness environment is presented. Finally, eye problems that are encountered during diving and altitude exposures are discussed.

Preliminary Planning Pertinent ocular items in a preliminary medical survey include contact lens wear; previous episodes of nontraumatic iritis; previous episodes of herpetic keratitis; and a history of corneal transplantation, retinal detachment, refractive surgery, or other ocular surgery. A positive response to these questions may alert the health care professional to specific ocular problems that may be encountered on the proposed trip. Congenital color vision deficiencies are common in the male population (8% in whites)32 and typically pose no functional problems in the wilderness. Ocular health should be reviewed as part of the medical survey, and a basic wilderness eye emergency kit should be assembled and taken on the trip; this is described in the next section.

The Wilderness Eye Emergency Kit Box 28-1 lists the suggested items for a basic wilderness ocular emergency kit. A topical fluoroquinolone (e.g., moxifloxacin) is the antibiotic eye drop of choice. These medications are preferred for the treatment of bacterial keratitis in a wilderness setting. Topical tetracaine and fluorescein strips are important for diagnosis. Topical prednisolone is an excellent ocular antiinflammatory medication. The choice of an oral antibiotic is based on the efficacy of the proposed antibiotic for the treatment of preseptal cellulitis, orbital cellulitis, and penetrating trauma to the globe. The fluoroquinolone family of antibiotics offers several good choices for these indications. The fourth-generation fluoroquinolone moxifloxacin provides good coverage against gram-positive, gramnegative, and anaerobic organisms, with a relatively mild side effect profile and once-daily dosing; it is the recommended firstline oral antibiotic.99 Gatifloxacin has recently been withdrawn from the market because of dysglycemic side effects. Trovafloxacin (500-mg tablets) is a systemic fluoroquinolone with excellent coverage against gram-positive, gram-negative, and anaerobic bacteria.61,138 It offers the convenience of once-daily dosing, but there have been a number of unpublished reports of hepatotoxicity with trovafloxacin that limit the usefulness of this medication.105 Levofloxacin (500-mg tablets) is a systemic fluoroquinolone with very good activity against a wide variety of gram-positive and gram-negative organisms but less anaerobic coverage than is offered by trovafloxacin.105 Ciprofloxacin has been shown to have excellent ocular penetration when given orally,80 but it is less efficacious against gram-positive organisms than is levofloxacin. Bacitracin is an antibiotic ointment that is suitable for use for patching corneal abrasions. Ophthalmic ointments are best applied with the use of downward pressure on the lower lid to pull it away from the eye followed by the application of a 1-cm (0.4-inch) ribbon of ointment to the conjunctiva of the lower lid. When released, the lid returns to its normal position, and normal blinking distributes the ointment over the corneal surface.

Oral prednisone has at least three possible eye-related treatment uses in the wilderness: (1) refractory iritis; (2) giant cell arteritis; and (3) orbital pseudotumor. Topical scopolamine 0.25% is used to reduce ciliary muscle spasm, which causes much of the discomfort that is associated with iritis and corneal abrasion. However, scopolamine has the disadvantages of dilating the pupil, thus making the eye very sensitive to bright light, and of preventing accommodation, thus making reading very difficult, for 5 to 7 days. Artificial tears are used to treat ocular surface drying and to flush conjunctival foreign bodies from the eye. Artificial tears are a better choice for these symptoms than are ophthalmic preparations that contain vasoconstrictors, because the latter medications have been shown to cause both acute and chronic conjunctivitis.131 Diclofenac 0.1% drops have been shown to decrease corneal sensitivity, especially when multiple drops are used.119,136,137 These drops have been found to be helpful for reducing the discomfort that is associated with traumatic corneal abrasion67 and excimer laser refractive surgery.46,139,144 In the unlikely event of angle-closure glaucoma in a wilderness setting, 2% pilocarpine may be used. The medications in Box 28-1 are listed in my recommended priority order. In the spirit of making do in the wilderness, all of the disorders mentioned in this chapter can be managed with only the aforementioned medications, but alternative therapies are also discussed. Many individuals suffer from seasonal allergies, including allergic conjunctivitis, and these may be exacerbated in the wilderness. Adding olopatadine 0.1%, lodoxamide 0.1%, nedocromil 2%, or ketotifen 0.025% to the wilderness eye kit provides treatment options for allergic conjunctivitis.77 Because this condition is frequently chronic, individuals may carry their own medications on trips.

Visual Acuity Measurement in the Wilderness Evaluation of visual acuity is an essential element of the eye examination. Serial measurements of visual acuity are used to monitor an individual’s progress while he or she is being treated for infectious, inflammatory, or traumatic eye disorders. Lack of an eye chart does not preclude the ability to obtain a quantitative measurement of visual acuity; rather, a near-vision card can be used for this purpose. Such a card should be held the prescribed distance from the eye; this is usually 35 cm (14 inches). If a near-vision card is not available, the ability to read print in a book is a useful alternative measure. If the individual’s glasses have been lost, use a piece of paper with a pinhole that has been created with the tip of a pen or pencil to help to compensate for the lost refractive correction. Individuals who are 40 years old and older may need a pinhole or reading correction to help them to focus on a near target. Although a marked decrease in visual acuity can be an important warning of a significant ocular disorder, visual acuity cannot always be considered a reliable indicator of the severity of disease. A corneal abrasion victim may initially have worse visual acuity than a person with a retinal detachment or corneal ulcer, despite the fact that the latter two entities are much more serious disorders.

General Therapeutic Approach The recommendations made in this chapter are not necessarily the preferred management of the disorders mentioned when one is not in the wilderness setting. Of special interest is the 561

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 28-1  The Wilderness Eye Emergency Kit Medications Moxifloxacin 0.5% drops Tetracaine 0.5% drops Prednisolone 1% drops Moxifloxacin 400-mg tabs Levofloxacin 500-mg tabs Bacitracin ointment Prednisone 20-mg tabs Artificial tears Scopolamine 0.25% drops Diclofenac 0.1% drops Pilocarpine 2% drops Miscellaneous Penlight with blue filter Fluorescein strips Cotton-tipped applicators Metal eye shield Tape (1-inch wide, plastic or nylon) Near-vision card Wound closure strips (0.25-inch wide) Magnifying glass Fine forceps

recommendation for an individual who is not an ophthalmologist to use a topical steroid for the management of several of the disorders discussed. The use of topical ocular steroids is generally best undertaken by ophthalmologists for two reasons. First, steroids are usually indicated only for relatively serious ocular disorders, which should be followed by an ophthalmologist when possible. Second, topical steroid use may result in elevated intraocular pressure, cataracts, and exacerbation of certain eye infections. All of the disorders for which steroids are recommended in this chapter should be referred to an ophthalmologist for follow up as soon as possible after the patient returns from the wilderness. Caution should be exercised when prescribing a topical steroid for more than 3 days of use. Although cataracts are typically associated with long-term steroid use, a significant rise in intraocular pressure may occur within just a few days after initiation of topical steroid therapy.77 The requirement for expedited evacuation is one of the questions that must be answered when treating an eye disease in the wilderness. In the following sections, the need for evacuation may be considered nonurgent unless an emergency (i.e., as soon as possible) or expedited (i.e., as soon as is deemed reasonable given the resources required to accomplish the task) evacuation is specified in the recommendations for treatment.

Acute Periocular Inflammation Causes of acute periocular inflammation are listed in Box 28-2. The term preseptal cellulitis means that the infectious process is confined to the tissues anterior to the orbital septum. Therefore, preseptal cellulitis manifests as erythema and edema of the eyelids without restricted ocular motility, proptosis, pupillary change, or decrease in visual acuity. However, some of these

BOX 28-2  Differential Diagnosis of Acute Periocular

Inflammation

Preseptal cellulitis Orbital cellulitis Dacryocystitis Orbital pseudotumor Insect envenomation

562

findings may be difficult to appreciate in the presence of marked lid edema. Historical clues include antecedent periocular trauma or insect bite or sting. Staphylococcus aureus and Streptococcus species are the most common causative organisms in adults.39 In the past, this disorder has been treated very aggressively because of the high incidence of Haemophilus influenzae infection, especially in pediatric patients, with subsequent septicemia and meningitis. The advent of H. influenzae type B vaccine has changed the microbiology of this disorder and may dictate changes in treatment strategies in the future.36 Persons who present with this disorder may be treated with 400 mg of moxifloxacin once a day and should have an expedited evacuation. Alternative antibiotic choices include 500 mg of levofloxacin once a day, 750 mg of ciprofloxacin twice a day, 500 mg of dicloxacillin every 6 hours, or 500 mg of cephalexin four times a day. Dacryocystitis, which is infection of the lacrimal sac, may mimic the findings of preseptal cellulitis; however, erythema, edema, and tenderness are localized to the area that is inferior to the medial aspect of the eye and over the nasolacrimal sac and duct. The presence of this condition usually indicates an obstruction in the opening between the lacrimal sac and the nasal cavity. Surgical intervention to restore the patency of this opening is usually undertaken after the acute infection is treated. The most common pathogens that cause acute dacryocystitis are S. aureus, Streptococcus species, and, in children, H. influenzae.98 Treatment should be initiated with 400 mg of moxifloxacin once a day and warm compresses. Alternative antibiotic choices include 500 mg of levofloxacin once a day, 750 mg of ciprofloxacin twice a day, or 875 mg of amoxicillin and 125 mg of clavulanate every 8 hours. Worsening of the condition after 24 to 48 hours should be managed with an expedited evacuation. Periocular insect envenomation is a preseptal cellulitis lookalike. Although secondary infection may follow envenomation, the envenomation itself may produce significant erythema and edema. Diagnostic clues include a history of insect bite or a periocular papular lesion at the site of the envenomation. Ice or cool compresses may be used to treat the envenomation, with 400 mg of moxifloxacin once a day, 500 mg of levofloxacin once a day, 500 mg of dicloxacillin every 6 hours, or 500 mg of cephalexin 4 times a day added if secondary infection is suspected. The term orbital cellulitis means that infection has spread to or originated in the tissues posterior to the orbital septum. This may be manifested as diplopia or restriction in ocular motility as the extraocular muscles are affected, proptosis as edema in the orbit pushes the globe forward, decreased vision as the optic nerve is affected, or pupillary change if innervation of the pupil is affected. Fever is suggestive of orbital cellulitis as part of the differential diagnosis of periocular inflammation. This condition is more commonly associated with sinusitis than with periocular trauma as an antecedent disorder.83 Most series report a 50% to 75% incidence of sinusitis or other upper respiratory infection in association with orbital cellulitis.146 The bacteria that most commonly cause orbital cellulitis are S. aureus, Streptococcus pyogenes, and Streptococcus pneumoniae.98 Anaerobes are frequently present in patients with chronic sinusitis and should be suspected in those with orbital cellulitis that is associated with longstanding sinus disease.98 If not treated aggressively, orbital cellulitis may be associated with a life-threatening infection of the central nervous system. Before antibiotics became available, approximately 19% of persons with orbital cellulitis died of intracranial complications, and 20% of survivors became blind in the involved eye.98 This disorder requires hospitalization and intravenous antibiotic therapy. Interim therapy should include 400 mg of moxifloxacin once a day. Alternative antibiotic choices are 500 mg of levofloxacin twice a day, 750 mg of ciprofloxacin twice a day, or 875 mg of amoxicillin and 125 mg of clavulanate every 8 hours. A decongestant should be added if sinusitis is present, and emergent evacuation should be undertaken. Orbital pseudotumor is an inflammatory disease of the orbit that may manifest very much like orbital cellulitis. The differentiation between these two entities may be difficult.83 There would typically not be a history of preceding sinusitis. A reasonable approach in the wilderness is to begin therapy with 400 mg of moxifloxacin once a day and then to arrange for emergent evacuation. Prednisone (80 mg/day) should be added if there is no

Periocular Trauma EYELID LACERATION The most important aspect of managing an eyelid laceration is to carefully exclude the presence of penetrating injury to the globe. Clues to the presence of an open globe are noted in the sections about Obvious Open Globe and Occult Ruptured Globe, later. A lid laceration that is horizontally oriented on the eyelid, that does not penetrate the full thickness of the lid, and that does not involve the lid margin is relatively easily managed. In the absence of an ability to properly irrigate, disinfect, and suture the laceration, it should be managed by irrigation with the cleanest disinfected water available, application of topical antibiotic drops (e.g., ciprofloxacin, ofloxacin, tobramycin) to the laceration, drying the surrounding skin surface, and closing the laceration with tape strips. The wound may then be treated with antibiotic ointment (e.g., bacitracin, erythromycin) four times a day for 3 to 4 days. Alternatively, the laceration may be left open, treated with antibiotic ointment four times a day, and repaired 1 or 2 days later.83 The laceration should be observed frequently while it is healing. If redness or discharge develops, the victim should be started on 400 mg of moxifloxacin once a day, 500 mg of levofloxacin once a day, or 500 mg of dicloxacillin every 6 hours. The wound closure tape should be removed from the laceration, and evacuation should be expedited, especially if the response to oral antibiotics is poor. Complicated lid lacerations, which are defined as stellate or complex, and those that involve the lid margin or the canthi (i.e., the medial or lateral end of the palpebral fissure) are more difficult to manage. These lacerations may result in secondary functional difficulties if ocular lubrication or lacrimal drainage becomes impaired. In addition, cosmesis may be poor if a meticulous repair is not done. These wounds should be managed by irrigation with the cleanest disinfected water available, application of antibiotic ointment, and coverage with a sterile dressing. Evacuation for definitive repair should be expedited.

CORNEAL FROSTBITE Corneal frostbite is an uncommon disease, but it has been reported during such activities as snowmobiling without protective eye goggles when participants keep their eyes open in conditions of high windchill factor.6 Symptoms and treatment are the same as those described in the section about Corneal Abrasion, later.

INSTILLATION OF ADHESIVE DROPS INTO THE EYE Inadvertent instillation of a “superglue” compound (i.e., a cyanoacrylate-type adhesive) into the eye may bind the lids tightly together. Overnight application of a pressure patch with eye pads that have been presoaked with water has been reported to make manual separation of the lids possible and to eliminate the need for general anesthetic and the surgical separation of the lids.109 Ophthalmic ointment inserted through any small opening in the adherent lids has also been reported to facilitate resolution.93 After the lids are separated, the eye should be checked for corneal abrasion.123

RETROBULBAR HEMORRHAGE Blunt or penetrating periocular trauma may result in orbital bleeding. If the bleeding is contained by the orbital septum, an

orbital compartment syndrome may ensue. Because the pressure in the orbital compartment is progressively elevated, intraocular pressure will also rise. If intraocular pressure rises to a highenough level, either central retinal artery occlusion or damage to the optic nerve may ensue, and vision may be permanently lost in the eye. Signs and symptoms of retrobulbar hemorrhage include pain, periorbital ecchymosis, progressive proptosis (i.e., bulging forward of the eye), decreased vision, diffuse subconjunctival hemorrhage, and an afferent pupillary defect. Definitive management of this disorder is a minor surgical procedure called lateral canthotomy (Figure 28-1) in which an incision is made at the lateral aspects of the eyelids to relieve pressure in the orbit.

Chemical Injury of the Eye The mainstay of management of any chemical eye injury is immediate and copious irrigation of the ocular surface with water from whatever source is most readily available. Lactated Ringer’s solution or normal saline is the preferred irrigation fluid, when available39; however, in the wilderness, bottled water may be the best option. If none of these fluids is available, treated (i.e., filtered and disinfected) water from a drinking container is the next best option, with untreated water being the last resort. Instillation of several drops of tetracaine will make the procedure much less uncomfortable for the victim. Irrigation should be continued for a minimum of 30 minutes.83 The two most damaging chemicals are strong acids and alkalis.83 Sulfuric acid from an exploding car battery is a typical acid, whereas cleaning products (e.g., drain cleaners) are typical alkalis. Caustic alkalis are more likely to damage the eye than are acids because of their profound and rapid ocular penetration. Do not attempt to neutralize the corneal surface with acidic or alkaline solutions. Chemicals other than acids and alkalis may be uncomfortable when they are encountered, but they are less likely to produce significant long-term damage. After a minimum of 30 minutes of flushing has been completed, the eye should be examined for retained particles; these should be removed with a moistened cotton-tipped applicator.83 Treatment for an acid- or alkali-induced injury includes moxifloxacin 0.5% drops (one drop four times a day) or bacitracin ointment every 1 to 2 hours while awake until fluorescein staining confirms that the corneal epithelial defect that typically accompanies these injuries has resolved. Topical prednisolone 1% should be added if there is significant inflammation. Prednisolone drops should be used every hour while awake for 3 days. Eye pain is managed with scopolamine drops four times a day for 3 days and oral pain medications.121 Frequent use of artificial tears may also help to relieve discomfort. Evacuation should be expedited if the cornea is found to be opaque, if a large epithelial defect is found on fluorescein staining, or if significant pain persists after 3 days. Another sign of serious injury is blanching of the conjunctiva in the limbal area.83 A special type of chemical injury to the eye is ocular envenomation from a spitting cobra.51,56,141 Ocular injury from cobra venom may be severe and result in blindness. Cobras can project this venom out to a range of 3 m (10 feet), and they typically aim directly for the victim’s eyes. Ocular surface envenomation causes severe conjunctival and corneal inflammation, edema, and erosions. Corneal erosions may progress to corneal ulceration, perforation, hypopyon, and endophthalmitis. Central corneal opacification may result despite aggressive therapy. One report described nine individuals who had suffered ocular surface cobra envenomations.141 Five had only severe conjunctivitis; corneal erosions developed in the other four. Two individuals were permanently blinded as a result. Therapy includes immediate flushing of the eyes as described previously. After this is done, check for a corneal abrasion, and treat it with moxifloxacin 0.5% drops if an erosion is present (one drop four times a day until the erosion is healed). Note that healing may be prolonged in toxin-induced corneal surface injuries. Immediate consultation with a toxicology consult service and a corneal or external disease subspecialist should be obtained, if possible, and an expedited evacuation should be arranged. Topical steroid therapy should be considered (one drop of prednisolone every hour 563

CHAPTER 28  The Eye in the Wilderness

response to antibiotic therapy, if there is no fever or sign of central nervous system involvement, and if evacuation has not been possible by 24 to 48 hours after presentation. If prednisone therapy is initiated, its efficacy should be evaluated after 48 hours. If there has been a decrease in pain, erythema, edema, or proptosis, therapy should be continued until evacuation is accomplished. If there has been no response after 48 hours, the prednisone may be discontinued without tapering.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

2

1

4

3

5

FIGURE 28-1  Lateral canthotomy and inferior cantholysis are indicated for casualties that manifest with orbital hemorrhage and evolving orbital compartment syndrome. Step 1, Infiltrate the lateral canthal area with a local anesthetic (e.g., 2% lidocaine with epinephrine) and use tetracaine drops in the eye for topical anesthesia. Step 2, Place a mosquito clamp on the lateral canthus that extends horizontally toward the orbital rim for a distance of 1 cm. Leave it in place for 30 seconds to assist with hemostasis. Step 3, Remove the clamp, and use a pair of fine (e.g., Stevens) scissors to divide the lateral canthal tissues along the line created by the clamp. This completes the lateral canthotomy. Step 4, Next, use the scissors to cut the inferior crus of the lateral canthal ligament. Position the scissors perpendicular to the canthotomy incision that was made in Step 3 (i.e., not along the lid margin), and cut the ligament. This completes the inferior lateral cantholysis. Step 5, The completed lateral canthotomy and cantholysis are shown. These procedures allow the orbital tissues to move forward slightly, and they help to relieve the pressure in the orbital compartment.

while awake) and discussed with the consultant. The decision to treat is based on the severity of symptoms and the presence or absence of a corneal erosion or ulcer. The value of the topical application of specific cobra antivenom has not been documented, so this therapy is not recommended. Systemic heparin therapy has been shown to be useful for prevention of corneal opacification in animal models of this injury.64,65 Another type of chemical injury of the eye may occur when the eyes are sprayed with skunk musk. Such an episode should be managed with immediate ocular irrigation as described previously. If discomfort persists beyond several hours, check for a corneal abrasion, and treat this with moxifloxacin 0.5% drops (one drop four times a day until the abrasion is healed). If fluorescein staining does not show an abrasion but significant discomfort persists, a 3-day course of prednisolone 1% drops (one drop four times a day for 3 days or until symptoms have resolved) may be of benefit. If pain is severe and unrelieved by prednisolone drops or if it persists after the 3-day course has been completed, consider an expedited evacuation and an ophthalmologic consultation.

Acute Loss of Vision in a White, Quiet Eye Vision may be variably decreased with many of the disease entities that are noted in the section about Acute Red Eye, later. The current section addresses sudden loss of vision that occurs in a white, quiet eye. A differential diagnosis is provided in Box 28-3. Disorders that cause this symptom are often difficult to diagnose without ophthalmic instruments, none of which is included in the kit described in Box 28-1. There are few treatments for most of these disorders that are likely to be effective in a wilderness setting. Although an afferent pupillary defect (e.g., Marcus Gunn pupil) may be present, this is a nonspecific finding that would be expected with most of the disorders listed in Box 28-3, except for vitreous hemorrhage and high-altitude retinal hemorrhage. An important question that must be asked in the face of acute loss of vision in a white, quiet eye is “Does this person have 564

giant cell arteritis?” Giant cell arteritis (GCA), which is also called temporal arteritis, can cause devastating anterior ischemic optic neuropathy that is often first noted on waking and that usually becomes permanent.49 Subsequent involvement of the second eye is common if GCA in the first-stricken eye is not promptly treated.49 Although visual loss has been reported to occur in both eyes simultaneously, there is typically a delay of 1 to 14 days before the second eye is affected.1 Loss of vision in the second eye can be prevented in most cases by prompt initiation of highdose corticosteroid therapy.1,49,59,104 Arteritic anterior ischemic optic neuropathy is typically a disease of older individuals, with one large study reporting a mean age of onset of 70 years and the age of the youngest patient as 53 years.1 Clues to diagnosis are temporal headache, jaw claudication, fever, weight loss, transient visual obscurations, and polymyalgia rheumatica (i.e., generalized myalgias).104 The visual obscurations seen with GCA usually last for 2 to 3 minutes.104 If a person is thought to be suffering from GCA, he or she should be started on 80 mg of prednisone once a day, and evacuation should be expedited. If prednisone or steroids of equal or greater systemic potency are not available, then the evacuation should be considered an emergency. If one suspects that loss of vision is the result of retinal detachment on the basis of a history of high myopia (i.e., extreme BOX 28-3  Differential Diagnosis of Acute Loss of

Vision in a White, Quiet Eye

Retinal detachment Central retinal artery occlusion Nonarteritic anterior ischemic optic neuropathy Optic neuritis Central retinal vein occlusion Arteritic anterior ischemic optic neuropathy Vitreous hemorrhage High-altitude retinal hemorrhage

Care should be taken when monocular visual loss occurs. Although central vision may still be normal in the fellow eye, depth perception may be impaired, and the victim may therefore be at increased risk of a fall during evacuation.

Acute Red Eye Box 28-4 provides a partial list of disorders that can result in an acute red eye. In the absence of a slit lamp, the diagnosis must rely on the basic techniques of history, penlight inspection, fluorescein staining, response to administration of topical anesthesia, and pupillary status. The discussion of the differential diagnosis of the acute red eye that follows makes use of these clinical findings to establish the diagnosis. An algorithmic representation is shown in Figure 28-2. The term fluorescein positive is used to denote an eye with a discrete area of staining noted with cobalt blue light after instillation of fluorescein dye. Some conditions, such as blepharitis, viral keratoconjunctivitis, and ultraviolet (UV) keratitis, may cause a pattern of punctate staining that is referred to as superficial punctate keratitis (SPK).

TRAUMATIC OCULAR DISORDERS Obvious Open Globe If there is a history of trauma and if penlight inspection of the eye reveals an obvious open globe (e.g., the eye in Figure 28-3), the examination should be discontinued and a protective rigid shield placed over the eye. Do not apply a pressure patch or instill any topical medication. There are two primary concerns during management of this condition. The first is to minimize manipulation or additional trauma to the eye that might raise intraocular pressure and result in expulsion of intraocular contents through the corneal or scleral defect. The second is to prevent development of post-traumatic endophthalmitis, which is an infection of the aqueous and vitreous humors of the eye. This typically has devastating visual results, with only 30% of victims in one study retaining visual acuity that is greater than or equal to 20/400.76 Staphylococcus epidermidis is the most common pathogen that is implicated in this condition, but Bacillus cereus is a very aggressive pathogen that is also often isolated.76 After the shield is placed, the victim should be started on 400 mg of moxifloxacin once a day or 500 mg of levofloxacin once a day; 750 mg of ciprofloxacin twice a day is another option. Penetration of antibiotic into the vitreous cavity is of major concern with penetrating eye trauma, so other antibiotics should not be substituted unless they are known to have adequate vitreal penetration. A person with an obvious open globe

BOX 28-4  Differential Diagnosis of the Acute Red Eye Obvious open globe Corneal abrasion Corneal ulcer Subconjunctival hemorrhage Traumatic iritis Hyphema Occult open globe Herpes simplex virus keratitis Corneal erosion Acute angle-closure glaucoma Iritis Scleritis Conjunctivitis Blepharitis Ultraviolet keratitis Episcleritis Conjunctival foreign body Dry eye Contact lens overwear syndrome

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CHAPTER 28  The Eye in the Wilderness

nearsightedness), floaters, or photopsias (i.e., flashing lights), expedited evacuation should be undertaken because of the need for surgical repair. Loss of central vision caused by a retinal detachment usually means that the macula is involved and that surgical repair is urgent rather than emergency. Ross and Kozy116 found that a delay to surgery of up to 1 week in macula-off rhegmatogenous retinal detachments did not affect final visual acuity. Expedited evacuation to a facility that has retinal surgery capability allows for more precise determination of the urgency for surgical repair. The presence of “floaters” in the field of vision is a very common occurrence among individuals who are middle aged or older. An acute awareness of floaters may be caused by certain activities, such as looking at a visually homogenous background (e.g., the sky). If the floaters are new in onset or suddenly more numerous than before or if they are accompanied by a sensation of flashing lights (i.e., photopsias), this suggests the possibility of posterior vitreous detachment (PVD), which is detachment of the vitreous face from the retina. PVDs are common, and they are usually not a problem, except for the annoying floaters; however, the suspicion of PVD should prompt a visit to the ophthalmologist as soon as is practical so that he or she can check to make sure that the PVD has not caused a retinal tear or detachment. Expedited evacuation from the wilderness environment is not required for floaters alone. If the victim is at a high altitude (i.e., >3048 m [10,000 feet]), high-altitude retinal hemorrhage, which is discussed later in this chapter, should be suspected; further ascent should be avoided.19 Descent of at least 915 m (3000 feet) should be undertaken as soon as is feasible.19 Another potentially treatable cause of sudden loss of vision in a white, quiet eye is central retinal artery occlusion (CRAO). Previous conventional therapy for CRAO of ocular massage, pentoxifylline, and anterior chamber paracentesis has been reported to be unsuccessful for restoring the vision in 40 of 41 patients with CRAO, even though 11 patients presented within 6 hours of visual loss and 17 patients presented within 12 hours.117 Primate retinas can tolerate no more than 100 minutes of is­ chemia caused by complete blockage of retinal blood flow.58 However, fluorescein angiography has shown that in humans CRAO is seldom complete and that therapy begun up to 6 hours after visual loss may be successful for restoring vision.117 Hyperbaric oxygen was reported to be successful for restoring vision on two separate occasions in one patient with recurrent branch retinal artery occlusions that were associated with Susac’s syndrome.81 Oxygen is supplied to the retina from both the retinal and choroidal circulations. Under normoxic conditions, approximately 60% of the retina’s oxygen is supplied by the choroidal circulation. Under hyperoxic conditions, the choroid is capable of supplying 100% of the oxygen required by the retina.81 When retinal arterial flow is interrupted, the retinal tissue undergoes a period of ischemia. Blood flow may be spontaneously reestablished, which frequently happens with arterial obstruction, or ischemia may continue until cell death and necrosis occur.87 The period of time during which the tissue is ischemic yet still capable of recovery is called the ischemic penumbra.87 Hyperbaric oxygen is not always required for a reversal of retinal ischemia. The author has treated a monocular patient who suffered CRAO in his only seeing eye and presented to the emergency department within an hour of visual loss. The victim’s vision improved from 20/400 to 20/25 within minutes after he received supplemental oxygen by mask. Unfortunately, however, his vision decreased rapidly to 20/400 whenever the supplemental oxygen was removed. The victim was heparinized and maintained on supplemental oxygen for approximately 10 hours, at which time the removal of oxygen no longer caused a decrease in vision. If oxygen is being carried for an extreme altitude summit attempt or for other purposes, a person with sudden painless loss of vision should be given a trial of oxygen administered in as high a concentration as possible to see if this therapy results in visual improvement. CRAO has been approved by the Undersea and Hyperbaric Medical Society as an indication for hyperbaric oxygen therapy.94 Other ocular indications for hyperbaric oxygen therapy have been summarized in a recent review article23 and textbook chapter.25 Ocular contraindications to and complications of hyperbaric oxygen therapy have also been recently summarized.22

PART 4  INJURIES AND MEDICAL INTERVENTIONS

History of trauma No

Yes

Fluorescein test

Obvious open globe

Positive

Negative or punctate staining only

No Fluorescein test Positive • Corneal abrasion • Corneal ulcer

Negative or variable

• Subconjunctival hemorrhage • Traumatic iritis • Hyphema • Occult ruptured globe

• Corneal ulcer • Corneal erosion • HSV keratitis

Response to topical anesthesia No relief

Pupillary status Normal or miotic

Dilated • Angle-closure glaucoma

• Iritis • Scleritis

Pain relieved (or no pain)

• Conjunctivitis • Blepharitis • UV keratitis • Conjunctival foreign body • Dry eye • Subconjunctival hemorrhage • Episcleritis • Contact lens overwear syndrome

FIGURE 28-2  Algorithm that shows the wilderness diagnostic procedure for the acute red eye.

requires surgical repair as soon as possible and should be evacuated as an emergency. Because there is a possibility that air may have been introduced into the eye, barometric pressure changes during evacuation should be minimized, if possible. However, this consideration is secondary to the need for expeditious transport to a facility where surgical repair can be performed. Emesis should be treated or prevented if antiemetic medications are available. The need for surgical intervention shortly after arrival at the hospital should be anticipated. The victim should not be allowed to become dehydrated as a result of a prolonged evacuation time from the wilderness setting, so plain water by mouth may be allowed up to several hours before arrival at the hospital. Occult Ruptured Globe A penetrating injury to the eye or a ruptured globe may not always be obvious. Clues to occult rupture include large subconjunctival hemorrhage with chemosis; dark uveal tissue that is present at the limbus; distorted pupil (Figure 28-4); fluorescein leak from a linear or punctate corneal epithelial defect; mechanism of injury (e.g., hammering metal on metal, impaling injury); or a decrease in vision. If an occult globe rupture is suspected, the victim should be treated as described previously for an

FIGURE 28-3  Obvious open globe (i.e., corneoscleral laceration). (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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obvious open globe. The relatively less severe appearance of the injury does not eliminate the threat of endophthalmitis, so systemic antibiotic therapy as noted previously should be initiated. Snakebite injuries to the eye are thankfully uncommon, but they may result in occult open globe injury as a result of penetration by teeth or fangs.5 If the snake is venomous, direct injection of toxin into the globe has been reported to cause necrosis, uveitis, and keratomalacia. Another type of penetrating ocular injury particular to the wilderness environment is injury to the eye from a fishhook that has become embedded in the globe or in the periocular tissues. Principles of management include protecting the eye from further injury by covering it with a shield, avoiding manipulation of the hook that may worsen known or suspected injury to the globe, beginning systemic antibiotics as soon as possible, and expediting evacuation of the victim to the care of an ophthalmologist. Corneal Abrasion A corneal abrasion is disruption of the protective epithelial covering of the cornea (Figure 28-5). This results in intense pain, tearing, light sensitivity (i.e., photophobia), and increased susceptibility to infection until the defect has healed, usually in 2 to 3 days. There is typically a history of antecedent trauma or

FIGURE 28-4  Occult open globe with uveal pigment at the limbus and a peaked pupil. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

contact lens wear. The sine qua non for this diagnosis is an epithelial defect on fluorescein staining. Standard treatment in the recent past consisted of antibiotic ointment followed by application of a pressure patch. A study showed that small (<10 mm2) and noninfected abrasions that were not related to contact lens wear healed significantly faster with less discomfort when they were not patched.69 Standard texts now note that patching is rarely used.39 In a wilderness setting, the nonpatching option has the additional advantages of not rendering the victim completely monocular and of not adversely affecting visual field and depth perception. If the nonpatching option is chosen, the victim should be treated with moxifloxacin 0.5% drops (one drop four times a day) or bacitracin ointment four times a day until the corneal epithelium is healed. Diclofenac drops four times a day should be helpful for reducing discomfort. Sunglasses may help to alleviate photophobia. Repeated use of a topical anesthetic for pain control is contraindicated. If the abrasion is contact-lens related, the eye should not be patched because of the increased risk of corneal ulcer that is present with a contactlens–related abrasion;111 contact-lens–related corneal abrasions should be treated with moxifloxacin 0.5% drops (one drop every 2 hours while awake) until the epithelial defect has resolved. An abrasion that is associated with vegetable matter should also not be patched.111 If the abrasion is large or if the victim’s discomfort is severe, scopolamine drops once or twice a day may be added to the antibiotic (wait 5 minutes between each drop). Much of the pain that is associated with corneal abrasion and ulcer is the result of ciliary muscle spasm, which is relieved by scopolamine. The rationale for using scopolamine only with a very painful abrasion in the wilderness is that this medication will cause the pupil to dilate (and the eye to become very sensitive to light) and lose accommodation (with a resultant decrease in near visual acuity) for approximately 5 to 7 days. Contact lenses should not be worn until the abrasion has resolved.39 An oral analgesic may be required for pain control. The victim should be monitored daily for development of a corneal ulcer, which is noted on penlight examination as a white or gray infiltrate on the cornea, and for progress in healing of the epithelium as measured by the resolution of fluorescein staining. Corneal Ulcer The term corneal ulcer, as used in this chapter, denotes acute bacterial, fungal, or protozoal infection of the cornea. Chronic corneal epithelial defects caused by a variety of autoimmune or inflammatory processes are also referred to with this term at times, but these disorders are beyond the scope of this chapter. Although a corneal ulcer (Figure 28-6) is an infectious process, it is often preceded by a traumatic corneal abrasion. The other predisposing condition for a corneal ulcer is contact lens wear, which results in microtrauma to the corneal epithelium and may allow bacteria or other microorganisms to infect the cornea. Corneal ulcers are typically significantly painful. A small white or gray infiltrate on the cornea can be appreciated by a careful penlight examination. If it is not treated aggressively, the small initial lesion may progress to the much larger infiltrate (see Figure 28-6), with a correspondingly more severe impact on visual acuity. Fluorescein staining reveals an epithelial defect overlying the infiltrate. The associated pain is usually significantly decreased

Traumatic Iritis The term iritis refers to inflammation of the iris or, more accurately, of the anterior uveal tract of the eye; it may also be called anterior uveitis or iridocyclitis. The defining feature of this condition is inflammatory cells in the anterior chamber of the eye, which must be visualized with a slit lamp. In the wilderness, this diagnosis must be presumptive. Iritis may accompany a corneal abrasion, or it may result from blunt trauma. The diagnosis rests primarily on the presence of significant post-traumatic pain without a corneal abrasion or ulcer noted on fluorescein staining or on pain that persists after the abrasion is healed. Treatment is with one drop of prednisolone four times a day for 3 days. One drop of scopolamine twice a day may be added if pain is severe enough to justify the blurred vision that results from this therapy. Expedited evacuation should be undertaken if severe pain persists. Subconjunctival Hemorrhage Subconjunctival hemorrhage (Figure 28-7) is a bright red area over the sclera of the eye that results from bleeding between the conjunctiva and the sclera. It is easily visible without the use of a slit lamp. This injury is innocuous and resolves over a period of several days to several weeks without treatment. In the presence of antecedent trauma, one should be alert for another more serious injury. In particular, if hemorrhage results in massive swelling of the conjunctiva (i.e., chemosis), then an occult globe rupture should be suspected. Hyphema The term hyphema is defined as blood in the anterior chamber. Although this is usually seen in the setting of acute trauma, it

FIGURE 28-6  Corneal ulcer. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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CHAPTER 28  The Eye in the Wilderness

FIGURE 28-5  Corneal abrasion. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

by applying a topical anesthetic, but ciliary spasm may cause pain relief to be incomplete. An inadequately treated corneal ulcer may result in visual loss from dense corneal scarring or ocular perforation with subsequent endophthalmitis. Management of this disorder in the past included hospital admission for treatment with concentrated and frequently administered aminoglycoside and cephalosporin topical drops. Outpatient therapy with fourth-generation fluoroquinolone eye drops has been shown to be comparable in efficacy with fortified antibiotic preparations.63,100 Thus, treatment for corneal ulcer should be with moxifloxacin 0.5% drops as follows: one drop every 5 minutes for five doses initially, then one drop every 30 minutes for 6 hours, and then one drop every hour thereafter around the clock.111 One drop of scopolamine given two to four times a day may help to relieve the discomfort that is caused by ciliary spasm. Repeated use of topical anesthetics for pain control is contraindicated. Moxifloxacin (400 mg by mouth once a day) may be added if evacuation is delayed and either the infiltrate or the victim’s pain is becoming worse.39 Systemic analgesia may be required if pain is severe. Expedited evacuation and immediate evaluation by an ophthalmologist are recommended.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 28-7  Subconjunctival hemorrhage. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

FIGURE 28-9  Herpes simplex virus keratitis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

may also be caused by other conditions, such as iris neovascularization. The eye should be examined with the victim sitting upright. If enough blood is present, it collects at the bottom of the anterior chamber and is visible as a layered hyphema (Figure 28-8). This may not be appreciated if the victim is examined while in a supine position or if the amount of blood is very small. Although most hyphemas resolve without sequelae, this disorder may be complicated by an acute rise in intraocular pressure or corneal blood staining. Treatment in the wilderness consists of activity restriction (i.e., walking only), prednisolone drops four times a day, avoidance of aspirin or nonsteroidal anti-inflammatory drugs, and use of a rigid eye shield until the hyphema has resolved. Do not use a pressure patch. Diamox (250  mg four times a day by mouth) should be added, if available, to treat potentially increased intraocular pressure. The victim should be maintained in a head-up or head-elevated posture, if possible, to promote settling of the hyphema and clearing of vision. Pain should be managed with acetaminophen or another analgesic medication that does not impair platelet function. Retinal injury or an occult ruptured globe may accompany traumatic hyphema. A hyphema victim requires ophthalmologic evaluation, so expedited evacuation should be undertaken. If a hyphema victim experiences improvement of vision followed by a sudden worsening of vision, this may indicate that a rebleed or retinal detachment has occurred, and emergency evacuation should be considered.

simplex virus keratitis. Treatment is with trifluridine 1% drops nine times a day.111 Treatment is continued until the corneal staining has resolved, at which time the frequency of dosing is reduced to four times a day for 1 week. Trifluorothymidine was not included in the list of eye medications to be taken on the expedition because trifluorothymidine drops require refrigeration. If a significant delay is anticipated before evacuation, herpes simplex virus keratitis may be treated by giving three to five drops of tetracaine 1 minute apart to anesthetize the cornea and then performing a gentle cotton-tipped applicator debridement of the epithelial lesion.111 The resulting epithelial defect should then be treated as described previously in the Corneal Abrasion section.

NONTRAUMATIC FLUORESCEIN-POSITIVE ACUTE RED EYE Herpes Simplex Virus Keratitis The essential element in this diagnosis is the characteristic dendritic epithelial pattern on fluorescein staining (Figure 28-9). There will often be a history of previous episodes of herpes

FIGURE 28-8  Hyphema. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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Corneal Erosion A corneal erosion is an epithelial defect that is caused by nontraumatic disruption of the corneal epithelium. The fluorescein staining pattern seen with corneal erosion may be identical to that seen with corneal abrasion; pain and photophobia are present with both disorders. The diagnosis is made when the apparent corneal abrasion has no history of trauma to explain its presence. There is often a history of previous similar episodes. The two primary causes of corneal erosion are corneal dystrophies and previous ocular trauma.104 Recurrent corneal erosions are believed to be caused by a defect in healing between the hemidesmosomes of the corneal epithelium and the underlying basement membrane.83 At night, the epithelium may become adherent to the closed eyelid during sleep. When the individual awakens and opens his or her eyes, the corneal epithelium is pulled away from the basement membrane by movement of the lid; this accounts for the typical history of acute onset of pain on awakening. Signs and symptoms include red eye, pain, tearing, foreign-body sensation, and usually an epithelial defect, although this may be a variable sign, depending on when the patient is evaluated.83 Treatment of these lesions may be difficult. The cornea should be inspected for a loose sheet of epithelium that remains partially attached to the corneal surface. If this is present, try to debride it with a cotton-tipped applicator after topical anesthesia with tetracaine. The lesion is then managed initially in the same manner as a corneal abrasion. There is a high rate of recurrence if follow-up treatment with 5% sodium chloride ointment each evening or anterior stromal puncture is not undertaken. Corneal Abrasion and Corneal Ulcer With Contact Lens Wear Both corneal abrasions and corneal ulcers may occur as complications of contact lens wear; management of these conditions has been described earlier. Contact-lens–related corneal abrasions have a relatively high incidence of progressing to corneal ulcers.69 Therefore, they should not be patched, and should receive topical antibiotic therapy with moxifloxacin 0.5% drops every 2 hours while awake until the epithelial defect has resolved. Contact lens wear in both eyes should be discontinued immediately. If an ulcer is related to contaminated lens solutions,

NONTRAUMATIC FLUORESCEIN-NEGATIVE ACUTE RED EYE WITH PAIN THAT IS NOT SIGNIFICANTLY IMPROVED BY TOPICAL ANESTHESIA Acute Angle-Closure Glaucoma This diagnosis is easily made when the intraocular pressure can be measured with a tonometer. Intraocular pressure is normally between 10 and 21 mm Hg. With acute angle-closure glaucoma, the pressure may increase to 50 or 60 mm Hg or more. Although handheld tonometers are available, they will not often be present outside of hospitals or clinics. The most important clues to the diagnosis of angle-closure glaucoma in the wilderness setting are the characteristics of the pain and the status of the pupil. Angleclosure glaucoma victims do not have the mild burning or foreign-body–type pain that is typically seen with conjunctivitis, blepharitis, or other external eye diseases. Angle-closure glaucoma produces pain that is usually deep and severe. Although corneal abrasions and corneal ulcers may also be accompanied by severe pain, the pain associated with these two disorders is usually significantly relieved by topical anesthetics. This is not true of the pain that is seen with acute glaucoma, scleritis, or iritis. With these disorders, the pain is rarely if ever significantly relieved by topical anesthetics. With acute angle-closure glaucoma, the pupil is usually found to be mid dilated (i.e., 6 to 7 mm), and vision is usually decreased. This disorder generally affects persons who are more than 50 years old,83 and it is more common among persons of Asian ethnic origins. There is often a history of previous transient episodes of eye pain. Nausea and vomiting may be present. An eye with acute angle-closure glaucoma is shown in Figure 28-10. Some wilderness expeditions now carry portable instruments such as a Tono-Pen to measure intraocular pressure. Updated operating instructions for the Tono-Pen can be found at http://www.tonopen.com. The usual treatment is with topical antiocular hypertensive medications and laser iridotomy, which allows the aqueous humor to bypass the pupillary block. This relieves the angle closure, with a resultant decrease in intraocular pressure.83 In the wilderness setting, treatment should be with 2% pilocarpine, with one drop given every 15 minutes for four doses104 and then one drop given four times a day in both eyes, because there is a high rate of the subsequent occurrence of angle-closure glaucoma in the second eye. Pilocarpine alone may be successful for relieving the angle closure and lowering the pressure, but this is not a reliably effective treatment, because ischemia of the pupillary sphincter muscle may prevent pilocarpine from exerting its miotic effect. Diamox (250 mg four times a day by mouth) should be added, if available. Emergency evacuation should occur if pain is not relieved, because even a single day of very high intraocular pressure may result in permanent damage to the optic nerve and loss of vision.

FIGURE 28-10  Angle-closure glaucoma. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

FIGURE 28-11  Nontraumatic iritis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Nontraumatic Iritis Signs and symptoms of nontraumatic iritis that may be appreciated without a slit lamp include pain, redness, photophobia, limbal flush, and decreased vision.104 There is often a history of previous episodes. An eye with nontraumatic iritis is shown in Figure 28-11 (the pupil is iatrogenically dilated). Iritis that is not associated with corneal trauma is typically more severe than that of the traumatic variety, but it may range from mild to very severe, and it is typically not significantly relieved by topical anesthesia. Fluorescein staining is negative, and the pupil is usually miotic, thereby helping to differentiate iritis from angleclosure glaucoma. Iritis is far more common than angle-closure glaucoma, and it may be associated with a number of systemic infectious and inflammatory diseases. In the wilderness setting, the emphasis should be on immediate treatment with prednisolone 1%, with one drop given every hour while awake. Scopolamine 0.25% (one drop one to four times a day) may be added for pain control and to prevent posterior synechiae (i.e., pupillary scarring) if inflammation is severe. If pain is not significantly decreased after 24 to 48 hours, 80 mg of oral prednisone per day should be added to the treatment regimen and maintained until evacuation. Evacuation should be expedited, because posterior synechiae and elevated intraocular pressure may develop. Scleritis It may be difficult to differentiate between nontraumatic iritis and scleritis without a slit lamp, but scleritis is much less common than iritis. The characteristics of the pain are similar, with photophobia, scleral injection, and tearing also being present.104 Scleritis is often associated with rheumatologic disease, and it may be either nodular or diffuse.104 The diffuse form of scleritis is shown in Figure 28-12. The initial treatment of scleritis in the wilderness setting involves topical prednisolone (one drop every hour while awake) and a nonsteroidal antiinflammatory drug.

FIGURE 28-12  Diffuse scleritis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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CHAPTER 28  The Eye in the Wilderness

infection in the first eye may be followed rapidly by a similar occurrence in the other eye.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Prednisone (80 mg/day) should be added if there is no improvement after 24 to 48 hours, and it should be maintained until an expedited evacuation is accomplished.

NONTRAUMATIC FLUORESCEIN-NEGATIVE ACUTE RED EYE WITH NO DISCOMFORT OR DISCOMFORT THAT IS IMPROVED BY TOPICAL ANESTHESIA Conjunctivitis One of the most common disorders in this diagnostic category is conjunctivitis. Etiologic agents of infectious conjunctivitis include bacteria, viruses, Chlamydiae, fungi, and parasites.83 Acute allergic conjunctivitis may also be encountered, especially in a wilderness setting. The keys to diagnosis are the presence of discharge or tearing, relatively mild burning or foreign-body– type discomfort that is relieved by topical anesthesia, and a negative or SPK fluorescein staining pattern. The diagnosis of conjunctivitis should be questioned in the absence of discharge or tearing. The primary exception to this statement is allergic conjunctivitis, which may not generate a significant discharge. In this case, bilaterality, significant ocular itching, and a history of ocular or systemic allergies help with making the diagnosis. With infectious conjunctivitis, there are often signs or symptoms of an accompanying upper respiratory infection or a history of contact with other persons who have recently suffered from conjunctivitis. Treatment of conjunctivitis in the wilderness setting is with moxifloxacin 0.5% drops (one drop four times a day for 5 days) if there is a yellowish discharge. Ciprofloxacin 0.3% drops, ofloxacin 0.3% drops, tobramycin 0.3% drops, or trimethoprim and polymyxin B drops are acceptable alternatives.83 This should be an adequate treatment time if the conjunctivitis is bacterial. Symptoms that persist for more than 5 days suggest a viral etiology. These symptoms may take several weeks to clear, just as some viral upper respiratory infections take several weeks to resolve. If there is only tearing or a watery discharge or if there is associated upper respiratory infection that suggests a viral etiology, treatment with artificial tears and cool compresses may be substituted for antibiotic therapy. The victim should be instructed regarding infection precautions, because viral conjunctivitis can spread rapidly through a group. This is especially true if the discomfort that is caused by conjunctivitis is severe and accompanied by significant photophobia. These symptoms suggest epidemic keratoconjunctivitis, which, in addition to having a prolonged course, is very uncomfortable because of the corneal involvement. The cornea of an eye with epidemic keratoconjunctivitis is shown in Figure 28-13. Sunglasses should be part of the treatment. One drop of scopolamine two to four times a day may be required to reduce discomfort. As noted previously, if the predominant ocular symptom is itching, allergic conjunctivitis should be suspected. Allergic conjunctivitis may be treated with cool compresses or systemic antihistamines. Severe ocular itching may be treated with a 3-day course of prednisolone (one drop four times a day).

FIGURE 28-13  Epidemic keratoconjunctivitis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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FIGURE 28-14  Blepharitis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Hyperacute conjunctivitis with marked lid edema, conjunctival hyperemia, chemosis, and copious purulent discharge should alert the health care provider to the possibility of a gonococcal etiology.83 Gonococcal conjunctivitis may progress to visionthreatening keratitis and should be treated aggressively with moxifloxacin (400 mg orally once a day), moxifloxacin drops four times a day, and expedited evacuation. If the conjunctivitis is chronic and associated with a preauricular node and conjunctival follicles, then the individual will require additional therapy with doxycycline (100 mg twice a day for 14 days) as treatment for a possible chlamydial infection.79 Sexual partners should also be treated for chlamydial infections; follow up with an ophthalmologist, when feasible, is also recommended. Both the bacterial and viral types of conjunctivitis are highly contagious. Individuals with infectious conjunctivitis should be informed of this fact, and the importance of infection precautions should be emphasized. Blepharitis Blepharitis is probably the most common external eye disease that is seen in the general ophthalmologist’s office.37 It is often misdiagnosed as conjunctivitis. Differentiation may often be made with the use of the patient’s history. Blepharitis tends to be a bilateral and chronic disease with recurrences and exacerbations. There is chronic flaking and irritation of the skin at the base of the eyelashes that may occasionally be complicated by a bacterial superinfection. An eye with blepharitis is shown in Figure 28-14. There may be an association with skin disorders, such as seborrheic dermatitis or acne rosacea.37 The victim often has a history of chronic ocular itching and burning. Fluctuating vision may be present as well.37 There is often a history of excessive mucus discharge in the eyes on waking. Treatment for blepharitis should focus on the lid margins. Bacitracin or erythromycin ophthalmic ointment should be applied thinly to the lid margins at bedtime for 4 weeks. Lid hygiene is directed at reducing the amount of debris on the lid margins and consists of warm, moist compresses applied to the eyelids one to four times a day for 5 to 10 minutes followed by gently wiping away the moistened lash debris. Artificial tears may relieve the sensation of “dry eye” that often accompanies blepharitis.37 Ultraviolet Keratitis The diagnosis of UV keratitis is easy to make in the presence of a severely sunburned face and bilateral red, painful eyes. The discomfort typically does not start until 6 to 10 hours after UV exposure, and it may awaken the victim.104 Symptoms range from mild irritation and foreign-body sensation to severe pain, photophobia, and lid spasm.104 Fluorescein staining usually reveals a punctate staining pattern. Treatment consists of moxifloxacin drops four times a day. Bacitracin or erythromycin ophthalmic ointment applied to the eye four times a day is an acceptable alternative. Sunglasses help with the severe light sensitivity that accompanies this disorder. In a severe case, one or both eyes may be patched to help with

FIGURE 28-15  Conjunctival foreign body. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

pain control, although it may be better to patch only the more severely affected eye so that the victim is not deprived of vision in both eyes.19 Scopolamine (one drop twice a day) may be added for pain control. Systemic analgesia may also be required. The victim should be reexamined every day until there is no longer an SPK pattern present on fluorescein staining, at which time antibiotic therapy may be discontinued. The duration of discomfort from UV keratitis is typically 24 to 48 hours.104 Conjunctival or Corneal Foreign Body The symptom of ocular foreign-body sensation does not necessarily mean that a conjunctival or corneal foreign body is present. Although the presence of a conjunctival foreign body may be strongly suspected on the basis of the abrupt onset of discomfort after a gust of wind or other mechanism for depositing foreign material in the eye, definitive diagnosis requires visualization of the offending material, which may sometimes be quite difficult. Figure 28-15 shows an eye with a conjunctival foreign body. The victim is often able to help with foreign-body localization before the instillation of topical anesthetic drops. Treatment consists of a careful search for the foreign body with the use of adequate lighting. Topical anesthesia makes the victim much more agreeable during the search and removal efforts. A handheld magnifying lens or a pair of reading glasses provides magnification to help with visualizing the foreign body. Eyelid eversion with a cotton-tipped applicator helps the examiner to identify foreign bodies that are located on the upper tarsal plate. After it has been located, the foreign body should be removed with fine forceps or a cotton-tipped applicator when the eye has been anesthetized and the cotton-tipped applicator moistened with tetracaine. The eye is then stained with fluorescein to check for a corneal abrasion. If no foreign body is visualized but the index of suspicion is high, vigorous irrigation with artificial tears or sweeps of the conjunctival fornices with a moistened cotton-tipped applicator after topical anesthesia may be successful for removing the foreign body. Several types of foreign bodies merit special mention. If the foreign body that is identified is one that may have penetrated into the eye (e.g., a large thorn), then the victim should be managed as described previously in the Obvious Open Globe section. Hot ashes or cinders from a campfire may strike the eye and result in both a foreign body and a thermal burn. Immediate instillation of topical anesthesia provides temporary pain relief to facilitate foreign-body removal and also stops ongoing thermal injury. Multiple or loose conjunctival foreign bodies may be best managed with saline irrigation.39 After the foreign body has been removed, the corneal abrasion that typically results from a thermal injury to the cornea should be managed as outlined previously in the Corneal Abrasion section. Dry Eye Symptomatic dry eye is commonly encountered in the wilderness, especially in mountainous areas where the air is very dry and where significant wind is often present.19 Dry eye is usually bilateral, and may result in secondary tearing.111 There may be a

Contact Lens Overwear Syndrome The considerations here are much as described in the Dry Eye section, except that the symptoms are magnified by the presence of contact lenses. Contact lens rewetting drops and sunglasses are the first line of management. If these measures are ineffective for relief of symptoms, then the contact lenses should be removed. If significant SPK is present on fluorescein staining, moxifloxacin drops (one drop four times a day) should be used until SPK has resolved.19 Contact lenses should not be replaced in the eye until the eye is symptom free. An individual who wears contact lenses in the wilderness should always carry a pair of glasses that can be used if contact lens problems arise. Episcleritis Episcleritis is a benign, self-limited, inflammatory condition of the lining of the eye between the conjunctiva and the sclera.83 There is usually sectoral redness without discharge (Figure 28-16), although the redness may be diffuse in some cases.39 There is often a history of previous episodes, and discomfort is typically mild or absent. Presence of severe pain, photophobia, or decreased vision suggests another diagnosis. Episcleritis is often misdiagnosed as conjunctivitis, but lack of a discharge and sectoral redness that are usually seen with episcleritis help to differentiate between the two disorders. Episcleritis is usually self-limited, and it resolves without treatment in 3 to 4 weeks.83 If symptoms are troublesome, the condition may be treated with prednisolone drops four times a day for 3 days.

Solar Retinopathy The retina is protected from UV radiation damage, because this high-energy radiation is absorbed by the cornea and the lens of the eye. However, visible and near-infrared light of sufficient intensity may reach the retina and cause photochemical damage.83 In the wilderness setting, this would most likely occur as the result of staring at the sun or a solar eclipse. Shortly after such an exposure, the individual may experience blurred or distorted vision, a central scotoma, or a headache. Visual acuity is often reduced to the 20/40 to 20/70 range. There is no effective therapy for this injury, but visual acuity may return to normal over a period of several months in mild cases.

FIGURE 28-16  Episcleritis. (Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

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CHAPTER 28  The Eye in the Wilderness

history of previous episodes of symptomatic dry eye. Individuals with chronic dry eye are usually middle aged or older, and they may have a history of autoimmune disorders. Treatment is with artificial tears that are used as often as needed to relieve symptoms. Dehydration may contribute to this condition, and adequate fluid intake should be maintained. The use of sunglasses may provide protection from the wind and be of significant benefit for management of this disorder. Highviscosity drops (e.g., Celluvisc) and lubricating ointments used at bedtime may also help to relieve symptoms.84 In more severe cases, reversible punctal occlusion may be considered as well.84

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Locating a Displaced Contact Lens Wearers of soft contact lenses may occasionally have one of their lenses become displaced, which results in blurred vision and a foreign-body sensation. When the lens is displaced, it may be hard to locate. The conjunctival fornix of the lower lid is easily examined by distracting the lens from the globe with gentle downward finger pressure applied to the lower lid. If the contact lens has been displaced into the superior conjunctival fornix, which is usually the case, it may be more difficult to locate. If visual inspection with a penlight and a handheld magnifying lens is not successful for finding the lens, gentle digital massage over the closed upper lid that is directed toward the medial canthus often results in the contact lens emerging at that location. Several minutes of massage may be required. A few drops of artificial tears often facilitate the process. If this maneuver is unproductive, the eye may be anesthetized with a drop of tetracaine, the upper lid distracted from the globe with upward finger pressure, and the fornix swept with a moistened cotton-tipped applicator.

Improvisation If you encounter a person with known or suspected globe rupture, it is of paramount importance to ensure that subsequent inadvertent trauma does not cause extrusion of the ocular contents. If an eye shield is not available, one may be fashioned with duct or rigger’s tape and any available rigid flat or concave object that can be placed over the eye. Examples include small cups or bowls to provide a good standoff distance between the eye and improvised shield. Improvised wound closure strips can be made by tearing rigger’s or duct tape into 1 4 -inch widths. Spectacles and sunglasses can be improvised by making a pinhole in a piece of paper or cardboard. (Make the pinholes before placing the paper or cardboard in front of the eyes.) Take note of the restriction in peripheral vision that is caused by use of pinhole glasses. If the purpose is to improvise sunglasses rather than to achieve a refractive effect, the pinhole can be larger or fashioned into a horizontal slit to improve peripheral vision. Improvised magnifying glasses for examining the eye or other small areas may be made by simply using a pair of reading or hyperopic glasses. Another refractive improvisation technique involves a handheld magnifying lens. This convex lens, with its plus refracting power, can be used to provide a variety of hyperopic refractive corrections by moving the lens to various distances in front of the eye.

The Eye at Altitude Ocular disorders that are associated with altitude exposures have been addressed in several recent review articles.19,70,84

TABLE 28-1  Pressures and Equivalent Oxygen

Fractions at Altitude

Feet

Meters

Sea level 4000 7000 10,000 15,000 20,000 25,000 29,028

Sea level 1219 2134 3048 4572 6096 7620 8848

Atmospheric Equivalent Partial Pressure Pressure of Oxygen of Oxygen (mm Hg) (%) (mm Hg) 760 656 586 523 429 347 282 253

20.9 18.0 16.1 14.4 11.8 9.5 7.8 7.0

159 137 122 109 89 73 60 53

HIGH-ALTITUDE RETINAL HEMORRHAGE There are many reports of retinal hemorrhages (Figure 28-17) in mountain climbers. These have been described as high-altitude retinal hemorrhages (HARHs) or as part of the more inclusive term altitude retinopathy.24 A classification for HARH has been developed by Weidman.142,143 Butler and colleagues24 reported a 29% incidence of HARH among climbers on a Mt Everest expedition at altitudes that ranged from 5300 to 8200 m (17,385 to 26,896 feet). McFadden and co-workers88 found that 56% of their subjects had HARH at an altitude of 5360 m (17,581 feet) and that one had a retinal nerve fiber layer infarct (i.e., a cotton wool spot) (Figure 28-18). They also reported that exercise at altitude was associated with both an increased incidence of HARH and fluorescein leakage from the retinal vessels. Hackett and Rennie53 described HARH in 4% of 140 trekkers examined at 4243 m (13,917 feet) at Pheriche in the Himalayas. These authors also found a significant correlation of retinal hemorrhages with symptoms of acute mountain sickness. Kobrick and Appleton72 found no retinal hemorrhages among eight subjects who were examined after 48 hours at 4573 m (15,000 feet) in a hypobaric chamber, although all subjects displayed the marked vascular engorgement and tortuosity that was typical of the eye at altitude (Figure 28-19). HARH developed in 19 of 21 climbers who climbed above 7600 m (25,000 feet). Fourteen of 19 climbers who climbed to between 4880 and 7600 m (16,000 and 25,000 feet) were found to have retinopathy.149 Differences in the incidence of HARH for exposures at similar altitudes may be the result of differences in time at altitude before examination, acclimatization schedule, exercise levels, examination techniques, and the presence of concurrent conditions that may predispose an individual to HARH.

ALTITUDE EXPOSURES AND OCULAR PHYSIOLOGY A number of significant effects on visual function that result from the hypoxia of altitude were described by Wilmer and Berens151 in their classic article, and they were also discussed later by Sharma.120 The decrease in ambient pressure at altitude causes hypobaric hypoxia despite a constant oxygen fraction of 0.21, as noted in Table 28-1. Retinal blood flow has been shown to increase by 128% after 4 days at 5300 m (17,384 feet).48 This increase in blood flow results in clinically observable changes, such as an increase in the diameter and tortuosity of retinal vessels and optic disc hyperemia, which are seen in most unacclimatized persons at altitudes of more than 4573 m (15,000 feet).48,72,88,110 Because of its avascularity, the cornea receives most of its oxygen supply from the surrounding atmosphere,127 so it may suffer hypoxic dysfunction, even if the inspired gas mix is not hypoxic, as noted in the section about Refractive Changes at Altitude After Refractive Surgery, later. This is an important factor when considering topics such as the suitability of contact lenses and refractive surgical procedures for mountaineers and aviators. 572

FIGURE 28-17  High-altitude retinal hemorrhages. (Courtesy Dr. M. McFadden, University of British Columbia, Vancouver, British Columbia. In association with Dr. C. Houston, Burlington, Vermont; Dr. G. Gray, Canadian Defense and Civil Institute of Environmental Medicine, Toronto, Ontario; and Drs. J. Sutton and P. Powells, McMaster University, Hamilton, Ontario, Canada.)

High-altitude retinal hemorrhage has been reported to be associated with both altitude headache and a history of vascular headache at sea level.118 Rimsza and colleagues112 noted that HARH may occur at lower altitudes among individuals with chronic lung disorders that interfere with oxygenation. Their case report described a woman with cystic fibrosis who had climbed as high as 3049 m (10,000 feet) but was at 1677 m (5500 feet) when she noted a sudden decrease in vision that was associated with preretinal hemorrhage of the right eye. They also noted that the ocular findings of cystic fibrosis are similar to those seen with altitude retinopathy.112 Although HARHs are often not associated with acute visual symptoms,24,110,150,155 they may result in a loss of visual acuity or paracentral scotomas.47,78,122,150 Lang and Kuba78 reported on a person who experienced decreased visual acuity and central scotoma from HARH as a result of a 7000-m (22,960-foot) altitude exposure. Permanent deficits in visual function are uncommon but have been reported.122,150 Shults and Swan122 reported that four survivors of an ill-fated Aconcagua expedition in Argentina

INTRAOCULAR GAS BUBBLES AT ALTITUDE Presence of an intraocular gas bubble presents a hazard for anyone who is exposed to a change in ambient pressure. Intraocular gases are frequently used to provide internal tamponade during and after vitreoretinal surgery. Three patients described by Hart and associates57 lost vision in their eyes with intraocular gas after subsequent nitrous oxide (N2O) general anesthesia. All three patients suffered visual loss as a result of presumed retinal artery occlusion caused by expansion of the intraocular gas by N2O administration during general anesthesia.57 N2O is a highly soluble inhalational anesthetic agent that diffuses rapidly down its concentration gradient into an intraocular gas bubble. N2O is known to increase intraocular gas bubble volume during general anesthesia.153 Resulting expansion of the bubble can lead to a rapid rise in intraocular pressure.128 Growth of intraocular gas bubbles can also be caused by exposure to reduced atmospheric pressure during air travel.73,91 Even small bubbles can cause symptomatic rises in intraocular pressure. The patient with residual intraocular gas who experiences pain or dimness of vision in an ascending airplane can obtain relief if the cabin altitude is decreased to 610 m (2000 feet).82 A patient who had a scleral buckle and pneumatic retinopexy with a residual gas bubble 2 weeks before a commercial airline flight experienced sudden blindness, presumably from gas

FIGURE 28-19  The normal fundus at sea level (left). The same fundus at 5400 m (17,712 feet; right). Note the vascular engorgement and tortuosity at altitude. (Courtesy Dr. M. McFadden, University of British Columbia, Vancouver, British Columbia. In association with Dr. C. Houston, Burlington, Vermont; Dr. G. Gray, Canadian Defense and Civil Institute of Environmental Medicine, Toronto, Ontario; and Drs. J. Sutton and P. Powells, McMaster University, Hamilton, Ontario, Canada.)

573

CHAPTER 28  The Eye in the Wilderness

FIGURE 28-18  Cotton wool spots seen at 5400 m (17,712 feet). This occurred in a climber after the Valsalva maneuver was performed and represents the most severe form of retinopathy. (Courtesy Dr. M. McFadden, University of British Columbia, Vancouver, British Columbia. In association with Dr. C. Houston, Burlington, Vermont; Dr. G. Gray, Canadian Defense and Civil Institute of Environmental Medicine, Toronto, Ontario; and Drs. J. Sutton and P. Powells, McMaster University, Hamilton, Ontario, Canada.)

in 1973 were found to have severe HARH after an altitude exposure of 6860 m (22,500 feet). Two of the survivors apparently suffered permanent paracentral scotomas. No reports were found of progressive decrease in visual acuity or of progressive enlargement of paracentral scotomas as a result of remaining at altitude after development of HARH.19 Wiedman150 reported a case in which further ascent after development of HARH resulted in additional lesions. HARH that results in decreased visual acuity should be a contraindication to further ascent.19 Butler and colleagues24 recommended that evacuation of individuals with decreases in visual function as a result of HARH (in the absence of high-altitude cerebral edema or high-altitude pulmonary edema) be considered nonemergent unless reexamination indicates progressive deterioration of vision or increasingly severe retinopathy. HARH resolves over a period of 2 to 8 weeks after the altitude exposure is terminated.150 Recognizing advancing grades of HARH may allow physicians to recommend initiating treatment with oxygen, steroids, diuretics, and immediate descent to prevent HARH progression, macular involvement, or potentially fatal high-altitude cerebral edema. High-altitude retinopathy is both a significant component of and a predictor of progressive altitude illness.149

PART 4  INJURIES AND MEDICAL INTERVENTIONS

bubble expansion with resultant central retinal artery occlusion when the aircraft ascended to a cabin pressure of 2440 m (8000 feet).107 The mechanism of this injury is presumed to be a rise in intraocular pressure that exceeded central artery pressure, thereby collapsing the artery. The patient’s symptoms were relieved when an onboard flight surgeon recognized the problem and cabin pressure was reset to 610 m (2000 feet).107 The same problem can occur if an individual with an intraocular gas bubble ascends certain altitudes during mountaineering.55 Fang and Huang41 reported a case of a 46-year-old man who ascended to an altitude of 1893 m (6210 feet) after vitreoretinal surgery with a residual perfluoropropane bubble in his right eye. He noted a sensation of fullness in his right eye that was accompanied by loss of vision. When he returned to sea level, his intraocular pressure was found to be 54 mm Hg. The cause of this vision loss was believed to be central retinal artery occlusion caused by expansion of intraocular gas during mountain travel.41

CORTICAL BLINDNESS AT HIGH ALTITUDE Hackett52 reported six cases of cortical blindness at high altitude. These victims were found to have intact pupillary reflexes. Descent, Gamow (hyperbaric) bag recompression, or supplemental oxygen breathing should be used in persons with such neurologic dysfunction at altitude.

OCULAR MOTILITY Kramar and colleagues75 reported that convergence insufficiency was found in women with altitude illness. Basnyat7 noted that lateral gaze palsy and other focal neurologic deficits, often in the absence of other symptoms of acute mountain sickness or highaltitude cerebral edema, are seen commonly by physicians who are working for the Himalayan Rescue Association. Rennie and Morrissey110 reported on a person with nystagmus at altitude that was associated with ataxia and intention tremor. Ocular motility abnormalities should be managed in the same way as cortical blindness at high altitude, which was described in the preceding section.

CONTACT LENSES IN MOUNTAINEERING 28,155

Contact lenses may be used successfully at high altitude. Clarke28 noted that contact lenses were used successfully by five members of the British Everest Expedition in 1975 up to altitudes of as high as 7317 m (24,000 feet). The use of contact lenses at altitude during trekking or mountaineering entails several considerations beyond those that are encountered with normal use. In general, overnight use of extended-wear contact lenses is not recommended because of the associated increased rate of microbial keratitis. Even soft contact lenses decrease oxygen that is available to the cornea. Lid closure during sleep further accentuates corneal hypoxia. However, removing contact lenses at night presents logistical problems in the mountaineering setting. Practicing acceptable lens hygiene during an expedition is difficult. The mountaineer who leaves contact lenses in a case that is filled with liquid solution in the tent outside of his or her sleeping bag at night may awaken to find the solution and lenses frozen solid. Finally, wearing contact lenses can make eyes more sensitive to glare.44 Guidelines for military personnel who are using contact lenses in austere environments have been developed in the past, and, although contact lenses are no longer recommended for use in deployed field settings in the military, these guidelines may be applied with caution to the expedition setting:19 1. Disposable extended-wear lenses may be left in the eye for up to 1 week. If the wearer is still in the field at the end of this period, the lenses should be removed and discarded. After an overnight period without lenses, new lenses may be inserted, with strict attention paid to contact lens hygiene. 2. Contact lens wearers should always have backup glasses available for use in the wilderness in case a lens is lost or becomes painful. 574

3. Individuals who wear contact lenses on expeditions should carry both fluoroquinolone eye drops and contact lens rewetting solution. Both types of drops may freeze if they are not protected from the cold. 4. Contact lens wearers often note that their eyes become dry. This discomfort may be alleviated with contact lens rewetting drops. 5. Contact lens wearers often note increased sensitivity to sunlight. Individuals who wear contact lenses in the field during daylight hours should carry sunglasses. Continuous wearing of disposable contact lenses for a week that is followed by discarding the lenses and insertion of fresh lenses after an overnight period without a lens is a controversial approach to contact lens wear in an expedition setting. Whether the reduction in lens handling offsets the increased risk of microbial keratitis that results from overnight wear is unknown. The decision to wear contact lenses while mountaineering should be made carefully. Microbial keratitis (corneal ulcers) can pose a significant threat to vision under the best of circumstances. Should this disorder occur with a 7- to 10-day delay to definitive ophthalmologic care, the danger of a permanent loss of vision is great. Any eye pain that occurs among contacts lens wearers in the wilderness should be managed as described previously in the Acute Red Eye section. Contact lenses that block out harmful UV rays are available (e.g., Acuvue, Precision UV), but sunglasses are still a good idea to help protect the eyes from drying wind effects and the eyelids from UV exposure, even if contacts are worn. Considering all the potential problems, a good pair of prescription glacier glasses or laser refractive surgery might be a more reasonable alternative than contact lenses as a long-term solution to the refractive needs of mountaineers. The excellent military experience with photorefractive keratectomy (PRK) and laser in-situ keratomileusis (LASIK) has led to a warfighter vision enhancement program that has largely obviated the need for contact lens use in deployed military settings.54,132 The effects of refractive surgery on the vision of individuals at altitude are discussed in the following section.

REFRACTIVE CHANGES AT ALTITUDE AFTER REFRACTIVE SURGERY An acute hyperopic shift in persons who have had radial keratotomy (RK) and who then experience altitude exposure was reported by Snyder and colleagues129 in 1988 and by White and Mader148 in 1993. This effect has been observed at altitudes of as low as 2744 m (9000 feet).129 A dramatic example of this phenomenon was that experienced by Dr. Beck Weathers in the Mt Everest tragedy of May 1996, during which eight climbers lost their lives. Dr. Weathers had undergone bilateral RK years before the expedition. He noted a decrease in vision, which started early during his ascent.74 Author Jon Krakauer recalls that “… as he was ascending from Camp Three to Camp Four, Beck later confessed to me, ‘my vision had gotten so bad that I couldn’t see more than a few feet.’ ”74 This decrease in vision forced Dr. Weathers to abandon his quest for the summit shortly after leaving Camp Four and nearly resulted in his death. Another report describes two expert climbers who experienced hyperopic shifts of 3 diopters or more during altitude exposures of 5000 m (16,400 feet) or higher on Mt McKinley and Mt Everest.29 Mader and White85 found that the magnitude of the hyperopic shift was 1.03 ± 0.16 diopters after 24 hours at 3659 m (12,000 feet) and 1.94 ± 0.26 diopters at 5183 m (17,000 feet). Ng and co-workers97 reported no refractive change after 6 hours in post-RK eyes at a simulated altitude of 3659 m (12,197 feet), which suggests that the hyperopic shift requires more than 6 hours to develop. Further studies by Mader and colleagues86 at 4299 m (14,100 feet) on Pike’s Peak revealed the following: (1) a subject who had undergone RK demonstrated a progressive hyperopic shift associated with flattened keratometry findings during a 72-hour exposure; (2) control eyes and eyes that had undergone laser refractive surgery (i.e., PRK) experienced no change in their refractive state; (3) peripheral corneal thickening was seen on pachymetry in all three groups; and (4) refraction, keratometry, and pachymetry all returned to baseline after a return to sea level. Winkle and associates152 demonstrated that exposing post-RK

sea level.13 These data suggest that a small refractive shift in the myopic direction may be present at extreme altitudes. Climbers who do not ascend beyond moderate altitudes should not experience a post-LASIK refractive shift.

GLAUCOMA AT ALTITUDE Mader and Tabin84 discuss the hazards of going to altitude with severe glaucoma. Even individuals who have mild, well-controlled glaucoma may suffer adverse effects at altitude if they are being treated with topical β-blockers. These drugs may produce systemic side effects of lethargy and exercise intolerance that may be exacerbated at altitude.84 Consideration should be given to other choices for topical therapy for persons who will be traveling to significant altitude. The hypoxia of altitude may also worsen glaucomatous optic neuropathy. One person with moderately severe glaucoma who was well controlled on two topical medications ascended to 6707 m (22,000 feet) on Cho Oyu in the Himalayas. He noticed a decrease in vision and descended. His intraocular pressure was normal when it was measured in Kathmandu, but a marked increase in optic nerve damage was later confirmed by visual field and optic nerve imaging studies.84

ULTRAVIOLET RADIATION DAMAGE UV radiation is divided into UVA (320 to 400 nm), UVB (290 to 320 nm), and UVC (100 to 290 nm). Almost all UVC radiation is absorbed by the earth’s ozone layer.101,134 The cornea absorbs all radiation with wavelengths of less than approximately 300 nm, and the lens absorbs almost all of the remaining UVB radiation that reaches it.134 UV radiation is increased with high-altitude, low-latitude, and highly reflective environments.101 Altitude exposures associated with mountaineering entail exposures to increases in the amount of both incident and reflected UV light (see Chapter 14). Acute exposure to high levels of UV radiation may result in UV photokeratitis,35,134 whereas chronic exposures may be associated with cortical lens opacities,30 posterior subcapsular lens opacities,12 pterygia,10 and squamous cell carcinoma of the conjunctiva.96 The Salisbury Eye Evaluation project145 quantified ocular UVB exposure with use of a UVB pyranometer. This study found that cataract incidence increased (odds ratio, 1.1; 95% confidence interval, 1.02 to 1.20) with the degree of UVB sun exposure from the lowest to the highest quartile. Diagnosis and management of UV keratitis were discussed previously in this chapter. The best strategy for dealing with UVradiation–induced disorders is prevention. Most experienced mountaineers and trekkers are well aware of the need for sunglasses with high ratings for UV absorption. UV attenuation in sunglasses depends on the size, shape, and wearing position as well as the absorption properties of the optical material used.114 Wearing a brimmed hat is another effective method of decreasing UV exposure to the eye.44,101,115 In conjunction with the use of topical sun-blocking agents, a hat may also help to prevent cutaneous neoplasms from being a lasting reminder of previous mountaineering expeditions.

SUNGLASSES SELECTION IN MOUNTAINEERING When selecting sunglasses for use in mountaineering, absorption of essentially all UV radiation is a key consideration, because radiation in this portion of the electromagnetic spectrum is not visible and serves only to produce adverse effects in the eye. Another critical consideration is the amount of visible light that is transmitted. Sunglasses that suffice for everyday use may not be adequate for use in the mountains, especially while on snow or glaciers. The comfort zone for luminance is approximately 350 to 2000 candelas/m2.134 An outdoor environment that consists of sunlit fields and foliage may have a luminance of 3000 to 7000 candelas/m2; a bright beach may have a luminance of 6000 to 15,000 candelas/m2. Standard sunglasses that transmit 15% to 25% of visible light reduce the luminance in these situations to within the comfort range. By contrast, bright sun reflected off of snow or clouds may result in luminances of 15,000 to 575

CHAPTER 28  The Eye in the Wilderness

corneas to 100% nitrogen through goggles at 1 atm for 2 hours caused a significant hyperopic shift of 1.24 diopters and corneal flattening of 1.19 diopters. Corneal thickness increased in both post-RK and control eyes but was not associated with a hyperopic shift in control eyes. This is strong evidence that the effect of altitude exposures on post-RK eyes is caused by hypoxia rather than by hypobarism, and it further illustrates that breathing a normoxic inspired gas mix will not protect against development of hypoxic corneal changes in post-RK eyes. The effect of the post-RK hyperopic shift seen at altitude depends on the postoperative refractive state (i.e., undercorrected patients may actually have their vision improve) and the accommodative abilities of the individual.85 The work of Mader and colleagues has provided compelling evidence that, for myopic mountaineers, PRK rather than RK should be the refractive surgical procedure of choice. Individuals who have undergone RK and who plan to undertake an altitude exposure of 2744 m (9000 feet) or higher while mountaineering should bring multiple spectacles with increasing plus lens power.85 To my knowledge, a post-RK hyperopic shift has not been reported among airline passengers or flight crew. This may be because the latent period required for this phenomenon to develop exceeds the duration of most commercial flights or because the approximate 2440-m (8000-foot) cabin pressure on most commercial flights does not produce sufficient corneal hypoxia for a hyperopic shift to occur. The altitude at which RK is performed also affects the surgical outcome. RK that is performed at altitude (i.e., 1753 m or 5750 feet) produces more of a hyperopic shift than does the same procedure performed at sea level.27,34,126 The average changes in spheric equivalent cycloplegic refraction were 5.09 ± 1.29 diopters and 6.50 ± 2.24 diopters among subjects who had undergone the same procedure by the same surgeon at sea level and at 1753 m (5750 feet), respectively.126 In another study, the mean spheric equivalent cycloplegic refraction changes were 4.40 ± 0.92 diopters and 6.03 ± 1.13 diopters in patients who had had RK at sea level in Istanbul, Turkey, and at 1720 m (5641 feet) in Van, Turkey, respectively (p <0.001). The procedures at both altitudes were performed by the same surgeon and using the same technique to demonstrate the potential need to adjust surgical nomograms for altitude.27 The most commonly performed laser refractive surgery at present is LASIK.84 White and Mader147 reported that a climber who had undergone LASIK developed blurred vision after reaching the summit of Alpamyo (5945 m [19,500 feet]). He noticed the blurred vision after spending two nights at 5488 m (18,000 feet), and his vision cleared 3 days after returning to 3048 m (10,000 feet).147 Recent studies have examined the effects of altitude exposure on individuals who have undergone this procedure. Six climbers who had bilateral LASIK subsequently undertook an ascent of Mt Everest.34 Visual acuities were measured at base camp (5365 m [17,600 feet]); subjective symptoms (but not measured acuities) were obtained at higher altitudes. All climbers ascended to at least 7927 m (26,000 feet), and four of the six reached the summit at 8852 m (29,035 feet). Five of the six climbers reported no visual changes at altitudes of up to 7927 m (26,000 feet). One climber reported mild blurring with ascent above 4878 m (16,000 feet) that improved with descent or prolonged stay at altitude. Two additional climbers reported visual blurring at altitudes of 8231 m (27,000 feet) and 8689 m (28,500 feet). The authors’ conclusion was that LASIK may be a good choice for individuals involved in high-altitude activities, but those who plan to achieve extreme altitudes of 7927 m (26,000 feet) and above should be aware of possible fluctuations of vision.34 In another study, two physicians who had undergone myopic LASIK 8 and 14 weeks previously subsequently undertook an ascent of Mt Aconcagua (6964 m [22,841 feet]). They prospectively assessed their vision at 610-m (2000-foot) intervals during ascent. Both climbers described moderate loss of distance acuity with preserved near and pinhole acuity. These findings are suggestive of a myopic shift at altitude. Blurred vision began to occur at 5488 m (18,000 feet) in the left eye and at the summit (6964 m [22,841 feet]) in the right eye in one climber; blurring was first noticed at 5488 m (18,000 feet) in the right eye in the second climber. These myopic shifts resolved after a return to

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 28-2  Sunglasses Selection Criteria for

Mountaineering

Subject

Characteristics

Ultraviolet light absorption Visible light transmittance Lens material Optical quality Frame design features

99% to 100% 5% to 10%* Polycarbonate or CR-39† Clear image without distortion‡ Large lenses; side shields or wraparound design; fit close to face; good stability on face during movement; lightweight; durable Gray§

Color

*Glasses with less than 8% transmittance of visible light should not be worn while driving. Sunglasses or any tinted lenses with a visible light transmittance of less than 80% should not be worn while driving at night.134 † Glass lenses typically have very good optical clarity and scratch resistance, but are heavier and more expensive. ‡ Hold the sunglasses at arm’s length, and then move them back and forth. If the objects are distorted or move erratically, the optical quality is probably less than desirable. In addition, compare the image quality of several different pairs of sunglasses to get a basis for comparison. § Colored lens tints can alter color perception and possibly compromise the visibility of traffic signals. Neutral gray absorbs light relatively constantly across the visible spectrum and avoids these problems.134

2

30,000 candelas/m . Sunglasses with visible light transmittance in the 5% to 10% range are needed to reduce luminance to a comfortable range in these circumstances. (The 1986 American National Standards Institute standards for nonprescription sunglasses recommend that tinted lenses with visible light transmittances of less than 8% not be used for driving.134) Side shields or deeply wrapped lens designs should be used.134 Infrared absorption is important in certain industrial occupations (e.g., for those who work with glass, iron, and steel),134 but this is less important in protective eyewear that is to be used outdoors. Table 28-2 provides desirable characteristics to consider when selecting sunglasses for mountaineering or other environments with high levels of luminance and UV radiation.19 Individuals who are involved in mountaineering expeditions should always carry spare sunglasses in case the primary pair is lost or broken.

PHOTOCHROMIC LENSES Photochromic lenses change transmittance or color when they are exposed to light or UV radiation.134 They are designed to transmit a greater percentage of incident light when indoors or in conditions of reduced illumination and a reduced amount of light when exposed to higher levels of illumination. This is accomplished in one example of glass lenses by incorporating inorganic silver halide into the lens. When the lens is exposed to sunlight, this compound decomposes into its component silver and halide ions, and the lens turns dark gray.134 When the lens is removed from sunlight, the process reverses. When selecting photochromic lenses, the adequacy of indoor light transmittance can be judged while trying them on. Outdoor transmittance should be approximately 5% to 10%, as noted in Table 28-2, if the glasses are to be used for mountaineering. Most photochromic lenses have outdoor transmittances of approximately 20%, which should suffice for less highly reflective outdoor environments.134 Several plastic photochromic lenses are now available. The darkening process in plastic lenses is accomplished with organic light-sensitive compounds that are suspended in a thin layer near the front of the lens. Plastic photochromic lenses generally do not darken well enough to be used as sunglasses in bright environments. In addition, unlike glass photochromic lenses, the photochromic reaction that is typically used in plastic lenses usually fades in 1 to 2 years.134

The Eye and Diving The ocular aspects of scuba diving and other hyperbaric exposures were reviewed in a 1995 article.18 The sections from that 576

paper that address the hyperbaric environment, ocular barotrauma, the ocular manifestations of decompression sickness (DCS) and arterial gas embolism, ophthalmic considerations in fitness-to-dive evaluations, and the differential diagnosis of decreased vision after diving are discussed here. An expanded discussion of these issues as well as additional material about diving after eye surgery, the effect of common eye medications on fitness to dive, and the use of hyperbaric oxygen to treat ocular disorders may be found in the review article.

THE HYPERBARIC ENVIRONMENT At sea level, the body is exposed to 1 atm of pressure. This magnitude of pressure may also be expressed as 760 mm Hg, 33 feet of sea water (fsw), and 14.7 pounds per square inch. The normal atmospheric pressure of 1 atm is often used as a reference point from which other pressures are measured. When one states that the intraocular pressure is 15 mm Hg, what is meant is that the intraocular pressure is 15 mm Hg greater than the surrounding environment. In fact, the absolute pressure inside the eye at sea level is 775 (760 + 15) mm Hg. The intraocular pressure that is measured with a tonometer is therefore a “gauge” pressure, which means that the pressure displayed is the actual pressure minus the atmospheric pressure.

OPHTHALMIC CONSIDERATIONS IN THE FITNESS-TO-DIVE EVALUATION A diver should have adequate visual acuity to be able to read his or her gauges and to function safely underwater. Possession of a driver’s license is a convenient indication that a potential diver has sufficient visual acuity to meet this standard.18 A person who has recently undergone ophthalmic surgery should refrain from diving until the recommended convalescence interval has passed.18 Individuals who suffer from glaucoma may dive safely unless they have had glaucoma filtering surgery performed.18 Systemic carbonic anhydrase inhibitors are best avoided by patients with glaucoma who wish to dive because of possible confusion between medication-induced paresthesias and DCS.18 Any individual who is suffering from an acute ocular disorder that causes significant pain, decreased visual acuity, or other disabling symptoms should refrain from diving until these symptoms have resolved.18 Individuals who have undergone surgical repair of retinal detachments may occasionally have gas bubbles placed in the eye to stent the retina against the retinal pigment epithelium. Intraocular gas bubbles are an absolute contraindication to both diving and hyperbaric chamber exposures. A study was done in which rabbit eyes were injected with perfluoropropane to a bubble size of 60% of the vitreous cavity. When the eyes that contained the bubbles were exposed to increased atmospheric pressure, intraocular pressure dropped as compared with the surrounding environment and then rose to more than 50  mm  Hg when the atmospheric pressure was returned to normal.66 The individual who dives with a gas bubble may experience severe pain on descent as a result of compression of the globe as the gas phase is compressed106 or on ascent after extra gas has diffused into the bubble and the absolute pressure is reduced on surfacing, thereby causing the bubble to grow and intraocular pressure to rise.

UNDERWATER REFRACTIVE CORRECTION If contact lenses are to be used for diving, soft contact lenses are preferred.31,38,68,89 Hard (polymethylmethacrylate) contact lenses have been associated with corneal edema during decompression and after dives.124,125 These changes are caused by formation of nitrogen bubbles in the precorneal tear film during decompression, which interferes with normal tear film physiology and results in epithelial edema. Bubble formation under contact lenses would be expected to be more common during dives with significant decompression stress. Although the increased gaseous diffusion properties of rigid gas-permeable contact lenses theoretically decrease the chance of bubble formation in the tear film, use of these lenses while

REFRACTIVE SURGERY AND DIVING Laser refractive surgery is a safe and effective means of correcting refractive errors in divers.18 PRK has been allowed in U.S. Navy divers since 1996. LASIK is now a more commonly performed procedure. Although this procedure presents the potential for both inflammation and infection under the corneal flap as well as traumatic dislocation of the flap, these conditions have not to date been reported as complications of diving. Visual acuity appears to be maintained in the hyperbaric environment. Huang and colleagues62 reported about three patients who had undergone bilateral myopic RK, two who had undergone bilateral myopic LASIK, and three control subjects. Eye examinations were performed at baseline, at 4 atm in a dry chamber, and on return to the surface. Acute hyperbaric stress did not appear to significantly alter refractive power after corneal surgery.62 I recommend a 2-week wait after PRK and a 1-month wait after LASIK before the individual returns to diving.16

OCULAR AND PERIOCULAR BAROTRAUMA The eye is normally filled with noncompressible fluid and solid tissues and therefore protected from barotrauma. However, when a mask is placed over the face, a different circumstance exists. The face mask is an air-filled space that is bounded on one side by the eyes and the ocular adnexa. As a diver descends, if he or she does not expel gas through the nose into the airspace of the face mask, a relative negative pressure develops in this space. If this negative pressure becomes great enough, the eyes and ocular adnexa are drawn toward the space. Marked lid edema with ecchymosis and subconjunctival hemorrhage may develop

CHAPTER 28  The Eye in the Wilderness

diving has been demonstrated to cause bubble formation under the lens and to lead to secondary corneal epithelial disruption.130 I have personally treated one diver with foreign-body sensation and blurred visual acuity that occurred during ascent while wearing gas-permeable contact lenses. Symptoms resolved on removal of the lens at the surface. Corneal edema was not observed in one series in which soft contact lenses were studied.124 The most frequent complication of soft contact lens use in diving is loss of the lens.68,71 The risk of lens loss can be minimized by ensuring a good seal on the face mask and by minimizing the amount of water that gets into the air space of the mask. Should the mask become displaced during the dive, narrowing of the palpebral fissures helps to decrease the chance of the contact lens floating off of the surface of the eye.68 Betts11 reported an incident in which bubbles formed under “micro-corneal” contact lenses. When leaving the hyperbaric chamber after a simulated dive, the diver complained of blurred vision in the right eye, which appeared to have a white film over it. The left eye was similarly affected but to a lesser extent. During examination with an ophthalmoscope, a haze of fine bubbles could be seen under the contact lens; these bubbles persisted on the surface of the cornea after the lens was removed. The bubbles did not move with blinking and were felt to be in the superficial layers of the cornea; they slowly resolved over 30 minutes. The author speculates that the observed difference in bubble formation between the two eyes may have been the result of a difference in lens fit.11 A prescription ground face mask is another refractive alternative, as is a face mask with a lens that is bonded onto the surface of the mask. However, masks and lenses may be lost in high swells or rough surf, thereby leaving the diver without refractive correction. When contemplating purchase of an expensive prescription face mask, one needs to be mindful of the corollary of Murphy’s Law that applies to diving: “Weight belts always fall on the face masks with prescription lenses.” Refractive corrections for presbyopia present special challenges underwater. Presbyopic divers with contact-lens–corrected myopia may require greater near-vision correction underwater than when viewing the same objects in air because of the increased percentage of shorter-wavelength light rays underwater. Divers with presbyopia should consider monovision correction to facilitate underwater visual tasks.14

FIGURE 28-20  Mask squeeze in a diver who descended to 45 fsw without exhaling into his mask. (Courtesy Kenneth W. Kizer, MD.)

as tissues and blood vessels are disrupted by this distention. These signs may be alarming to the diver, but they typically resolve without sequelae. In a more severe case, such as that which may occur when an unconscious diver sinks a significant distance in the water column, more serious injury (e.g., hyphema) may occur.45 A diver with face mask barotrauma is shown in Figure 28-20. In some settings, facial barotrauma may be quite severe. The first reported “squeeze” that occurred during diving took place on October 4, 1841, as part of the Royal George salvage work off of Portsmouth Harbor, England. Ten months later, on the same project, another diver suffered a severe squeeze when his air hose burst. Colonel Pasley, who was the director of salvage operations, told of removing the diver’s helmet: “… his face and neck were much swollen, and blood was issuing from his mouth and ears profusely, his eye closed and protruding; he vomited a great deal of blood on being laid on the deck.” Severe squeezes during the early days of hard-hat diving resulted from a combined failure of both nonreturn valves and air supply hoses.103 Barotrauma is also possible in persons with gas bubbles in the anterior chamber or vitreous cavity. Pressure-induced changes in the volume of this bubble may result in retinal, uveal, or vitreous hemorrhage as well as in partial collapse of the globe. Permanent loss of vision may ensue. One person who attempted to dive while an iatrogenic bubble was present in the vitreous cavity noted immediate onset of very severe eye pain on descent and quickly aborted his dive.106 Persons with intraocular gas should not be allowed to dive as long as the bubble remains in the eye. The need to add extra gas to the face mask during descent makes it obvious that swim goggles, which cover only the eyes and not the nose, should never be used for diving. Face mask barotrauma may also result in damage to the periocular tissues. Bove and Butler20 reported on a diver who noted numbness and paresthesias in the distribution of the infraorbital nerve that resulted from maxillary sinus barotrauma. Butler and Gurney21 described a diver who noted the onset of pain during a dive. After the dive, she noted a bulging sensation of the eye and diplopia. Ophthalmologic examination revealed a tropia, and subperiosteal orbital hemorrhage was found with magnetic resonance imaging.21

DECOMPRESSION SICKNESS Ocular involvement in DCS was first reported by Sir Robert Boyle, who observed gas bubbles in the anterior chamber of the eye of a viper that had been experimentally exposed to increased 577

PART 4  INJURIES AND MEDICAL INTERVENTIONS

pressure.17 Ocular manifestations of DCS are infrequently reported in the ophthalmic literature,18 but there are a number of reports of ocular involvement with DCS in the dive medicine literature.15,18,40,113 Reported manifestations include nystagmus, diplopia, scotomas, homonymous hemianopias, orbicularis oculi pain, cortical blindness, convergence insufficiency, optic neuropathy, and central retinal artery occlusion.18 The incidence of visual symptoms in patients with DCS was found to be 7% in one large series.113 Physicians should also be aware of the possibility of DCS occurring after altitude exposures.15,133 Altitude DCS that presents as optic neuropathy has been reported.15 The risk of DCS may be increased if an altitude exposure occurs after diving without allowing for sufficient time for excess nitrogen taken up during the dive to leave the body.18 Fitzpatrick42 reviewed 143 cases of altitude-induced type II neurologic DCS. Visual disturbances were identified in 38 cases, for a prevalence of 26.6%. The most commonly reported visual symptoms were blurred vision (61%), loss of vision (34%), and scintillation or scotoma (32%). Forty-five percent of the cases occurred at altitude, 24% occurred within the first hour after the exposure, and 21% occurred 1 to 6 hours after the exposure. No cases were reported to have begun more than 24 hours after the exposure.42 Special attention should be paid to the possibility that DCS after a hypobaric exposure may manifest with symptoms that subsequently resolve, only to recur days to even weeks later. Steigleman and coworkers133 reported a 20-year-old aircrew student who had pain on ascent during altitude exposure. Pain resolved on descent but recurred 3 weeks later, when he experienced severe retro-orbital pain and moderate vision loss in the left eye. His signs and symptoms resolved completely in the first U.S. Navy Treatment Table 6, but they recurred several days later. He eventually underwent a total of four treatment tables, and experienced complete resolution of his signs and symptoms.133 DCS is treated with oxygen breathing and recompression on an emergency basis. Ophthalmologists seldom encounter this disease in an acute setting, because most divers know to seek recompression therapy for signs or symptoms of DCS. Because treatment usually results in resolution of all symptoms, most persons with visual symptoms before treatment are asymptomatic after recompression treatment and are therefore not referred to ophthalmologists.17 If an ophthalmologist encounters a person with acute ocular disturbances that are consistent with DCS after a hyperbaric or hypobaric exposure, the victim should be referred as an emergency to the nearest available recompression chamber and diving medicine specialist, because DCS may worsen rapidly if it is not treated. Physicians who are unsure about the location of the nearest diving medicine specialist or recompression chamber can call the Divers Alert Network at Duke University in Durham, North Carolina at 919-684-9111. An incomplete response to treatment or recurrence of symptoms after treatment may bring a victim with ocular DCS to the ophthalmologist on a nonemergency basis. The victim should be managed in conjunction with a dive medicine specialist. Recompression therapy and hyperbaric oxygen should be administered even when a significant delay has occurred between the onset of symptoms and initial evaluation of the victim, because treatment may be effective despite delays of up to several weeks.15,18,140

completed two series of chamber dives in accordance with the Professional Association of Diving Instructors tables.90 The first dive series was to 70 fsw for 15, 29, and 40 minutes. The second was maximum-duration no-stop diving at 40 fsw (140 minutes), 70 fsw (40 minutes), 90 fsw (25 minutes), and 120 fsw (13 minutes). Tear-film bubble assessment was observed to be more sensitive for detecting decompression stress than was the conventional Doppler ultrasonic surveillance of the precordial region.90 Bennett and colleagues9 observed 42 recreational divers after a single day of diving and 11 divers after repetitive multiday diving. After diving, bubble counts increased significantly (p <0.01) as compared with predive values. Single-day divers reached a maximum bubble count at 48 hours of 1 bubble per eye (range, 0 to 2.25 bubbles). Bubble counts were not significantly correlated with inert gas load, body mass index, age, or diving experience.9 Another study subjected 11 volunteers to pressures of 4 bar for 15 minutes. During the predive examinations, there was only one individual with one bubble observed. Postdive examinations found a mean of 6 bubbles per eye (range, 3 to 12 bubbles; p <0.001).135 Whether these observations will eventually be useful for clinicians or decompression researchers remains to be determined.8

THE OCULAR TEAR FILM AS AN INDICATOR OF DECOMPRESSION STRESS

Retrochiasmal defects such as hemianopias and cortical blindness may be seen with arterial gas embolism. Central retinal artery occlusion may also result from gas emboli in the ophthalmic artery.18 Management is similar to that for DCS, with emergency recompression and hyperbaric oxygen therapy indicated in all cases.

There has been interest in observing bubble formation in the ocular tear film and using the presence and numbers of bubbles observed after hyperbaric exposures as an indicator of the magnitude of decompression stress encountered. Nine healthy adult volunteers made a series of dives to 50 fsw and 90 fsw.92 In the first series, all subjects spent the 15-minute bottom time resting, whereas on the second series they exercised on a bicycle ergometer. Dive profiles were accomplished in accordance with the Canadian Defense and Civil Institute of Environmental Medicine tables. On the resting profiles, the divers were found to have no bubbles on postdive eye examination, whereas on the exercising profiles bubbles were present.92 In another study, 11 divers 578

OCULAR FUNDUS LESIONS IN DIVERS Fluorescein angiography of divers has documented retinal pigment epithelial abnormalities that are indistinguishable from those that are seen in eyes with choroidal ischemia.108 These changes were attributed to decompression-induced intravascular gaseous microemboli. The incidence of these lesions was related to the duration of diving and a history of DCS. Other abnormalities that were noted more frequently in divers were low retinal capillary density at the fovea, microaneurysms, and small areas of capillary nonperfusion. Retinal pigment epithelium defects were seen in 1 of 23 nondivers and in one-half of the divers. All observed changes were noted by the authors to be consistent with obstruction of the retinal and choroidal circulations. Although no diver was reported to have suffered a loss of visual acuity as a result of these abnormalities, the long-term effects of this phenomenon remain to be studied. Another study60 reported fundus fluorescein angiography that was performed on 26 divers who had reportedly used safe diving practices for at least 10 years and on 7 control subjects. There was no significant difference in the incidence of macular abnormalities between divers and nondivers in this study. The authors concluded that adherence to safe diving practice confers some protection against the macular abnormalities that are known to occur in divers with a history of DCS.60 A third study95 compared fluorescein angiograms of 55 Royal Navy divers with those of 24 nondivers. No differences were found between divers and nondivers, and prevalence of abnormalities was not correlated with diving experience. Visual fields were normal in all control subjects and divers. Twenty-five percent of both control subjects and divers had retinal pigment epithelium defects. The authors believed that their divers, as members of the Royal Navy, may have followed safer diving practices and thus avoided the lesions that were observed in other studies.95

ARTERIAL GAS EMBOLISM

HYPEROXIC MYOPIA Individuals who undergo prolonged exposures to hyperoxic gas mixtures may experience lenticular oxygen toxicity that is initially manifested by a myopic refractive shift. This myopic shift is progressive and usually reversible if the hyperoxic exposures are discontinued.4 Although this condition is most common among patients who are undergoing repeated hyperbaric oxygen

OCULAR JELLYFISH STINGS Divers and swimmers may occasionally be stung by jellyfish on and around the eyes. The pain from this injury may be severe, but is typically self-limited, and usually resolves within 24 to 48 hours. Glasser and colleagues50 described a series of five cases that were associated with unusually severe and prolonged iritis and elevations of intraocular pressure. Intraocular pressures ranged from 32 to 48 mm Hg and were treated successfully with topical β-blockers and oral carbonic anhydrase inhibitors. One patient developed chronic unilateral glaucoma. The iritis persisted for up to 8 weeks. This report illustrates the potential for serious long-term sequelae as a result of ocular jellyfish stings. All patients with ocular jellyfish stings that do not resolve within 24 to 48 hours should be seen urgently by an ophthalmologist.50

DIFFERENTIAL DIAGNOSIS OF DECREASED VISION AFTER DIVING DCS and arterial gas embolism should be considered whenever vision is acutely decreased after diving because of the possible emergency need for recompression therapy, especially if any other manifestation of DCS or arterial gas embolism is present. Other disorders may also affect vision after a dive. Corneal edema that results from formation of gas bubbles under polymethylmethacrylate and rigid gas-permeable contact lenses may cause decreased vision. An individual who wears soft contact lenses and who complains of blurred vision after a dive may have a lost or displaced lens. Another possible cause of nondysbaric decreased vision after a dive is epithelial keratopathy induced by chemical agents that are used to reduce face mask fogging. The time-honored application of saliva or toothpaste to the interior surface of the mask reduces but does not eliminate fogging. This led to development of commercial antifog agents that are designed to be applied to the inside surfaces of face masks. These agents may contain volatile compounds that are potentially toxic to the corneal epithelium, including glycols, alcohols, and phenol derivatives. Exposure to these compounds may result in blurred vision, photophobia, tearing, and blepharospasm that may not develop until several hours after the dive.154 Slit-lamp examination typically reveals diffuse superficial punctate keratopathy. Development of this syndrome commonly results from improper use of the antifog agent, such as overly generous application or the failure to rinse the mask before use. I have personally treated several persons with recurrent mild ocular irritation and blurring of vision after dives during which soft contact lenses were worn. The lenses were noted to be tightly adherent to the cornea, probably as a result of a decrease in water content in the lens after contact with hypertonic sea water. Symptoms were relieved with a few drops of isotonic artificial tears. Decreased movement of soft contact lenses on the cornea has been reported to occur after exposure to swimming pool water as well.33

BOX 28-5  Differential Diagnosis of Decreased Vision

CHAPTER 28  The Eye in the Wilderness

exposures in a chamber for medical conditions,3,4 it has also been reported in a scuba diver doing a series of prolonged dives using a gas mix with a constant partial pressure of oxygen of 1.3 atm.26 This condition has also been noted among caisson workers.102

After Diving

Decompression sickness Arterial gas embolism Bubbles under contact lenses Displaced contact lens Antifog agent keratopathy Contact lens adherence syndrome Transdermal scopolamine Hyperoxic myopia Oxymetazoline optic neuropathy Diving-induced migraine phenomena Eye disorders not related to diving

Divers sometimes use a transdermal scopolamine patch placed behind the ear to prevent motion sickness. This may result in mydriasis, decreased accommodation, and blurred vision in the ipsilateral eye. Hyperoxic myopia may be a possible cause of vision loss if the diver has had recurrent or prolonged exposures to elevated partial pressures of oxygen.26 Divers often use oxymetazoline nasal spray to assist with shrinking mucous membranes to equalize pressure in the middle ear. Vasoconstriction caused by this medication has been reported to cause anterior ischemic optic neuropathy. Fivgas and Newman43 described a 43-year-old woman who was evaluated for sequential bilateral vision loss after using oxymetazoline nasal spray. Visual loss in both eyes was temporally associated with use of the medication. A thorough evaluation for other causes of optic neuropathy was negative.43 Migraine-like phenomena have been reported after hyperbaric exposures. Anderson and co-workers2 described four individuals who had migrainous signs or symptoms after hyperbaric exposure. Three of the four individuals had a history of migraine headaches, and they noted sudden appearance of scintillating scotomas 10 to 90 minutes after surfacing, with no other manifestations of DCS. Three of the four patients experienced resolution of symptoms with surface oxygen only, and one patient was recompressed as well. These events may represent a migraine event that is temporally associated with diving, or they may be an atypical manifestation of DCS.2 Finally, loss of vision may be caused by ocular disorders that occurred during or shortly after the dive but that were not a direct result of the dive itself. A differential diagnosis of decreased vision after diving is presented in Box 28-5. Acknowledgments. The author thanks Drs. Steve Chalfin, Dave Harris, and Dave Perlman for their much-appreciated contributions to preparing this chapter.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 29 

Foot Problems and Care GRANT S. LIPMAN AND BRIAN J. KRABAK “There’s language in her eye, her cheek, her lip; Nay, her foot speaks.” WILLIAM SHAKESPEARE

The American Alpine Club has estimated there are more than 100,000 climbers in the United States with 1 to 2 million days in the mountains a year.24 Combined with the 73.3 million people (roughly one-third of the population) in the United States who went hiking in 2002,3 it is no surprise that friction blisters are arguably the most common medical problem encountered in the wilderness. For some, a foot blister may be considered merely a nuisance; for others, it may ruin an outing, necessitate immobility, or even lead to cellulitis or sepsis (Figure 29-1).2,29 Blistering rates in the hiking community range from 7% to 54%,14,80 with incidence often inversely proportional to the experience levels of the hikers studied. Blister occurrence in marathons range from 0.2% to 39%,47 whereas in multiday adventure events, foot care represents the most common (32% to 45%) reported injury.48,79 In the authors’ experience providing medical support for more than 1800 miles of ultraendurance races in four countries with more than 1200 documented medical visits, 70% of chief complaints were related to foot care.39 In the military, foot problems have historically been recognized as one of the most common training complications and preventable debilitating injuries. In 1895, the Duke of Connaught reported 824 cases of blistered feet during maneuvers in the New Forest.78 Cadets at the U.S. Military Academy undertaking a 21-km (13-mile) hike reported a 48% occurrence of blisters,37 and over 65% of military personnel after a 10-km (6.2-mile) road march had observed blisters.42 Although most blisters are of minor medical significance, they can impair concentration, decrease athletic performance, and potentially lead to debilitating infections. A studied Navy recruit population was estimated to have an 84% incidence of cellulitis secondary to foot blisters, with an average loss of 8 full days of training per case.29 A recent study of over 2,000 U.S. Marine recruits showed that those with blisters were 50% more likely to experience additional training-related injuries.9

Blister Pathophysiology The earliest etymology of the word friction, described from 1704, is “to rub; to crumble; they injure.”50 The mechanism of a friction blister injury is the repeated action of skin rubbing against another surface. As the external contact of either sock or footwear moves across the skin, the frictional force (Ff) opposes this movement. Amonton described the magnitude of frictional resistance in 1699 as “directly proportional to the load and independent of the area of contact between the surfaces.” Frictional force increases with increasing external force. When external force exceeds the frictional force, movement occurs at the interface. In addition to magnitude of the frictional force, frequency of the cycling of the object across the skin leads to higher probability of blister development.56 There is an inverse relationship between these two variables; at higher frictional forces, it takes fewer cycles to form blisters.1,11,12,56 The skin surface is subjected to normal forces (Fn), the perpendicular or “force of contact,”38as well as nonperpendicular or tangential shear forces (Figure 29-2). The magnitude and relationship of a frictional force is defined by the following formula:8 Ff = µ • Fn, where µ is the coefficient of friction or the ratio of the shear force to normal force that needs to be overcome to initiate movement of the materials relative to the skin.67 There is wide variation in the coefficients of friction between the skin and various substances (Figure 29-3, online), and frictional 580

properties of the skin depend on inherent suppleness and hydration, as well as a host of external factors, including temperature and humidity.84 Shear forces extend horizontally between skin layers (Figure 29-4), skin and sock interface, between socks, and between socks and footwear. When the forces overcome resistance, sliding occurs. Repeated sliding at a friction point causes exfoliation of the stratum corneum and erythema in and around this zone.38,56 This is experienced as a initial sensation of heat—the “hot spot.” Continued friction on a hot spot causes epidermal cells in the stratum spinosum to delaminate and split.2,76 With continued rubbing, a sensation of stinging or burning occurs as a narrow pale area forms around the central reddened region. This enlarges inward.38 This skin becomes elevated as the underlying epidermis fills with fluid, and a blister is created (Figure 29-5).76 The intact superficial cells of the stratum corneum and stratum granulosum form the blister’s “roof.” The separated cleft in the area under the blister roof quickly fills with a low-protein electrolyte-rich transudate as a result of hydrostatic pressure.13 The underlying basal skin layer and associated epidermal–dermal interface is usually unaffected and undamaged. Healing of the blister is rapid if one can reduce further friction and exacerbation of the injury. At 6 hours, cells at the base of the blister increase uptake of amino acids and nucleosides, precursors of RNA and DNA. After 24 hours, there is high mitotic activity in the blister wound, and at 48 hours, new stratum granulosum can be seen. By 120 hours, a new stratum corneum is made.20 In the presence of continued friction and pressure, as is often the case in the backcountry, where continued ambulation and activity are required, the body needs outside assistance to heal.

Blister Prevention The perpendicular directed normal force between the foot and the insole is determined by the weight of the hiker and the weight being carried. Reducing the magnitude of the forces on the feet that cause a friction blister can be as simple as reducing the carried load36 either by shedding a few pounds of adipose tissue or taking a few items out of the backpack. Another way to minimize force on the feet is to use a padded insole or arch support. There are myriad generic and custom moldable insoles on the market. Although an insole or orthotic does not technically reduce the perpendicular forces on the feet, it helps to evenly distribute pressure over the plantar surface of the foot. Greater pressure occurs when there is a high load on a smaller surface area of the foot, which may cause that area of skin to be susceptible to blister formation. Either increasing or decreasing the ease with which two surfaces rub against each other can reduce the chances of blister development. If the coefficient of friction is small, the resulting Ff will be minimized, with greater ease of sliding and reduction of the shear forces and chances for blister formation. Another option is to maximize frictional forces through well-fitted footwear, resulting in little or no movement at the skin–surface interface.

REDUCTION OF MOVEMENT WITHIN THE FOOTWEAR SYSTEM Shoes or boots should fit properly and comfortably. Shoes that are too tight can increase contact points of pressure on the foot.

For online-only figures, please go to www.expertconsult.com

MINIMIZING MOISTURE

FIGURE 29-1  Aggressively spreading leg cellulitis. (Courtesy Grant S. Lipman, MD.)

Those that are too loose can allow excess movement that allows generation of frictional forces. Narrow shoes can cause blisters on the large and small toes. Loose shoes can create blisters on the tips of toes from sliding and jamming the tips into the toe box. A toe box that is too shallow can cause blisters on the tops of the toes from repeated contact. It is important to fit a shoe in the evening, because feet tend to swell throughout the day and the fit will be similar to the natural swelling that feet undergo while active. When trying on shoes or boots, wear the same socks and/or insoles or orthotics that you will be using on the trails. Size boots to compensate for thicker socks. Allowing for ample time to break in a new set of footwear before use increases flexibility in the material, thereby reducing potential high-friction areas against the foot.

INCREASING MOVEMENT WITHIN THE FOOTWEAR SYSTEM—SOCKS Various sock layer combinations can create a nonspecific weak shear layer, exploiting the coefficients of friction and minimizing the friction forces against the skin of the foot itself. The goal is to have friction occur between the two layers of socks, not between the skin and socks. A smooth, thin, snug-fitting synthetic sock worn as an inner layer against the foot will move with the foot, whereas a thick, woven sock tends to move with the footwear and cushions against shocks. Socks that have a low frictional coefficient worn close to the foot have been found by computer modeling to reduce plantar shear stress. This reduction in shear force is compounded by also wearing a sock that has high friction against the insole.16 This combination is commonly used by many outdoor enthusiasts and has been found to produce the least amount of blisters in military populations.35 The thinner synthetic liner sock will also assist in humidity control by retaining less moisture and wicking moisture and perspiration away from the skin surface.26,27 A longitudinal double-blind study was conducted to determine the effect of sock fiber on frequency and size of blisters. Two different visually identical socks were tested—one with Friction force Resultant vector direction Object on skin

Epidermis Dermis Subcutaneous tissue

Repetitive rubbing on moist skin produces higher Ff than on very wet or dry skin.2,56,76 Cutaneous hydration leads to increased contact area, adhesion, and maceration, resulting in more frequent blisters (Figure 29-6). Very wet skin has a low incidence of blister formation, likely due to the lubricating effects of water on the skin surface. Frictional forces on dry skin may exfoliate superficial cells of the stratum corneum, lubricating the feet in a manner analogous to the lubricating effects of graphite powder.38 High-technology oversocks combine waterproof materials with traditional socks to help keep feet dry when repeatedly exposed to water. Combining Gore-Tex oversocks with wicking liner socks and foot antiperspirant are tricks to reduce foot moisture. Consider the addition of gaiters to help eliminate dirt, gravel, sand, and rocks from entering the sock-shoe system. Consistently moist skin or sweaty feet may require frequent changing of socks.

FEET PREPARATION Repeated low-intensity Ff exposure results in cellular proliferation and epidermal thickening. These adaptations to underlying skin may reduce the likelihood of developing blisters. A soft and supple foot will be more adept at withstanding frictional stress than will cracked, horny feet. Many podiatrists and ultraendurance athletes recommend preparing feet with Bag Balm, a moisturizer, Vaseline, or other softening agent for months before an event (Figure 29-7, online). Other clinicians and athletes have the opinion that “dry is better” and take serial footbaths in povidone-iodine or tannic acid.47 Calluses should be filed down with a pumice stone or emery board to prevent them from tearing off, which would leave an open wound. Blisters deep to a callus are extremely painful and difficult to drain (Figure 29-8). Toenails should be kept short and beveled downward to reduce the incidence of subungual hematomas. Before a big event, consider having a professional manicure. Having this done at least a week before the planned outing allows time for the manipulations to the epidermis and cuticles to heal, to prevent potential bacterial entry and infection on the trail.

BLISTER PREVENTION COMPOUNDS The key to preventing blisters involves decreasing shear forces on the skin. Despite extensive studies regarding the impact of shear forces on development of blisters, there are few studies examining the efficacy of various modalities (e.g., powders, antiperspirants, lubricants, tapes, pads). Theoretically, each of these offers a distinct advantage. Lubricants, tapes, and pads are proposed to decrease the friction that leads to blisters, whereas powders and antiperspirants are thought to limit perspiration and

Shear force Resultant vector direction Object on skin

Epidermis Dermis Subcutaneous tissue

FIGURE 29-2  Cross-section illustration of skin and resultant vector direction of a friction force and vector direction of a shear force. (Reproduced with permission from Polliack AA, Scheinberg S: A new technology for reducing shear and friction forces on the skin: Implications for blister care in the wilderness setting, Wilderness Environ Med 17:109, 2006.)

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CHAPTER 29  Foot Problems and Care

100% acrylic fibers, the other with 100% natural cotton fibers. Acrylic fiber socks were associated with fewer blister events and size when compared with cotton fiber socks.26

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Stratum corneum

Stratum lucidum Stratum granulosum

Stratum spinosum

Stratum basale FIGURE org.)

29-4  Epidermal

FIGURE 29-6  Moist macerated feet. (Courtesy Mark Ellis, MD.) layers.

(From

http://www.ratbehavior.

resulting cutaneous hydration associated with activity that lead to increased blister incidence. Antiperspirant mechanism of action is by the metallic salt that dissolves at the skin surface, forming an acidic solution that hydrolyzes upon contact with more alkaline sweat, precipitating and “plugging” the acrosyringium of the eccrine sweat gland.60,61

PREVENTIVE TAPING AND PADS A preventive barrier between the footwear and potential point of blister formation is a proactive treatment that can prevent a blister. Barriers are best used as preventive measures before blisters form, either at the beginning of the day’s activities or as soon as a hot spot develops. The barrier needs to be adhesive so it can remain fixed to skin, despite the action of frictional forces, heat, or humidity that will likely occur inside the footwear acting on the barrier. The concept of prevention is to have a layer over the skin such that the following resulting shear will occur between the barrier and the footwear, not the footwear and the skin. The shelves of drugstores and running stores are filled with products that can be applied in areas that historically have developed blisters. These include Micropore paper tape, cloth tape, Elastikon, Kinesio tape, Moleskin, Spenco Blister Pads, Blist-O-Ban, and duct tape (Table 29-1). Use of an adhesive-like tincture of benzoin or Pedi-Pre Tape spray adherent will help keep the barrier fixed to the skin. ENGO Performance Patches are smooth fabric-film composite patches that go on the inside of the shoe or insole. Silicone gel toecaps and sheaths reduce friction at the tips and between toes. Taping is a relatively easy and cost-effective method to prevent hot spots and subsequent blister injuries at various sites on the foot. Ideally, taping products should be thin, easy to apply, adhere well, and provide limited seams that may themselves be friction points. Paper-like tape (Figure 29-9, online) can be easily

Blister cleft Basal layer

placed over and around the toes, heel, plantar, and dorsal aspects of the foot (Figure 29-10). Due to its low cost, ease of use, and silky feel, it is the authors’ first-line product to apply on a hot spot to prevent blister formation. Elastikon is a sturdier and wider tape that may be used over the planter surfaces of the feet, heels, and dorsa of the feet. Because of the rough feel of this tape, it should not be used in the spaces between digits. Duct tape is used with variable success in areas such as the heel of a foot. However, there are innate qualities that make this product less than ideal for blister prevention. It is nonporous, leading to increased moisture content and maceration of skin beneath the tape; it wrinkles easily, leading to pressure points (Figure 29-11); and the adhesive backing sticks too well, often removing epidermis along with the tape. Detailed descriptions on taping

FIGURE 29-8  Subcallus blister. (Courtesy Grant S. Lipman, MD.)

Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum

FIGURE 29-5  Longitudinal section of the epidermis showing a friction blister. (Reproduced with permission from Knapik JJ, Reynolds KL, Duplantis KL, et al: Friction blisters: Pathophysiology, prevention and treatment, Sports Med 20:136, 1995.)

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FIGURE 29-10  Paper-tape prophylactically applied to heels to prevent hot spots. (Courtesy Ashlie Emmett.)

Product

Description

Advantage

Blist-O-Ban

Ultrathin patented BursaMed dome reported to decrease the forces along the skin by deflecting forces away from the skin. Useful over hot spots or mild blisters. Sterile hypoallergenic plaster reported to protect vulnerable skin from friction damage. Polyethylene tape with flexible shell and pressure-sensitive adhesive quality; however, not very breathable and difficult to remove; may be used over any surface. Flexible tape made of a porous high-twist, cotton elastic cloth tape with a rubber-based adhesive; useful over heels and plantar surface of foot. Slightly thicker tape with zinc oxide and rayon backing; may be used over any part of the foot. Breathable pressure-sensitive adhesive tape. Useful for preventive taping and underneath thicker tape; however, not well suited for wet environments. A heavy cotton fabric sheared on one side with adhesive backing on the other. Useful over relatively even surfaces to offset the direct pressure on large blisters. Series of products ranging from nonwoven cotton tape to a hydrogel pad designed to assist with fluid absorption and wound healing. The pads are very useful for complicated blisters without any skin cover.

Ultrathin, easy to apply, hypoallergenic, multiday use, water resistant Easy to apply, water resistant, flexible, multiday use Strong, easy to apply, multiday use

Compeed Duct tape Elastikon Leukotape Micropore paper tape Moleskin Spenco 2nd Skin

Breathable, easy to apply to uneven surfaces Breathable, easy to apply Easy to apply and remove, hypoallergenic, multiday use Easy to apply, hypoallergenic Easy to apply, hypoallergenic, multiday use

techniques are discussed in the blister treatment section of this chapter. Like taping, pads (which are a combination of adhesive dressing with a central thicker composite pad) are relatively easy to apply to prevent or treat developing blisters. Pads can be extremely easy to apply over relatively smooth surfaces such as the Achilles region or metatarsal area. However, these products are usually bulkier than tape, making them more difficult to apply on uneven surfaces or in small areas, such as between the toes. Improper application can lead to excessive friction around the product and further epidermal injury. Pads are exponentially more expensive than tape and potentially take up more space in the pack, limiting their use on multiday trips, where weight and space may be at a premium. A product made popular by British athletes, Compeed, is notorious for its strong adhesion qualities (Figure 29-12), which becomes apparent when removing layers of epidermis along with the bandage after activity (Figure 29-13). There are very few studies assessing the efficacy of any these products in preventing blister formation.63,70 The relatively new adhesive bandage Blist-O-Ban has been prospectively studied affixed at specific sites (e.g., heel or metatarsal head). The product appears to decrease the incidence of new blisters in treated feet compared with untreated feet and adheres well in humid conditions. However, these studies did not address blister formation in common areas, such as the toes and intertriginous spaces, that can be difficult to treat with abrasive or bulky dressings. Any chapter on foot care would be remiss without mentioning Moleskin, the ubiquitous product that has been a fixture in hikers’

first-aid kits for generations (Table 29-2). The technique of using Moleskin is to affix a doughnut-shaped patch around a hot spot or blister, securing the material with the irritated epidermis in the opening, in the hope that friction will act on the perimeter of feltlike material rather than the original spot. Although large or open heel blisters may benefit from being surrounded by

FIGURE 29-11  Wrinkled duct tape that can promote blister formation.

FIGURE 29-13  Torn epidermis resulting from Compeed bandage removal. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-12  Removing a Compeed bandage that had been placed over a blister, showing strong adhesive qualities. (Courtesy Grant S. Lipman, MD.)

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CHAPTER 29  Foot Problems and Care

TABLE 29-1  Foot Care Tapes and Pads

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 29-2  Personal Foot Care Kit Safety pins Alcohol swabs/squares Benzoin swabs /squares Spenco 2nd Skin burn pads (in resealable bag) Lubricant (e.g., Hydropel) Paper tape 10-cm (4-inch) Elastikon roll Small roll of duct tape Small scissors 18-gauge needle

Moleskin or Molefoam (Figure 29-14), the authors do not recommend this family of products for treatment or prevention of hot spots or blister treatment. Anecdotally, it has a high failure rate, is difficult to anchor, and the volume of the product in a wellfitted shoe box may cause a “contrecoup” blister on the toes or even under the Moleskin product itself because of its high coefficient of friction.59

ANTIPERSPIRANTS/POWDERS Antiperspirants and powders (Table 29-3) have been proposed as preventive measures to decrease the amount of moisture at the foot-sock interface. Limited studies provide conflicting findings in regard to blister prevention and the impact on foot perspiration. A small prospective, nonblinded study assessed the effectiveness of two different antiperspirants (aluminum based) in reducing sweat accumulation and preventing blisters. Each of the subjects applied one of the antiperspirants and then completed a 1-hour treadmill march in a warm environment. Overall, both groups experienced a significant decrease (greater than 50%) in foot-sweat accumulation and a nonsignificant trend toward fewer blisters. However, there was an increase in the incidence of irritant dermatitis.17 A randomized study of 23 healthy males examined the impact of antiperspirants with emollients by applying one of three preparations (a 20% aluminumbased antiperspirant with emollient additive; emollient alone; or nothing) for 4 days before ambulating on a treadmill in a warm environment while carrying a load over a 4-hour period. All groups experienced a similar incidence of blisters and sweat accumulation with no reported skin irritation.64 The largest of the prevention studies was a double-blind trial of 667 U.S. military cadets randomized to either a 20% aluminumbased antiperspirant or placebo for 5 days before a 21-km (13mile) hike. For compliant subjects who used the preparation for at least 3 nights, the incidence of blister formation was 21% in the antiperspirant group versus 48% for the placebo group. However, these results were tempered by a 57% incidence of skin irritation in the antiperspirant group compared with only 6% in the placebo group.37 The gained antiperspirant benefit from antiperspirant may not be worth the risk for resulting irritation.

FIGURE 29-14  Moleskin “doughnut” placed around a large open heel blister. (Courtesy Paul Langer, DPM.)

Overall, there are conflicting data to support or refute the use of antiperspirants in preventing foot blisters. In theory, antiperspirants reduce the amount of perspiration and resulting friction, leading to reduced blister formation. However, this must be balanced with the high incidence of skin irritation. Further research is needed to better define the proper dilution of compounds in the antiperspirants and frequency of application to decrease the incidence of foot blisters. Antiperspirants are most likely helpful for those who suffer from excessively sweaty feet (hyperhidrosis). If the decision is made to use an antiperspirant, a trial should be attempted at least a week before the planned outing to avoid having skin irritation in an outdoor setting. A variety of powders are designed to help with foot odor and perspiration. These powders are typically composed of an astringent to assist with itching and an inorganic compound (talc, sodium bicarbonate) to assist with wetness. Despite widespread marketing of these compounds, there is no published scientific evidence to suggest that these products prevent foot blisters.6 In addition, it has been suggested that powders may increase the risk for blisters because of their tendency to clump with perspiration. Despite anecdotal support for use of powders, they are likely best used to dry out feet in the evening, rather than being used on the trail.

LUBRICANTS Lubricants ostensibly prevent blister formation by decreasing friction at the foot-contact material interface. Lubricants have been developed that are more advanced than traditional Vaseline,

TABLE 29-3  Foot Care Antiperspirants and Powders Product

Description

Advantages

Ingredients

Pedifix Neat Feat antiperspirant spray Dr Scholl’s foot powder Gold Bond powder

Antiperspirant foot spray designed to eliminate odor, prevent irritation, and cool feet. Powder used to control foot odor, cool and soothe irritated skin, and absorb wetness. Medicated body powder used to prevent skin irritation and relieve itching.

Aluminum, oils

Odor-Eaters foot powder

Powder combining special ingredients with baking soda to control odor and protect against wetness.

Spray makes application extremely easy Absorbs moisture, controls foot odor and odor-causing bacteria. Absorbs moisture, controls foot odor and odor-causing bacteria, provides itch relief, and cools and soothes irritated skin Odor and wetness protection

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“Special cooling product” Zinc oxide and menthol Unique combination of odor-destroying ingredients and baking soda

Product

Description

Advantages

Application

Ingredients

Bodyglide

Hypoallergenic, non–petroleum based moisturizer that helps prevent against friction, rubbing from footwear, and blister formation.

Nongreasy, nonfragrant, sweat and water resistant

Hydropel

Silicone-based skin lubricant used to prevent blisters, chafing, and chapping of skin in extreme environments. Skin gel composed of antifungal and antibacterial ingredients used to prevent blisters, chafing, and chapping of skin in dry and water environments.

Nongreasy, nonfragrant, sweat and water resistant

Packaged as an applicator (i.e., deodorant stick) that can make it slightly awkward for application to the foot Ointment allows easy application to any body part

Allantoin 0.5; Aloe barbadensis (Aloe vera) leaf extract, C18-36 acid triglycerides, caprylic/capric triglycerides, tocopheryl acetate, tribehenin Dimethicone 30%, petrolatum, aluminum starch, octenylsuccinate

Nongreasy, sweat and water resistant

Tolnaftate 1%, triclosan, silicone, petrolatum, aloe, vitamin E, soybean oil, and oil fragrance

Relative ease of application to any body part depending upon product used Easy to apply to any body part; however, the product is greasy

Dimethicone, aloe vera extract, vitamin E

Sportslick

Sportshield

Vaseline

Silicon-based liquid roll-on or towelette used to minimize friction that causes blisters, chafing, and irritation. Petroleum-based product used to minimize friction that causes blisters, chafing, and irritation.

Skin gel composed of antifungal and antibacterial ingredients used to prevent blisters, chafing, and chapping of skin in dry and water environments Nongreasy, water resistant, and odorless Water resistant, odorless

Blister Treatment

which is greasy and tends to attract grit particles that irritate and may increase friction and blister production (Table 29-4). Lubricating agents that have a subjective “greasiness” leave skin with a higher coefficient of friction than those with a sensation of “slipperiness.”54 Advanced lubricants use silicone and petrolatum mixes that have a silky feel and are thought to work by altering skin smoothness and moisture content of the skin. Several studies have shown that after applying lubricating substances to skin, there is an initial decrease of the coefficient of friction, but that within an hour, it returns to baseline with a subsequent increase in friction 35% over baseline over the next 4 to 6 hours (Figure 29-15).12,54 The studies suggest that with prolonged exercise, the use of lubricants might contribute to blister formation, so if used, they need to be reapplied frequently. More recently, analysis of the effect of skin creams on the skin of a rat model found that the cream appeared to reduce roughness of the surface while increasing hydrophilic properties of the skin. In addition, the authors noted an increase in the coefficient of friction for the cream-treated skin when the thickness of the cream was lower than a specific thickness.77 Future clinical studies are needed to assess if newer-generation lubricants or creams prevent blisters, need re-application at certain intervals, or actually contribute to blister formation. Percent change in friction coefficient

100% pure petroleum jelly

Treating a blister as soon as possible improves outcome, reduces pain, and minimizes complications from either subsequent tissue damage or infection. In the early stages of blister formation, the initial sensation of warmth from the hot spot is a warning sign. Prompt attention and rapid treatment can stop the abrasive process to prevent progressive blister formation. Options for hot spot treatment include the blister-preventive taping/lubricating measures mentioned earlier in the chapter. Proper blister care is not complicated, yet may be time intensive depending on the extent of damage to the feet. Individuals should become familiar with techniques before heading outside and facing a blister predicament. The authors’ medical experiences with ultraendurance Racing the Planet events have shown that implementation of mandatory personal foot care kits for competitors and the expectation of self-care takes a huge burden off the medical team (Table 29-5). The blister treatment techniques discussed in this chapter have been easily taught and mastered by numerous ultraendurance race participants. There is no one correct way to care for feet. For every technique and product mentioned, there are several different options. The goals of blister treatment are to optimize comfort for

50 Petrolatum Heavy mineral oil Glycerin Baseline

40 30 20 10 0 –10 –20 –30 –1

0

1

2

3

4

5

6

Time after application (hrs) Time = –1 is immediately prior to application; time = 0 is immediately after application FIGURE 29-15  Effect of lubricant cosmetic ingredient on skin friction coefficient. Amount applied to each material: approximately 2 mg cm-2. (Reproduced with permission from Sivamani RK, Goodman J, Gitis NV, et al: Coefficient of friction: Tribological studies in man—an overview, Skin Res Technol 9:227, 2003.)

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CHAPTER 29  Foot Problems and Care

TABLE 29-4  Foot Care Lubricants

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 29-5  Expedition Foot Care Kit Foot Care Materials Alcohol swabs/towelettes Micropore paper tape, 2.5 cm (1 inch) Micropore paper tape, 5 cm (2 inch) Paper towels/gauze for draining blister fluid Elastikon tape, 5 cm (2 inch) (or other tape of choice) Elastikon tape, 10 cm (4 inch) (or other tape of choice) Pedi-Pre adherent spray or benzoin swabs/towelettes Adhesive felt, 0.6 cm (0.25 inch) Spenco 2nd Skin 2.5-cm (1-inch) squares Spenco 2nd Skin 7.5 cm (3-inch) circles Athletic tape Hydropel Duct tape Instruments Tissue scissors Bandage scissors Nail file Blades, sterile No. 15 Hypodermic needles, 18 gauge Hypodermic needles, 25 gauge, 3.2 cm (1.25 inch) Syringes, 3 mL and 5 mL Safety pins Miscellaneous Ankle/SAM Splints Isopropyl alcohol liquid, bottle Povidone-iodine sticks Povidone-iodine liquid, bottle Elastic wrap, 10 cm (4 inches) Antibiotic or antiseptic cream Antiinflammatory cream Gloves, latex-free, nonsterile Chemical ice packs Antiseptic hand-washing cleanser Washbasin for cleaning feet Garbage bags Sharps container Cephalexin, 500-mg pills Amoxicillin-clavulanic acid, 875-mg pills Levofloxacin, 750-mg pills Ceftriaxone, 1-g ampules Lidocaine 1%, ampules IV catheters, 18 gauge and 20 gauge IV starter kit and tubing. 1000 mL dextrose 5% in normal saline and normal saline

Before taping, ensure that the skin is clean of dirt and grit and as dry as possible, which will enhance natural adhesion of tape. Consider using an adhesive substance, such as benzoin, to ensure security of the applied dressing. Extra care must be given to securing the tape, possibly using duct tape or extra tape as an anchor. As a general rule, try not to remove blister tape unless it is peeling off or there is increasing discomfort at the tape site. Some clinicians advocate removing tape during multistage events.82 However, leaving tape on as long as possible during repetitive activity minimizes the risk for “deroofing” the blister on tape removal. When tape is to be removed (ideally after the activity is finished and feet will not be subjected to further abuse), soaking the bandages before removal will loosen adhesion and minimize chances of ripping open intact blisters.

BASIC BLISTER TREATMENT The pain from a blister is due to pressure on an incompressible fluid between skin layers. As abrasion and pressure build, there is further pain and separation of skin layers and increasing potential for rupturing the blister, which would leave exposed raw and sensitive skin. The best protection for a blister is its own “roof,” so efforts should be taken to maintain this natural skin protection. The best method for treating a blister is to drain the fluid. Small friction blisters that are not causing significant discomfort can be left intact. If the blister is punctured with a needle and drained, it will often refill within a few hours. If a large hole is made that allows continuous fluid drainage, there is the risk for losing integrity of the blister and having the blister’s roof tear off, leaving a large damaged area. The authors’ recommendation is to use a safety pin or similar-sized needle to create an optimumsized hole. To clean a blister, wash gently around it with soap and water, being careful not to break the skin. If unbroken, use a sterilized needle or knifepoint to prick the lower edge of the blister to remove fluid. Do not remove the skin; cover the blister with an absorbent adhesive bandage or similar dressing, extending beyond the edge of the blister.18 Prepare the blister skin and safety pin with an alcohol pad. Alcohol pads commonly have two hinged sheets; one sheet can be used to clean the blister-draining implement and the other to clean the skin. Puncture the blister with the prepared pin at a distal point (away from the midline). This will allow natural foot pressure to continually squeeze out fluid. If more drainage is required, use several small holes rather than one large hole, limiting risk for deroofing the blister. Gently blot out the expressed fluid (Figures 29-16 and 29-17). Cover the now-flattened blister with paper tape that is cut to overlap the edge of the blister (Figure 29-18). This very important step protects the roof of the blister when the overlying tape is removed. Cover paper tape with benzoin adhesive and allow it to become tacky. As a final layer, apply shaped adhesive tape over the paper-taped blister

IV, Intravenous.

continued activity, maximize prevention of infection, assist with epidermal recovery, and prevent further blister enlargement when resting and “staying off your feet” is not an option.

GENERAL TAPING RULES Any tape used for blister treatment or prevention should be applied as smoothly as possible. The tape ideally acts as a second layer of skin, so rubbing acts on the tape, not on the underlying skin. Any folds or wrinkles in the tape should be avoided because they may lead to high-pressure and friction areas. Cut the tape corners to round them and to avoid “dog-ears” that have a tendency to roll off under a sock. All tape should be cut long enough to extend well beyond the border of the blister and any blister pads underneath the tape. Try to not overlap tape, and avoid circumferential wrapping of the feet that may lead to venous congestion and swelling. 586

FIGURE 29-16  A toe blister. (Courtesy Grant S. Lipman, MD.)

CHAPTER 29  Foot Problems and Care

FIGURE 29-17  Expressing fluid from a toe blister. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-20  Removal of the torn roof of an open blister. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-18  Paper tape covering of a drained blister. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-21  Spenco 2nd Skin cut to size, slightly overlapping the open blister circumference. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-22  A blister at the end of a toe. (Courtesy Grant S. Lipman, MD.) FIGURE 29-19  Elastikon tape layer over paper-taped blister. The elastic quality of the tape allows smooth application and contours to the foot. (Courtesy Grant S. Lipman, MD.)

(Figure 29-19). Blisters that recur under intact tape can be drained with a prepared safety pin through the tape.

of hydrocolloid Spenco pads absorbs moisture and promotes collagen production and healing while providing cooling relief and padding. Finish dressing the blister by covering the Spenco with paper tape, a benzoin adhesive layer, and finishing with shaped Elastikon tape or tape product of choice (basic blister treatment).

OPEN BLISTER TREATMENT

TOE BLISTERS

Using scissors, carefully unroof the blister (Figure 29-20), completely trimming off the dead skin. Devitalized skin is insensate and not painful to remove. Place a piece of Spenco 2nd Skin pads over the exposed base of the blister, extending slightly beyond the external margins (Figure 29-21). The moisture content

Only paper tape should be used on toe blisters, because tape with rough texture can cause irritation, abrasion, and blisters on neighboring toes. Drain a clean blister with a prepared safety pin. If a blister is at the end of a toe (Figure 29-22), apply a piece of paper tape longitudinally covering the distal phalanx 587

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 29-23  Paper tape–wrapped toe blister. This wrapping technique can also be applied to hot spots, as well as prophylactically to help avoid toe hot spots and blisters. (Courtesy Ashlie Emmett.)

FIGURE 29-25  A 10-cm (4-inch) Elastikon tape is prepared for heel cup application; the tape is cut longitudinally with a central connected piece. Note the rounded edges of the tape to minimize the edges peeling off. (Courtesy Grant S. Lipman, MD.)

from the dorsum to the plantar aspect. A second strip of paper tape is used as an anchor, encircling the toe circumferentially (Figure 29-23). If there is an isolated blister in the web space, just applying the circumferential wrap should be sufficient. Care should be taken to not overlap the tape multiple times, constricting the digit, and to leave the tape end on the dorsum of the foot, to avoid irritating neighboring toes. Pinch the tape closed, and trim any dog-ears or wrinkles.

HEEL BLISTERS Heel blisters are notorious for the pain and large size (Figure 29-24). The authors have witnessed exasperated persons cut out the heel of a shoe to remove the instigating point of friction. A “heel cup” is a useful technique to provide a large surface area over the blister, while providing a large anchoring surface to compensate for the large shear stresses. A large 10-cm (4-inch) piece of Elastikon is cut to cover the calcaneus, and the corners are rounded off. A horizontal incision is cut almost completely through the tape, leaving an anchoring piece in the middle like a large sideways H (Figure 29-25). The upper portion is wrapped around the upper heel (Figure 29-26), and the lower “wings” are wrapped over the plantar heel and up over the ends of the upper portion, anchoring them down (Figure 29-27).

FIGURE 29-24  Heel blisters are notorious for pain. (Courtesy Grant S. Lipman, MD.)

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FIGURE 29-26  Wrapping the wings of a heel cup up under the malleoli will help to stabilize the bandage inside the footwear. (Courtesy Ashlie Emmett.)

BALL-OF-FOOT BLISTERS Blisters occurring on the ball of the foot may be very painful, because this is a large weight-bearing surface (Figure 29-28). These blisters are often difficult to reach. Taping across the ball and up the sides of the foot is an option, but because the tape is running perpendicular to the mechanical movement of the foot

FIGURE 29-27  A completed heel cup covering a heel blister. (Courtesy DJ Kennedy, MD.)

CHAPTER 29  Foot Problems and Care

FIGURE 29-28.  Ball-of-foot blister. (Courtesy Paul Langer, DPM.)

in the shoe, it has a tendency to pull off. The authors prefer a method we have dubbed “desert origami.” The blister is drained and treated using either the open or closed method described earlier. Figure 29-29 shows a dumbbell or butterfly shape cut out of Elastikon tape with a thin connector piece. This provides three important functions. The tape has a large surface area to cover and protect the blister; it has a large surface area to be anchored on the dorsum of the foot; and the thin strip of material connecting the two halves of tape passes between the web space of the toes, causing minimal irritation and avoiding further webspace blisters. In some cases, a piece of Elastikon tape may be used over the instep to secure the “origami” (Figure 29-30).

SUBUNGAL HEMATOMAS A subungual hematoma is a collection of blood that develops underneath the nail bed. The mounting pressure makes this very painful. It is common to acquire a subungual hematoma on downhill hikes or runs when the toes are repetitively jammed into the toe box. A toenail that has been beveled downward at a 45-degree angle seems to direct pressure upward rather than back into the toe matrix. Some people find silicone toe caps useful to prevent these injuries. Other athletes have gone so far as to have all their nails removed prophylactically. This is a drastic measure. Subungual hematomas are easily treated. An 18-gauge hypodermic needle is held perpendicular to the proximal nail bed over the area of greatest fullness (Figure 29-31). With gentle downward pressure, hold the needle between the thumb and first finger (Figure 29-32). Twirl the needle back and forth between the thumb and finger and it easily drills into and through

FIGURE 29-30  A well-wrapped ball-of-foot blister stabilized with a perpendicular piece of Elastikon tape. (Courtesy Mark Ellis, MD.)

the nail, releasing the hematoma (Figure 29-33, online). The release of blood under pressure through the 18-gauge hole may be dramatic, causing it to squirt, so one should use appropriate universal precautions. The 18-gauge needle should be recapped and likely will need to be reused for the same patient, because these blisters have a tendency to recur.

FIGURE 29-31  A subungual hematoma about to be drained with an 18-gauge hypodermic needle. (Courtesy Brandee Waite, MD.)

FIGURE 29-29  “Desert origami.” Note the rounded corners of tape prepared to minimize the edges peeling off. (Courtesy Grant S. Lipman, MD.)

FIGURE 29-32  Moderate downward pressure applied to a rotating 18-gauge hypodermic needle will drill a hole and release the blood under a toenail. (Courtesy Brandee Waite, MD.)

589

PART 4  INJURIES AND MEDICAL INTERVENTIONS FIGURE 29-34  Needle-and-thread blister technique. (Courtesy Brian Krabak, MD.)

ADVANCED BLISTER CARE TREATMENTS In the needle-and-thread technique (Figure 29-34), a needle and thread are cleaned with alcohol and passed through the blister, leaving 2.5 to 5 cm (1 to 2 inches) of thread hanging out on either side of the blister. The thread acts as a wick to continually drain fluid and quickly dry the blister. Although this method seems to work well, it is only cautiously mentioned, because any route for fluid out of a blister is a potential entry point for bacteria. Techniques to chemically treat blisters have variable rates of success, yet consistently high levels of procedural pain. One method to seal a blister’s roof uses benzoin. After the blister has been drained, benzoin or “liquid bandage” is directly injected into the blister cavity, then pressure is applied to the roof of the blister. This seals or “glues” the blister together. A similar technique has been attempted (cutting off the blister roof, blotting away the blister fluid, and then gluing the blister’s roof down) in a prospective study using 2-octylcyanoacrylate (tissue glue). There was no significant difference in either the intervention or control groups in mean blister size or time of return to normal activity; however, the 2-octylcyanoacrylate arm was associated with significant procedural discomfort.42 A particularly uncomfortable technique made popular by the Marathon des Sables is the application of merbromin (Figure 29-35) to a manually deroofed blister. This mercury salt compound effectively dries out the blister base, allowing further activity on a now callus-like epidermis (Figure 29-36). Of note, this product was moved from the “generally recognized as safe” into the “untested” classification by the U.S. Food and Drug

FIGURE 29-35  Mercurochrome brand antiseptic. (Courtesy Grant S. Lipman, MD.)

590

FIGURE 29-36  Mercurochrome applied to a large open heel blister with resulting red staining and desiccated skin. (Courtesy Grant S. Lipman, MD.)

Administration in 1998 over concerns about mercury toxicity,49 effectively stopping its U.S. distribution. It is widely available in many other countries.

BLOOD-FILLED BLISTERS Blood-filled blisters represent injury to the dermal plexus (Figure 29-37). This blister represents a potential route for bacteria to enter the wound and bloodstream, which can lead to cellulitis or sepsis. Blood blisters should be left intact unless they are large, fluctuant, and at risk for spontaneous rupture. To drain a blood blister, use a povidone-iodine preparation and clean gloves and instruments following the techniques described previously (Figure 29-38). Consider applying antiseptic ointment to the drained blister before taping. Recheck the blister site frequently for redness, streaking, or pus, in which case any infection should be treated promptly with an antibiotic.

FIGURE 29-37  Large fluctuant blood blister. (Courtesy DJ Kennedy, MD.)

INFECTED BLISTERS A blister with murky, hazy fluid or pus may be infected. The blister should be opened (deroofed), irrigated with povidoneiodine (Figure 29-39, online), and then have antiseptic or antibiotic ointment applied to the cavity before being covered with the “open blister” technique. This blister’s roof is more sensitive than most devitalized blister skin. An infected blister surrounded by tender, warm, red skin or streaking may represent cellulitis. This blister should be opened and managed as described, with the addition of an antibiotic. If the patient begins to show signs of worsening local infection or systemic symptoms, such as chills, fevers, nausea, or weakness, definitive care should be sought as soon as possible.

SUBCALLUS BLISTERS Blisters deep to a callus should not be drained. These blisters are difficult to access, yield little blister fluid, and quickly refill after drainage. Drainage can introduce infection to the deep space. These blisters are painful, but there is no other good treatment option beyond taping as for a basic blister and allowing the fluid to be absorbed by the body. These painful and difficultto-manage blisters are examples of why it is beneficial to minimize blisters with a pumice stone or emery board before an outing.

Common Foot/Ankle Injuries The wilderness physician should be prepared to evaluate and treat common foot and ankle injuries. The majority of these injuries are not life threatening and can be managed conservatively while in the wilderness. However, foot and ankle injuries can have a significant impact on activity level during and immediately following an expedition. Therefore, once stabilized, the focus should be to successfully return the individual home for proper follow-up care.

LIGAMENT INJURIES The majority of ligament injuries involve the ankle joint. Ankle sprains represent approximately 14% to 21% of sports injuries.44 A sprain typically involves the lateral ankle complex (85%) compared with the medial complex or syndesmosis.21 Anatomically, the distal fibula extends more inferiorly than does the tibia, contributing to lateral ankle instability. The lateral ankle ligaments (anterior talofibular ligament [ATFL], calcaneofibular ligament [CFL], posterior talofibular ligament [PTFL]) are quite small compared with the thicker medial deltoid ligament. The syndesmotic ligament includes an interosseous membrane connecting the distal tibia, fibula, ATFL, and PTFL. The typical mechanism of injury involves excessive inversion and plantar flexion of the foot, resulting in a torn lateral

SOFT TISSUE INJURIES Many soft tissue injuries to the foot and ankle involve tendon injuries. Lower extremity tendon injuries occur from excessive overuse and/or improperly fitting equipment. Individuals who are poorly conditioned, insufficiently prepared, or overtrained are at risk for injury.69 Injury often occurs because of tendon sheath inflammation or degeneration of the tendon over time. Fortunately, unless there is subsequent tendon tear, these can be treated conservatively with nonsteroidal antiinflammatory drugs, physical therapy, and/or corticosteroid injections. Treatment should focus on any biomechanical deficits that contributed to the injury, including inflexibility or strength issues. 591

CHAPTER 29  Foot Problems and Care

FIGURE 29-38  The blood blister was drained with povidone-iodine skin preparation to minimize spontaneous rupture and resultant infection. The drained blister is dressed with paper tape in preparation for a heel cup. (Courtesy DJ Kennedy, MD.)

ligament. The majority of lateral ankle sprains involve the ATFL but may include the CFL up to 50% of the time. The PTFL is involved in fewer than 10% of all lateral ankle injuries.22 Patients often describe a “popping” sensation when twisting an ankle, probably on an uneven surface. There will be immediate pain and swelling on the lateral aspect of the ankle, with difficulty bearing weight on the affected leg. Palpation reveals tenderness involving the lateral ligament complex but should not include the fibula away from the ankle joint, the medial ankle, calcaneus, or proximal fifth metatarsal bone. Tenderness in these other areas and inability to bear weight would suggest more severe injury, such as a fracture, as defined by the Ottawa ankle rules.40,73 The extent of ligamentous instability should be assessed for the ATFL with the anterior drawer test (when the foot is plantarflexed about 30 degrees, the calcaneus is cupped and moved anteriorly while the distal tibia is stabilized) and the CFL with the talar tilt test (when the foot is at 0 degrees of plantar flexion, the calcaneus is cupped and inverted while the distal tibia is stabilized). Medial ankle sprains are much less common than are lateral ankle sprains but are more severe. The typical mechanism of injury involves excessive external rotation leading to a torn deltoid ligament and possible proximal fibula fracture. Patients describe exquisite pain on the medial aspect of the ankle and possibly over the proximal fibula due to concurrent fracture. They will usually not be able to bear weight due to pain. Palpation reveals marked tenderness involving the medial ankle at the distal tibia and proximal fibula if there is a concurrent fracture. Eversion stress of the ankle joint (foot plantar flexed, foot everted) produces pain and may reveal instability compared with the noninjured ankle joint. Like medial ankle sprains, syndesmotic or “high ankle” sprains are less common, but more severe. The mechanism of injury involves excessive external rotation and dorsiflexion of the ankle joint, leading to a torn syndesmosis.22 Individuals describe pain between the distal tibia and fibula with inability to bear weight. Palpation l reveals tenderness along the distal tibia–fibula joint. External rotation stress test (foot is externally rotated while held at 0 degrees of plantar flexion) and squeeze test (squeezing the midshaft of the tibia and fibula) reproduce pain in the distal tibia–fibula joint. Once an ankle sprain is suspected, treatment focuses on pain control and joint stabilization. It is not necessary to “grade” the ankle sprain, although appreciating the severity of injury may alter treatment recommendations while in the wilderness setting. Swelling may initially be minimized through use of a cold compress made of chemical ice packs or snow; a cold running river can work just as well. Pain medication should be considered depending on the individual’s symptoms. Ideally, the wilderness provider will have an ankle brace, elastic wrap, tape (athletic tape or Coban), or similar device (SAM Splint) to provide support for the injured ankle.4 Appropriately sized sticks placed on either side of the ankle joint may work as splints, if no other supportive device is available. When not ambulating, the limb should be elevated to limit swelling. Weight bearing should be limited as much as possible, which may be challenging in the wilderness. Evacuation may be necessary if a severe injury or fracture is suspected and the patient is unable to ambulate. A proper rehabilitation program focusing on proprioceptive and strength training41 should help prevent future injures.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

ACHILLES TENDINOPATHY

BONE INJURIES

Achilles tendinopathy may range from mild tendonitis to complete rupture of the tendon necessitating surgical repair. It is estimated that 6.5% to 18% of runners experience Achilles tendon injury.69 Injury is often due to excessive loading of the tendon with rapid deceleration or acceleration, such as walking up or down a steep hill. Contributing factors may include inappropriate footwear (stiff support around ankle), hyperpronation, and obesity.81 Pain and swelling occur around the distal aspect of the tendon, approximately 2 to 6  cm (.8 to 2.4 inches) above its insertion into the calcaneus. If there is complete rupture, individuals describe a popping sensation in the Achilles tendon and inability to take a step, and they may note an obvious defect in the tendon. Palpation of the region reveals tenderness, swelling, or defect in cases of rupture. A positive Thompson test (lack of ankle plantar flexion with compression of the gastrocnemius complex) suggests complete rupture of the Achilles tendon. Treatment options depend on the severity of injury. In mild tendinopathies and incomplete tears, ice and pain medication help manage the symptoms.72 A heel cup or use of layered felt pad/Moleskin under the heel may be helpful to decrease the amount of plantar flexion at the ankle, resulting in less stress to the tendon. Frequent rest breaks from activity and stretching of the Achilles tendon may help manage the symptoms. An individual suspected of a complete tendon rupture should have the ankle joint immobilized with the ankle in plantar flexion, if possible. Anyone suspected of an acute Achilles tendon rupture should be evaluated as soon as possible by an orthopedic surgeon.

The reader is referred to Chapter 27 for a complete discussion regarding management and treatment of fractures. This section focuses on two common injuries involving the foot region: stress fractures of the metatarsal bones and sesamoiditis. Both of these diagnoses contribute to metatarsal pain or metatarsalgia.

PLANTAR FASCIITIS The plantar fascia is thick tissue that stretches along the bottom of the foot from the heel bone toward the toes, with some fibers close to the skin. It provides support for the foot and helps to maintain dynamic alignment of the foot and leg while walking and running. Overuse and repetitive microtrauma cause inflammation and degeneration of the fibers. When this tissue becomes painful and stiff, it is described as plantar fasciitis. In the general population, increased risk is seen with obesity, heel spurs, poor strength and flexibility, and prolonged standing.65 In athletes, especially runners, there is increased risk with flat feet, higharched feet, limited ankle flexibility (from tight Achilles tendons), incorrect running shoe fit, inadequate warm-up, and excessive training (especially with sudden increases in distance). Persons with plantar fasciitis describe sharp pain on the plantar aspect of the foot. It is worse when beginning to walk after sitting or lying down, especially on first getting out of bed in the morning. The symptoms usually get worse at the beginning of a workout but improve with time. Worsening heel pain with continued ambulation could be indicative of an underlying stress fracture of the calcaneus. On examination, there is usually a discrete area that is tender to touch over the medial part of the heel bone. The discomfort can extend over the length of the fibers under the foot. There should not be tenderness involving the calcaneus away from the insertion of the plantar fascia. Limited big toe extension is often seen with plantar fascial tightness. The treatment of plantar fasciitis is not emergent. The condition frequently should improve with conservative treatment.46,83 In the acute setting, management addresses both symptoms and mechanical factors. Initial therapy includes protection with activity modification. Ice massage, especially after activity or at the end of the day, may be helpful. Antiinflammatory medications may be used briefly (1 to 2 weeks) if there is a suspected inflammatory component. Arch support with taping and/or the use of heel cups has been helpful in some patients. Some individuals respond to night splints, which are thought to assist in maintaining a stretch to the plantar fascia throughout the night. The use of custom orthotics is controversial, although helpful for some patients. Recalcitrant symptoms may require other interventions, including the use of physical therapy, night splints, injections, and surgery (rare). 592

STRESS FRACTURES Stress fractures are common in athletic and military individuals. They occur when an excessive load is placed on normal bone because of repetitive stress or a normal stress is placed on abnormal bone.7 Stress fracture of the foot most often involves the metatarsal region of the foot (march fracture) but can involve the calcaneus or talus. Metatarsal stress fractures typically involve the second metatarsal, followed by the third and first metatarsal bones. The majority of studies looking at the incidence of stress fractures in the foot suggest an incidence of 5% to 35% depending on the specific population and anatomic location.51,58 Various extrinsic and intrinsic factors have been described as contributing to development of stress fractures. Extrinsic factors include excessive training, incorrect footwear, or new footwear. Intrinsic factors include pes planus,62 pes cavus, excessive forefoot varus, tight Achilles tendon, and weak hip musculature. Individuals experiencing stress fractures will report a variety of symptoms depending on the location of the injury. They often first describe diffuse pain in the region of the stress fracture that localizes to a specific area over time. The pain is worsened with continued weight-bearing activity and relieved by rest. On physical examination, pain along the bone localized to a specific area corresponding to the area of reported pain suggests a stress fracture. Swelling may be noted over the dorsum of the foot for metatarsal stress fracture or around the ankle for talus or calcaneal stress fractures. Inspection should reveal normal anatomic alignment of the foot and ankle structures. Thorough neuromuscular examination should be performed to rule out other injuries. Treatment should focus on the specific symptoms in relation to the area suspected of having the underlying fracture. The use of medication, ice, and elevation helps with pain and swelling. In the case of metatarsal stress fractures, some individuals may be able to tolerate continued ambulation if the pain is not too severe. Individuals with severe metatarsal pain or pain involving the talus and/or calcaneus may not be able to bear weight. These individuals may be placed in a posterior splint for protection, and evacuation may be warranted, depending on severity of the symptoms. Fortunately, metatarsal stress fractures resolve over 4 to 6 weeks once the individual is able to rest. Calcaneal and talus stress fractures typically take longer to heal. All individuals should seek definitive evaluation once removed from the wilderness setting.

SESAMOIDITIS Sesamoiditis involves injury to the sesamoid bones under the first metatarsal head. Although the term would suggest inflammation, this most likely represents a stress fracture to the sesamoid bones. Individuals describe pain localizing to the plantar surface of the first metatarsal region. Pain occurs with continued weight bearing and improves with rest. On physical examination, there is swelling involving the first metatarsal region. There is pain with palpation that may move slightly with extension and flexion of the first great toe. Treatment should focus on decreasing pressure to the sesamoid region. Strategies include use of doughnut-shaped padding around the area to relieve pressure to the sesamoid and deceased weight bearing.

ORTHOTICS Foot orthoses have been commonly used to manage various lower extremity injuries. Despite their widespread use, there are conflicting data regarding the efficacy of these devices and their use in preventing blister formation or injury occurrence. Some clinicians question the putative benefits of modern-day running shoes. These authors note that despite the continued

BUNIONS

but may occur along the plantar surface (moccasin) or instep (vesiculobullous) of the foot. There is increased prevalence of tinea pedis in athletes compared with the general population.23 Reported prevalence rates vary by sport, with a preponderance in runners (22% to 31%) and soccer players (61%).10 Trichophyton rubrum and T. mentagrophytes cause most cases; less common causes include Epidermophyton floccosum or Candida. Unique factors in the athlete contributing to the development of athlete’s foot include excessive sweating, exposure to water, occlusive athletic footwear, and skin trauma. Typical symptoms include pain, itching, and burning with observed red, dry, or cracking skin or scaling of affected areas. The foot may develop erythematous plaques, fissures, vesicles, or bullae. Superinfection with bacteria may cause skin to appear shiny, taut, red, with progressively more severe pain. Prevention and aggressive treatment are crucial to managing these foot infections. Preventive strategies include keeping feet dry by using synthetic socks (rather than cotton), changing socks often, well-ventilated shoes, and dusting over-the-counter antifungal powders into shoes. Treatment options include antifungal ointments or powders, such as azoles, tolnaftate, or allylamines, for 4 weeks. Nonadherence to a 4-week treatment course leads to recurrence. For more complex cases, oral drug therapy, such as with itraconazole, fluconazole, or terbinafine, may be necessary.

PLANTAR WARTS A plantar wart (verruca plantaris) is a benign epithelial tumor caused by the human papillomavirus, found on the plantar surface (sole) of the foot and toes (Figure 29-40). This highly contagious virus is able to survive several months without a host. Skin that is moist, cracked, or with an open blister is most susceptible to infection. Avoiding direct skin-to-skin contact with a wart minimizes the chances of transmission. The lesion appears as a flesh-colored, white, brown, or grey area, is usually hard and granulated, and can have a spongy cauliflower-like appearance. The wart may have punctate bleeding when irritated. Plantar warts can be differentiated from calluses or corns by recognizing the skin striations that go around plantar warts, rather than continuing through them (because the skin’s DNA is altered by the virus). After infection, it may take several weeks or months for a wart to become visible, because pressure on the foot causes layers of hardened epithelium to form over the deep infection. Plantar warts are self-limited and resolve on average within 15 weeks.25 Irritation and pain exacerbated by physical activity drive many to seek treatment. Although no single therapy has been proved to provide complete remission, treatment may decrease duration and reduce transmission.25 Treatment of warts in the field is usually limited to providing symptomatic relief by padding the surrounding area with a doughnut cut out of Moleskin or

A bunion or hallux valgus deformity manifests as an abnormal alignment of the foot, typically involving the first metatarsal phalangeal joint. A bunionette, or tailor’s bunion, will involve the fifth metatarsal phalangeal joint. Most experts believe that there is a genetic predisposition to bunions.28,33 Bunions slowly develop over time, leading to alignment changes in the foot, including a valgus deformity, widening of the forefoot, and pes planus. Eventually, the metatarsal phalangeal joint develops degenerative arthritis. Bunions can be painful with hiking or running because of the altered foot biomechanics. Blisters may form over the bunion as a result of excessive friction. Ideally, preventive strategies such as appropriate-fitting shoes with a wide toe box and orthotics may help avoid symptoms.28 Preventive treatment of the bunion skin with strategies for blister care mentioned in this chapter may be helpful as well. Treatment is focused on alleviating the symptoms through the use of rest, ice to the area, blister care, and decreased weight bearing.

TINEA PEDIS Tinea pedis, or “athlete’s foot,” is a fungal infection of the foot. It most commonly occurs in the web spaces between the toes

FIGURE 29-40  Verruca plantaris (plantar warts) on the sole of the foot. (Reproduced with permission from Bacelieri R, Johnson SM: Cutaneous warts: An evidence-based approach to therapy, Am Fam Physician 72:647, 2005.)

593

CHAPTER 29  Foot Problems and Care

modifications to shoes, there are limited data to suggest decreased injury rates to runners. Although detailed discussion of orthoses is beyond the scope of this chapter, several key points may help the sports physician and athlete in deciding whether to recommend and use them. Several theories have been proposed to suggest how orthoses help to prevent lower extremity injuries. These theories focus on the areas of kinematics, shock attenuation, and neuromotor control. In the kinematic model,32,52 abnormal pronation at the subtalar joint coupled with abnormal tibial rotation leads to lower extremity injuries. In the shock attenuation model,55 excessive impact forces on the lower extremity contribute to injury. Finally, the neuromotor control model52,57 suggests that inappropriate muscle activity and fatigue contribute to injury. A recent metaanalysis found there is a significant amount of variability in study design and how patients have responded to the use of orthoses.52 It appears that noncustom orthoses produce greater rearfoot and tibial motion control compared with controls. Custom-molded orthoses appear to be more effective in decreasing the loading rate and impact forces on the lower extremity, compared with controls. Orthoses appear to increase the activation of lower extremity muscles, including the tibialis anterior, peroneus longus, medial gastrocnemius, and thigh muscles. What is not clear is whether these changes prevent future lower extremity injuries. Several studies suggest that the use of running shoes and orthoses may actually contribute to lower extremity injuries. Analysis of gait patterns and forces in the lower extremity of barefoot and shod (shoed) runners34,43,53 suggest that barefoot runners strike in the midfoot and forefoot, compared with shod runners, who strike at the heel.19,43 As a result, in barefoot runners there are lesser impact forces,34,43 lesser contact times, better transfer of energy to rotational energy, and more natural motion to the lower extremity. In addition, proponents of barefoot running suggest that immobilizing the foot through use of shoes or orthoses leads to deconditioning and atrophy of lower extremity muscles, contributing to injury. Whether or not an individual should use an orthotic is between the user and his or her physician. For persons without injury, orthoses are probably not needed. More importantly, an appropriate training schedule to slowly stress the bones, muscles, ligaments, and skin of the lower extremities will help prevent injuries. The above studies suggest that athletes could help in conditioning by incorporating minimal or barefoot running into their training program, as long as it is instituted in a safe manner. For individuals with recurrent or prolonged injuries, correction of flexibility and strength deficits and review of training schedules should help with treating injuries. Addition of orthotics may play a role in treating specific injuries, depending upon lower extremity biomechanical or neuromuscular control issues.

Molefoam placed around the affected area to minimize direct pressure. Salicylic acid therapy is considered first-line medical treatment;5 and if used while active, the area should be covered with duct tape (occlusion therapy). Debridement of the offending area is discouraged, because it may lead to superinfection or autoinoculation of surrounding skin. If the plantar wart remains bothersome, a visit to a podiatrist is recommended.

HYPERHIDROSIS Hyperhidrosis is the distressing condition of sweating in excess of what is needed for thermoregulation.31 It is usually in a focal distribution, affecting the axillae, palms, and/or soles. The cause is unknown (idiopathic) in the majority of cases, but it can be attributed to sympathetic overactivity and rarely, to an underlying pathologic state. Generalized sweating other than in focal areas suggests an etiology of secondary hyperhidrosis that may represent significant disease and should be investigated by a physician. The onset of idiopathic hyperhidrosis is often in adolescence and may persist throughout adult life. Sweating is usually exacerbated by heat or emotional stimuli and has both emotional and physiologic consequences, because continuously wet feet predispose to maceration, blisters, and infection. The mainstay of treatment is frequent changing into dry socks and application of a topical antiperspirant. Most over-the-counter antiperspirants contain small concentrations of a metal salt, and may be successful in alleviating mild symptoms. Prescriptionstrength antiperspirants are available; unfortunately, effectiveness is often limited by resulting skin irritation. To minimize irritation, the strong antiperspirant should be applied to dry skin between

sweating episodes. Some clinicians recommend applying in the evening (when hyperhidrosis is at a minimum) and washing off in the morning.75 Some experts advocate applying baking soda in the morning to neutralize any remaining noxious compound.68 Iontophoresis is a treatment that temporarily blocks sweat glands by delivering a low voltage of direct current to intact skin. The foot acts as a conductor between positively and negatively charged buckets of water; the minerals in the water (released by the current) are thought to affect the sweat ducts. This technology has been described since the 1950s, and the equipment is available for home use. Several small clinical trials have shown up to an 85% success rate (involving both hands and feet),15,30,74 but iontophoresis has been described as mildly painful and is a time-consuming process. More invasive options for treating severe plantar hyperhidrosis include surgery (lumbar sympathectomy) and botulinum toxin injection. Injection of botulinum toxin blocks release of neuronal acetylcholine, and several small trials studying palmar hyperhidrosis have demonstrated successful outcomes.45,71 Lumbar sympathectomy is a relatively new procedure reserved for the most severe and refractory cases of plantar hyperidrosis. Clipping the sympathetic chain has a success rate of 90%; some of the initial concerning negative outcomes (hypotension and male infertility and sexual dysfunction) have not been validated.66

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 30 

Wilderness Dentistry HENRY J. HERRMANN AND CYNTHIA L. IDZIK-STARR

This chapter discusses the signs, symptoms, diagnosis, and treatment of a wide variety of emergencies, from minor to life threatening, associated with the mouth and its related structures. The common toothache can cause excruciating pain and ruin an otherwise wonderful wilderness experience. Major oral trauma and severe dental infections, although rare, can cause significant morbidity or even become life threatening. A basic knowledge of dental conditions can prove very useful to anyone venturing into the backcountry. This chapter also covers administration of local anesthesia for dental emergencies and suggests what to add to the first-aid kit to assist in handling and treating dental emergencies.

History and Examination History taking for dental emergencies proceeds as with any other condition. In emergency situations, the chief complaint and history of the present illness deserve greater emphasis than family, personal, and social history and review of systems. However, the presence of complicating medical factors or chronic illness may prove very important in choosing the proper treatment. Many commonly used medications have bearing on dental diagnosis and treatment. Emphasis on the need for subacute bacterial endocarditis (SBE) prophylaxis, bleeding disorders, immunosuppression, allergies, and current medications is a good start. The American Academy of Orthopaedic Surgeons2 recently changed their recommendations to state that persons with total joint replacements should receive antibiotic prophylaxis before invasive procedures. The American Heart Association recommendations for SBE prophylaxis have also changed recently 594

and are listed in Boxes 30-1 to 30-3. Note that premedication is no longer recommended for patients with most types of heart murmurs.50 Begin with open-ended questions before focusing attention with more specific questions. As information is collected, one can begin to focus attention on the more specific characteristics of pain to help attain a diagnosis. It is useful to know when symptoms started, frequency, severity, duration, how they change over time, what brings them on, and what allows relief. The examination focus depends somewhat on the examiner’s suspicions. However, in all cases a systematic approach to examination in oral and maxillofacial emergencies allows efficient collection of all relevant data. Begin the examination with a general appraisal of the victim that optimally includes temperature, blood pressure, and pulse rate. How sick is the patient? Observe the head, neck, and face, especially noting any asymmetry. Palpate to appreciate point tenderness, crepitus, foreign bodies, or swelling. Palpate the temporomandibular joints, muscles, lymph nodes, and areas of suspected injury. Observe the victim slowly open and close his or her mouth, observing for degree of opening, range of motion, and deviation on opening. Begin the intraoral examination with the lips, then move back to the cheeks, floor of the mouth, tongue, hard palate, soft palate, and pharynx. In addition to inspection, palpation is very important. Swelling may turn out to be rock hard (bone) or fluctuant (abscess). Bimanual palpation is helpful when examining the lips, cheeks, and floor of the mouth. The gingiva is observed for color, firmness, recession, and swelling. Gentle probing reveals the depth of the gingival pocket and the presence or absence of

For online-only figures, please go to www.expertconsult.com

BOX 30-3  Antibiotic Prophylactic Regimens for Dental

Antibiotic prophylaxis for dental procedures is reasonable only for patients with cardiac conditions associated with the highest risk for adverse outcomes from endocarditis Prosthetic cardiac valve or prosthetic material used in valve repair Previous endocarditis Congenital heart disease only in the following categories: Unrepaired cyanotic congenital heart disease, including those with palliative shunts and conduits Completely repaired congenital heart disease with prosthetic material or device, whether placed by surgery or catheter, during the first 6 months after the procedure (prophylaxis is reasonable because endothelialization of prosthetic material occurs within 6 months after the procedure) Repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization) Cardiac transplantation recipients with cardiac valvular disease

Oral Amoxicillin Adults: 2 g Children: 50 mg/kg

Procedures for Patients With Cardiac Conditions

Data from Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis: Guidelines from the American Heart Association—A guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group, J Am Dent Assoc 139:3S, 2008.

bleeding. The teeth are inspected for caries, fractures, presence of plaque and calculus, wear, and loose restorations. Test for tooth mobility by using moderate force in a side-to-side direction. Gentle percussion of the teeth with a metal instrument reveals injury or disease of the supporting structures. Inspect occlusion by retracting the lips and then having the victim occlude the teeth (bite). The victim may feel pain when biting on a specific tooth, or you may see that the teeth do not come together normally. Radiographs and other technology-dependent diagnostic tests are valuable but for purposes of this chapter are assumed to be unavailable. Gather the results of your history, examination, and tests to formulate the proper diagnosis.

Maxillofacial Pain The causes of maxillofacial pain are myriad, and the diagnosis of head and neck syndromes can be exceedingly difficult.32,33 The most common painful conditions are covered below. If the BOX 30-2  Dental Procedures for Which Prophylaxis Is

Reasonable in Patients With the Cardiac Conditions Listed in Box 30-1

All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth, or perforation of the oral mucosa Antibiotic prophylaxis is NOT recommended for the following dental procedures or events: Routine anesthetic injections through noninfected tissue Taking dental radiographs Placement or adjustment of removable prosthodontic or orthodontic appliances Placement of orthodontic brackets Shedding of deciduous teeth Bleeding from trauma to the lips or oral mucosa Data from Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis: Guidelines from the American Heart Association—A guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group, J Am Dent Assoc 139:3S, 2008.

Procedures (Single Dose 30 to 60 Minutes Before Procedure)

If Unable to Take Oral Medication Adults: ampicillin 2 g IM or IV, or cefazolin or ceftriaxone 1 g IM or IV Children: ampicillin 50 mg/kg IM or IV, or cefazolin or ceftriaxone 50 mg/kg IM or IV Allergic to Penicillins or Ampicillin Cephalexin* Adults: 2 g PO Children: 50 mg/kg PO OR Clindamycin Adults: 600 mg PO Children: 20 mg/kg PO OR Azithromycin or clarithromycin: Adults: 500 mg PO Children: 15 mg/kg PO Allergic to Penicillins or Ampicillin and Unable to Take Oral Medication Cefazolin or ceftriaxone Adults: 1 g IM or IV Children: 50 mg/kg IM or IV OR Clindamycin Adults: 600 mg IM or IV Children: 20 mg/kg IM or IV Data from Wilson W, Taubert KA, Gewitz M, et al: Prevention of infective endocarditis: Guidelines from the American Heart Association—A guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group, J Am Dent Assoc 139:3S, 2008. *Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage. IM, Intramuscularly; IV, intravenously; PO, orally.

victim’s symptoms do not seem consistent with a dental origin, other causes should be suspected. Examples of disorders that are sometimes confused with dental pain are myofascial pain, maxillary sinusitis, temporal arteritis, and trigeminal neuralgia. Box 30-4 lists others. Table 30-1 shows the characteristics of specific types of tooth-related pain that can assist the examiner in sorting out a diagnosis.

PULPITIS The common toothache is caused by inflammation of the dental pulp. It may be difficult for the victim to identify the offending tooth due to convergence of neurons in the trigeminal spinal tract nucleus.9,26 The painful tooth is rarely sensitive to percussion or palpation. An obvious cause, such as a large carious lesion, is sometimes found on examination of the mouth, but often all of the teeth appear intact. If inflammation is mild, the condition is characterized by pain that is elicited only by cold or sweets and disappears within seconds when the stimulus is removed. Moderate pulpitis is characterized by sensitivity to hot as well as cold, greater discomfort, and an increasing interval between the removal of the stimulus and resolution of the pain. In its most severe form, pulpitis causes intense, continuous, and debilitating pain.6,9,33 Emergency treatment recommendations are given in the following sections. 595

CHAPTER 30  Wilderness Dentistry

BOX 30-1  Antibiotic Prophylaxis for Dental

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 30-4  Some Conditions That Cause Facial Pain Pulpitis (acute, chronic, hyperplastic) Periapical osteitis (acute, chronic) Cracked tooth syndrome Periodontal infections Periodontal abscess Acute necrotizing ulcerative gingivitis Primary herpetic gingivostomatitis Pericoronitis Temporomandibular disorders Maxillary sinusitis Neurologic pain Trigeminal neuralgia Trigeminal neuritis Herpes zoster neuritis Postherpetic neuralgia Atypical facial pain Psychogenic facial pain Dental causalgia (atypical odontalgia) Vascular pain Migraine headache Temporal arteritis Cluster headache Referred pain Referred pulpitis Referred pain of subacute thyroiditis Referred pain of myocardial infarction or angina pectoris

Mild Pulpitis (Characterized by Transient Thermal Sensitivity) Examine the mouth visually. Structures will likely appear within normal limits. However, if a defect is found in a tooth, it can be temporarily filled. Reassure the victim that although this condition is annoying, rapid progression is unlikely. Moderate Pulpitis (Longer Episodes of Pain) Proceed as for mild pulpitis. Treat with a non-narcotic analgesic (ibuprofen 600 mg orally [PO] every 6 hours as needed for pain), and reduce physical activity. If a large defect (cavity) is found in the offending tooth, a cotton pellet with eugenol can be applied to the exposed pulp. Then fill the defect with zinc oxide/eugenol cement (Intermediate Restorative Material [IRM]) or Cavit. Severe Pulpitis (Intense, Continuous Pain) The preferred approach is pain relief using a local anesthetic, followed by evacuation of the victim.35,47 A nerve block with bupivacaine (Marcaine) 2% with 1 : 200,000 epinephrine can provide up to 8 hours of excellent pain relief without central nervous system depression (see Local Anesthesia, later). Nonsteroidal antiinflammatory drugs (NSAIDs) will probably give little relief. Large doses of narcotics should not be used because they are likely to compromise the victim’s ability to participate in evacuation. Sometimes application of cold (continuously sipping cold water) provides relief to the hyperemic pulp. In an extraordinary circumstance, an experienced rescuer could locate the offending tooth, expose the pulp, remove the inflamed pulpal tissue with a barbed broach, and cover the opening with a temporary filling material. Extraction is also an option in a case of severe pulpitis but is usually contraindicated for a number of reasons (see Exodontia, later).

TABLE 30-1  Characteristics of Dental Conditions That Cause Pain Irreversible (Moderate to Severe) Pulpitis

Necrotic Teeth (Periapical Osteitis)

Episodes last a few to several seconds None or may be preceded by gingival recession or lost restoration

Episodes last a few to several minutes Yes. Probably preceded by symptoms of mild pulpitis

Patient usually points to the general area but may not know the specific tooth Mild to moderate

Patient usually points to the general area but may not know the specific tooth Moderate to severe

Pain comes on quickly, lasts several days None or possible history of pulpitis symptoms, or history of restoration months before Patient usually points to a specific tooth

Dull throbbing pain

Sharp, quick, shock-like feeling

Sharp, followed by lingering pain

Moderate to severe. Mild if abscess is draining Constant ache that will not let up

Spontaneous or chewing

Cold, including air Sweets

Cold, including air, heat Sometimes biting, sometimes spontaneous

Biting or even mild pressure as with the patient’s tongue

Erupting Teeth

Reversible or Mild Pulpitis

Sudden/lasts for several days Possibly

Location

Tissue in area of eruption

Severity

Mild to moderate

Type

Trigger

Onset/ Duration Previous history

596

Cracked Tooth Syndrome

Periodontal Infection

Fractured Teeth

Episodes last a few seconds

Gradual progression, lasts for days Often recurrent, but this may be the first episode

Sudden onset

None or possible history of sudden crack while chewing Patient may not even be able to tell if it is an upper or lower tooth Mild to severe

Sharp, shock-like pain

Biting hard or chewy food in just the right way

Usually easy for the patient to point to the exact area of pain and swelling Mild to moderate Dull throbbing pain. Usually the patient knows it is coming from the gingiva, not the tooth Spontaneous, touch increases pain

May have a previous history of sensitivity to cold Patient can usually point to a specific tooth Moderate to severe Sharp pain on release of pressure

Pain on biting on a specific cusp

Inflammation of the supporting structures at the root of a tooth is characterized by constant, often throbbing, pain. Unlike pulpitis, the affected tooth is easily located. The victim can usually point to the exact source of the pain, or the examiner may gently tap individual teeth, observing for tenderness. The area over the apex of the tooth is usually tender to palpation, but there is no frank swelling. Although trauma to a tooth can result in periapical inflammation, the most common cause is egress of bacteria and breakdown products from the necrotic pulp. Minor swelling around the apex extrudes the tooth slightly, causing increased forces on the tooth during occlusion, and thus intensifies the pain. Emergency treatment includes an analgesic (ibuprofen 600 mg PO every 6 hours as needed for pain) or a local anesthetic and a soft diet. Ideally, the contacting areas of the opposing tooth are reduced to relieve occlusal forces.6,9 Because this usually is impractical in the field, the victim can be given a strip of webbing or something similar to place between the teeth on the nonpainful side. This will keep the offending tooth out of occlusion and reduce the pain.

CRACKED TOOTH SYNDROME The victim complains of momentary, sharp pain when chewing certain foods or on releasing the bite. Often the victim reports that the tooth feels “weak” or that “it only hurts when I bite on something hard just the right way.” These symptoms occur when forces of the proper magnitude and direction open the incomplete fracture in the tooth.37 The pain can vary with a cracked tooth depending on how deep the crack is and how close it comes to the pulp. Significantly, there is no pain on chewing soft foods. Often the victim has large restorations or a habit of chewing ice or clenching and grinding.22 This condition usually progresses slowly. Reducing the occlusion on the cracked tooth will relieve some pain but again is often impractical in the field. The victim should be advised to avoid chewing on the affected side and to seek definitive dental treatment as soon as possible.

ODONTOGENIC REFERRED PAIN Pain originating in the pulp of the tooth can sometimes be referred to distant sites. Common referral patterns are the following: maxillary incisors to the forehead, maxillary canine to the infraorbital area, maxillary molars to the temple or ear area, mandibular anterior teeth to the mental foramen area, mandibular premolars to the posterior jaw, and mandibular molars to the angle of the jaw, the ear, or the neck. Sometimes the victim swears the pain is coming from a tooth several teeth in front or behind the source of pain. Pulpitis pain can be referred from an upper tooth to a lower tooth, or vice versa, but never crosses the midline. Many cases have been presented in the dental literature detailing how experienced practitioners have treated the wrong tooth or performed multiple dental treatments when the source of pain was not a tooth.26,30 If in doubt about the diagnosis, ensure that you do no harm.

MAXILLARY SINUSITIS The pain of maxillary sinusitis can be referred to a maxillary posterior tooth. It is usually described as a relatively continuous throbbing ache that is intensified by postural change. A typical statement is, “My tooth really hurt when we were hiking down the hill. I could feel it pound with every step. When we got to camp, I lay down, but it got even worse.” The pain may be unilateral or bilateral. It is usually located in the infraorbital region and is often referred to the cheeks, frontal region, and the maxillary premolars and molars. A complaint of multiple toothaches in the maxilla, with no evidence of carious teeth, should immediately raise suspicion for maxillary sinusitis. In addition to pain, there is tenderness elicited by pressure infraorbitally or over the bony prominence above the first molar. The victim also generally has an elevated temperature and nasal or postnasal discharge.

Treatment of maxillary sinusitis includes an analgesic (ibuprofen 600 mg PO every 6 hours as needed for pain), inhalation of steam, oxymetazoline (Afrin) 0.05% 1 spray in each nostril twice a day to shrink the nasal membranes and improve sinus drainage, and an antibiotic. Appropriate choices include amoxicillin 875 mg with clavulanic acid 125 mg (Augmentin) PO twice a day for 10 days or trimethoprim 160 mg with sulfamethoxazole 800 mg (Septra DS) PO twice a day for 10 days. Azithromycin (Zithromax) 500 mg PO the first day and then 250 mg PO for 4 days is a convenient alternative.1,19

TEMPOROMANDIBULAR DISORDER Temporomandibular disorder (TMD) is a cluster of conditions, multifactorial in origin, and with overlapping symptoms that often respond to a variety of therapies, including placebos.31 If the victim answers “yes” to any of the following questions, he or she may suffer from TMD: Does it hurt to open the mouth widely or yawn? Do you have earaches or pain in front of your ear? Is your pain worse in the morning? Have you had trauma to your face or jaw? Do you have temporal pain or headaches? Has your jaw ever gotten stuck open or closed? Does your jaw pop or click on opening or closing? Included under the term TMD are two groups of sufferers: those with primary masticatory muscle involvement (myofascial pain and dysfunction [MPD]) and those with internal derangements of the temporomandibular joint (TMJ). Patients also may present with a combination of both types. Internal derangements, traumatic injuries, and dislocation of the joint are covered in Chapter 31. Myofascial Pain and Dysfunction Muscle hyperactivity is an important etiologic factor in MPD. In some persons this may result from parafunction (gum chewing, clenching or grinding the teeth). Occlusal interferences can also cause muscle hyperactivity. This occurs when a lower tooth contacts an upper tooth prematurely during mouth closure and a reflex causes jaw muscle contraction that shifts the mandible in such a way as to avoid the premature contact. For this reason this condition is often referred to as an “occluso-muscle disorder.” Psychological stress is also an important factor in causing excessive muscle tension.25 Participants in wilderness activities are exposed to many of the risk factors for MPD. The high physiologic and psychological demands of many expeditions lead to considerable stress. Increased jaw function, such as that required to chew granola, beef jerky, and other dried foods common on wilderness expeditions, is another factor that may precipitate an acute episode of MPD. Symptoms of MPD include pain in the muscles of mastication that is usually unilateral and increased with chewing, headache, earache, limitation of jaw movement, and a change in the bite. Pain originating in the muscles of mastication is often referred to the teeth, so the chief complaint may be a toothache.26,40 The victim may have a history of acute onset, or a long saga of exacerbation, remission, and various treatments. The examiner may find objective signs, such as tenderness of the jaw muscles to palpation, muscle spasm or “knots,” and abnormal jaw movements, such as inability to open the mouth widely, or deviation of the chin to one side on opening. Tenderness to palpation of the TMJ or joint noise suggest the victim has an internal derangement of the joint.25 Emergency treatment consists of resting the muscles (soft diet and control of tooth clenching and grinding habits) and the application of moist heat. Holding a soft material such as a folded gauze between the front teeth or use of an athletic mouth guard often gives immediate relief because it keeps the teeth from touching and allows the muscles to relax. An analgesic should be given on a scheduled basis (ibuprofen 600 mg PO every 6 hours), rather than as needed, to break the cycle of muscle pain and spasm. A muscle relaxant, such as cyclobenzaprine hydrochloride (Flexeril) 10 mg PO 3 times a day, or sedatives, such as diazepam (Valium) 2 to 10 mg PO 3 times a day, may be helpful if the primary treatment is ineffective. Muscle relaxants and sedatives, especially in higher doses, can cause significant central nervous system 597

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PERIAPICAL OSTEITIS

PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 30-1  Aphthous ulcer on the tongue.

depression, so they should be used in the lowest effective dosage and only if more conservative therapy has failed.10,31,42

Miscellaneous Lesions APHTHOUS ULCERS It is thought that aphthous ulcers may represent a local immune response with various triggers such as stress; trauma; immunosuppression; nutritional deficiencies of vitamin B12, folic acid, or iron; acidic foods; and food allergies; to name a few. The lesions are round or ovoid in shape with a yellowish center and a red border and usually occur on nonkeratinized, movable mucosa (Figure 30-1). They can be quite painful. The victim usually gives a history of similar ulcerations. There are three types of aphthous ulcers. Minor aphthae are less than 0.6 cm (0.2 inch) in size and usually last 10 to 14 days. Major aphthae are larger than 0.6 cm (0.2 inch) and may last weeks or months. Herpetiform aphthae are clusters of small, shallow ulcers that resemble intraoral herpes. Many treatments have been proposed, but none has been found predictably effective. The best approach appears to be application of a topical corticosteroid to reduce pain and hasten healing by 3 to 4 days. Mix fluocinonide (Lidex) 0.05% ointment with Orabase and place the mixture gently over each ulcer 6 to 8 times per day, especially after meals and before bedtime. Do not mix the medications until you are ready to apply them, and do not rub the mixture into the lesions. Other options include premixed preparations, such as Kenalog in Orabase, applied to the ulcer 6 to 8 times per day, which is more convenient but delivers only about 10% of the antiinflammatory effect, or dexamethasone (Decadron) elixir (0.5 mg/5 mL, rinse with 5 mL for 2 minutes and expectorate 4 times a day). Finally, a systemic corticosteroid (prednisone, 40 mg PO once daily for 3 days, then taper) may be used for a very severe case. If these preparations are not available, tincture of benzoin or a topical anesthetic (viscous lidocaine 2%) can be applied to the dried surface of the ulcer before meals and at bedtime to control the pain.15,45

jaws (BRONJ) may occur after bone is exposed by acute trauma, by chronic trauma such as from an ill-fitting dental prosthesis, from dental surgery, or after tooth extraction. The incidence after tooth extraction in patients that have taken oral bisphosphonates is less than 1%. The risk for BRONJ in patients that have received intravenous therapy is estimated between 0.8% and 12%.3 The diagnosis of BRONJ is made when exposed, necrotic bone persists for at least 8 weeks in a patient currently or previously treated with a bisphosphonate who has no history of radiation treatment to the jaws. Small lesions may be asymptomatic (Figure 30-2, online), whereas some exposed areas become infected, as evidenced by pain, erythema of the surrounding soft tissue, and possible purulent drainage. Prevention of BRONJ focuses on avoiding bone exposure in patients at risk. Emergency management consists of eliminating pain, controlling infection, and limiting the progression of bone necrosis. Asymptomatic lesions are treated with an antibacterial mouth rinse such as chlorhexidine. BRONJ that is painful and infected is treated with an antibacterial mouth rinse as well as an antibiotic, such as penicillin V potassium 500 mg PO 4 times a day, cephalexin (Keflex) 500 mg PO 4 times a day, or clindamycin 150 mg PO 4 times a day, and pain control. Evacuation for surgical care is indicated in cases of BRONJ complicated by any one of the following: pathologic fracture, extraoral fistula, or necrosis extending to the inferior border of the mandible.3,27,38

MUCOCELE Mucocele, or mucous retention phenomenon, occurs when the duct of a minor salivary gland is blocked or traumatized, resulting in accumulation of saliva beneath the mucosa. It most commonly occurs in the lower lip. A mucocele in the floor of the mouth is called a ranula. Most mucoceles are a few millimeters in diameter, lie just under the surface, and have a translucent or bluish tint. They often form, spontaneously drain, then reform again and again. Most will eventually disappear without surgical intervention. No emergency treatment is necessary (Figure 30-3).

Maxillofacial Infections VIRAL INFECTIONS Herpes labialis (cold sore, fever blister) is the most common oral viral infection. It is characterized by yellow, fluid-filled vesicles that rupture to leave ragged ulcers on the lips (Figures 30-4 and 30-5). Other locations for recurrent herpetic outbreaks include the palate, tongue, and buccal mucosa. The victim can be given valacyclovir (Valtrex) 2 g PO twice daily for 1 day, with doses taken about 12 hours apart.43 It is important to begin treatment as soon as the victim becomes aware of a prodromal “tingle” or paresthesia. There is some evidence that the same regimen of valacyclovir can prevent outbreaks from occurring.8,29 However,

TRAUMATIC ULCERS Traumatic ulcerations are similar to aphthous ulcers but are usually more irregular in outline and lack the red border. They occur from chronic rubbing such as from a sharp tooth against the tongue or an ill-fitting denture against the palate. Topical anesthetic (viscous lidocaine 2%) can be used, but the most important treatment is to remove the source of irritation.

BISPHOSPHONATE-RELATED OSTEONECROSIS OF THE JAWS Oral bisphosphonates such as alendronate (Fosamax) are widely used to treat osteoporosis, and intravenous bisphosphonates, such as zoledronic acid (Zometa) are used to manage skeletal involvement in various cancers. A side effect of these medications can be delayed healing of exposed bone in the maxillofacial region. Altered bone metabolism persists long after the medications have been discontinued. Bisphosphonate-related osteonecrosis of the 598

FIGURE 30-3  Mucocele commonly occurs on the inside of the lower lip.

CHAPTER 30  Wilderness Dentistry

FIGURE 30-4  Herpes labialis in the healing stage. FIGURE 30-6  Thrush.

more conservative methods, such as the use of sun-blocking agents on the lips, are preferred.44 Primary herpetic gingivostomatitis is characterized by a thin zone of very red, painful gingiva just next to the teeth. Other areas of mucosa, such as the tongue, may also be involved, and close inspection may reveal tiny vesicles or ulcers. Sore throat, lymphadenopathy, and low-grade fever are also present. This and other viral infections of the oral cavity are self-limited. The victim should be reassured that the condition will resolve in about 10 days. Treatment involves the use of an analgesic (ibuprofen 600 mg PO every 6 hours as needed for pain and fever) and soothing mouth rinses, such as warm saline or a mixture of equal amounts of diphenhydramine (Benadryl) elixir 12.5 mg/5 mL with kaolin-pectin (Kaopectate) and viscous lidocaine 2% (rinse and expectorate 5 mL every 2 hours).

BACTERIAL INFECTIONS

YEAST INFECTIONS Oral yeast infections occur most commonly in persons who are debilitated, immunocompromised, suffer from xerostomia, or are taking an antibiotic or corticosteroid. Classic oral candidiasis (thrush) is characterized by white patches on the mucosa that can be rubbed off, leaving a red and raw surface (Figure 30-6). Candidiasis can also manifest as erythematous mucosa, without any white patches, or as chronic angular cheilitis (Figures 30-7 and 30-8; Figure 30-8, online). Candidiasis is treated with an antimycotic mouth rinse (nystatin oral suspension 100,000 U/mL, rinse with 5 mL for 2 minutes and swallow, 4 times a day for 10 days) or lozenges (clotrimazole [Mycelex] troche, 1 troche 4 times a day, leave in mouth 5 minutes, and expectorate remains). In the field, nystatin preparations meant for vaginal treatment (Nystatin vaginal suppository used as an oral lozenge 3 times a day for 10 days) can be used.

Acute Apical Abscess/Cellulitis An acute apical infection begins with bacteria invading the dental pulp. The infection then spreads to surrounding bone through the apical foramen and then along the path of least resistance. Because the apices of most teeth are located closer to the facial aspect of the jaw, swelling is much more common in the facial soft tissues, as opposed to those on the lingual or palatal side. The victim presents with pain and swelling, often fluctuant and usually in the buccal vestibule (Figure 30-9). There is often a history of prior toothache, but at this stage tooth pain is often absent. The offending tooth can be localized by percussion, site of the swelling, condition of the teeth, and by radiographs if available. The affected tooth does not respond at all to hot or cold. The victim may be dehydrated because of decreased fluid intake. Primary treatment for an apical abscess is drainage.28,41 This can be accomplished with incision, extraction, or endodontic

FIGURE 30-5  Herpes labialis showing vesicles.

FIGURE 30-7  Angular cheilitis.

A bacterial infection in the maxillofacial region can become a serious health threat. In a wilderness setting, it should be taken seriously. Most odontogenic infections are caused by mixed populations of aerobic and anaerobic bacteria. These organisms are almost always present as normal oral flora, but because of a change in the relative numbers of various bacteria or because of a change in the oral environment, an infection can become aggressive. The behavior of an organism, such as the production of collagenase or hyaluronidase, determines the clinical presentation. Thus an infection may manifest as diffuse cellulitis or localize as an abscess. Oral infections usually spread slowly, but rapid spread to a deep facial space can occur. Regional lymphadenop­athy is common, whereas severe systemic symptoms are rare. Although bone is often involved, osteomyelitis is uncommon.39

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

and a knife handle or the beak of a hemostat is used to spread the incision. A T-shaped drain may be improvised from a piece of latex glove and retained without sutures (Figure 30-10). Hydration, a soft diet, an analgesic (ibuprofen 600 mg PO every 6 hours as needed for pain), and warm saline rinses are helpful postoperative measures.

FIGURE 30-9  An apical abscess manifesting with swelling in the buccal vestibule.

therapy. The treatment chosen depends on the equipment and personnel available, advisability of retaining the offending tooth, and ultimately on clinical judgment. An antibiotic is necessary only if complicating factors exist11,28,41,46 (Box 30-5). Penicillin V potassium 500 mg PO 4 times a day is the most commonly used antibiotic in dental practice, but a cephalosporin, such as cephalexin (Keflex) 500 mg PO 4 times a day, typically carried on wilderness expeditions, is acceptable. Clindamycin 150 mg PO 4 times a day is a good alternative.23,41,46 Combination antibiotic therapy is not indicated except for life-threatening sepsis or when organisms particularly sensitive to combination therapy have been identified. There is some evidence that hesitation to obtain drainage combined with overreliance on chemotherapy can lead to serious exacerbation of dental infections.11 Incision and Drainage Incision and drainage (I&D) is often the treatment of choice in an emergency situation. An I&D procedure can be performed by a nondentist using commonly available supplies. It is indicated for fluctuant swelling due to an apical abscess and may also be effective for nonfluctuant swelling associated with infection. Infiltration of a local anesthetic helps to reduce the pain of incision. If unavailable, adequate anesthesia can often be obtained by applying cold to the area to be incised, using ice, snow, or frigid water. An incision is made down to the bone in one swift motion, BOX 30-5  Indications for Antibiotic Use in Dental

Emergencies

Prophylaxis for persons at risk for bacterial endocarditis (see   Box 30-1) Prophylaxis for persons having prosthetic joint implants within the past 2 years Local infections If the victim is immunocompromised If drainage cannot be established If there will be a long delay before definitive care If infection persists after local treatment Disseminated infections Lymphadenopathy Fascial plane involvement Trismus Systemic symptoms (fever, chills, malaise) Compound maxillofacial fractures, including all fractures of tooth-supporting bone Exarticulation (avulsion) of teeth Soft tissue wounds open for 6 hours or more before closure Surgical procedures under nonsterile conditions

600

Deep Fascial Space Infections An acute apical infection occasionally spreads beyond the local region. The rescuer should be suspicious of any dental infection that causes swelling or tenderness in the floor of the mouth, swelling of the tongue, dysphagia, breathing difficulty, or trismus, or that fails to respond to appropriate therapy. The most commonly involved fascial spaces are the canine, buccal, masticator, and submandibular spaces.12 The canine space is located lateral to the nose. Infection originates in the maxillary canine tooth and swelling causes the eye to close. The infection is drained through an intraoral approach over the root of the canine tooth. Buccal space infection is characterized by rounded swelling of the cheek (Figure 30-11). The offending teeth are the maxillary and mandibular molars. Drainage is obtained extraorally through an incision below the lower border of the mandible, so that the scar will eventually be hidden or minimal. The masticator space is divided into the masseteric, pterygoid, superficial temporal, and deep temporal spaces, all of which communicate. The hallmark of involvement is trismus. Swelling may be minimal owing to the deep location of the abscess. The masseteric and pterygoid spaces are drained at the angle of the mandible, whereas the temporal space may be drained from an intraoral approach or through an incision just superior to the zygomatic arch. The mylohyoid muscle divides the floor of the mouth into the sublingual and submandibular spaces. These communicate posteriorly and with their counterparts across the midline. An infection originating in a mandibular tooth can involve these spaces. If only the sublingual space is infected, an intraoral approach is used for drainage, avoiding damage to Wharton’s duct. If the submandibular space is involved, an extraoral approach is used. All incisions in the facial area are made parallel to branches of the facial nerve.12,24 Fascial space infections are potentially life threatening. The likelihood of widespread sepsis increases, cavernous sinus venous thrombosis and mediastinitis are possible, and the airway may become compromised.13,17 The most feared infection is Ludwig’s angina, a bilateral submandibular space infection that elevates the tongue, obstructs breathing, and is associated with a high mortality rate (Figure 30-12). A mild dental infection can progress to a life-threatening emergency in as little as 48 hours.17 Treatment of fascial space infections includes airway management, proper hydration and electrolyte balance, aggressive incision and drainage, intravenous antibiotics, and pain control. Because these objectives are best met in a controlled environment, any person with a suspected fascial space infection should be evacuated immediately. Chronic Apical Abscess The hallmark of chronic apical infection is a draining fistula or “gum boil” (Figure 30-13, online). Because the bacteria have a route to escape, they do not cause pressure or pain, although the tooth may be mildly sensitive when eating. Such an abscess is not an emergency except in the unlikely event of an acute flare-up. Antibiotics are not indicated. An infected deciduous tooth also usually manifests with a fistula and a mild amount of swelling at most. Happily for the child, severe pain is rarely present. Emergency care involves an antibiotic, with the dosage adjusted for the child’s weight, and I&D only if the abscess is not draining. Extract the tooth only if it is very loose and it will be weeks until comprehensive care is available. Periodontal Abscess A periodontal abscess is an accumulation of pus between the gingiva and the tooth. Swelling is near the gingival margin rather than in the vestibule, as would be the case with a

B

C

D

E

F

CHAPTER 30  Wilderness Dentistry

A

FIGURE 30-10  Incision and drainage technique. A, Fluctuant abscess. B, Abscess incised with scalpel. Purulent drainage is removed by suction or caught in gauze sponges. C, Cross section showing incision carried to the bone. D, The incision is spread with a hemostat. E, A T-shaped drain often stays in place without sutures. F, Drain in place. (Redrawn from Ingle JI, Beveridge EE: Endodontics, ed 2, Philadelphia, 1976, Lea & Febiger, with permission.)

periapical abscess. The tooth is sensitive to percussion but responds appropriately to hot and cold. There is always a potential communication between the abscess and the mouth. The passage can be found by probing the gingival margin with a small, blunt instrument, using a local anesthetic if available. Gentle probing establishes drainage; no incision is necessary. Hot saline rinses are prescribed, and rapid recovery is almost invariable. Pericoronitis Pericoronitis is an infection of the gingival flap over a partially erupted tooth. The most common site is the mandibular third molar. Pericoronitis is usually caused by streptococci and seldom produces purulence. The condition may mimic streptococcal pharyngitis or tonsillitis. The primary site of infection is always

FIGURE 30-11  A buccal space infection.

tender, and trismus is a common sign. Field treatment consists of saline irrigation of the space under the flap using a syringe. Place the victim on hot saline rinses every 2 hours, and begin antibiotic therapy. Acute Necrotizing Ulcerative Gingivitis Acute necrotizing ulcerative gingivitis, also known as trench mouth, is characterized by ulceration and blunting of the interdental papillae. The gingiva between the teeth appears punched out and is covered by a gray/white pseudomembrane, whereas the surrounding gingival tissue is very red. The victim’s primary complaint is pain, but he or she may also report gingival

FIGURE 30-12  Ludwig’s angina.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

bleeding, metallic taste, and foul odor. This infection is caused by fusiform bacteria and spirochetes. It usually occurs in young adults with poor oral hygiene, stress, and suboptimal nutrition (conditions that may be present during difficult wilderness expeditions). The most important treatment is gentle debridement of plaque, calculus, and food from around the teeth. Resolution may require several sessions of careful cleaning 1 to 2 days apart. Each session of debridement results in some healing, which allows more aggressive treatment the next time. The victim is also given an antibiotic (metronidazole [Flagyl] 500 mg PO 4 times a day) and analgesics (ibuprofen 600 mg PO every 6 hours as needed for pain) and instructed to keep the area clean with good brushing, flossing, and rinsing (warm saline or diluted hydrogen peroxide, if available).6

Exodontia A dental extraction is considered definitive treatment and should be attempted in the field only under extraordinary circumstances (Box 30-6). Extraction requires training, specialized instruments, and profound anesthesia, which may be difficult to obtain. As discussed above in the section on facial pain, symptoms that seem to be coming from a maxillary molar may actually originate in a lower molar or from a muscular trigger point. Never extract a tooth without a definitive diagnosis. Premedication with a sedative or narcotic may be necessary, as may dental radiographs. Intraoperative and postoperative complications are common. Providers of emergency care should focus on treating pain and infection with local anesthetics, analgesics (ibuprofen 600 mg PO every 6 hours as needed for pain, or hydrocodone 7.5 mg and acetaminophen 750 mg [Vicodin ES] PO every 4 to 6 hours as needed for pain), I&D, and antibiotics (see Acute Apical Abscess/ Cellulitis, earlier) as appropriate for each case.6,35,41 Extraction or other definitive care can then be rendered after evacuation; the tooth can often be saved. Other factors to consider before exodontia are degree of mouth opening possible, relationship of the root to the maxillary sinus, condition of the clinical crown, alignment of the tooth in the dental arch, and history of previous endodontic treatment (after root canal treatment, a tooth is usually very brittle).21 Along with the considerations for extracting the tooth, weigh the possible complications arising from extraction, such as fractured roots, fractured alveolus, fractured mandible or tuberosity, damage to adjacent teeth and restorations, soft tissue injury, loss of root tip in sinus, prolonged bleeding, and infection.

BOX 30-6  Factors to Consider Before Extraction

of Teeth

Desires of the victim Victim’s medical history Available alternative treatments Difficulty/desirability of evacuation Certainty of diagnosis (Are you sure you have the correct tooth?) Possible complications if the tooth is not extracted Factors relating to the difficulty of the procedure Mobility or immobility of the tooth Position of the tooth Condition of tooth structure above the gingiva Patient’s mouth-opening ability Available supplies and instruments Experience of rescuers Possible complications arising from the extraction Fractured root(s) Fractured alveolus Soft tissue injury Root tip lost in the sinus Prolonged bleeding Localized osteitis (dry socket)

602

FIGURE 30-14  No. 151 universal mandibular forceps.

If, after careful consideration of all factors, extraction is deemed the best course of treatment, proceed as follows. Review the victim’s medical history. There are dental implications for many frequently prescribed medications.7 Chapter 34 discusses chronic diseases and wilderness activities. Do not assume that the victim is free of bleeding disorders, severe cardiovascular disease, and the like. A discussion of dental surgery for the patient on anticoagulant therapy and maximum international normalized ratio (INR) values for various procedures is beyond the scope of this chapter. Suffice it to say, you do not want to exceed those values in a wilderness setting! Persons with certain cardiac conditions or recent prosthetic implants should be premedicated with an antibiotic2,50 (see Boxes 30-1 to 30-3). Consider the emotional state of the victim, and decide if sedation is prudent. Plan the procedure, and gather all necessary equipment. Secure a good light source and a means to keeping the field dry—either suction or plenty of gauze. It is important to have the victim’s head supported. Therefore it may be best to place the victim in a supine position with the head slightly elevated. Obtain good local anesthesia, and test by touching the soft tissues with a sharp instrument. A 10 × 10-cm (4 × 4-inch) gauze curtain placed in the rear of the victim’s mouth prevents aspiration of teeth and debris. Teeth are inflexible and brittle. Heavy forces, especially if applied quickly (high acceleration), break teeth. Bone has more flexibility, the degree of which depends on the individual patient. Judiciously applied, moderate forces slowly expand the bone. The tooth will eventually be delivered in the same direction as if it continued to erupt. However, do not attempt to “pull” the tooth in that direction initially. The direction of force needed to loosen a tooth depends on the anatomy of the root. A straight, conical root can be loosened by twisting forces. This technique often works well on the upper front teeth. Sometimes a tooth can be removed by alternating 30 seconds of steady pressure toward the cheek with 30 seconds of steady pressure in the opposite direction, until the root gradually loosens.52 A variety of instruments can be used to apply force to the tooth. Elevators are firmly wedged between tooth and bone in the interproximal area. Avoid putting pressure on the adjacent tooth. Forceps should be applied as far apically as possible. Spend plenty of time working the forceps well under the gingiva. Lower molars are often removed with “cowhorn” forceps, which, in addition to applying the usual forces, are designed to apply force to the tooth in a coronal direction simply by squeezing the handles. However, an experienced exodontist using careful technique and a single forceps (the No. 151 universal extraction forceps) (Figure 30-14) will have success extracting almost any nonimpacted tooth, whereas a reckless operator using dozens of specialized instruments will have difficulty.21,52 Despite the utmost care, a tooth may break during the extraction procedure. If this occurs, stop and take a minute to reevaluate the situation. The root canal will probably now be exposed. If you are treating a case of infection, perhaps drainage can be obtained through the root canal. If you are treating a case of severe pulpitis, perhaps the pulpal tissue can now be removed. Remember that you are rendering emergency care, and it may not be necessary to remove the remaining root at that time. Some teeth are impossible to remove without sectioning or can be removed in only one direction. Once the tooth has been removed, look at the end of the root to confirm that the entire root was extracted. Any remaining fragments can be removed at another time if necessary. Compress the expanded socket using the thumb and forefinger. If the

Dental Trauma Wilderness recreation creates many opportunities for traumatic injury. One recent survey of 9543 consecutive trauma patients registered with an oral and maxillofacial surgery service found that 31% were sports related. Of those, 44% could be considered “backcountry” trauma, mostly resulting from skiing and snowboarding. The study was done in Innsbruck, Austria.49 It is essential to quickly evaluate the general condition of an injured victim (see Chapter 21). The primary survey identifies and corrects any inadequacy in respiration or circulation. The mouth and pharynx should be examined for foreign bodies such as blood clots, tooth or bone fragments, or dentures. If the airway is still obstructed, it may be necessary to perform a chin lift or jaw thrust or insert an oropharyngeal airway to hold the tongue forward (see Chapter 20). Care should be taken not to hyperextend the neck because of the possibility of a cervical spine fracture. If there is no indication of a neck fracture, sometimes merely placing the victim on his or her side rather than in a supine position facilitates respiratory exchange. If all these measures fail, endotracheal intubation or performance of a cricothyrotomy or, less commonly, a tracheotomy may be necessary.5 Once a victim’s airway is secured and he or she is hemodynamically stable, perform a secondary survey. Question the victim about the time and nature of the accident, symptoms, loss of consciousness, nausea, vomiting, visual disturbances, and headache. A baseline mental status examination and cranial nerve assessment may be warranted. Clean the face, mouth, head, and neck of blood and debris. This unmasks soft tissue injuries and facilitates diagnosis. Gently reflect the lips with teeth closed to examine soft tissues and occlusion. Examine any lacerations carefully to determine if they penetrate through the lip or contain foreign material. Examine all of the teeth for fractures. A blow to the chin or whiplash injury may produce fractures of the posterior teeth as the mandible is forcibly closed. Examine fractured teeth carefully for pulp exposure. This will require drying the tooth with gauze. Tap each tooth with an instrument handle. Tenderness denotes injury to the periodontal ligament, whereas a high-pitched, metallic sound indicates ankylosis as occurs in lateral luxation or intrusion. Test each tooth for abnormal mobility. Electrical pulp vitality testing, dental radiographs, and soft tissue radiographs should be obtained if available.4,16

BOX 30-7  Classification of Dental Trauma

CHAPTER 30  Wilderness Dentistry

gingiva is quite loose, placing a suture may help speed healing. Have the victim apply direct pressure to the wound by biting firmly on a gauze pack for 30 minutes while sitting in an upright position. Complete hemostasis may require several hours of steady pressure. Caution the victim to avoid rinsing, spitting, toothbrushing, and smoking for 24 hours. Apply cold packs for 15 minutes on and 15 minutes off for the first day, and use an appropriate analgesic to reduce swelling and pain. Beginning the day after surgery, have the victim rinse with warm saline to cleanse the area. A common postoperative complication is persistent bleeding several hours after the extraction, accompanied by a poorly organized clot that looks like a piece of raw liver growing out of the socket. Remove the “liver clot,” and have the victim apply firm, uninterrupted pressure to the socket by biting on a gauze pack or a wet tea bag (tannic acid in the tea helps to promote clotting) for 20 minutes. If the victim cannot do this, the rescuer will have to apply manual pressure. If bleeding continues after 20 minutes, consider packing the socket (Gelfoam, Surgicel, or sterile gauze) or suturing. Then resume direct pressure. Another postextraction complication is acute alveolar osteitis, or “dry socket.” The victim reports moderate to severe pain, foul odor, and a bad taste, beginning about 3 days after a dental extraction. Examination reveals an empty socket and exposed bone due to loss of the blood clot, but no suppuration. Treatment consists of anesthetizing the area, gentle irrigation with warm saline, followed by packing with a strip of gauze dipped in eugenol. Administer an oral analgesic. Change the pack every 24 to 48 hours until the symptoms subside, which may take up to 10 days. The victim should avoid alcohol, smoking, and carbonated beverages during treatment.

Injuries to the hard dental tissues and pulp Crown infraction Uncomplicated crown fracture Complicated crown fracture Uncomplicated crown–root fracture Complicated crown–root fracture Root fracture Injuries to the periodontal tissues Concussion Subluxation Intrusive luxation Lateral luxation Extrusive luxation Exarticulation Injuries to the supporting bone Comminution of alveolar socket Fracture of alveolar socket wall Fracture of alveolar process Fracture of jaw Injuries to soft tissues From Andreasen JO, Andreasen FM: Textbook and color atlas of traumatic injuries to the teeth, ed 3, St Louis, 1994, Mosby.

See Chapter 31 for injuries to the face, head, and jaws. A classification of traumatic injuries to the teeth and supporting structures is given in Box 30-7. Note that these injuries often occur in combination, with one tooth exhibiting two or more injuries, or several teeth exhibiting various sequelae of trauma. Each injury requires definitive treatment, but proper emergency care improves the prognosis and makes the victim more comfortable. Treatment of most injuries requires, or is at least facilitated by, infiltration of a local anesthetic.

SPECIFIC DENTAL INJURIES Crown Infraction Blows to the teeth sometimes produce small craze lines in the enamel. These superficial fractures look like tiny surface cracks on an old porcelain dish. Reassure the victim that minimal damage has occurred and treatment is not necessary. Uncomplicated Crown Fracture The tooth has been fractured, but no pulp tissue is visible. The tooth may be sensitive to cold, but otherwise all test results are within normal limits. Account for and save the missing fragment if possible. No emergency treatment may be necessary. Irritating sharp edges can be smoothed with a fingernail file. If thermal sensitivity is moderate to severe, a soothing topical antiinflammatory dressing (IRM) can be held in place with aluminum foil or adhesive tape. Uncomplicated Crown–Root Fracture Diagnosis and treatment of this condition are identical to the uncomplicated crown fracture, except that the fracture is nearly vertical, leaving a small, chisel-shaped fragment attached only by the palatal gingiva (Figure 30-15). Removal of this mobile fragment makes the victim much more comfortable. Complicated Crown Fracture In this injury, the pulp has been exposed. A small exposure that has not been grossly contaminated is capped with calcium hydroxide (Dycal) or IRM. If the exposure is larger than 1 mm or if the pulp tissue has been exposed for more than 24 hours, amputate approximately 2 mm of tissue with a sharp, sterile instrument. If bleeding continues for more than a few minutes, use a cotton pellet soaked in local anesthetic solution, hydrogen peroxide, or Dycal to obtain hemostasis. Fill the top of the canal with Dycal or IRM, and protect the tooth as for a crown fracture (Figure 30-16). 603

PART 4  INJURIES AND MEDICAL INTERVENTIONS

treatment (to prevent inflammatory root resorption) and orthodontic extrusion should begin within 2 weeks of injury. Intrusion is associated with a poor long-term prognosis.4 Extrusion The extruded tooth is partially displaced from its socket and extremely mobile. Gentle, steady pressure is used to reposition the tooth, allowing time to displace the blood that has collected in the apical region of the socket. After reduction, the tooth is nonrigidly splinted for 2 to 3 weeks.

B

A

FIGURE 30-15  Crown-root fracture. The mobile fragment (A) should be removed. The larger fragment (B) should be left in place.

Complicated Crown–Root Fracture The tooth has been fractured obliquely, resulting in a mobile fragment attached to the palatal gingiva as well as a pulp exposure. First, remove the mobile fragment as in a crown–root fracture, then treat the pulp exposure as in a complicated crown fracture.4 It is possible to glue tooth fragments together with 2-octyl cyanoacrylate (Dermabond) for a day or two.20 Root Fracture A root fracture may be difficult to diagnose without radiographs. There is slight to severe malposition of the crown, but this could be caused by extrusion of the entire tooth or a root fracture with luxation of the coronal portion. Reposition the tooth as precisely as possible, and splint rigidly (see Splinting, later). Hard tissue union of the fragments usually occurs within 3 months. If the coronal portion of the tooth proves impossible to stabilize and definitive treatment is days away, remove the mobile fragment, but do not attempt to extract the apical fragment.4,16 Concussion and Subluxation Injuries to the tooth’s supporting structures (periodontal ligament, bone, and gingiva) cause sensitivity to percussion. The tooth remains in its proper position. In subluxation the tooth is abnormally mobile, whereas mobility is normal with concussion. Hemorrhage from the gingival crevice sometimes occurs. Emergency treatment consists of shortening the opposing tooth so that the victim can occlude comfortably. Intrusion A tooth that has been driven into the bone by a vertical force demonstrates little mobility and a high-pitched, metallic tone on percussion. Emergency treatment is palliative only. Endodontic

A

Exarticulation When a tooth is totally avulsed from bone, the prognosis after replantation depends on the health of the periodontal ligament cells, some of which are still attached to the root surface and some of which line the socket wall.14,36 To preserve the vitality of these cells, certain guidelines should be observed. Keep the time before replantation to a minimum. Immediate replacement is ideal (Figure 30-18). If the tooth must be stored, keep it moist. Less than 20 minutes in air is associated with a good prognosis and longer than 1 hour with a poor prognosis.4,14 If possible, the tooth should be stored in a Save-A-Tooth, which uses a soft mesh to suspend the tooth in Hanks’ balanced salt solution. Alternative transport mediums are whole milk, saline, the victim’s saliva, sports drinks, and water, in that order of preference. The concept is to preserve the health of the periodontal ligament cells in the most isotonic, pH-balanced solution at hand. If no container is available, use a plastic bag, plastic wrap, or saturated cloth to keep the tooth from drying. Handle the tooth by the crown only. Never scrub, curette, or use a disinfectant on the root surface; gently rinse with saline to remove debris. When removing clotted blood from the socket, use gentle irrigation and suction, and avoid scraping the socket walls. Examine the socket for fracture of the alveolar wall. If present, reduce the fractured bone with a blunt instrument. Ease the tooth back into place with slow, steady pressure. After replantation, splint the tooth nonrigidly for

B

FIGURE 30-16  A, Complicated crown fracture. B, Treated with a temporary filling.

604

Lateral Luxation In this injury, the tooth is often displaced by a horizontal blow, yet it is not mobile because the apex is locked into its new position in the alveolar bone. A high, metallic tone on percussion is another clue that this has occurred. This injury and its treatment are painful. Figure 30-17 shows how two fingers are used to reduce the tooth. One finger guides the apex down and back, while the other repositions the crown. This requires judicious, but sometimes quite firm, application of force. The tooth may snap back into position and be quite stable. Check the tooth the next day. Breakdown of marginal bone and inflammation may cause the tooth to become mobile. Splinting is necessary if mobility is present, whether this occurs immediately after reduction or is detected later.16

FIGURE 30-17  Two fingers are used to reduce lateral luxation.

Patient Instructions After all of the preceding intraoral injuries, the patient should be placed on a soft diet for 10 to 14 days and instructed to brush gently but thoroughly with a soft toothbrush after every meal. The patient should also rinse twice each day with a chlorhexidinecontaining mouthwash if available, or warm saline if not.

A

B FIGURE 30-18  A, Two teeth have been avulsed. B, The teeth have been replanted.

1 week. Suture any gingival lacerations after splinting. Administer an antibiotic for 5 days, and give appropriate antitetanus prophylaxis. Endodontic therapy should be instituted within 2 weeks.4,36 The preferred approach to tooth avulsion or severe luxation is immediate reduction in the field, followed by evacuation for definitive treatment. The next most desirable option is to store the tooth properly and transport victim and tooth for replantation within a few hours of injury. If the extraoral dry time exceeds 60 minutes, the periodontal ligament cells are presumed necrotic and should be removed by curettage. The root is then treated before replantation. Sodium fluoride 2.4% with a pH of 5.5 has been shown to improve prognosis, as have enamel matrix proteins (Emdogain).48 If field conditions prevent all of the aforementioned treatments, a delayed replantation procedure is indicated. Store the tooth dry. Three weeks after the injury, the necrotic pulp tissue is removed and the tooth is disinfected, fluoridated, and surgically replanted. The aim of delayed replantation is to produce ankylosis between tooth and bone.4

Proper Reduction It is sometimes difficult to know when a displaced tooth has been returned to its proper position. Usually a tooth should be positioned similarly to its contralateral mate. Sometimes asking the victim can help; it may be that one tooth has always been longer than the others, or in a different position. However, occlusion is always the best guide to proper position. If the victim bites and contacts only the injured tooth, further positioning is necessary. In many cases, it is not possible to reposition the tooth completely because of swelling or organized clot formation. Therefore some adjustment of the opposing tooth (try using an emery board or pocket knife file) may be necessary to allow proper occlusion. If the injured tooth receives additional trauma each time the victim bites, it will be uncomfortable and healing will not occur. Splinting When the goal of splinting is to establish a normal, fibrous union between the tooth and the bone, a short-term, nonrigid technique is used. When hard tissue union is desired (e.g., root fracture or alveolar segment fracture), longer-term rigid splinting is used.4 Ideally, a single avulsed or loosened tooth is usually bonded to the adjacent tooth or teeth with the acid etch and composite technique.4,16 For fractures of the jaws or alveolar segments, arch bars and wire splints are often used. The rescuer lacking adequate materials must use ingenuity and improvisation to splint teeth. During a very short evacuation, the victim could hold the tooth in approximate position by closing (biting gently) on a gauze pad. Softened wax can be adapted to a loosened tooth and the teeth on either side to lend support. If the victim has an athletic mouth guard with him or her, this can also be used. Figure 30-19 shows how a suture can be used to hold a tooth in place for a period of a few days. For a sturdier splint, a crude arch bar can be cut from a SAM Splint or made from a paper clip and dead-soft wire obtained from copper wiring or twist ties. Injuries to Primary Teeth Injuries to the deciduous teeth offer unique challenges, not the least of which is behavioral management of a young child. Splinting is very difficult because of the small amount of tooth structure available. In general, heroic efforts should not be made to save primary teeth.4,16 Exarticulated deciduous teeth should not be replanted. Severely extruded teeth, infected teeth, or those intruded into the developing permanent tooth

Comminution of Alveolar Socket or Fracture of the Alveolar Socket Wall The bone of the alveolar socket is fractured into one or more segments. Stabilize the associated teeth. Alveolar Segment Fracture This condition is characterized by displacement of two or more teeth as a unit. The teeth are not mobile with respect to one another. The apices may be locked into their abnormal position as in lateral luxation. The segment is repositioned (this may be painful even with local anesthesia), and rigid splinting is placed for 4 to 6 weeks.

SOFT TISSUE INJURIES Wounds of the oral mucosa and face should be treated after repair of the dental injuries and jaw fractures. Time is more critical when treating intraoral, hard tissue injuries. Also, lacerations

FIGURE 30-19  A suture can be used to hold a replanted tooth in place.

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CHAPTER 30  Wilderness Dentistry

are likely to be reopened if closed before intraoral manipulations. See Chapter 31 for diagnosis and treatment of facial soft tissue injuries and Chapter 22 for wound care.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

should be extracted. Because the permanent tooth follicle lies to the lingual side of the primary tooth root, the typical frontal impact displaces the crown toward the palate, but levers the root apex away from the permanent tooth (Figure 30-20). Most minor subluxations and luxations require only symptomatic treatment. As long as the displaced tooth does not interfere with occlusion, reduction is contraindicated. Spontaneous repositioning often occurs over a period of weeks. Fragments of primary roots need not be extracted because normal resorption will still occur.

DISLODGED FILLINGS, CROWNS, AND BRIDGES No emergency treatment is necessary for a dislodged filling, small piece of tooth, crown, or bridge in the absence of other symptoms. Often the best course of action is to file off any excessively sharp areas of the tooth that are irritating the victim’s soft tissues, and otherwise leave the tooth alone. If you are going to attempt a temporary filling or crown recementation procedure, make sure you do not create an occlusal problem by leaving the restoration too high. This will only make the patient more uncomfortable.

APPLIANCE SORES Complete dentures, removable partial dentures, retainers, mouth guards, and the like can cause mucosal sores if their fit changes even a small amount. The mucosa will appear red or even ulcerated. Often the patient can do without the appliance until definitive treatment is available. If not, it is necessary to file or scrape away a small amount of material where the appliance is rubbing the mucosa. Finding the proper area of the appliance to relieve can be a challenge. Mark the sore spot (a tiny piece of adhesive tape, sticky side out, or a slurry of water and grape drink mix are options), insert the dried appliance, and remove. Hopefully the mark will have transferred to the appliance, showing the proper place to adjust.

ORTHODONTIC EMERGENCIES Orthodontic appliances can cause soft tissue irritation or ulceration. Cover the offending fixture with soft wax. Sometimes a protruding wire can be bent until the sharp portion faces away from the soft tissues. If a bracket or wire becomes excessively loose, it can usually be removed with judicious tinkering. If a wire needs to be cut and small wire cutters are unavailable, try fingernail clippers or repeatedly bending the appliance until the metal fatigues and breaks.

FIGURE 30-21  Technique for infiltration of a local anesthetic.

Local Anesthesia Local anesthesia is a prerequisite to many emergency dental, oral, and maxillofacial procedures. Anesthesia of any upper tooth and the associated buccal soft tissues can be obtained by infiltration. Approximately 2 mL of a local anesthetic solution is placed as close to the apex of the tooth as possible, just above the periosteum. By holding the syringe parallel to the long axis of the tooth, the needle tip is guided in the proper direction (Figure 30-21). Articaine (Septocaine) 4% with 1 : 100,000 epinephrine has become the most widely used local anesthetic in dentistry.51 Two percent lidocaine with 1 : 100,000 epinephrine is also commonly used, and bupivacaine (Marcaine) 2% with 1 : 200,000 epinephrine is useful for long-term pain relief. Other available local anesthetics can be substituted. The mental nerve block is a simple method for obtaining anesthesia of the teeth and buccal mucosa from the second premolar forward. Proceed as for the infiltration, except that the target area is the mental foramen, located between apices of the lower first and second premolars (Figure 30-22). After depositing the solution, gently massage the area for about 30 seconds. The inferior alveolar nerve block is more difficult to learn but produces anesthesia of all the lower teeth up to the midline, as well as the buccal soft tissues forward of the mental foramen.

Permanent tooth bud

B

Primary tooth

A

FIGURE 30-20  When a child falls forward, the typical direction of force is shown by arrow A, and the apex of the deciduous tooth is levered away from the developing permanent tooth bud, as shown by arrow B.

606

FIGURE 30-22  Technique for blocking the inferior alveolar nerve near the mental foramen. The shaded teeth will be anesthetized.

1/2

Finger

1/2

*

FIGURE 30-23  When administering the inferior alveolar block, the target area lies on the medial surface of the mandibular ramus, halfway between the rescuer’s thumb and forefinger.

The lingual nerve is also blocked by this injection, producing numbness of the anterior two-thirds of the tongue and lingual gingiva. Figure 30-23 shows how the deepest concavity on the anterior border of the mandibular ramus is palpated by the thumb while the deepest concavity on the posterior border is palpated by the index finger. The target area is then halfway between the rescuer’s thumb and index finger.47 Figure 30-24 shows how the syringe is kept parallel to the plane of the lower teeth and how to puncture the mucosa just medial to the rescuer’s thumbnail. When bone is contacted in the target area, the anesthetic solution is deposited. Experienced dentists miss the target area, and thus fail to produce adequate anesthesia, in approximately 10% of injections.

Dental First-Aid Kit Most supplies needed to treat dental emergencies can be found in a good, general purpose first-aid kit. These include antibiotics and analgesics, gauze, tweezers, scalpel, hemostat, and sutures. Items specific to dental emergencies can be added to a wilderness first-aid kit without a large sacrifice of space or weight. Cavit is temporary filling material that requires no mixing and is easy to use. Squeeze a small amount of the material from the tube and place it in the tooth. Wet a dental packing instrument (or cotton-tipped applicator or toothpick) to prevent sticking and pack the Cavit well. Then remove any excess. Have

I

Prevention The vast majority of dental emergencies can be prevented, beginning with pretrip planning. Before any extended travel to a remote area, all persons should have a thorough dental examination, radiographs, periodontal care, and treatment of potentially troublesome teeth. The Peace Corps requires certification that examination and treatment have been performed before assignment to developing countries. The National Science Foundation has similar requirements and in addition requires impacted and unopposed third molars to be extracted before travel to Antarctica. Once in the wilderness, minimal precautions can have significant effects. Lip balm with sunscreen can inhibit herpes labialis outbreaks. Routine personal oral hygiene will prevent many odontogenic infections and painful inflammatory conditions. Ideal care should include twice-daily toothbrushing and flossing. Toothpaste is not essential because mechanical removal of plaque and stimulation of the gingiva are the most important aspects of oral care. The fuzzy end of a hickory twig or even a finger can be used if a toothbrush is not available. In the wilderness, daily oral hygiene not only helps prevent dental emergencies but contributes to an overall sense of well-being and helps buoy morale when, for example, an expedition is tent-bound by bad weather. Helmets are essential for preventing trauma in rock climbing, whitewater kayaking, and mountain biking. It is estimated that custom-made mouth guards prevent over 200,000 injuries every year in interscholastic sports.34 Their use in backcountry recreation, now almost nonexistent, would probably prevent many dental injuries if used in appropriate circumstances. Despite commercial claims to the contrary, there is no scientific evidence that mouth guards can prevent traumatic brain injury.18

REFERENCES FIGURE 30-24  Keep the syringe parallel to the plane of the lower teeth.

Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 30  Wilderness Dentistry

Thumb

the victim bite to displace material that would interfere with occlusion. The filling material will set in a few minutes after contact with saliva. Zinc oxide/eugenol cements (IRM) consist of a liquid and powder. Start with two drops of the liquid and begin mixing in the powder. Keep adding powder to make a dough that is not sticky yet will hold together. Dip the instruments in some powder to keep the mixture from sticking. Insert and shape the filling material as explained previously. Zinc oxide/eugenol cements have several advantages compared with Cavit. They are significantly stronger and can be mixed to a doughy stage for filling or slightly thinner for use as cement. Most important is the soothing effect of eugenol on teeth with pulpitis. However, the liquid often leaks from its container, lending a pervasive odor to the backpack and tent; wind tends to blow the powder away; and the material is difficult to mix and is a sticky mess to insert into the tooth. A more complete kit for extended expeditions should include a No. 151 universal extraction forceps (see Figure 30-13, online) and a straight elevator for extracting teeth. A mouth mirror, Orabase with benzocaine, orthodontic wax, dental floss, dental syringe, 30-gauge needles, and anesthetic cartridges complete the kit. These items fit in a small case and weigh about 14 oz. A custom dental first-aid kit is preferred over commercial dental “travel kits,” which contain unnecessary items and lack essential ones. In an outdoor situation, techniques must often be adapted or improvised depending on the items available. For example, Figure 30-18 shows how a suture can be used to splint an avulsed or extruded tooth. A temporary filling can be fashioned from softened candle wax, an emery board can be used to smooth a sharp tooth, or a pocket knife can be used to perform a drainage procedure.

CHAPTER 31 

Management of Facial Injuries VICKI MAZZORANA

Wilderness medicine is defined in terms of the amount of time that an individual is remote from definitive hospital-based care. This definition allows for the inclusion of disaster medicine, military or tactical medicine, rural emergency medical services systems, and traditional wilderness medicine. These fields have in common their resource-constrained environments, necessity for expanded prehospital patient care, and delayed access to definitive care. These conditions require integrating evacuation and rescue training, evaluating environmental threats, and understanding and ability to make use of resources during disasters. A more expansive definition of wilderness medicine also includes the type of injury, setting in which the injury occurred, and, more specifically, how a particular injury relates to human interaction with the environment.41 In all of these environments and situations, facial injuries occur and require urgent initial management to diminish morbidity, mortality, and the disruption of recreational activities. The Joint Theater Trauma Registry is responsible for collecting and organizing medical treatment data about patients from combat operations who are treated at U.S. medical facilities. Although the head, face, and neck account for only 12% of the body surface area, approximately 40% of all injuries that are sustained during military conflicts are to this region. This proportion is higher than previous military conflicts, and it is most likely the result of improved body armor and the relative lack of protective devices for the head and face.32,38,50 Soldiers are at high risk for sustaining oral and facial trauma during training and assaults.52 Traumatic facial injuries account for significant morbidity and mortality among U.S. armed forces, so improved functional protection for the vulnerable facial region must be developed. Experience and data gathered during military conflict have provided tremendous value with regard to further education of medical providers about emergency care of facial trauma. Research published by the military has been instrumental to advancing trauma care principles and guidelines used to manage trauma in both civilian and military populations. In addition to military-related injuries, sports-related accidents are responsible for a significant number of orofacial injuries. Skiing, bicycling, soccer, and mountain biking account for more than 60% of sports-related accidents. Traumatic injuries as a result of falls, collisions, and self-inflicted injuries result in facial bone fractures, dentoalveolar trauma, and soft-tissue damage. The injury pattern depends on the sporting activity, with high-speed and high-impact sports causing more fractures and low-speed and low-impact sports producing more dental injuries.48 A growing number of people are participating in a wide variety of outdoor recreational activities that take them farther away from definitive medical services.14,46 Wilderness recreation and adventure activities create many situations that place individuals at risk for facial traumatic injury. The National Outdoor Leadership School (NOLS) collects and publishes data about injuries, illnesses, nearmiss incidents, nonmedical incidents, and evacuation profiles among their participants. Per recent unpublished NOLS data, facial trauma accounted for 4% of all reported injury incidents over a period of 25 years from 1984 to 2009; the majority of these were soft-tissue injuries. The NOLS commitment to risk management and developing strategies aimed at preventing serious injuries and fatalities while meeting educational objectives has provided a better understanding of injury patterns.26

History and Examination Before evaluating and treating a patient with injuries in the wilderness, the setting and situation must be evaluated to determine the safety of the environment. Evaluating a patient with facial 608

trauma proceeds as it does with any other medical condition. In emergency situations, obtaining the chief complaint and history of the present illness takes place simultaneously with the performance of the primary survey. The primary survey evaluates and treats inadequacies in the areas of airway, breathing, and circulation. The patient’s baseline mental status is assessed and any neurologic disabilities are identified. Examine the mouth and pharynx for foreign bodies such as blood clots, tooth or bone fragments, and dentures. If the airway is obstructed, perform a chin lift or a jaw thrust, or insert an oropharyngeal airway to hold the tongue forward. If there is a potential cervical spine fracture, keep the head and neck in a neutral position without hyperextension. Position the patient to maintain the airway and to facilitate respiratory exchange; in many instances, this will be the prone position. Raise the head above the heart to decrease bleeding and swelling, or position the victim seated with the head forward so that blood drains from the mouth or nose. If these measures fail, perform endotracheal intubation or cricothyrotomy. Do not leave the patient unattended, especially in a supine position. After the airway is secured and the victim is stabilized, perform a secondary survey to obtain an abbreviated history of the present injury or illness and to extract pertinent information, such as allergies, medications, medical history, the presence of complicating medical factors or chronic illnesses, last oral intake, and events leading up to the injury. If the victim has sustained significant head or facial trauma, determine if he or she experienced a loss of consciousness or has symptoms of nausea, vomiting, visual disturbances, or headache. Assess the patient’s pain, and ask about its character, onset, location, radiation, and duration. Determine if anything exacerbates or relieves the pain. The focus of the examination depends somewhat on the provider’s clinical impression. However, in all cases, a systematic approach to examination in oral and maxillofacial emergencies allows for efficient collection of relevant information. Start the examination with a general appraisal that includes the vital signs. Clean the face, mouth, head, and neck of blood and debris; this unmasks soft-tissue injuries and facilitates diagnosis. Next, observe the head, neck, and face, and note any asymmetry. Palpate all facial bones, temporomandibular joints, muscles, and areas of suspected injury for tenderness, crepitus, swelling, instability, dislocation, fracture, and foreign bodies. Bimanually palpate the lips, the cheeks, and the floor of the mouth. Observe the patient slowly opening the mouth, and examine for range of motion and any deviation with opening. Evaluate facial soft-tissue swelling for hematoma formation, especially in areas that are associated with underlying cartilage, such as the ear and nose. Perform an intraoral examination of the lips, cheeks, mouth, tongue, hard palate, soft palate, and pharynx. Examine facial lacerations carefully to determine if they penetrate through the skin into the oral cavity or if they contain foreign material. Gently retract the lips with the teeth closed to examine soft tissues and occlusion. Examine dentition for fractures and mobility. Observe the gingiva for bleeding, swelling, trauma, color, firmness, and recession.

Temporomandibular Joint Disorders Temporomandibular joint (TMJ) dislocation is more commonly referred to as mandibular dislocation. Dislocation of the mandibular condyles causes an inability to close the mouth and may result from external trauma or, more frequently, from mandible hyperextension. This may occur in any environment while yawning, taking a large bite when eating, vomiting, laughing, or

Temporal bone

CHAPTER 31  Management of Facial Injuries

performing oral sex. This condition may be bilateral or, less often, unilateral, and it frequently recurs.8 Although posterior, lateral, and superior dislocations occur, anterior TMJ dislocation is most common, and it occurs when the mandibular condylar heads and their respective cartilaginous discs move anteriorly along the articular eminence out of the glenoid fossa and become locked in the anterior–superior aspect of the articular eminence of the temporal bone. Dislocation is complicated by involuntary spasms of the muscles of mastication, including the masseter, temporalis, and medial pterygoid, thereby making it extremely difficult for the condyles to return to their normal position during reduction.1,8,37 Diagnosis of TMJ dislocation is not difficult, but, without the benefit of a medical history can be confused with an acute dystonic reaction. Patients present with difficulty speaking, acute jaw pain anterior to the ear, malocclusion, and inability to open or close the mouth. They may be extremely uncomfortable and anxious. Patients present with an open mouth and a prominent-appearing lower jaw. If the dislocation is unilateral, the chin will appear to deviate to the side opposite the dislocation. More frequently, dislocation is bilateral without chin deviation. Clinically, the patient may have a palpably absent condyle within the glenoid fossa and visible periauricular depression.8,27,28 Ideally, with traumatic dislocation, radiographs are performed to eliminate a condylar fracture. In the wilderness environment, radiography is impossible, and fracture exclusion must be done on the basis of clinical examination alone. In the wilderness, a variety of methods may be attempted to reduce anterior mandibular dislocations without procedural sedation or local anesthesia. The goal of the reduction process is to relocate the mandibular condyle to the glenoid fossa and out of its current location anterior to the articular eminence of the temporal bone. This requires relaxing the muscles of mastication, and is accompanied by properly positioning the provider and patient so that direct pressure can be placed on the mandible during relocation.8 Multiple reduction techniques are used that do not require conscious sedation or local anesthesia (Figure 31-1). To perform the classic reduction technique, seat the patient lower than you and stabilize his or her head. Stand facing the seated patient, and ask the patient to open his or her mouth widely against resistance; this reduces muscle tone of the elevator muscles through reciprocal inhibition and allows for concurrent manual reduction. Simultaneously exert maximal downward reduction force with the use of gloved thumbs on the patient’s lower molars or mandibular ridge while exerting steady and constant downward pressure by moving the mandible down, then posteriorly, and then up with the remainder of the fingers

FIGURE 31-2  Classic technique for the reduction of anterior mandibular dislocation.

and hand around the jaw and chin, levering upward. The downward pressure clears the condyle of the articular eminence, whereas the posterior pressure repositions the condyle within the glenoid fossa. This technique may be difficult if muscle spasm is severe8,28 (Figure 31-2). For the recumbent approach, lay the patient on his or her back, and, standing either behind or in front of the patient, apply caudal pressure on the mandibular ridge8 (Figure 31-3). For the posterior approach, seat the patient either on the floor or a chair, and stand behind and above the patient. Place the thumbs on the retromolar gum posterior to the patient’s last molar along the mandibular ramus, and exert downward pressure on the mandible8 (Figure 31-4). For the ipsilateral approach, use a sequential combination of intraoral and extraoral manipulation. Focus on one side of the jaw at a time. Stand on the side of the patient, and, while stabilizing the patient’s head with one hand, use the thumb of the other hand to exert external downward pressure on the displaced mandibular condyle, which is located anterior and inferior to the

Articular eminence

Mandibular fossa 1

Mandibular condyle 2

3

4

5

FIGURE 31-1  Reduction of temporomandibular joint dislocation. The temporomandibular joint is shown in both normal and dislocated positions. 1, Closed position, with the mandibular condyle resting in the mandibular fossa behind the articular eminence. 2, In the maximally open position, the condyle is just under and slightly behind the eminence. 3, In the dislocated position, the condyle moves forward and upward slightly above the eminence; muscle spasm then occurs. 4, To reduce dislocation, place the thumbs intraorally and lateral to the lower molars, and apply downward pressure to the lower molar ridge area near the jaw angle in a downward and backward direction. 5, When the condyle has cleared the articular eminence, muscle contraction will return the jaw to a normal closed position. The patient sits on a low chair with the back straight. Face the patient, wrap the thumbs with gauze for protection, place them in the mouth on the back molars, and then push down and back. A rocking motion may help. (From Amsterdam JT: Oral medicine. In Marx JA, Hockberger RS, Walls RM, editors: Rosen’s emergency medicine: Concepts and clinical practices, ed 6, Philadelphia, 2006, Mosby, p 1041.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 31-5  Ipsilateral extraoral approach for reduction of anterior mandibular dislocation.

zygomatic arch. If this is unsuccessful, exert downward pressure intraorally on the ipsilateral lower molar teeth or the mandibular ridge. If this is still unsuccessful, a combination of intraoral downward pressure on the posterior molars along with external downward pressure on the mandibular condyle may be successful8,43 (Figure 31-5). For an alternative manual method, place your fingers over the periauricular-dislocated condyle, and then gently massage the musculature posteriorly and inferiorly to induce relaxation of the muscles and reduction of the condyle into the glenoid fossa.8,21 For the wrist pivot method, face the seated patient while standing, and place your thumbs on the apex of the patient’s chin while wrapping the remainder of the fingers laterally over the mandible onto the inferior molars of the patient. With this method, push upward with the thumbs on the patient’s chin while

at the same time pushing downward on the body of the mandible with the remaining fingers in a pivoting action. Flex your wrists, and move in the direction of ulnar deviation. The pivoting action uses the angle of the jaw as a fulcrum, and this results in rotation of the mandibular condyles back into the glenoid fossa. To prevent injury to the mandible, this technique must be applied to both sides of the jaw concurrently8,27 (Figure 31-6). For the gag reflex method, elicit a patient’s gag reflex by stimulating the soft palate. This results in mastication muscle relaxation and the descent of the mandible caudally as part of the reflex. During the gag reflex, the jaw muscles relax, thereby causing transient descent of the mandible inferiorly and forcing the condyle to relocate back into the glenoid fossa.2,8 Alternatively, have the patient open his or her mouth widely or against resistance to cause reciprocal relaxation of the elevator muscles to allow for simultaneous manual reduction. With the nerve block method, the peripheral masseteric nerve is anesthetized where it has passed through the mandibular notch and before it penetrates the masseter. The deep temporal nerve may be anesthetized by locating the anterior temporalis muscle within a depression just above the zygomatic bone. The greater wing of the sphenoid bone is located deep below this portion of the muscle. The anesthetic needle is directed into this area until the needle hits the sphenoid bone and the anesthetic is deposited.

FIGURE 31-4  Posterior approach for reduction of anterior mandibular dislocation.

FIGURE 31-6  Wrist pivot method for reduction of anterior mandibular dislocation.

FIGURE 31-3  Recumbent approach for the reduction of anterior mandibular dislocation.

610

These blocks result in reduction of pain and muscle spasm, thereby allowing manual reduction. Administration of a local anesthetic agent around the TMJ capsule may diminish joint pain, but it will not diminish muscular pain or spasm51 (Figure 31-7). Complications of the various reduction techniques include intraoral trauma from significant downward pressure on the teeth and gums, fractures, joint cartilaginous injuries, and torn ligaments and muscles. More frequently, the provider’s fingers are injured during the intraoral relocation techniques when the jaw snaps shut after successful reduction and relocation. Using gloves, gauze, bite blocks, and plastic finger splints as well as placing the thumbs on the mandibular ridge rather than the teeth or gums during the reduction process can prevent this.8 After reduction, advise patients to apply ice or cool compresses to the TMJ, to avoid hyperextending the mandible, to take nonsteroidal antiinflammatory agents such as ibuprofen, and to maintain a soft diet for a week. Wrap a bandage around the head and jaw to prevent mandible hyperextension and to limit jaw movement.8,16

Internal Derangements of the Temporomandibular Joint Between the movable mandibular condyloid process and the articular eminence of the temporal bone, there is a cartilaginous disc that is interposed between these articulating components.

A

Epistaxis Although most cases of nosebleed are trivial, some become life threatening, because aspiration can lead to respiratory compromise, and extensive blood loss can result in hemodynamic collapse. Therefore, the condition should never be neglected. It is more common among the young and elderly. Most causes are traumatic and occur in winter.37 Spontaneous epistaxis is more common in environments that are cold, dry, dusty, or smoke filled. Anterior nosebleeds may be managed definitively in the wilderness, but posterior bleeds require immediate evacuation as a result of continued hemorrhage and the potential for airway compromise.29 The nasal mucosa is highly vascular, with superficial exposed blood vessels that arise from the terminal branches of both the internal and external carotid arteries that serve to warm and

B

FIGURE 31-8  A, The normal temporomandibular joint with cartilaginous disc. B, In a closed lock, the ligaments have stretched, and the disc is trapped anterior to the condyle.

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CHAPTER 31  Management of Facial Injuries

FIGURE 31-7  Masseteric nerve block for reduction of anterior mandibular dislocation. The index finger locates the zygomatic arch and moves inferiorly until it reaches the mandibular notch at a point halfway between the thumb and the middle finger. The needle is introduced posterior to the index finger to hit the neck of the condyle.

The disc stabilizes the joint and allows for rotational movements. The intra-articular cartilaginous disc may displace anteriorly, which results in joint dysfunction and abnormal joint sounds such as clicking or popping. When closing the mouth, if the cartilaginous disc of the TMJ displaces anteriorly relative to the mandibular condyle with reduction to its normal position when the mouth opens, clicking of the joint may occur. This may manifest itself as a pop, which is the noise that is heard when the condyle moves under the anteriorly displaced disc; this may or may not be associated with joint pain and dysfunction25 (Figure 31-8). However, if the cartilaginous disc is displaced but does not reduce and return to its normal position on mouth opening, then the patient may experience occlusive instability associated with jaw locking. There are two types of lockjaw. With closed lock, the mandibular condyle is unable to slide under the anteriorly displaced disc. With open lock, the mandibular condyle is unable to slide back over the disc into its normal position.36 Clinically, there is joint tenderness on palpation, and the chin may be deviated toward the affected side on attempted mouth opening. Functionally, the disc is trapped anterior to the mandibular condyle, and the ligaments are stretched and become inflamed. This can occur spontaneously while eating or talking, but it may be present on awakening from sleep, and it may be associated with mandibular trauma. The provider can attempt to instruct the patient to reduce a closed lock. To do this, the patient should close the mouth until the teeth almost touch, move the mandible laterally as far as possible to the affected side, and finally swing the mouth fully open.36 If these maneuvers fail, consider manual reduction using techniques that were described for TMJ reduction. Myospasm of the muscles of mastication may cause similar restriction in mandibular function, but typically the affected muscles are firm and extremely tender; alternatively, with closed lock, the muscles are usually normal.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

humidify inspired air. Epistaxis is normally classified into anterior or posterior, depending on the anatomic location of the bleed. A particularly rich collection of vessels and a common site of anterior nosebleed is Kiesselbach’s plexus on the lower anterior part of the nasal septum (i.e., Little’s area). This area accounts for 90% of epistaxis. Posterior bleeding originates primarily from a branch of the sphenopalatine artery called the posterior nasal artery, which forms part of Woodruff’s plexus19,49 (Figure 31-9). Initial evaluation requires first determining if the patient’s bleeding is unilateral or bilateral and whether it is coming from an anterior or posterior site. A nosebleed usually occurs on one side of the nasal cavity. However, with profuse bleeding, blood can pass behind the nasal septum and also appear on the unaffected side. Most individuals bleed from an anterior site, which is visualized on intranasal speculum examination, whereas with posterior epistaxis the bleeding point cannot be seen on intranasal examination. Evaluate and treat a nosebleed by having the patient sit upright with his or her head tipped slightly forward. This maneuver will decrease blood flow through the nasopharynx and allow blood to drip passively out of the nose rather than flow posteriorly into the throat and cause choking, aspiration, and vomiting swallowed blood. Have the patient blow the nose to remove any clots immediately before examination. Warm saline lavage of each nostril may accelerate activation of the clotting cascade and allow for better visualization of the bleeding areas.49 Bleeding may resume, but there will be improved access and visibility for the application of a vasoconstrictor or chemical cautery. Ask the patient if he or she has put anything up the nose to stop the bleeding so that it can be removed before additional packing is placed. Examine the nasal cavity with a nasal speculum to determine the site of bleeding. Instruct the patient to pinch the fleshy alae tightly against the cartilaginous septum portion of the nose between the thumb and index finger for at least 10 to 20 minutes. Applying cold compresses to the nose and instructing the patient to suck on ice can improve this.39 Pinching the bony bridge of the nose does not provide direct pressure on the bleeding vessels. Alternatively, hands-free techniques that involve the use of external pressure devices fashioned from taping together two tongue depressors or a commercially available nose clip also work well.19 If a bleeding point is localized and nose pinching does not stop the bleeding, apply local anesthetics and vasoconstrictors to the nasal mucosa over Little’s area. Anesthetic preparations include topical tetracaine 1%, cocaine 1% to 4%, lidocaine 5%, ephedrine 5%, and aqueous epinephrine 1:1000. Vasoconstrictive nasal sprays include phenylephrine 0.5% (Neo-Synephrine) and oxymetazoline 0.05% (Afrin). Apply anesthetics and vasoconstrictors by drip or spray, on a cotton pledget, or with a cotton-tipped

applicator. Objects placed in the nose should have a string attached or include another method of easy removal and they should be aimed posteriorly. Avoid pushing material laterally into the turbinates or superiorly toward the cribriform plate. Leave the vasoconstrictor in place for 10 minutes to 24 hours.29 Epistaxis that is refractory to pressure and topical vasoconstrictors may require chemical cauterization with use of a silver nitrate stick of 75% concentration that reacts to the mucosal lining to produce local chemical damage. After applying a topical anesthetic, apply a cautery stick to the bleeding point with firm pressure for 5 to 10 seconds. Apply the cautery only to one side of the septum, and be careful to not perforate the septum by applying too much pressure.13 When there is more vigorous anterior nasal bleeding, nose pinching, topical chemical vasoconstrictors, and cautery may not be effective. In such an instance, inject the anterior bleeding site with 0.5 to 1 mL of lidocaine 0.5%, 1%, or 2% that contains 1:100,000 epinephrine. This has a tamponading effect as well as a vasoconstrictive effect. Alternatively, directly over the bleeding site, insert into the nares a small piece of absorbable or degradable material that does not require removal. Such materials include oxidized regenerated cellulose (Oxycel or Surgicel), purified bovine collagen foam or paste (Gelfoam), microfibrillar collagen (Avitene), porcine gelatin (Surgiflo), bovine gelatin-human thrombin (FloSeal), QuikClot, recombinant factor VIIa, topical thrombin, hemostatic matrix, nosebleed gauze, and fibrin glue.19,33,34,39 After the bleeding has stopped, instruct the patient to not blow the nose or probe the area for 48 hours. Increase the humidity, warm the inspired air, and moisturize the nasal mucosa with topical gels, lotions, and ointments to help prevent recurrent bleeding. Treat persistent epistaxis by packing the anterior cavity, posterior cavity, or a combination of both. If the site of bleeding is not controlled by the previous methods, insert a lubricated anterior nasal sponge or tampon. Improvise with gynecologic tampons, sponges, and gauze. Current commercial options include Merocel, Medtronic, Rapid Rhino, ArthroCare, Weimert Epistaxis Packing, and Rhino Rocket34 (Figure 31-10). If a nasal tampon fails to halt the bleeding, then formal anterior packing is necessary. The basic technique involves placing 12-mm (0.5-inch) petrolatum- or antibiotic-impregnated strip gauze into the nasal cavity. The adult patient requires 90 to 120 cm (3 to 4 feet) of such gauze to pack the nose adequately and to tamponade the bleeding. Layer the gauze in tiers that start on the nasal floor and proceed to the roof of the nose. Leave both ends of the gauze outside of the nose and taped to the face to prevent inadvertent aspiration. Improvised anterior nasal tamponade can be accomplished with a Foley catheter (Figures 31-11 and 31-12).

Septal branch of anterior ethmoidal artery

Frontal sinus

Anterior ethmoidal artery

Ethmoid bone Sphenopalatine artery (septal branch)

Watershed area (Kiesselbach’s plexus) Septal cartilage

Frontal sinus

Posterior ethmoidal artery Sphenoid sinus Sella turcica

Sphenoid sinus

Sphenopalatine artery (lateral nasal branch)

Vomer

Eustachian tube

Septal branch of superior labial artery

A

Palate

Great palatine artery

B

Site of posterier epistaxis

FIGURE 31-9  A, Vascular supply to the septum. The most common site of anterior epistaxis is within the area that is labeled Kiesselbach’s plexus. B, Vascular supply to the lateral wall. The most common site of posterior epistaxis is the sphenopalatine artery as it emerges posterior to the middle turbinate. (From Maceri DR: Epistaxis and nasal trauma. In Cummings CW, editor: Otolaryngology: Head and neck surgery, ed 2, St Louis, 1993, Mosby, p 728.)

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CHAPTER 31  Management of Facial Injuries

A C

D

E

B

FIGURE 31-10  Commercial nasal packings are commonly used in place of the traditional gauze packing. A, Rhino Rocket. B, Epi-Stop Balloon Catheter. C, Rapid Rhino. D, Rapid-Pac. E, Rapid Rhino Dual Nasal Pack. (A and B courtesy Shippert Medical, Centennial, Colorado; C to E courtesy ArthroCare Corporation, Austin, Tex.)

A

C

B

D

FIGURE 31-11  The key to placing an anterior nasal pack that will control epistaxis adequately and stay in place is to lay the packing into the nasal cavity in an “accordion” manner so that part of each layer of packing lies anteriorly, thereby preventing the gauze from falling posteriorly into the nasopharynx. A, Grasp the first layer of 0.25-inch Vaseline gauze strip approximately 2 to 3 cm (0.8 to 1.2 inches) from its end. B, Place the first layer on the floor of the nose through the nasal speculum (not pictured), and then withdraw the bayonet forceps and the nasal speculum. C, Reintroduce the nasal speculum on top of the first layer of packing, and place a second layer in an identical manner. After several layers have been placed, it is often useful to reintroduce the bayonet forceps to push the previously placed packing down onto the floor of the nose to make it tighter and more secure. D, A complete anterior nasal pack can tamponade a bleeding point anywhere in the anterior nasal cavity and will stay in place until the clinician or patient removes it.

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

Facial Bone Fractures Examine any person who is suffering from head or facial injury for facial fractures. Forehead fractures that involve the frontal sinus potentially involve the brain; this area is considered a part of the skull, and fracture here may suggest underlying brain injury. Orbital fractures frequently involve injury to the eye and its supporting structures.

MIDFACE: NOSE

FIGURE 31-12  A Foley catheter is placed into the nasopharynx, inflated with water, and retracted into position. The distal tip of the catheter has been cut off. Place an anterior pack (not shown) around the catheter. Protect the ala and the columella with gauze padding, and apply a plastic umbilical clamp or nasogastric clamp to the catheter to maintain slight tension on the balloon.

Nasal packing blocks sinus drainage and can predispose the patient to sinusitis. Therefore, place the patient on a prophylactic antistaphylococcal antibiotic such as 875 mg of amoxicillin with 125 mg of clavulanic acid (Augmentin) by mouth three times daily, 500 mg of dicloxacillin by mouth four times daily, 150 to 450 mg of clindamycin by mouth four times daily, or 160 mg of trimethoprim and 800 mg of sulfamethoxazole (Bactrim) by mouth twice daily until the packing is removed after 48 hours.29 If the site of bleeding is posterior and not possible to visualize, insert a formal posterior nasal pack, commercially available nasal balloon device, or Foley catheter. These methods rely on direct pressure or blood accumulation within the nasal cavity, which leads to tamponade. Placing a formal posterior nasal pack is difficult and involves gently inserting a lubricated soft tube into each nostril until the ends can be visualized in the back of the throat, then grasping this with a hemostat and bringing it out through the mouth. Use Foley catheters, nasogastric tubes, chest tubes, or improvised substitutes. Prepare a cylindric pack of 10 × 10-cm (4 × 4-inch) gauze, and hold it in shape by tying three silk sutures around it and leaving the ends approximately 10-cm (4-inches) long. The pack should be the same diameter as a circle made by the patient’s thumb and forefinger (i.e., the “OK” sign). Attach the two end sutures to the oral ends of the catheters. Pull the nasal ends of the catheters carefully back out of the nose until the pack is firmly positioned against the posterior aspect of the nasal cavity above the soft palate. Detach the sutures from the catheters, and tie them over a bolster that is placed underneath the nose. Secure the middle suture externally on the outside of the mouth to allow for removal 48 hours later (Figure 31-13). Commercially available preshaped nasal balloons (e.g., Brighton, Nasostat, Naso-Blymp, Simpson plug, and EpiStat nasal catheter) are manufactured specifically for treatment of posterior epistaxis. They have a postnasal balloon and mobile anterior balloon that are inflated independently. These are contraindicated in the case of severe head trauma, basilar skull fracture, or suspected craniofacial fractures that involve cerebrospinal fluid rhinorrhea19,34 (Figure 31-14). A standard urinary 14F to 16F Foley catheter with a 30-mL balloon can function as a posterior pack. Trim the distal tip of the catheter to prevent irritation. Insert the lubricated catheter through the nose into the posterior pharynx until it is visualized in the oropharynx; inflate it with a minimum of 3 to 5 mL of air or saline, gently pull it forward into the nasopharynx until the balloon engages, and then hold it in position by clamping the external end with a hemostat or an umbilical clamp. Balloons that are filled with air tend to deflate over time, and those that are filled with water may rupture and allow for aspiration.13,49 Pack the anterior nasal cavity with a nasal sponge or gauze. Hot-water irrigation has been documented as an alternative strategy for posterior epistaxis. Occlude the posterior pharynx with a balloon catheter, and then irrigate the nares with heated water (i.e., 45° C to 50° C [113° F to 122° F]). This reduces blood flow by causing mucosal edema and it clears blood clots from the nose.19,34 614

Nasal fractures are the most common midface fracture. The projected and prominent nasal vault is a delicate, pyramid-shaped structure that is comprised of paired nasal bones centrally and the frontal processes of the maxilla laterally. The remainder of the nose is composed of interconnecting cartilaginous structures that provide stability and support to the nasal septum. Typically nasal fractures manifest with midface swelling, epistaxis, periorbital ecchymosis, subconjunctival hemorrhage, and deformity. Facial swelling may preclude appreciation of obvious deformity. Functional changes in breathing and loss of the sense of smell may occur. Sweet or salty watery drainage suggests a cerebrospinal fluid leak.10 After soft-tissue injuries and epistaxis have been appropriately managed, examine the nose to determine the extent of nasal trauma. This requires an internal examination using a nasal speculum as well as an external examination. Cerebrospinal fluid rhinorrhea, which is appreciated on internal nasal examination as clear fluid, is indicative of more serious intracranial trauma. Cerebrospinal fluid separates from blood when it is placed on filter paper, and produces a clinically detectable ring sign, a double-ring sign, or a halo sign. When palpating the bridge of the nose, the provider may appreciate bony crepitus, nasal segment mobility, point tenderness, and displacement that may not be visible on external examination. Remove intranasal clots with cotton swabs. Close deep intranasal lacerations with absorbable sutures or cover with Oxycel, Gelfoam, Surgicel, or Avitene to control bleeding.31 Advise patients to apply ice to the area and to keep the head elevated to reduce soft-tissue swelling. Most surgeons prefer to treat nasal fractures after the swelling has subsided 5 to 10 days after the injury. Immediate treatment and evacuation are not necessary unless there are complications such as persistent epistaxis, difficulty breathing, or deeper lacerations that require definitive repair. If the nose appears to be straight after the swelling has subsided and the patient can breathe easily through both nostrils, further treatment may not be necessary. If the nose remains crooked after the swelling has resolved or if the patient experiences breathing problems, refer him or her to an otolaryngologist or a plastic surgeon within 3 to 5 days so that the bones do not heal while misaligned. Children with nasal fractures may have premature closure of sutures and uneven growth; therefore, a consultant should evaluate the injury, preferably within 4 days of its occurrence10,30 (Figure 31-15). Although digital pressure may reduce the deformity involved with simple nasal fractures, potential litigation issues exist, because the extent of the injury may not be appreciated immediately, and the patient may have a bad cosmetic outcome.31,37 Make a protective splint by cutting a triangular piece of a SAM splint that is large enough to fit the contour of the nose. Rest the splint on the adjacent part of the face without placing pressure on the nasal bridge. Secure the splint with strips of adhesive tape. Do not pack the nose unless this is necessary to control epistaxis or to drain a septal hematoma. Administer 500 mg of penicillin V potassium or amoxicillin by mouth four times a day for 5 days.10 Anterior nasal septal trauma may cause tearing of the submucosal blood vessels. If the mucosa remains intact, blood will accumulate between the septal cartilage and the mucoperichondrium and cause formation of a hematoma, either immediately or within the first 24 to 72 hours after the injury. Septal hematoma appears as a deviation, bulging, or widening of the nasal septum. Symptoms include nasal obstruction, pain, rhinorrhea, and fever (Figure 31-16).

CHAPTER 31  Management of Facial Injuries

Rubber catheter in nostril

Catheter in nostril

Palate

Turbinates

Nasopharynx

Palate

Tongue

Tongue

Ring forceps

Gauze wrapped around cotton ball

B

A

* 4” x 4” pad

Folded gauze pad

Fold

Long tapes

*

Roll

Two ties

Umbilical tape

C

Palate Traction

Gauze roll Silk ties Tongue

*

D

E

*

F

FIGURE 31-13  Traditional posterior nasal pack. A, After applying topical anesthesia, pass a red rubber catheter through the nose, and carefully grasp it in the oropharynx with ringed forceps and bring it out through the mouth. B, Make a posterior nasal pack by wrapping a cotton ball in a 4 × 4-inch gauze pad and tying two long silk sutures or umbilical tapes around the neck of the pack. Leave one tie long so that it can be taped to the cheek until it is needed for removal of the pack. C, Alternatively, fold a gauze pad, roll it into a cylinder, and tie it with two strings. Use two of the long strings to tie the pack to the tip of the catheter, and use the other two to remove the pack. D, As an option, use a second catheter that has been passed through the nonbleeding side and brought out through the mouth to retract the palate forward to help with the placement of the pack (not shown). E, Remove the optional “retraction” catheter after the pack is in the proper position. Digitally guide the pack into the nasopharynx. F, Use a gauze roll to secure the pack to the nose, and tape the rescue ties to the cheek.

Inspect the nasal septum for asymmetry, swelling, pain, and a fluctuant area. The mucosa of the fluctuant area will usually have a bluish or reddish hue. The bulging area of the septum, when compressed with a cotton-tipped applicator, feels boggy and may be temporarily indented by the pressure. Increased mobility that occurs with palpation with the applicator suggests septal fracture. Insert gloved small fingers into each side of the nostrils, and palpate the entire septum for swelling, fluctuance, and crepitus. The nasal cartilage receives nourishment from the surrounding perichondrium and the supporting tissues. Septal hematoma separates the cartilage from the nutrient-rich perichondrium and requires urgent drainage to prevent complications. Unrecognized

or untreated septal hematoma can lead to septal perforation, necrosis, and loss of nasal support, which results in the saddlenose deformity. Bacterial growth of Staphylococcus aureus, Streptococcus pneumoniae, and group A β-hemolytic streptococcus within stagnant blood may form an abscess, which will destroy the septum.10 Before drainage, anesthetize the bulging area by infiltrating with a local anesthetic such as lidocaine 1% or by applying a topical anesthetic such as benzocaine 20%. Aspirate the hematoma with an 18-gauge needle attached to a syringe, or make a small incision at the most inferior aspect of the hematoma. Evacuate the blood clot, and reapproximate the perichondrium to the cartilage. It may be necessary to excise a small amount of mucosa 615

PART 4  INJURIES AND MEDICAL INTERVENTIONS

A

B

FIGURE 31-14  A, The Epi-Max balloon catheter. The balloon tamponade device serves as both an anterior and a posterior pack. It is easily inserted, and is often successful for temporarily controlling posterior epistaxis in the emergency department. Such devices rarely fail for initial control of bleeding in the emergency department. B, The inflated Epi-Max. If the balloon pack is used for more than a few days, protect the nasal opening with a piece of gauze, because skin breakdown is possible. (Courtesy Shippert Medical, Centennial, Colo.)

to prevent premature closure and blood reaccumulation. Pack the nasal cavity with 0.5-inch antiseptic-impregnated gauze or petrolatum to prevent recurrent bleeding and to maintain apposition of the perichondrium to the cartilage (Figure 31-17).

Hematoma

MIDFACE: MAXILLA Fractures of the maxilla are less common than are other facial fractures. On the basis of the areas of structural weakness in the maxilla, the Le Fort classification of maxillary fractures was established.22 The Le Fort I transverse fracture is the most common type of maxillary fracture. The fracture occurs above the apices of the teeth and runs transversely through the maxilla; this involves the alveolar process, walls of the maxillary sinuses, palate, and pterygoid processes. The Le Fort II pyramidal fracture starts in the nasal bones and the frontal processes of the maxilla and then passes laterally and inferiorly through the lacrimal bones, inferior orbital rims, and orbital floors near the zygomaticomaxillary suture. It continues posteriorly along the lateral walls of the maxilla, through the pterygoid plates, and into the pterygomaxillary fossa. The Le Fort III craniofacial disjunction fracture occurs through the zygomaticofrontal and frontomaxillary nasofrontal sutures, orbital floors, cribriform plate of the nose, and ethmoid and sphenoid sinuses. The fracture forces with this type

FIGURE 31-16  Nasal septal hematoma that requires drainage.

A

Unilateral fracture of nasal pyramid

B

Dislocation of septum

C FIGURE 31-15  Nondisplaced and minimally displaced nasal fractures often do not require manipulation, but the true extent of the deformity is often difficult to appreciate initially. Note that the septum may also require subsequent intervention. The reduction of a depressed and dislocated nasal bone fracture is usually performed after 3 to 7 days, when swelling has subsided and the true deformity is obvious.

616

D

FIGURE 31-17  A, A small left-sided septal hematoma. B, After applying the appropriate topical anesthesia (which can be supplemented with local infiltration, if necessary), make a horizontal incision through the mucosa and the perichondrium that cover the hematoma. C, Use a small cup forceps or scissors to remove enough mucosa to prevent premature closure of the wound and reaccumulation of hematoma.  D, Place a sterile rubber band as a drain, and pack the naris.

Le Fort II

Le Fort III FIGURE 31-18  Classification of midface fractures. (Redrawn from the American Association of Oral and Maxillofacial Surgeons: Oral and maxillofacial surgery services in the emergency department, Rosemont, Ill, 1992, American Association of Oral and Maxillofacial Surgeons. With permission.)

are so great that there is a complete separation of the facial bones from the cranial base47 (Figure 31-18). Clinical findings in maxillary fractures vary on the basis of the mechanism of trauma. Inspect the face for asymmetry, hematomas, ecchymosis, swelling, bleeding from the nose or conjunctivae, intraoral tears, ecchymosis of the palatal mucosa, and malocclusion. Palpate for crepitus, deformities, and step-offs of the orbital rims, nasal bones, zygomatic arches, zygomas, and intraoral prominences of the maxilla. Examine the maxilla for possible fracture by grasping the anterior segment between the thumb and forefinger and gently rocking the jaw anteroposteriorly and laterally. If a bilateral Le Fort I transverse fracture is present, the entire maxilla will move. With a unilateral fracture, the two halves of the maxilla may move independently. With a Le Fort II pyramidal fracture, palpation will identify movement at the nasofrontal junction and the medial portion of the inferior orbital rims. Rock the maxilla gently while the bridge of the nose is grasped between the thumb and forefinger of the opposite hand. Any movement of the nasal complex is indicative of a pyramidal fracture. Palpate the infraorbital rim for the presence of a step deformity. A fracture that involves the infraorbital foramen may injure the infraorbital nerve and result in numbness below the eye, above the upper lip, and the lateral aspect of the nose. Manipulation of the Le Fort III craniofacial disjunction fracture results in separation and movement of the entire midface. This complex injury often accompanies intracranial trauma. There is usually subconjunctival hemorrhage, ecchymosis, and bilateral periorbital edema that causes eyelid closure. Fractures that involve dural tears and laceration of the meninges cause cerebrospinal fluid to leak from the nose (i.e., rhinorrhea). When cerebrospinal fluid rhinorrhea is suspected, the nose should not be packed, and prophylactic antibiotics (e.g., 500 mg of oral azithromycin daily) should be initiated. As a result of potential airway compromise, a posteriorly displaced Le Fort fracture should be disimpacted by using forward

LOWER FACE: MANDIBLE Signs and symptoms of mandibular fractures include trismus, edema, excess salivation, intraoral and extraoral lacerations, buccal or lingual ecchymosis, malocclusion, crepitus, mental nerve paresthesias, facial asymmetry, jaw deviation with mouth opening, and a palpable step defect along the inferior border of the mandible.6,18 Mandibular fractures are typically described on the basis of their anatomic location within the mandible47 (Figure 31-19).

Region of the coronoid process

Region of the ramus

Region of the alveolar process Region of the symphysis

Region of the body

Region of the condylar process

Region of the angle

FIGURE 31-19  Anatomic regions of the mandible. (Modified from Dingman RO, Natvig P: Surgery of facial fractures, Philadelphia, 1964, Saunders.)

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Le Fort I

traction. If the mandible is intact, hold the maxilla in place by forcing mouth props (either commercially available or improvised) between the upper and lower molars. Significant bleeding from the nasal cavities may occur with midface fractures. However, any nasal cavity tamponade will displace the mobile maxilla inferiorly unless the fracture is first stabilized from below with mouth props. Orbitozygomatic and naso-orbital-ethmoid complex fractures involve the nasal skeleton, medial orbital walls, and interorbital area. Clinical signs and symptoms include periorbital ecchymosis, proptosis, dystopia, anosmia, nasal obstruction, enopthalmos, subcutaneous emphysema, subconjunctival hemorrhage, edema, lacerations, flattened nasal bridge, cerebrospinal fluid rhinorrhea, and blindness. The medial canthal ligament attachments may become disrupted, which results in telecanthus or abnormally widely spaced eyes.22,47 Zygomaticomaxillary and zygomatic arch fractures usually result from a blow to the cheek, but they may be caused by falls. Findings include unilateral epistaxis, subconjunctival hemorrhage, and ecchymosis and swelling of the lids, conjunctivae, and sclera. Orbital floor disruption results in double vision as a result of displacement of the globe or extraocular muscle entrapment. Ocular injuries such as ruptured globe, retinal detachment, vitreous hemorrhage, lens dislocation, and hyphema may be associated with these fractures. Numbness and paresthesias in the distribution of the infraorbital nerve may be present. Cheekbone depression results in a flat-appearing face with dimpling over the arch. Trismus and pain with mandibular movement may occur. The coronoid process of the mandible is located beneath the zygomatic arch. Therefore, this fracture may result in inability to fully open the mouth.7,18,47 Complex facial bone fractures may impede the airway by allowing the tongue to fall backward or by causing soft-tissue swelling around the upper airway, thereby causing immediate or delayed airway obstruction. Fractures that involve the base of the skull may result in cerebrospinal fluid rhinorrhea or otorrhea. Hemorrhage may occur as a result of injury of the facial vasculature. Indications for immediate evacuation include midface fractures, displaced mandibular fractures, and zygomatic complex fractures. Pending evacuation, initiate antibiotic prophylaxis with 500 mg of penicillin V potassium by mouth four times a day, and medicate for pain.17 Strong narcotics are avoided if there is an associated head injury to avoid respiratory depression in an obtunded patient.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Inspect the skin, mucosa, dentition, and associated alveolar and basilar structures. If there is no obvious tooth or bony displacement, perform a bimanual examination. Place the thumbs on the occlusal edges of the teeth and the forefingers bilaterally on the inferior border of the mandible to evaluate for crepitus, instability, tenderness, and mobility. It is particularly important to evaluate any area of contusion in the soft tissue. In addition to abnormal movement, a grating sound can occasionally be heard when a fracture is present. Palpate the inferior border of the mandible for step-off defects and the mandibular condyles for limitation of mobility. Evaluate the TMJ by placing a finger in the external auditory canal.44 Normally the condyles can be palpated by placing a forefinger in front of the external auditory meatus. If the condyle cannot be palpated or if it does not move significantly when the mouth is opened, a fracture may be present. Place a tongue blade in the patient’s mouth across the posterior molars, and ask him or her to bite down and then to resist when you attempt to pull out the blade. If this is accomplished without too much pain, a fracture is unlikely to be present. A unilateral condylar fracture is suspected when there is a shift of the midline of the mandible to the fractured and painful side on mouth opening. Bilateral condylar fractures often result in anterior open bite and premature contact of the posterior teeth (Figure 31-20). Airway distress may occur with bilateral mandibular body or angle fractures. Hemotympanum and lacerations of the external auditory meatus indicate fractures of the temporal bone with condyle displacement. To evaluate occlusion, have the patient bite the teeth together. Any deviation of the bite or change in the level of the occlusal plane, especially in the mandible, should raise suspicion regarding a fracture. There will usually be a tear in the gingival tissues with bleeding and ecchymosis at the site of the discontinuity. Sublingual hematoma is a common sign of a mandibular fracture. In edentulous areas, there will also be a discrepancy in the level of the bone, and this is often accompanied by a disruption in the mucosa18 (Figure 31-21). Definitive repair of a mandibular fracture is not a surgical emergency. Delay in repair does not increase the risk of infectious complications, but persons who are treated after 3 days have a higher incidence of operative technical complications. Treatment within 24 to 36 hours after injury minimizes patient discomfort and avoids significant soft-tissue edema and fibrinous deposition within the fracture.4,22 Even if perfect alignment is not achieved, fixation makes the patient more comfortable, reduces bleeding, and avoids further displacement of fragments. Fractures that pass through the tooth-supporting portion of the mandible are quickly stabilized with a bridle wire or more securely held with an arch bar. More rigid fixation can be obtained with intermaxillary wiring, which involves placing arch bars on the upper and lower arches,

FIGURE 31-20  Condylar fracture. With a condylar fracture, the joint is positioned normally, but the muscles of mastication have pulled the posterior portion of the mandible upward to create premature contact of the posterior teeth.

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A

B FIGURE 31-21  Mandibular fracture. A, Note the malocclusion before reduction. B, Normal.

placing the teeth in proper occlusion, and then connecting the upper arch bar to the lower bar with elastics or thin wire.30 Temporarily immobilize more posteriorly located fractures with a Barton bandage; this pulls the mandible in a superior direction, obtains dental occlusion, and diminishes pain. Form the bandage by wrapping a 0.25- to 0.5-inch gauze bandage or ace wrap underneath the jaw and then alternating around the top of the head and back of the neck, with care taken to supply enough force to maintain occlusion.16 Do not pull the chin posteriorly, because this may displace the fracture and compromise the airway (Figure 31-22). Mandibular fractures are considered open and thus can be contaminated by oral flora. Thus, prophylactic antibiotics are needed. The most frequently recommended treatments are 500 mg of penicillin or 150 to 450 mg of clindamycin by mouth four times daily for 5 to 7 days.

FIGURE 31-22  Barton bandage. A simple bandage can be used to temporarily stabilize a jaw fracture.

During evaluation and treatment of facial soft-tissue injuries, it is important to remember that these wounds may have significant psychosocial and emotional impacts on the patient, with cosmesis being a priority. Treatment of these wounds in the wilderness environment must take into consideration the longterm sequelae associated with an unfavorable cosmetic result. Providers must discuss the risks and benefits associated with wilderness treatment versus evacuation and care in a more traditional setting. Soft-tissue facial injuries—including abrasions, contusions, lacerations, and avulsions—can be treated locally. Cover all such wounds with an antibiotic or antiseptic ointment such as mupirocin, bacitracin, or erythromycin, and gently wash the area four times daily with mild soap and warm water to prevent infection and crusting. Manage contusions conservatively, because they are frequently associated with tissue disruption, and this results in devitalized tissue and depressed scars. Apply cool compresses or ice, and have the patient sleep with the head of the bed elevated to diminish periorbital swelling, ecchymosis, and edema.23 Superficial lacerations are easily repaired primarily, but more complex lacerations that involve underlying muscles, nerves, and ducts must be identified at the time of injury and referred for appropriate definitive care. Complicated wounds with associated devitalized tissue may necessitate delayed primary closure or closure by secondary intention. Thoroughly clean, irrigate, and debride all soft-tissue injuries with a brush and decontaminated water to remove foreign material and to prevent tattooing and infection.42 Use a local anesthetic agent without epinephrine for adequate scrubbing. When treating wounds in the wilderness, it is important to be aware that infection rates do not differ for wounds that are cleaned with decontaminated water or sterile saline.12 Keep tissue debridement to a minimum. Significant tissue loss or avulsion typically necessitates specialty referral to achieve the best cosmetic result. Any injury that involves the eyelids, auricular helical rims, nasal alar rims, or vermilion border has potential significant cosmetic and functional implications and must be evaluated and managed with extreme caution. Treat epistaxis, dental injuries, and facial fractures before repairing facial and intraoral lacerations, because manipulation may reopen repaired wounds. Direct pressure achieves hemostasis. Do not close small wounds of the oral mucosa, because, as a result of high vascularity, these wounds heal quickly. Close larger wounds with 5-0 or 6-0 absorbable sutures. Consult an oral surgeon for definitive ductal repair if a cheek laceration involves Stensen’s duct. Close deep lacerations of the muscular soft palate in layers. Clean, simple, superficial, uncontaminated facial wounds that are less than 6 hours old may be closed with surgical glue or adhesive tape strips if they are not under tension.20 Irrigate and explore complex deeper wounds for the presence of underlying foreign bodies and fractures. Close nongaping wounds with nonabsorbable 5-0 or 6-0 interrupted sutures in a single-layer closure. Remove sutures after 3 to 5 days, at which time adhesive tape strips can be used to stabilize the wound margins. Place absorbable subcuticular buried sutures to close any potential space and to relieve tension on skin in gaping deep lacerations. Laceration repair of the lip, tongue, eyelid, nose, and ear may be more complicated. Soft-tissue lacerations may involve deeper structures, including the facial nerve or salivary glands and ducts, thus requiring referral and advanced management techniques.24

Lips Lips are mobile muscular folds that have three distinct regions: oral mucosa, skin, and a noncornified layer of stratified epithelium called the vermilion. Lip repair may be difficult if the laceration involves the vermilion border, which is the junction between the skin and the vermilion. Realigning this border and restoring the natural architecture of the philtrum is crucial to successful cosmetic repair. Close lip lacerations that include the muscular layer in multiple layers to prevent divots from forming and to

FIGURE 31-23  Lip laceration that involves the vermilion border.

maximize function. Do not use wound adhesives for lip lacerations. During repair of a through-and-through lip laceration, realign and stabilize the vermilion border, and then close the inner mucosal layer with 4-0 absorbable sutures. Next, irrigate the wound thoroughly, and close the remainder of the laceration from an extraoral approach. Close the muscular layer with 6-0 absorbable suture and the external skin with 6-0 or 7-0 nonabsorbable suture. Through-and-through lacerations of the lower lip that do not involve the vermilion border occur when the lower incisors impale tissue during facial blunt trauma. First, cleanse and close the mucosal layer from an intraoral approach. Irrigate to remove foreign material and oral bacteria, and then rescrub the extraoral wound. Close the remainder of the layers, finishing with the skin. Large soft-tissue avulsions of the lip may require a plastic surgeon to achieve the best cosmetic result5 (Figure 31-23). A mental nerve block anesthetizes the chin and the lower lip; an infraorbital nerve block anesthetizes the cheek, upper lip, lower eyelid, and lateral aspect of the nose. These blocks provide adequate anesthesia without tissue distortion and are easily performed. The mental nerve exits the mandible through the mental foramen in the midpupillary line 1 cm (0.4 inch) inferior to the apex of the second bicuspid. While retracting the lower lip with the nondominant hand, insert the needle 5 mm (2 inches) inferior to the tooth, and inject 2 cc of anesthetic. The infraorbital nerve exits the infraorbital foramen 1 cm (0.4 inch) below the infraorbital ridge. Place the third finger of the nondominant hand on the infraorbital foramen, and use the second finger and thumb to lift the upper lip. Insert the needle over the canine tooth at the level of the gingival buccal sulcus. Aspirate while advancing toward the foramen, and inject 2 cc of anesthetic (Figures 31-24 and 31-25).

Tongue Tongue lacerations may be difficult to suture. Traction must be maintained during repair. Simple, small, linear lacerations that are less than 1-cm (0.4-inch) long and located centrally usually heal well without suturing. Suture all lacerations that are deep, that gape, or that bisect the tongue. Apply local anesthesia by topically applying gauze soaked with lidocaine 4% to the tongue for 5 minutes, locally infiltrate the wound with lidocaine 1% with buffered epinephrine, or perform an inferior alveolar or lingual nerve block. The inferior alveolar and lingual nerves are terminal branches of the trigeminal nerve. Palpate the vertical ridge of the anterior border of the mandibular ramus with your thumb. Using a tongue blade, push away the buccal surface of the cheek to expose the target area. Position the syringe barrel over the opposite premolar and parallel to the occlusive surface of the lower teeth. Insert the needle into the oral mucosa medial to the ridge, 1 cm (0.4 inch) above the occlusive surface of the mandibular 619

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Soft-Tissue Injuries

PART 4  INJURIES AND MEDICAL INTERVENTIONS

third molar. Aspirate while slowly advancing the needle 2 cm (0.8 inch), and inject 2 cc of anesthetic to block the inferior alveolar nerve. The lingual nerve runs with the inferior alveolar nerve at the mandibular foramen. It supplies the anterior twothirds of the tongue, floor of the mouth, and gums. Block the lingual nerve by withdrawing the needle 1 cm (0.4 inch) while aspirating, and then injecting another 1 cc of anesthetic. Use absorbable 4-0 or 5-0 suture to close tongue lacerations.5 Prescribe a liquid or soft diet after any intraoral repair. Advise the patient to gently swish and spit four times a day and after eating with warm saline, antiseptic mouthwash, chlorhexidine gluconate 0.12%, or half-strength hydrogen peroxide (Figure 31-26).

Eyelid A

B FIGURE 31-24  Mental nerve block. A and B, Infiltrate the anesthetic at the mental foramen opening. To prevent neurovascular damage, do not introduce the needle into the foramen.

It is essential that providers recognize eyelid lacerations that require referral to an ophthalmologist. Simple upper and lower lid lacerations may be managed without consultation, but complex lacerations that involve tissue avulsion, the tarsal plate, lid margins, orbital septum, levator palpebrae superioris, or lacrimal drainage system may require semiurgent ophthalmologic referral for definitive care. Presence of a penetrating globe injury must be appreciated.24 Upper eyelid lacerations with exposure of orbital fat and ptosis in the presence of a horizontal lid laceration suggest levator palpebrae superioris muscle damage.9 Lacerations that involve the lateral aspect of the upper lid may involve the lacrimal gland, which may be mistaken for orbital fat and inadvertently excised. Evaluate for laceration of the canalicular drainage system by instilling fluorescein into the eye and then assessing for its presence within the wound.5 Any laceration that involves the medial portions of the upper and lower eyelid or that is located medial to the puncta should be assumed to involve the canalicular system and requires evacuation and ophthalmology referral. If it is unrecognized or untreated, laceration or obstruction of the lacrimal ducts will cause tears to overflow.42 Stenting the canalicular system is required to prevent obstruction. Apply iced saline gauze to the medial corner of the lid to decrease edema pending evacuation. Superficial lacerations that comprise less than 25% of the lid are candidates for healing by secondary intention and may be treated conservatively without suture repair. Clean and irrigate the wounds with clean, disinfected water, and instill topical antibiotic drops (e.g., ciprofloxacin, ofloxacin, tobramycin) into the wound.5 Apply tape strips to approximate the wound edges if the laceration cannot be properly sutured. Alternatively, leave the wound open, and then repair it 1 to 2 days later. Lid margin lacerations require a three-layer closure. Close the conjunctival

Area of anesthesia

A

B

C

FIGURE 31-25  Infraorbital nerve block. A, The unilateral infraorbital nerve block anesthetizes the lower eyelid and upper lip. B, The nerve is located directly under the pupil when the patient is looking forward. C, Avoid the orbit by keeping the needle tip under the orbital rim. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

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Inferior alveolar nerve

B Inferior alveolar artery

CHAPTER 31  Management of Facial Injuries

A

Finger on pterygomandibular triangle Coranoid notch

Mandible

Inferior alveolar nerve Needle enters 1 cm above tooth surface

Lingual nerve

Second premolar First premolar

C

D

FIGURE 31-26  Inferior alveolar and lingual nerve blocks. A, Pterygomandibular triangle. B, Identify the anterior border of the ramus of the mandible with the left index finger or thumb. C, Grasp the ramus with the intraorally placed thumb and an extraorally placed index finger to allow visualization of the pterygomandibular triangle. D, The syringe is angled, with the barrel of the syringe overlying the first and second premolar teeth on the opposite side of the mandible. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

side and the tarsal plate with 6-0 or 7-0 absorbable sutures, and close the external surface with a nonabsorbable monofilament suture. Repair other simple superficial lacerations that do not involve the lid margin with either 6-0 or 7-0 absorbable or nonabsorbable sutures (Figure 31-27).

Nose Repairing simple superficial nasal lacerations with interrupted 5-0 or 6-0 nonabsorbable sutures or tissue adhesive is not difficult, but complex nasal lacerations that involve the nasal mucous membrane and cartilaginous framework are technically more difficult. Lacerations that involve the nostril margin or the alar rim require precise alignment for a satisfactory cosmetic result and to prevent notching (Figure 31-28). Close full-thickness lacerations that involve the cartilage with a three-layered closure by beginning with placement of absorbable intranasal sutures. Contraction and retraction of the nasal margin will occur if the inner nasal mucosa is not appropriately aligned. Reapproximate cartilage with 4-0 or 5-0 absorbable sutures, and then close the skin. Anesthetize the infraorbital nerve or the supraorbital nerve with lidocaine 1%.5 The supraorbital nerve exits the skull at the supraorbital foramen, and then branches cephalad into medial and lateral branches to supply the forehead and anterior scalp. The supratrochlear nerve supplies the mid forehead, and it lies under the medial 1 cm (0.4 inch) of the eyebrow. It exits the skull 0.5 to 1.0 cm (0.2 to 0.4 inch) medial to the supraorbital foramen. The infratrochlear nerve exits the orbit superior to the medial canthus and travels inferiorly to supply the medial eyelid, lateral

FIGURE 31-27  Eyelid laceration that involves the tarsal plate and the lacrimal apparatus. (Courtesy Dr. Chang Hee Kim.)

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

FIGURE 31-28  Nasal laceration that involves the alar cartilage. (Courtesy Dr. Ross Stutman.)

nose superior to the medial canthus, medial conjunctiva, and lacrimal apparatus. Use the nondominant hand to locate the supraorbital notch, insert the needle into the lateral edge of the middle one-third of the eyebrow, and advance it while aspirating toward the medial canthus. At this point, inject 2 cc of anesthesia (Figure 31-29).

Ear The ears lie laterally along the sides of the face, with the auditory canal exiting through the mastoid process of the temporal bone. The external skeleton of the auricle or pinna is the external expansion of the elastic cartilaginous canal, which is covered by a firmly attached perichondrium and closely apposed skin that is rolled into a prominent outer rim with a helical shape (helix) and with an inner parallel second ridge (antihelix) that defines the inner concha. There is a potential space between the avascular cartilage and the perichondrium that may allow blood accumulation. The earlobe contains subcutaneous fat and lacks cartilage. The external auditory canal, middle ear, cochlea, semicircular canals, and superior origin of the eustachian tube all lie within the temporal bone. External injury of the ear may be associated with hearing loss, facial nerve palsy, tympanic membrane rupture, and temporal bone fracture. Evaluate ear trauma with an otoscope to observe the integrity of the external canal and to assess for hemotympanum and otorrhea, which suggests an underlying brain injury that requires evacuation. Trauma to the external cartilaginous ear may result in lacerations, tissue avulsion, and formation of hematoma within the ear itself. Shearing forces of moderate intensity—which occur frequently during fights, wrestling, and mixed martial arts— may cause blood extravasation and hematoma formation in the

FIGURE 31-29  Supraorbital, supratrochlear, and infratrochlear nerve blocks. This is the site for local injection of the supratrochlear and infratrochlear nerves as well as for the lateral and medial branches of the supraorbital nerve. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

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subperichondrial potential space, thereby separating the perichondrium from the cartilage. If the hematoma is not treated acutely, neocartilage formation develops at the site of the clot, subsequently deforming the ear and leading to a “cauliflower ear.”30 Local anesthesia of the ear may be required to close lacerations, drain auricular hematomas, and for other painful procedures. The ear is richly innervated by the greater auricular nerve, the lesser auricular nerve, the auricular branch of the vagus nerve, and the auriculotemporal nerve. Partial or complete anesthesia of the ear can be accomplished with the use of a variety of field blocks. Inject approximately 2 to 4 mL of lidocaine 1% without epinephrine or bupivacaine 0.25% with a 25- to 27-gauge needle subcutaneously into the skin around the ear (Figure 31-30). Simple superficial skin wounds of the ear are closed in a single layer of 6-0 or 7-0 nonabsorbable suture. Repairing complex ear lacerations requires adequate coverage of exposed cartilage to prevent infection, chondritis, and cartilage necrosis. Repair lacerations of the auricular helical rim with a three-layer process that involves the precisely realigning the auricular cartilage to prevent notching (Figure 31-31). During the initial wound care of through-and-through lacerations, cleanse and irrigate the ear without dissecting the cartilage from the perichondrium. Trim devitalized tissue while making every effort to keep debridement at a minimum to prevent a poor cosmetic result. Reapproximate cartilage with 5-0 or 6-0 absorbable sutures placed through the anterior and posterior perichondrium as well as through the cartilage. This provides stability and strength, prevents tearing, and ensures a nutrient supply to the avascular cartilage. Suture the anterior and posterior skin with 6-0 or 7-0 nonabsorbable interrupted sutures. Treating auricular hematoma involves complete evacuation of the subperichondrial hematoma, elimination of dead space, and reapproximation of the perichondrium to the underlying cartilage. This allows the ear to heal with the best cosmetic result. Prevent reaccumulation of the hematoma by applying a compressive dressing, and reexamine this frequently, with reaspiration as necessary. If the provider does not have the tools necessary to drain or aspirate the hematoma within 7 to 10 days, then patient evacuation is necessary, because the new perichondrial growth must be debrided to prevent disfigurement and deformity of the ear caused by cartilaginous necrosis, chondritis, or fibrosis35 (Figure 31-32). Draining an auricular hematoma may be performed either by aspiration or by incision and drainage. Aspirate by perforating the hematoma with a 20-gauge needle, and compress the hematoma between the thumb and the forefinger until all of the blood is evacuated (Figure 31-33). If the hematoma is less than 7 to 10 days old and if aspiration is unsuccessful, then incision and drainage may be required. Anesthetize the pinna by locally infiltrating lidocaine 1% or 2% without epinephrine, or perform an auricular block. With a no. 15 blade, incise the hematoma, and follow along a natural anatomic crease or curvature of the pinna. The incision length should be long enough that simple compression is sufficient to adequately evacuate the hematoma. Gently peel the skin and perichondrium off of the hematoma and the underlying cartilage. Completely evacuate the hematoma, and irrigate the remaining pocket with normal saline (Figure 31-34). After removing the hematoma by aspiration or incision, apply topical antibiotic or antiseptic ointment, and reapproximate the perichondrium to the cartilage. Reexamine the ear frequently for reaccumulation of the hematoma. Cover the wound with a nonadhesive dressing, and place petrolatum-coated cotton within all fissures and folds of the ear until the dressing is level with the helix. Place dry cotton gauze behind the ear, and fit it to the shape of the pinna to provide padding and to prevent the ear from being compressed against the skull. Place dry cotton gauze anterior to the ear, and secure it with a circumferential compressive head bandage that does not include the other ear. Compressive ear dressings prevent hematoma formation and deformity. Evacuate for consultation and definitive repair if there is significant tissue and cartilage loss that precludes a cosmetic closure30,42 (Figure 31-35). After draining the hematoma and reapproximating the auricular layers, blood and fluid can reaccumulate. A number of

CHAPTER 31  Management of Facial Injuries

A

C

B

D

FIGURE 31-30  Field blocks of the auricle. A, One method makes use of approximately 3 to 4 mL of anesthetic, both in the posterior sulcus and at a point just anterior to the tragus. B, An alternative field block technique that involves depositing 2 to 3 mL of anesthetic with each needle pass. C and D, The locations of anesthetic injections. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders)

FIGURE 31-31  Ear laceration that involves the auricular cartilage. (Courtesy Dr. Ross Stutman.)

FIGURE 31-32  Auricular hematoma that requires drainage. (Courtesy Dr. Alicia Pilarsky.)

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Perichondrium

Cartilage

B

A

FIGURE 31-33  Auricular hematoma aspiration. A, Subperichondrial hematoma within the concha of the ear. B, Needle aspiration of an auricular hematoma. A topical antiseptic is used to clean the ear, but local anesthesia is seldom required. While stabilizing the pinna with the thumb and fingers, puncture the most fluctuant part of the hematoma with a 20-gauge needle. Use the thumb to “milk” the hematoma into the syringe until the entire hematoma has been evacuated. Be very careful to not puncture your thumb with the needle. The thumb maintains continuous pressure on the ear for 3 minutes after the needle has been withdrawn. A pressure dressing is then applied, and the ear is checked for reaccumulation of blood in 24 hours. Reaspiration may be required, and persistent accumulations require incision and drainage. (B redrawn with permission from Ruddy RM: Aspiration of an auricular hematoma. In Fleisher GR, Ludwig S, Henretig FM, et al, editors: Textbook of pediatric emergency medicine, ed 5, Philadelphia, 2006, Lippincott Williams & Wilkins, p 1889.)

methods are available to eliminate the dead space and to prevent hematoma recurrence. Data suggest that one technique that involves incision and drainage of the hematoma followed by the placement of absorbable mattress sutures resulted in fewer reaccumulations and complications and eliminated the need for bulky bolstering. To perform this technique, after incision, drainage, and irrigation of the hematoma, manipulate the ear into the Perichondrium Cartilage Incise Hematoma

A

B

Cheek

Skin

Incision site Posterior auricular

C

Anterior auricular

D

FIGURE 31-34  Auricular hematoma incision. A, Hematoma separates the perichondrium from the cartilage. B, Incision (arrows) made along the skin curvature at the posterior edge of the hematoma. The hematoma is evacuated, and the area is irrigated. C, Two anterior dental rolls are secured with sutures to a posterior dental roll to maintain normal anatomy of the pinna. D, A side view illustrates the position of sutures and dental rolls in relation to the incision site. Note that the perichondrium is in apposition with the cartilage. (From Clemons JE, Seveneid LR: Otohematoma. In Cummings CW, editor: Otolaryngology: Head and neck surgery, ed 2, St Louis, 1993, Mosby, p 2866.)

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preinjury appearance. Weave absorbable 4-0 Vicryl or chromic suture from posterior to anterior through the skin and cartilage as many times as is necessary to achieve the appropriate appearance of the ear contour while apposing the skin to the cartilage. Place topical antibiotic or antiseptic ointment on both sides of the ear, and apply a loose head dressing (rather than a compressive dressing) for the next 24 to 48 hours.15 If medical-grade soft silicone putty is available, the lateral part of the external auditory meatus and contours of the lateral surface of the pinna are filled with the putty, which hardens after a few minutes. From the anterior aspect of the pinna, fold the malleable silicone backward to cover the medial surface and mold to the pinna before placing a head bandage.11 A technically more complicated alternative technique is to suture dental rolls over the area. To accomplish this, pass a 4-0 nylon suture through the entire thickness of the ear over the hematoma. Wrap the suture around a dental roll on the posterior aspect of the ear, and then pass the needle back through the pinna. Wrap and tie the suture around a second dental roll on the anterior aspect of the pinna. A second suture may be placed to secure a third dental roll. The dressing should firmly reapproximate the perichondrium to the cartilage without vascular compromise.40

Contusions and lacerations of the cheek or parotid region may involve other structures, including the external auditory meatus, TMJ, underlying zygomatic or maxilla bones, parotid gland, Stensen’s duct, branches of the facial nerve, and transverse facial artery. Failure to recognize these injuries may lead to significant morbidity. Injuries to these structures require repair that occurs concurrently with laceration repair. The parotid gland sits anterior to the masseter muscle. The parotid duct arises from the anterior aspect of the gland and runs superficially over the masseter muscle. The duct pierces the buccinator muscle and oral mucosa at the level of the second maxillary molar. A line that connects the mid portion of the upper lip with the tragus delineates the path of the parotid duct over the cheek. The duct runs in proximity to the transverse facial artery and the buccal branch of the facial nerve. Suspect damage to the parotid duct if there is saliva leakage from the wound when Stensen’s duct is irrigated with saline. A sialocele, cutaneous fistula, or salivary duct cyst may occur as a result of salivary fluid retention if a parotid duct injury is not initially recognized45 (Figure 31-36). Injuries to branches of the facial nerve (cranial nerve VII) frequently occur in association with a parotid duct injury. Delay the injection of local anesthetic until facial nerve function has been evaluated. Evaluate facial nerve damage by observing the

A

CHAPTER 31  Management of Facial Injuries

3 layers of gauze

Cotton soaked in mineral oil or saline-soaked packing gauze covering a small dry cotton pledget that has been placed in the ear canal.

B

Fluffed gauze

C

Elastic or gauze roll

D

FIGURE 31-35  Compression dressing of the ear. After the successful aspiration of an auricular hematoma, use a compression dressing to prevent reaccumulation of the hematoma or fluid. A, First, place dry cotton into the ear canal, and then carefully mold a conforming material into all of the convolutions of the auricle. One may use petroleum-jelly–impregnated gauze, saline-soaked 0.25-inch packing gauze, or cotton soaked in mineral oil or saline. Inset, Note the gauze pack behind the pinna and the use of saline-soaked packing gauze to conform to the auricle. B, When the convolutions are fully packed, place a posterior gauze pack behind the ear. A V-shaped section has been cut from the gauze to allow it to fit easily behind the ear. C, Place multiple layers of fluffed gauze over the packed ear, and hold the entire dressing in place with Kling Gauze or an elastic gauze roll. Do not wrap this too tight. D, The ear is thus compressed between two layers of gauze, and the packing ensures even distribution of pressure to all parts of the auricle. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

patient moving his or her eyebrows, eyelids, and mouth. Evacuate any patient for immediate repair of any facial nerve injury behind a vertical line through the lateral canthus of the eye, because nerve transection requires early repair to maximize the chance for functional neural regeneration. The face has an excellent vascular supply, which allows for wound closure with a minimal fear of infection if treatment can be accomplished within 6 hours of the injury. Topical antibiotics are useful, but do not initiate prophylactic oral antibiotics, because these wounds rarely become infected. More complicated wounds—including those that involve the cartilage of the ear or nose, through-and-through lip or buccal mucosa lacerations, bites, and wounds with any evidence of maceration, contamination, or devascularization—require prophylactic oral antibiotic treatment on the basis of the normal bacterial flora that are associated with the affected site, with consideration given to the mechanism of trauma. Inspect all facial wounds frequently for evidence of vascular compromise, infection, or both. Significant infections require bandage removal, possible surgical drainage, and intravenous antibiotics.

Foreign Bodies In contrast with children, adults insert foreign bodies into the nose and ear deliberately to control nosebleeds or to clean and relieve irritation in the nose and ear.3 Insects may find their way

into the nose and ear and prove to be quite distressing to the patient, although this is not associated with trauma. The patient can usually blow out insects from within the nostril by occluding the unaffected nostril and blowing, and this rarely requires provider instrumentation. Insects within the ear may be problematic, because the inner ear canal is extremely sensitive. The patient is usually aware that something is in the ear. If the insect is alive, the patient may be extremely agitated and feel movement of the insect or hear buzzing. This may be associated with pain, fullness, impaired hearing, itching, canal edema, and drainage. The insect may damage the canal and cause bleeding, tympanic membrane perforation, and infection. Tympanic perforation may cause tinnitus, vertigo, and hearing loss. Before examining the ear, it is important to ascertain if any attempts have been made to remove the foreign body by the patient, because this may have caused further problems, including ear canal injury, tympanic membrane perforation, or worsening foreign body impaction. Ear canal irrigation may cause enlargement of some foreign bodies. Within the external auditory ear canal, there are two areas of anatomic narrowing where foreign objects usually become stuck. These include the point of bony narrowing called the isthmus at the junction between the bone and the cartilage and the area near the inner end of the cartilaginous portion of the canal lateral to the tympanic membrane.37 Examine the ear with adequate lighting, an otoscope, and a large-size speculum to visualize the 625

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Speculum

1 C 2

Lacrimal apparatus

B

3

5

A

4

Syringe

FIGURE 31-36  Structures that may be injured by facial lacerations. A, The lacrimal drainage system. B, The parotid duct. C, A line drawn through the lateral canthus of the eye. Facial nerve injuries posterior to this line should be repaired as soon as possible. 1 through 5, Branches of cranial nerve VII. (Redrawn from the American Association of Oral and Maxillofacial Surgeons: Oral and maxillofacial surgery services in the emergency department, Rosemont, Ill, 1992, American Association of Oral and Maxillofacial Surgeons. With permission.)

ear canal and allow injection of a local anesthetic. Grasp the superior pinna and retract it in a posterior-superior direction to straighten the tortuous canal and to achieve a more complete view of the external auditory canal. Kill or immobilize an insect within the ear canal to decrease patient distress and to facilitate removal. Immobilizing agents include lidocaine 2% gel, lidocaine 10% spray or liquid, mineral oil combined with lidocaine 2% or 4%, and alcohol. If attempts are made to remove a moving insect, the insect or the device may cause ear damage. With appropriate tools, foreign body removal may be attempted in the wilderness. Instill a topical anesthetic such as lidocaine 1% to 2% within the canal to minimize patient discomfort and to reduce the risks of iatrogenic trauma. Unfortunately, topical anesthetics are poorly absorbed through the impermeable keratinized epithelial surface of the external auditory canal. Auralgan, which is a combination of benzocaine and other ingredients, does not provide adequate anesthesia for painful procedures. Local anesthetic injection within the canal is painful and difficult to perform, and it frequently does not provide adequate anesthesia of the inner ear and the tympanic membrane. A common technique that is used to provide local anesthesia of the canal requires the insertion of a large speculum immediately inside the auditory meatus to facilitate use of a 25- to 27-gauge needle that is 3 to 5 cm (1.2 to 2 inches) in length to inject 0.25 to 0.5 mL of lidocaine 1% or a 1:10 mixture of sodium bicarbonate 8.4% with lidocaine into the subcutaneous tissue, stopping after a small bulge in the skin is raised. Inject all four quadrants as well as deeper tissues along the anterior wall and at the posterior wall of the bone–cartilage junction (Figure 31-37). Another technique involves injecting approximately 0.5 to 1.0 mL of lidocaine 1% externally into each of five points around the auditory meatus and the tragus (Figure 31-38). Various instruments can be used to successfully remove a foreign body from the ear canal. Instrument choice depends on the tools that are available. Alligator forceps, bayonet forceps, and right-angle probes are frequently used. Foreign-body removal is often successful by using indirect irrigation of the canal. If tympanic membrane perforation is 626

FIGURE 31-37  Four-quadrant field block anesthesia of the external auditory canal. Local anesthetic is injected subcutaneously into the four quadrants of the lateral portion of the ear canal. The largest speculum that will fit is used to guide the injections. The speculum is withdrawn slightly and tilted toward each of the four quadrants, and the needle is then inserted subcutaneously (x). Inject a very small amount of anesthetic (i.e., 0.25 to 0.50 mL) to produce a slight bulge in the soft tissue. A total of 1.5 to 2.0 mL of anesthetic is usually sufficient to anesthetize the ear canal and to allow for painless removal of a foreign body. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

suspected, this technique is contraindicated. Using of a 20-mL syringe and a 14- or 16-gauge catheter, direct a stream of roomtemperature water or saline around the (nonvegetable) foreign body. Irrigation that is directed past the object will collide with the tympanic membrane and bounce against the posterior aspect of the foreign body, thereby driving it out of the canal. This technique has a low complication rate and is well tolerated.3 Cyanoacrylate-adhesive–tipped swabs have been used to remove foreign objects from the ear. Complications associated with this method include contaminating the ear canal with glue that is difficult to remove and the accidental perforation of the tympanic membrane.

FIGURE 31-38  External auditory canal anesthesia: diagram of injection sites for an alternative technique to anesthetize the ear canal and the central concha. Each site should be injected with approximately 0.5 mL of lidocaine 1%. Do not perform these injections if external signs of infection are present. (From Roberts JR, Hedges JR: Clinical procedures in emergency medicine, ed 5, St Louis, 2009, Saunders.)

Temporomandibular Joint Relocation Supplies Bite blocks Plastic finger splints Mandible Dislocation and Fracture Supplies Barton bandage 0.25- to 0.5-inch bandaging gauze Nasal Fracture and Epistaxis Supplies Nasal speculum and light source Nasal clips and tongue depressors Cotton pledgets and cotton-tipped applicators Silver nitrate sticks Topical anesthetics: Tetracaine 1% Cocaine 1% to 4% Lidocaine 5% Ephedrine 5% Aqueous epinephrine 1 : 1000 Benzocaine 20% Vasoconstrictive nasal sprays: Phenylephrine 0.5% (Neo-Synephrine) Oxymetazoline 0.05% (Afrin) Commercial nasal tampons or sponges Nasal balloon devices Petroleum-jelly–impregnated gauze Absorbable degradable nasal packing materials Foley catheters Wound Evaluation and Repair Fine nonabsorbable nylon 6-0 and 7-0 sutures Fine absorbable chromic 6-0 and 7-0 sutures Surgical glue Adhesive strips No. 15 scalpel blade 18-gauge needles Ophthalmoscope Fluorescein paper and blue light Traumatic Ear Injury Evaluation Otoscope Alligator forceps, bayonet forceps, and right-angle probes Viscous lidocaine Medical-grade soft silicone putty Cotton pledgets Prophylactic Antibiotics Oral antibiotics: Keflex Augmentin Dicloxacillin Clindamycin Bactrim Penicillin Amoxicillin Topical steroids containing antibiotic suspension drops: Hydrocortisone with ciprofloxacin Topical antibiotic drops: Ciprofloxacin Ofloxacin Tobramycin

After successfully removing an insect, inspect the external auditory canal for trauma and retained material. Evaluate the tympanic membrane for perforation caused by the insect itself or by removal attempts. Confirm that there is not any tympanic membrane perforation. If the irrigation method was implemented, instill several drops of isopropanol within the canal to facilitate moisture evaporation. Initiate a prophylactic oral antibiotic (e.g., 500 mg of cephalexin by mouth twice daily) if the tympanic membrane was ruptured or perforated, because the middle ear is at risk for infection. Administer topical steroid–containing antibiotic suspension drops (e.g., hydrocortisone with ciprofloxacin) to alleviate pain and to potentially decrease the risk of developing otitis externa as a result of the foreign body and removal efforts.

Facial Trauma: Wilderness Medical Kit (Box 31-1) TMJ relocation supplies include bite blocks and plastic finger splints. A Barton bandage and 0.25- to 0.5-inch bandaging gauze stabilize the dislocated or fractured mandible. Nasal fracture and epistaxis evaluation and treatment require a nasal speculum and a light source. Nasal clips and tongue depressors are used to pinch the nose and to diminish bleeding. Cotton pledgets and cotton-tipped applicators are used to apply topical anesthetics, which include tetracaine 1%, cocaine 1% to 4%, lidocaine 5%, ephedrine 5%, aqueous epinephrine 1:1000, and benzocaine 20%. Vasoconstrictive nasal sprays include phenylephrine 0.5%, (Neo-Synephrine) and oxymetazoline 0.05% (Afrin). Silver nitrate sticks can be used for precise cauterization. Commercial nasal tampons or sponges, nasal balloon devices, petroleum-jelly–impregnated gauze, absorbable degradable nasal packing materials, and Foley catheters can be used to tamponade bleeding. Facial laceration repair and wound care require fine nonabsorbable nylon 6-0 and 7-0 and fine absorbable chromic 6-0 and 7-0 suture, surgical glue, and adhesive strips. A No. 15 scalpel blade or an 18-gauge needle may be used to evacuate a hematoma. Lacrimal duct injury and eye injury evaluation require an ophthalmoscope, fluorescein paper, and a blue light. Traumatic ear injury evaluation requires an otoscope. Foreignbody extraction tools include alligator forceps, bayonet forceps and right-angle probes. Viscous lidocaine provides local anesthesia. Medical-grade soft silicone putty and cotton pledgets may be used to prevent hematoma reaccumulation. Prophylactic oral antibiotics that are used for patients with facial trauma include cephalexin, amoxicillin clavulanate, dicloxacillin, clindamycin, trimethoprine-sulfamethoxazole, penicillin, and amoxicillin. Topical-steroid–containing antibiotic suspension drops (e.g., hydrocortisone with ciprofloxacin) and topical antibiotic drops (e.g., ciprofloxacin, ofloxacin, tobramycin) are currently used.

Prevention Prevent significant head and facial trauma by wearing a helmet for recreational activities such as technical rock climbing, rock scrambling, mountaineering, caving, skiing, snowboarding, biking, whitewater kayaking and rafting, and horseback riding. Wear safety goggles and custom-fitted mouth protective devices when training for and participating in contact sports or any activity that may injure the eyes, mouth, and face. Wear properly fitted protective equipment such as helmets, face masks, padded chin straps, and mouth guards for all sporting activities to prevent orofacial trauma.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 31  Management of Facial Injuries

BOX 31-1  Facial Trauma Wilderness Medical Kits

CHAPTER 32 

Wilderness Cardiology AARON L. BAGGISH AND BENJAMIN D. LEVINE

The wilderness environment places great demands on the cardiovascular system. Certain wilderness activities, such as diving and high-altitude mountaineering, pose specific challenges to the cardiovascular system by imposing additional environmental stressors, such as water immersion and hypoxia, respectively, on top of the physical demands of the specific activity. In addition, many wilderness endeavors involve prolonged exposure to high or low ambient temperatures, posing challenges to thermoregulation. As the popularity of wilderness adventure continues to grow, the number of people with established cardiovascular disease who partake in wilderness adventure activities will also increase. Probably the most important consideration related to wilderness activities for persons with known cardiovascular disease is remoteness of the environment, making modern medical technology and “usual” advanced care partly or completely inaccessible. Any person with cardiovascular disease who wishes to participate in wilderness activities needs to accept the risk that a cardiovascular event occurring in a remote environment may have a more adverse outcome compared with a similar event that transpires in the city. This chapter reviews basic cardiovascular physiologic adaptations to the wilderness environment. Although basic cardiovascular responses to exercise are central to all wilderness activities, a detailed discussion of exercise physiology is beyond the scope of this chapter; the reader is referred elsewhere, including Chapter 98, for this information.30 In addition, we review cardiovascular conditions of relevance to wilderness travelers and physicians, with emphasis on basic management of common cardiovascular emergencies in the wilderness setting.

Cardiovascular System Responses to Specific Wilderness Environments HYPERBARIA (UNDERWATER DIVING) Diving places a unique combination of physical stressors on the cardiovascular system. The physiologic stress of diving arises from the combination of immersion underwater and sustained moderate-intensity exercise. Immersion significantly reduces the effect of gravity on the diver’s body and therefore on the lower extremity venous blood pool when the diver is upright.19 This results in central redistribution of blood, with increases in intrathoracic blood volume and right atrial and ventricular filling pressures.20 The direction and magnitude of the fluid shift induced by water immersion depend on the position of the diver in the water. If the diver is upright, then the extensively researched physiology of upright water immersion applies. However, if the diver is horizontal or head down, entirely different hydrostatic gradients are induced, and these may be dynamic as the diver changes position in the water. For upright divers, as dictated by the Frank-Starling phenomenon, the increase in cardiac preload leads to immediate increases in stroke volume, cardiac output, and myocardial work. Patients with cardiomyopathy with or without prior congestive heart failure may be especially sensitive to cardiac volume overload and may become acutely symptomatic with these sudden shifts in volume status. Physical exertion is also an important contributor to the overall cardiovascular stress of underwater exercise. Divers typically use large muscle groups at low intensity to propel themselves through the water, although this depends on the experience 628

of the diver and the nature of the dive. This action may be continuous for the entire duration of the dive. The cardiovascular system facilitates this activity by increasing heart rate, stroke volume, and cardiac output. This translates into mildly increased myocardial oxygen demand and may cause myocardial ischemia in patients with underlying coronary artery disease (CAD) who are not well compensated. Fear, excitement, and emotional stressors may compound the physical stresses of diving, especially for inexperienced divers. It should be noted that the underwater environment is particularly remote. In particular, if underwater decompression stops are indicated, emergency ascent and access to medications (such as nitroglycerin) or medical care can be quite complicated. As with many other wilderness activities, it is not only the stress of the activity that is problematic, but also the risk for a cardiovascular event occurring in a remote setting. The diving reflex is a unique autonomic reflex response to water immersion that has direct relevance to the safety of this popular sport. It was first described in 1870 by the French physiologist Paul Bert, when he observed that heart rate slowed dramatically during forced water submersion. The full diving reflex response involves transient slowing of the heart rate (typically by 20 to 30 beats/min) with subsequent reduction in cardiac output and peripheral vasoconstriction to maintain systemic blood pressure.6 The reflex is mediated by increased vagal nerve activity. Heart rates lower than 10 beats/min have been measured in accomplished breath-hold divers.18 Although typically well tolerated, such intense bradycardia may result in supraventricular and ventricular escape arrhythmias in susceptible individuals.40 Individuals with underlying heart disease may tolerate diving poorly, as evidenced by data that document a significant percentage of diving fatalities attributable to cardiac causes. Depending on the age of the population, sudden cardiac death (SCD) and myocardial infarction account for 12% to 27% of diving fatalities.15 It is important to emphasize that this statistic does not mean that diving “caused” the fatality but rather that acute coronary events occur in middle-age divers who may not have access to usual emergency care if an event occurs during diving. Adequate screening for underlying cardiovascular disease is essential at a reasonable interval before any diving excursion, especially in patients with known disease. Individuals with significant cardiovascular disease, including incompletely revascularized CAD and cardiomyopathy/congestive heart failure, are typically at high risk for complications during diving and should be given restrictive recommendations. In addition, patients who have undergone coronary artery bypass grafting and have had chest tubes placed occasionally have scarring and air trapping that could place such individuals at risk for pneumothorax during compressed-air diving. At the very least, a chest radiograph should document no evidence for scarring before allowing such patients to dive; occasionally other tests for air trapping, such as chest computed tomography, could be indicated. Recommendations used to advise patients with cardiac disease who want to participate in competitive sports may be useful for diving and other wilderness activities as well.36 If patients have normal left ventricular function, are well revascularized, and have no provocable ischemia or arrhythmias, consideration could be given to individual patients to be allowed to dive. It must be emphasized that divers, should they become incapacitated during a dive, put not only themselves at risk, but also their diving partners. Therefore some recommendations may be more restrictive than just for individual assumption of risk.

Heart rate

Stroke volume

Muscle flow

Cardiac output

Blood pressure

Peripheral resistance

CHAPTER 32  Wilderness Cardiology

Sea level

Acute hypoxia

Chronic hypoxia

Sea level

Acute hypoxia

Chronic hypoxia

FIGURE 32-1  Changes in cardiovascular parameters during acute and sustained exposure to hypoxia. (Modified from Baggish AL, Levine BD: The cardiovascular system at high altitude. In Horbein TF, Schoene RB: High altitude: An exploration of human adaptation, New York, [in press], Marcel Dekker, Inc.)

HYPOXIA (HIGH-ALTITUDE ACTIVITY) The cardiovascular system’s response to hypoxia is a dynamic process that begins immediately on exposure and evolves over days, weeks, and years of prolonged exposure. Although the temporal nature of this response has inherent interindividual variability, it is useful to consider the response in two distinct phases: acute hypoxia and sustained hypoxia. Important changes in cardiovascular function during acute and sustained hypoxia are summarized in Figure 32-1. Acute hypoxia decreases alveolar and arterial oxygen content, leading to sympathetic nervous system activation.26,37 This activation is the key element of the acute hypoxic response of the cardiovascular system. Increased sympathetic activity (with or without vagal withdrawal) leads to increased heart rate and thus increased cardiac output. However, peripheral vasoconstriction, the expected vascular response to increased sympathetic tone, appears to be blunted by the release of local vasodilatory substances, constituting a phenomenon equivalent to the “functional sympatholysis” that occurs during sustained endurance exercise.23 Cardiac output increases while systemic vascular resistance and blood pressure decrease transiently. Acute hypoxia also causes dilation of the coronary arteries, although in patients with CAD who may have endothelial dysfunction, appropriate coronary dilation may not occur and may even be associated with paradoxical vasoconstriction.5 As hypoxia becomes sustained, arterial oxygen concentration (CaO2) increases secondary to hemoconcentration, ventilatory

acclimatization, and increases in red cell mass. These changes lead to some abatement of the hyperdynamic state of the circulatory system. Ventricular contractile function remains normal, but reductions in plasma volume and ventricular filling lead to decreased stoke volume as predicted by the Frank-Starling mechanism.24 Persistent sympathetic hyperactivity leads to downregulation of cardiac β-receptors45 and increased vagal activity,10 which combine to promote a reduction in resting heart rate. However, resting heart rate remains elevated during sustained hypoxia when compared with sea-level conditions. These heart rate and stroke volume reductions lead to an overall fall in cardiac output, especially at maximal exercise. In the systemic circulation, blood pressure gradually rises as the peripheral mechanisms responsible for local vasodilation diminish. For patients with hypertension, this sympathetic activation may result in substantial increases in blood pressure during high-altitude excursions. High-altitude activities, such as hiking, trekking, and mountaineering, also generally include sustained, low-intensity exercise for prolonged periods of time. The combination of reduced arterial oxygen content and perhaps paradoxical vasoconstriction during exercise (increased myocardial oxygen demand) results in provocation of myocardial ischemia with acute altitude exposure at work rates somewhat less than that provoked at sea level.32 However, with at least 5 days of acclimatization, responses near those noted at sea level can be restored. Mountain walking, even at the relatively moderate altitudes seen in the Alps, is associated with a slightly increased risk for SCD,11 although this 629

PART 4  INJURIES AND MEDICAL INTERVENTIONS

risk seems greatest in persons who are least fit. Overall, there is one SCD per 780,000 hiking hours and one SCD per 1,630,000 skiing hours in the Alps,11 and one “cardiac event” per 957,000 hours of mountain activities,41 which increases substantially in individuals over the age of 50 to 60 years. This risk seems somewhat higher than the one death per 3,000,000 jogging hours reported by Thompson and colleagues.43 For patients with known CAD, if they are adequately revascularized, exercise at high altitude appears reasonably safe.17,42

HYPERTHERMIA The healthy human body is capable of tolerating and even successfully performing vigorous physical exercise during exposure to high ambient temperature. The hypothalamic thermoregulatory center prevents elevation of core body temperature during ambient heat exposure by causing peripheral vasodilation and increased sweat production. Humans thermoregulate predominantly by sending blood to the skin; during an acute heat stress, up to 8 to 10 L/min of cardiac output may be directed to the skin (and therefore unavailable to other organs) to maintain body temperature. Especially for persons with compromised circulation, such as with heart failure (HF),4,13 heat exposure may be poorly tolerated. With ample oral hydration and electrolyte repletion, moderate physical exercise can be performed in the face of significant thermal exposure for extended periods, although safe performance requires adequate heat acclimatization. The absolute intensity and duration of work that can be performed in the heat by a given individual are dictated by numerous factors, including prior heat acclimatization, physical fitness, and ambient temperature and relative humidity. Heatstroke occurs when the cooling system fails and core body temperature rises. Heatstroke is defined clinically as a core body temperature that rises above 42° C (107.6° F), with signs and symptoms including hot, dry skin and central nervous system abnormalities such as delirium, convulsions, or coma.9 Cardiovascular complications of heatstroke include atrial fibrillation, various electrocardiographic abnormalities (T-wave changes and prolongation of the QT interval), pulmonary edema, pericardial effusion, right ventricular dysfunction, hypotension, and ventricular arrhythmias.46

HYPOTHERMIA Classically hypothermia is defined as a core body temperature of less than 35° C (95° F). Hypothermia may develop in numerous wilderness scenarios, including but not limited to cold-water immersion, snow burial, and exercise in cool to cold ambient temperatures. Unlike heat exposure, humans do not acclimatize to an appreciable degree to cold exposure, so survival in the cold depends on behavior (e.g., clothing, shelter). The initial response to cold exposure is increased sympathetic nervous system activity leading to peripheral vasoconstriction and tachycardia.28 This causes a rise in systemic arterial blood pressure and a tendency toward central redistribution of blood volume. Acute exercise in the cold, especially in patients with CAD, is associated with increased risk for acute coronary events. With sustained mild hypothermia (core body temperature of 33° to 35° C [91.4° to 95° F]), this central volume shift promotes diuresis, which can lead to dehydration. As hypothermia becomes more pronounced (moderate hypothermia is 30° to 33° C [86° to 91.4° F]), heart rate and cardiac output fall and the electrocardiogram may show characteristic findings of prolonged QT interval or Osborn waves. Bradycardia, caused by direct slowing of sinoatrial function and concomitant changes in tissue pH, oxygen concentration, and electrolyte concentrations, becomes more marked as core temperature continues to drop.33 The drops in core temperature and pulse rate typically observe a linear relationship; deviations from this relationship, particularly tachycardia in the moderately hypothermic patient, should raise suspicion of a secondary process, such as toxin ingestion or hypovolemia. Premature atrial and/or ventricular beats and atrial fibrillation commonly occur in the moderately hypothermic person. In severe hypothermia (<30° C [86° F]), there are significant reductions in stroke volume, heart rate, and blood pressure. All 630

types of atrial and ventricular tachyarrhythmias can occur during severe hypothermia.14 It should be noted that rough handling or jostling of the severely hypothermic patient could trigger arrhythmias, so care should be taken to avoid unnecessary physical manipulation of the hypothermic patient.28 At temperatures below 25° C (77° F), spontaneous ventricular fibrillation and/or asystole may occur. As discussed in further detail below, victims of hypothermia may tolerate periods of cardiac arrest longer than do victims under normothermic conditions. Thus the appropriate window for initiating and continuing resuscitation for a hypothermic patient may exceed that in other cardiac arrest situations.

Screening and Preparation for Wilderness Travel ASYMPTOMATIC WILDERNESS ADVENTURERS Participation in wilderness activities can place considerable stress on the cardiovascular system. Before wilderness activity, healthy individuals without known preexisting cardiovascular disease should seek medical consultation with a clinician familiar with the demands of the wilderness environment. This recommendation is similar to that for individuals considering starting an intensive exercise program or participation in competitive sports. Assessment of the asymptomatic individual should focus on determining risk for underlying, previously unrecognized cardiovascular conditions. A detailed medical history focused on prior exercise experience, wilderness adventure experience, medications, allergies, a detailed family history of cardiovascular disease or premature sudden/unexplained death should be obtained. Individuals should be specifically questioned about established cardiovascular risk factors, including tobacco use, hypertension, diabetes, family history of premature coronary disease, and dyslipidemia. A comprehensive physical examination should be performed, beginning with a basic assessment of vital signs to exclude systemic hypertension and arrhythmia. Auscultation of the heart and lungs should be performed to exclude congenital or acquired valvular heart lesions and pulmonary vascular congestion. Peripheral pulse examination should be performed to detect the presence of atherosclerotic peripheral vascular disease and aortic coarctation. Although not specifically designed for wilderness travelers, the American College of Cardiology/American Heart Association’s athletic pre-participation medical history and physical examination template may prove to be a useful guide for clinicians in this setting.35 Asymptomatic wilderness travelers with a normal medical history and physical examination typically tolerate wilderness activity without cardiovascular complications and should not be restricted from any specific activities based on cardiac risk. Individuals with abnormalities detected during the medical history or physical examination may require further testing. Some combination of 12-lead electrocardiography, transthoracic echocardiography, exercise stress testing, and ambulatory rhythm monitoring may be useful in such individuals. The decision to perform one or more of these diagnostic tests must be individualized based on characteristics of the patient.

ESTABLISHED CORONARY ARTERY DISEASE Atherosclerotic coronary artery disease (ACAD) is the leading cause of death in middle-age and older individuals in the developed world. Atherosclerosis is the process of arterial lumen narrowing caused by accumulation of lipids, inflammatory cells, and calcium within the walls of an artery. ACAD leads to clinically relevant myocardial ischemia in one of two principal fashions. ACAD may progress steadily and often slowly over a period of months to years to the point at which arterial lumen narrowing is sufficient to cause myocardial demand–related ischemia. In this setting, ACAD manifests as exertional chest discomfort, referred to as angina pectoris. Patients with angina pectoris are managed clinically with medications to reduce myocardial oxygen demand (e.g., β-blockers, nitrates), prescribed exercise

A

B FIGURE 32-2  Representative example of 12-lead electrocardiogram at rest (A) and peak exercise (B) in a 56-year-old man with cardiac risk factors of diabetes and dyslipidemia who underwent screening before high-altitude travel. B demonstrates ST-segment depression of greater than 1 mm in numerous contiguous ECG leads. This patient was found to have multivessel coronary artery disease with high-risk features necessitating coronary artery bypass grafting surgery.

BOX 32-1  Baseline Patient Characteristics

Necessitating Myocardial Imaging as an Adjunct to Exercise Stress Testing for Establishing a Diagnosis of Myocardial Ischemia

• Prior percutaneous (PCI) or surgical revascularization (CABG) if ECG is abnormal • Preexcitation (Wolff-Parkinson-White) syndrome • Resting ST-segment depression ≥1 mm • Electronically paced rhythm • Left bundle branch block • Resting repolarization abnormalities due to LVH or digitalis use CABG, Coronary artery bypass grafting; ECG, electrocardiogram; LVH, left ventricular hypertrophy; PCI, percutaneous coronary intervention.

triggered during stress testing. As such, we emphasize several principles to our ACAD patients who choose to engage in wilderness activity. First, we encourage all ACAD patients to be knowledgeable about the typical symptoms of this disease (e.g., exertional chest pain/pressure/tightness, inappropriate exertional dyspnea). Development of any of these symptoms during wilderness activity should prompt the patient to abort the activity and to seek immediate medical attention. Second, we encourage all ACAD patients to prepare as fully as possible for the physical demands of wilderness activity. This is best accomplished by using a progressive exercise-training program designed to mimic the specific challenges of the planned wilderness activity. Third, we emphasize the value of allowing ample time for wilderness environment acclimatization. Acclimatization techniques vary by activity and environment and may include gradual or staged high-altitude ascent or prolonged, low-intensity exercise under hot conditions.

CARDIOMYOPATHY/CONGESTIVE HEART FAILURE Cardiomyopathy refers to abnormal function of the heart muscle. Cardiomyopathy may be inherited/congenital (e.g., hypertrophic cardiomyopathy, familial dilated cardiomyopathy) or acquired (e.g., ischemic cardiomyopathy, cardiomyopathy secondary to a pathologic valvular condition) and thus can affect individuals of all ages. Risk associated with wilderness activity among patients with cardiomyopathy is determined by etiology and severity. Certain forms of cardiomyopathy (e.g., hypertrophic cardiomyopathy) are associated with increased risk for SCD in the context of vigorous physical activity. Patients with these forms of cardiomyopathy should either be excluded from wilderness activity or counseled extensively about the inherent risks associated with physical activity and wilderness isolation. In addition to sudden death risk, cardiomyopathy may lead to development of heart failure (HF). HF is a syndrome defined as inability of the circulatory system to provide adequate circulation of blood to meet the demands of the body and to fill adequately at a low enough pressure to avoid congestion. HF severity can be assessed based on symptom severity and the results of an assessment of cardiac structure and function. Recently updated practice guidelines present an HF severity classification scheme that incorporates symptom severity and cardiac structural/functional parameters (Table 32-1).25 Cardinal symptoms of HF include dyspnea, fatigue, exercise intolerance, and systemic venous congestion manifesting most commonly as peripheral edema. Noninvasive imaging such as echocardiography can provide important information such as left ventricular size and ejection fraction. Individuals with Class D HF are typically not capable of wilderness activity, and exposure to hypoxia, hyperbaria, or thermal extremes should be avoided. Individuals at risk for HF with (Class B) or without (Class A) documented structural or function cardiac abnormalities should undergo assessment of functional capacity by exercise testing before participating in wilderness activity. Class A and B patients that demonstrate normal, age-appropriate exercise capacity during formal testing can be expected to 631

CHAPTER 32  Wilderness Cardiology

therapy, aggressive risk factor modification, and symptom-driven revascularization. Alternatively, ACAD may manifest with sudden and complete occlusion of a coronary artery. This phenomenon is triggered by ulceration or rupture of an atherosclerotic plaque with subsequent development of a platelet-rich clot. This dramatic and often catastrophic ACAD presentation leads to myocardial infarction and/or a malignant ventricular arrhythmia. Effective management of plaque rupture and complete coronary arterial occlusion requires pharmacologic (systemic thrombolytics) or mechanical reperfusion (percutaneous coronary angioplasty and stenting), which are typically not feasible in the wilderness environment. Individuals with coronary artery disease should not necessarily be restricted from wilderness activity. Patients with clinically stable ACAD (i.e., patients fully revascularized or incompletely revascularized but without recent change in anginal threshold) who are on a well-tolerated medical regimen should not universally be excluded from wilderness activity. We recommend that all individuals with established ACAD undergo some form of exercise stress testing before wilderness activity, because exercise stress testing provides an accurate assessment of both exercise capacity and the efficacy of medical therapy. Stress testing using continuous 12-lead electrocardiographic monitoring can be done using a number of exercise modalities, including treadmill running/walking and upright or supine cycle ergometry. Typical electrocardiographic findings of myocardial ischemia are illustrated in Figure 32-2. The choice of exercise modality can be made based on patient and clinician preferences. Concomitant myocardial imaging may be necessary to achieve adequate diagnostic accuracy in patients with certain pretest features (Box 32-1). Imaging can be performed using nuclear perfusion tracers or echocardiography as dictated by available expertise. Individuals with clinically stable ACAD who have normal left ventricular function and no myocardial ischemia during exercise testing performed at least to a workload commensurate with the demands of the expected activity should not be restricted from wilderness activity based on cardiovascular disease. It should be emphasized, however, that no laboratory-based exercise test is a perfect simulator of the wilderness environment. The combination of intense physical exercise and environmental extremes may precipitate myocardial ischemia that could not be

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 32-1  ACC/AHA Classification of the Stages

of Heart Failure

Heart Failure Stage

Definition

At Risk for Heart Failure Stage A Patients at high risk for developing heart failure in the future but no functional or structural heart disorder Stage B Structural heart disorder but no symptoms of prior heart failure at any stage Heart Failure Present Stage C Previous or current symptoms of heart failure in the context of an underlying structural heart disorder Stage D Advanced disease requiring hospital-based support, a heart transplant, or palliative care ACC, American College of Cardiology; AHA, American Heart Association.

tolerate wilderness activity without complications and thus do not require restriction. The most difficult clinical decisions arise when clinician advisors are confronted with individuals with Class C disease. Class C individuals, particularly those with stable disease, can tolerate moderate-intensity exercise in controlled environments, such as cardiac rehabilitation programs, and may express interest in wilderness activity. It must be emphasized that these patients are at considerable risk for decompensation if activity intensity exceeds a certain threshold. Because this threshold differs markedly among Class C patients and may change rapidly in any given individual, we advise conservative recommendations in this patient population. In our opinion, the majority of Class C HF patients should be restricted from aggressive or extreme wilderness activities that significantly increase stress on the cardiovascular system. Clearance to perform low-intensity wilderness activity in this patient population must be considered carefully on a case-by-case basis.

CONGENITAL HEART DISEASE Congenital heart disease (CHD) is a term that includes a wide array of cardiac abnormalities that are present at birth. CHD can include abnormalities of the heart muscle, cardiac valves, coronary arteries, and electrical conduction system and may be confined to the heart or a component of a systemic disorder. From a functional perspective, CHD can be categorized as either cyanotic or acyanotic. Cyanotic CHD is characterized by reduced arterial oxygen saturation due to right-to-left intracardiac shunting with direct venous to arterial transit of blood. Cyanotic CHD is relatively rare and involves complex and severe structural cardiac malformations, such as tetralogy of Fallot. Most individuals with cyanotic CHD present early in life because of failure to thrive or markedly reduced exercise capacity and are treated with surgical reconstruction. Individuals with complex cyanotic CHD are at high risk for decompensation during wilderness activity and should be restricted from wilderness activity for this reason. Among patients with successful surgical correction of cyanotic CHD, the risk associated with wilderness activity is highly variable. For example, patients who have undergone a surgical Fontan procedure and who do not have right-to-left shunting tolerate acute exposure to high altitude surprisingly well.21 Nevertheless, the impact of chronic exposure to high altitude in such patients has not been well defined. The decision to prohibit or restrict activity in this patient population should be made on a case-by-case basis in consultation with a cardiovascular specialist with expertise in CHD. Acyanotic CHD, defined by the presence of an abnormality associated with normal arterial oxygen saturation, is more common than is cyanotic disease. Common causes of acyanotic CHD include atrial and ventricular septal defects. In these conditions, intracardiac shunting of blood travels in a left-to-right direction and does not produce arterial hypoxemia. Many individuals have their acyanotic CHD go undetected through childhood and adulthood and can be expected to have normal exercise capacity and life expectancy. However, normal development and previous clinical stability in a patient with acyanotic heart disease do not 632

necessarily indicate an acceptable risk for wilderness activity. This is particularly true of wilderness activity that involves exposure to hypoxia, such as that which occurs during high-altitude travel. Hypoxia facilitates pulmonary vasoconstriction, leading to increased pulmonary vascular resistance. The increased pulmonary vascular resistance and resultant increase in right ventricular and atrial pressures may lead to right-to-left intracardiac shunting and conversion to cyanotic CHD physiology. The risk associated with wilderness travel among patients with common acyanotic CHD is variable and largely determined by the specific form and severity of the intracardiac lesion. Before wilderness activity, individuals with acyanotic CHD should consult with a cardiovascular specialist with expertise in CHD. Two other conditions deserve specific comment. One rare condition, consisting of congenital absence of the right pulmonary artery, places patients at grave risk for high-altitude pulmonary edema, even at relatively low altitudes. It is crucial for practitioners of wilderness medicine to be aware of this condition and counsel such patients to avoid high-altitude exposure. The second is patent foramen ovale. This condition is quite common, present in perhaps 5% of the adult population, and has been associated with acute mountain sickness and high-altitude pulmonary edema.1,31 However, there is no evidence that closing a patent foramen ovale has any effect on exercise performance at altitude or the risk for high-altitude illness, and such a procedure should be avoided unless there are other strong clinical conditions. For individuals with a known patent foramen ovale wishing to go to high altitude, consideration should be given for high-altitude pulmonary edema prophylaxis with a pulmonary vasodilator such as nifedipine39 or tadalafil.34

ARRHYTHMIAS Disturbance of cardiac rhythm, arrhythmia, is a common form of cardiac disease. Arrhythmias are commonly categorized by their site of anatomic origin. Supraventricular arrhythmias arise from foci above the atrioventricular node, typically in the atria or adjacent vessels, such as the pulmonary veins. In contrast, ventricular arrhythmias originate below the atrioventricular node within the ventricular myocardium or His-Purkinje conduction fibers. The clinical implications of cardiac arrhythmia are highly variable and constitute a full spectrum of severity. In general, supraventricular arrhythmias are better tolerated than are ventricular arrhythmias. Many individuals experience completely asymptomatic supraventricular arrhythmias. Individuals with a history of asymptomatic supraventricular arrhythmias who are free of other forms of cardiac disease may participate fully in wilderness activity. Patients with a history of symptomatic supraventricular arrhythmias, including those taking medications for maintenance of sinus rhythm and/or heart rate control, should undergo exercise testing to assess for rhythm stability and circulatory sufficiency during high-intensity exercise. Carrying an extra “pill in the pocket,” such as a short-acting β-blocker like propranolol, may be a useful precaution for such patients. Some patients with paroxysmal or chronic supraventricular arrhythmias are managed with anticoagulation (e.g., aspirin, warfarin). These patients may be susceptible to bleeding complications of trauma and should be advised to take appropriate precautions in the wilderness environment. Patients with a history of ventricular arrhythmia, fibrillation, or tachycardia should be considered at risk for recurrence unless the underlying cause of the rhythm has been identified and corrected. We typically recommend restriction from high-intensity exercise, including competitive sports and wilderness activity, in such patients.

IMPLANTABLE CARDIOVERTERDEFIBRILLATORS AND PACEMAKERS Implantable cardioverter-defibrillators (ICDs) are placed for the primary and secondary prevention of SCD in patients susceptible to malignant ventricular arrhythmias. Recent expansion of ICD appropriateness criteria has lead to continually increasing numbers of patients with these devices.16 By definition, individuals with ICDs are at high risk for arrhythmia and subsequent device discharge during strenuous activity and therefore should avoid all

HYPERTENSION Because blood pressure rises with chronic altitude exposure, hypertension that is well controlled at sea level may become uncontrolled at high altitude. Patients with hypertension, especially those with other comorbidities, are advised to carry a small, wrist type of blood pressure cuff to check their blood pressure and to discuss with their physicians strategies to increase the dose of current medications or add a new drug if necessary. Drugs with combined α/β-blocking effects, such as carvedilol or labetalol, may be especially effective at high altitude.

Basic Management of Cardiovascular Emergencies in the Wilderness Environment CHEST PAIN Myocardial ischemia most commonly manifests with chest discomfort. The quality of this discomfort varies among individuals and may be reported as heaviness, tightness, or a dull ache. The chest discomfort attributable to myocardial ischemia is often accompanied by other symptoms, including diaphoresis, nausea, dyspnea, or pain in adjacent anatomic structures, including the neck, jaw, or left arm. Among wilderness adventurers, new-onset chest discomfort without a clear musculoskeletal cause should be considered an ominous sign. It should be assumed that nontraumatic chest discomfort is indicative of an active coronary artery process until proved otherwise. Definitive and effective therapy for active myocardial ischemia requires access to hospitalbased resources.2,3 As such, wilderness travelers who experience chest discomfort suspected to be of myocardial ischemic origin should place emphasis on gaining access to a capable medical facility with minimal delay. In some cases, assistance from search and rescue programs with the capability to provide rapid transport may be appropriate. In the field, acetylsalicylic acid (aspirin), preferably in a chewable, rapidly absorbed form, should be given immediately once myocardial ischemia is suspected. Nitroglycerinbased agents, additional anticoagulants, including low-molecularweight heparin, and analgesic medications may be appropriate if administered in the field by a clinician trained in their use.

ARRHYTHMIAS A rapid but regular heart rate with normal sinoatrial node origin (sinus tachycardia) may be caused by appropriate physiologic

response to the intense physical or emotional stress of the wilderness environment. In contrast, pathologic tachyarrhythmias may develop suddenly and may originate in the atria, atrioventricular node, or ventricles. Sinus tachycardia is typically associated with a clear stimulus, develops gradually as the stimulus intensifies, and abates gradually once the stimulus is removed, although it may also be a sign of inadequate compensation to altitude or heat. Sinus tachycardia is generally not associated with additional symptoms unless an individual harbors significant occult or previously documented heart disease. In contrast, pathologic tachyarrhythmias may begin suddenly either at rest or during exertion and typically fail to resolve gradually with activity cessation. They are often accompanied by symptoms that include lightheadedness, palpitations, or chest discomfort. Resolution of tachyarrhythmia is typically abrupt. Differentiation between normal sinus tachycardia and a pathologic tachyarrhythmia can be difficult in the wilderness setting. A prior medical history of confirmed pathologic arrhythmia (e.g., Wolff-Parkinson-White syndrome, atrial fibrillation, or atrial flutter) or underlying structural heart disease can be helpful. Brief physical examination may provide additional clues. The patient’s pulse should be assessed for rate, regularity, and beat-to-beat variability. The jugular venous column should be inspected for the presence of atrioventricular dissociation or flutter waves. Direct auscultation of the heart using either a stethoscope or the simple placement of an ear on the patient’s bare chest can provide clues about rhythm origin. These clues include paradoxical splitting of the second heart sound (characteristic of the left bundle branch block that accompanies ventricular tachycardia, or supraventricular tachycardia with aberrancy) or the presence of Rytand’s murmur (a murmur of varying intensity that indicates advanced heart block). Management of the symptomatic patient with suspected pathologic tachyarrhythmia should focus on rapid transportation to a medical facility with advanced cardiac life support capabilities.8 When transportation to professional medical attention is not an immediate option, several therapeutic maneuvers can be attempted. Carotid sinus massage can be used to terminate several forms of tachyarrhythmia. External pressure on the carotid sinus stimulates baroreceptors that trigger increased vagus nerve activity and decreased sympathetic nervous system activity, thereby potentially terminating the arrhythmia. The patient with tachyarrhythmia should be placed in a supine or lateral decubitus position with the neck fully extended and turned away from the care provider. The carotid pulse should be palpated close to the angle of the jaw to approximate the common carotid artery bifurcation. Firm pressure should then be applied with a gentle rotating motion for 5 seconds. If there is no response, the procedure should be attempted on the patient’s other side. The procedure should never be performed on both sides simultaneously. In patients who do not respond to carotid sinus massage, alternative vagus nerve stimulation maneuvers may be attempted. Prolonged breath holding, a Valsalva maneuver, putting the face in cold water (to induce the “diving reflex”), or a strong cough against a closed glottis may also cause a vagal response adequate to terminate a tachyarrhythmia.

SYNCOPE Syncope is defined as transient loss of consciousness accompanied by loss of postural tone. Syncope occurs because of rapid reduction in cerebral blood flow culminating in significant central nervous system hypoperfusion. There are numerous causes of syncope. Syncope may be attributable to an underlying cardiovascular pathologic condition, including structural, valvular, or electrical heart disease. Such underlying processes need to be considered when evaluating any patient with a prior syncopal event. Most commonly, syncope occurs in healthy individuals without explanatory heart disease and is attributable to autonomic mechanisms (vasovagal or neurally mediated syncope). The physiology of neurally mediated syncope is beyond the scope of this text; the interested reader is referred to several excellent reviews of this topic.27,29,38 Neurally mediated syncope is common among physically fit individuals who may choose to engage in wilderness activity12 633

CHAPTER 32  Wilderness Cardiology

high-intensity exercise. Device discharge may be painful and may render the recipient temporarily incapacitated. Accordingly, all wilderness activities during which transient compromises in cognitive or motor function may have grave consequences to the patient or partners are contraindicated in patients with ICDs. Examples include underwater diving, rock climbing, and hang gliding. Lowto moderate-intensity exercise may be appropriate for patients with ICDs. We encourage careful assessment of heart rate and rhythm response during formal exercise testing in ICD patients who choose to pursue such activities. Cardiac pacemakers are used in patients with native conduction system disease and associated symptoms. Although individuals with pacemakers have no specific exercise limitations as a result of the presence of their devices, early-generation pacemakers were not designed to accommodate the physiologic demands of exercise and left recipients with reduced exercise capacity. Recent advances in pacemaker technology have been substantial. With respect to exercise capacity and wilderness activity, the most important advances involve the ability of newer devices to augment heart rate and cardiac output during volitional exercise. Devices now sense the need for heart rate/cardiac output augmentation by tracking some combination of patient body motion, respiratory rate, and properties of the intact native conduction system. The presence of a pacemaker should not constitute grounds for restriction from wilderness activity. However, patients should undergo device interrogation for battery life and sensing/ pacing thresholds before participation.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

and has been reported to occur during the early phases of altitude acclimatization as a result of plasma volume loss, hyperventilation, and perhaps hypoxia-mediated vasodilation. Individuals with a predisposition for neurally mediated syncope may be at increased risk for syncope during wilderness activity that produces dehydration (prolonged strenuous exercise) and/or significant peripheral vascular dilation (thermal exposure). The individual with neurally mediated syncope will typically report presyncopal feelings of warmth, diaphoresis, or light-headedness, which culminate in loss of consciousness ranging from several seconds to minutes. Management of wilderness syncope begins with removal of the patient from dangerous conditions. Individuals who succumb to syncope should be removed immediately from locations (e.g., partial water submersion, precarious heights) in which transient loss of consciousness could lead to trauma or further complications. Patients should be assessed for spontaneous ventilation and the presence of a regular pulse in a central artery. If spontaneous cardiorespiratory function is confirmed, it is best to observe the unconscious individual for several minutes to allow for spontaneous resumption of normal cognition and motor function. Once revived, efforts to correct or minimize the potential syncopal trigger, such as rehydration, active cooling, or activity cessation, are warranted. A physician should assess all individuals who have syncope during wilderness activity in a full-service medical facility as soon as possible to exclude an underlying cardiac pathologic condition. This assessment should include a detailed history, physical examination, and 12-lead electrocardiogram with further diagnostic evaluation on a case-by-case basis, unless typical “vasovagal” circumstances and symptoms are present.

CARDIAC ARREST The initial approach to the patient in the wilderness with presumed cardiac arrest, typically individuals with sudden collapse or those who suffer prolonged and severe hypoxia (e.g., avalanche burial, drowning) should be to confirm the absence of spontaneous circulatory activity. This is performed by manual palpation of a large central artery such as the carotid or femoral artery and simultaneous inspection of skin tone, motor activity, and chest wall motion. In patients with a palpable pulse but evidence of primary respiratory collapse, maneuvers to clear the upper and lower airways can be initiated. Once the absence of spontaneous circulatory activity is confirmed, resuscitation in the form of basic life support measures should be initiated immediately. Historically, basic life support has been dictated by the ABC acronym that referred to the resuscitation sequence of airway, breathing, and circulation. The approach to basic resuscitation has recently undergone important modifications. The most recent American Heart Association/American College of Cardiology consensus guidelines advocate a CAB or circulation– airway–breathing approach to basic life support.7 This strategy involves immediate initiation of chest compressions for unconscious patients without spontaneous or normal cardiorespiratory function. The logic for this paradigm shift is that there is ample oxygen present in the lungs and arterial system for several minutes following cardiac arrest to avoid ischemia if blood can reach the target organs. Thus immediate circulation of blood via chest compressions will facilitate optimal oxygenation of the brain and other key organs sooner than the conventional airwayfirst approach. The currently recommended sequence of adult basic life support can be summarized as follows: 1. Recognition of cardiac arrest: Individuals with witnessed collapse or found unconscious should be assessed for responsiveness. Loud verbal engagement with concomitant physical stimulation (shoulder tapping) in the form of the question, “Are you all right?” is recommended. The responder should simultaneously assess the victim’s breathing. If the victim fails to respond and is found to have absent or abnormal breathing, cardiac arrest should be assumed and resuscitation should proceed. 2. Defibrillation: When accessible, an automated external defibrillator should be applied to evaluate for the presence of a cardiac rhythm that may respond to electrical therapy. 634

This is rarely an option in the wilderness environment. An acceptable, although infrequently successful method of terminating a malignant tachyarrhythmia, is the precordial thump. To perform a precordial thump, the patient’s chest should be cleared of clothing to facilitate accurate assessment of anatomy. Next, one or two firm blows should be delivered to the middle to lower one-third of the sternum with a closed fist from a height of 8 to 10 inches above the chest. A central artery should again be palpated for a pulse. If unsuccessful after one attempt, the effort should be abandoned and further life-support initiated. 3. Chest compressions—“C”: Chest compressions should be initiated immediately after confirmation of confirmed cardiac arrest and an unsuccessful precordial thump. The rescuer should place the heel of one hand on the lower one-half of the victim’s sternum and the heel of the other hand on top of the first so that the hands are overlapped and parallel. Briefly, the adult sternum should be depressed at least 2 inches with chest compression and chest recoil/ relaxation times approximately equal. Compressions should be performed at a rate of at least 100 per minute. The initial sequence of compressions should be performed continuously for 1 minute. 3. Airway—“A”: Assurance of airway patency remains an important component of the overall resuscitation effort. In the wilderness environment, use of the head tilt–chin lift maneuver is the optimal manual strategy for opening a victim’s airway. Individuals with appropriate training may consider using an oral or nasopharyngeal airway. Cricoid pressure is not recommended. 4. Breathing—“B”: Rescue breathing should be performed by mouth-to-mouth, mouth-to-barrier, or mouth-to-mask ventilation. Breathing should be initiated after compressions. To provide mouth-to-mouth rescue breaths, the victim’s airway should be opened using the head tilt–chin lift maneuver. The victim’s nose should be pinched to create an airtight mouth-to-mouth seal. One breath should be given over a 1-second interval. The rescuer should take and provide a “regular” (not a deep) breath to avoid getting dizzy or light-headed and to prevent overinflation of the victim’s lungs. The most common cause of ventilation difficulty is an improperly opened airway. If the victim’s chest does not rise with the first rescue breath, the head should be repositioned by performing the head tilt–chin lift again and then giving the second rescue breath. Giving compressions and rescue breaths in a 30 : 2 ratio is recommended during resuscitation. Rescuers are advised to switch roles frequently to minimize the fatigue that is inherent in the delivery of effective chest compressions. A brief resuscitation pause to assess for the presence of spontaneous pulses should be performed every 2 minutes. The success of cardiac arrest resuscitation typically requires access to advanced cardiac life support equipment and trained personnel. This may not be a reality when cardiac arrest occurs in wilderness environments. Cardiac arrest patients who do not respond to resuscitation efforts during the first 15 to 30 minutes of basic life support are very unlikely to recover any significant degree of brain function, even if spontaneous cardiopulmonary function is restored. The decision of when to terminate resuscitation in a wilderness setting is challenging. Recommendations for this task have been developed.22 In general, it is reasonable to terminate resuscitation efforts after 30 minutes if a spontaneous pulse has not been restored. An extension beyond this time limit should be considered for the hypothermic patient because hypothermia may extend the window of potential central nervous system survival. Current resuscitation guidelines provide recommendations for specific wilderness situations (Table 32-2).44 Finally, there are certain situations in which resuscitation may be deferred in the wilderness environment. These include the following: (1) Any situation in which resuscitation efforts would put rescuers at risk, (2) a victim with a core body temperature of less than 15° C (59° F), (3) a victim with a frozen chest wall, (4) a victim who has been submersed in cold water for more than 60 minutes, (5) a victim with an obvious lethal injury such

TABLE 32-2  Considerations for Resuscitation of Cardiac Arrest Victims in Specific Wilderness Situations Wilderness Situation Trauma

Hypothermia

Avalanche burial Drowning

Lightning strikes

Special Considerations • A jaw thrust, not a head tilt–chin lift maneuver, should be used to establish a patent airway. • Ventilation should be performed using a barrier device whenever possible, especially if the victim’s face is bloody. • Visible hemorrhage should be controlled with direct pressure and compressions to minimize blood loss. • Wet garments should be removed if they can be replaced with dry insulating cover, ideally during early stages of the resuscitation efforts. • Consider prolonged resuscitation effort (>30 min) if it can serve as a bridge to a medical facility with active rewarming capabilities. • Resuscitation should not be conducted in a location with continued snow instability that could put care providers at risk. • Decision to initiate resuscitation efforts must be tailored to victim’s burial time. All individuals without clear evidence of fatal trauma (e.g., decapitation) should receive resuscitation for burial times <30 min. • Rescuers must take great care to avoid personal during the retrieval of a submerged or potentially drowned victim. • Standard resuscitation sequence applies. Rescuers should be aware that victims with respiratory arrest but intact circulation (spontaneous pulse) may respond promptly to several mechanical ventilations. • Rescuers must take great care to avoid personal risk in the care of a victim struck by lightning by avoiding lightning strikes to themselves. • Concomitant trauma to the head and spinal column is a common side effect of lightning strikes and should be assumed in all victims.

as decapitation, and (6) a situation in which resuscitation would significantly delay evacuation of a hypothermic patient to controlled rewarming.22

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 33 



Wilderness Neurology CHARLES CLARKE

It is essential for practitioners in wilderness settings to have a working knowledge of neurology and to be able to diagnose and treat patients without recourse to specialist investigation, especially computed tomography and magnetic resonance imaging. Circumstances will vary depending on terrain, weather, and the availability of emergency transport (Figure 33-1, online). This chapter focuses on common neurologic problems. Important neurologic problems within wilderness medicine are divided into three main groups: • Specific neurologic conditions that are the results of an extreme environmental stressor. Examples include cerebral edema in high-altitude mountaineers and trekkers; nitrogen narcosis in divers at great depths; and decompression sickness when surfacing after a dive. These conditions typically require specialist knowledge to recognize and treat, and they form an important group of neurologic emergencies. Conditions discussed in other chapters include high-altitude cerebral edema (HACE) and acute mountain sickness; diving medical emergencies; hypothermia; frostbite; nonfreezing cold injuries; heat-related illnesses; insect, plant, animal, and marine toxins; lightning strikes; carbon monoxide poisoning; and drowning. • Incidental neurologic conditions that occur in a wilderness setting. Examples include migraine or tension headache, syncope or a suspected seizure, Bell’s palsy, meningitis, transient cerebral ischemia, stroke, head injury, and brain tumor. These are the primary subject matters of this chapter. When a diagnosis is not obvious, management can be difficult, and it tends to differ from practice in a clinical setting. If evacuation to a hospital is felt to be necessary, decisions can affect not only the patient but also their companions and sometimes the entire enterprise. Careful risk evaluation is essential.

• Advice and management related to preexisting neurologic conditions. Examples include handling recurrent seizures in known cases of epilepsy or advising whether or not a person should take part in a trek in a remote area when he or she has been previously diagnosed with multiple sclerosis.

Preliminaries: History and Examination The majority of neurologic conditions can be diagnosed with the use of a minimum of tools with a combination of history, observation, and physical examination. Clinical diagnosis in neurology is highly reliable; in no other branch of medicine are disease patterns and physical signs more consistent and dependable. This section outlines the rudiments of diagnosis, and stresses that a brief examination in combination with a succinct and practical formulation are essential. Written records should be maintained in all circumstances. In the event of any substantive illness and after any accident, one should inform the relevant insurance company, because many policies exclude coverage for late complications unless illnesses or accidents have been reported promptly. This holds true beyond neurology per se. There is no substitute for a careful history from the patient, his or her companions, or witnesses. Until the practitioner learns the actual story of what happened, he or she should not jump to medical conclusions. For example, the person who has fallen to the ground while shaking has not necessarily suffered a seizure; there is a broad differential diagnosis. Nervous system examination need not be lengthy or complex. A short neurologic examination (Box 33-1) takes less than 5

For online-only figures, please go to www.expertconsult.com

635

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 33-1  Five-Part Short Neurologic Examination 1. Look at the patient. • Appearance, injuries, level of consciousness, and cognition • Speech • Gait • Arm swinging 2. Examine the patient’s head. • Fundi, if an ophthalmoscope is available • Pupils • Eye movements • Facial weakness and movements • Tongue 3. Examine the patient’s upper limbs. • Posture of outstretched arms • Wasting and fasciculations • Power and tone • Coordination • Deep tendon reflexes 4. Examine the patient’s lower limbs. • Power • Tone • Deep tendon reflexes • Plantar responses 5. Inquire about the patient’s sensation. • Usually one can simply ask the patient.

minutes. Much can be done without any special equipment; a tendon hammer can be improvised easily, and lack of an ophthalmoscope rarely makes a great difference to diagnosis and management. Try to answer the following critical questions, using the story and examination findings: • What are the sites of the lesions? • What is the likely pathology? • Does a recognizable disease fit this pattern? • Broadly, is this really serious, and what is the sensible way going forward? Pattern recognition—and thus some experience—is vital. Try to take matters as simply as possible, gauge whether or not the case is truly serious, and review physical signs regularly. In wilderness settings, one may only be able to reach tentative conclusions. The substantial majority of all neurology cases turn out not to be sinister, and fortunately there are few true neurologic field emergencies where immediate action is vital.

Incidental Neurologic Conditions DIAGNOSING AND MANAGING HEADACHE Headache is one of the most common symptoms in medicine and a frequent problem in wilderness settings. Its significance ranges from an infrequent and trivial problem to a persistent unpleasant symptom to a marker of serious disease. In wilderness practice, complex headache classifications are of little value.

HEADACHE MECHANISMS Pain receptors are located at the base of the brain in the arteries and veins and throughout the meninges, extracranial vessels, scalp, neck and facial muscles, paranasal sinuses, eyes, and teeth. The brain itself is nearly devoid of pain receptors. Head pain is mediated via mechanical and chemical receptors, including the stretching of the meninges as well as neurotransmitters such as 5-hydroxytryptamine and histamine and their receptors and pathways. Nerve impulses travel from the peripheral structures above via the fifth and ninth cranial nerves and upper cervical sensory roots, and they pass centrally through the thalamus to the sensory cortex. The vast majority of headaches are 636

benign. However, the diagnostic issue is the question of serious disease.

COMMON HEADACHE Almost all headaches without other neurologic signs and with a duration of hours to days are of a band-like or generalized nature, often with a history of some weeks or a background history of several years. These headaches are usually the result of muscle tension or migraine. Migraine associates visual symptoms, nausea, and vomiting with the headaches. Emotional depression is common with any longstanding headache, but it is unwise to assume automatically that a psychological cause lies at the root of a headache. Headaches are not caused by essential hypertension. Malignant hypertension or accelerated hypertension with hypertensive encephalopathy can cause headache, but this is a rarity. Eye strain from refractive error does not itself cause headache. New prescription lenses sometimes provoke head pain, which is generally loosely regarded as being the result of eye strain and which is mediated via the pupils readjusting to a new refractive situation. In wilderness settings in snow, at sea, or in the desert, ultraviolet radiation and glare cause headache. In snow, this is as a part of snowblindness; painful keratoconjunctivitis can develop. Acute mountain sickness is a common cause of headache above 3000 m (9843 feet), and it may be premonitory for HACE. Headache is also said by some to be a feature of dehydration.

SUDDEN HEADACHE OF SHORT DURATION If pain is focal (e.g., localized to the upper face and lasting minutes to hours), consider sinusitis, glaucoma, and cluster headache. The sudden headache associated with subarachnoid hemorrhage, severe migraine, bacterial meningitis, and cervical arterial dissection is discussed later in this chapter.

HEADACHE CAUSED BY INCREASED INTRACRANIAL PRESSURE Intracranial mass lesions displace and stretch the meninges and the basal vessels. Pain is provoked when these structures are shifted either by a mass or by changes in cerebrospinal fluid pressure, such as may be caused by coughing. Cerebral edema around brain tumors causes the further shift of intracranial structures. Pressure headaches typically worsen when a patient is lying down or with movement; this feature is also seen commonly with migraine, acute mountain sickness, and HACE. Many textbooks indicate that any new headache that is present on waking and made worse by coughing, straining, or sneezing may be the result of a mass lesion, but it should be noted that benign headaches (e.g., migraine) are often made worse with head movement. Vomiting often accompanies pressure headaches. Pressure headaches appear early during the pathologic process and over the course of days or weeks when they are caused by posterior fossa masses or hydrocephalus, but they typically develop over months or years when they are caused by hemisphere tumors. Pressure headaches with ataxia occur with HACE. A rare cause of prostrating headache with lower-limb weakness is an intraventricular tumor that causes intermittent hydrocephalus.

HEADACHE OF SUBACUTE ONSET The onset and progression of a headache over days or weeks with or without features of a pressure headache should raise suspicion of an intracranial mass or serious intracranial disease. Encephalitis, viral meningitis, and chronic meningitis should be considered when a headache increases over the course of several days.

HEADACHE WITH SCALP TENDERNESS Patches of exquisite tenderness overlying superficial scalp arteries may be caused by giant cell arteritis (temporal arteritis) in patients who are more than 50 years old, and they almost never appear among younger persons.

The vast majority of headaches that occur after trauma—even those that last for several months—are not caused by serious intracranial pathology. However, subdural and extradural hematoma (see Chapter 21) must be considered in the aftermath of head injury. Both are rare in the absence of corroborating physical signs.

A SINGLE EPISODE OF SUDDEN SEVERE HEADACHE The common emergency of a single episode of sudden severe headache is caused by migraine or another benign type of headache (e.g., cluster), or it may be the result of serious events such as subarachnoid hemorrhage (SAH), cervical arterial dissection, or the onset of meningitis. The term thunderclap headache is used to describe such a devastating sudden headache without a clear cause. This is usually migrainous, but it also may indicate the onset of subarachnoid bleeding. Particular attention should be paid to the sudden onset, which is suggestive of SAH. The mode of onset, time to peak, duration, associated symptoms, and the patient’s headache history should be explored. The patient with SAH usually will indicate precisely the time of onset of a sudden headache. High fever, neck stiffness, vomiting, meningeal irritation, and a rash suggest bacterial meningitis, which requires immediate treatment. For nonfebrile persons, careful reassessment over the course of 12 hours can usually sort out whether a sudden headache was a migraine or part of SAH. Bacterial meningitis is often obvious at the onset. Cervical arterial dissection is discussed briefly in this chapter (see Stroke, later).

Wilderness Guidelines for the Diagnosis of Headache With any headache, first establish whether there is fever, a rash, or any “hard” neurologic signs, such as diplopia, papilledema, hemiparesis, or ataxia. If any of these is present, serious pathology must be considered. Papilledema may be difficult to detect with certainty in isolated circumstances. Easily visible retinal hemorrhages almost always accompany true disc edema. Consider the following questions: 1. Is this headache a migraine? The development of sudden headache, no matter how severe, that involves flashing lights, nausea, and vomiting is very likely to be migraine. Some migraines are devastating. Subarachnoid bleeding does not typically cause migrainous visual symptoms. In any event, in wilderness settings, management is expectant, because immediate evacuation is unlikely to be possible. Treat the patient with an analgesic (e.g., acetaminophen) and an antiemetic (e.g., metoclopramide, ondansetron). Await and expect recovery. After 12 to 24 hours, the majority of migraines will have resolved. If the patient becomes drowsy with neck stiffness, subarachnoid bleeding should be considered. 2. Does the headache appear to be a tension headache or a chronic daily headache? Band-like (i.e., around the head) headaches without any other clinical features and the absence of neurologic signs are distinctly unlikely to be the result of anything sinister. Again, await events. 3. Is the headache localized? Sinusitis, glaucoma, dental pain, and cluster headache need to be considered. With glaucoma, the eyeball will typically be painful, and vision may be altered. Sinusitis can cause severe pain that is usually well localized within and around the infected sinus. Cluster headache causes pain of exceptional severity, often at night, and is typically perceived around and behind the eye. Cluster headache, no matter how severe, tends to resolve after 4 to 6 hours. 4. Are the headaches subacute (i.e., have they gradually worsened over days to weeks)? This is a cause for concern and requires careful reeva­ luation for emerging physical signs. For example, in a situation that involves chronic meningitis (e.g., tuberculous meningitis), headache can precede the onset of neck

stiffness and emerging signs (e.g., hemiparesis, cranial nerve lesions) by several weeks.

Blackouts and Episodes of Impaired Consciousness The word blackout is used here as a general term to mean an episode of altered consciousness. Typically, no sinister cause is found, and simple syncope is the most common reason. In the United Kingdom, among persons who are initially diagnosed with a seizure in the emergency department or by paramedics, only about 20% have epilepsy. The differential diagnosis lies between vasovagal syncope, seizure, cardiac arrhythmia, non­epileptic attack disorder, and rarer causes of impaired consciousness.

Epilepsy A seizure (i.e., a convulsion or “fit”) is caused by a paroxysmal discharge of cerebral neurons. Epilepsy is the continuing tendency to have seizures, even if a long interval separates the attacks. A generalized convulsion (i.e., a grand mal seizure) is the most common recognized event. More than 2% of the population in developed countries is known to have two or more seizures during their lifetimes; among 0.5%, epilepsy is an active problem. Around 200,000 people in the United Kingdom and around 1.5 million people in the United States take antiepileptic drugs.

CLASSIFICATION The terms that are used to classify epilepsy include idiopathic, symptomatic, cryptogenic, primary generalized, focal (partial), and secondarily generalized. The clinical patterns of the main types of attack are described here. A generalized (i.e., grand mal or tonic-clonic) seizure is a convulsion that involves bilateral motor manifestations (i.e., convulsive features) and a loss of consciousness. With a primary generalized seizure, the origin of the abnormal electrical spikeand-wave activity seen with electroencephalography during the event is bilateral. A partial (focal) seizure occurs when the electrical abnormality remains localized to one part of the cerebral cortex. With a simple partial seizure, there is no loss of awareness (e.g., one limb jerking in a Jacksonian seizure). With a complex partial seizure, there is a loss of awareness (e.g., a temporal lobe seizure). A secondary generalized seizure is a grand mal fit that began as a focal seizure.

DIAGNOSING A SEIZURE Eyewitness accounts may be unclear and colored by the drama of the situation. Some stages of a seizure may be absent. With a primary generalized seizure, the typical stages are first the warning (i.e., a perception that something is about to happen but without a specific aura), which leads to the tonic (i.e., stiff or rigid) phase, during which the patient falls unconscious to the ground, sometimes first uttering a cry. Injuries are common, and the tongue may be severely bitten. Incontinence of urine, feces, or both may follow. The clonic (convulsive) phase begins, with bilateral rhythmic limb jerking and foaming at the mouth. This convulsive phase lasts from a few seconds to several minutes. The patient is typically cyanotic during the attack. Postictal drowsiness, confusion, or coma follows; this sometimes lasts for several hours, but it typically lasts for several minutes. With a partial seizure, the sequence of events depends on the site of the seizure origin in the cortex. The patient may have an aura before the seizure begins. An aura is a specific and patterned sensation that is caused by a focal cortical electrical discharge. With a simple Jacksonian partial motor seizure that has its origin within the motor cortex, the patient may sense a vague warning (as with a primary generalized seizure) that is followed by a specific aura (e.g., unusual sensations in one limb). This is followed by the onset of rhythmic jerking, typically in one hand or foot. Jerking spreads to the entire limb or to both the upper and lower limbs and possibly the face on the same side. This progression is 637

CHAPTER 33  Wilderness Neurology

HEADACHE AFTER HEAD INJURY

PART 4  INJURIES AND MEDICAL INTERVENTIONS

known as the “march” of the seizure. Consciousness is not lost during a simple partial seizure. In place of postictal drowsiness or coma, weakness of the limbs that were involved with the seizure may follow. This is known as Todd’s paralysis, and it may last for several hours. A stroke may be suspected if early stages of the seizure were not witnessed or if they are unclear. With a complex partial seizure of temporal lobe origin, the patient may experience an aura of familiarity with his or her surroundings, which is known as déjà vu; this is followed by an “absence attack” during which the patient is generally unaware or disoriented. As the seizure develops, the patient looks distant (i.e., appears to be in a trance-like state) and does not respond to stimuli. Facial or lip twitching may occur. Recovery is typically rapid, with the patient regaining full awareness in a matter of seconds or minutes (and rarely in more than 10 minutes). A focal seizure may progress to become secondarily generalized. For example, a Jacksonian motor seizure may develop into a grand mal fit. The usual differential diagnosis of a seizure is between syncope and a nonepileptic attack. There are many causes of loss of consciousness or sudden attacks; these are described later in this chapter. Assuming that one knows what to expect, they are usually recognizable.

EMERGENCY MANAGEMENT OF SEIZURES In the field, a seizure may well take place in a sensational situation, such as on a glacier, on a steep path, on a climb, or at sea. The doctor’s actions are frequently very much in the public view, and there is often an expectation that skilled and urgent treatment must be seen to be underway. The reality is that careful observation is usually the most important activity. Immediately establish and maintain a patent airway. Do not force the patient’s mouth open. Wooden mouth wedges, tongue forceps, and excessive restraint are likely to cause more injuries than will any seizure. Deep cyanosis is typical during a grand mal fit. The spontaneous return of normal breathing and oxygenation will remedy the problem. If an attack lasts for more than a few seconds, stay with the patient, summon help, assist with breathing, and establish intravenous access, if possible. The latter is unlikely to be necessary, but it prepares the patient for the medical emergency of status epilepticus. Most seizures resolve spontaneously. Status Epilepticus Status epilepticus, which is also known as status (Box 33-2), involves the occurrence of continuous seizures (two or more) without fully recovering consciousness. More than 50% of cases of status occur without a previous history of epilepsy. Status is associated with a mortality rate of 10% to 15%. Around 25% of patients with apparent refractory status have pseudostatus, which is also known as nonepileptic attack disorder (NEAD). Although the apparent status is factitious, there are great difficulties when it comes to making a confident diagnosis in this emergency situation. Not all status is convulsive. With absence status, the patient is in a continuous, distant, and stuporous state. The term focal status describes continuous jerking of a limb or other focal seizure activity. Epilepsia partialis continua is continuous seizure activity in one discrete part of the body (e.g., a finger, one side of the face) without a loss of consciousness. This is typically the result of a cortical neoplasm or, in the elderly, a cortical infarction. One should have an established protocol. Box 33-2 describes such a protocol that has been adapted for wilderness use. For the emergency kit, one method is to carry injectable and rectal diazepam, injectable lorazepam, injectable phenytoin, and buccal midazolam with a bag-valve-mask device and several airways. One also needs to cope with the aftermath, so oral antiepileptic drugs (e.g., phenytoin, carbamazepine) should be available for continuing therapy.

MANAGING A PROBABLE FIRST-TIME SEIZURE Although no hard-and-fast rules can be laid down, a definite unprovoked first grand mal seizure is usually sufficient reason to 638

BOX 33-2  Status Epilepticus Before all else, do the following: • Preserve and maintain the airway. • Treat convulsions rapidly. • Check for head and other injuries. • Protect and stay with the patient. • Establish intravenous access, if possible. Drugs: • Give diazepam (5-10 mg IV at 5 mg/min or less every 5-10 min to a maximum of 30 mg). • Use rectal diazepam (10-20 mg) or buccal midazolam (10 mg repeated once after 10 min if intravenous access is impossible.) • Order two people to act as assistants. • Administer oxygen and monitor the pulse and blood pressure, if possible. • Give intravenous glucose and thiamine. If status epilepticus persists, consider other antiepileptic drugs: • Lorazepam (4 mg at 2 mg/min IV every 10-15 min to a maximum of 8 mg) • Phenytoin (intravenous bolus not exceeding 50 mg/min and an adult dose of 10-20 mg/kg) • Phenobarbital (intravenous bolus of 60 mg/min or less and an adult dose of 10-20 mg/kg to a maximum of 30 mg/kg) • Valproate (intravenous adult dose of 15-45 mg/kg at 6 mg/ kg/min or less) • Remember the potential unwanted effects of antiepileptic drugs, such as hypotension, cardiac dysrhythmias, and cardiorespiratory arrest. • Continue to monitor the patient as best as possible Doses from Clarke C, Howard R, Shorvon S, et al: Neurology: A Queen Square textbook, Oxford, UK, 2009, Wiley Blackwell Publishing, p. 235. IV, Intravenously.

evacuate a patient. However, even in this situation, the yield of investigation is low, and the tendency exists to overdiagnose epilepsy. Often, despite a good history from an eyewitness, one may remain in some doubt about the nature of an attack. When there is uncertainty, it is useful to recall the benign outcome of the majority of blackouts and to remember that it may be reasonable to await events. It is usually prudent to not use antiepileptic drugs until a diagnosis of epilepsy is certain, despite pressure from either the patient or his or her team members to administer them.

Syncope and Related Phenomena Transient disturbances of awareness, losses of consciousness, and falls are common clinical problems. It should be possible to distinguish between a seizure, syncope, and other types of attack with the use of descriptions and eyewitness accounts.

SIMPLE SYNCOPE, CARDIAC SYNCOPE, POSTURAL HYPOTENSION, AND DROP ATTACKS Fainting is the result of sudden reflex bradycardia with vasodilatation of peripheral and splanchnic vasculature. This is simple syncope, which is also known as neurocardiogenic syncope, and it is a common response to prolonged standing, fear, venipuncture, or pain. Syncope almost never occurs when an individual is in the recumbent posture, unless the vagal response is profound. The subject falls to the ground and is unconscious for less than 2 minutes, and recovery is rapid. Jerking movements may occur, especially if the patient is trapped in a sitting position; this can briefly resemble a grand mal seizure. Incontinence of urine may occur. Cardiac syncope caused by arrhythmia is potentially serious and often treatable. Typically the onset is abrupt and involves pallor and an irregular or nonpalpable pulse. Asystole or ventricular tachycardia generally causes cardiac syncope. A useful

DROP ATTACKS AND HYDROCEPHALUS Drop attacks are sudden-onset, unexpected episodes of lowerlimb weakness with falling that occur primarily among women who are more than 60 years old. Awareness is preserved. There is a sudden unprovoked loss of lower-limb tone that is presumably of brainstem origin. Patients are frequently injured. Sudden attacks of leg weakness may also occur with hydrocephalus, presumably as a result of brainstem compression.

SYNCOPE: MANAGEMENT The immediate management of syncope or impending syncope is to lay the patient down, lift the patient’s legs, and record the pulse. For the rare circumstances in which brain blood flow cannot be restored (e.g., when a person is propped upright in a chair), brain infarction can follow syncope. Syncope in its various forms can usually be distinguished from epilepsy. Witnessed accounts are invaluable. Postepisode confusion with amnesia suggests a seizure, as do foaming at the mouth and substantive tongue biting. Pallor is typical with syncope.

OTHER CAUSES OF SUDDEN ATTACKS AND “FUNNY TURNS” Pseudoseizure is mentioned first because it is common during stressful situations. There are no truly diagnostic features of pseudoseizures. However, immediate loss of consciousness without a prelude that is followed by bizarre flailing limb movements that do not look truly convulsive are most common. Cyanosis is rare, and frothing at the mouth unusual. Pseudoseizure can be a difficult diagnosis, and status epilepticus can be successfully mimicked. Hypoglycemia A sudden fall in blood glucose level can cause loss of consciousness, sometimes with a convulsion. Hypoglycemic attacks unrelated to diabetes mellitus are rare. Patients with diabetes frequently recognize the times at which they are hypoglycemic. There is usually some warning, such as hunger, malaise, shaking, or sweating. Prompt recovery occurs with intravenous or oral glucose or an alternative form of sugar administration. Occasionally, injection with glucagon is necessary to elevate the blood glucose level. Prolonged hypoglycemia can cause widespread cerebral damage. Feeling faint after fasting does not necessarily (or usually) indicate anything serious. Transient Ischemic Attack Posterior circulation transient ischemia rarely leads to an isolated loss of consciousness, and potential cases are usually excluded from research data related to transient ischemic attack (TIA). Choking, Apnea Attacks, and Breath Holding When a large food bolus blocks the larynx, the person becomes blue and, more importantly, silent. Death may follow if the blockage is not relieved promptly as a result of the Heimlich maneuver, gravity, or back blows. Partial obstruction causes intense coughing and laryngeal spasm. Apnea episodes commonly occur during sleep at altitude; they are rarely of significance, but they

do alarm the individual’s companions. They may contribute to the hypoventilation that is associated with the headache of acute mountain sickness. Breath-holding attacks are primarily a pediatric attention-seeking problem. Panic and Hyperventilation Panic attacks are usually associated with autonomic disturbances such as tachycardia, sweating, and piloerection. Consciousness is usually preserved, so these attacks are easily recognized. Hyperventilation is common. Overbreathing causes respiratory alkalosis, which leads to dizziness, anxiety, and sometimes circumoral or peripheral tingling and carpopedal spasm. Occasionally there is brief loss of consciousness. For the rare situation in which there is underlying chronic hypocalcemia, hyperventilation can generate a grand mal seizure. Basilar Migraine Basilar migraine involves migraine-like symptoms of lightheadedness, vertigo, limb numbness, and speech disturbance, sometimes without headache. Consciousness can be briefly lost. Severe Vertigo When vertigo is sudden in onset, as with Ménière’s disease, it can be sufficiently severe to cause prostration and transient loss of consciousness. Carcinoid Syndrome, Pheochromocytoma, and Scombroid Poisoning The flushing and palpitation caused by these sudden biochemical insults are sometimes mistaken for anxiety, allergy, or possibly a partial seizure. Drug Reactions Acute dystonic reactions, such as drug-induced oculogyric crises, are sometimes mistaken for a form of seizure. Consciousness is preserved. Paroxysmal Dyskinesias Paroxysmal dyskinesias are exceptionally rare causes of sudden episodes of abnormal limb movement. Narcolepsy, Excessive Daytime Drowsiness, and Cataplexy Narcoleptic attacks are episodes of irresistible sleep that occur in inappropriate circumstances. Cataplexy is the sudden loss of lower limb tone (i.e., falling with intact awareness). Attacks are often triggered by surprise, laughing, or crying. Narcolepsy and cataplexy may coexist, and they are sometimes accompanied by other sleep-related phenomena, such as vivid hypnagogic (on falling asleep) or hypnapompic (on waking) hallucinations and sleep paralysis, the latter being a frightening inability to move. These sleep-related phenomena can occur in isolation, and they are of no major medical consequence. When treatment is necessary, modafinil, methylphenidate, or dexamfetamine are used for narcolepsy and cataplexy.

Sleep Problems with sleep are common in wilderness settings, often as a result of a combination of crossing time zones, physical discomfort, worry or depression, and disrupted daily routine (e.g., long watches at sea, predawn starts on climbs, precarious bivouac sites). At altitude, hypoxia causes disrupted sleep patterns, irregular respirations, and episodes of harmless (if not contributory to high-altitude pulmonary edema or HACE) sleep apnea. At sea in a small vessel, the need to remain in wet clothing so that one may be available instantly on deck contributes to sleep being uncomfortable and fitful. Sleep is necessary. It is essential for preserving recent memory and to refresh emotional equilibrium and stamina. Poorly understood pathways, such as the hypothalamic hypocretin (orexin) neuropeptide system between the cerebral cortex and reticular formation, are involved in sleep–wake cycles. Prolonged sleep deprivation causes exhaustion, poor judgment, elementary mistakes, and even mild confusion. Seizures may be 639

CHAPTER 33  Wilderness Neurology

working rule in the field is that supraventricular tachycardias are usually obvious to the patient as palpitations and lightheadedness, and they rarely produce loss of consciousness. Syncope can occur after micturition in men, particularly at night, and in either sex when venous return to the heart is obstructed by breath holding and severe coughing. “Effort syncope” is of cardiac origin. Postural hypotension is also a cause of syncope. This typically occurs among the elderly, among those with autonomic neurop­ athy, and as a result of the effects of phenothiazines, levodopa, or tricyclic antidepressants. Postural hypotension symptoms also occur during acclimatization to altitude. Carotid sinus problems can occasionally cause syncope, but these are difficult to diagnose. Syncope can also occur with severe anemia and blood loss.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

provoked in persons with a low seizure threshold. Sleepwalking, jerking episodes, and movements in sleep, which are common events among the normal population, may become more evident and worrisome in the close confines of a tent than they are at home. Vivid dreams and nightmares are common with both sleep deprivation and stressful situations. Dreams may relate to real dangers, such as the typical nightmares of slipping off a narrow ledge or falling overboard at sea. Alternatively, they may be pleasant; a person may dream that he or she is at a poolside sipping a cocktail, only to wake to discover he or she is tied into a bivouac the size of a crow’s nest. This phenomenon is known colloquially as a reverse-mare.

SLEEP MANAGEMENT 1. Ensure that team members have adequate sleep duration. Leaders are at particular risk, because they tend to take responsibilities to bed with them. 2. Ensure that sleeping accommodations are as comfortable as possible. Simple measures such as a proper pillow, warm headgear, dry nightclothes, and earplugs can be remarkably helpful. There is no need to be uncomfortable. A pee bottle for nocturnal micturition obviates the need to leave a tent or cabin, but it may require prior negotiation with companions. 3. Avoid sedatives unless they are really necessary. Recognize repeated early morning awakening as a prominent feature of depression. 4. Avoid caffeine, if possible, for 6 hours or more before sleeping. 5. Never suggest stimulant drugs (e.g., amphetamines), because these may lead to poor judgment. A cup of strong coffee on waking is preferable.

Meningitis and Encephalitis MENINGITIS Bacterial infections within the nervous system pose difficult dilemmas in any setting, but they require a particularly pragmatic approach when one is far from help. Bacterial meningitis is fatal unless it is treated promptly. Bacterial meningitis may be difficult to distinguish from self-limited viral infection. Microorganisms reach the meninges either by direct extension from the ears or nasopharynx, as a result of cranial injury or congenital defect, or via the bloodstream. Patients who are at particular risk are those with compromised immune systems. With acute bacterial meningitis, the pia-arachnoid becomes congested with neutrophils, and a thin layer of pus forms. Pus can organize to form adhesions that lead to cranial nerve palsies and hydrocephalus. With chronic infection (typically with tuberculosis), the brain surface becomes covered in sticky grey-green exudate with numerous meningeal tubercles. Adhesions are invariable. Brain edema occurs with any bacterial meningitis.

THE MENINGITIC SYNDROME The classic diagnostic triad for meningeal irritation is headache, stiff neck, and fever. With acute bacterial meningitis, there are usually intense malaise, fever, rigors, headache, photophobia, and vomiting that develop within hours or even minutes of infection. The patient is irritable and prefers to lie still. Neck stiffness and a positive Kernig’s sign (i.e., neck and back pain when the hip and knee are flexed with the patient supine) usually appear within hours. Brudzinski’s sign (i.e., spontaneous flexion of hips and knees when the neck is flexed with the patient supine) may also be present. The diagnostic conundrum is that sometimes with bacterial meningitis there are few prominent meningitic features, and the clinical picture may resemble viral meningitis. For example, neck stiffness may not be evident. A mild form of the meningitic triad is reliable as an indicator of meningeal irritation but not of its cause. If in doubt, treat the patient for bacterial meningitis. 640

TABLE 33-1  Some Clinical Clues to Meningitis Petechial rash Skull fracture Ear disease Congenital central nervous system lesion Immunocompromised patient Pleuritic pain with or without rash International travel Environmental issues (e.g., polluted water, canals, sewage)

Meningococcal meningitis Pneumococcal infection

Human-immunodeficiencyvirus–related opportunistic infection Enterovirus infection Possible malaria or poliomyelitis Leptospirosis

CLUES TO SPECIFIC VARIETIES OF BACTERIAL MENINGITIS Possible infecting organisms are shown in Table 33-1. However, in wilderness practice, treatment for an unknown pyogenic organism will be required.

EMERGENCY WILDERNESS MANAGEMENT OF MENINGITIS If acute bacterial meningitis is suspected, treatment must be started immediately and before evacuation is even considered. Table 33-2 indicates a practical treatment approach, but it is important that up-to-date information about treatment protocols, potential allergies, and drug side effects is sought before embarking for a remote area. Evidence suggests that the administration of steroids (e.g., 10 mg of intravenous dexamethasone very 6 hours for 4 days) commencing with the first antibiotic dose reduces complications such as brain edema and delayed deafness.

VIRAL, SUBACUTE, AND CHRONIC MENINGITIS AND ENCEPHALITIS Most cases of viral meningitis begin to improve after several days. Meningitis that has a more chronic course (e.g., with neck stiffness and drowsiness over several days or weeks) may be caused by tuberculosis, another chronic meningeal infection (e.g., cryptococcus, brain abscess, encephalitis), or a general medical condition (e.g., endocarditis). Evacuation will usually be required in these situations. TABLE 33-2  Antibiotics for the Treatment of

Possible Acute Bacterial Meningitis

Suspected Organism

Antibiotic

Unknown pyogenic

Cefotaxime (2 g IV every 4 hr) or ceftriaxone (2 g IV every 12 hr) for 7-14 days

Meningococcus

Benzylpenicillin*

Pneumococcus

Cefotaxime* or ceftriaxone* for 14 days Cefotaxime* or ceftriaxone* for 14 days

Haemophilus

Alternative (e.g., in the case of allergy) Benzylpenicillin (penicillin G; 2.4 g given IV every 4 hr for 7-14 days) with chloramphenicol (50-100 mg/kg/day divided given every 6 hr to a maximum of 4 g/day) Cefotaxime* or ceftriaxone* Benzylpenicillin* for 14 days Chloramphenicol* for 14 days

Doses from Clarke C, Howard R, Shorvon S, et al: Neurology: A Queen Square textbook, Oxford, UK, 2009, Wiley Blackwell Publishing, p. 292. *Dosing information for these medications can be found in the text of this chapter. IV, Intravenously.

The approach to these conditions in a wilderness environment differs little from usual emergency management, although caring for a patient with any impairment of consciousness can be quite challenging in a tent or at sea. Even in the wilderness, drug or alcohol intoxication remains a likely cause of stupor or coma. At altitude, cerebral edema should be considered; the presentation is typically with headache and ataxia that precede coma. In any environment in which hypothermia is a possibility, measure the body temperature. Hypothermic patients look very similar to drug-intoxicated persons, with midpoint reactive pupils and the absence of lateralizing signs. Indeed, these conditions may coexist. Malaria remains the most common cause of coma worldwide.

Transient Cerebral Ischemia and Stroke Stroke, which is defined briefly as an acute focal neurologic deficit that results from vascular disease, is distinctly rare among the typical fit, young, normotensive population that embarks on ventures into remote areas. However, two factors make it essential for a wilderness physician to consider how to manage stroke or TIA. One thing to consider is that increasing numbers of older people take part in wilderness travel and that stroke is a common event among persons who are more than 60 years old. The second reason is more subtle. Transient episodes that might be thromboembolic TIAs are not uncommon, and they often cause diagnostic difficulty. Many of these events turn out to not reflect serious vascular pathology. They are either migrainous as a result of transient hypotension, or, if they occur at high altitude, they may be associated with polycythemia and increased blood viscosity. Thus, an episode that is labeled initially as thromboembolic TIA with a prognosis of nearly 20% of stroke at 3 months may well turn out to have a much more benign cause. Rarely, other brain pathology such as a tumor or a subdural hematoma manifests with a TIA-like event.

DIAGNOSIS OF TRANSIENT ISCHEMIC ATTACK TIAs cause a sudden loss of function, usually within seconds and without a prelude. By definition, they last less than 24 hours, and they usually last only minutes or hours at most (Table 33-3). There is usually no difficulty distinguishing TIA from a focal seizure, because TIA symptoms are usually negative in the sense that there is weakness, visual loss, or aphasia; alternatively, epileptic events cause convulsive movements. Positive visual symptoms (e.g., lights, flashes) and headache point to migraine. Amaurosis fugax, which is defined as a sudden loss of vision in one eye that lasts minutes to hours, can be caused by thromboembolism. For circumstances in which an episode has been witnessed, arterial emboli have been seen to pass through the retinal circulation. Amaurosis fugax also occurs as a migraine phenomenon. An episode of isolated loss of consciousness is rarely if ever caused by TIA. Transient global amnesia or a sudden loss of memory and orientation that lasts minutes to hours is usually not a prelude to stroke and is excluded as a form of TIA.

TABLE 33-3  Features of Transient Ischemic Attacks Anterior (Carotid) Circulation

Posterior (Vertebrobasilar) Circulation

Amaurosis fugax Aphasia Hemiparesis Hemisensory loss Hemianopic visual loss

Diplopia, vertigo, and vomiting Choking and dysarthria Ataxia Hemisensory loss Hemianopic or bilateral visual loss Tetraparesis

MANAGING TRANSIENT ISCHEMIC ATTACK AND STROKE Thorough vascular and cardiac examinations are essential. After a TIA, there are no abnormal neurologic signs. After a stroke, hemiplegia (i.e., profound, total weakness) and aphasia may be evident, or there may be a less severe residual deficit (e.g., hemiparesis). Stroke With a diagnosis of such gravity as stroke, there will be discussion about evacuation. The team doctor should accompany the patient. Carrying a stroke patient over rough terrain may not be a good plan. However, there is no reason why such a patient should not travel by air. After a major or minor stroke, pay special attention to the patient’s airway and swallowing, and give him or her oxygen, if available. Establish a roster of care assistants. Do not leave the patient alone. Remember the need for regular turning, passive physiotherapy, and general encouragement. The underlying cause of a stroke is unlikely to be diagnosed clinically. One simply cannot distinguish reliably on clinical grounds between hemorrhage, infarction, or rarer causes of stroke (e.g., arteriovenous malformation, vasculitis). Cervical arterial dissection is a common cause of stroke among persons who are less than 35 years old, and this sometimes follows head injury or jarring of the neck. Subarachnoid hemorrhage will usually be obvious; it is diagnosed in the presence of sudden headache, impaired consciousness, and neck stiffness, unless the patient has become comatose immediately. Investigation and drug therapy are simplified by wilderness or other remote or austere circumstances. Imaging and speedy thrombolysis are out of the question. With stroke, although there are theoretic discussions about the risk of aspirin worsening a cerebral hemorrhage or the possible complications of giving antiplatelet therapy to a patient with an unsuspected cerebral arteriovenous malformation, the reality is that thromboembolic stroke is the most common cause of stroke, and aspirin (300 mg initially and 75 mg thereafter each day by mouth) may improve the outcome. The National Institute for Clinical Excellence in England recommends the combination of 75 mg of aspirin daily with 200 mg of modified-release dipyridamole twice daily for prophylaxis after thromboembolic stroke; 75 mg of clopidogrel can be used in place of aspirin. Treat excessive levels of hypertension, and aim for a blood pressure of 140/90 mm Hg. Transient Ischemic Attack If one diagnoses a thromboembolic TIA, consider prompt evacuation and further investigation. Give aspirin by mouth (300 mg initially and 75 mg daily thereafter) unless there are contraindications, such as active indigestion, a history of peptic ulcer, or aspirin allergy. Treat hypertension as for stroke.

TRANSIENT ISCHEMIC ATTACK AND STROKE IN SPECIAL CIRCUMSTANCES Sudden neurologic events occur after underwater dives and at high altitude. Diving problems, decompression sickness, and the dangers of syncopal episodes after shallow dives are discussed in Chapter 77. There are numerous case reports of TIA and stroke-like events occurring at altitudes of more than 5000 m (16,404 feet), some in the setting of HACE and others presumably brought on by dehydration and polycythemia caused by chronic hypoxia. With HACE, a stroke-like event may be the first sign of brain edema, and it may occur out of the blue in well-acclimatized climbers at extreme altitudes (i.e., usually above 6500 m [21,325 feet]). This is in contrast with the typical cases of HACE that occur at around 5000 m (16,404 feet) with headaches and ataxia, when there is an apparent failure of acclimatization. Papilledema in a well-acclimatized man at 7600 m (24,934 feet) with sudden ataxia is illustrated in Figure 33-2. Transient TIA-like episodes of aphasia, visual disturbances, and unilateral weakness are also well described, again mostly at extreme altitudes above 6500 m (21,325 feet). 641

CHAPTER 33  Wilderness Neurology

Confusion and Coma

PART 4  INJURIES AND MEDICAL INTERVENTIONS

elbow. This may resolve with the use of an elbow splint and elbow pads and by avoiding leaning on the elbows; however, after it has been established for more than a week, it may require surgical ulnar nerve decompression and transposition.

RADIAL NERVE PALSY: COMPRESSION IN THE SPIRAL GROOVE OF THE HUMERUS The radial nerve lesion known as Saturday night palsy is typically caused when an individual falls asleep with one arm draped over a hard chair. The patient awakes thinking that he or she may have had a stroke. Weakness of wrist and finger extension causes profound disability, but there is typically little or no sensory loss. Weakness almost always resolves spontaneously in about 3 to 6 weeks. FIGURE 33-2  Papilledema in a sherpa climbing at 7600 m (24,934 feet) on Mt Everest’s southwest face in 1975. Photo taken at 6100 m (20,013 feet). (Courtesy Dr. Charles Clarke.)

BACKPACKS: NUMB HANDS, BACKPACK PALSY, AND NEUROGENIC THORACIC OUTLET SYNDROME

1. If someone has a stroke at altitude, use oxygen by mask, if available. Administer 4 mg of dexamethasone by mouth four times daily, reducing this to zero over 5 days. Give 300 mg of aspirin by mouth followed by 75 mg daily unless there are contraindications, such as diabetes, active indigestion, or a history of peptic ulceration. Anticipate the gastrointestinal side effects of indigestion, and administer an H2 antagonist (e.g., 150 mg of ranitidine twice daily by mouth). 2. With a TIA-like event at altitude, hydrate the patient. Consider a short course of dexamethasone, and use aspirin as for stroke at altitude, as described previously. Climbing expedition physicians have performed therapeutic phlebotomy to reduce polycythemia in these situations, which is a reasonable enough practice if it can be performed safely. One withdraws one-half a liter of blood and replaces it with normal saline, with the entire process occurring over the course of 4 hours.

Transient numb and weak hands occur when rucksack shoulder straps are too tight or when a load is too heavy. Symptoms usually resolve within a few days, but occasionally there occurs damage to a branch of the brachial plexus. It is often hard to determine the precise nerve that has been affected. True rucksack or backpack palsy was first described as being caused by the compression of the long thoracic nerve. This is a rarity that causes weakness of the serratus anterior muscle and leads to a “winged” scapula, which is diagnosed when the patient pushes the palm of each hand against a wall; the weak scapula protrudes from the back. Neurogenic thoracic outlet syndrome is a C8 or T1 nerve root lesion caused by a cervical rib or a fibrous band that can become symptomatic as a result of compression by a backpack strap above the clavicle.

Weak and Numb Hands, Foot Drop, Pressure Palsies, Back Pain, and Cervical Disc Disease

Painful tingling of the outer thigh in the distribution of the lateral cutaneous (femoral) nerve of the thigh is common, especially among persons who are obese. It is also sometimes seen when the thigh swells after strenuous exercise. The problem usually resolves over a few days, and no treatment is necessary.

Focal neuropathies, which are caused by local damage to peripheral nerves and focal radiculopathies (i.e., nerve root lesions), are seen frequently in wilderness settings because of unusual postures, uncomfortable sleeping positions, wearing backpacks, carrying gear, excessive exercise, and fluid retention at altitude.

MEDIAN NERVE COMPRESSION AT THE WRIST: CARPAL TUNNEL SYNDROME This common cause of nocturnal tingling in the hands is in a median nerve distribution and involves clumsiness with weakness, typically of thumb movements (e.g., when opening bottles). It is less well known that pain in the forearm is often prominent and that numbness may extend above the wrist or be rather vague and poorly localized. Weakness of the abductor pollicis brevis (i.e., moving the thumb at right angles to the palm) is the earliest motor sign. A wrist splint that holds the wrist in slight extension at night is helpful. Elevation of the arm at night also helps, but this may not be feasible in a tent. Steroid injection into the wrist along the median nerve is not a simple or risk-free procedure. If symptoms persist long term, nerve conduction studies should be advised on return. Surgical carpal tunnel decompression is almost always curative, but it is certainly not meant to occur in the outback.

ULNAR NERVE COMPRESSION AT THE ELBOW Transient tingling in an ulnar nerve distribution is almost universal in uncomfortable beds, and it is of little importance. However, persistent tingling that progresses to a weakness of finger abduction implies substantial compression of the ulnar nerve at the 642

THIGH PAIN AND TINGLING: MERALGIA PARESTHETICA

FOOT DROP: PERONEAL AND SCIATIC NERVE LESIONS Peroneal (lateral popliteal) nerve palsy is the third most common focal motor neuropathy, after compression of the median and ulnar nerves. The peroneal nerve is compressed behind the head of the fibula at the knee. There is foot drop, which is usually noticed after an unusual posture such as squatting. There is profound weakness of the tibialis anterior, extensor hallucis longus, and peroneal muscles. The patient cannot dorsiflex and evert the ankle or extend the great toe. Deep tendon reflexes remain intact. The small patch of numbness above the lateral malleolus is often barely noticeable. The usual course is one of spontaneous recovery over a few weeks. An ankle splint that supports the foot comfortably at a right angle to the tibia may be useful. This cause of foot drop needs to be distinguished from anterior compartment syndrome, which is a surgical emergency. Sciatic nerve palsy, which is caused by pressure in the gluteal region or a misplaced intramuscular injection, causes weakness of the hamstrings and of all muscles below the knee. Transient minor sciatic palsy is the “dead leg” that results from sitting on the edge of an uncomfortable chair and that resolves within minutes. By contrast, established sciatic nerve lesions tend to remain painful.

LUMBAR BACK PAIN: LATERAL AND CENTRAL DISC PROTRUSION Acute low back pain of disc or facet origin is common, and it is discussed in Chapter 21. One valuable emergency treatment is gentle spinal manipulation if pain and circumstances allow. My

CERVICAL DISC LESIONS Acute neck pain is covered in Chapter 21. The potential neurologic sequelae of degenerative cervical disc disease are lateral disc protrusion that causes a cervical root lesion and central disc protrusion that causes spinal cord compression and paraparesis. Lateral cervical disc protrusion can be intensely painful, but it is usually self-limited. Central cervical disc protrusions are frequently painless, may cause no neck symptoms, and are usually progressive; they require urgent specialist treatment.

ACUTE LATERAL CERVICAL DISC PROTRUSION Sudden pain in the neck and down the arm is typical with acute lateral cervical disc protrusion, and neck movement is restricted. Pain may be excruciating and require opiate analgesia. The C7 root is most commonly affected. Root pain radiates to the myotome—in this case, the triceps, muscles deep to the scapula, and the forearm extensors, all of which may be weak—with tingling and numbness in the C7 dermatome, which includes the middle finger. The triceps reflex is also lost. Lay the patient down, and immobilize his or her neck. An inflatable or makeshift neck splint prevents neck motion. Check that all passive upper-limb joint movements are free, and keep exercising the upper limb passively several times daily to prevent stiffness and potential frozen shoulder. The acute pain, which may be intense and require opiates, usually resolves within 1 week. During the days before imaging, these cases would usually only be investigated after several weeks. A minority of these patients require surgery.

NEURALGIC AMYOTROPHY (ACUTE BRACHIAL NEURITIS) This intensely painful condition, which is presumed to be an acute demyelinating brachial plexopathy with an allergic basis, is mentioned because it is frequently misdiagnosed as an acute cervical root lesion. Severe acute pain develops around the shoulder girdle, and is followed by weakness and wasting of the supraspinatus, infraspinatus, deltoid, and serratus anterior muscles, all during the course of a week. Gradual resolution over many months is the rule. Pain may require the administration of opiates. Steroids (e.g., 50 mg of prednisolone for 5 days) are often given, although there is little evidence base for this therapy.

CENTRAL CERVICAL DISC PROTRUSION (CERVICAL MYELOPATHY), CORD COMPRESSION, AND PARAPARESIS The typical presentation of a central cervical disc compressing the spinal cord is of ascending lower-limb numbness, spasticity,

and weakness with loss of bladder control. Spastic paraparesis implies possible spinal cord compression, which is a potential neurosurgical emergency. Although there are many causes of spastic paraparesis, precise diagnosis is impossible in a wilderness setting. Evacuation will usually be mandatory.

CRANIAL NERVE PALSIES AND VERTIGO Cranial nerve VII is by far the most commonly affected, and this is manifested as Bell’s palsy, described later. Loss of the sense of smell is sometimes a sequel to upper respiratory infection. If that is the cause, the ability to smell returns over a few weeks. Anosmia as a result of severance of the olfactory nerves as they pierce the cribriform plate can follow head injury and become permanent. A lesion of any other single cranial nerve usually merits specialist investigation, but this is seldom a neurologic emergency. One exception that requires urgent investigation is a painful oculomotor nerve palsy, when the eye points down and out with a pupil that is large and fixed. Aneurysm of the posterior communicating artery is the diagnosis until proved otherwise. Visual failure is discussed in Chapter 28.

Bell’s Palsy This common acute unilateral facial weakness with a lower motor neuron pattern is probably the result of herpes simplex virus infection. Rare causes include malignant infiltration of cranial nerve VII, sarcoidosis, and seroconversion in a patient with human immunodeficiency virus infection. In practical terms, a patient with Bell’s palsy awakens with unilateral facial weakness and often thinks that he or she may have suffered a stroke. Pain behind the ear is usual. There is drooling from the side of the mouth and inability to close the eye. Unilateral hyperacusis and a loss of taste may be present. Other cranial nerves are unaffected, and there are no other neurologic findings. A useful rule is that facial weakness with anything else is not Bell’s palsy. Spontaneous resolution within 6 weeks is usual in approximately 80% of cases. Essential emergency treatment is to protect the eye by taping the lid closed. Treat superficial eye infection with antibiotic drops or ointment. Drug treatment with oral acyc­ lovir (200 mg by mouth five times daily for 5 days) and steroids (a 5-day course of 60 mg of oral prednisolone daily) is often given. Bell’s palsy often causes alarm because of its unsightly appearance, and there is often pressure to treat, despite a lack of evidence base for drugs making much of a difference.

Acute Vertigo Sudden rotary vertigo is a distinctly unpleasant symptom; the distress that it causes usually outweighs the seriousness of any underlying condition. Vestibular neuritis (VN) is a presumed viral infection and thus in one way similar to Bell’s palsy. VN causes severe prostrating rotary vertigo with vomiting. Jerk nystagmus (i.e., oscillating fast– slow nystagmus) is typically present. Severe symptoms last for a few days before their gradual resolution. Vestibular sedatives (e.g., 15 mg of cinnarizine every 6 hours) are sometimes helpful for reducing the severity of the vertigo. Benign paroxysmal positional vertigo (BPPV) is believed to be caused by loose otolith fragments in the semicircular canals. The onset of rotary vertigo is typically sudden and provoked by head movement (e.g., rising from bed). Neurologic examination is typically negative until positional testing is carried out. To carry out positional testing, the patient is positioned sitting upright on a chair. The examiner holds the patient’s head and moves the patient’s body briskly so that the patient’s head and trunk become horizontal, first to one side and then to the other. For patients with BPPV, this provokes vertigo and rotary nystagmus that fatigues. The ear that is lowest usually contains the affected semicircular canal (labyrinth). To treat BPPV, various particlepositioning maneuvers have been developed in which the head is moved into and held in a dependent position. These are sometimes curative immediately, and they are safe and well 643

CHAPTER 33  Wilderness Neurology

preferred method is to lay the patient supine on a firm, flat surface. Examine the patient neurologically, and check hip, knee, and ankle joint movements. Sitting astride the supine patient, grasp one knee and thigh in a firm but gentle elbow lock. Firmly flex and rotate the hip so that the patient’s flexed knee, which is held in your elbow, points toward the opposite hip of the patient. Although this is primarily a treatment for facet joint problems, it is generally worth trying. Keep all patients with back pain active if at all possible. Lateral lumbar disc protrusion typically causes an L5 or S1 nerve root lesion. There is acute low back pain, sciatica, and a limitation of straight-leg raising. The ankle jerk is lost with an S1 lesion. With an L5 lesion, extension of the great toe becomes weak. The usual course, even when there is substantial weakness, is for spontaneous recovery that occurs over days to weeks. When weakness is progressive, emergency surgery may be required, so evacuation is advisable. Central lumbosacral disc protrusion is a distinctly uncommon surgical emergency. Back pain is followed by sacral and perineal numbness and flaccid weakness of the lower limbs, usually for several hours, with the retention of urine; this is known as cauda equina syndrome. Even with prompt surgery, many of these patients have residual deficits and thus should be evacuated.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

worth trying. Lay the patient down supine, with his or her head protruding over an “examination couch” of some kind. Support the head in both hands, and turn the head gently so that the affected labyrinth is lower. Briskly extend the patient’s neck for a few seconds, and then lift the patient back to the upright position. Vestibular sedatives (e.g., 15 mg of cinnarizine every 6 hours) are of limited value for the treatment of BPPV, but they are often prescribed anyway. Vertigo may occur as part of migraine and also with Ménière’s disease, with the latter involving attacks of tinnitus and deafness. Structural or vascular disease of the brainstem and the vestibular system can also cause vertigo, but it rarely occurs in isolation from other symptoms. Working guidelines for vertigo are as follows: • The diagnosis is likely to be VN or BPPV if there are no other neurologic symptoms or signs. • If there are additional signs (e.g., cerebellar ataxia, diplopia), urgent investigation and evacuation may be necessary, because a structural lesion such as infarction, tumor, or demyelination is likely. • In the absence of additional signs, first completely examine the patient. If there are nystagmus and sustained vertigo without other neurologic signs, then the diagnosis is likely to be VN. Most cases of vertigo are improved by head movement, so keep the patient as active as possible. • If there is neither vertigo nor nystagmus at rest without other neurologic signs but one can elicit provoked positional vertigo or nystagmus, BPPV is the likely diagnosis. Try the postural treatment maneuver described previously. If this does not cure the problem immediately, repeat the procedure more vigorously, because this may dislodge the otolith fragment.

Preexisting Neurologic Conditions During the last 20 years, there have been substantial changes in the prevailing attitude toward people with chronic diseases taking part in many sports and participating in adventurous activities that entail risk. We have moved from a proscriptive attitude, when many people who suffered from chronic illness were dissuaded from participating, to one where participation is actively encouraged. The overall experience gained suggests that the harmful effects of the wilderness environment are few and that, in general, any medical risks (i.e., those that would cause an underlying condition to become worse or cause death) are outweighed by the usual risks of operating in a hostile environment. For example, the environmental dangers of avalanche, rockfall, crossing glaciers, desert travel, or sailing are generally accepted as part of the activity, and appropriate precautions are taken. High risk is clearly apparent when mountaineering at extreme altitudes, where death rates of entirely fit lead climbers can be 5%; this is a daunting figure. To put matters in perspective, such risk levels far outweigh the chances of most chronic medical conditions deteriorating in any serious way. On the positive side, one sees wilderness activities enhancing the lives of people with disabilities and chronic illnesses as well as broadening their horizons. Many years ago, I signed with trepidation a medical-fitness form to agree that a 20-year-old woman with seizures and hydrocephalus was healthy enough to crew in The Tall Ships Race; I recall the joy in her eyes when she returned. When giving advice, one should be encouraging but carefully outline the risks. Established neurologic conditions rarely cause substantive problems. People who have epilepsy, brain tumors, multiple sclerosis, and cerebrovascular disease may take part in mountain expeditions. In one instance, a climber with a cerebral glioma went to Mt Everest and participated up to 7000 m (22,966 feet). There are no absolute rules. There is a range of medical opinions, and there are different ethical and cultural approaches to consider. Issues of potential medical malpractice need to be addressed as well. Travel insurance companies are often reluctant to accept any increased level of risk and may deny policies to these individuals. 644

EPILEPSY Well-controlled epilepsy should not be a bar to wilderness activity. The general risk assessment must include the question of danger to the patient as well as to other members of the party. Rock climbing, sea kayaking, and diving (other than snorkeling in company) are usually prohibited. For example, when a patient with a history of seizures is assessed for suitability to join a trek at altitudes of 4500 to 5500 m (14,764 to 18,045 feet), consider the following: • Certainty of diagnosis. Epilepsy tends to be overdiagnosed. Have all appropriate investigations (e.g., electroencephalography, imaging) been carried out? Has there been a diagnostic assessment by a specialist in epilepsy? If not, suggest one. • Seizure control. More than one seizure every few months, previous status epilepticus, and poor drug compliance would be reasons to reject an applicant for participation in most wilderness activities. • Liaison with the treating neurologist. This is done to achieve recommendations about further antiepileptic drug treatment in the event of a seizure. There is no evidence that seizures are provoked by exercise, acute mountain sickness, or cerebral edema.

CEREBROVASCULAR DISEASE Hypertension that is well controlled at home usually remains so in wilderness settings and at altitude. Patients who have recovered well after ischemic or hemorrhagic stroke do not appear to be at any increased risk. I know of several cases of professional mountaineers who have returned to climbing after recovery from a minor stroke. In my experience, two areas cause particular difficulty. One is the applicant to an expedition who may have had a previous TIA. Some difficulties with reaching a diagnosis have been outlined previously. My advice and practice are as follows: • To ensure that the problem was fully investigated, one should review the original notes and any subsequent vascular images, carotid ultrasound studies, and cardiac assessments. • It is reasonable to accept that stroke risk is low if investigations were both detailed and negative and if the TIA event took place more than 6 months previously. With a more recent unexplained (and presumed thromboembolic) TIA, I feel uneasy, especially if the event was in a carotid artery distribution. I would tend to caution the applicant, including perhaps recommending against the wilderness activity. A second specific situation relates to a previous TIA-like event that has taken place at high altitude (usually over 7000 m [22,966 feet]). This quandary is not uncommon, and examples include transient hemiparesis or aphasia on a previous expedition. Should the patient once again travel to a high altitude? Such events can be caused by hyperviscosity, by incipient brain edema, or occasionally by thromboembolism, or they may have a benign cause such as migraine. Practical Guidelines: 1. The typical mountaineer understands the major risks and is in general averse to restrictive advice. If it is explained that the medical risks are far smaller than the physical and environmental risks, he or she will usually go climbing and overcome any hesitation related to a potential medical problem. 2. Conversely, the typical trekker is on holiday and generally risk averse. If one explains that there are, for example, risks of cerebral edema or stroke, most casual recreationists adopt a cautious attitude.

Multiple Sclerosis, Parkinson’s Disease, and Other Degenerative Conditions Multiple sclerosis patients run marathons and take part in many wilderness activities. With relapsing and remitting multiple

sclerosis, a relapse is likely to be manageable in the field with rest, steroids, and the treatment of any infection. For patients with chronic progressive multiple sclerosis, a significant increase in disability is unlikely during an expedition. Each case must be assessed individually, with clear explanations given regarding the potential lack of hospital treatment. Disability caused by multiple sclerosis sometimes worsens with heat; this is known as Uhthoff’s phenomenon. This is the result of slow conduction in nerve-fiber pathways that have been stripped of myelin. This is a temporary problem, and it occurs as body temperature increases. Weakness, ataxia, and visual symptoms may be provoked by strenuous exercise, exposure to high environmental temperature, or fever. Problems settle within a matter of hours with rest and cooling. Patients with Parkinson’s disease who have the condition in a mild form have normal exercise tolerance and preserved motor skills, and sometimes they are able to rock climb at a high standard; such exercise may in fact be emotionally therapeutic. Just as other neurodegenerative conditions do not prevent an active

lifestyle, automatic restrictions should not be placed on these patients. To put matters another way, for patients with progressive conditions that in due course will be fatal, the physician can sometimes suggest a life-enhancing experience that can help make the patient’s life more challenging, uplifting, and worthwhile. In my experience, patients and their relatives seldom mention the possibility of taking part in an adventure activity or of pursuing a long-dreamed-of journey. This is an area that it is well worth the physician exploring. The wilderness may be a hostile environment, but it may provide immense pleasure. We should make every effort to offer its potential rewards to enthusiastic and willing persons who are chronically ill.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 34 



Chronic Diseases and Wilderness Activities COLIN K. GRISSOM, ANDREW M. LUKS, AND THOMAS G. DELOUGHERY

The focus of this chapter is on the prevention and treatment of complications due to chronic medical conditions during wilderness activities. For the purposes of this chapter, wilderness activities are defined as any excursion into an outdoor environment where usual medical services are not available, and include outings ranging from a day to several months. Wilderness activities may occur close to home, in the country of residence, in foreign developed countries, or in foreign developing countries. Issues relating to chronic medical conditions during wilderness activities are important to primary care and specialty physicians because patients often seek advice on whether a certain wilderness trip or activity is appropriate, given their medical condition, and how they should manage their disease while in the wilderness. Medical problems may occur during wilderness activities as a result of an acute injury, acquired infectious illness, or environmentally caused illness (heat, cold, or high-altitude illness). A preexisting medical condition may also cause complications during a trip or activity or may predispose the patient to environmentally caused illness. The few studies that report the epidemiology of medical problems in the wilderness show that most are due to traumatic injuries, and most deaths are due to falls or drowning.46,68,121 Cardiac disease is the most common medical illness that causes death in the wilderness. Cardiac disease, asthma, and diabetes are also reported as causes of medical illness during wilderness activities. Medical illness due to environmental exposure, such as heat, cold, or altitude illness, depends on the environment.46,96 The first issue to consider in evaluating a patient with a chronic medical condition who is planning a wilderness trip or activity is how the environment will affect the patient and his or her medical condition. In a wilderness environment, patients with chronic medical conditions will potentially be exposed to heat, cold, high altitude, and a greater level of exercise. Wilderness activities occur in remote areas where medical care is impossible to obtain. These factors require evaluation in relation to the patient’s chronic medical condition. First, the physician and patient need to address whether the planned wilderness activity is appropriate for the patient. Second, the physician should

provide advice to the patient on how to manage his or her medical condition in the remote wilderness environment. Deciding on whether a potential wilderness activity is appropriate for a patient is a shared responsibility between the physician and patient. “Wilderness” implies that medical care will be remote, so if a major medical problem arises, the consequence may be severe or even include risk for death. Risk is an inherent part of any wilderness activity, so persons who venture into the wilderness should make conscious decisions about acceptable levels of risk and how they can exercise good judgment to reduce those risks. The same process is used with regard to a chronic medical condition: acknowledging risk, deciding whether it is acceptable, and changing behavior to minimize risk. Although it is important for the physician to help the patient understand issues and to make medically responsible recommendations, he or she should recognize patient autonomy and leave most decisions to the patient.

Considerations for Wilderness Travel INCREASED PHYSICAL ACTIVITY Although some wilderness activities are of the sedentary variety (e.g., car-based safaris), many other activities involve physical exertion. The level of exertion may be comparable with that which the person already performs on a regular basis but may, in some cases, involve more activity than the person’s typical baseline. As a result, all wilderness travelers with underlying medical problems must consider the level of activity on their planned trip and whether they are capable of doing the work necessary for that activity. Many commercial outfitters label trips with a difficulty rating that takes into account the level of exertion, remoteness, and exposure to high altitude. Ratings generally include easy, moderate, and strenuous categories. This can be useful to the physician evaluating the patient before the trip, especially if the physician is not familiar with the environment

For online-only figures, please go to www.expertconsult.com

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PART 4  INJURIES AND MEDICAL INTERVENTIONS

or the activity that will be pursued, although the physician must be aware that these ratings are not based on hard criteria and what constitutes a “moderate” trip for one company may be labeled as a “strenuous” trip by another. Some companies that offer adventure trips require potential clients to complete a medical history questionnaire and may also have a consultant physician review the questionnaire and provide advice to select clients.77,78 Erb47 has developed a scale of trip difficulty and correlated that with objective parameters of exercise capacity required to complete that type of activity (see Table 101-2, Chapter 101). “Extreme-performance ventures” are the most physically demanding and require above-average exercise capacity for participation. This category would include activities such as mountaineering at high altitude and alpine climbing. “Highperformance ventures,” such as high-altitude trekking or hunting, or jungle trekking are the next most demanding category of activities and require an average exercise capacity. The third level of wilderness trips, “recreational activities” requires just belowaverage exercise capacity and includes activities such as hiking on mild-moderate terrain in a variety of environments. The last category of wilderness trips is “therapeutic activities,” which may be appropriate for persons with chronic cardiovascular or pulmonary disease that limit activity. Even though Erb defines categories of wilderness trips and assigns objective exercise capacity parameters to them, formal cardiac stress testing or cardiopulmonary exercise testing is not required in most cases to determine if a patient has adequate exercise capacity to complete a planned wilderness trip. The most important predictor is successful completion by the patient of similar activities in the past. Still, formal cardiopulmonary exercise testing may be useful in patients with chronic medical conditions to define maximum exercise capacity objectively to select the appropriate level of a wilderness trip. This helps to ensure a more enjoyable and safe experience for patients and their trip partners.

COLD

TRIP PREPARATION

HEAT

Patients with chronic medical conditions have an obligation to inform the other people involved in a trip, or the trip leader in the case of a commercial trip, about medical issues that might affect their ability to complete the planned itinerary. This is important because chronic medical conditions may influence not only the patient but also other members of the party. Notification will allow the trip leaders or other participants to anticipate situations in which the underlying medical problem may worsen, facilitate monitoring of the patient’s condition, and allow preparations to alter the group’s plans or arrange an evacuation when serious problems arise. It is also important that everyone in the group accept the limitations of a chronic medical condition and make conservative decisions during the trip that prevent the patients from overexerting themselves. Pretrip preparation includes identifying the closest medical facility and resources available should evacuation become necessary. Rescue insurance and repatriation medical insurance are available and should be strongly considered by the patient. Patients should carry an adequate supply of medications and keep medications with them at all times to ensure that they do not become lost (e.g., pack in carry-on baggage rather than checked baggage). Patients should travel with a list of their medications and a concise list of their medical issues, including a baseline electrocardiogram for patients with cardiac problems, and contact information for their regular health care providers. They must also recognize that in remote settings they may encounter facilities not equipped for or physicians lacking experience dealing with complex medical problems.

Peripheral vasodilation is a primary response to heat exposure that leads to sweat production and evaporative heat loss. In highhumidity conditions, however, heat loss from sweating is diminished. Radiant heat loss has no usefulness when environmental temperature exceeds skin temperature. Unlike cold adaptation, heat adaptation depends more on physiologic acclimatization than on behavior. Prior heat exposure reduces the skin temperature at which vasodilation and sweating occur, thus initiating cooling earlier. Physical training improves heat tolerance through the same mechanisms and improves efficiency of the cardiovascular system. Poor physical fitness, obesity, lack of heat acclimatization, and dehydration decrease heat tolerance. Chronic medical conditions increase the risk for heatstroke, whereas increased temperature may exacerbate chronic medical conditions: • Diabetes (the disease may predispose to dehydration whereas dehydration may increase the risk for hyper­ glycemia) • Cardiovascular disease (limited cardiac output in the face of peripheral vasodilation decreases heat tolerance and may lead to syncope or presyncopal symptoms) • Skin disease (inadequate sweating predisposes to heatstroke) • Anticholinergic drugs or diuretics (decrease heat tolerance) • Sickle cell trait (increased risk for heatstroke and rhabdomyolysis with physical exertion) • Obesity (low ratio of body surface to mass increases risk for hyperthermia) Susceptible individuals can improve heat tolerance through a program of heat acclimatization before or during their trip.5 Before a wilderness trip to a hot environment, exercising daily in the heat for limited periods of at least 1 hour’s duration for at least several days improves heat tolerance. If such pretrip training is not feasible, then the individual should restrict exertion to limited periods during cool parts of the day for the first week of the trip. Regardless of the acclimatization program, once a trip commences, individuals should maintain volume status through adequate intake of water or electrolyte drinks with copious clear urine output being a good indicator of adequate hydration status.

Environmental Extremes and Chronic Medical Conditions Thermoregulation, hypothermia, heat illnesses, and high altitude are extensively reviewed elsewhere in this textbook. For the purpose of understanding how these environmental extremes might affect chronic medical conditions, some key points are worth emphasizing. 646

Exposure to cold causes peripheral vasoconstriction, increased systemic blood pressure, and tachycardia and, as a result, increases myocardial oxygen consumption. When core body temperature drops below normal, shivering ensues as a metabolically demanding activity that occurs as a means to generate heat and defend against further drops in temperature. Although such physiologic responses are important for protecting the individual, learned behavioral responses, such as avoiding moisture or donning dry clothing, also play an important role during cold exposure. Even with appropriate preparation, however, some chronic medical conditions still increase the risk for accidental hypothermia or frostbite. Alternatively, cold conditions may exacerbate the underlying chronic medical condition. Situations in which such problems may arise include the following: • Cardiovascular disease (angina or congestive heart failure may occur because of increased systemic vascular resistance, afterload, and myocardial oxygen demand) • Hypertension (exacerbated by cold-induced peripheral vasoconstriction) • Peripheral arterial disease (increased risk for frostbite) • Raynaud’s phenomenon (increased frequency of Raynaud’s attacks and potentially increased risk for frostbite) • Asthma (cold air– and exercise-induced bronchospasm) • Older adults (impaired thermogenesis) • Endocrine disease (impaired thermogenesis) • Iron deficiency (impaired thermogenesis) • Neuromuscular disease (impaired shivering thermo­genesis) • Malnutrition (decreased body surface area to mass ratio increases risk for heat loss and hypothermia) • Diabetes (hypoglycemia may impair thermogenesis; peripheral neuropathy may predispose to cold injury)

HIGH ALTITUDE The primary physiologic insult at high altitude is hypobaric hypoxia. This leads to a decrease in the partial pressure of inspired oxygen (PIO2), which in turn leads to drops in the alveolar and arterial PO2. For persons with normal gas exchange, significant decreases in arterial oxygen saturation will not occur on acute exposure until they are higher than approximately 3000 m (9,843 feet), because of the sigmoidal shape of the oxyhemoglobin dissociation curve. In acclimatized individuals, arterial oxygen saturation (SaO2) decreases below 90% at elevations above approximately 3500 m (11,483 feet). Any individual with gas exchange abnormalities or right-to-left shunts at sea level may become very hypoxemic at significantly lower elevations, whereas individuals with diseases exacerbated by hypoxia (e.g., severe coronary artery disease or heart failure) may have significant problems in this environment as well. Regardless of their underlying health status, all individuals undergo physiologic responses that facilitate acclimatization to hypobaric hypoxia. Individuals with certain chronic conditions, however, may either fail to mount these responses or may suffer adverse consequences as a result of the responses. For example, low arterial PO2 triggers an increase in minute ventilation, referred to as the hypoxic ventilatory response. This response, which occurs within hours of ascent to altitudes greater than 2000 m (6562 feet) and varies in magnitude between individuals, helps to raise alveolar and arterial oxygen tensions and may affect susceptibility to altitude illness. Persons with chronic diseases that restrict ventilatory capacity (e.g., very severe chronic obstructive pulmonary disease [COPD], obesity hypoventilation syndrome, and neuromuscular diseases with respiratory system involvement) may be unable to raise their minute ventilation and may experience severe hypoxemia and exercise intolerance. Low alveolar oxygen tensions also trigger hypoxic pulmonary vasoconstriction and a rise in pulmonary artery pressure. The response is seen above 2,000 m (6562 feet) in elevation and varies in magnitude between individuals. Most people tolerate the rise in pulmonary artery pressure, but individuals with underlying pulmonary hypertension or right-to-left shunts may be at risk for high-altitude pulmonary edema, worsening right heart function, or increased hypoxemia. Important cardiovascular responses also occur that may not be tolerated well by all individuals. Increased sympathetic tone occurs acutely after ascent to high altitude and increases heart rate and blood pressure. Heart rate and blood pressure gradually decrease over several days at high altitude, but remain higher than sea level baseline values for the duration of stay at high altitude. Despite the increase in sympathetic tone, most persons with mild to moderate cardiovascular disease do well after ascent to moderate altitudes of approximately 2500 m (8202 feet),99,137 although individuals with unstable angina, severe cardiomyo­ pathy, or poorly controlled hypertension might not tolerate such changes. Increased erythropoiesis is a long-term adaptation to high altitude requiring weeks to complete that increases red cell mass and oxygen-carrying capacity of the blood. Persons with severe iron deficiency or chronic marrow suppression are unable to increase erythropoiesis to complete the normal long-term hematologic acclimatization. The following chronic diseases may worsen at high altitude or predispose to impaired tolerance of hypobaric hypoxia: • COPD (inadequate ventilatory acclimatization, worsened hypoxemia) • Asthma (potential for exacerbation due to hyperventilation of cold, dry air) • Cardiac disease (cardiac ischemia or congestive heart failure precipitated by hypoxia) • Pulmonary hypertension (hypoxia precipitates rise in pulmonary artery pressure that may predispose to high-altitude pulmonary edema or worsening right heart function)

• Obesity (hypoventilation increases risk for hypoxemia and high-altitude illness) • Neuromuscular disease (respiratory muscle involvement impairs ventilatory responses and acclimatization) • Hematologic disease (hypoxia may worsen sickle cell disease, thalassemia; anemia or marrow suppression can impair erythropoietic responses)

Chronic Medical Conditions and Wilderness Travel ASTHMA Asthma is a disorder of reversible airflow limitation marked by the presence of cough, wheezing, chest tightness, and shortness of breath. Affected individuals can have long symptom-free periods punctuated by exacerbations and worsening symptoms that are often triggered by stimuli such as respiratory infections, exercise, or allergen exposures. Given the high prevalence of the disorder in the general population, it is likely that many wilderness travelers suffer from this disorder. Despite this fact, little data are available as to how wilderness travel affects these patients. In the only prospective study of asthma patients engaged in wilderness travel, Golan and colleagues66 studied 203 patients with mild to moderate asthma presenting to a travel clinic before departure. Forty-three percent of these individuals reported an exacerbation during their trip, whereas 20% reported worsening asthma control and 16% reported the worst exacerbation of their life. The leading risk factors for exacerbations during the trips were frequent rescue inhaler use (>3 times per week) before the trip and participation in intensive physical activity during the trip itself. Pretrip exercise testing with pretest and post-test spirometry was not useful in predicting which patients would develop an exacerbation. Because the potential for exacerbations exists and pretrip identification of patients likely to experience such problems is difficult, all asthma patients should strongly consider pretravel evaluation to ensure that their disease is under adequate control at the time of their trip and to establish the means to monitor for and respond to exacerbations. Treatment of a patient with asthma planning a wilderness activity should begin with the basic elements of treatment for any patient with asthma: monitoring of symptoms, pharmacologic therapy, avoidance of triggers, and patient education. A pretrip evaluation for asthma is an opportunity to ensure that the patient has optimal baseline treatment for asthma, which will also help prevent asthma attacks during the sojourn. Although not necessary before every short day-long or weekend excursion, such evaluations should take place before any long trips, particularly those to international and/or remote destinations. The first part of this evaluation is to review the state of the patient’s current symptoms and determine if the patient is on the appropriate pharmacologic regimen. The National Institutes of Health’s Guidelines for the Diagnosis and Management of Asthma118 provides definitions of categories of severity for patients with asthma and the appropriate treatment (Box 34-1 and Table 34-1). Pretrip evaluation for a patient with asthma should include a review of these guidelines in relation to the patient’s symptoms and consideration of escalating therapy before a wilderness trip. For example, a patient who usually uses inhaled bronchodilators only on an as-needed basis for mild persistent asthma may consider adding an inhaled corticosteroid for improved control, although this practice has never been formally studied for wilderness travel. Because a primary trigger for asthma on a wilderness trip may be exercise, consideration can be given to adding the leukotriene receptor blocker montelukast to the patient’s controller regimen, because this has been shown to be effective adjunctive therapy for exercise-induced asthma.97 Patients can also use short-acting β2 agonists before and during exercise.114 Individuals reporting worsening control or who are in the midst of a severe exacerbation should strongly consider postponing their trip until symptoms are under better control. As noted above, many exacerbations are triggered by identifiable factors such as allergens, respiratory infections, irritants, 647

CHAPTER 34  Chronic Diseases and Wilderness Activities

Individuals engaged in prolonged bouts of exercise (lasting several hours or more) should supplement water intake with meals or salty foods to maintain electrolyte balance and prevent hyponatremia.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

BOX 34-1  Classification of Asthma Severity in Patients

12 Years of Age and Older

Mild Intermittent (Step 1 Treatment) Symptoms <2 days/wk Nights with symptoms: <2/mo Short-acting β-agonist use <2 days/wk No interference with normal activity Normal FEV1 between exacerbations FEV1 >80% predicted FEV1/FVC normal Mild Persistent (Step 2 Treatment) Symptoms >2 times a wk but less than daily Nights with symptoms: 3-4/mo Short-acting β-agonist use >2 days/wk but not daily and not more than once per day Minor limitation of normal activity FEV1 >80% predicted FEV1/FVC normal Moderate Persistent (Step 3 Treatment) Daily symptoms, exacerbations affect activity Daily use of short-acting β-agonist Nights with symptoms: >1 wk but not nightly Some limitation of normal activity FEV1 >60% but <80% FEV1/FVC reduced 5% Severe Persistent (Step 4 or 5 Treatment) Continual symptoms throughout the day, limited physical activity Frequent exacerbations Extremely limited activities Nights with symptoms: often 7/wk Short-acting β-agonist use several times per day FEV1 <60% predicted FEV1/FVC reduced >5% FEV1, Forced expiratory volume in 1 second; FVC, forced vital capacity. Modified from National Asthma Education and Prevention Program: Expert panel report 3 (EPR-3): Guidelines for the diagnosis and management of asthma—summary report 2007, J Allergy Clin Immunol 120:S94, 2007.

chemicals, exercise, and emotional stress. The pretravel assessment also provides an opportunity to review the triggers that could contribute to worsening control during the trip. Patients should realize, however, that on certain wilderness trips it may be difficult to avoid certain triggers, such as breathing cold, dry air during exercise on a mountaineering expedition. In such cases, effort can be made instead to minimize exposure by, for example, wearing and breathing through a balaclava or pretreating with asthma medications before exertion. Asthma patients should also anticipate exposure to triggers that might not be an issue at home. For example, adventure travel often requires transit through major international cites, such as Bangkok, Thailand, or Kathmandu, Nepal, where local air quality may be poor and contribute to worsening control before the actual adventure activity begins. Another important part of the pretravel assessment is to devise a program for objectively monitoring disease status during the trip. Asthma patients commonly monitor asthma control using measurements of peak expiratory flow (PEF), an objective parameter measured after the patient inhales to total lung capacity and then forcefully exhales into a peak flow meter. Patients establish their baseline peak flows when their disease is under good control by performing the maneuver several times a day and recording the results in a diary. Typically, PEF is highest in the morning and lowest in the afternoon. The highest measured PEF becomes the baseline for the patient, and comparison of further measurements with that baseline can be used to identify disease exacerbation and therefore escalate therapy. The National Institutes of Health’s Guidelines for the Diagnosis and Management 648

of Asthma118 recommends using a zone scheme for categorizing results of PEF: green is a PEF greater than 80% of personal best, yellow is a PEF 50% to 80% of personal best, and red is a PEF less than 50% of personal best. A PEF in the green zone indicates the patient should continue maintenance medications, whereas a PEF in the yellow or red zone requires adjustments in treatment according to a predetermined plan, as well as seeking evaluation by a physician. This type of self-monitoring could easily be used on a wilderness trip. For example, a predetermined treatment plan for PEF in the yellow zone associated with symptoms of asthma might include acute treatment with an inhaled short-acting β2-adrenergic agonist followed by reevaluation in 1 hour, and if not improved to the green zone, initiation of oral corticosteroids and an increase in the dose of inhaled corticosteroids. A treatment plan for PEF in the red zone associated with symptoms of an asthma exacerbation would specify immediate therapy with inhaled β2 agonists, to be repeated at frequent intervals, and initiating an oral corticosteroid. Persistent symptoms associated with PEF in the red zone suggest that evacuation from the wilderness environment should be initiated. An alternative to peak-flow monitoring is the PiKo-1, which measures both PEF and forced expiratory volume in 1 second (FEV1). This electronic device has a 2-year battery life and is small and easy to pack. Patients should be aware that the PiKo-1 and PEF meters, particularly variable orifice peak flow meters, may generate readings significantly lower than actual PEF under conditions of cold temperatures or high altitude.127,132 If concern exists about such problems on a trip, the individual should rely on an assessment of trends in the measured PEF rather than the absolute values. In addition to devising a monitoring plan and means for recording the data (e.g., an asthma diary), the health care TABLE 34-1  Stepwise Approach to Managing

Asthma in Patients 12 Years of Age   and Older

Intermittent Asthma Short-acting β2-agonist as needed Persistent Asthma Step 2 Preferred: Low-dose inhaled corticosteroid Alternative: Cromolyn, leukotriene receptor antagonist, nedocromil, or theophylline Step 3 Preferred: Low-dose inhaled corticosteroid plus long-acting β2-agonist OR medium-dose inhaled corticosteroid Alternative: Low-dose inhaled corticosteroid plus either leukotriene receptor antagonist or theophylline Step 4 Preferred: Medium-dose inhaled corticosteroid plus long-acting β2-agonist Alterative: Medium-dose inhaled corticosteroid plus either leukotriene receptor antagonist or theophylline Step 5 Preferred: High-dose inhaled corticosteroid plus long-acting β2-agonist AND consider omalizumab for patients who have allergies Step 6 Preferred: High-dose inhaled corticosteroid plus long-acting β2-agonist plus oral corticosteroid AND consider omalizumab for patients who have allergies Each step: Patient education, environmental control, and management of comorbidities. Steps 2-4: Consider subcutaneous allergen immunotherapy for patients who have allergic asthma. Quick relief of symptoms for all patients: Short acting β2-agonist as needed for symptoms. Intensity of treatment depends on severity of symptoms: up to three treatments at 20-min intervals as needed. Short course of oral systemic corticosteroids may be needed. Use of short-acting β2-agonist >2 days/wk for symptom relief (not prevention of exercise-induced bronchospasm) generally indicates inadequate control and the need to step up treatment. Step down if possible if asthma is well controlled at least 3 mo. Step 1

Modified from National Asthma Education and Prevention Program: Expert panel report 3 (EPR-3): Guidelines for the diagnosis and management of asthma—summary report 2007, J Allergy Clin Immunol 120:S94, 2007.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE COPD is a syndrome of progressive airflow limitation caused by chronic inflammation of the airways and lung parenchyma with

a prevalence of approximately 4 to 7 per 1000 persons in developed countries.6 The extent to which COPD limits an individual’s planned wilderness activities is a function of disease severity, assessment of which can be made using criteria specified by the Global Initiative for Chronic Obstructive Lung Disease (GOLD).133 According to these guidelines, disease severity is graded based on the decrement in the patient’s postbronchodilator FEV1 of a forced vital capacity (FVC) maneuver (Table 34-2). Patients who fall in the mild disease category (FEV1 ≥80% predicted) will probably do well on a wilderness activity, provided the planned activity does not far exceed their usual exercise tolerance. Once patients meet the criteria for moderate disease (FEV1 50% to 80% predicted), careful evaluation is warranted to determine their suitability for the planned activity. Cardiopulmonary exercise testing4 should be considered to determine exercise capacity, which can then be compared with the expected level of exertion on the planned trip. Of note, patients whose disease may not appear too severe based on their pulmonary function test results may have significant air trapping during exercise that impairs pulmonary mechanics and leads to significant exercise limitation.124Patients in the severe (FEV1 30% to 50% predicted) or very severe (FEV1 ≤30% predicted) categories, or those with carbon dioxide retention or right heart failure, should be advised against any wilderness activity in which exertion above their baseline level of tolerance is expected, or if the planned trip is to a higher altitude than their current residence. Such patients may, however, tolerate car or horse-led activities such as safaris or fishing that do not require much in the way of physical exertion. In considering suitability for travel, it is important to remember that many patients with COPD have comorbid conditions, such as coronary artery disease, that may also affect their tolerance for a planned activity and that will require attention in the pretravel assessment. Once a decision is made that a patient can undertake a given activity, pretrip pulmonary evaluation is warranted to evaluate several important aspects of disease management around the time of the trip. The first element of this evaluation is to review the patient’s pharmacologic regimen. Inhaled bronchodilators (selective β2-agonists or anticholinergics) are the foundation of pharmacotherapy for COPD because of their capacity to alleviate symptoms, decrease frequency of disease exacerbations, and improve exercise tolerance by decreasing hyperinflation and airflow limitation.25,157 These medications have clear benefits, even in patients who may not meet official pulmonary function testing criteria for bronchodilator responsiveness (increase in FEV1 or FVC by 200 mL and 12% compared with prebronchodilator testing). As indicated in Table 34-2, patients with mild disease are typically on a regimen of short-acting bronchodilators used on an as-needed basis. The selective β2-agonist albuterol and the anticholinergic ipratropium bromide are equally effective for this purpose.157 In addition to as-needed short-acting bronchodilators, there is a need for patients with moderate disease severity to be started on scheduled long-acting bronchodilator therapy with either a long-acting β-agonist (salmeterol or formoterol) or the

TABLE 34-2  Global Initiative for Chronic Obstructive Lung Disease (GOLD) Classification of Severity of COPD

and Therapy

Stage 0: At Risk

Stage I: Mild

Stage II: Moderate

Stage III: Severe

Chronic symptoms Risk factors Normal spirometry

FEV1/FVC <0.7 FEV1 ≥80%

FEV1/FVC <0.7 50%≥ FEV1 ≤80%

FEV1/FVC <0.7 30%≤ FEV1 ≤50%

Stage IV: Very Severe FEV1/FVC <0.7 FEV1 ≤30% Or FEV1 ≤50% with chronic respiratory failure (PaO2 <60 mm Hg with or without PaCO2>50 mm Hg on room air at sea level)

Avoidance of risk factors; influenza vaccination Add short-acting bronchodilator when needed Add regular treatment with one or more long-acting bronchodilators, and add rehabilitation Add inhaled corticosteroids if repeated exacerbations Add long-term oxygen if chronic respiratory failure Consider surgical treatments

Modified from Rabe KF, Hurd S, Anzueto A, et al: Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary, Am J Respir Crit Care Med 176:532, 2007. COPD, Chronic obstructive pulmonary disease; FEV1, forced expiratory volume in 1 second, reported as percentage predicted; FVC, forced vital capacity.

649

CHAPTER 34  Chronic Diseases and Wilderness Activities

provider should observe the patient’s inhaler technique and correct any deficiencies, because inhaled medications are of less benefit when not administered properly. Finally, all patients should travel with an adequate supply of rescue inhalers (e.g., short-acting bronchodilators) and a supply of prednisone to treat an exacerbation during the trip. If traveling in a cold environment, patients should be instructed to keep their inhalers warm, because cold exposure can decrease their effectiveness. With regard to specific types of wilderness activities, two types of activities that warrant further attention in the asthma patient are high-altitude travel and diving. The effect of high-altitude exposure on asthmatic patients has not been well studied, but available evidence suggests that patients with mild to moderate disease, well controlled at the time of their trip, can tolerate significant altitude exposure. Several studies have shown that exposure to elevations as high as 5000 m (16,404 feet) is associated with decreased bronchial hyperresponsiveness.2,32 A small study of patients with mild to moderate disease climbing Mt Kilimanjaro found a non–statistically significant improvement in PEF between 2700 and 4700 m (8858 and 15,420 feet), no difference in the incidence of acute mountain sickness or summit success compared with nonasthmatic patients, and no evidence of exacerbations during the excursion.156 Because of interindividual disease heterogeneity, however, it is difficult to draw broad conclusions that apply to all patients. In the end, how a patient fares at altitude may be a function of the particular triggers for their disease. Patients whose disease is triggered primarily by allergens may fare well at altitude,166 where, for example, the number of dust mites decreases with increasing elevation, whereas patients whose disease is triggered by breathing cold, dry air may have difficulty during mountaineering or ski excursions that include significant exposure to such conditions. Epidemiologic evidence suggests that asthma incidence is increased among cross-country skiers and ski mountaineers, athletes whose activities entail high levels of minute ventilation in cold, dry environments.42,94 The primary concern with scuba diving in patients with asthma is that active airflow obstruction could lead to air trapping and significantly increase the risk for pulmonary barotrauma with changes in barometric pressure on ascent back to the surface of the water. As discussed further in Chapter 77, asthma was previously considered an absolute contraindication to diving but is now permitted provided the patient is (1) an asymptomatic adult with a childhood history of asthma, (2) has well-controlled disease with known triggers, (3) has normal pulmonary function tests with a less than 20% change in peak expiratory flow after exercise, and (4) no evidence of cold- or exercise-induced bronchospasm.

PART 4  INJURIES AND MEDICAL INTERVENTIONS

long-acting anticholinergic tiotropium. Patients are typically started on a single agent, but combination therapy with a β-agonist and anticholinergic can be used in those who fail to respond to monotherapy. Inhaled corticosteroids are considered for patients with poor symptom control on such therapy or frequent exacerbations, or whose disease falls in the severe or very severe categories.51 Patients whose symptoms are not under good control before their planned wilderness trip may require escalation of therapy. Any such changes should be made several weeks before the planned departure, because the benefits of tiotropium may not occur for a week after starting therapy, whereas those of corticosteroids may require up to several weeks. Although theophylline is sometimes used as an adjunctive therapy in patients whose disease is not well controlled with the other agents, it has a narrow therapeutic window and increased risk for toxicity compared with other therapies and should not be added to a patient’s regimen before a wilderness trip. Patients already taking theo­ phylline on a regular basis should have their levels checked before departure and should be counseled regarding how to recognize symptoms and signs of toxicity. As with asthma patients, COPD patients are at risk for disease exacerbations. Often triggered by viral or bacterial infections, these exacerbations are characterized by increased dyspnea and a change in the frequency or character of sputum production and can lead to worsening hypoxemia and overt respiratory failure. The literature does not contain information on the incidence of COPD exacerbations during wilderness travel and, as a result, all COPD patients traveling into the wilderness should prepare for the possibility of this complication. They should arrange an evacuation plan in the event of severe symptoms and carry a supply of rescue medications, including short-acting bronchodilators, prednisone, and oral antibiotics (azithromycin, levofloxacin, doxycycline, or trimethoprim-sulfamethoxazole). In hospital settings, short-acting bronchodilators are often given in the form of nebulized solutions. Such treatments are infeasible in the field, but with proper technique, metered-dose inhaler therapy can be of equal efficacy. Similarly, prednisone has good oral bioavailability and can be substituted for the intravenous formulations that are commonly used in the inpatient setting. Patients on formoterol should be aware that its onset of action is fast enough that it can be used as a rescue inhaler if albuterol is not available, although its long half-life precludes use for more than every 12 hours. Salmeterol’s onset time is too slow to be of use in rescue situations. COPD patients with a baseline resting arterial partial pressure of oxygen (PaO2) less than 55 mm Hg or SpO2 less than 88% should be treated with continuous supplemental oxygen, because this has been shown to have a mortality benefit in this patient population. These patients should continue supplemental oxygen on any planned wilderness trip, whereas patients not regularly on oxygen, but whose exacerbations are associated with worsening hypoxemia, might consider supplemental oxygen for the purpose of their trip. The traditional supplemental medical oxygen delivery system is a continuous flow of 100% oxygen from a compressed gas cylinder delivered by nasal cannula. The disadvantage to this system is its inefficient use of oxygen, because only a small percentage of the oxygen delivered to the nose actually reaches the lungs. In a wilderness setting, the weight and space required to carry medical oxygen cylinders create a significant burden and limit the trip duration. A more efficient alternative is for the patient to use a pneumatic nonelectronic demand valve that delivers flow of oxygen only on inspiration.163 Portable liquid oxygen units with demand valves are an alternative to oxygen cylinders and offer the advantage of lighter weight for a comparable amount of oxygen but are more expensive. Any patient using a demand valve system for a wilderness trip should be evaluated during rest and during exercise to ensure that adequate oxygenation is maintained.162 Finally, portable oxygen concentrators are available that obviate the need for liquid or compressed gas cylinders and increase patient mobility. However, their usefulness is limited by short battery life.101 Depending on the length of the planned trip, access to power sources, or ability to carry spare batteries, they may not represent a suitable alternative. 650

Patients seeking to travel with supplemental oxygen need to be aware of important logistic issues that may affect their plans. For those traveling by car to their destination, there should be few problems bringing oxygen to their destination, but persons traveling by airplane may encounter significant problems. As a general rule, patients are not allowed to bring liquid or compressed gas oxygen cylinders on board aircraft as either carry-on or checked baggage. The Federal Aviation Administration permits the use of small portable oxygen concentrators on aircraft in the United States, but use may not be permitted on all airlines worldwide. Unfortunately, standard practices for supplemental oxygen vary across the airline industry, with the availability of service, feasibility of using personal systems, and the fees varying between countries, airlines, and domestic and international flights.104,172 Patients planning to obtain oxygen sources on arrival at their destination will need to confirm whether such sources are available, because access will vary based on whether the person is traveling in the developed or developing world. Even in the developed world, access to supplies might be limited in more remote settings. Similar to asthma patients, two specific wilderness activities that deserve further attention in patients with COPD are highaltitude travel and diving. The biggest concern with regard to high-altitude travel is the potential for worsening hypoxemia. Few data are available about COPD patients in actual mountain environments, but data from the literature on COPD patients and commercial airline flights clearly indicate that patients with FEV1 values of 1 to 1.5 L experience significant hypoxemia when exposed to altitudes equivalent to 2440 m (8005 feet), with further drops in their PaO2 with minimal exertion, such as walking on flat ground or cycling at very modest work rates (20 to 30 W).101,103 Patients already using supplemental oxygen at home should increase their flow rates at high altitude and can consider portable pulse oximetry as a means to decide on the appropriate adjustment. Depending on their baseline disease severity, patients not already on supplemental oxygen should undergo pretravel assessment to determine the need for oxygen at high altitude. This can be done using either high altitude simulation testing40 or a variety of prediction rules that take into account various factors such as the PaO2 on room air at sea level, the FEV1, or the target altitude.31,67,116 Patients who develop symptomatic hypoxemia (PaO2 <50 to 55 mm Hg) during the high altitude simulation testing or who are predicted to have a PaO2 less than 50 to 55 mm Hg using one of the other prediction tools should be strongly encouraged to use supplemental oxygen at high altitude. Decisions to use oxygen should not be based on the PaO2 alone but should reflect whether or not the patient develops associated symptoms (dyspnea, light-headedness, dizziness, altered mental status, exercise intolerance). Patients who become hypoxemic (PaO2 <50 to 55 mm Hg) but remain asymptomatic with preserved exertion tolerance can travel without supplemental oxygen. They should monitor symptoms and oxygen saturation on arrival at high altitude using portable pulse oximetry or through periodic clinic visits and should carry a prescription for supplemental oxygen that can be filled at their destination if they develop problems following arrival. Patients whose PaO2 remains above these thresholds can travel without supplemental oxygen but may also consider monitoring symptoms and SpO2 during their sojourn.101 There are no data on the frequency of exacerbations at high altitude, whereas data on measures of airflow obstruction are limited and conflicting. As a result, any COPD patient traveling to high altitude must be prepared for the possibility of exacerbations as described above. There is no evidence to suggest that patients with severe bullous disease are at increased risk for pneumothorax at high altitude, despite the fall in barometric pressure.103 Diving carries the same concerns for COPD patients as it does for asthma patients. Airflow obstruction could lead to significant air trapping, which would increase the risk for barotrauma when trapped air expands in response to barometric pressure changes on ascent. Any blebs or bullae that do not adequately communicate with the environment could also expand and rupture with ascent to the surface. For these reasons, COPD is considered a contraindication to diving.

Sleep-disordered breathing refers to respiratory disturbances that occur during sleep and includes entities such as obstructive sleep apnea (OSA), central sleep apnea (CSA), and sleep-related hypoventilation. OSA is the most common form of sleepdisordered breathing and is marked by the presence of repeated reductions (hypopneas) or cessation (apnea) of airflow that occur as a result of either partial or complete occlusion of the upper airway during sleep. Present in up to 28% of the general population, the disease is more common in men and among older individuals and may occur in people who lack other underlying medical problems.178 CSA is also marked by recurrent apneas or hypopneas, but, unlike in OSA, alterations in airflow occur because of changes in respiratory signaling and effort rather than upper airway occlusion. Although idiopathic forms of the disease occur, it is most frequently seen among individuals with severe cardiomyopathy. As indicated in Chapter 1, CSA is also common among otherwise healthy people at high altitude. Sleep-related hypoventilation refers to abnormally high arterial carbon dioxide tension levels during sleep and is usually seen in the context of severe obesity, obstructive lung diseases, and various neuromuscular disorders, such as muscular dystrophy or amyotrophic lateral sclerosis. The various forms of sleep-disordered breathing are significant not only because of their ability to disrupt sleep quality but also due to their adverse effects on daytime function, including, for example, excessive daytime somnolence and impaired concentration. In addition to treatments directed at the underlying disease (e.g., heart failure), the standard treatment approach for each of these disorders is nocturnal use of intermittent non­ invasive positive pressure ventilation (NIPPV) or continuous positive airway pressure (CPAP). Individuals with these disorders who seek to travel into wilderness environments must consider several key issues before their trip, including (1) what will happen to the underlying disorder in that environment, (2) whether it is necessary to continue treatment while engaged in the wilderness activity, and (3) how to facilitate continued treatment if such treatment is deemed necessary. With regard to the first question, little is known about what happens to the various patterns of sleep-disordered breathing in the wilderness. There is little theoretic basis to expect changes in the incidence and severity of these problems when sleep is conducted at or near the same elevation at which the patient normally resides. Although changes in the severity of preexisting CSA following ascent to high altitude have not been studied, limited data suggest that the severity of OSA decreases considerably with ascent to high altitude. In one study of normal individuals, the OSA index fell from 5.5 + 6.9 events/hr to 0.1 + 0.3 events/hr at 5050  m (16,568 feet),22 whereas in a study of adults with moderate OSA at baseline, the obstructive respiratory disturbance index fell from 25.5 + 14.4 events/hr to 0.5 + 0.5 events/ hr at 2750  m (9022 feet).21 Of note, however, was the fact that in both studies, the decrease in obstructive events was offset by marked increases in the frequency of central apneas. The reason for the observed changes was not elucidated in these studies, but they may be due to alterations in air density, increased respiratory drives, and increased upper airway tone.21 Because the various forms of sleep-disordered breathing are generally associated with intermittent nocturnal hypoxemia, it can be expected that high-altitude travel will lead to greater degrees of nocturnal desaturation, with the magnitude of hypoxemia likely being a function of the altitude attained, as well as the duration of apneas and hypopneas. Whether individuals with sleep-disordered breathing should continue treatment while engaged in wilderness activity will be a function of the severity of their disease and associated symptoms and characteristics of their planned activities. For example, individuals with OSA but minimal or no daytime symptoms may be able to forego CPAP for several days while away on a trip, although excessive snoring may be a nuisance to other people on their excursion. On the other hand, individuals with severe daytime symptoms or who expect to perform activities that require high levels of concentration may find it necessary to continue therapy.

For individuals who plan to continue NIPPV or CPAP, the most important issue will be ensuring reliable access to power supplies. When such access is available (e.g., hotel, generators), travel should be relatively straightforward, because most machines are small and light enough to facilitate travel and can be brought on airplanes as carry-on luggage. Significant challenges arise, however, when power access is not available. Some manufacturers now make devices with rechargeable lithium batteries, but battery life is short, and use for more than 1 to 2 days would require access to recharging facilities or ample numbers of back-up batteries. An alternative is to obtain a special power cord from the device manufacturer that allows one to draw power off a 12-volt battery (deep cycle marine batteries offer the best battery life), but this option is limited by the size and weight of these batteries, expense, and logistic issues associated with obtaining a battery at the destination or traveling with one in hand.146 Individuals should contact the device manufacturer for information about the power consumption of their device to guide anticipated battery needs and should be aware that use of heated humidity systems will increase power needs. Finally, although most commercially available machines can run off the voltage levels used with outlets in the United States (110 to 120 V) and Europe (220 to 240 V), individuals should confirm the range for their machine and ensure that they are carrying the appropriate plug adapters.

DIABETES Approximately 17.9 million people with a diagnosis of diabetes live in the United States (6% of the U.S. population), so it is likely that diabetes will be encountered in persons pursuing wilderness activities.119 Diabetes encompasses the disorders of type 1 diabetes, previously known as insulin-dependent or juvenile-onset diabetes, and type 2 diabetes, previously known as non–insulindependent or adult-onset diabetes. Approximately 5% to 10% of diabetic patients have type 1 disease, and 80% have type 2, with the remainder of cases due to other causes. The pathophysiology of type 1 diabetes results from inadequate insulin production, whereas the pathophysiology of type 2 diabetes is due to peripheral resistance to insulin action. Patients with type 1 diabetes must be treated with insulin, whereas type 2 diabetes may be treated with diet and exercise, oral and injectable hypoglycemic agents, or insulin. A number of issues need consideration for diabetics pursuing wilderness activities. Diabetics may be remote from medical help and need to ensure that adequate medication is available. Carrying two or three times as much medication and devices (syringes, glucometer, glucose and ketone test strips) as anticipated and splitting up medication and medical device supplies among group members will mitigate against theft, loss, or unanticipated delays on longer trips (Table 34-3). Anticipate erratic meals, time changes, and increased levels of physical activity, and factor how they may change medication regimens. Engaging in nonroutine activities also creates certain safety issues for the patient with diabetes, so advising the patient on how to manage diabetes appropriately during exercise in an outdoor environment is essential. High-risk wilderness activities, such as mountaineering or rock climbing, where loss of focus and concentration may result in death, would not be appropriate for a diabetic patient who is susceptible to hypoglycemia, unless the person is constantly monitored by a climbing partner, does not climb in the lead, and is always secured by a rope. Similarly, solo wilderness activities may not be appropriate for diabetic patients who may become hypoglycemic. Patients with both type 1 and type 2 diabetes require evaluation for several issues before a wilderness trip. The extent of increased exercise that will be undertaken on the trip needs to be determined in relation to the patient’s current level of physical activity and his or her glucose control. Increased physical activity is beneficial for diabetic patients, particularly those with type 2 disease, and wilderness activities may be encouraged as part of lifestyle modification. In addition to exercise, the specific activity and associated travel are likely to effect a change in diet. Screening for conditions associated with diabetes, such as cardiovascular disease, peripheral and autonomic neuropathies, proliferative 651

CHAPTER 34  Chronic Diseases and Wilderness Activities

SLEEP APNEA

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 34-3  Diabetes-Specific Supplies Insulin Supplies Insulin Insulin pens and needles (if applicable) Pump supplies (if applicable) Syringes Glucose meter Glucose strips and lance/lancets Ketone strips Carbohydrates Dextrose tablets (rapid-acting carbohydrate) Dried fruit and cookies (slower-acting carbohydrates) Glucagon kit (this must be protected from breakage and from freezing of the vehicle) Intravenous setup Single-use sterile needles and syringes Insulated packs Letter from physician

Three times the amount anticipated for each type of insulin, stored at nonextreme temperatures One extra pen and three times the anticipated number of needles Three to five times the amount anticipated Enough to cover the entire trip if on the pen or pump; two to three times the anticipated requirement if using syringes alone Two different meters with extra batteries for each Three times anticipated number of strips for each meter, two lances, and three times the anticipated number of lancets; a supply of visually read strips should also be taken as a backup in the event of meter failure Two packages One package (50 g) per day Several individually wrapped packages per day Two kits One complete kit Several 18-g and 10-mL syringes, respectively, in the event that medical treatment is required in a hospital or clinic with limited resources Enough to carry all supplies Listing supplies and their necessity, for international border crossings

Modified from Brubaker PL: Adventure travel and type 1 diabetes: The complicating effects of high altitude, Diabetes Care 28:2563, 2005. Note: Supplies should be packed and carried in a minimum of two independent sites (carried personally at all times by two people or by one person with the second set in a separate travel bag and/or at a nearby hotel).

retinopathy, and nephropathy, should be done. These conditions may significantly influence the ability of diabetic patients to pursue wilderness activities safely and may require further evaluation and testing before the trip. Last, the effect of the change in environment on the diabetic patient is considered, including potential problems with exposure to heat or cold. The effect of increased exercise is important for both type 1 and type 2 diabetic patients because it may precipitate hypoglycemia or hyperglycemia, depending on the timing of the last dose of insulin and blood glucose level at the onset of exercise.70,173 The normal response to exercise in nondiabetic persons is a decrease in insulin secretion as serum glucose levels fall because of uptake of glucose by exercising muscle, and an increase in hepatic glucose release in response to catecholamines, glucagon, and growth hormone to maintain blood glucose levels. Patients with type 1 diabetes who are hypoinsulinemic when they exercise (as may occur if they excessively decrease their insulin in an effort to accommodate the increased physical activity) may become hyperglycemic because of increased hepatic release of glucose into the blood in addition to insufficient insulin to allow glucose to enter the cells. Thus hyperglycemia results in decreased exercise capacity, because exercising muscle is depleted of glucose as a result of insufficient insulin to enable glucose to enter the cells. Under these conditions, the substrate for fuel becomes free fatty acids released from adipocytes, with generation of ketone bodies by the liver. Hypovolemia may occur due to glycosuria; if the process persists, diabetic ketoacidosis may ensue. Patients with type 1 diabetes who have exogenous insulin in excess may become hypoglycemic when they exercise. Exercise results in an increase in insulin secretion, rather than the expected physiologic decrease in insulin with exercise. The increased insulin levels enhance glucose uptake by the muscles and decreases release of glucose from the liver. Both result in a fall in blood glucose to a greater degree than in nondiabetic persons during exercise. Type 1 diabetic patients also have defective glucagon secretion that will augment defective counter-regulatory responses to hypoglycemia. Delayed hypoglycemia may occur hours after exercise as the resting muscle takes up glucose from the blood to replenish glycogen stores. Because insulin is metabolized by the kidneys, dehydration can result in decreased renal insulin clearance and prolong insulin action. Therefore monitoring glucose levels, nutrition and hydration, and adjusting the dose of insulin are also important after exercise. Another factor contributing to hypoglycemia in the exercising patient with type 1 diabetes is increased exogenous insulin 652

mobilization from subcutaneous tissue because of increased blood flow.60,85 Inadvertent intramuscular injection would exaggerate this phenomenon. It is important for patients with type 1 diabetes to administer their dose of subcutaneous insulin before exercise in a location away from exercising muscle. They should avoid injections into the arms and legs, instead using the abdomen or back of the neck. Insulin absorption is fastest and most consistent when it is injected into the abdomen. Absorption is generally slower from the arms and slowest from the thighs or buttocks, but the rate may be more inconsistent depending on the type of exercise. If the planned exercise uses primarily arm muscles, such as sport climbing, then it may be beneficial to give the insulin injection in the abdomen to avoid increased absorption from the exercising arm muscles. Likewise, if the planned activity is hiking or skiing, then it would be beneficial to use the arm or abdomen to avoid increased absorption from the exercising leg muscles. Absorption of subcutaneous insulin during exercise may also depend on the type of insulin used. A study of the long-acting insulin analog glargine, injected subcutaneously into the thigh on the evening before an intense 30-minute exercise session in patients with type 1 diabetes, did not show an increased rate of absorption, but plasma glucose fell during exercise.130 Another measure to prevent exercise-associated hypoglycemia is to reduce the dose of insulin that will be in effect during exercise.109 The best strategy for a patient with type 1 diabetes is to monitor blood glucose before, during, and after exercise to predict changes, and adjust insulin doses accordingly. This means that before a wilderness trip, the type 1 diabetic patient should exercise daily at a level of physical activity similar to that anticipated on the wilderness trip, so that adjustments in insulin dosing can be made. Differences in nutritional intake, in addition to increased exercise, during the wilderness trip should also be anticipated when planning insulin regimens. Patients with type 1 diabetes may engage in strenuous physical activity without experiencing problems, but it is important for the patient to focus on the timing of exercise in relation to meals and insulin dosing.86,159 It is also important to anticipate the nature of the exercise that will be undertaken. Long endurance activities have different implications for type 1 diabetes management (more risk for hypoglycemia) than do short bursts of high-intensity exercise (more risk for hyperglycemia).70 Another consideration is whether regular insulin or a rapidly acting insulin analog (lispro or aspart) is used for prandial dosing. Rapidly acting insulin alters the timing of exercise-related hypoglycemia. Patients who exercise early in the postprandial period (1 to 3 hours after a meal) require a decrease in the dose of

once a day. A mirror may be required to visualize the plantar surface. Any sign of inflammation, including blistering or abrasion, should be promptly addressed. The importance of well broken in footwear and the need to wear clean and dry socks at all times should be emphasized. Diabetic patients should be advised to never walk barefoot. Autonomic neuropathy also poses problems with increased activity in a wilderness environment. Cardiac responsiveness may be delayed during rapidly changing exercise levels. Gastroparesis may make absorption of carbohydrates unpredictable and could result in a mismatch in timing between insulin and glucose peak. Certain drugs that may be used at high altitude also need special consideration in diabetics. Acetazolamide is commonly used for prevention of acute mountain sickness through a mechanism of inhibition of renal carbonic anhydrase, causing bicarbonate diuresis and non–anion gap metabolic acidosis that result in compensatory hyperventilation. Acetazolamide could worsen metabolic acidosis and promote volume depletion in diabetic patients. Dexamethasone is commonly used to treat severe acute mountain sickness or high-altitude cerebral edema and, as a glucocorticoid, increases insulin resistance and predisposes to hyperglycemia. Lastly, metformin is commonly used to treat type 2 diabetes. It is contraindicated in clinical conditions that may cause hypoxemia. This may be a consideration in travel to high altitude. Ensuring that insulin does not freeze and glucose testing equipment works properly are also important for the insulindependent diabetic patient in the wilderness. Strategies to ensure that insulin does not freeze include carrying the medication inside a jacket next to the body or storing the insulin in an insulated container and putting the container in the sleeping bag at night. Glucose testing equipment should be reliable, rapid, and used frequently to help identify impending hypoglycemia and increase carbohydrate ingestion before incapacitation occurs. The accuracy of glucose testing equipment can be affected by high altitude and cold. Both overestimation and underestimation of glycemia and of standard glucose control solutions have been reported for all types of glucose meters.19 Glucose meters using the oxygen-insensitive enzyme glucose dehydrogenase may perform better at high altitude than those using the enzyme glucose oxidase, but both types perform poorly at low temperatures.123 High glucose levels seem to be misreported to a greater extent at altitude than are low to normal glucose levels.19 The use of multiple meters with control glucose solutions can lend some confidence. Carrying glucose monitoring equipment next to the skin may prevent the problems associated with battery malfunction at cold temperatures. Provided that the insulin-treated patient with diabetes has reviewed all the factors associated with a wilderness trip that may be complicated by diabetes and has chosen to undertake the preparation required and accept the risks, a treatment plan needs to be generated. The most challenging wilderness trips for maintaining glucose control in diabetic patients are those where the level of exercise is consistently increased above usual. Intensive diabetes management can be achieved with multiple daily injections of insulin or an insulin pump and numerous checks of blood glucose throughout the day (Tables 34-4 and 34-5). A standard strategy to offset the increased efficiency of insulin due to exercise is to ingest 15 to 30  g (0.5 to 1  oz) of carbohydrate for every half hour of moderate aerobic exercise. Monitoring blood glucose during periods of exercise of several hours’ duration is important.70,173 Adjusting the dose of insulin downward may be required if carbohydrate supplementation does not prevent hypoglycemia. It may be necessary to decrease the dose of insulin by 30% or more.41,109 Blood glucose should be checked more often early during a wilderness trip to assess how to balance insulin, carbohydrate intake, and exercise. It is also critical to prevent delayed hypoglycemia associated with exercise that often occurs after muscle and liver glycogen stores have been depleted and not replenished. The use of intermediate-acting insulin may need to be shifted from the afternoon or early evening to bedtime, or a long-acting insulin preparation that does not peak may be used. Adequate hydration is essential to ensure that the duration of action of insulin is not increased. 653

CHAPTER 34  Chronic Diseases and Wilderness Activities

rapidly acting insulin, whereas those who exercise later (3 to 5 hours) require a smaller or no change.79 A predictable exercise schedule on a wilderness trip would be useful for the patient with type 1 diabetes, although this may be difficult depending on the type of trip and the environment. Other members of the group need to be aware of signs and symptoms of hypoglycemia in the diabetic patient and how to render appropriate treatment. This is especially important for patients with type 1 diabetes, but also is significant for patients with type 2 diabetes who are on oral hypoglycemic drugs or insulin, because this group of diabetic patients also experiences a decrease in serum glucose during exercise.131,173 Preventive measures include ingesting extra food in the form of 15 to 30 g (0.5 to 1 oz) of quickly absorbed carbohydrate (e.g., glucose tablets, whole milk, hard candies, or juice), which should be taken 15 to 30 minutes before exercise and approximately every 30 minutes during exercise.69,70 Patients are also at risk for late hypoglycemia (i.e., 4 to 8 hours after the termination of exercise) because of replenishment of depleted glycogen stores. This can usually be avoided by ingesting slowly absorbed carbohydrates (dried fruit, granola bars, or trail mix) immediately after exercise.152 Fluid intake should also be increased to ensure adequate hydration, because dehydration prolongs insulin action by decreasing insulin clearance from the blood. The acute symptoms of hypoglycemia are mediated by the adrenergic autonomic nervous system and are manifested by shakiness, tremors, palpitations, cold sweats, hunger, confusion, and nervousness/anxiety. If these are ignored, not sensed (owing to hypoglycemic unawareness), or cannot be treated immediately, the person may experience neuroglycopenic symptoms because of inadequate amounts of glucose reaching the brain. Neuroglycopenic symptoms consist of headache, loss of concentration, irritability, and, if allowed to proceed long enough, even seizures and loss of consciousness. Hypothermia is a common sign of hypoglycemia. All persons with diabetes should be questioned about their history of hypoglycemic reactions (frequency and severity) as well as their ability to sense the reactions (history of hypoglycemic unawareness). Travel into the wilderness should be discouraged in persons with a history of severe or frequent reactions or a history of hypoglycemic unawareness. Companions should be taught to recognize the signs and be knowledgeable in the treatment of hypoglycemia. If the person with diabetes is alert and cooperative, he or she may be treated with 15 g (0.5 oz) of a rapidly absorbed carbohydrate (e.g., glucose tablets, juice, or hard candies). The blood glucose should be checked in 15 minutes to ensure that the glucose level has increased to a safe level (>100 mg/dL) before continuing with the physical activity. The person should be closely watched for evidence of recurrent symptoms. If the person becomes uncooperative or loses consciousness, a glucagon injection kit should be available. Glucagon releases glucose stored in the liver and helps raise the glucose level to the point at which the person becomes alert and treatment may be continued with an oral, rapid-acting carbohydrate. The dose of glucagon is 1 mg (1 ampule) given either subcutaneously or intramuscularly. Another route for delivering glucose is to deposit glucose formulations, such as table sugar, under the tongue. Activity limitations for diabetic patients also depend on associated complications. Patients with proliferative retinopathy should avoid activities that can rapidly or explosively elevate intraocular pressure because vitreous hemorrhage may occur. Bleeding from damaged retinal capillaries may also occur during a Valsalva maneuver, while lifting heavy objects, or during a collision. An expert should do an examination for early signs of retinopathy at least once a year.41,169 Patients with peripheral neuropathy are at risk for pressure ulceration to the feet and should avoid traumatic weight-bearing exercise (long-distance running or prolonged downhill skiing). Well-fitting protective footgear helps prevent this complication. Diabetic patients with peripheral neuropathy are also more susceptible to cold injury of the feet in a cold environment, and patients, as well as group members, need to monitor their feet meticulously. In a cold-weather environment, it is especially important to have well-insulated warm footgear with dry socks. Diabetic patients should check all surfaces of their feet at least

PART 4  INJURIES AND MEDICAL INTERVENTIONS

TABLE 34-4  Matching Insulin Treatment Schedules With Exercise Schedules Treatment Type

Advantages

Disadvantages

Standard: two injections, mixed intermediate- and short-acting insulins Intensive: three or more injections a day Extended: glargine for basal plus lispro/aspart for meals Continuous infusion (pump)

Easy to perform

Poor match with exercise, rigid time restraints, least likely to give good metabolic control and health More frequent testing, harder to learn

Better control, more flexible timing, less hypoglycemia in the evening Least amount of time rigidity, most protection against hypoglycemia, excellent metabolic control Most flexible (no injections most days), low hypoglycemia risk overnight, best metabolic control Basal insulin infusion rate can be adjusted to accommodate increased insulin sensitivity due to increased activity

Much more effort to master and do well Needs expensive device, harder to master, must remove pump for some activities; need to carry syringes in case of mechanical failure Risk for infusion site infections

Modified from Draznin MB: Type 1 diabetes and sports participation: Strategies for training and competing safely, Phys Sportsmed 28:49, 2000.

Diabetic patients may pursue the same wilderness activities as do other individuals, provided they have the experience necessary to participate safely. This includes activities such as highaltitude mountaineering.95 On an expedition to Cho Oyu, an 8201-m (26,906-foot) peak in the Nepal Himalayas, six type 1 diabetic patients participated in the expedition and one reached the summit.125,126 These climbers were highly motivated and adhered to careful glucose monitoring, and all completed the expedition safely and free from long-term complications. Their cardiovascular parameters were comparable with those of nondiabetic control subjects on the same expedition, although the patients with diabetes did have a worsening in metabolic control and required higher insulin doses than at sea level.

PERIPHERAL ARTERIAL DISEASE Peripheral arterial disease (PAD) is caused by atherosclerotic occlusion of the arteries of the legs. The most common symptomatic presentation is intermittent claudication, which is leg muscle discomfort on exertion that is relieved with rest. Many patients present with atypical symptoms, including leg fatigue, difficulty walking, and leg pain not typical of cluadication.175 Among men over the age of 60 years, 2% to 3% have symptomatic PAD, as do 1% to 2% of women. The prevalence of asymptomatic PAD, proved by a reduced ankle–brachial index less than or equal to 0.9 (measurement described below), is three to four times as great as that of symptomatic disease.151 Approximately 25% of patients with peripheral arterial disease have symptoms of claudication, and approximately 10% have critical ischemia.155 Because PAD is common, it may be present in persons intending

to pursue wilderness activities, especially elders and those with other manifestations of systemic atherosclerosis. Severity of PAD is closely associated with the risk for myocardial infarction, is­ chemic stroke, and death from vascular causes. The major risk factors for PAD are older age (>40 years), cigarette smoking, and diabetes mellitus. Hyperlipidemia, hypertension, and hyperhomocysteinemia are also important risk factors.76 When evaluating a patient with PAD for a wilderness activity, it is helpful to characterize the severity of the disease and how it affects functional capacity. The most useful method for evaluating severity is the ankle-to-arm ratio of systolic blood pressure (ankle–brachial index), which is easily obtained with a standard blood pressure cuff and a Doppler device.76,175 Systolic blood pressure is measured by Doppler ultrasonography in each arm and in the dorsalis pedis and posterior tibial arteries in each ankle. The higher of the two arm pressures is selected, as is the higher of the two pressures in each ankle to calculate a left and right ankle–brachial index. An ankle-to-arm pressure ratio of 0.91 to 1.3 is normal. A ratio of 0.41 to 0.9 indicates mild to moderate peripheral arterial disease, and less than 0.4 is severe. A ratio of greater than 1.3 indicates a calcified noncompressible vessel. Patients with claudication, defined as walking-induced pain in one or both legs (primarily in the calves) that does not go away with continued walking and is relieved by rest, typically have ankle–brachial indexes in the mild to moderate range. Patients with critical ischemia have ankle–brachial indexes in the severe range. Increased exercise is associated with wilderness activities. This may be a limiting factor for patients with peripheral vascular disease who suffer claudication. Hiking or trekking, however, are

TABLE 34-5  Types, Names, and Uses of Insulin Insulin

Onset

Peak

Duration

Uses

Notes

Rapid-acting (insulin analogs lispro, aspart, glulicine)

≤0.5 hr

0.5-3 hr

3-5 hr

Short-acting (human regular) Intermediate-acting (human NPH)

0.5-1 hr

2-5 hr

Up to 12 hr

Insulin of choice for pumps. Rapid action may not be desirable during periods of physical activity because it may lead to more hypoglycemia May last too long, leading to hypoglycemia

1.5-4 hr

4-12 hr

Up to 24 hr

Meal coverage if taken up to 15 min before eating; adjust for elevated blood glucose levels Meal coverage if taken 30-45 min before eating Meal coverage (lunch) if taken in the morning

Long-acting (insulin analogs glargine, detemir)

0.8-4 hr

None

Up to 24 hr

Basal

More active early in the dosage or can linger longer than anticipated; either can cause hypoglycemia Once-a-day injection; cannot be mixed with other insulins; soluble until injected

Modified from Draznin MB: Type 1 diabetes and sports participation: Strategies for training and competing safely, Phys Sportsmed 28:49, 2000; Hirsch IB: Insulin analogues, N Engl J Med 352:174, 2005; and Vijan S: Type 2 diabetes, Ann Intern Med 152:ITC31, 2010. NPH, Neutral protamine Hagedorn. Notes: A typical intensive schedule of injections would be a mixture of NPH with lispro before breakfast, lispro alone at dinner, and NPH at bedtime. Testing is done before meals and at bedtime regardless of the type of insulin used. To establish the dose (given by injection or by pump) for long-acting insulin plus lispro for meals, the patient also tests blood glucose 2 hr after each meal for 3 to 4 wk. Careful record keeping will determine if assumptions are correct and which doses work best. Testing should be done initially every 30 to 60 min during exercise to determine the effect of the activity on the blood glucose levels. Testing should be done every 2 hr after the completion of exercise for 6 to 12 hr to monitor for late-onset hypoglycemia. The time course of action of each insulin may vary among persons or at different times in the same person. Because of this variation, the time periods indicated here should be considered general guidelines only.

654

Patients with symptomatic PAD can pursue activities in the wilderness that are appropriate for their functional capacity. Such activities should include walking or hiking and allow for periods of rest when necessary. An exercise program along with drug therapy can improve ability to participate in wilderness activities. Environmental extremes such as cold and high altitude may worsen limb ischemia and predispose to frostbite.

RAYNAUD’S PHENOMENON Raynaud’s phenomenon is a disorder of abnormal vasomotor control marked by the onset of pallor or cyanosis in the distal extremities due to vasospasm and decreased arterial blood flow.177 It can occur as an isolated problem (primary Raynaud’s phenomenon) or as part of collagen vascular diseases such as systemic sclerosis or systemic lupus erythematosus (secondary Raynaud’s phenomenon). Primary Raynaud’s phenomenon is more common in women than men and occurs in approximately 5% of the U.S. population.177 Raynaud’s phenomenon is an episodic phenomenon with attacks usually occurring in response to triggers such as cold (exposure of the extremity to cold or a when the patient’s body becomes cold), moisture, vibration, and emotional stress. Attacks begin with an ischemic phase marked by well-demarcated pallor that progresses to cyanosis of the digits (Figure 34-1). Changes typically start in one or several digits and spread symmetrically to all digits in the hands and/or feet, with the hands being a more common site of involvement than the feet in most individuals. These symptoms are often accompanied by pain, numbness, and burning sensations and are usually, although not always, followed by a hyperemic phase as circulation is restored to the affected areas. The classic threephase color change occurs in approximately two-thirds of affected patients, whereas the rest have only pallor and cyanosis.14 In most cases the attack is self-limited and resolves after rewarming the hands or feet. In severe secondary Raynaud’s phenomenon, superficial ulceration or deep tissue necrosis with gangrene and amputation can occur. Certain aspects of wilderness travel may pose risks for patients with Raynaud’s phenomenon. Intense vasoconstriction can make the hands nonfunctional for performing basic tasks essential for survival in a cold-weather environment, such as zipping a coat, lacing boots, or putting on crampons. Affected individuals may be forced to rely on others to accomplish these tasks. Concern has also been raised about the risk for frostbite in Raynaud’s patients, because they have been shown to have lower finger temperatures with body cooling,136 slower rate of skin temperature rise with rewarming,170 and diminished cold-induced vasodilation (“hunting response”)83 when compared with healthy controls. Few studies, however, have determined whether the incidence of frostbite is increased relative to normal controls. Ervasti and colleagues49 compared Finnish military recruits with and without the disorder and found that the odds ratio for all degrees of frostbite among people with Raynaud’s phenomenon was 2.05 (95% CI, 1.72 to 2.44). The risk for “deep frostbite”

FIGURE 34-1  Active Raynaud’s phenomenon. Sharply demarcated pallor resulting from the closure of digital arteries in the second, third, and fourth fingers of both hands. Cyanosis of the fifth fingers on both hands. Note the bandages over fingers covering nonhealing wounds due to arterial insufficiency. (Courtesy Colin K. Grissom, MD.)

655

CHAPTER 34  Chronic Diseases and Wilderness Activities

reasonable activities for patients with claudication if they engage in a regular exercise training program. The benefit of exercise in improving functional capacity in patients with claudication is well proved,73,155 and greater physical activity is associated with lower mortality.63 One meta-analysis concluded that exercise training improved pain-free walking time in patients with claudication by an average of 180% and improved maximal walking time by an average of 120%.62 Exercise at least 2 times per week, even in the presence of pain from intermittent claudication, increases walking time. Walking through the claudication pain is not harmful and increases walking distance.73 Even self-directed walking exercise programs of 3 times weekly prevent functional decline in patients with symptomatic and asymptomatic PAD.113 Exercise-induced increases in functional capacity and lessening of claudication symptoms are primarily due to improvements in endothelial vasodilator function, skeletal muscle metabolism, blood viscosity, and biomechanics of walking. Increases in leg blood flow and oxygen delivery may also occur but do not appear to account for the large improvements in exercise capacity that are observed. A supervised exercise program several times per week is recommended, but a regular self-directed exercise program can also have benefit.113 The key elements of each session include a warm-up period followed by walking on a track or treadmill at a workload that causes claudication in about 5 minutes. One continues at that workload until claudication of moderate severity occurs, then rests standing or sitting for a brief period to allow symptoms to subside, and repeats the exercise–rest pattern for the duration of the session, lasting initially approximately 30 minutes but working up to about an hour. This exercise strategy might also be used while hiking, repeating periods of exercise and rest as gauged by claudication symptoms, and could potentially lead to improvements in exercise capacity over time. A walking or hiking exercise program needs to be done regularly and sustained over months, or the benefits diminish. Patients with PAD who wish to pursue wilderness activities or an exercise program should undergo evaluation for heart disease, hypertension, hyperlipidemia, and diabetes. Appropriate treatment and risk factor modification (including smoking cessation) should be initiated.73 In addition, an exercise test with 12-lead electrocardiographic monitoring should be performed to evaluate for cardiac ischemia. Patients with claudication may be limited by leg pain during a maximal exercise test, thus limiting stress on the heart, but information gained regarding heart rate and blood pressure response, work level at which claudication occurs, and exercise capacity is useful for estimating the type of wilderness activity that may be pursued and in formulating a prescription for exercise training. Treatment of claudication should include a formal walkingbased exercise program. In addition, several options exist for drug therapy. The Eighth ACCP Consensus Conference on Antithrombotic and Thrombolytic Therapy recommends lifelong antiplatelet therapy in patients with PAD: aspirin or clopidogrel for persons with coronary artery or cerebrovascular disease, and aspirin rather than clopidogrel for all others.151 Clopidogrel is a thienopyridine drug that inhibits platelet activation and is an alternative to aspirin, and it has fewer hematologic side effects than the related drug ticlopidine. Aspirin is significantly less expensive than clopidogrel and ticlopidine.73 Clopidogrel has U.S. Food and Drug Administration (FDA) approval for prevention of ischemic events in patients with PAD.76,151 Cilostazol and pentoxifylline are the two drugs approved in the United States for treating claudication. Cilostazol is a phosphodiesterase inhibitor that suppresses platelet aggregation and is a direct arterial vasodilator. Cilostazol improves both pain-free and maximal treadmill walking distances in patients with stable moderate to severe claudication161 and is recommended for patients with more severe disabling claudication.151 Because other oral phosphodiesterase inhibitors used for inotropic therapy have caused increased mortality in patients with advanced heart failure, cilostazol is contraindicated in heart failure of any severity. Pentoxifylline is a methylxanthine derivative that improves deformability of red cells, lowers plasma fibrinogen concentrations, and has antiplatelet effects. It is not as effective in improving walking ability as is cilostazol.36 The Eighth ACCP Consensus Conference did not recommend pentoxifylline for treatment of PAD.151

PART 4  INJURIES AND MEDICAL INTERVENTIONS

(blisters, ulcers, and gangrene), however, was not different between the two groups. In another study of high-altitude travelers with primary Raynaud’s phenomenon, Luks and colleagues102 reported an incidence rate of 15%, but this study lacked a control group and the data were based on self-report rather than formal confirmation. In addition to the issues of cold exposure in the wilderness, there is also theoretic concern that high-altitude travel could adversely affect Raynaud’s phenomenon patients. Any impairment in oxygen delivery stemming from arterial vasoconstriction might be worsened by low ambient oxygen conditions at high altitude, thereby increasing the severity or frequency of attacks and the risk for frostbite and/or gangrene. In the only study to address this question, Luks and colleagues102 surveyed 142 people with Raynaud’s phenomenon, 98% of whom had primary disease, and did not find evidence of worse problems at high altitude. Survey respondents spent 5 to 7 days per month at elevations greater than 2400 m (7874 feet) and engaged in a wide variety of activities, including winter sports (89% of respondents). Only 22% reported changing their pattern of activities in the mountains because of their disease. Of note, there was significant heterogeneity in the respondents’ perceptions of the frequency, duration, and severity of their disease at altitude, compared with their home elevation. Although the survey approach made it difficult to separate out the effects of hypobaria and cold at high altitude, this study does at least suggest that motivated individuals with primary Raynaud’s phenomenon can safely engage in many different activities, including winter sports at high elevations. To prevent problems in cold or high-altitude environments, Raynaud’s patients should take steps to minimize the risk for serious attacks. For example, they might choose to travel in warmer climates or in the summer rather than the winter months. If winter activities are pursued, a location with a less severe winter environment can be chosen. For example, high-altitude mountaineering in South America is more equatorial and takes place in a warmer climate than does mountaineering in North America, Asia, or Europe. Appropriate cold-weather gear and clothing are essential to keep the entire body warm and help mitigate attacks. High-quality plastic mountaineering boots or ski boots and expedition-type mittens or gloves with space for disposable chemical hand warmers help in winter environments. Once on a trip, patients might avail themselves of a variety of strategies to prevent attacks. In the study by Luks and colleagues,102 for example, 89% of the respondents used multiple strategies on any given trip, with the most common tactics being wearing gloves or mittens at all times, chemical hand warmers, the use of liner gloves, and limiting exposure to moisture. Climbers with Raynaud’s phenomenon should also exercise good judgment and retreat early, before becoming overextended and exhausted. Nicotine and other drugs with peripheral vasoconstrictive effects, such as over-the-counter decongestants, should be avoided. Patients might also consider the use of pharmacologic prophylaxis. Calcium channel blockers160 and phosphodiesterase inhibitors,24 for example, have been shown to decrease the frequency and severity of episodes of Raynaud’s phenomenon and may be used on an as-needed basis during the trip.24 Other pharmacologic agents that can be used for prevention include the α1-antagonist prazosin, the serotonin uptake inhibitor fluoxetine, the angiotensin receptor inhibitor losartan, and the direct vasodilator isoxsuprine.75,174 Calcium channel blockers are the pharmacologic agents of choice, but for those intolerant of calcium channel blockers, other agents may be tried. Benefits may also be idiosyncratic, so lack of response to calcium channel blockers is also an indication to try an alternative agent. Once an attack sets in, efforts should be made to warm the affected extremities and, in some cases, the entire body. By way of example, individuals can move to a warmer environment, don dry gloves and/or change into dry clothing, use chemical hand warmers, or place hands in warm water or on a warm surface.

OSTEOARTHRITIS Osteoarthritis is a major cause of disability in adults and most commonly affects the joints of the hands, hips, knees, and 656

cervical and lumbar spine. Uncommonly affected joints include the shoulder, elbow, and wrist. Factors in the evolution of osteoarthritis include initiation in either previously injured or susceptible joints; development, which is biochemically mediated and biomechanically driven; and clinical expression, which may be modified by factors such as weight and sex.34 The primary symptom of osteoarthritis is pain that is typically exacerbated by activity and relieved by rest. With more advanced disease, pain may occur with progressively less activity. Osteoarthritis can be inflammatory or noninflammatory. Patients with noninflammatory osteoarthritis complain primarily of joint pain and disability. Physical findings in affected joints include tenderness, bony prominence, and crepitus. Patients with inflammatory osteoarthritis complain of articular swelling, morning stiffness, and night pain. Signs of inflammation include joint effusion on examination or radiography, warmth on palpation of the joint, and synovitis on arthroscopic examination. The degree of disability caused by hip or knee osteoarthritis is an important consideration for wilderness activities. Patients should be guided toward activities that are within their functional capability. Wilderness activities that cause increased weight bearing on lower extremity joints should be avoided. For example, hiking or trekking with a light pack or bicycling are recommended over activities, such as a multiday backpacking trip or mountaineering, where carrying heavy loads might be required. Risk for development of hip or knee osteoarthritis is also relevant to wilderness activities. There is increased risk for lower limb osteoarthritis associated with repetitive, high-impact sports, and that risk is increased with joint injury.34 When assessing risk for osteoarthritis from wilderness activities, the nature and intensity of the activity, presence of previous injury, and body mass index should all be considered. Recreational running does not appear to increase the risk for knee osteoarthritis,34,92 but how this applies to trail running is not known. The evidence that obesity is strongly associated with development of knee, and probably hip, osteoarthritis and that weight loss improves joint pain and function82,120 are relevant to wilderness activities where carrying heavy loads is required. Wilderness activities that repeatedly require carrying a heavy pack, or squatting and kneeling maneuvers, may cause progression of knee or hip osteoarthritis, especially if there has been previous injury to a joint or associated joint muscles, ligaments, or tendons.150 Very little information is available on the development of hand arthritis with wilderness activities such as climbing. One study suggests that rock climbing at a high standard for over 10 years may increase risk for osteoarthritis in certain joints of the hands.139 Measures that can be taken to improve functional capacity for wilderness activities include nonpharmacologic and pharmacologic treatments. The goal of management of osteoarthritis is to control pain and improve function and health-related quality of life with avoidance of therapeutic toxicity. Potential treatments include weight loss, exercise, biomechanical techniques, pharmacologic therapy, and surgery. Table 34-6 outlines a stepwise approach to management of osteoarthritis depending on severity.82 Exercise is the primary nonpharmacologic intervention for lower limb osteoarthritis that is directly related to wilderness activities. There is good evidence that strengthening and aerobic exercise can reduce pain and improve function and health status in patients with knee osteoarthritis.57 The evidence for hip osteoarthritis is not as compelling,58 but exercise is still recommended.50,138 Well-conditioned muscles and muscular balance are needed to attenuate impact loads and provide joint stability. Muscular conditioning may prevent exercise-related osteoarthritis.150 Muscular conditioning is achieved through well-designed exercise programs performed with supervision or as home exercise routines that include range-of-motion and flexibility exercise, muscle conditioning, and aerobic cardiovascular exercise.52,53,167 Biomechanical treatments for knee osteoarthritis are relevant to wilderness activities such as hiking and trekking and are helpful at reducing symptoms. For appropriate application, consultation with a physiatrist or sports medicine physician may be required. Shock-absorbing footwear reduces impact loading, heel wedges reduce loading of the medial knee joint surface, neoprene support sleeves increase proprioception and reduce

Osteoarthritis

Symptom Severity Nonpharmacologic Management Education, exercise, weight loss, appropriate footwear

Mild

↓ Further Nonpharmacologic Management Physiotherapy, braces Simple analgesics Acetaminophen ↓ Pharmacologic Management NSAIDs, opioids If effusion is present, aspirate and inject intra-articular corticosteroids ↓ Surgery Osteotomy, joint replacement

Severe

NSAIDs, Nonsteroidal antiinflammatory drugs.

feelings of instability, dynamic bracing controls lateral instability, and taping allows repositioning of the patella.52,53 Hiking poles are an additional method to help unload lower extremity joints while hiking or trekking and may be helpful for patients with osteoarthritis of the hip and knee. During downhill walking when not carrying an external load, the use of poles reduces forces on the knees,59,143 and with an external load, reduces forces on the ankles, knees, and hips.13 The major pharmacologic treatments for osteoarthritis include analgesics, nonsteroidal antiinflammatory drugs (NSAIDs), and intra-articular corticosteroids. The major goal of treatment with these agents is relief of pain, which usually is achieved with nonopioid analgesics. The nonprescription analgesic acetaminophen at doses up to 4 g/day is the recommended primary treatment.15,82,179 Patients with osteoarthritis who have mild to moderate pain will obtain a similar degree of pain relief with acetaminophen as with NSAIDs.52,53 Although it is one of the safest analgesics, acetaminophen can prolong the half-life of warfarin and can cause hepatic toxicity at therapeutic doses in patients with chronic alcohol abuse. For patients who do not obtain adequate symptom relief with nonopioid analgesics, self-limited use of nonselective NSAIDs is an alternative after considering the risk for upper gastrointestinal and renal toxicity. Cyclooxygenase-2–selective NSAIDs are an alternative with less potential risk for gastrointestinal toxicity, but with an increased risk for serious cardiovascular events. The risk for adverse cardiovascular events may also apply to the nonselective NSAIDs, and they are recommended only for short-term use in the relief of pain12 (updated information is available at the FDA website: Rheumatology Information: Therapeutics for Osteoarthritis, http://www.fda.gov/Drugs/ResourcesForYou/ HealthProfessionals/ucm106969.htm). An alternative to NSAIDs for osteoarthritis pain not relieved by acetaminophen is the centrally acting oral analgesic tramadol. This is a synthetic opioid agonist that inhibits reuptake of norepinephrine and serotonin and has been approved by the FDA for treatment of moderate to severe pain. The efficacy of tramadol has been found to be comparable with that of ibuprofen in patients with hip and knee osteoarthritis.52,53,171 Another alternative therapy for osteoarthritis is the combination of glucosamine and chondroitin. These are compounds extracted from animal products that are absorbed by the gastrointestinal tract and appear to be capable of increasing proteoglycan synthesis in articular cartilage. One meta-analysis concluded that, despite methodologic flaws in many studies, these

compounds are probably efficacious for treatment of osteoarthritis and have no significant side effects.35,82,110 Relevant to wilderness activities, glucosamine and chondroitin were effective in relieving symptoms of knee osteoarthritis in active members of the U.S. Navy diving and special warfare community.98 In persons with osteoarthritis of the hand or knee who have mild to moderate pain, use of topical analgesics, such as capsaicin cream, is appropriate as adjunctive treatment or monotherapy.35,82 Evidence supports short-term (up to 2 weeks) improvement in symptoms of osteoarthritis of the knee after intra-articular corticosteroid injection. Significant improvement may also occur for up to 16 to 24 weeks with a dose equivalent to 50 mg of prednisone.3,35,82 There is concern that multiple injections of intraarticular corticosteroids may promote disease progression; further study is required. Corticosteroid injection for knee osteoarthritis to provide benefit for the duration of a wilderness trip for up to 2 weeks seems reasonable105 and may provide enough pain relief and increase in function to make wilderness activity safer and more enjoyable. Surgical treatment of osteoarthritis is usually considered after failure of nonsurgical treatments. Four categories of surgical treatment are available: osteotomy, arthroscopy, arthrodesis, and arthroplasty. Osteotomies are performed in persons with early osteoarthritis and may relieve symptoms and slow the rate of progression. Arthroscopic debridement and lavage can also successfully alleviate symptoms, particularly in the case of degenerative meniscal tears in the presence of mechanical symptoms. When there is substantial joint space narrowing, however, arthroscopic surgery has limited benefit. Arthrodesis, or joint fusion, successfully alleviates pain and is commonly performed in the spine and in small joints of the carpus, hand, and foot. Arthrodesis of the major proximal joints of the upper and lower extremities is not well tolerated because of the functional deficits associated with loss of motion. Total joint arthroplasty represents the most significant advancement in the treatment of osteoarthritis in the past century. It is the mainstay of surgical treatment for advanced osteoarthritis of the hip, knee, and glenohumeral joints. For older persons, total joint replacement is a highly successful procedure that will probably last for the duration of their lives. The pain and disability of end-stage osteoarthritis can be eliminated, restoring patients to near-normal function. However, a total joint replacement may not be sufficiently durable in persons with life expectancies exceeding 20 years and those who wish to participate in highdemand activities. After total joint arthroplasty, patients should be encouraged to remain physically active for general health and also for the quality of their bones. There is evidence that increased bone quality improves prosthesis fixation and decreases the incidence of early loosening. To recommend a certain activity after total knee or hip replacement, factors such as wear, joint load, intensity, and the type of prosthesis must be taken into account for each patient and sport. Because load exponentially influences the amount of wear, only activities with low joint loading, such as swimming, cycling, or walking, should be performed regularly for exercise. If an activity is performed intermittently for recreation, then activities with higher joint loads, such as skiing or hiking, may be acceptable. It is unwise to start technically demanding wilderness activities after total joint replacement because the joint loads and the risk for injuries are generally higher for these activities in unskilled individuals. Activity recommendations differ after total knee and total hip replacement. During activities such as hiking or jogging, high joint loads occur between 40 and 60 degrees of knee flexion, where many knee designs are not conforming and high stress will occur. It is prudent to be more conservative after total knee arthroplasty than after total hip arthroplasty for activities that exhibit high joint loads in knee flexion. After total knee replacement, patients should alternate activities such as walking and cycling. For mountain hiking, patients are advised to avoid descents or at least use hiking poles. Jogging or sports involving running should be discouraged after total knee replacement,89,90 although some higher-impact activity, such as tennis, may be well tolerated.147 657

CHAPTER 34  Chronic Diseases and Wilderness Activities

TABLE 34-6  Stepwise Management of

PART 4  INJURIES AND MEDICAL INTERVENTIONS

HEMATOLOGY Anemia The most common hematologic condition encountered is anemia. Although specific anemias have certain concerns discussed below, the universal effect of mild to moderate anemia is reduction in exercise capacity. As a rule, for every 1% fall in hematocrit  2 max ) decreases 1% and maximum oxygen consumption ( VO endurance decreases by 2%.23,45,65,164 Thus anemic patients should be counseled that their ability to perform strenuous exercise will be less than that of traveling companions; they may not be able to keep up the same pace or hike as far. Thalassemia Trait.  Thalassemia trait is the most common inherited hemoglobin disorder and can be encountered in patients from diverse ethnic origins. β-Thalassemia trait is autosomal dominant and results in mild microcytic anemia (mean corpuscular volume [MCV] approximately 60 to 70 fL) and hematocrit in 30% range. It is diagnosed by hemoglobin electrophoresis showing elevated hemoglobin A2 in the presence of normal iron stores. The genetics of α-thalassemia trait are more complex, with the most common forms being electrophorectically silent and autosomal dominant. α-Thalassemia trait leads to microcytosis (MCV approximately 70 fL) with hematocrit at the lower end of normal range. A severe recessive variant, hemoglobin H disease, predominantly affects people of Southeast Asian origin. This type of α-thalassemia results in hemolytic anemia with hematocrits that can be in the high 20% to low 30% range. The presence of either α- or β-thalassemia trait does not lead to any specific problems except for the anemia. Diagnosis is important to avoid inappropriate therapy with iron or unnecessary genetic counseling. Iron Deficiency.  Iron deficiency is very common, affecting up to 40% of women and 1% to 5% of men. In athletes, especially runners, the incidence is increased to 50% to 80% of women and 10% to 17% of men.117,140 This increase in iron deficiency may reflect iron loss through gastrointestinal bleeding,26,29,111 sweat losses, urinary iron loss via hemolysis,26,72 and blockage of iron absorption by inflammation.128 Iron deficiency has multiple impacts on exercise ability. As noted above, lower hematocrit decreases exercise ability. Iron lack has a negative effect on exercise beyond the decrement in hematocrit. Studies have  2 max , exercise endurshown that repletion of iron improves VO ance, and strength, suggesting that lack of tissue stores of iron is detrimental.17,18,20,61,140 This may be due to iron deficiency first leading to loss of muscle iron stores because of the bone marrow iron demand.87 Iron deficiency has been shown to impair cold tolerance, perhaps because of alteration in thyroid hormone metabolism.7,16 Going to altitude puts additional stresses on body iron stores. Although the initial increase in hematocrit at altitude is due to contraction of plasma volume, red cell production increases several days later. Studies have shown that after as little as 1 week at altitude, serum ferritin falls as iron is consumed to make more red cells.9,74,134 For example, Berglund and associates9 showed that after 10 days of breathing 14% oxygen, a 10% increase in hemoglobin was associated with a 46% decrease in ferritin. Although serum ferritin is the best test for iron deficiency, the range of “normal” listed on the laboratory report may not be the appropriate level for athletes. Improvement can be seen in exercise ability and fatigue with the ferritin above 50 ng/mL.168 Climbers with low ferritin levels may not be able to mount an adequate hematocrit response to altitude and may have impaired exercise ability. In one study, climbers with ferritin levels above 50 to 100 ng/mL were the ones who performed the best.134 In theory, 250 mg of storage iron is required for every 1 g/dL increase in hemoglobin; that amount of iron is equivalent to 25 to 32 ng/ mL of serum ferritin. It has been suggested that “ideal” hemoglobin for altitude should be 2.5 gm/dL higher than the usual range; increasing the hemoglobin by that amount would require a serum ferritin level of 62 to 80 ng/mL.9 Iron replacement therapy should be prescribed for any person with a serum ferritin under 50 ng/mL who is planning a high- or 658

extreme-performance expedition or if serum ferritin is under 100 mg/mL in a person planning a prolonged trip to altitude. Given that 100 mg of oral iron decreases iron deficiency and improves vigor in women undergoing basic training for 9 weeks, women undergoing major treks or expeditions can consider this option.112 The best method of iron replacement is still controversial. One approach is to start with a single pill that contains at least 60 mg of elemental iron once a day; the gut cannot absorb more iron, and additional doses can lead to GI intolerance. Taking the pills with vitamin C can aid absorption. People taking iron should avoid certain foods, such as fiber and tea, within several hours of iron ingestion. Those who need iron replacement but who cannot tolerate or absorb oral iron can accomplish intravenous iron therapy.54 Hemolytic Anemias.  Many patients have well-compensated congenital hemolytic anemias. The laboratory findings are mild to moderate anemia with elevated reticulocyte count, indirect bilirubin, and lactate dehydrogenase. Red cell membrane defects, such as hereditary spherocytosis, are the most common causes of inherited hemolytic anemia. Any patient with hemolysis is prone to folate deficiency, so adequate intake (400 to 800 mcg/day) should be part of nutrition planning. Patients with hemolytic anemia may have increased hemolysis with fevers. The incidence of gallstones is increased in these patients, so consideration should be given to obtaining a screening ultrasound before prolonged expeditions away from medical care. Glucose-6-Phosphate Dehydrogenase Deficiency.  Glucose6-phosphate dehydrogenase (G6PD) deficiency is an important cause of hereditary hemolytic syndromes with wilderness implications.10 G6PD deficiency is gender linked and most commonly affects males. The defect is in the hexose monophosphate shunt and renders the red cell unable to withstand oxidative stress. Most people with this disease have hemolysis only with such stressors as infections and intake of oxidative drugs. The two main subtypes of G6PD deficiency are African and Mediterranean. In the African type, the enzyme is unstable and older cells have diminished activity. Therefore, when these patients suffer hemolysis, it is self-limited because as the reticulocyte count increases, G6PD activity returns to normal. The Mediterranean type is caused by a defective enzyme and so tends to be more severe because with oxidative stress, G6PD activity does not keep pace with the reticulocyte count increase, and fatal hemolysis may result. G6PD deficiency is of concern because many medicines used in travel medicine can lead to sudden and severe hemolysis (Box 34-2). Many patients are unaware that they are

BOX 34-2  Drugs That May Precipitate a Hemolytic

Crisis with G6PD Deficiency

Acetanilide Dapsone Furazolidone Isobutyl nitrate Methylene blue Nalidixic acid Naphthalene Nitrofurantoin Pamaquine Phenazopyridine Phenylhydrazine Primaquine Quinolones Sulfacetamide Sulfamethoxazole Sulfanilamide Sulfapyridine G6PD, Glucose-6-phosphate dehydrogenase.

Site of Bleed

Hemostatic Level

Hemophilia A

Hemophilia B

Joint

80% acutely, then 40% every other day until resolved 40%-50%

40 units/kg initially, then 20 units/kg every other day until healed 20-40 units/kg per day until healed

100%* Initially 80%-100%, then 30% until healing Initially 100%, then 50% until healing Initially 100%, then 30% until healing Initially 100%, then 50%-100% for 14 d Initially 100%, then 80%-100% until wound healing begins, then 30% until suture removed

50 units/kg* 40-50 units/kg, then 30-40 units per day

80 units/kg initially, then 40 units/kg every other day or third day as needed 40-60 units/kg, then 20-30 every other day as needed 100 units/kg* 80-100 units/kg, then 35-40 units every day 100 units/kg, then 30-40 units every day 100 units/kg, then 30-40 units every day 100 units/kg, then 50 units/kg every day

Muscle Oral Nose Gastrointestinal Genitourinary Central nervous system Surgery/trauma

50 units/kg, then 30-40 units/kg per day 50 units/kg, then 30-40 units/kg per day 50 units/kg, then 25 units/kg every 12 hr 50 units/kg, then 40-50 units every 12 hr adjusted according to healing

100 units/kg, then 50 units every day adjusted according to healing

Modifed from de Wit R, Sleijfer S, Kaye SB, et al: Bleomycin and scuba diving: Where is the harm? Lancet Oncol 8:954, 2007. *Antifibrinolytic agents are useful for oral bleeding. Note: For severe or persistent minor bleeding, factor levels should be followed.

G6PD deficient; their first symptom may be fulminant hemolysis with antimalarial drugs. In the field, acute hemolysis manifests as back pain and dark urine. Management is stopping the suspect drug and hydrating the patient. Ingestion of fava beans (an oxidative stress) in patients with the Mediterranean type of G6PD deficiency may cause severe hemolysis, which may prove fatal. Sickle Cell Anemia and Trait.  Eight percent of black patients and 0.08% to 0.5% of whites have sickle cell trait.56,107,149 Mostly clinically silent, there is a potential for problems in the wilderness. Sickling can occur in trait patients under moderately hypoxic conditions. Multiple case reports describe splenic crisis occurring at altitude or during airplane travel.56,107 Patients present with acute onset of severe left upper quadrant pain that may have a pleuritic component, nausea, and vomiting. Therapy is descent, oxygen, and pain control. Rarely in cases of large splenic infarction, splenectomy may be required. Patients with sickle trait are more prone to dehydration due to a renal concentration defect. Maintenance of adequate fluid intake is very important. One study showed that just 45 minutes of exercise without fluids led to sickling in trait patients walking briskly in warm (33° C [91.4° F]) weather.8 Because patients cannot maximally concentrate their urine, the color of the urine cannot be used as a guide to hydration. If patients with sickle trait develop diarrhea or vomiting, very close attention should be paid to hydration status. Concern about the risk for “sudden death” in people with sickle cell trait with strenuous exercise is valid.43,142 Data collected in the 1960s from army recruits in boot camp showed a 28-fold increased risk for death (absolute risk 1 : 3200).148 Review of these cases revealed that most patients had heatstroke, with resulting severe rhabdomyolysis causing their deaths. Practical advice for patients with sickle cell trait is to be cautious about dehydration and to avoid strenuous exercise in the heat, especially if they are deconditioned. Cramping of the legs can be an early warning sign of sickling and a sign to immediately stop exercising and begin to rehydrate.142 Patients with sickle cell anemia often have end-organ damage that may complicate wilderness travel. Older patients may have chronic pain syndromes because of multiple bony infarcts. The leading causes of overall mortality in adults are complications of pulmonary hypertension, which result in hypoxia and impair lung function. Pain crises are unpredictable and can be provoked by heat extremes, dehydration, or hypoxia—all features found in wilderness travel. Patients with sickle cell anemia who are going on limited trips to the wilderness need to be reminded about the importance of adequate fluid intake and to bring sufficient pain medicine to manage both chronic pain and any crisis. When considering longer-term or adventure travel, patients should be screened for pulmonary hypertension. Physician documentation about the patient’s narcotics supply and needs should be carried. Patients should be reminded to comply with folic acid supplementation.

Because most adults with sickle cell anemia are functionally asplenic, they should take the same precautions as outlined below for asplenic patients. Hemophilia Deficiency of factor VIII or IX occurs in 1 of 5000 males.153 Patients with severe hemophilia are at risk for severe bleeding, even with minor trauma. Bleeding most often occurs in muscles and joints, but intracranial hemorrhage is the leading cause of fatal hemorrhage. Patient can have severe arthritis because of repeated bleeding. A rough rule is that patients with less than 1% of normal levels of factor VIII or IX can have spontaneous bleeding, those with 1% to 15% of normal levels may have bleeding with minor trauma, and those with greater than 15% of normal factor levels may have bleeding with major trauma. Factor concentrates to correct the coagulation defects are available. A suggested dosing scheme is given in Table 34-7. The World Federation of Hemophilia website is an invaluable guide to resources available for the traveler in many different countries (http://www.wfh.org/). Hemophilia does not preclude travel or expedition travel. However, patients with hemophilia who are planning travel should take factor replacement with them, especially if they will be away from health care facilities. Only certain factors listed in Box 34-3 can be stored without refrigeration. The patient should also have the supplies necessary, such as alcohol wipes and needles, to inject the factors. At least one member of the traveling party should also be trained to infuse factor in case the patient is incapacitated. The biggest functional limitation to the hemophilia patient is joint disease. Arthritis due to joint bleeds is very common and BOX 34-3  Factor Concentrates That Do Not Require

Refrigeration

Factor VIII Concentrates Recombinant ReFacto Hemophil M Monarc-M Koa¯ te-DVI Alphanate Factor IX Concentrates BeneFix Mononine AlphaNine SD Profilnine SD Bypassing Factor for Factor VIII or IX Inhibitor Patients NovoSeven (rVIIa)

659

CHAPTER 34  Chronic Diseases and Wilderness Activities

TABLE 34-7  Guidelines for Factor Replacement

PART 4  INJURIES AND MEDICAL INTERVENTIONS

can be disabling. Joint bleeds can occur with minor injuries or ankle twists. Before travel, patients should work to strengthen their muscles to provide joint protection. Simple measures to prevent ankle sprains, such as wearing high-top boots, should also be taken. Damaged joints should be splinted to prevent reinjury.

TABLE 34-8  Maintenance Warfarin Adjustment

von Willebrand’s Disease The most common inherited bleeding disorder is von Willebrand’s disease; this may affect up to 1 in 1000 people. It is characterized by easy bruising and mucocutaneous bleeding. Joint bleeding is unusual for most patients. Patients with von Willebrand’s disease can have significant bleeding with trauma. There are multiple types of von Willebrand disease, but the 80% of patients with type 1 respond to desmopressin, which is available as a nasal spray (Stimate). The dose of Stimate is one squirt in each nostril, with the effect lasting up to 24 hours. One needs to be specific when prescribing Stimate, because generic nasal desmopressin that is used for enuresis has too little desmopressin per dose to be effective for bleeding disorders. Estrogens can also raise levels of von Willebrand’s factor; use of oral contraceptives can normalize levels in mildly affected women. The patient with rarer types of von Willebrand disease may require specific replacement therapy with Humate-P, a factor concentrate that contains von Willebrand’s factor. This concentrate must be kept refrigerated.

1.1-1.4

Thrombocytopenia Immune thrombocytopenia is the most common autoimmune hematologic disease; it occurs in one in 50,000 people. Patients with modest (>30,000 platelets/µL) thrombocytopenia are not at greater risk for bleeding except with extreme trauma, so no specific precautions are needed. Patients with chronic immune thrombocytopenia and stable platelet counts can be cleared for wilderness travel. For the patient with a history of recurrent severe thrombocytopenia who is planning prolonged travel, a dose of “pulse” dexamethasone (40 mg orally × 4 days) can be prescribed to be carried and started if the patient notices sudden onset of petechiae and bleeding. There are multiple causes of congenital thrombocytopenia and platelet function defects. Some patients have mild thrombocytopenia with no bleeding defects, whereas other may have both platelet number and function defects. One group of such patients are those with mildly decreased platelets (75,000 to 150,000/µL) but no bleeding defects. These patients require no special precautions. Most patients with congenital platelet defects have a mild bleeding diathesis. Many of these patients respond to desmopressin and can carry the nasal form (Stimate) with them. Anticoagulation Indications for chronic anticoagulation are increasing, especially because of recommendations for lifelong anticoagulation for idiopathic and recurrent deep vein thrombosis (DVT). Patients on warfarin and other oral anticoagulants pose special challenges.135 A varied diet, increased exertion, and potential travel-related illness can dramatically alter the level of anticoagulation. Unless the patient has access to a point-of-care international normalized ratio (INR) monitor, there may be no way to monitor the level of anticoagulation. Well-controlled patients with stable INR can safely go several weeks without an INR check. This assumes that their diet is the same as their regular diet and there are no concurrent illnesses. For patients who plan to travel longer or for those who will be away from health care, the use of point-of-care INR monitors is advised. The patient should be very familiar with how to operate the machine and be able (or have a nomogram) to adjust their warfarin dose. A suggested nomogram is given in Table 34-8. Vitamin K tablets should be carried to allow treatment of very high INR. Another option for long-term therapy is to consider the use of low-molecular-weight (LMW) heparin injections. The dosing is weight based and does not need monitoring. The tradeoff is the extra space required to pack the syringes and inconvenience of proper needle disposal. For the patient who has an absolute requirement for stable anticoagulation, use of LMW 660

Nomogram

International Normalized Ratio (INR)

1.5-1.9 2.0-3.0 3.1-3.9 4.0-5.0 >5.0

Dose Change Day 1: Add 10%-20% total weekly dose (TWD)* Weekly: Increase TWD by 10%-20% Return: 1 wk Day 1: Add 5%-10% of TWD Weekly: Increase TWD by 5%-10% Return: 2 wk No Change Return: 4 wk Day 1: Subtract 5%-10% TWD Weekly: Reduce TWD by 10%-20% Return: 2 wk Day 1: No warfarin Weekly: Reduce TWD by 10%-20% Return: 1 wk Stop warfarin until INR <3.0 Decrease TWD by 20%-50% Return daily

From DeLoughery TG: Oral anticoagulants. In Goodnight SH, Hathaway WE, editors: Disorders of hemostasis and thrombosis: A clinical guide, New York, 2001, McGraw-Hill Professional, pp 533-566. With permission. *TWD, Total weekly dose.

heparin is the safest alternative. In the future, availability of new oral anticoagulants that neither require monitoring nor have food or drug interactions will make management of travelers who need chronic anticoagulation much simpler. Travel Thrombosis Airplane travel has been considered a risk factor for DVT for over 40 years, but it is only recently that flight has been rigorously studied as a DVT risk factor. Case-controlled studies suggest a relative risk for thrombosis of threefold to fourfold with prolonged (>4 to 6 hours) travel, with a higher risk for travel times over 8 hours.1,28,84,158 The absolute risk for thrombosis is uncertain. For example, the overall risk for symptomatic pulmonary embolism is estimated to be 0.4 per million passengers, rising to 4 per million in the highest risk group. One study showed a DVT risk of 1 in 4600 following flight.88,93,129 In contrast, small prospective trials showed a calf vein thrombosis rate of 2% to 10%.144,145 The presence of risk factors, such as history of DVT or underlying hypercoagulable state, is important. Up to 70% to 90% of those with thrombosis had other risk factors for thrombosis.80,108 Pathogenesis of “traveler’s thrombosis” is controversial. Venous stasis appears to be the primary risk factor. Prolonged sitting is a risk factor for thrombosis, perhaps by increasing venous stasis. Although mild hypoxia due to the low air cabin pressure is often blamed in the popular press, there are currently no data to show activation of coagulation with mild hypoxic exposure.37 Preexisting risk factors for thrombosis are important. Most studies indicate that people who develop travel-related thrombosis have other risk factors such as history of thrombosis or estrogen use. The presence of long travel and these thrombotic risk factors raise the risk for thrombosis by 16-fold.108 The best method of prophylaxis is still to be determined. Ideally people should try to be up and exercising their legs at least once an hour. However, given crowded cabins and the security climate, this is unrealistic. Aspirin remains a popular recommendation but has been demonstrated in a randomized trial not to be effective for preventing traveler’s thrombosis and so should not be relied on for this purpose.27,64 Elastic stockings provide protection in trials but have the side effect of discomfort and superficial thrombosis.145 A single prophylactic dose of LMW heparin before the flight is effective, but this is inconvenient for most people. A reasonable approach is to first assess a patient’s risk for thrombosis when traveling by plane for over 6 hours (Box 34-4). For most low-risk people, one could encourage foot movement and avoiding dehydration. For medium- and high-risk patients, stockings (knee-high 20 to 30 mm Hg compression pressure)

Older than age 65 Cancer Carrier of a hypercoagulable state Estrogen use History of lower extremity deep vein thrombosis Lower leg cast Obesity (>2 × ideal body weight) Recent surgery (previous 6 weeks)

should be recommended. In addition, the feasibility of adding LMW heparin on a case-by-case basis for high-risk patients should be considered. The Asplenic Patient Asplenic patients pose unique travel risks. Asplenic patients may have no other health problems but are at risk for overwhelming infections from a diverse group of infectious agents. The risk for overwhelming sepsis varies by indications for splenectomy but appears to be about 1%.11,91 Use of pneumococcal vaccine and recognition of this syndrome have helped lessen the risk, but travel can expose asplenic persons to novel (for them) infectious organisms. The classic bacterial pathogen is the pneumococcus, but in older patients gram-negative bacteria are a common cause of infections.44 Unusual organisms causing overwhelming infections, such as Capnocytophaga from dog bite or babesiosis from tick bite, have been reported.38,176 Asplenic patients need to be counseled about the risk for overwhelming infections and should be vaccinated against pneumococcus, meningococcus, and Haemophilus influenzae.71,115 Patients previously vaccinated for pneumococcus should be revaccinated every 3 to 5 years.91 In addition, due to concerns about greater severity of malaria, they should be scrupulous with antimalarial prophylaxis.106,122 The role of prophylactic antibiotics is controversial for adults, but patients under the age of 18 should be on penicillin VK 250  mg orally twice a day. Patients should be advised to start antibiotics and seek medical care if they get a fever, shaking chills or lower-respiratory tract infections. A reasonable oral antibiotic for self-medicating is amoxicillin/clavulanic acid 875  mg twice a day.33 Patients who are bitten by dogs should also take antibiotics. Asplenic patients should wear an identification bracelet to alert health care providers.48

Chemotherapy can cause a variety of long-term side effects (Box 34-5). Anthracyclines such as Adriamycin can lead to cardiac damage that may be well compensated until another stressor, such as altitude, is added. The risk for chronic heart failure is highest with doses over 300 mg/m2 but can be seen with any dose. Agents such as vincristine can lead to neuropathy that causes loss of dexterity. Of particular concern is bleomycin, an antineoplastic agent that is part of a curative regimen for both germ cell tumors and Hodgkin’s disease. Bleomycin can lead to subtle lung damage that results in loss of diffusing capacity. For very competitive athletes with germ cell tumors, effective non–bleomycin-containing regimens can be used. Bleomycin can also interact with high concentrations of oxygen to cause fulminant lung toxicity. Fatal cases have been reported up to many months after cessation of therapy. Controversy remains as to whether patients who have had bleomycin can safely go scuba diving because of the high pressures of oxygen to which they will be exposed. For example, during a dive to 20 m (65.6 feet), the PIO2 is 0.63 atm. It will be 0.84 atm at 30 meters, potentially leading to lung toxicity.81 This notion has recently been challenged, such that diving can be considered for patients 6 months after receiving bleomycin if they did not suffer pulmonary toxicity.39 Patients who have received bleomycin should wear an identification bracelet in case emergency surgery is needed, so that the lowest possible oxygen concentration is used. The cancer survivor planning to go on a high- or extremeperformance expedition should undergo careful screening. Patients who have received anthracyclines should have cardiac function screened, and pulmonary function needs to be checked in patients who have received bleomycin or other potential pulmonary toxic agents. Any patient who received upper chest or neck radiation should have thyroid function screened. Certain agents used for hematologic malignancies, especially chronic lymphocytic leukemia, can lead to profound and prolonged T-cell immunosuppression that persists for months to years and puts patients at risk for unusual infections. These agents are fludarabine, cladribine, and alemtuzumab. The degrees of immunosuppression can be monitored by measuring CD4 counts. Patients with counts under 200/µL are severely immunocompromised, and travel is not recommended.30,141 Patients with higher CD4 counts still may have residual immunosuppression and may be prone to zoster outbreaks for years after chemotherapy. Increasingly, patients are using oral “targeted” agents for cancer, such as imatinib for chronic myelogenous leukemia and sorafenib for renal tumors. Patients need to be sure that they have an adequate supply of these medications for the trip and “guard” them closely, because they are not available in most countries and often cost several thousands of dollars for a month’s supply.

ONCOLOGY

BOX 34-5  Chemotherapy Agents: Long-Term

The numbers of cancer survivors is increasing, and many of these patients pursue wilderness activities. Chemotherapy can lead to short-term side effects such as nausea and neutropenia, but many side-effects can last months or years after chemotherapy has ended.

Cardiac Dysfunction *Anthracyclines (doxorubicin, daunorubicin, epirubicin, mitoxantrone, idarubicin)

Chemotherapy Common side effects of most chemotherapeutic agents are nausea and marrow suppression. The nausea is short term and managed with 5-hydroxytryptamine blockers. The highest-risk time for neutropenia is usually 10 to 21 days after onset of chemotherapy. Patients may want to hike or go camping between chemotherapy sessions. Neutropenic patients can be cleared for this type of activity as long as they can seek medical care if they become febrile. A good rule of thumb is that patients should not be more than 2 hours away from an emergency department. The vast majority of infections these patients get are due to endogenous organisms and not from the environment, but some precautions, such as wearing a mask when in crowded areas and avoiding ingestion of fresh fruits or vegetables, should be suggested. Thrombocytopenia is more rare with most chemotherapy regimens. Platelet transfusion should be performed for platelet counts under 10,000/µL.

Side Effects

Pulmonary Toxicity *Bleomycin *Radiation therapy *Nitrosoureas Cyclophosphamide Methotrexate Neuropathy *Cisplatin *Oxaliplatin *Vincristine *Taxol Raynaud’s Phenomenon Bleomycin Cisplatin *Common.

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CHAPTER 34  Chronic Diseases and Wilderness Activities

BOX 34-4  Risk Factors for Traveler’s Thrombosis

PART 4  INJURIES AND MEDICAL INTERVENTIONS

Stem Cell (“Bone Marrow”) Transplantation Stem cell transplantation is an increasingly common therapy. Currently three different types of stem cell transplants are performed. Autologous transplants involve harvesting and preserving the patient’s stem cells and then administering radiation and/or chemotherapy (conditioning) to ablate the marrow. This is followed by reinfusion of the stored stem cells. Allogeneic transplant involves infusion of another person’s marrow. Increasingly, nonmyeloablative allogeneic transplants (“mini-transplants”), which involve only modest conditioning, are being used. “Conditioning” is a course of chemotherapy or radiation therapy intended to eradicate the immune system and any cancer in preparation for a bone marrow transplant. The major long-term complication of allogeneic transplant is graft-versus-host disease (GVHD) due to the donor immune system attacking the recipient. Chronic GVHD can be debilitating and lead to chronic skin disease, restrictive pulmonary disease, and increased propensity for infection. When counseling the stem cell transplant patient about travel, one needs to know what type of transplant the patient received, time since transplant, and whether they are suffering from GVHD. In general a patient who has received an autologous transplant and has recovered his or her blood counts can be cleared for travel 6 months after transplant. For the patient who has received an allogeneic transplant, the main concerns are restoration of immunity and presence of GVHD. A reasonable rule of thumb is that patients will be immunosuppressed for 12 to 24 months after they stop taking immunosuppressants and should always be treated as functionally asplenic. The transplant (especially allogeneic) patient who is considering a high- or extreme-performance trip should undergo pulmonary and cardiac screening. Timing of travel immunizations for transplant patients is an uncertain area.33,100 If given too soon, the immature immune system will not mount a response. Live vaccines are also a concern if immune function is not normal. An approach is given in Table 34-9. Patients with stem cell transplants who remain on immunosuppression have special concerns. It should be remembered that their family members and close contacts should also not receive live vaccines for fear of disease transmission to these patients. New medications can interfere with immunosuppression, so consideration should be given to starting any new medications (such as malaria prophylaxis) at home to monitor levels of immunosuppressive medications.

SOLID ORGAN TRANSPLANT RECIPIENTS Solid organ transplant recipients include persons who have received heart, lung, kidney, liver, or pancreas transplants. Concerns for the solid organ transplant recipient engaging in wilderness activities include risk for infection, availability of local

medical care knowledgeable in the care of transplant recipients when traveling outside of the United States, carrying adequate supplies of medication and storage of medications on extended trips (immunosuppressive medications and prophylactic medications for infection), and increased level of physical activity. Improvements in immunosuppressive agents have decreased the incidence of rejection of transplanted organs in solid organ transplant recipients but have increased the risks for infection and malignancy.55 Newer immunosuppressive approaches, including use of sirolimus, mycophenolate mofetil, and T-cell and B-cell depletion, have largely replaced high-dose corticosteroids and azathioprine. Sources of infections include donor-derived infections, recipient-derived infections, nosocomial infections, and community-acquired infections. A predictable timeline for risk for infection is dictated by the time from transplant and the immunosuppressive regimen (Figure 34-2). In the first month after transplant donor-derived infection, recipient-derived infection, and nosocomial infection are the categories for infection risk. In the first 6 months after transplantation infectious risk is determined by whether Pneumocystis (trimethoprim-sulfamethoxazole) and antiviral prophylaxis medications (valacyclovir, high-dose acyclovir, ganciclovir, or valganciclovir) are used. After 6 months, the primary risk is community-acquired infections, some of which are “unusual” pathogens (e.g., aspergillus, atypical molds, Mucor species, Nocardia, Rhodococcus, and rare viruses). Wilderness activities and travel in rural areas or Third World countries can increase risk for exposure to potential infectious pathogens. Transplant recipients should wash their hands after food preparation and after contact with soil or feces. They should avoid well water and lake water (which may contain Cryptosporidium or Giardia species), undercooked meats, unwashed fruits and vegetables, and unpasteurized dairy products (which may contain Escherichia coli or Listeria monocytogenes).55 Despite these concerns, solid organ transplant recipients can travel safely outside the United States or Canada. In one study of 303 solid organ transplant recipients, 94% of whom were further than 1 year from transplant, only 24 (8%) became ill during travel.165 The most common illness was upper respiratory infection. Illness during travel was more common among those who visited high– infection risk areas (18.4% became ill during travel to Asia, Central or South America, Africa, or the Middle East), compared with low–infection risk areas (6.1% became ill). No travelers were diagnosed with “tropical” infections. Three of 24 ill travelers returned home early. Two travelers to high–infection risk areas developed transplant-related illness, one with post-transplant lymphoproliferative disease and the other with acute allograft rejection. Only 18% of travelers in this series were in rural areas, and only one traveler was camping, so risk for infection may be greater during some wilderness activities.

TABLE 34-9  Post–Bone Marrow Transplant Vaccine Recommendations Vaccine

Allogeneic Transplant

Autologous Transplant

Timing

Tetanus toxoid Diphtheria Inactivated poliovirus Pneumococcal H. influenzae Influenza Measles Rubella Hepatitis B Hepatitis A Inactivated polio Oral polio MMR Typhoid (tY21a) Varicella Yellow fever Japanese encephalitis V Meningococcal vaccine

Recommended Recommended Recommended Recommended Recommended Recommended No earlier than 24 mo No earlier than 24 mo

Recommended Recommended Recommended Recommended Recommended Recommended

6-12 6-12 6-12 6-12

No No No No No

earlier earlier earlier earlier earlier

than than than than than

24 24 24 24 24

mo mo mo mo mo

mo mo mo mo

6-12 mo 6-12 mo 6-12 mo

6-12 mo 6-12 mo

From Committee to Advise on Tropical Medicine and Travel (CATMAT): The immunocompromised traveler: An Advisory Committee Statement (ACS), Can Commun Dis Rep 33:1, 2007; and Ljungman P, Cordonnier C, Einsele H, et al: Vaccination of hematopoietic cell transplant recipients, Bone Marrow Transplant 44:521, 2009.

662

Live

Yes Yes

Yes Yes Yes Yes Yes

Nosocomial, technical (donor or recipient)

Activation of latent infection (relapsed, residual, opportunistic)

Transplant

CHAPTER 34  Chronic Diseases and Wilderness Activities

Doner-derived infection

Community-acquired

Dynamic assessment of risk infection Common infections in solid-organ transplant recipients

Recipient-derived <1 month infection Infection with antimicrobialresistant species: MRSA VRE Candida species (non-albicans) Aspiration Catheter infection Wound infection Anastomotic leaks and ischemia Clostridium difficile colitis Donor-derived infection (uncommon): HSV, LCMV, rhabdovirus (rabies), West Nile virus, HIV, Trypanosoma cruzi Recipient-derived infection (colonization): Aspergillus, Pseudomonas

1-6 months With PCP and antiviral (CMV, HBV) prophylaxis: Polyomavirus BK infection, nephropathy C. difficile colitis HCV infection Adenovirus infection, influenza Cryptococcus neoformans infection Mycobacterium tuberculosis infection Anastomotic complications Without prophylaxis: Pneumocystis Infection with herpesviruses (HSV, VZV, CMV, EBV) HBV infection Infection with Listeria, Nocardia, Toxoplasma, Strongyloides, Leishmania, T. cruzi

>6 months Community-acquired pneumonia, urinary tract infection Infection with aspergillus, atypical molds, Mucor species Infection with Nocardia, Rhodococcus species Late viral infections: CMV infection (colitis and retinitis) Hepatitis (HBV, HCV) HSV encephalitis Community-acquired (SARS, West Nile virus infection) JC polyomavirus infection (PML) Skin cancer, lymphoma (PTLD)

FIGURE 34-2  Changing timeline of infection after organ transplant. Infections occur in a generally predictable pattern after solid-organ transplant. The development of infection is delayed by prophylaxis and accelerated by intensified immunosuppression, drug toxic effects that may cause leukopenia, or immunomodulatory viral infections such as infection with cytomegalovirus (CMV), hepatitis C virus (HCV), or Epstein-Barr virus (EBV). At the time of transplantation, a patient’s short-term and long-term risks for infection can be stratified according to donor and recipient screening, the technical outcome of surgery, and the intensity of immunosuppression required to prevent graft rejection. Subsequently, ongoing assessment of the risk for infection is used to adjust both prophylaxis and immunosuppressive therapy. HBV, Hepatitis B virus; HIV, human immunodeficiency virus; HSV, herpes simplex virus; LCMV, lymphocytic choriomeningitis virus; MRSA, methicillin-resistant Staphylococcus aureus; VRE, vancomycin-resistant Enterococcus faecalis; PCP, Pneumocystis carinii pneumonia; PML, progressive multifocal leukoencephalopathy; PTLD, posttransplantation lymphoproliferative disorder; SARS, severe acute respiratory syndrome; VZV, varicella-zoster virus. (Data from Fishman JA: Infection in solid-organ transplant recipients, N Engl J Med 357:2601, 2007.)

Vaccination is an important element of prevention of infection for transplant recipients. Immunization status should be carefully reviewed before transplant to ensure that all immunizations are up to date and any needed vaccinations administered while the patient is immunocompetent. Vaccination is generally less effective during immunosuppression. Pneumococcal vaccine is recommended every 3 to 5 years, and influenza vaccine is recommended annually. The immunologic protection from vaccines may be limited.55 Other vaccines are appropriate for patients who travel to regions where certain illnesses are endemic, and patients should seek advice from transplant and travel medicine specialists. Live vaccines are generally contraindicated after transplantation, because they may cause disseminated infection in immunocompromised hosts.55 Wilderness activities commonly require increased exercise; solid organ transplant recipients in general have lower-thanpredicted exercise capacity.154 This includes recipients of heart, lung, liver, and kidney transplants. Although maximal oxygen consumption is decreased, cardiopulmonary function is appropriate for the level of work performed. Cardiac output is normal in response to exercise, oxygen desaturation does not occur, and ventilation is not a limiting factor. Anemia may play a role in decreasing oxygen-carrying capacity, although the degree of anemia is generally mild and does not explain the decrease in exercise capacity. Peripheral muscle work capacity or oxygen utilization by the tissues are proposed as causes of decreased

exercise capacity. Indeed, many solid organ transplant recipients have endured long illnesses before transplant and have deconditioned muscle. Supervised exercise programs improve maximum oxygen consumption, but it still may be lower than predicted.154 Immunosuppressive drugs have also been suggested as a cause of peripheral myopathy. Despite results from studies showing decreased maximal exercise capacity in solid organ transplant recipients, clearly some are capable of high-performance athletic endeavors, including mountaineering, competitive recreational sports, and even competition at the Olympic level. Most transplant recipients return to a level of function at least as good as before transplant. In general, solid organ transplant recipients are capable of pursuing wilderness activities but should consult with their transplant specialist medical providers for recommendations on specific issues. If traveling outside the United States, the transplant recipient should wait until his or her immunosuppressive regimen is stable at least 6 months out from transplant and consult with a travel medicine specialist for specific vaccination and prophylaxis recommendations.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 35 

Mental Health in the Wilderness BARRY MORENZ

Wilderness environments often have beneficial effects on the overall emotional health of many individuals. Individuals who choose to pursue wilderness activities are often seeking relief from the stress of their hectic urban lives (Figure 35-1). However, remote wilderness environments can present unique stresses of their own. Mental health and mental health problems might improve in the wilderness, but psychiatric problems can emerge or become worse in response to the demands of wilderness experiences. This chapter discusses the diagnosis and management of emotional problems in the wilderness, including the use of psychotropic medications, both in people who have preexisting psychological difficulties and in those who develop new emotional problems in the wilderness. The Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision1 (DSM-IV-TR) is the most recent and widely used compendium of the nosology of psychiatric disorders. Most mental health problems can be thought of as falling into six broad groups of disorders: (1) anxiety disorders; (2) mood disorders; (3) psychotic disorders; (4) organic mental disorders; (5) personality disorders; and (6) substance abuse disorders. Specific diagnostic assessment with the use of the DSM-IV-TR and psychological testing in a wilderness setting is not practical. Appropriate triage and management in a wilderness setting depends on classifying emotional and behavioral problems as falling into one or more of these broad categories. Separating normal from abnormal human behaviors is the first step in the triage of emotional problems. It is not straightforward to differentiate what may be considered an adaptive response to the challenge of a wilderness experience from responses that are maladaptive and signal the onset of new emotional problems or the exacerbation of preexisting psychiatric problems. For example, at the end of a physically challenging day of backpacking with a group, one member of the group breaks down in tears. Such crying may be a healthy and adaptive response, or it may be a sign of depression or panic. The process of crying can relieve stress and result in the tearful backpacker receiving needed emotional support. Alternatively, such tears may suggest that the person feels mentally and physically overwhelmed. The person might be approaching a panic state, and, if appropriate interventions are not undertaken, the person’s mental state will deteriorate. The challenge is to determine whether a pat on the back and some encouraging words are all that are needed or if the individual has to be assisted out of the wilderness to prevent further emotional deterioration. In the following sections, four important topical areas for assessment and management of emotional problems in the wilderness are discussed: (1) the common characteristics of the six major categories of psychiatric disorders; (2) suicide and violence potential; (3) psychosomatic complaints; and (4) response to crisis (i.e., disasters and survival psychology). At the end of the chapter, Table 35-1 summarizes the triage of psychiatric problems in the wilderness.

Psychiatric Disorders ANXIETY DISORDERS Anxiety is a universal emotion that is usually a normal and adaptive response to everyday life. Anxiety motivates us in myriad ways to complete tasks, study for tests, have a reliable belay partner when rock climbing, and work to earn a living. The experience of anxiety is physical as well as psychological. Increased heart rate, blood pressure, and respirations; sweaty palms; and muscular tension are common physical manifestations 664

that accompany the psychological feelings of anxiety and tension. Rarely is anyone totally free of anxiety; however, for most people, anxiety is mild. There are many ritualized and socially condoned means of diminishing everyday forms of anxiety, such as jogging, athletics, socializing with friends, drinking alcohol, and engaging in sexual activity. In response to threat or danger, an extreme form of anxiety that is triggered in everyone is the fight-or-flight response. This response occurs automatically and without conscious control. Athletes, extreme sports enthusiasts, military combatants, crime victims, and anyone confronting serious injury or death will have this response triggered. The fight-or-flight response is mediated through the autonomic nervous system, which, when triggered, causes blood to be diverted from the internal organs to the skeletal musculature. Heart rate, blood pressure, and respiration rate dramatically increase. A person in a fight-or-flight state often acts with little or no reflective thinking to preserve his or her life or the lives of others. Memories of these episodes may be unreliable, because an individual is often on “automatic pilot.” Episodes of autonomic arousal in response to danger or threat are normal. However, some people experience anxiety in ways that interfere with their ability to function, to complete everyday tasks, and to respond appropriately to danger. The several types of anxiety disorders include generalized anxiety disorder, specific phobias, panic disorder, obsessive– compulsive disorder (OCD), and acute and post-traumatic stress disorder (see Response to Crisis, later). People with generalized anxiety disorder worry a lot. Their anxiety is out of proportion as compared with what most people would experience in similar circumstances. The afflicted individual may find it difficult to keep worrisome thoughts from interfering with attention that needs to be paid to current activities. The focus of the worries among people with generalized anxiety disorders are mundane and include such concerns as getting up on time for work, making appointments, and doing chores. These individuals experience somatic symptoms, such as sweating, nausea, and diarrhea. The prevalence of generalized anxiety disorders is approximately 1.5%.5 In a wilderness setting, the foci of worries might be bear attacks, getting lost, not keeping up, flash floods, and so forth. These anxieties will likely diminish the person’s enjoyment of a wilderness experience, affect his or her concentration, and drain his or her energies. People with generalized anxiety may negatively affect group morale. However, generalized anxiety problems are not emergencies; they are chronic problems that can be managed in the field. People with a generalized anxiety disorder require ample reassurance. A good leader can provide reassurance and appoint other group members to assist with reassuring the anxiety-ridden individual.4 Building rapport and trust with the afflicted person is a good first step to helping them. Trying to talk someone out of his or her worries is unlikely to be productive. In the field, a benzodiazepine (e.g., 0.5 to 2 mg of lorazepam two to three times a day) can be useful.11 Side effects include sedation, memory difficulties, and impairment of motor coordination. Sustained benzodiazepine use can lead to physical dependence and withdrawal symptoms with abrupt discontinuation. Thus, such medications must be used cautiously in the field, but they can provide short-term relief of anxiety-related symptoms. Probably one of the more common specific phobias encountered during a wilderness outing is a fear of heights or exposure (e.g., to an edge with a drop-off). Other common phobias are to snakes, spiders, and water. A specific phobia is an unreasonable fear in anticipation of or on exposure to a particular object

OBSESSIVE–COMPULSIVE DISORDER: REPETITIVE BEHAVIORS FIGURE 35-1  A Sierra Club group enjoys camping in the Grand Canyon.

or situation.1 The intensity of anxiety with the exposure may vary from relatively mild to extreme panic. In some instances, phobias to heights cannot be overcome in the wilderness. For instance, a trail that crosses a bridge over a chasm or that involves a section of precipitous exposure might be more than can be managed by an individual with a specific phobia to heights. I have personally guided people who were so terrified of exposure that they were unable to complete some trails. Sometimes, gentle reassurance or distraction may be all that is required. Engaging height-phobic people in distracting conversations while backpacking in areas that involve dizzying exposure can be successful. However, if an individual is likely to respond with extreme anxiety and become unbalanced, then it is not safe to use such psychotherapeutic measures. Individuals with panic disorders experience recurrent and unexpected panic attacks. A panic attack occurs during a discrete period of time that lasts approximately 10 to 30 minutes, and is manifested by one or more of the following symptoms: pounding heart, sweating, trembling, chest pain, nausea, dizziness, numbness, chills, hot flushes, and shortness of breath. During a panic attack, a person may fear that he or she is dying, having a heart attack, going crazy, or losing control. Such individuals often visit emergency departments out of fear that they have had a heart attack or that something is seriously physically wrong. Any person with one of the anxiety disorders described in this section may experience a panic attack, but the person with a panic disorder experiences recurrent and unexpected panic attacks. These attacks occur without warning and seem to come “out of the blue,” which is in contrast with being in response to a specific trigger (e.g., as with specific phobias, which were described previously). As a result of recurrent attacks, people may develop avoidant behaviors, because they do not want to be in situations in which escape might be difficult or embarrassing or in which help might not be available (e.g., agoraphobia). When these people are caught in these situations, they have a desperate desire to flee. Agoraphobia may lead people with panic disorders to avoid leaving their homes, or they may leave only in the company of trusted companions. Panic disorders occur in approximately 1.6% to 5% of the population.5 Treatment with selective serotonin reuptake inhibitors (e.g., fluoxetine, sertraline) or benzodiazepines (e.g., alprazolam, clonazepam) or with a combination of the two and with psychotherapeutic intervention can be successful for controlling panic disorder and agoraphobia.5 People with panic disorder whose symptoms are not problematic may safely enjoy a wilderness adventure without difficulty. However, remote locations, bad weather, or physical challenges may increase the stress on such individuals, thereby causing them to experience a resurgence of symptoms. Having panic attacks in the wilderness may precipitate agoraphobia. The afflicted person may want to escape from the wilderness, and he or she may be completely intolerant of being left alone, even for brief periods. A person who is having a panic attack in the wilderness may present a diagnostic dilemma. He or she may look like he or she is having a heart attack or experiencing acute respiratory distress

A person on a wilderness trip is observed constantly stopping to wash his hands in a stream or lake or with water that he is carrying. His hands are observed to be raw from frequent washing, and the time consumed by this activity is slowing the group’s progress to a crawl. When asked about the hand washing, the individual apologizes and acknowledges that the behavior is irrational but explains that he is deathly afraid of germs and cannot cease the behavior. Another person on a wilderness trip is frequently overheard counting in a whispered voice. When asked about the counting, the individual (with considerable embarrassment) explains that she is afraid that she will attack someone, so every time that she has a violent thought, she counts to 100. The obsessions and compulsions of a person with OCD are usually seen as irrational by the person who is experiencing them, but at the same time he or she feels helpless to stop them. If a person with OCD is prevented from performing ritualistic obsessions and compulsions, he or she may near panic or experience full panic attacks. A person with OCD may not be able to adhere to the requirements of a wilderness trip. For instance, the chronic hand washer may slow a group so profoundly that the group cannot make reasonable progress. The example of the person who tries to control his or her anxiety about acting violently by counting may present less of a problem. People with OCD are not typically violent, but a person who is observed to be constantly counting to ward off violent behaviors may have difficulty fitting in with a group. In the general population, the prevalence of OCD is 1% to 2.5%.5 People with OCD are often successfully treated with clomipramine and psychotherapy.5 It is unlikely that OCD symptoms will appear suddenly on a wilderness trip. Frank disclosure to a wilderness group about the OCD symptoms of a member of the group can diminish the group’s anxieties about the person’s odd behaviors and make the afflicted person less likely to be isolated by the group.

MOOD DISORDERS Sadness, moodiness, happiness, and elation are normal emotions within the human experience. However, when they become extreme and prolonged and interfere with normal functioning, they are considered mood disorders. People with severe depression or unstable bipolar disorder (i.e., manic–depressive illness) will not usually venture into the wilderness. However, people who are being successfully treated or who have relatively mild symptoms may participate in wilderness adventures. Seriously depressed people feel sad, useless, and bad about themselves and the world. Their view of the world is dark, and they have difficulty believing that their lives will improve. Depressed people have difficulty sleeping, lose their appetites, have poor energy levels, lose concentration, withdraw socially, cry for no reason, and have difficulty enjoying anything. The most common diagnostic term for this type of depression is major depression; the prevalence of this disorder is approximately 2.5% to 10%.5 At their worst, people with severe depression may become psychotic and suicidal (see Suicide and Violence Potential as well as Psychotic Disorders, later).1 People who are having mild problems are unlikely to develop severe symptoms rapidly, because severe symptoms gradually appear over a period of weeks or months. The more likely problem on 665

CHAPTER 35  Mental Health in the Wilderness

caused by pulmonary edema. A careful history that indicates that the person has a history of panic disorder and does not have a history of heart disease may help. However, for an older person who may have risk factors for heart disease, the distinction between panic disorder and symptoms of a myocardial infarction may be nominal. People who have a panic attack usually begin to calm down within 30 minutes to 1 hour. Symptoms often respond to a benzodiazepine (e.g., lorazepam), reassurance, and support. Providing regular doses of benzodiazepines to an individual with a panic disorder or increasing the dosage of currently prescribed benzodiazepines may be enough to allow for the completion of the trip.

PART 4 INJURIES AND MEDICAL INTERVENTIONS

a wilderness adventure is finding someone who started out with mild symptoms that are becoming worse. Such individuals may already be taking antidepressant medications (e.g., citalopram, paroxetine). These medications work slowly over a period of weeks, so a change in dose in the midst of a wilderness trip probably would probably not provide significant benefit. The most common problem that the wilderness group may face with a depressed person is that person’s overall impact on group morale. Emotional outbursts, crying for no apparent reason, and offhand comments about suicide will likely concern and distress others in the group. If group members provide encouragement and emotional support, this may help the depressed person to get through the trip safely. However, severe symptoms may not respond to ordinary support. A lack of response can anger others, who may begin to feel conflicted, because they recognize that they are punishing someone who is already suffering. As the symptoms grow worse, it may become necessary to hasten the depressed person’s departure from the wilderness, especially if there is suicidal ideation. Individuals with bipolar disorder experience episodes of major depression that alternate with periods of mania over a period of months, often with normal functioning occurring between the abnormal episodes. The prevalence of bipolar disorder is approximately 1%.5 During periods of normal mood or during the early stages of a manic phase (i.e., hypomania), bipolar persons may participate in wilderness adventures with no difficulty. During a period of hypomania, a person is very positive, productive, hardworking, energetic, and expansive. However, as the person becomes manic, problems become readily apparent. There is often rapid and pressured speech that is difficult to interrupt. Sufferers might not sleep at all, or they may be excessively gregarious and begin to believe that they have superhuman powers. An individual may try to awaken a wilderness group in the middle of the night to hike up a nearby peak. When rebuffed, the manic person might take off alone with no water or protection from the weather because of the belief that he or she is superhuman. A guide described a participant on a wilderness trip who became manic and could not be dissuaded from climbing to the top of a mountain to talk with God. An individual with mania who is in the wilderness should be considered a medical emergency and should be evacuated as rapidly as possible. Careful questioning may reveal that the manic person is taking psychiatric medications such as mood stabilizers (e.g., lithium, divalproex), antipsychotic medications (e.g., risperidone, olanzapine), or both. People who take lithium must avoid dehydration, which can result in lithium toxicity. Lithium toxicity begins with tremulousness and can proceed to seizures and death. If lithium toxicity is suspected, the lithium should be stopped and the person should be well hydrated. The patient may require dialysis to resolve the toxicity, so evacuation is required. People with bipolar disorder sometimes stop their medications because they enjoy how they feel when they are hypomanic. The use of a benzodiazepine (e.g., lorazepam) or an antipsychotic medication (e.g., risperidone) can control some of the symptoms. Risperidone (2 to 6 mg) and lorazepam (4 to 8 mg) spread over the course of a day may be required to keep a manic individual calm.5 It may be possible to coax a manic person out of the wilderness with the use of encouragement and enticements. Manic indivi­ duals can be extremely irritable and sometimes aggressive. Weapons should be confiscated. If a manic individual will not voluntarily leave the wilderness, then assistance—including law enforcement—should be obtained as soon as possible. An evacuation may require the individual to be forcibly restrained and medicated. While waiting for help to arrive, members of the group must constantly contain the manic individual’s excesses to keep both the affected individual and the group safe.

PSYCHOTIC DISORDERS Individuals with severe mental illnesses (e.g., schizophrenia, schizoaffective disorder) do not typically venture into the wilderness, especially if they are in a deteriorated state. Their overall functioning is too low for them to organize themselves to the point that they could join a wilderness group. Those 666

persons who have been able to benefit from treatment, usually in the form of antipsychotic medications, sometimes venture with groups into the wild. There is an approximate 1% prevalence of schizophrenia worldwide.5 Tragically, the illness often manifests during young adulthood. The hallmark of these disorders is a substantial period, usually of at least 1 month, during which the individual becomes unable to rationally perceive reality. A person who believes that a sinister group worshiping the devil has implanted a transmitter in his mouth (delusion) and who hears mysterious people talking about him and saying that he is pathetic and should kill himself (auditory hallucination) is considered psychotic. People with delusions and hallucinations cannot be talked out of them. People who are successfully treated with medications may still have some unusual or even delusional beliefs, but the psychotic symptoms have receded into the background and are not an active concern for the individual. In addition to psychotic symptoms, people with schizophrenia or a schizoaffective disorder often seem awkward or distant interpersonally. Their thoughts may be jumbled and disorganized. Concrete thinking that is literal or obvious with little ability for abstraction is common. If they are receiving adequate treatment, such individuals might enjoy a wilderness adventure with no difficulty, although their personal contribution to the group may be nominal. Antipsychotic medications—especially older ones such as haloperidol—that are required for the treatment of symptoms cause a wide range of side effects, including extrapyramidal symptoms (e.g., Parkinsonism), acute dystonias, insomnia, sedation, and orthostatic hypotension.11 Side effects alone may preclude a person from participating in a wilderness adventure, but people who have been taking medication for weeks or months may have adapted to the side effects. Newer antipsychotic medications (e.g., aripiprazole [Abilify]) have fewer side effects. Problems arise for the wilderness group if a member of the group becomes acutely or floridly psychotic. Symptoms may range from mild issues (e.g., a person asking the group why they are always talking about him) to paranoid beliefs that snipers are in the woods trying to kill the psychotic individual. Very mild symptoms may be tolerable, or the individual may respond to periodic gentle reassurance (i.e., reality orientation). An increase in the dose of the individual’s already-prescribed antipsychotic medication may help, or a benzodiazepine may have a calming effect, at least temporarily. If psychotic symptoms become more severe with prominent paranoia or agitation or if the victim begins to make bizarre accusations toward others in the group, the situation should be treated as a medical emergency, and the person should be evacuated as soon as possible. Psychotic individuals’ behaviors may be unpredictable and violent toward themselves or others. The many causes of psychotic symptoms include schizophrenia, schizoaffective disorder, mania, illicit drugs (e.g., methamphetamine), and organic causes (e.g., brain tumor, metabolic disturbance). A good history may help with the differential diagnosis, but it may be difficult in the field to determine the cause of psychosis.

ORGANIC MENTAL DISORDERS There any many medical problems in the wilderness that can cause behavioral symptoms, and these range from mild confusion that is associated with high-altitude hypoxemia to delirium that is associated with high-altitude cerebral edema. A person in the wilderness may have fallen and hit his or her head on a rock, which initially results in a minor scrape and a headache; however, this may progress to a subdural hematoma and delirium that may become life threatening. It is crucial to recognize which signs of delirium in the wilderness are true medical emergencies. A person with delirium has a fluctuating level of consciousness; he or she may be awake and alert for a few minutes and then become inexplicably sleepy. People with delirium are often confused and disoriented with regard to date, time, and place. Concentration, memory, and calculation ability may be impaired, and visual, tactile, or other types of hallucinations may appear. Paranoid delusions might be reported.5 The key sign for differentiating delirium from psychosis is that the psychotic person remains alert with no change in level of consciousness, whereas

PERSONALITY DISORDERS Personality disorders are psychiatric disturbances that can cause considerable difficulty in the wilderness, although they rarely present as emergencies. Personality disorders are common, with an approximate 12% prevalence.5 There are 10 different categories of personality disorders that are described in the DSM-IV-TR. People with personality disorders have enduring maladaptive patterns of behavior that usually date from adolescence. The use of a narrow set of adaptive strategies inflexibly leads these individuals to have chronic problems at school and work and in their interpersonal relationships. Ironically, people with personality disorders do not tend to see themselves as having problems; rather, they blame others for their difficulties. Individuals with personality disorders unwittingly create their own special circle of misery. Depression and substance abuse are common in this population. People with schizoid personality disorders are loners, and they tend to avoid relating to others, except on a shallow and superficial level. People who are schizotypal have odd and eccentric preoccupations and manners. They may be enamored of astrology, spiritual vortices, or numerology, and they tend to relate in an awkward or uncomfortable way. Annoying, aloof, and unable to join in comfortably with a group, these individuals do not usually cause major problems. People with a paranoid personality disorder are constantly suspicious of others and believe that others have malevolent intentions toward them. Their suspicions are not totally absurd, as they are with someone who is psychotic. For example, these individuals may believe that fellow travelers do not like them or will steal from them, but they do not believe that transmitters have been implanted in their brains or that the Federal Bureau of Investigation is conspiring to kill them. A person with persistent suspicions of others can be problematic for a wilderness group, because the successful functioning of such a group depends on trust among its members. Group leaders need to work doubly hard to draw such individuals into the group and to avoid having the group isolate these people; such isolation serves only to amplify the paranoia and discomfort between the affected person and the group. Another group of personality disorders is sometimes referred to as the “dramatic and erratic” personality disorders. The person with narcissistic personality disorder is one who considers himself or herself special and unusually talented and therefore deserving of special praise or attention. The person with a histrionic

personality disorder is colorful and dramatic and demands to be the center of attention. He or she may be perceived as vain and shallow and often exaggerates physical complaints. For example, a small blister can cause excruciating pain and discomfort for this type of individual. The person with a borderline personality disorder is unstable and has a fragile sense of identity. Relations with a borderline person tend to be stormy; he or she may be exquisitely sensitive and react with rage at the slightest sign of rejection. The person with an antisocial personality disorder is a “confidence man” who may manipulate, intimidate, or steal to obtain what he wants. He can be superficially charming, but he is irresponsible, unreliable, and sometimes aggressive and violent if his wishes are thwarted. A third group of personality disorders includes the avoidant, dependent, and obsessive–compulsive personality disorders. The person with an avoidant personality disorder is constitutionally shy but desires relationships with others. The person with a dependent personality disorder is someone who looks to others to make decisions and to care for them. The person with an obsessive–compulsive personality disorder is task oriented and hardworking, but he or she is also perfectionist, moralistic, and humorless. The obsessive–compulsive personality disorder is to be contrasted with OCD, which was described previously. A psychologically intuitive leader may be able to run interference between the afflicted person and the rest of the group. At other times, the maladjusted individual can be so disruptive that the leader or the rest of the group must insist that the person leave. If this is the case, the person should be assisted with exiting the wilderness. These individuals may not willingly accept being dismissed from the group, and they may become physically or verbally combative. They may be enraged and report that they are going to kill themselves, sue, or seek some other form of retaliation. Nevertheless, if the individual cannot safely function as part of a wilderness group, the leader must remain firm in dismissing the person from the group and assisting him or her safely out of the wilderness.

SUBSTANCE ABUSE DISORDERS People who abuse illicit drugs or alcohol should not be on wilderness adventures; they are a hazard to themselves and others. It is not uncommon for a wilderness traveler to appropriately enjoy a small quantity of alcohol after a long day. However, the use of methamphetamines, cocaine, heroin, lysergic acid diethylamide, and other illicit drugs on a wilderness trip is dangerous. If someone is unwilling or unable to stop using these drugs, then he or she should be escorted out of the wilderness. More problematic is a person who is prescribed narcotic medications (e.g., oxycodone, OxyContin) to control pain. Narcotics are central nervous system depressants that can impair concentration and coordination. In modest doses, such medications may be reasonable; however, at higher doses or if the individual is abusing prescription narcotics, then it is not safe to have him or her continue a wilderness journey, and he or she must be escorted out of the wilderness. Some people may be unaware that they have a substance abuse problem when they start a wilderness trip until they start to experience physical or psychological withdrawal. A careful history can establish if someone is experiencing alcohol or drug withdrawal. Alcohol withdrawal is considered a medical emergency because of seizures, psychotic symptoms, and delirium tremens.2 Withdrawal symptoms usually start with shakiness and increased heart rate and blood pressure. Withdrawal from barbiturates or benzodiazepines can manifest similarly to alcohol withdrawal, and can also be life threatening. If withdrawal is suspected, a benzodiazepine (e.g., lorazepam) can be given; several milligrams may be needed before the vital signs stabilize. Alcohol can be used to stop withdrawal symptoms, if necessary and available. People who abuse cocaine, methamphetamines, or narcotics will not experience life-threatening withdrawal, but their symptoms can be extremely uncomfortable and disabling. Withdrawal from substances such as cocaine (i.e., crashing) is associated with extreme irritability and fatigue. Aches and pains that are typical of influenza are seen in association with withdrawal from narcotics. Withdrawal symptoms may last several 667

CHAPTER 35  Mental Health in the Wilderness

the delirious person’s level of consciousness fluctuates over minutes or hours. If delirium is suspected, a cause must be determined as rapidly as possible. Dehydration, hypoglycemia, high-altitude cerebral edema, head injury, meningitis, encephalitis, drug or alcohol withdrawal, and heat illness—to name but a few conditions—can cause delirium. In their confusion, people with delirium can easily injure themselves, so they must be watched constantly. Especially with delirious patients, physical restraint may be needed. In the wilderness, physical restraint can be accomplished by applying duct tape over cloth (so that the person does not injure himself or herself by struggling against the restraints) to each limb and possibly to the trunk as well, with the person being restrained in a side- or face-down position to prevent aspiration. Physical restraint is certainly potentially hazardous and should only be done as a last resort. Grand Canyon rangers have had to physically duct tape combative and delirious individuals (who have become that way as a result of dehydration) to litters before putting them on a helicopter for evacuation. If an easily treatable cause of the delirium cannot be identified and treated, then evacuation is necessary. I personally reviewed a Grand Canyon backpack trip during which a member of the group became increasingly unsteady and confused as he progressed down the canyon. He would be fine for a few hours and then would become obtunded. He fainted and fell a couple of times, but he was not seriously injured from the falls. Shortly after the group made it to a beach on the Colorado River, the man became semicomatose. A helicopter eventually evacuated the victim to a nearby hospital, where he was treated successfully in an intensive care unit for pulmonary edema.

PART 4 INJURIES AND MEDICAL INTERVENTIONS

days. Individuals who are experiencing alcohol or drug withdrawal should be evacuated. On a wilderness trip, someone may experiment with natural plants in hopes of achieving an induced high. Tea made with jimson weed or certain other plants can induce florid psychosis and delirium. Such individuals may shed clothes, develop severe sunburns, become dehydrated, and expose themselves to all manner of risks. Plants that can cause psychotic symptoms and delirium are common (see Chapter 64) and should be avoided.2 People who are experiencing psychotic symptoms or delirium as a result of the ingestion of toxic plants must be watched constantly until evacuation to a hospital can be arranged.

Suicide, Violence Potential, and Anger Management Suicide is a major public health problem. The suicide rate in the United States is approximately 11.1 per 100,000, with a recent increase in suicides occurring among young people.5 Depression and alcoholism are frequently associated with suicide. People who are depressed, lonely, or physically ill sometimes commit suicide. Rejection, unemployment, and legal problems are often associated with suicide. In the context of a wilderness trip, factors to consider are depression and recent loss. For example, a wilderness traveler who has been divorced, widowed, or fired from his or her job shortly before the trip may be at higher risk for suicide. A family history of suicide or a history of suicidal behavior increases suicide risk. If there is a concern that someone might be suicidal, then he or she should be asked about suicidal thinking in a straightforward and concerned manner. Asking about suicide does not increase suicide risk. People who kill themselves often think about or become preoccupied with ending their lives. They plan how they will kill themselves, so they should be asked about their plans for suicide. If the suicide potential is judged to be significant, then the person must be watched closely. People who are delirious or psychotic can suddenly become impulsively suicidal in the midst of their confusion and frenzy. Suicidal individuals should be evacuated. More than 40 people have killed themselves below the rims of the Grand Canyon, some in spectacular fashion. Wilderness locations can be inviting places for people to end their lives because of the beauty and the access to effective means (e.g., high cliffs). Many more people think about suicide than those who attempt or complete suicide; however, there is not yet any reliable means for quantitatively assessing the seriousness of someone’s suicide risk. Caution should be the watchword when someone is assessed as being even mildly suicidal in a wilderness setting. Anger is an adaptive and universal human experience. With modulation, expressions of anger can signal distress, conflict, fatigue, or fear. Allowing people who are not typically angry to have time to cool off and then approaching them in a supportive and concerned manner can lead to rapid resolution of the conflict. Asking an individual who has been angry how he or she is doing can be a good beginning to dealing with someone who is angry. These individuals may report fatigue, fear about some aspect of the journey, or conflict with someone in the group. Active and nonjudgmental listening can often identify the problem and help lead to a resolution. For example, the wilderness trip may need to be slowed down to allow rest for someone who has become exhausted or to provide empathy for a person who is struggling to keep up on the journey. More problematic are people with psychiatric disorders, especially those with borderline or antisocial personality disorders, who have maladaptive ways of expressing anger and hostility. These individuals may be chronically angry, hostile, sarcastic, and even menacing on a wilderness journey. Management of this type of anger should be characterized as attempting damage control. Intensive psychotherapy with the use of cognitive behavioral techniques can be useful, but this is beyond what can be provided in the field.5 People with these more serious forms of anger can have a very negative impact on a group, sometimes splitting the group into factions and causing an absence of camaraderie and an undercurrent of tension. Periodically taking problematic individuals aside in private, providing support, and allowing persons to ventilate 668

while setting firm limits on their more troublesome behaviors can help to diminish the impact that these individuals might have on a group. For extreme behaviors that involve blatant threats or actual violence, more draconian interventions may be needed; these are described later in this chapter. The culture in the United States is much more violent than those of other industrialized nations. Rape, child abuse, homicide, and other violent crimes are far too common. Men are 10 times more likely than women to be violent, and young men are particularly prone to violence.5 Substance abuse is highly correlated with violence. People who have a history of acting violently in the past are more likely to do so in the future, and people who are going to be violent often signal their intentions. They act aggressively, clench their fists or jaws, and speak loudly or shout. They may have thoughts of acting violently, so they should be asked if they are thinking about hurting anyone. People who have a personality disorder or who are psychotic are at an elevated risk for violence. If a concern exists about someone being violent in the wilderness, weapons should be removed, if possible, and everyone should be vigilant. The potentially violent person should be evacuated or assisted out of the wilderness, with the help of law enforcement personnel if necessary.

Somatic Complaints Some people are more sensitive to physical irritations and discomfort than are others. For most people, a headache, a scrape, or a sore muscle is not cause for alarm. However, for some individuals, a headache is a sure sign of a brain tumor, the scrape will undoubtedly become gangrenous, and sore muscles are evidence of a smoldering systemic illness. Simple reassurance that there is no major pathologic process present may be enough for many people, but others continue to worry despite solid medical evidence to the contrary; these people suffer from hypochondriasis.1 Insomnia, gastric distress, and fatigue are common complaints that are associated with travel and are usually not cause for concern. However, persons who tend to magnify the significance of common somatic complaints worry excessively and may voice their concerns to the entire group. Occasionally, this can have the effect of creating a kind of “mass hysteria,” where other members of the group begin to experience the same symptoms. For a person who is very worried about his or her health, repeated reassurance might be successful for ameliorating the problem. The difficulty lies in discriminating symptoms of little consequence from genuine and potentially serious organic medical problems. A woman on a wilderness trip in the mountains had a minor fall and became nonresponsive to painful stimuli. She was evacuated to a hospital, where she was released from the emergency department with no ill effects and no cause for her unresponsiveness being found. This woman probably had a conversion disorder, which is rare but can manifest as sudden blindness, paraplegia, or unresponsiveness with no apparent etiology. Taking a good history to exclude an organic explanation for symptoms is important before concluding that the complaints are primarily of psychological origin. The Grand Canyon Park Service Rangers at Phantom Ranch and Indian Gardens regularly respond to individuals who report that they cannot physically hike out of the canyon. After taking a history to exclude organic illness, the rangers use a firm approach and tell these individuals that they can and will hike themselves out of the canyon. These individuals are encouraged to hike slowly, to avoid hiking during the hottest part of the day, and to remain hydrated, but they are not given a helicopter or mule ride to the rim.

Insomnia Complaints of insomnia are exceedingly common, with a 1-year prevalence rate of 30% to 45%.1 Although individuals may complain about poor sleep and daytime sleepiness, sleep laboratory assessments frequently demonstrate that these individuals sleep better than they subjectively report. Common insomnia-related complaints include difficulty falling asleep, frequent awakenings, and early awakenings. As people age, they normally sleep less and more lightly, and they have more frequent awakenings; this

Response to Crisis DISASTERS Avalanches, storms, rockfalls, climbing, whitewater accidents, and many other untoward events can lead to the death or serious injury of one or more group members. People who venture into the wilderness usually do not anticipate someone being seriously injured or killed (Figure 35-2). Even persons who have taken wilderness first-aid courses do not enter the wilderness expecting the worst, or else no one would participate in these types of activities. There are many descriptions of outdoor trips that have involved crises.10 Humans wrap a cloak of denial around themselves. Thus, when a crisis or tragedy occurs, it is almost always an emotional shock. When you watch your climbing partner fall and die or when your friend drowns when his kayak flips in whitewater, there is a reaction of horror, dread, and disbelief. The situation is overwhelming, and survivors or witnesses of these types of

FIGURE 35-2  A Sierra Club group enjoys dinner in the Wind Rivers Wilderness.

tragedies often describe a sense of unreality that is associated with the horrible event. People who are involved in tragedies often need to replay the event to put it into some type of meaningful personal context. People who are relatively intact psychologically and who have good social support can usually mentally process a trauma successfully without long-term mental health problems. As the size of a disaster grows and its impact on a person or a community’s support networks increases, the likelihood of long-term mental health problems grows. People who handle trauma by psychological avoidance and casting blame may have poorer outcomes.13 In response to natural disasters, some individuals develop acute stress disorder or post-traumatic stress disorder (PTSD). Estimates of the frequency of these disorders after disasters— either manmade or natural—vary from 2% to more than 50%.13 The symptoms that are typical of these disorders include efforts to avoid reminders of the traumatic event and markedly increased anxiety during exposure to such reminders. The affected person may be flooded with uncontrollable memories, including bad dreams and flashbacks (i.e., feeling and behaving as if the trauma was happening again). The person may feel a sense of emotional detachment from others. He or she may have difficulty concentrating and sleeping, feel restless, and be easily startled. Symptoms can begin immediately after a disaster. If they persist for more than 2 days but for less than 1 month, the disorder is called acute stress disorder; if the symptoms are present for more than 1 month, the disorder is called PTSD.1 For most people, symptoms diminish as time passes, although there is commonly intensification of symptoms around the time of the 1-year anniversary of the tragedy. Symptoms may become chronic and require ongoing psychiatric care. I have personally evaluated men who were held as prisoners of war during World Wars I and II and who were subjected to cruel deprivation or torture. Some did not experience symptoms of PTSD until they retired, which was many years after they were traumatized (i.e., delayed PTSD).1 There is no evidence-based consensus for mental health interventions during the immediate aftermath of a disaster. Available evidence indicates that psychological debriefing is not associated with benefits and may in fact complicate recovery after a disaster. Debriefing, which usually involves some review of the disaster, may increase physiologic hyperreactivity, increase the coding of traumatic memories, and promote rumination about the tragedy; debriefing can thus interfere with more adaptive and natural healing mechanisms (e.g., avoiding thinking about the trauma). If debriefing is used, it should be voluntary, involve clinical assessment, and only be performed by experienced and welltrained individuals. Clearly, more systematic research is needed in this area.13 However, despite a lack of systematic research, there have been attempts to promulgate a clinical consensus regarding desirable mental health interventions in the wake of disasters on the basis of current empiric evidence.8 The immediate and first response to a wilderness disaster should emphasize ensuring the safety and security of the survivors; this includes provision of food, water, warmth, and shelter. Second, efforts should be made to calm everyone who was involved in the disaster. Survivors should be accurately informed about what has 669

CHAPTER 35  Mental Health in the Wilderness

leads to frequent sleep complaints in the elderly. Even for persons without baseline sleep problems, traveling long distances across several time zones to wilderness locations might lead to insomnia problems as a result of the disruption of their circadian rhythms. Individuals with insomnia often have poor sleep hygiene. They nap during the day, drink caffeine and alcohol, do not exercise, undertake stimulating activities like watching television while falling asleep, have irregular sleep schedules, and sleep in noisy and uncomfortable settings. In wilderness settings, sleep problems can be accentuated as a result of heat, cold, humidity, altitude, uncomfortable sleeping arrangements, and fears of bugs, snakes, and wild animals. However, wilderness settings can also have a salutary effect on sleep as a result of the associated quiet, darkness, exercise, and freedom from the stresses of work and other responsibilities. Several suggestions can be made for persons who report difficulty with sleep in wilderness settings: no napping, no caffeine or alcohol, regular exercise, comfortable sleeping space in a tent or cabin, reassurance regarding wild animals, and a regimented wake time. It is best for people to cue their biologic sleep rhythm to the time that they usually awaken. In other words, if someone normally awakens at 6 AM, then they should get out of bed and begin their day at 6 AM in the local time zone, even if they only slept a couple of hours the night before. By cueing to this awake time, sleep quality should gradually improve over subsequent nights. No one can sleep in a tent with a gale force wind blowing all night, but losing a night of sleep will not have any substantial effect on functional ability the next day, other than some increased sleepiness. Sleep medicines are commonly used for insomnia, but these can have deleterious effects on wakefulness and coordination. Uncommon side effects are unusual behaviors (e.g., driving a car in the middle of the night with no destination) that are associated with memory loss for the event. Thus, medications to relieve insomnia should only be used if more conservative sleep hygiene suggestions fail. Sleep disorders such as narcolepsy, sleepwalking, and sleep apnea could prove hazardous in a wilderness setting. Narcolepsy is characterized by sudden sleep attacks, even during the day, during which the afflicted person suddenly falls asleep with little or no warning. Narcoleptics are also subject to cataplexy, which means that they suddenly lose muscle tone, often in response to strong emotion. People who sleepwalk may not be aware of their behavior, which occurs during the deepest phase of sleep. Narcolepsy and cataplexy could present serious hazards on wilderness journeys, where individuals could inadvertently fall off a cliff or cause someone else to fall and injure themselves. Sleep apnea is associated with airway blockage that is caused by enlarged tonsils or the uvula. This causes hundreds of awakenings each night of which the afflicted individual may or may not be aware. Sufferers often snore, complain of fatigue and sleepiness, and are at risk for heart failure and stroke. At higher altitudes, symptoms associated with sleep apnea may worsen as a result of hypoxia and lead the individual to be severely sleep deprived. They may have difficulty paying attention or even fall asleep in hazardous situations.

PART 4 INJURIES AND MEDICAL INTERVENTIONS

happened and about what rescue efforts are underway. It is important to advise survivors about the status of others who were involved in the disaster and about the safety of family and loved ones. Communication with loved ones should be facilitated as soon as possible. Victims should be provided with a calm setting to decrease arousal as much as possible. Encouraging deep breathing and muscle relaxation may be helpful. Reassurance should be provided regarding any distortions that a survivor may experience, such as feelings of weakness or guilt or catastrophic perceptions that the world is a malevolent and dangerous place. Medication use is controversial, with selective serotonin reuptake inhibitors demonstrating some benefit during the weeks and months after the disaster. However, using psychotropic medications during the immediate aftermath may not be necessary and may even be harmful, particularly if the sedative properties interfere with survival behavior or motivation. It is expected that survivors will be very emotional after a disaster, but the experience of those emotions may be naturally adaptive, so artificially dampening them with medications can be counterproductive. Survivors should be approached with the expectation that they will recover psychologically, and they should be reassured about their future mental health. Further interventions are required in the initial aftermath of a disaster. Promoting a sense of selfefficacy is recognized as an important component of recovery efforts, and this includes providing survivors with continuing information about the effects of the disaster and the means to contact other survivors. Making psychological intervention accessible can be very useful during the weeks and months after a disaster. Specialized crisis counseling services were developed after Hurricane Katrina that proved very useful.7 Cognitive behavioral treatments have also demonstrated considerable value for survivors of disasters. Finally, promoting a sense of connectedness with the broader community and instilling a sense of hope (i.e., avoiding social withdrawal and hopelessness) can be crucial for people who are recovering from a disaster. Pragmatically, a feeling of hope can come from prompt reparation payments, which may allow someone to rebuild a home that was destroyed in a disaster.

SURVIVAL PSYCHOLOGY It is not uncommon for people to become lost in the wilderness. Human spatial orientation abilities are limited; we often function under the illusion that we know exactly where we are when that is absolutely not the case.3 People rationalize disorientation in the wilderness by explaining away inconsistencies between their topographic map and the actual landmarks before them. As a person becomes convinced that he or she is completely lost, he or she may experience intense fear, panic, and disorientation that are unique to this type of dilemma. Lost people have been shown to tend to walk in circles.12 Even people with considerable experience in the wilderness may demonstrate inexplicable behaviors, such as abandoning provisioned backpacks or other potentially valuable items. Some have even removed clothing, which increased their exposure to the elements.3 After becoming lost, some persons develop a strategy and carry it through; however, when this plan fails, these individuals may abandon hope and resign themselves to fate. Ironically, children who are less than 6 years old fare better when they are lost as compared with older children and adults. The explanation for this paradox might be that younger children act on instinct and seek shelter when cold and water when thirsty, whereas older children and adults panic and sometimes overlook obvious and simple means to help them to survive.3 In groups that become lost, good leadership is often a key component of the survival of the group. Perhaps the most famous survival story is that of Ernest Shackleton’s ill-fated voyage to reach the South Pole in 1914. His ship, the Endurance, broke up in the ice. Under his leadership, the group survived months of incredible hardship. Against all odds, all 27 men survived.9

Leadership and Teamwork Wilderness activities are usually not solo affairs. Outdoor adventures can range from a 5-mile day hike with a social group to 670

an expedition that involves dozens of people who climb to the summit of Mt Everest. For adventures to be successful and safe, planning, preparation, leadership, and guidance are required. People who share wilderness activities together experience the same types of group interactions that occur among co-workers, families, and many other groups. A safe and rewarding wilderness adventure begins before the actual trip. Careful planning includes attention being given to numerous issues, including food, equipment, maps, screening of participants, impact on the environment, and necessary permits.4 The planning process itself may involve a group working together. Subsequent to the adventure, some type of communication may be essential to bring spiritual, emotional, or logistical closure to the experience. The manner in which groups interact can result in a safe, challenging, and rewarding adventure or a conflicted, dangerous, and disorganized affair. Trips in the wilderness sometimes involve people who may not know one another very well yet who are thrown into close quarters and frequent close contact for an extended period. Regular close contact inevitably leads to annoyances and conflicts, but can also result in pleasurable camaraderie. Leadership is one key ingredient to a successful wilderness experience. A group in the wilderness without a leader and a plan can be a recipe for disaster. Groups without direction and guidance tend to deteriorate; they often break into factions or drift aimlessly. Morale suffers and tempers flare as arguments and fights erupt. Such situations tend to bring out the worst in individuals. However, an effective leader can bring out the best in everyone. The type of leadership that is needed for a day hike differs from that needed for a difficult expedition. However, even the short hike needs coordination. What if someone breaks his or her leg on the hike? Who will go for help, administer first aid, and reassure upset members of the group? Leadership skills should be taught and developed; otherwise, the leader will make the same mistakes repeatedly.4 Good leaders have a vision for the outings, but they are flexible enough to adapt according to the exigencies of evolving circumstances. Successful leaders care about their people and build teams that make use of the strengths of each member of the group. Caring, sensitivity, and empathic listening are crucial components of a successful and effective leader. When effective leaders convey caring and empathy to an entire group, the results are increased cohesiveness and solidarity. Sometimes leaders emerge during a crisis or disaster and are critical to the survival of a group.9 Leadership and interactions among group members evolve during the course of a trip. Leadership is often fluid, because people with different skills take leadership roles in different functional areas, such as building fires, reading maps, and maintaining good humor and morale. People can be remarkably courageous, kind, and ingenious, but they can also be petty, mean, and destructive. A group on a wilderness journey is a microcosm of society; in other words, the group is complex and multifaceted. This type of situation reflects the full range of strengths and weaknesses of both men and women.

Triage Although mental illness is common, most emotional problems in the wilderness are mild and do not require evacuation or restraint. One of the most serious errors that can be made when assessing an individual with apparent mental problems is to fail to exclude an organic cause of his or her change in mental status. People can become agitated and irritable in response to encephalitis or dehydration. It is important to not forego the fundamentals of assessment, such as taking the vital signs and obtaining a thorough history. As with the assessment and treatment of any medical problem in the wilderness, a careful systematic approach will yield the best triage decisions. To help with this assessment, Table 35-1 provides a summary of the recommendations made in this chapter regarding simple triage and treatment decisions for a variety of mental health problems in the wilderness. In addition, the General Health Questionnaire— especially the 28-item version—is a widely used and studied mental health screening tool that is adaptable for use in wilderness settings.6

Anxiety disorders Mood disorders, mild Mood disorders, severe (e.g., mania, suicidal ideation, violence) Psychotic disorders Organic mental disorders Personality disorders, mild Personality disorders, severe (e.g., violence, extreme behaviors) Substance abuse (i.e., no delirium or psychosis) Substance abuse or withdrawal, severe (e.g., unstable vital signs, delirium, psychosis) Suicidal or violent behaviors Somatic symptoms of psychological origin Disasters and post-traumatic stress disorder Wilderness survival

Provide reassurance, support, and lorazepam Provide support and encouragement Observe constantly, contain or restrain, give lorazepam and haloperidol, and evacuate Observe constantly, contain or restrain, give lorazepam and haloperidol, and evacuate Identify the cause and eliminate it if possible, observe constantly, contain or restrain, give lorazepam and haloperidol, and evacuate Avoid overreacting to annoying behaviors and intercede to prevent conflicts within the group Expel the individual from the group if possible or obtain assistance and terminate the outing Confiscate drugs and alcohol Give lorazepam for withdrawal and haloperidol for psychosis or delirium, observe constantly, contain or restrain, and evacuate Observe constantly, contain or restrain, give lorazepam and haloperidol, and evacuate Exclude an organic cause and provide support, reassurance, and firm expectations Ensure physical and psychological security and safety, provide support, and discuss the disaster as guided by the victim Stop, take time to develop a plan, attend to physical security (e.g., shelter, warmth, water), and avoid panic

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 35  Mental Health in the Wilderness

TABLE 35-1  Mental Health Triage in the Wilderness

CHAPTER 36 

Wilderness Emergency Medical Services and Response Systems FRANKLIN R. HUBBELL

The “wilderness” in wilderness medicine has broadened in scope. Skills that are learned for providing wilderness medical care now apply equally to several other situations. These wilderness skills have proved invaluable in the context of military operations as well as in disaster settings. The military has special needs for providing care during combat, and the disaster arena requires not only the knowledge and skills of providing immediate longterm victim care but also knowledge regarding preparedness and self-preservation. Major disasters from 2000 to 2010: 2001—Gujarat earthquake, India 20,000 deaths 2003—Bam earthquake, Iran 30,000 deaths 2004—Indian Ocean earthquake and 230,000 deaths tsunami 2005—Kashmir earthquake, Pakistan 85,000 deaths 2005—Hurricane Katrina, United States 1800 deaths 2008—Sichuan China earthquake 70,000 deaths 2008—Cyclone Nargis, Burma (Myanmar) 150,000 deaths 2010—Haitian earthquake 270,000+ deaths These natural disasters have cost hundreds of thousands of lives, displaced and made homeless millions of people (mostly the poorest of the poor), and cost billions of dollars; they have a global impact that will continue for decades. Tens of thousands of volunteers and other relief workers sprang into action and made tremendous personal sacrifices to assist at the disaster sites. Disaster medicine is by far the largest arena in which the skills of wilderness, extended care, and remote medicine are practiced. Wilderness and mountain rescues performed around the world require a great deal of training and skill to be successful, but these activities pale in comparison with the efforts that are involved in disaster relief. As a result of increasing recognition and use of wilderness medical skills in disaster settings, this chapter focuses on wilderness and mountain rescue training and response systems, and includes essential information about disaster training and response systems. Regardless of the situation, the starting point is always with immediate dangers and self-preservation. We begin with the knowledge and skills necessary to minimize the inherent risks that come with disaster response and relief work. This brief section provides a list of the principles to consider with regard to being prepared to respond, help, and unselfishly serve others in their time of need. The principles that will help one to prepare to respond and serve are: Safety Shelter Sustenance Sanitation Staying Well Stress and Sanity

Safety Make a plan. First and foremost, the basis of personal and team safety is having a well thought-out plan, putting it into action, and sticking to it, if possible. There is safety in numbers. Always try to travel in a group, and try to work together as a group. Keep the team together. Travel during the day. Traveling during the day is inherently much safer than traveling at night. 674

Know where you are going. Know how to get there; know how to use a map, compass, and global positioning system; know who is going to meet you when you arrive at your destination. Are there any local concerns? Find out well in advance if there are any local issues with regard to safety or if there are dangerous areas that should be avoided. Ask questions. Don’t guess. Most people are happy to answer questions and to be helpful. Have an evacuation plan. You need to know what to do if someone in your group becomes sick or injured. The plan should include how to evacuate them to home or to a wellstaffed and up-to-date medical facility. It is a good idea to have some form of evacuation insurance from a group such as Global Rescue, the American Alpine Club, or the Divers Alert Network. If you have evacuation insurance, make sure to carry the details of the policy on one’s person at all times, with appropriate contact information and telephone numbers. Never leave it at home or back at base camp. This information needs to be available at the time of the crisis so that the plan can be easily and accurately activated.

Shelter When one goes into areas of destruction, it is not wise to count on housing being available. Each person needs to carry his or her own shelter; in tropical climates, it is recommended to sleep under mosquito netting at night to avoid bug bites. Check the weather conditions, and carry an appropriate sleeping bag or bedroll for the anticipated climate conditions. Remember, in the tropics, 15.5° C (60° F) is considered cold. A sleep sack may be sufficient, but a bedroll or a sleeping bag should still be packed. Know how to and be prepared to bivouac, and be able to make an emergency shelter from a sheet of plastic or tarp.

Sustenance Food and water: As with shelter, one cannot assume that there will be potable water or adequate food supplies. It is not reasonable to use up the resources of the people whom you have come to help. Food: Carry enough food for the team (preferably food that does not require a lot of cooking or preparation time). It is best to carry food that can be eaten without cooking, such as protein bars, or food that cooks quickly in boiling water, such as macaroni and cheese, instant potatoes, rice, or premade meals. Water: One must be prepared to disinfect all drinking water.

Sanitation Sanitation is more than just hand washing. It involves the following: Wearing gloves when examining and treating patients Having a plan to properly dispose of human waste Staying clean Keep the perineum area clean to avoid rashes and a painful, itchy anus. Applying a thin layer of petroleum jelly to the

Staying Well Immunizations/vaccinations: Go to the Centers for Disease Control and Prevention website (http://www.cdc.gov) and click on “Travelers’ Health” for information about travel vaccines and common diseases in the intended area of travel. Team members should have received the usual childhood vaccinations plus hepatitis A and B, inactivated poliovirus vaccine, and typhoid immunization. Make sure that tetanus and diphtheria immunizations are up to date, and consider yellow fever and meningococcal vaccines. Antimalarials: Malaria is treatable but not necessarily curable. Obtaining malaria prophylaxis is common sense. Use insect repellents and insecticides. Do everything possible to avoid being bitten by insects. Use insect repellents, wear appropriate protective clothing, and sleep under mosquito netting.

Stress and Sanity Post-traumatic stress disorder: One of the most difficult tasks is trying to determine whether you are emotionally prepared to face destruction and human suffering. During the deployment, gather several times daily to share experiences, expectations, and concerns in a format that is comfortable and nonconfrontational and that invites open and honest communication. Have a plan to get together and share stories after everyone has returned home. Post-traumatic stress disorder can be prevented and is treated by talking about the tough work, the difficult things that you saw and did, and the sense of disappointment or even failure that can haunt you after you are back home. Today, medicine is replete with improving communications, computer-assisted diagnosis, futuristic imaging technology, faster and luxurious emergency medical vehicles, and highly skilled trainees. However, the physical world that we explore is still rugged and enduring: majestic mountains, spectacular shorelines, wild rivers, dense tropical rain forests, polar ice sheets without horizons, arid deserts, vast oceans, and hazards beyond imagination. We enter and must sometimes be rescued, treated, and saved. First response is critical. The wilderness will always have the ability to place humans in situations in which immediate help is simply not available. When in the wilderness—whether it is preexisting or created by a disaster—people must know how to survive and be able to perform emergency medicine barehanded, without all of the technical wizardry that exists in a modern ambulance or an emergency department. The anatomy of disaster response and its limitations are very similar to those found on a mountain or backcountry rescue. Time and distance work against rescuers, when notification of the emergency can be delayed and initial information may be inaccurate. The weather conditions at the site of the emergency may be poor, hostile, and rapidly changing. Terrain can make travel very difficult, slow, or even impossible. Manpower, equipment, and resources will be very limited and hard to obtain. Human responders require specialized training, skills, and knowledge of everything from self-preservation skills to emergency care skills in an extended care environment. What continues to change as emergency medical service (EMS) evolves is the scope of practice of prehospital medicine. The important expansion features are patient complexity and time to definitive care.

The usual method of assessing EMS needs is to consider the quantity of knowledge needed to provide emergency care on the basis of the complexity of the medial problems. Education begins with first aid and basic life-saving concepts and then progresses as the complexity of patient care increases. Each next level requires more hours of study to obtain the knowledge necessary to treat specific medical problems. For example, First Responder training takes about 60 hours; basic emergency medical technician (EMT-Basic) training takes 120 hours or more, EMTIntermediate training takes about 220 hours or more, and EMT-Paramedic takes more than 1000 hours. Another way to look at the provision of emergency medical care is to consider how long it will take to bring the patient to definitive care and how the patient’s condition will change over time. When taking time into consideration, there are four distinct areas of patient care, each of which requires its own unique knowledge and skill set. The four time-dependent areas of patient care are the “first 5 minutes”; emergency care delivered during the “golden hour;” “extended care” during the ensuing hours; and, finally, “remote care,” when there is no definitive care available. First response: 5 minutes Emergency care: 1 hour Extended care: 24 hours Remote medicine: No definitive care available

First Response First responders are the first to arrive on the scene. They provide the initial assessment and emergency care; they can be fire, police, rescue, EMS, or military personnel, or they may be Good Samaritans who have arrived at the scene of a crisis. In a wilderness, remote, or disaster situation, they may be search and rescue team members or fellow hikers. This is when the skills of rapid assessment, recognition, and treatment of potentially lifethreatening problems frequently make the difference between life and death. It is within the first 5 minutes of an encounter during which the greatest good is typically done for the greatest number of people.

Prehospital Emergency Care The “golden hour” is best served by well-trained, staffed, and funded EMS systems that are capable of rapid response and transport to hospitals where there are adequate emergency departments. The name states the goal: it should take less than 1 hour from the onset of injury or illness for the patient to be treated and transported to definitive care.

Extended Emergency Care Standards for long-term or extended patient care were developed for wilderness, rural, and marine environments as well as for the military and for disaster response teams. This level of emergency medical training takes into consideration what to do when patient care extends beyond the golden hour.

Remote Medicine Remote medicine is enacted in remote locations, during expeditions when there is delay to rescue, and when there is no place to take a victim. Whether an accident or medical crisis occurs in the wilderness, in the backcountry, on the high seas, or at a disaster site away from access to immediate assistance, the chain of events set in motion hopefully leads to a successful rescue and lives saved. However, how it unfolds varies tremendously, depending on the part of the world in which the critical events occur. Currently no national or international standards exist for wilderness EMS and response. Instead, the configurations of personnel and policies reflect local, national, and international influences. In the United States, wilderness EMS is the most diverse, because it is provided by a broad range of agencies and by individuals with a wide variety of training and certification levels that range from first aid to paramedic. Canadian wilderness EMS is generally 675

CHAPTER 36  Wilderness Emergency Medical Services and Response Systems

area will help to avoid chafing. Bring toilet paper and personal wipes. Women need to bring a personal supply of tampons, sanitary napkins, or pads. Bathe in small amounts of water, and do so daily if possible. Rinse out clothing every day with soap and water. Check the skin several times a day for ticks, bug bites, and rashes.

PART 5  RESCUE AND SURVIVAL

provided through the military, whereas in European wilderness situations civilian physicians have a prominent role. The skills that have been developed for providing long-term patient care in the wilderness are proving to be beneficial in medical and rescue assistance in the disaster response and relief setting. Although there is not a great effort to produce national or international standards for wilderness or disaster relief, there are national and international organizations that have their own command structures, response systems, and response criteria. It may be that organizations or structures such as the American Red Cross, Federal Emergency Management Agency, or Department of Homeland Security will address these issues and develop standards for communications, response, and medical and rescue techniques. The challenge will be to create a system-wide or nationwide set of standards that can be used when diverse entities come together during an emergency to provide relief so that they will be able to function well together. In the world of mountain rescue, the American Alpine Club’s Safety Committee gathers, reviews, and analyzes mountaineering accidents that have occurred throughout North America and publishes an annual report entitled Accidents in North American Mountaineering. The data collected illustrate both the necessary diversity of wilderness and mountain rescues and current limitations of the field (Box 36-1). Several states have established (or are in the process of establishing) working protocols for providing care in the wilderness or “extended care” environment. With increased natural and human-made disasters, EMS systems worldwide have suddenly found themselves essentially operating in a “wilderness” setting as a result of prolonged exposure to a hostile environment, delayed evacuation and transport times, and a lack of medical resources and direction. Prehospital personnel in extended care situations find themselves providing care for much longer than the golden hour and discover that their street-oriented skills are often inadequate. Internationally, the Union Internationale des Associations d’Alpinisme (i.e., the International Mountaineering and Climbing Federation, http://www.uiaa.ch), which is headquartered in Bern, Switzerland, has established criteria and courses for postgraduate training in mountain medicine for physicians. After BOX 36-1  Mountain Search and Rescue Factors in the

United States

1. Search and rescue is the responsibility of national parks, state parks, county sheriffs, or state conservation officers, depending on the state or park. 2. Most backcountry and technical rescues are carried out by volunteer rescue groups. 3. Ninety percent of all rescues are carried out on foot rather than with airlifts by helicopter or fixed-wing aircraft. 4. At least 95% of rescues are performed without physicians present, instead making use of the skills of First Responders, emergency medical technicians, and paramedics, who may or may not be trained in wilderness medicine and rescue techniques. 5. Only two major climbing areas—Yosemite and Grand Teton National Parks—use helicopters extensively. 6. Only Denali National Park uses fixed-wing aircraft extensively and helicopters occasionally. 7. Only three national parks have rangers who are trained specifically for technical rescue, advanced medical support, and helicopter operations: Yosemite, Grand Teton, and Mt Rainier National Parks. 8. National and state parks are not mandated with a “duty to rescue.” However, virtually all parks provide rescue service, and most parks have a budget for these activities. 9. Many roadside climbing areas and popular backcountry areas are not within the jurisdictions of parks. Technical and backcountry rescues carried out at these locations are often performed by local rescue squads, fire departments, and ambulance units, usually without the benefit of specialized training or technical backcountry skills.

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fulfilling these requirements, physicians in the European Union become certified in wilderness medicine and can practice the relevant skills in an appropriate arena. There is now a similar program for physicians being offered in the United States by the Wilderness Medical Society (http://www.wms.org). The Society has produced a curriculum to address various wilderness medical topics for a total of about 100 contact hours. On completion and qualification, the individual becomes a Fellow of the Academy of Wilderness Medicine. In the United States, the foundation has been set for national standards for providing emergency care and rescue by adoption and implementation of the Incident Command System (ICS). This system of command and communication was developed by the U.S. Forest Service for coordinating forest firefighting tactics in the western United States, where many different agencies had to work together while fighting large-scale forest fires. The ICS command system has been improved and adopted by many state and local agencies, and has quickly become the command system standard for all emergency response organizations, especially when it becomes necessary to orchestrate the operations of several agencies that are working together. The assimilation of ICS into police, fire, rescue, and EMS has offered a solution to the single biggest problem facing these services: how to coordinate and interface a variety of teams that are working on the same rescue effort. When each team works within its own set of operating procedures, standing orders, leadership protocols, terminology, and egos, it is often virtually impossible to effectively and safely coordinate a major rescue effort. The ICS works well, and organizations such as the National Fire Academy and various state police, fire, rescue, and EMS offices nationwide have adopted and implemented this system at all levels of emergency response. ICS is now the standard for responding to any emergency situation, whether it is a single department answering a call about a minor motor vehicle crash or a complex search and rescue effort involving many agencies and rescue teams. ICS is the foundation of emergency response because it establishes a common language and command structure that allows everyone involved to anticipate how the effort is going to proceed, what their individual and team jobs are, who is in charge, and how to communicate with each other. As the ICS becomes widely adopted and used, it will help to establish a national standard on which national prehospital standards— including wilderness and extended care protocols—can be built. Most states have produced a set of working protocols for providing prehospital emergency care. However, few have attempted to write protocols for providing emergency care in the wilderness or in the extended care environment. At the time of this writing, Maine, New Hampshire, and Alaska have tackled some of the issues associated with providing wilderness care. New Hampshire is the only state that has written a complete set of emergency medical protocols for the wilderness, extended, or long-term patient care environment. Wilderness emergency medicine is a combination of emergency medical training and outdoor wilderness skills. Although it is essential to blend these elements, it is not necessarily natural or easy to do so. The art and science of prehospital emergency medicine began more than 40 years ago in the United States, and has evolved into a highly regimented and well-defined subspecialty of emergency medicine. Today there are highly trained First Responders, including EMTs and paramedics, as well as organized EMS systems. Each state has an independent EMS system and its own regulations; a truly national standard does not yet exist. The only national prehospital EMS standard that currently exists is the testing and evaluation and certification standards developed by the National Registry of EMTs. A national standard for prehospital care has emerged in the EMS Agenda for the Future, which was first published in 1996. This is an effort to steer EMS across the United States toward a more consistent and cohesive set of skills, protocols, and scopes of practice. It is an excellent document that will hopefully lay a foundation for standards of care; however, at this time, it does not contain a wilderness or extended care section. The National Registry of EMTs offers individual state EMS systems standardized written and practical examinations for

BOX 36-2  Rescue Personnel and Training

Sequence of Events During Backcountry Rescue

1. The critical event occurs; this is an injury or illness that requires assistance and evacuation. 2. A decision is made to get help, and someone goes for help. 3. The emergency medical system is notified of the emergency. 4. The emergency medical system is activated or dispatched. 5. Eventually, the extended rescue team is notified and mobilized. 6. The rescue team assembles, organizes, and then leaves the trailhead; this may be preceded by a hasty team. 7. The team locates the victim. 8. The team provides appropriate extended emergency care. 9. The team organizes and evacuates the victim to the appropriate facility. 10. The team returns to base, is debriefed, and prepares for the next rescue.

The principles and standards of a wilderness or mountain rescue (i.e., extended care rescue)—including organization, specialized skills and knowledge, and essential components of the team— can best be illustrated by reviewing the sequence of events during a typical backcountry rescue in North America (Box 36-3).

OCCURRENCE OF THE CRITICAL EVENT The critical event occurs when an individual who is participating in an activity away from immediate help is suddenly stricken by injury or illness. The key factor is immobilization. The fact that the injured or ill person cannot self-evacuate or move to seek shelter or stay warm results in the need for a rescue. After the

in the United States

1. Most technical rescue personnel in the United States are climbers or skiers who have added wilderness rescue techniques and medical training to their skills. 2. Currently, there are about 800,000 certified and licensed basic emergency medical technicians (EMT-Basics), EMTIntermediates, and EMT-Paramedics in the United States. 3. A growing number of wilderness EMTs are trained in the skills of extended victim care in the backcountry environment. There are an increasing number of courses available for training. 4. Key skill elements of medical training for wilderness medical and rescue training include: a. Thorough victim assessment and monitoring skills b. Technical skills and the authority to perform: (1) Airway management, including endotracheal intubation, laryngeal mask airway, Combitube, and other advanced airway skills (2) Shock management, including include intravenous therapy (3) Use of the pneumatic antishock garment (these garments are no longer recommended for treatment of shock, but they are still useful for management of a fractured pelvis or intra-abdominal bleeding) (4) Oxygen administration and its limitations (5) Use of appropriate medications: (a) Epinephrine for anaphylactic reactions (b) Antibiotics for major open or penetrating wounds, protruding intestines, and compound fractures (c) Acetazolamide, steroids, nifedipine, and furosemide for acute high-altitude problems (d) Pain medications for musculoskeletal trauma (e) Albuterol for bronchodilation (f) Aspirin and nitroglycerin for chest pain (6) Field rewarming techniques (7) Field reduction of angulated fractures and dislocations c. Victim packaging and transportation skills 5. Key skill elements of technical training for rescue personnel in the United States include: a. Appropriate climbing skills for terrain (e.g., rock, ice, snow, glacier) b. Radio communication skills and protocols c. Helicopter and fixed-wing protocols d. Training for and expertise in the use of the Incident Command System in field protocols

BOX 36-3  Sequence of Events in Backcountry Rescue

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First Responders, EMT-Basics, EMT-Intermediates, and EMTParamedics. This guarantees that, regardless of where someone was trained, he or she will be tested using the same standard. Because a central agency to monitor persons who have been trained in providing wilderness care does not exist, there is no registry of trained individuals. Organizations have been training people in wilderness medicine for the past 35 years. Currently, there are more than 100 different organizations, schools, and individuals who offer various forms of wilderness medical training. It is reasonable to estimate that more than 500,000 persons have some sort of certificate training in prehospital wilderness EMS. Training programs that focus on rapid response, rapid intervention, and rapid transport to advanced care facilities exist nationwide. Prehospital personnel are prepared to work within the framework of the golden hour, when time is precious and critical actions save lives. This is a nationally accepted urban standard to which all EMS personnel are currently trained. Although this standard is appropriate for evaluating and training urban EMS personnel and response systems, it is often not adequate for rural, wilderness, mountain, or extended EMS personnel and response systems. In these situations, patient care is measured in hours and days rather than in minutes. Traditional EMS recognizes rapid notification (i.e., the 9-1-1 system), dispatch, response, assessment, thorough prehospital care, transport, evaluation, and critical care in a hospital emergency department. Rapidity is the most critical factor that distinguishes urban emergency medical care from wilderness emergency medical care. However, time is not the only difference. Wilderness emergency medicine is governed by a complex set of medical skills and protocols, equipment requirements, and other specialized skills, including different attitudes or psychological requirements, each of which combines premeditated action with improvisation. A productive mental attitude comes largely from the individual’s training, expertise, and experience in the outdoors. In mountain and wilderness outdoor activities, including mountain and wilderness rescue, haste truly makes waste, which may, in certain circumstances, cost lives. As a result, wilderness and mountain rescue teams must achieve a balance between the urgency of the situation and the necessity for adequate preparation. This is not an easy or natural blend of emotions and skills. On the one hand, trained EMS professionals are always primed and ready to go and feel comfortable moving rapidly, acting quickly, and thinking on their feet. On the other hand, skilled outdoors people are always eager and willing to travel into the backcountry, but they understand the necessity of thorough preparedness. This attitude ensures not only that each team is prepared but also that each individual is prepared. The team must be organized from a leadership perspective and know where it is headed, what injuries to anticipate, and how weather will affect the rescue. The team counts on each individual member being physically and mentally prepared. This difficult task requires recognition of the differences between short-term and long-term care during a rescue so that a safe and successful extended care rescue can be achieved. Box 36-2 outlines key skills that training needs to include.

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victim or others in the party realize this, the need to seek help becomes obvious.

MAKING THE DECISION TO GET HELP Before anyone leaves to seek assistance, the victim’s companions should perform a physical examination, record the victim’s vital signs, determine the level of consciousness, and provide appropriate emergency care, which may entail moving the victim into protective shelter. Victim information should be summarized in a note that accompanies the individuals who are going for help. A map depicting the victim’s exact location and a list of the other party members that notes their level of preparedness to endure the environmental conditions should be included. The individuals who are going for help should carry appropriate provisions. To prepare information adequately generally takes 30 minutes to 1 hour. However, thorough preparation rarely occurs. Often someone suddenly yells, “I’ll get help” and then disappears, running down the trail with sparse vital knowledge. With improvements in and availability of communications technology, such as cellular phones and global positioning systems, backcountry adventurers may have more rapid access to the EMS system from the mountains. Whether this will increase the number of inappropriate callouts remains to be determined. Recent reports indicate that reliance on fallible technology may be responsible for outdoors people using poor judgment in terms of trip planning. Because they assume that help is just a phone call away, hikers are taking more risks.

NOTIFYING THE EMERGENCY MEDICAL SYSTEM Eventually the messenger notifies someone in authority that an emergency has occurred and that help is needed. Usually the request is made to a central 9-1-1 system. If no central service is available, a local dispatch agency is notified. The agency contacts the closest emergency medical service, which can be a rescue squad, ambulance corps, fire department, or first response team. Activating the Emergency Medical System Notification of an emergency usually occurs by means of pagers worn by individual members. An alert tone is followed by an oral message that describes the emergency, its location, and the type of response required. At this point, a wide variety of events can occur that involve agencies both within and outside of the EMS system. Even in areas of the United States with well-organized extended care rescue teams, the team may be notified last. Ideally, the team should be notified immediately, but all too often this is not the case. Instead, local agency responders are notified and rush around trying to determine how quickly they can reach the victim. Notifying and Mobilizing the Extended Rescue Team The first step is to notify team members. In many parts of the United States, organized and coordinated extended rescue teams do not exist, so a “team” is created out of a group of relatively untrained volunteers who are willing to hike in and assist. The task of further organizing and coordinating the rescue effort generally falls on the shoulders of a local rescue squad, fire service, or police department, which may or may not be willing and prepared to manage and execute an extended or technical rescue. For parts of the United States in which backcountry use is common and backcountry accidents occur regularly, extended care rescue teams have generally evolved from local EMS squads with skilled outdoor enthusiasts. Some teams that offer local search and rescue capabilities may be coordinated locally (e.g., the Appalachian Mountain Club, Stonehearth Open Learning Opportunities, Mountain Rescue Service in the White Mountains of New Hampshire); other teams may be part of a nationwide system that responds to incidents throughout the country and that is coordinated on a regional or national level (e.g., the National Cave Rescue Commission). The future may involve the Federal Emergency Management Agency or even the Department 678

of Homeland Security. Coordination of extended care rescue teams may also come under the jurisdiction of a law enforcement body, such as state conservation officers (e.g., New Hampshire Fish and Game), a sheriff’s department (e.g., the Los Angeles County Sheriff in California), or a statewide coordinating system (e.g., the Pennsylvania Search and Rescue Council). Organized teams can be quite sophisticated with regard to their dispatching function so that all members can be notified simultaneously, or they may use a more “low-tech” telephone tree to call out members.

ASSEMBLING AND ORGANIZING THE RESCUE TEAM After members are notified, they assemble at a common location (i.e., a rescue station) to organize the rescue effort. The first task is to define the type of rescue and to establish equipment needs. Estimating the time that it will take to effect the rescue and assessing the need for other agency involvement and assistance are also primary tasks. The questions to be answered and variables to be considered may include: 1. Time of day: Will this be a night rescue? 2. Weather: What are the current weather conditions at the rescue location? What is the forecast? 3. When did the accident occur? 4. What are the supposed injuries? 5. How many victims are there? 6. How many people are in the party? 7. How well prepared are they? 8. Does anyone in the party have medical expertise? 9. Do we know the exact location, or is this a search and rescue? 10. Is a “hasty team” needed? Has it left for the scene yet? 11. Is each of the team members prepared? Does each have personal equipment, a bivouac kit, a headlamp, food, and water? 12. Is each member trained and skilled in this particular type of rescue? 13. Who is on the medical team? 14. Who is on the evacuation team? 15. Is the team equipment organized and divided up? 16. How urgent is the situation? Is a helicopter required? If so, is one available? 17. Are the weather conditions appropriate for an air rescue? 18. Will multiple agencies be involved? If so, are radio frequencies coordinated? After the team is assembled and all pertinent issues have been addressed satisfactorily, then the team is transported to the trailhead (i.e., the launch point) to begin the search. Commonly a hasty team will start out ahead of the main team. When the hasty team has enough information to locate the victim, team members travel as lightly as possible, with only enough gear to ensure their own safety and to equip them to manage the victim’s primary injuries. The goal is to reach the victim as quickly as is reasonably possible and to deliver primary care; the hasty team will then apprise the rest of the team regarding the victim’s condition, equipment needs, and environmental concerns.

LOCATING THE VICTIM How long it takes to locate the victim varies tremendously, depending on distance, terrain, weather conditions, mode of transportation, and whether the victim’s exact location is known. A general rule of thumb for a team that is responding on foot is that it will take 1 hour for each mile traveled through the backcountry. If a search is involved, all bets are off. A search and rescue effort can involve many agencies, individuals, and days (see Chapter 37).

PROVIDING APPROPRIATE EXTENDED EMERGENCY CARE After the victim has been located, appropriate medical care can be provided. The rescue team should ensure its own safety; wet

EVACUATING THE VICTIM TO THE APPROPRIATE FACILITY While providing emergency care, part of the team is designated as the evacuation team. This group has evaluated the various options for evacuation. To properly evaluate the situation, the first information that the group needs is provided by the medical team leader, who needs to know the status of the victim to establish the pace. If the victim’s condition is stable, time is less important; if the victim’s condition is critical, time is also critical. The evacuation team must explore different options. If speed is a consideration, weather conditions are reviewed, and availability of a helicopter-assisted rescue is determined. If a helicopter is not an option, the fastest route out is established. If time or speed is not critical, the safest means of evacuation that is easiest on the victim and rescuers is defined. A general rule for duration of an evacuation is that it will take 1 to 2 hours for every 1 mile to be covered, which requires six well-rested litter bearers for every 1 mile. Thus, a 4-mile carryout will require a 24-member litter team and can take 4 to 8 hours to complete. Eventually, the team reaches a trailhead, and the victim is transferred to an ambulance for transport to a hospital emergency facility.

RETURNING TO BASE The team returns to base to reorganize equipment in preparation for the next extended rescue and to debrief. Because people are exhausted and hungry, the debriefing session is often canceled. However, establishing a mechanism to debrief after the rescue effort is imperative so that team members can learn from the shared experience, discuss victim care, and work through problems. Whenever several different emergency organizations with disparate rescue and emergency personnel combine to perform a complex rescue, there may be tension, conflicting egos, and concerns about the medical care provided or the evacuation plan used. These problems deserve to be discussed and managed in real time as expediently as possible so that teams will cooperate successfully in the future, improve their performance, and provide the best possible patient care during the next rescue. This process minimizes the burnout syndrome that can occur with volunteer teams.

Team Organization and Function Organization of an extended care rescue team is based on both training of individuals and type of rescue. The structures of teams can vary from loosely knit groups of friends with no leadership hierarchy to paramilitary organizations with rigid leadership roles. Team members require personal knowledge, experience, and expertise with regard to the particular aspect of extended care

BOX 36-4  Victim Assessment Primary Survey: Locating and Treating Life-Threatening Problems A: Airway Management Is the airway open? Is the airway going to stay open? B: Breathing Is air moving in and out? Is the airway quiet or silent? Is breathing effortless? Is the respiratory system intact? Is breathing adequate to support life? C: Circulation Is there a pulse? Is bleeding well controlled? Is capillary refill normal (i.e., <2 sec)? Is circulation adequate to support life? D: Disability Conscious versus unconscious Level of consciousness: AVPU (awake, verbal, painful, unconscious) or Glasgow Coma Scale Cervical spine stabilization E: Environment Internal versus external Is the victim warm and dry? Is the victim protected from the cold ground? Is the victim protected from the elements? Secondary Survey: What Is Wrong and How Serious Is It? Vital Signs: Indicate the Condition of the Victim Respiratory rate and effort Pulse rate and character Blood pressure: systolic/diastolic Level of consciousness: AVPU (awake, verbal, painful, unconscious) or Glasgow Coma Scale Tissue perfusion: skin color, temperature, and moisture Capillary refill (<2 sec) Victim examination: head-to-toe examination to locate injuries AMPLE History Allergies Medicines Past medical history Last in and out: food/drink and voiding Events leading up SOAP Note: To Record and Organize Victim Data Subjective: age, gender, mechanism of injury, and chief complaint Objective: vital signs, victim examination, and AMPLE history Assessment: problem list Plan: plan for each problem “Re-SOAPing” the Patient Subjective: Is the victim comfortable, too hot, too cold, hungry, thirsty, or in need of urination or defecation? Objective: Vital signs: are they stable? Record these. Victim examination: recheck all dressings, bandages, and splints. Are they still controlling bleeding? Are they too tight or too loose? (Swelling limbs can cause bandages or splints to impede circulation, thereby resulting in ischemic injuries or worsening frostbite or snakebite.) Assessment: Has the initial assessment changed? Plan: Is the rate of evacuation still the same?

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clothes should be replaced with warm, dry clothing, and members should check for emerging problems within their group. While the medical team cares for the victim, the evacuation team secures shelter, prepares warm drinks, establishes and maintains communications, and plans and organizes the evacuation. Companions of the victim may have been affected by the environment while waiting for the rescue team to arrive and may require assistance. They may need to be assessed and treated for hypothermia, frostbite, heatstroke, heat exhaustion, or dehydration. Regardless of what transpired before the medical team arrived, a complete victim assessment is essential. Do not assume that all of the injuries have been found or that all medical conditions have been managed properly (Box 36-4). In the extended care environment, the victim must be monitored for changing conditions that indicate an underlying problem. Awareness of environmental emergencies is particularly important, with constant care needed to prevent hypothermia, frostbite, heatstroke, heat exhaustion, and dehydration. To do this, it is necessary to monitor the victim and write a new SOAP note or to “re-SOAP” the patient every 15 minutes.

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and rescue in which they will participate as well as knowledge and expertise concerning the principles of extended emergency care, extended rescue techniques, and technical rescue skills.

PERSONAL KNOWLEDGE, EXPERIENCE, AND EXPERTISE Individuals who want to be part of an extended rescue team need to acquire outdoor skills before they become part of a rescue team. Every member must have extensive knowledge of likely environmental emergencies, including hypothermia, frostbite, heat syndromes, snakebite, dehydration, and lightning strike. Each individual must also understand the general principles of weather behavior. Rescuers need to be comfortable with route finding, maps and compasses, personal preparedness, and bivouac and survival skills. The knowledge, skills, and equipment that a skilled outdoors person should possess are often referred to as “the 10 essentials” (Boxes 36-5 and 36-6). The same skills, knowledge, and equipment that are commonly used by the outdoor enthusiast are essential on a mountain rescue.

EXTENDED RESCUE TECHNIQUES AND SKILLS Specific skills and techniques that are applicable to a particular situation include those of search and rescue, vertical and technical rock climbing, and white-water navigation. Snow or winter camping or avalanche rescue may be required, depending on the environment. Extended rescue teams should require their members to have, at a minimum, the working knowledge and equipment described in Box 36-7. Knowledge is acquired over time. Specific medical, rescue, and technical skills are obtained and retained through courses,

BOX 36-5  The 10 Essentials 1. Attitude Positive belief that you can make things better; the will to survive 2. Fuel to burn: food High-carbohydrate foods that require no preparation High-carbohydrate foods that can be made into beverages 3. Quench your thirst: water with appropriate electrolyte supplementation A minimum of 2 L per day to survive and 4 L per day to thrive Up to 3 L per hour if active Ability to make more disinfected water and to supply electrolytes 4. Stay warm and dry: clothing Warm clothing that retains heat, even when wet Waterproof raingear, both top and bottom 5. Get dry: shelter Ability to improvise shelter or to bivouac A bivouac kit (see Box 36-6) 6. Get warm: fire Ability to heat water (e.g., stove, candle, fire) Ability to build a fire (e.g., waterproof matches, tinder) Ability to make kindling or tinder (e.g., folding knife) 7. Know where you are going: navigation Map, compass skills, and route-finding skills Ability to move about at night (e.g., headlamp) 8. Know the environment: weather Basic understanding of weather patterns Knowledge of how to react in severe weather (e.g., lightning) 9. Getting help: signaling Whistle (preferably plastic) 10. Providing help: first-aid kit Basic small personal trauma kit

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BOX 36-6  Bivouac Kit All of these items fit neatly into a small stuff sack that is 15.2 cm  (6 inches) long and weighs less than 2.2 kg (1 lb) when filled. Two large garbage bags (emergency shelter or raingear) 10-foot sheet of plastic and 100 feet of parachute cord (shelter) Emergency space blanket (shelter, ground cloth) Stocking cap (warmth) Spare socks (warmth; can act as spare mittens) Metal cup (to warm liquids) Gelatin (to make a drink) Two plumber’s candles (to warm water or start a fire) Waterproof matches or lighter Knife Compass Whistle

continuous training, and refresher programs. The Appendix at the conclusion of this chapter provides a list of schools, institutes, and organizations that are involved in wilderness medicine and mountaineering research, standards development, and training programs.

WILDERNESS AND MOUNTAIN RESCUE TEAM ORGANIZATION The organization of wilderness and mountain rescue teams is the area in which there exists the greatest diversity, because no universal standard has been established. Teams vary from local mountain rescue teams with extreme skills and qualifications for providing mountain rescue care to informal collections of friends without leadership. Other more professional teams are operated under the jurisdiction of law-enforcement agencies and involve paramilitary hierarchy and leadership. This diversity is particularly noticeable in the United States, because most teams are composed of volunteers who are not reimbursed for their rescue efforts. In Europe, mountain rescue teams are professional and employ full-time personnel. They charge for rescue efforts, with the fees providing money for personnel, equipment, helicopters, technical gear, and ongoing training. As with any profession, standards have evolved. As a result, there are more standards in Europe than in the United States. Still, there is variation across Europe from country to country, especially with regard to leadership and organization. In many parts of the world, especially remote and wild areas, organized and available rescue teams do not exist. If someone is in need of help, the expedition team necessarily becomes the rescue team.

Training of Wilderness Emergency Medical Technicians The best way to develop an appreciation for the vast difference between what is required of the traditional (urban) EMT and what is required of the extended care or wilderness EMT (WEMT) is to compare their respective course curricula. The Department of Transportation (DOT) is responsible for developing and updating the EMT-Basic, EMT-Intermediate, and EMT-Paramedic curricula in the United States. These curricula are considered the minimum national standards for EMT students to qualify for the National Registry or for an individual state practical and written examination. Passage of such an examination enables a student to become certified as a National Registry or state EMTBasic, EMT-Intermediate, or EMT-Paramedic. A national standard for WEMT curricula does not exist. Despite lack of a DOT-like standard, there are several similar curricula for wilderness emergency care at the EMT level. On the basis of recommendations from the Wilderness Medical Society and other groups that address wilderness prehospital emergency medicine,

Mountaineering Skills Understanding fabrics, clothing systems, and their seasonal variations (see Chapter 70) Fabrics and fibers Layering techniques Vapor barrier systems Waterproof fabrics and raingear systems Footgear Personal protection equipment Helmets Harnesses Gloves Goggles or sunglasses Hearing protection Backcountry equipment Internal or external frame packs and soft packs Shelter (natural and human made) Specialty equipment: snow shoes, crampons, ice axes, stoves, and skis Backcountry travel Route finding Map and compass: map reading, dead reckoning, and types of maps; compass reading, bearings, magnetic versus true bearing, triangulation, and global positioning systems Survival skills: the 10 essentials Shelter and warmth; emergency bivouac kits Food and water Understanding how backcountry travel and rescue vary with seasons Understanding how backcountry travel and rescue vary with different environments: Alpine Desert Forest Water (e.g., swamp, river, lake, ocean) Tropics High altitude Low-impact camping and rescue work Basics of weather and weather forecasting Principles of barometric pressure Clouds and their significance in weather forecasting Prevailing weather patterns in the rescue area Personal fitness Physical conditioning Nutrition and hydration requirements for different   activities Mountain and Extended Emergency Medical Skills Emergency medical training should be at a minimal level of first responder or higher (i.e., emergency medical technician, paramedic, registered nurse, nurse practitioner, physician’s assistant, or physician). Regardless of the level, training must include specific information about wilderness and extended emergency care procedures. Topics of Extended Care Training and Principles Should Include the Following: Patient assessment system Cardiopulmonary resuscitation Airway management, including endotracheal intubation and needle decompression for tension pneumothorax Shock and control of bleeding, including intravenous therapy for fluid resuscitation Long-term wound care and prevention of infection

Musculoskeletal injury management, including specific information about diagnosis and long-term management of: Sprains and strains Fractures, including how to reduce or realign angulated fractures Diagnosis and reduction of dislocations Management of compound fractures Management of chest injuries, including decompression of a tension pneumothorax using needle thoracostomy Spinal cord injury diagnosis and management Head injury, including recognition and management of increasing intracranial pressure Management of environmental emergencies Hypothermia and frostbite, including use of intravenous fluids Heatstroke and heat exhaustion, including use of intravenous fluids Dehydration and nutrition, both acute and during evacuation Lightning injuries Animal attacks, insect bites, and reptile and marine envenomations, including anaphylactic reactions and use of epinephrine and antihistamines Contact dermatitis, such as that caused by poison ivy, poison oak, and poison sumac Sunburn and snowblindness High-altitude injuries, including acute mountain sickness, pulmonary edema, and cerebral edema Drowning Diagnosis and management of acute medical emergencies: Chest pain (e.g., myocardial infarction, angina, costochondritis) Shortness of breath (e.g., asthma, anaphylaxis, pneumothorax) Seizures and cerebrovascular accidents Acute abdomen (e.g., peritonitis, constipation, diarrhea) Pyelonephritis Septic shock Victim lifting and handling techniques Improvising techniques (i.e., “emergency medicine barehanded”; see Chapter 19) Training involving the Incident Command System Blood-borne pathogens and infectious disease prevention Monitoring of bodily functions (i.e., hunger, thirst, and bodily waste management) General understanding and appreciation for the difference between urban (short-term) and wilderness (long-term) emergency care Mountain and Extended Rescue Skills Understanding equipment that is used in wilderness search and rescue operations, including its maintenance and care Ropes, slings, carabiners, harnesses, and helmets Litters, litter harnesses, and haul systems Litter patient packaging equipment Basic radio communications Care and maintenance of communications equipment Procedures and protocols Basic helicopter operations and procedures Approaching a helicopter Safety considerations Landing zones Haul techniques Interagency relations Basic understanding of search procedures Basic understanding of rescue procedures Basic understanding of the Incident Command System and its use in search and rescue management How to care for and handle ropes Continued

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BOX 36-7  Knowledge, Skills, and Equipment Needed by Extended Rescue Teams

PART 5  RESCUE AND SURVIVAL

BOX 36-7  Knowledge, Skills, and Equipment Needed by Extended Rescue Teams—cont’d Rappelling, belaying, and braking techniques Knots Figure-8 Figure-8 follow through Figure-8 on a bight Double figure-8 Double fisherman’s Prusik Tensionless hitch (i.e., a round turn and two half hitches) Water knot Half hitch and full hitch Bowline Alpine butterfly

these curricula adhere to the same principles of long-term patient care, so can be used for comparison with the standard DOT curriculum. A WEMT course typically contains all of the material in the DOT EMT course curriculum plus the things that are necessary for acquiring the attendant skills for long-term wilderness emergency care. Typical EMT courses require about 100 hours, with an additional 10 hours of emergency department observation time. The WEMT module carries an additional 48 to 80 hours of training. There are EMT wilderness modules available that are postgraduate courses that have been designed to train EMTs in long-term patient care. A typical WEMT course outline appears in Box 36-8. The topics in boldface are unique to WEMT programs; the other topics are required in a DOT EMT course. Hours per topic illustrate the time required for both EMT and WEMT training. This outline is arranged in the current DOT EMT recommended format, with the WEMT material added on a per-topic basis; topics are not necessarily listed in the order that they would be taught in a particular course. An explanation of the extended emergency medical care material that must be learned by WEMTs follows.

Introduction to Emergency Care “Wilderness versus urban emergency care” is an introductory presentation that illustrates the differences between urban (i.e., golden hour) emergency care and extended or wilderness emergency care. For WEMTs, it will be necessary in certain instances to learn two different modalities of therapy: one for short-term care (i.e., <1 hour) and one for long-term or extended care (i.e., several hours to days). “Backcountry rescue gear inspection” is a hands-on review of gear for outdoor practice sessions and backcountry mock rescues. The course staff must inspect the participants’ boots, clothing, raingear, and rescue equipment to determine their adequacy for the particular environment in which they will be deployed. Inspecting equipment not only ensures the safety of each individual in the course but also teaches a standard for preparedness, awareness, and attention to detail that is critical to wilderness travel and emergency care. “Medical-legal issues” is usually offered early in a course so that participants are aware of legal concerns that surround practicing medicine as EMTs and WEMTs. WEMTs need to be aware of protocols that exist where they will become licensed. “The human animal—our natural physiologic limits” is an overview of how humans fit into the natural environment, including their daily nutritional and fluid requirements and their natural limitations in different settings. The WEMT must understand physiologic limits (e.g., those of endurance, temperature, and altitude) and the consequences that occur when these limits are exceeded.

PATIENT ASSESSMENT SYSTEMS “Patient assessment in the wilderness and practice” takes the newly learned skills of patient assessment and adapts them to 682

Specific rescue training Water search White-water safety and rescue Avalanche safety and rescue Technical or vertical (rock) safety and rescue Cave safety and rescue Leadership Leadership and “followship” training Ability to use the Incident Command System

the backcountry. The WEMT must be knowledgeable and skillful with regard to wilderness patient assessment, a step-by-step approach to the first 5 minutes of scene safety, and patient care. The WEMT will develop an awareness of potential life-threatening dangers in the environment, how to ensure personal safety and the safety of others, how to approach a victim safely, how to perform primary and secondary surveys to determine the extent and severity of injuries, and what impact the environment might have on the victim.

AIRWAYS, OXYGEN, AND MECHANICAL AIDS TO BREATHING “Airways, oxygen, cardiopulmonary resuscitation, and mechanical aids to breathing in the wilderness environment—uses and limitations” addresses one of the most important lifesaving and life-maintaining skills in emergency medicine: the ability to establish and maintain a patent airway. Unfortunately, most EMTs are not provided with the training and tools they need to properly maintain an open airway in an unconscious victim. Failure to maintain an open airway by using the recovery position, endotracheal intubation, laryngeal mask airway, or Combitube can be disastrous. Endotracheal intubation is commonly used by EMTIntermediates, EMT-Paramedics, and other advanced life support personnel in cardiac arrest settings and for unconscious and unresponsive victims. In the extended care environment, use of intubation by endotracheal tube, laryngeal mask airway, or Combitube in a cardiac arrest situation is not nearly as common as it is for the normothermic, unconscious, and unresponsive person, who has probably suffered head trauma. In this situation, without the ability to perform intubation, the only way to maintain a patent airway while lifting, moving, and transporting a victim in a litter is to place the victim on his or her side in the recovery position. In the recovery position, gravity pulls the tongue forward and allows secretions to drain from the mouth. Oropharyngeal, nasopharyngeal, and tongue-pinning techniques may temporarily keep the tongue from occluding the airway, but are ineffective for preventing vomitus, blood, or saliva from entering the airway. In addition, during evacuation in a litter, constant monitoring of a victim’s airway is virtually impossible, which makes proper airway management and monitoring of paramount importance. The WEMT should know how to establish and maintain a patent airway; this includes using positioning and placement of advanced airways. “Oxygen administration” presents the use of supplemental oxygen, for which both EMTs and WEMTs follow the same general guidelines. Although oxygen is an important part of prehospital care, its use has significant logistic limitations in the backcountry. Carrying large quantities of oxygen into the backcountry is impossible. Small D and E cylinders can be carried, but each provides high-flow oxygen for only 20 to 30 minutes. Oxygen is a compressed gas in a tank, so as it expands, it cools dramatically; this may contribute to hypothermia. To prevent this, the gas should be preheated by wrapping the oxygen tubing around a chemical heat pack during administration.

Per Topic

1. Introduction to emergency care Wilderness versus urban emergency care (1 hr) Backcountry rescue gear inspection (1 hr) Medical-legal issues (1 hr) Blood-borne pathogens Overview of human systems—anatomy and physiology (2 hr) The human animal—our natural physiologic limits   (2 hr) 2. Patient assessment systems Primary survey—airway, breathing, and circulation (1 hr) Secondary survey (1 hr) Patient assessment practice (2 hr) Patient assessment in the wilderness and practice   (3 hr) 3. Cardiopulmonary resuscitation (8 hr) Mannequin practice and certification (8 hr) Cardiopulmonary resuscitation teaching, practice, and testing to American Heart Association standards 4. Airways, oxygen, and mechanical aids to breathing   (3 hr) Airways, oxygen, cardiopulmonary resuscitation, and mechanical aids to breathing in the wilderness environment—uses and limitations (6 hr) Airways: oropharyngeal, nasopharyngeal, endotracheal intubation, and laryngeal mask airway Oxygen administration Suction techniques 5. Bleeding and shock (3 hr) Shock, intravenous fluids, and long-term patient care   (4 hr) Practice starting intravenous infusions and fluid administration (4 hr) Use of pneumatic antishock garments (3 hr) Use of pneumatic antishock garments in the wilderness   (1 hr) 6. Soft-tissue injuries (3 hr) Long-term wound care (1 hr) 7. Principles of musculoskeletal care Fractures of the upper extremities (3 hr) Fractures of the pelvis, hip, and lower extremities (3 hr) Fracture laboratory—practice in assessment and management (3 hr) Musculoskeletal trauma management in the wilderness (3 hr)

“Suction techniques” presents the use of suction devices that are used to clear the airway; this information is similar for EMTs and WEMTs. Hand-operated (as distinct from battery-operated) suction devices are usually used in extended care scenarios.

BLEEDING AND SHOCK “Shock, intravenous fluids, and long-term patient care” and “Practice starting intravenous infusions and fluid administration” provide information about the care of victims who are in shock or who are suffering from environmental emergencies that cause volume depletion (e.g., heatstroke, hypothermia). For the urban management of shock, the essential component is recognition. After shock has been recognized, the victim can be rapidly transported to an emergency department or intercepted by paramedics for definitive care, which primarily involves fluid resuscitation. In the extended care environment, WEMTs must be able to manage the volume-contracted patient by providing appropriate definitive care and fluid resuscitation. During extended evacuations, WEMTs should know how to administer intravenous fluids to stabilize hypovolemia. This includes starting

8. Injuries of the head, face, eyes, neck, and spine (3 hr) Practical laboratory: spinal cord injury management (3 hr) Head trauma, increased intracranial pressure (1 hr) Spinal cord injury management: long-term care and improvising (1 hr) 9. Injuries to the chest, abdomen, and genitalia (3 hr) Chest trauma in the wilderness (3 hr) 10. Medical emergencies I (3 hr) Poisoning, bites and stings, heart attack, stroke, and dyspnea Medical emergencies II (3 hr) Diabetes, acute abdomen, communicable diseases, seizure, substance abuse, and pediatric emergencies Medical emergencies in the wilderness (3 hr) 11. Emergency childbirth (3 hr) 12. Burns and hazardous materials (3 hr) Long-term care of burns (1 hr) 13. Environmental emergencies (3 hr) Hypothermia, frostbite, and immersion foot (4 hr) Heatstroke, heat exhaustion, and dehydration (4 hr) Drowning (2 hr) High-altitude emergencies (2 hr) Barotrauma (2 hr) Animals that bite and sting (2 hr) Plants—contact dermatitis (2 hr) Marine animals that bite and sting (2 hr) 14. Psychological aspects of emergency care (3 hr) 15. Lifting and moving patients (3 hr) Use of Stokes litters and improvising litters (3 hr) Principles of backcountry evacuation (4 hr) Search and rescue organization and execution (4 hr) Wilderness mock rescue with or without overnight (8-12 hr) 16. Principles of vehicle extrication (4 hr) Practice laboratory (3-8 hr) 17. Leadership and “followship” skills The Incident Command System 18. Ambulance operations I (3 hr) Ambulance operations II (3 hr) Helicopter-assisted rescues (3 hr) 19. Review (3-6 hr) Testing—written and practical examinations (16-20 hr) 20. Emergency department observation time (10 hr)

a peripheral intravenous line, maintaining catheter placement, using proper fluids, and prewarming and maintaining warm solutions before and during administration. “Use of pneumatic antishock garments in the wilderness” discusses the use of these garments for victims with pelvic fractures. Treating shock with pneumatic antishock garments (PASGs) is no longer recommended. As long as an intravenous line can be established and maintained, fluid administration is the definitive method for management of shock. However, the WEMT must be aware that the PASG has other uses. In the extended care situation, the PASG may be invaluable as a splint to stabilize a fractured pelvis, thereby contributing to control of internal bleeding. It may also be used as an improvised air splint for a fractured femur. An added benefit is that the PASG may facilitate a more comfortable and well-padded ride for the victim in the litter during evacuation. However, WEMTs must recognize the limitations of PASGs. The primary drawback in the backcountry is the potential for cold injury. After the apparatus is inflated, the decrease in peripheral circulation greatly increases the risk for cold injuries or frostbite to the lower extremities; this can be prevented by properly packing the feet with chemical heat packs 683

CHAPTER 36  Wilderness Emergency Medical Services and Response Systems

BOX 36-8  Emergency Medical Technician and Wilderness Emergency Medical Technician Course Curricula and Hours

PART 5  RESCUE AND SURVIVAL

and adequately insulating the lower extremities in the litter. Careful monitoring of the lower extremities every 15 minutes is essential.

SOFT-TISSUE INJURIES “Long-term wound care” covers proper wound management after bleeding has been controlled and further care if more than 12 hours will be required to bring the victim to definitive care. The principles of long-term wound care are to stabilize wounds and to prevent and control infection. To prevent infection, the WEMT must know how to sterilize or disinfect fluid and how to properly debride and rinse out a contaminated wound. When the wound is cleaned and debrided, the edges can be approximated but not tightly closed, because this may increase the risk of abscess formation and life-threatening infection. Training in the use of suturing techniques to close wounds is not currently recommended, because suturing is usually for cosmetic reasons and can almost always be done later, thereby lessening the risk of infection caused by tightly closing the wound. Even the most fastidiously cleaned wound can become infected, particularly in a remote setting, because of constant exposure to microbes. Recognition of wound infections and appropriate management are important. The WEMT must learn to use specific antibiotics in extended care settings of more than 3 days and for prophylaxis with grossly contaminated wounds and compound fractures. Antibiotic therapy is not controversial, because various safe broad-spectrum antibiotics can cover most wound infections with minimal risk of a severe allergic reaction. In many circumstances, the benefits of antibiotic administration clearly outweigh the risks.

PRINCIPLES OF MUSCULOSKELETAL CARE “Musculoskeletal trauma management in the wilderness” presents the treatment of injuries. In an urban setting, the primary concern with fracture and dislocation care is that the injury site be splinted properly to prevent further injury. In the extended care environment, the primary concern is to maintain proper circulation distal to the site of injury; this may require straightening an angulated fracture or reducing a dislocation. When an angulated fracture occurs, distal circulation can be impaired, which puts the soft tissues at considerable risk for ischemic injury or frostbite. Under normal circumstances, it would take hours for moderate ischemia to cause irreparable soft-tissue injury; however, in the backcountry, prolonged time under hostile weather conditions frequently occurs, which decreases the amount of heat and oxygen that are transferred to the extremity. Knowing how to properly straighten out an angulated fracture significantly decreases the risk for secondary ischemic injury and frostbite, controls bleeding at the fracture site, and diminishes pain. It is much easier to splint and stabilize a fracture in proper position if it is in an anatomic position than if it is angulated. About an additional 3 hours of training are needed to teach a WEMT how to straighten angulated fractures and how to reduce dislocations. Without a radiograph, it is impossible to see the exact positioning of bone fragments or disarticulated joints, thus making it difficult to know exactly how to manipulate the bone. The concern is that, if a jagged bone end is moved improperly, secondary injury might occur because part of a neurovascular bundle might be severed, a fascial sheath that surrounds a muscle might be cut, or the bone ends might erupt through the skin. Fortunately, all of these structures are richly endowed with pain receptors. If the sharp end of a bone fragment begins to impinge, it causes a dramatic increase in pain at the site. A commonly used technique is to straighten the angulated site slowly while maintaining constant gentle traction. With each 1 to 2 cm (0.4 to 0.8 inch) of movement, the victim is asked if the new position is better or worse (i.e., if it causes less or more pain). If the pain diminishes with movement, the reduction is proceeding properly; if pain increases, all movement is stopped, and the extremity is returned to the previous position of improvement. While still 684

under gentle traction, the extremity is repositioned, and another attempt at reduction is made. As long as nothing is forced and movement is achieved slowly under gentle traction, angulated fractures can be easily realigned and dislocations reduced without the need for pain medication or any risk of further injury. Musculoskeletal injuries in the long-term care setting must be carefully monitored. It is essential to reinspect the injury site at reasonable intervals for circulation, sensation, and motion. Fracture sites swell; as a result, even the best splint can act as an inadvertent tourniquet. Immobilized extremities cool as a result of lack of activity and impaired circulation, which also increase the risk for ischemic injury or frostbite.

INJURIES OF THE HEAD, FACE, EYES, NECK, AND SPINE “Head trauma, increasing intracranial pressure” addresses one of the leading causes of death as a result of backcountry accidents. Many who die from head trauma in the wilderness would have survived in an urban setting because of rapid access to definitive care. The WEMT must be able to recognize a potentially serious head injury long before the victim is at risk for brainstem herniation. In the extended care environment, there are few situations in which the team should hurry. One such situation is the presence of significant head trauma, for which the only appropriate care may be rapid evacuation to a facility where the victim can be treated by a neurosurgeon. It is important to establish and monitor the level of consciousness. The AVPU scale—awake, verbal, pain, unresponsive—is used. Within the primary survey, an initial evaluation of disability or neurologic status is made. After that, the level of consciousness is reevaluated every 15 minutes to observe for evidence of increasing intracranial pressure.

INJURIES TO THE CHEST, ABDOMEN, AND GENITALIA Chest trauma can result in a pneumothorax that can evolve into a tension pneumothorax. WEMTs need to be taught how to inspect, palpate, percuss, and auscultate the chest to identify significant injuries. It is not difficult to train an individual to detect breath sounds, determine the presence of a pneumothorax, and monitor a pneumothorax for its development into a tension pneumothorax. Unlike increasing intracranial pressure, for which there is little to do but evacuate the victim, a tension pneumothorax can be relieved, thereby increasing the chance of survival. The easiest and most effective technique that a WEMT may learn is needle thoracostomy in the fifth intercostal space in the midaxillary line.

MEDICAL EMERGENCIES Diagnosing medical emergencies in the wilderness requires WEMTs to be aware of essential signs and symptoms.

ENVIRONMENTAL EMERGENCIES The typical EMT course includes 3 to 6 hours of training in the management of environmental emergencies. A WEMT course will have a minimum of 22 hours of additional training in environmental emergencies. “Hypothermia, frostbite, and nonfreezing cold injuries” covers cold injuries, which are among the most common environmental injuries seen in the backcountry. The WEMT must understand principles of thermoregulation; heat production and heat loss; recognition of hypothermia, frostbite, and immersion foot; and appropriate care. “Heatstroke, heat exhaustion, and dehydration” provides necessary information about the balance of heat production and heat loss in a hot environment and the fluid requirements necessary to support physiologic cooling. WEMTs need to know how to recognize and provide long-term care for victims of heat exhaustion, heatstroke, and dehydration.

“Use of Stokes litters and improvising litters” discusses the primary device for evacuation from the backcountry. Even when a helicopter is used, the victim is usually “packaged” in a litter before being loaded. WEMTs must know the specific techniques for victim packaging in a litter to protect and support injuries. Proper carrying techniques and methods of belaying a litter up or down a steep slope are critical to the safety of everyone involved.

AMBULANCE OPERATIONS “Helicopter-assisted rescues” describes the use of helicopters in backcountry rescue efforts and evacuation. WEMT training should address the dangers, hazards, and limitations of helicopters.

SELF-PRESERVATION Whether incidents or disasters to which they are responding are caused by nature or man, rescuers in remote places must know how to take care of themselves from the moment they arrive until the time that they return to safety. The classic mistake is when responders assume that there will be someone waiting to make sure that they have potable water, safe food, adequate shelter, and basic protection from the elements and from violence. This is never a safe assumption. When responding to a mountain rescue, each member is responsible for carrying a bivouac kit that contains all of the necessities to sustain life in the wild for at least 24 hours. When responding to a disaster, each individual needs to be prepared to survive on his or her own for at least 3 days. Each member has to be potentially self-sufficient, carrying the essentials for survival in a disaster team bivouac kit. The kit must provide shelter and protection from the elements, and must include tools that allow the individual to have the ability to produce potable water, calorie-rich foods, navigation, and light in the dark. Self-preservation is not an easy task. In the case of wilderness rescue, participants are often outdoors people who, before getting involved in search and rescue activities, have already obtained wilderness skills. Alternatively, as teams form to respond to a larger disaster, they may be highly skilled medically but without essential survival skills (e.g., how to make potable water, choose safe foods, or establish a bivouac). The essentials of personal survival include: • Water: Humans need at least 2 L of water per day to survive, 4 L to maintain health, and much more if they are sweating heavily. Water can be a source of infectious diseases such as giardiasis, hepatitis, amebiasis, and cholera, any of which can cause major diarrhea and abdominal pain. It is absolutely essential to be able to produce safe and potable water. Three ways to produce potable water are boiling, chemical disinfection, and filtering. Drinking potentially unsafe water puts the entire team at risk. Electrolytes must be properly replaced. • Food: One must know what is safe to eat, how to properly prepare meals, and how to maintain a clean “kitchen.” If refrigeration is not available, meat has to be kept alive until it is ready to be cooked. Safe food rules include the following: Eat only vegetables or fruits that can be peeled; leave them in their peels until they are ready to eat. Eat vegetables that have been cooked and that are served hot. Never eat raw, lightly cooked, or cold meats. Meat should be cooked until it is well done and then served hot. • Shelter: Shelter involves both a roof over your head and clothing on your back. It is not enough to carry a tent; one also must have the skill to improvise or bivouac (i.e., build an emergency camp).

• Navigation: Know how to use a compass and read a map. You should be able to walk a straight line guided by a compass and to determine the distance traveled. Other important items in the survival kit include sources of light, fire-building materials, signaling devices, knife, parachute cord, spare socks, hat, and a metal cup to make warm water (see Box 36-5). • Attitude: The most important aspect of survival is attitude and confidence. Practice and experience build confidence, and maintaining a positive attitude will help to ensure not only that you survive but that you also thrive.

APPENDIX The following is a list of organizations and committees dedicated to some aspect of extended medical, rescue, and technical training. Many are also active in mountain, wilderness, marine, or disaster rescue and management efforts. Advanced Wilderness Life Support University of Utah School of Medicine 358 South 700 East B509 Salt Lake City, UT 84102 888-521-2957 http://www.awls.org Resource: Teaches advance wilderness life support certification programs and practical approaches to the prevention and treatment of injuries and illnesses related to the wilderness environment. Aerie Backcountry Medicine 240 North Higgins, Suite 16 Missoula, MT 59807 406-542-9972 E-mail: [email protected] http://www.aeriemed.com Resource: Emphasizes prevention, treatment, and improvisation; offers wilderness emergency medical technician, wilderness First Responder, wilderness first aid, avalanche, and swift-water rescue courses. American Alpine Club 710 Tenth Street, Suite 100 Golden, CO 80401 303-384-0110 http://www.americanalpineclub.org Resource: Publishes the American Alpine Journal and the annual Accidents in North American Mountaineering; has committees that are dedicated to establishing and promoting standards of safety and education in mountaineering. American Mountain Guides Association Street address: 1209 Pearl Street, Suites 12 and 14 Boulder, CO 80302 Mailing address: P.O. Box 1739 Boulder, CO 80306 Phone: 303-271-0984 Fax: 303-271-1377 http://www.amga.com Resource: Dedicated to establishing and maintaining standards for mountaineering and professional mountain guides; publishes the quarterly Mountain Bulletin. Appalachian Mountain Club 5 Joy Street Boston, MA 02108 617-523-0655 E-mail: [email protected] http://www.outdoors.org Resource: Active mountain rescue team that offers a variety of workshops that address outdoor skills, environmental issues, and wilderness medical and rescue skills; publishes the quarterly Appalachia. 685

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LIFTING AND MOVING PATIENTS

PART 5  RESCUE AND SURVIVAL

International Society for Mountain Medicine P.O. Box 31142 Colorado Springs, CO 80931-1142 Phone: 719-572-1372 Fax: 719-572-1514 or 800-967-7494 (in the United States) E-mail: [email protected] http://www.ismmed.org Resource: An international organization that is dedicated to research and education in mountaineering; publishes the quarterly Newsletter of the ISMM. Mountain Rescue Association P.O. Box 880868 San Diego, CA 92168-0868 Fax: 619-374-7072 http://www.mra.org Resource: National wilderness rescue organization that is dedicated to the development of standards and the certification of mountain rescue teams. Nantahala Outdoor Center 13077 Highway 19 W Bryson City, NC 28713-9165 Phone: 888-905-7238 or 828-488-2176 http://www.noc.com Resource: Offers a variety of courses about white-water rescue and wilderness medical and rescue training. National Association for Search and Rescue P.O. Box 232020 Centreville, VA 20120-2020 703-222-6277 or 877-893-0702 E-mail: [email protected] http://www.nasar.org Resource: National information resource for search and rescue as well as for certifications in various search functions; publishes the quarterly Response. National Cave Rescue Commission c/o National Speleological Society Cave Avenue Huntsville, AL 35810 205-852-1300 Emergency: National Rescue Coordination: 800-851-3051 http://www.caves.org/io/ncrc Resource: Active national cave rescue team. National Ski Patrol System, Inc. Ski Patrol Building, Suite 100 133 South Van Gordon Street Lakewood, CO 80228 Phone: 303-988-1111 Fax: 800-222-4754 E-mail: [email protected] http://www.nsp.org Resource: Active rescue teams and ski patrols; offers an outdoor emergency care course, various ski patrol certifications, avalanche training, and introductory mountaineering training. Stonehearth Open Learning Opportunities P.O. Box 3150 Conway, NH 03818 603-447-6711 or 888-SOLO-MED E-mail: [email protected] http://www.soloschools.com Resource: An international organization that is dedicated to developing and offering a variety of courses and certifications in wilderness and marine medicine, rescue, leadership, and outdoor skills; an active mountain rescue team; publishes the bimonthly Wilderness Medicine Newsletter. Union Internationale des Associations d’Alpinisme (International Mountaineering and Climbing Federation) Monbijoustrasse 61 Postfach CH-3000 Bern 23/Switzerland

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Phone: 41 (0)31 370 1828 Fax: 41 (0)31 370 1838 E-mail: [email protected] http://www.uiaa.ch Resource: An international organization that is dedicated to promotion of standards, safety, awareness, and education in mountaineering worldwide; produces multiple publications about mountain safety and medicine. U.S. Coast Guard Headquarters 2100 Second Street, SW Washington, DC 20593-0001 202-267-1012 (Boating Operations) http://www.uscg.mil Resource: Active national marine rescue military organization; source of information and various boating-related certifications. Wilderness Medical Associates 400 Riverside Street, Suite A-6 Portland, ME 04103 Phone: 207-797-6005 or 888-WILD-MED (945-3633 within the United States and Canada) Fax: 207-797-6007 E-mail: [email protected] http://www.wildmed.com Resource: Offers a variety of courses and certifications in wilderness medical and rescue courses. Wilderness Medical Society 810 E. 10th Street, P.O. Box 1897 Lawrence, KS 66044 Phone: 800-627-0629 Fax: 785-843-1853 E-mail: [email protected] http://www.wms.org Resource: A physician-based national wilderness medical organization with various committees that are dedicated to education about wilderness emergency medicine; particular attention is paid to education for physicians; publishes the quarterly newsletter Wilderness Medicine and the peer-reviewed journal Wilderness and Environmental Medicine. Wilderness Medicine Institute of the National Outdoor Leadership School 284 Lincoln Street Lander, WY 82520-2848 Phone: 800-710-NOLS Fax: 307-332-1220 http://www.nols.edu/wmi Resource: Offers a variety of courses and certifications in wilderness medicine and rescue.

DISASTER PREPAREDNESS IN THE UNITED STATES Department of Homeland Security (http://dhs.gov) Federal Emergency Management Agency (http://fema.gov) Emergency Management Institute, provides on-line training Department of Health and Human Services (http://dhhs.gov) Disaster Medical Assistance Teams National Nursing Response Teams National Pharmacy Response Teams Veterinary Medical Assistance Teams Disaster Mortuary Operational Response Teams National Medical Response Teams

OFFICE OF THE U.S. SURGEON GENERAL Medical Reserve Corps (medicalreservecorps.gov)

SUGGESTED READINGS Complete Suggested Readings for this chapter can be found online at www.expertconsult.com.

CHAPTER 37 



Search and Rescue DONALD C. COOPER, PATRICK H. LAVALLA, AND ROBERT C. STOFFEL

As ever-increasing numbers of outdoor users turn to the wilderness for recreation, the medical community and search and rescue (SAR) organizations are contending with a growing number of lost, sick, and injured persons. Wilderness search, rescue, and medical intervention are unique in several ways. All aspects of SAR are enormously time consuming. Simply raising the alarm for someone lost or injured in an isolated area may take hours, days, or even weeks. Organizing a response, including obtaining equipment and transportation for responders, requires a variable amount of time, depending on the level of preparedness of the response organization. Locating, gaining access to, stabilizing, and transporting a victim to definitive care can be a lengthy process. Because it takes many people to perform a wilderness rescue (six or eight people are required to carry a litter 1 mile), logistic considerations such as food, shelter, and transportation for responders quickly create their own problems. SAR personnel are subjected to the same risks and environmental stresses that compromise victims. To obviate further tragedy, they must have a heightened awareness of potential danger, adverse conditions, and personal limitations. In addition to basic and advanced life support training, rescuers must have extensive wilderness experience—or experience in the particular environment in which they will be operating—that combines practicality with creativity and resourcefulness. SAR personnel must have training in survival, improvisation, communications, leadership, navigation (e.g., map, compass, and Global Positioning System [GPS]), first aid, and specific SAR techniques. Many interventions, such as cardiopulmonary resuscitation, defibrillation, tube thoracostomy, tracheal intubation, and intravenous therapy, are difficult— if not impossible—in the wilderness setting. Examinations may be hampered by the bulky clothing necessary to keep the victim warm and dry. Medications and equipment are subject to rough handling and extremes of temperature, which may render them ineffective, unsterile, or inoperative (see Appendix: Drug Storage and Stability). Finally, decision making that optimizes patient care while not unduly risking the well-being of SAR personnel requires experienced leadership grounded in both common sense and technical skill. Perhaps the demands of SAR were best summarized by the wise rescuer who said that climbers, divers, hikers, and other outdoor enthusiasts get to choose where they practice their skills, but SAR personnel have no such choice. The situation, usually urgent, dictates where and when rescuers practice their art. The same situation that already compromised at least one person’s health or well-being subsequently endangers the SAR participants. This chapter introduces medical personnel to some of the unique search, rescue, and medical problems encountered in wilderness, remote (including urban disaster environments), and backcountry situations. The rudiments of SAR coordination, resources, and specialized problems are discussed. This information will help medical personnel understand how the SAR community works and provide an educational foundation to help prevent situations requiring undue risk or SAR personnel themselves from having to be rescued.

Search and Rescue: An Overview SAR systems provide the response for overdue, lost, injured, or stranded persons, usually in connection with outdoor activities and environments. In the context of SAR, wilderness can take on

several meanings. For instance, most consider wilderness to be regions that are uninhabited and uncultivated. Personnel may be called out to search a natural area such as a large park or desert, but it is equally likely that a search will be urban, in an area devastated by a natural disaster such as an earthquake or hurricane. Because most of the population in the United States resides in urban areas, emergency responders and SAR personnel are far more likely to encounter urban wilderness than a natural one. However, this chapter focuses on the nonurban setting. Types of SAR emergencies vary nationally and internationally, as do the responders. Programs, equipment, and personnel differ geographically in accordance with local needs and available resources. SAR can generally be defined as “finding and aiding people in distress—relieving pain and suffering.”6 However, contemporary references find it most useful to define search and rescue separately (Box 37-1).19 SAR often involves a great many volunteers and entails a multitude of skills. The Bhola (now Bangladesh) cyclone in 1970 (500,000 died); the collapse of the Banqiao, China, Dam in 1975 (230,000 died; 11 million were affected); the Tangshan, China, earthquake in 1976 (250,000 died); the eruption of Mt St Helens (1980); the terrorist attacks on the World Trade Centers (2001); multiple Atlantic hurricanes that struck the southeastern United States in 2004 and 2005, including Katrina; the Indonesian earthquake and subsequent tsunamis of 2004; and the 2010 Haiti earthquake (250,000 died) are all examples of significant, yet vastly different threats, hazards, and environments requiring widely diverse sets of SAR skills. SAR operations benefit comprehensive emergency management, providing a training ground and experience builder for disaster response capability at the most elementary level. The management concepts used in SAR operations establish foundation principles for providing response capability to large-scale emergencies and disasters. Nearly every type of hazard mentioned in comprehensive emergency management plans (local and state disaster coordination plans, mandatory in all states) and international treaties require planning for search and rescue.28 Management of these SAR operations can range from directing the actions of a few responders in a small community to managing an effort involving thousands of responders in a large urban disaster. Often, large situations involve several political subdivisions (e.g., cities, counties, states, countries) and coordination of air, ground, and/or marine resources. Local governments and other agencies that participate in SAR must coordinate diverse, multiskilled responders. In addition, many agencies that collectively support multiorganizational SAR responses operate under their own specific statutory authority.46,47

BOX 37-1  Search and Rescue Defined Search—An operation using available personnel and facilities to locate persons in distress. Rescue—An operation to retrieve persons in distress, provide for their initial medical or other needs, and deliver them to a place of safety. From the International Maritime Organization and International Civil Aviation Organization (IMO/ICAO): International aeronautical and maritime search and rescue manual, vol I, Organization and management, vol II, Mission co-ordination, and vol III, Mobile facilities, London/Montreal, 1999, International Maritime Organization and International Civil Aviation Organization.

For online-only figures, please go to www.expertconsult.com

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PART 5  RESCUE AND SURVIVAL

Time is almost always a factor in SAR operations, which tends to focus efforts on a quick conclusion. The general idea is to find or rescue the missing, lost, or injured subject before he or she succumbs to the effects of the environment, injuries, or a specific hazard.

INTERNATIONAL AGREEMENTS International conventions are often what countries use to establish rules between them. The Convention on International Aviation, the International Convention on Maritime Search and Rescue, and the International Convention for the Safety of Life at Sea (SOLAS) include rules requiring countries that are parties to these agreements to provide aeronautic and maritime SAR coordination and services for their territories and territorial seas. Coverage of the high seas is apportioned among the member countries by these instruments as well. To carry out its SAR responsibilities, a country usually establishes a national SAR organization or joins one or more other countries to form a regional SAR organization. In the United States, the national SAR organization is called the National Search and Rescue Committee (NSARC). While airborne, virtually all commercial aircraft on international routes are under positive control (e.g., followed by radar and in direct communication with air traffic controllers) by air traffic services (ATS) units. The International Civil Aviation Organization (ICAO) has linked ATS units into a worldwide system. Consequently, SAR agencies are usually notified very quickly when an international commercial flight has an emergency. Commercial aircraft on domestic routes and general aviation aircraft may not be under positive control, which can result in delayed reporting of their emergencies. The international aeronautic distress frequency is 121.5 MHz, and it is monitored by ATS, some commercial airliners, and other aeronautic facilities where needed to ensure immediate reception of distress calls. Emergency locator transmitters (ELTs) are carried in most aircraft and are required in most aircraft flown in the United States (see COSPAS-SARSAT). Additional information on international SAR may be found at the International Maritime Organization (IMO) website (http:// www.imo.org) and ICAO website (http://www.icao.int).

INTERNATIONAL STAGES OF SAR OPERATIONS The international SAR community has developed an approach to organizing operations that has evolved over the past several decades. This system is documented in the International Aeronautical and Maritime Search and Rescue (IAMSAR) Manual,19 which was developed jointly by the ICAO and the IMO. Each of the three IAMSAR Manual volumes is written with specific SAR system duties in mind and can be used as a stand-alone document or in conjunction with the other two volumes as a means to attain a full view of the SAR system. Volume I, Organization and Management, discusses the global SAR system concept, establishment and improvement of national and regional SAR systems, and cooperation with neighboring countries to provide effective and economical SAR services. Volume II, Mission Co-ordination, assists personnel who plan and coordinate SAR operations and exercises. Volume III, Mobile Facilities, is intended to be carried aboard rescue units, aircraft, and vessels to help with performance of search, rescue, or on-scene coordinator functions and with aspects of SAR that pertain to their own emergencies. The IAMSAR Manual describes a series of five stages of a SAR operation through which most SAR events pass: Awareness, Initial Action, Planning, Operations, and Conclusion. The manual suggests that, “These stages should be interpreted with flexibility, as many of the actions described may be performed simultaneously or in a different order to suit specific circumstances.”19 The reason the IAMSAR Manual does not have a “Preplanning” stage is twofold. First, the five stages of a SAR operation are about what happens in a specific incident. Preplanning can address types of incidents, but not specific incidents. Second, the preplanning function is addressed in what are called plans of operations or operations plans (OPLANs); see Appendix C of the IAMSAR 688

Manual, volume II. These are standing plans for how to deal with various kinds of situations. Awareness Stage A SAR organization cannot respond to an incident until it becomes aware that someone is in need of assistance. At this stage, information is received that someone (or an aircraft or vessel) is, or will be, in distress. There may not be enough information to initiate action, or action may not be necessary yet. Initial Action Stage When enough information is available, immediate action may be necessary. The first action is always to evaluate the information available, attempt to gain more, and determine the degree of the emergency. The “phase” of the emergency is used by the SAR authority to describe the level of confidence in the available information and the level of concern it raises about the safety of an aircraft or vessel and the persons on board. The IAMSAR Manual describes three emergency phases: uncertainty, alert, and distress. • Uncertainty phase: A situation wherein doubt exists as to the safety of an aircraft or vessel and the persons on board • Alert phase: A situation wherein apprehension exists as to the safety of an aircraft or vessel and the persons on board • Distress phase: A situation wherein there is reasonable certainty that a vessel or other craft, including an aircraft or person, is threatened by grave and imminent danger and requires immediate assistance An overdue aircraft, as an example, may be late for a wide range of reasons. The phases of the emergency allow personnel in charge to establish and communicate a summary of the available information that matches its validity, the urgency of action, and the extent of the response required. The IAMSAR Manual requires specific initial actions based on the established emergency phase. Planning Stage Planning operations is essential, especially when the location of the distress situation is unknown. “Proper and accurate planning is critical to SAR mission success; if the wrong area is searched, there is no hope that search personnel will find the survivors, regardless of the quality of their search techniques or the amount of their search effort.”19 The IAMSAR Manual suggests the use of computers for operational planning but also includes basic information on manual methods of planning searches. Operations Stage The operations stage encompasses all the physical activities involved in finding, providing assistance to, and rescuing people in distress. In short, this phase is where the plans are carried out. Conclusion Stage The conclusion stage is entered when it is determined that no one is in distress, when the search or rescue is concluded, or when nothing was found and the search is called off. This phase is when all SAR resources are notified that the mission is concluded.

COSPAS-SARSAT The SARSAT system (search and rescue satellite-aided tracking) was developed in a joint effort by the United States, Canada, and France. In the United States, the National Oceanic and Atmos­ pheric Administration (NOAA) is the lead agency and coordinates national participation in SARSAT and associated international programs. The COSPAS system (cosmicheskaya sistyema poiska avariynich sudov; in English, “space system for the search of vessels in distress”) (Box 37-2) was developed by the Soviet Union. These four nations (United States, Canada, France, and now Russia) banded together in 1979 to form COSPAS-SARSAT. In 1982, the first satellite was launched and the first life saved using the system, and the system was declared fully operational in 1984. The COSPAS-SARSAT system ceased satellite processing of the original 121.5/243-MHz beacons on February 1, 2009. Second-generation 406-MHz beacons were introduced in 1997

COSPAS—cosmicheskaya sistyema poiska avariynich sudov (Russian; in English, “space system for the search of vessels in distress”) ELT—emergency locator transmitter EPIRB—emergency position-indicating radio beacon PLB—personal locator beacon SARSAT—search and rescue satellite-aided tracking From the National Oceanic and Atmospheric Administration: National Environmental Satellite, Data and Information Service, Search and Rescue Satellite-Aided Tracking (SARSAT). http://www.sarsat.noaa.gov/.

that allow transmission in the 406-MHz message of encoded position data acquired by the beacons from global satellite navigation systems such as GPS, using internal or external navigation receivers. As of this writing, the 4 original member nations have been joined by 36 other nations and 2 regional organizations that operate 76 ground stations and 30 mission control centers worldwide or serve as search and rescue points of contact (SPOCs). As of December 2008, the COPAS-SARSAT system had provided assistance in rescuing about 27,000 persons in over 7,200 incidents. Visit http://www.cospas-sarsat.org or http://www.sarsat. noaa.gov for more details. The system uses satellites to detect and locate emergency beacons carried by ships, aircraft, and individuals transmitting on 406 MHz. The system consists of a network of satellites, ground stations, mission control centers, and rescue coordination centers. When an emergency beacon is activated, the signal is received by a satellite and relayed to the nearest available ground station. The ground station, called a local user terminal (LUT), processes the signal and calculates the position from which it originated. This position is transmitted to a mission control center (MCC), where it is joined with identification data and other information on that beacon. The MCC then transmits an alert message to the appropriate rescue coordination center (RCC), based primarily on the geographic location of the beacon. If the location of the beacon is in another country’s search and rescue region (SRR), then the alert is transmitted to the appropriate MCC. Distress Radio Beacons The most recognizable component of the SARSAT system is the distress radio beacon, also known as a “beacon.” There are generally three types of beacons used to transmit distress: emergency position-indicating radio beacons (EPIRBs) designed for maritime use, emergency locator transmitters (ELTs) designed for aviation use, and personal locator beacons (PLBs) designed for use by individuals and land-based applications. Although the three types of devices are physically different owing to the differing environments in which they must operate, they all work on the same principle and in the same way. When turned on (automatically or manually), each transmits alert signals on specific frequencies intended to be received by COSPAS-SARSAT satellites. Only a few frequencies are used by these beacons: • 121.5 and 243 MHz are used by many existing analog beacons, but the COSPAS-SARSAT system ceased satellite processing of these signals in 2009. Other devices (such as man-overboard systems and homing transmitters) that operate at 121.5 MHz and do not rely on satellite detection are not affected by the cessation of satellite processing of 121.5 MHz. The 121.5 frequency is still used in aviation for voice communication of an emergency. • 406 MHz is used in digital beacons and is the only type of beacon currently detected by the COSPAS-SARSAT satellite system. Emergency Position-Indicating Radio Beacons.  There are several types of EPIRBS in use for maritime applications. The U.S. Coast Guard (USCG) maintains an outstanding website with more information on EPIRBs: http://www.navcen.uscg.gov/ marcomms/gmdss/epirb.htm. Emergency Locator Transmitters.  ELTs were the first emergency beacons developed, and most aircraft are required to carry

them. ELTs were originally intended for use on the 121.5-MHz frequency to alert aircraft flying overhead. Obviously, a major limitation to these is that another aircraft must be within range and listening to 121.5 MHz to receive the signal. One of the reasons the COSPAS-SARSAT system was developed was to provide a better receiving source for these signals. Another reason was to provide location data for each activation (something that overflying aircraft were unable to do). Different types of ELTs are currently in use. There are about 170,000 of the older-generation 121.5-MHz ELTs in service in the United States. Unfortunately, these have proved to be highly ineffective. They have a 99% false-alert rate, activate properly in only 12% of crashes, and provide no identification data. To fix this problem, 406-MHz ELTs were developed to work specifically with the COSPAS-SARSAT system. These ELTs have unique identifiers and dramatically reduce the false-alert impact on SAR resources, have a higher accident survivability success rate, and decrease the time required to reach accident victims by an average of 6 hours. Most aircraft operators are now mandated to carry an ELT. Although 121.5/243-MHz ELTs used by some aircraft may still be used, the COSPAS-SARSAT system ceased satellite processing of these beacons in 2009, and alerts from these devices (and from 121.5/243-MHz EPIRBs) are no longer acted on unless detected by an overflying aircraft or ground-based receivers. This is why all beacon owners and users should replace their 121.5/243-MHz beacons with 406 MHz beacons as soon as possible. Personal Locator Beacons.  PLBs are portable units that operate much the same as EPIRBs or ELTs. These beacons are designed to be carried by an individual person instead of on a boat or aircraft. Unlike ELTs and some EPIRBs, they can only be activated manually and operate exclusively on 406 MHz in the United States. Similar to EPIRBs and ELTs, all PLBs also have a built-in, low-power homing beacon that transmits on 121.5 MHz. This allows rescue forces to home in on a beacon once the 406-MHz satellite system has put them within 3.2 to 4.8 km (2 to 3 miles). Some newer PLBs also allow GPS units to be integrated into the distress signal. This GPS-encoded position dramatically improves the location accuracy down to the 100-m level. In the United States, PLBs were in limited use until July 1, 2003, after which they were fully authorized for nationwide use. NOAA encourages all PLB users to be acutely aware of the responsibility that comes with owning one of these devices. PLBs are a distress-alerting tool and work exceptionally well. PLB users should familiarize themselves with proper testing and operating procedures to prevent false activation and be careful to avoid their use in nonemergency situations.30

SEARCH AND RESCUE IN THE UNITED STATES SAR involves many agencies and volunteers. The federal government assumes some responsibility for overall coordination, especially of federal or military resources requested by local or state agencies. U.S. National Search and Rescue Plan The U.S. National Search and Rescue Plan (NSP) was first published in 1956. It provides guidance to signatory federal agencies (Departments of Transportation, Homeland Security, Interior, Defense, and Commerce, as well as the Federal Communications Commission [FCC], and the National Aeronautics and Space Administration [NASA]) for coordinating civil SAR services to meet domestic needs and international commitments. The federal government assists with coordination of certain SAR services, including any federal or military resources that are requested by local or state agencies. NSARC32 is responsible for coordinating and improving federal involvement in civil SAR for aeronautic, maritime, and land communities within the United States. It is also the federal-level committee formed to oversee the NSP and coordinate civil SAR matters of interagency interest within the United States. Member agencies of NSARC are the signatories of the NSP. More information about NSARC may be obtained from the committee’s website at http://www.uscg.mil/NSARC. 689

CHAPTER 37  Search and Rescue

BOX 37-2  COSPAS-SARSAT Abbreviations

PART 5  RESCUE AND SURVIVAL

The NSP defines an SRR as “an area of defined dimensions, recognized by IMO or ICAO, associated with a rescue coordination center (RCC), within which SAR services are provided.”32 An RCC is a unit responsible for promoting efficient organization of SAR services and for coordinating the conduct of SAR operations within an SRR. For every SRR, there is one RCC, and the goal is to have no overlaps or gaps between SRRs around the world. The ultimate goal, of course, is to ensure SAR services are available to those in need of them. To this end, SRRs are not considered to be either jurisdictional or territorial in nature. They do not supersede territorial sovereignty, not even for SAR missions. However, clearances for entry into territorial waters or airspace are usually expedited and/or relaxed for SAR activities. In addition, the SAR mission coordinator (SMC) for an incident may not be located with the RCC responsible for the SRR. The SMC may be located anywhere. For example, when the Achille Lauro caught fire and sank in international waters off Somalia in 1994, the SMC was located at RCC Stavanger, Norway, which had received the vessel’s radio distress calls and was able to establish communications with her and other vessels in the area to coordinate the rescue of passengers. In the United States, there are two types of SRRs: maritime and aeronautic. Although only the ocean areas surrounding the United States and its territories fall within the maritime SRRs (marine vessels cannot sail on land), both the ocean and land areas of the United States fall within aeronautic SRRs (aircraft can fly over both water and land). The maritime SRRs surrounding the United States include, in the Pacific: Juneau, Honolulu, Seattle, and Alameda; and in the Atlantic: Boston, Norfolk, Miami, New Orleans, and San Juan. The oceans surrounding the United States and its territories also fall within aeronautic SRRs whose names and limits coincide with their maritime counterparts. However, with the exception of U.S. islands (e.g., Hawaiian, Puerto Rico) that are contained entirely within maritime SRRs and the Great Lakes (Cleveland Maritime SRR), all U.S. land falls within either the Elmendorff Air Force Base (Anchorage, Alaska) Aeronautical SRR (Alaska) or the Tyndall Air Force Base (Panama City, Florida) Aeronautical SRR (continental United States). According to the NSP, a SAR coordinator is “a federal person or agency with overall responsibility for establishing and providing SAR services for a search and rescue region(s) for which the U.S. has primary responsibility.”32 The SAR coordinators for the United States are as follows: • U.S. Air Force: Recognized SAR coordinator for the U.S. aeronautic SRR corresponding to the continental United States other than Alaska • U.S. Pacific Command: Recognized SAR coordinator for the U.S. aeronautic SRR corresponding to Alaska • U.S. Coast Guard: Recognized SAR coordinator for all other U.S. aeronautic and maritime SRRs. This includes the State of Hawaii, as well as waters over which the United States has jurisdiction, such as navigable waters of the United States. Outside these SAR coordinators, state and local authorities are responsible for land-based SAR and designate a person to be “SAR coordinator” within their respective jurisdictions. The NSP covers most types of SAR operations, such as land, maritime, aeronautic, urban, mass rescue, and those associated with what the document defines as “Incidents of National Significance.” However, it does not cover air ambulance service that does not result from a SAR or recovery operation, rescue from space, military operations, salvage operations, civil disturbances, or “Operations and coordination in addition to those…that might be carried out concurrently with civil SAR operations on scene, such as could occur during a disaster or terrorism response situation, or an Incident of National Significance.”32 Although not considered a federal SAR coordinator, the U.S. Department of the Interior National Park Service (NPS) provides SAR and other emergency services on lands and waters administered by the NPS. These services often include SAR operations, including emergency medical aid conducted in a wide variety of environments, such as remote and rural areas, lakes, rivers and oceans, and deserts, mountains, and caves. They also often require extended response times and use of specialized equipment. In small parks, this may be achieved through agreements 690

with surrounding emergency service providers. Outside national parks, state and local authorities or SAR units often accept responsibility for providing SAR services. Because of the unique scale and SAR challenges in Alaska, the USCG is often the lead federal agency for inland SAR incidents in certain areas of the state, including the Alaska Peninsula (south of 58 degrees N), the Aleutian Islands, and other coastal islands. The reason for this is simple: In these areas, USCG assets can often respond much more quickly than can those available through the U.S. Alaska Rescue Coordination Center at Ft Richardson, Alaska, north of Anchorage. For Alaskan inland areas, SAR is carried out by Air National Guard units, the Alaska State Troopers, and local borough SAR organizations. Because of the unforgiving environment, all federal, state, and local agencies work together closely in response to SAR missions in Alaska. Many U.S. states have chosen to retain established SAR responsibilities within their boundaries for incidents primarily local or intrastate in character. In such cases, agreements have been made between federal SAR coordinators and relevant state organizations.32 These local and state SAR coordinators, if established, become important contacts for federal SAR coordinators. National Response Framework The National Response Framework (NRF)47—its previous iteration was referred to as the “National Response Plan”—is a guide that details how the U.S. government conducts all-hazards response, from the smallest incident to the largest catastrophe. It establishes a comprehensive, national, all-hazards approach to domestic incident response and identifies the key response principles, as well as the roles and structures that organize national response. The document describes how communities, states, the federal government and private-sector and nongovernmental partners apply these principles for a coordinated, effective national response (Box 37-3). In addition, it describes special circumstances in which the federal government exercises a larger role, including incidents in which federal interests are involved and catastrophic incidents for which a state would require significant support. It lays the groundwork for first responders, decision makers, and supporting entities to provide a unified national response. The NRF is addressed to senior elected and appointed leaders, such as federal department or agency heads, state governors, mayors, tribal leaders, or city managers—those who have a responsibility to provide for effective emergency management. It also informs emergency management practitioners, explaining the operating structures and tools used routinely by first responders and emergency managers at all levels of government. The NRF retains the same core principles of the National Incident Management System (NIMS), in which first responders from different jurisdictions and disciplines can work together more closely to effectively respond to natural disasters and emergencies, including acts of terrorism. The NRF Resource Center (http://www.fema.gov/NRF) is an online reference center that provides access to the NRF and supporting documents. The National SAR Supplement NSARC also directs preparation of the National SAR Supplement (NSS) to the IAMSAR Manual—under revision in 2010 to be renamed the National SAR Manual—which provides guidance to federal agencies concerning implementation of the NSP. The NSS provides specific additional national standards and guidance that build on the baseline established by the IAMSAR Manual. It

BOX 37-3  Key Principles of the National Response

Framework

• Engaged partnerships • Tiered response • Scalable, flexible, and adaptable operational capabilities • Unity of effort through unified command From the U.S. Department of Homeland Security: The national response framework, Washington, DC, 2008. http://www.fema.gov/emergency/nrf/.

Catastrophic Incident SAR Addendum to the National SAR Supplement The tragedies of September 11, 2001, Hurricane Katrina in 2005, and other calamitous events continue to challenge federal, state, tribal, territorial, and local SAR responders in the planning and execution of large-scale SAR operations. NSARC realized the federal government’s response to large-scale catastrophic incident SAR (CISAR) needed to improve. As a result, the CISAR Addendum to the NSS33 was developed to provide guidance for SAR (Box 37-4) operations during catastrophic incidents to complement the overarching strategy for a national response to a catastrophic incident provided in the Catastrophic Incident Annex of the NRF. CISAR consists of civil SAR operations carried out as all or part of the response to an emergency or disaster declared by the president, under provisions of the NRF and its emergency support function (ESF) No. 9, Search and Rescue. This CISAR Addendum does not supersede other federal, state, tribal, or territorial SAR plans. There are many different federal, state, tribal, territorial, and local SAR response cultures. Each possesses unique capabilities, language, and responsibilities. During a catastrophic incident, NSARC member departments and agencies are required to conduct multiagency SAR operations within a unified command (e.g., a command in which responding agencies and/or jurisdictions with responsibility for the incident share incident management). The CISAR Addendum is intended to (1) provide a concise description of the federal government’s civil SAR response to catastrophic incidents; (2) guide federal authorities involved in the response; and (3) inform states, tribes, and territories about what to expect from federal SAR responders.33 The primary federal agency responsible for CISAR operations depends on the nature of the SAR operation to be conducted. ESF No. 9 of the NRF lists the Federal Emergency Management Agency (FEMA) and its Urban Search and Rescue Response System as being responsible for urban SAR; the USCG as being responsible for maritime, coastal, and waterborne SAR; and the U.S. Departments of the Interior and Defense (DOD) as being responsible for land SAR during a CISAR event. Regardless of which federal agency takes the lead, the primary agency works closely with the respective federal SAR coordinator in the affected area.

BOX 37-4  “Catastrophic Incident” as Defined in the

U.S. National Response Framework

Any natural or manmade incident, including terrorism, that   results in extraordinary levels of mass casualties, damage, or disruption severely affecting the population, infrastructure, environment, economy, national morale, and/or government functions. From the U.S. Department of Homeland Security: The national response framework, Washington, DC, 2008. http://www.fema.gov/emergency/nrf/ and The U.S. Department of Homeland Security: The national response framework, Washington, DC, 2008. http://www.fema.gov/emergency/nrf/.

U.S. Rescue Coordination Centers The USCG and Air Force both operate RCCs in the United States, but each service takes a slightly different approach. The Air Force RCC (AFRCC) coordinates inland SAR activities in the continental United States but does not directly conduct SAR operations. In most situations, the Civil Air Patrol (CAP), state police, or local rescue services carry out the actual SAR operations. In contrast, the USCG not only coordinates but also conducts maritime SAR missions. U.S. Air Force Rescue Coordination Center.  Established in 1947 to meet the growing demand for SAR and its legislated responsibility, the original three AFRCCs have evolved into a single RCC located under the 1st Air Force (AFNORTH) at Tyndall Air Force Base, Florida. As the U.S. inland SAR coordinator, the AFRCC serves as the single agency responsible for coordinating on-land federal SAR activities in the 48 contiguous states, Mexico, and Canada. Since the center opened in 1974, the AFRCC recorded the prosecution of more than 60,000 SAR missions, resulting in more than 13,900 lives saved.42 The AFRCC functions around the clock and is staffed by people trained and experienced in the coordination of SAR operations. The center is equipped with extensive audio and digital communications equipment and maintains a comprehensive resource file listing federal, state, local, and volunteer organizations that conduct or assist in SAR. There are four types of authorized AFRCC missions: search, rescue, medivac, and mercy. Search.  Once a distress situation is determined to exist but a location is unknown, federal SAR forces may be activated to search for, locate, and relieve the distress situation. The object of these searches may be in the form of overdue aircraft, ELTs, hunters, hikers, or children. Rescue.  A rescue mission entails the use of federal SAR forces to recover persons in distress whose location in a remote area is known, but who need assistance. This may be in the form of transportation to safety or to an adequate medical facility. These requests are normally received by the AFRCC from park service personnel or the local law enforcement authority. Medivac.  The transportation by federal assets of persons from one medical facility to another is defined as aeromedical evacuation, or medivac. Requests are normally received from a local hospital when no commercial transportation is available, the person’s life is in jeopardy, and time is critical. Each request is evaluated, and the decision to use federal resources is weighted heavily by the attending physician’s medical opinions. Mercy.  A mission to transport blood, organs, serum, medical equipment, or personnel to relieve a specific time-critical, lifethreatening situation is referred to as a mercy mission. Requests are normally referred from a local hospital authority or, in some cases, the American Red Cross when commercial transportation is not available. Although the AFRCC will accept and act on initial notification from any person or agency, it will attempt to determine the urgency and the facts pertaining to the situation before obliging itself. Several aspects of the situation are considered before a mission is opened, including the following: 1. Medical evaluation and urgency 2. State agreement requirements 3. Posse Comitatus Act 4. Conflict of interest with commercial resources 5. Resource availability The medical condition of the victim or victims is the most important aspect of mission consideration. The AFRCC will consider a request valid only when there is an immediate threat to life, limb, or sight. A mission will be started only to prevent death or aggravation of a serious injury or illness. The observations and opinions of a physician at the incident site weigh heavily on the decision to open a mission, and a flight surgeon is on call at the AFRCC when a local physician is unavailable. Each state has an agreement on file in the AFRCC describing the responsible agency and coordinating requirements for the various types of SAR missions. Each request for federal assistance is evaluated to ensure the requirements stipulated in the relevant 691

CHAPTER 37  Search and Rescue

provides guidance to all federal forces, military and civilian, that support civil SAR operations.31 Specifically, the NSS is designed to serve as both a training and operational tool for civil SAR operations. SAR planning is both an art and a science, relying greatly on the creativity and experience of the personnel involved. Because of the many variables encountered during SAR operations and the individuality of each SAR case, the guidance provided in the NSS must be tempered with sound judgment, having due regard for the individual situation. Very little in the NSS is mandatory because it is not intended to relieve SAR personnel of the need for initiative and sound judgment.31 Each of the signatory agencies of the NSARC (and NSP) are encouraged to develop an addendum to the NSS for their agency. Such documents could include policies, information, procedures, and so forth on civil SAR matters applicable to the agency concerned and consistent with the IAMSAR Manual and NSS.

PART 5  RESCUE AND SURVIVAL

agreement are met. Title 18 USC 1385 (the Posse Comitatus Act) prohibits military participation in civil law enforcement activities. Although there are some exceptions to the prohibition, as a general rule, DOD forces, including the CAP, will be restricted from participating in searches in which the person being sought is evading searchers, or is a fugitive, or when foul play is considered. On medivac or mercy missions in which the patient is not eligible for DOD medical benefits, federal assets cannot be used when commercial resources are available. Even when a patient is unable to pay or is destitute, commercial resources will be checked for availability and provided the opportunity to accept the mission before allocating federal resources. Although any SAR-capable asset belonging to the federal government may be requested, each resource is evaluated for distance from the distress location, special equipment requirements, urgency of the situation, and which resource can best accomplish the mission. Military forces may be called on to assist in civilian SAR missions. However, their participation in these activities must not interfere with their primary military mission. Once the decision has been made to use federal resources, a mission number is assigned and SAR forces are selected based on the geographic location and mission requirements. The Air Force coordinator then works closely with the responsible agency in an attempt to provide the resources best suited to accomplish the mission.42 Additional information on the AFRCC can be found at http:// www.1af.acc.af.mil/units/afrcc/. U.S. Coast Guard Rescue Coordination Centers.  The USCG, now a division of the U.S. Department of Homeland Security (DHS), is designated as the federal SAR coordinator for the maritime SRRs surrounding the United States and large portions of the high seas. The USCG is responsible for providing and coordinating SAR services over 28 million square miles of the world’s oceans, mostly in the northern hemisphere. This responsibility is divided into several districts, which are further divided into sectors (several per district) and stations. A 24-hour alert status is maintained year-round at all levels; Coast Guard resources can be under way or airborne within minutes of notification of a SAR incident. At its headquarters, each district maintains a fully staffed operations/command center responsible for coordinating operations within the area or district on a 24-hour basis. When coordinating SAR missions, these operations centers are called RCCs. Although minor SAR incidents are often resolved at the station or sector level, the district assumes the duties of the SAR mission coordinator in more complex or large-scale missions.43 The USCG arguably prosecutes more SAR missions than does any other organization or agency. It is also notable that the USCG, although considered an important part of the U.S. military forces, is a separate federal agency now under the DHS, not under the DOD, as is the Air Force. An important global SAR-related service of the USCG is the automated mutual-assistance vessel rescue (AMVER) system. AMVER is a global system that involves ships, regardless of flag, voluntarily providing information about their capabilities (e.g., medical personnel on board, rescue equipment), sail plans for voyages, and regular reports of their locations to a computer system that tracks their whereabouts. When a situation arises that requires SAR capabilities, a surface picture is produced that graphically shows the locations of all AMVER participants in the vicinity. The RCC can use this information to select the best one or several ships to respond to the emergency and allow all others to continue their voyages. Today, about 12,000 ships from more than 140 countries participate in AMVER. On average, 3600 ships are on the AMVER plot each day, with more than 100,000 voyages tracked annually. The AMVER system has saved more than 2000 lives since 1990 and 450 in 2007 alone.44 A “preventive SAR” service provided by the USCG as a direct result of the Titanic disaster is the International Ice Patrol, with operations funded by SOLAS signatories.18 Since 1913, the Ice Patrol has amassed an enviable safety record, with not a single reported loss of life or property caused by collision with an iceberg outside the advertised limits of all known ice in 692

the vicinity of the Grand Banks. However, the potential for a catastrophe still exists, and the Ice Patrol continues its mission using high-tech sensors and computer models.43 The USCG also performs or coordinates the medical evacuation of seriously ill or injured persons from vessels at sea if the patient’s condition warrants and USCG assets are within range. For less serious situations, USCG flight surgeons offer medical advice by radio. On rare occasion, the RCC may coordinate with a U.S. Navy ship to allow a USCG medivac helicopter to refuel to extend its range. On rare occasion, the RCC may coordinate with the Air Force to dispatch pararescue personnel to parachute to the vessel and stabilize the patient. In either case, these actions are taken only in the most serious situations, when one or more lives depend on such drastic actions. If a vessel is reported overdue or unreported (i.e., failed to check in when expected), USCG assets may or may not launch immediately, depending on whether the overdue craft is thought to be in immediate danger. Regardless, an extensive investigative effort is initiated immediately. During this investigation, a preliminary communications check and extended communications check (EXCOM) will likely take place. These actually include more than just contacting intended destinations. They also include interviewing persons who may be knowledgeable about the craft, as well as dispatching USCG vehicles or small boats to physically check harbors, marinas, launching ramps, and the like. In addition, an urgent all-ships broadcast is initiated, requesting information on any recent or future sightings that might be the missing vessel, and extended communications checks are repeated on a regular basis.12 If none of these communications and investigation efforts produces positive results (i.e., locating the vessel or indications that the persons on board are not in immediate danger), a search is undertaken. Search planning is conducted by the RCC staff, but additional assets can be requested from other agencies (e.g., U.S. Air Force and Navy) or foreign governments in a position to assist. With assistance from the USCG’s Search and Rescue Optimal Planning System (SAROPS), the RCC develops scenarios based on the available information. These scenarios are then weighted according to a subjective estimate of how likely each one is to represent the true situation. Further analysis of available information leads to development of probability maps (using SAROPS), from which SAROPS computes an optimal (maximum probability of success) search plan. Orders are then issued to all participating units. The search continues until either the survivors are found and rescued or it is deemed that further searching would be fruitless.12 Because SAR regions are not construed as boundaries to effective SAR action, and because the aeronautic SRRs are surrounded by the maritime SRRs, coordination between the AFRCC and the Coast Guard RCCs is a daily occurrence. Missions that involve portions of both regions will be coordinated through the AFRCC or the appropriate Coast Guard RCC. It is not unusual for the Coast Guard to call on the AFRCC for a particular resource needed to prosecute a mission in the maritime region or, conversely, for the AFRCC to use a Coast Guard resource in the aeronautic region. Additional information about the USCG can be found at http:// www.uscg.mil/. Federal Aviation Administration.  The Federal Aviation Administration (FAA), through its air route traffic control centers (ARTCCs) and flight service stations, monitors and flight-follows aircraft filing flight plans in the aeronautic SAR regions. In some cases, individual citizens contact an FAA facility when they have knowledge of a probable SAR situation involving aircraft. Therefore the FAA is usually the first agency to alert the AFRCC of a distressed or overdue aircraft. The AFRCC is tied directly into the FAA’s computer network, and FAA facilities use this system to alert the AFRCC. Once the AFRCC is alerted, the FAA and AFRCC work together to determine the urgency of the situation and locate the aircraft. Initially, radio communications are reviewed to determine the last known location of the distressed aircraft. Concurrently, other FAA facilities begin a check of all possible airports where the aircraft might have landed. In the meantime, the AFRCC contacts

Civil Air Patrol.  In 1948, the CAP was permanently chartered by the U.S. Congress as the official auxiliary of the U.S. Air Force. As such, this nonprofit organization of volunteers was charged with three primary missions: development of aviation through aerospace education, a cadet youth program, and emergency services. As of this writing, the CAP boasts more than 64,000 members, including more than 27,000 cadets between the ages of 12 and 20 years; the world’s largest fleet of single-engine, piston aircraft; and access to 1000 emergency service vehicles. It is proud of the fact that it saves 100 lives per year.5 Under their emergency services mission, the CAP provides SAR mission coordinators, search aircraft, ground teams, personnel on alert status, and an extensive communications network to emergency response efforts. Further, they provide services to national relief organizations during a disaster; transportation of time-sensitive medical materials (e.g., blood and human tissue); and aerial reconnaissance, airborne communications support, and airlift of law enforcement personnel in the national counterdrug effort. When CAP resources are engaged in a SAR mission, they are reimbursed by the U.S. Air Force for communications expenses, fuel and oil, and a share of aircraft maintenance expenses. In addition, CAP members are covered by the Federal Worker’s Compensation Act in the event of an injury while participating in a SAR mission. The CAP is the AFRCC’s prime air resource for the inland area. The AFRCC maintains an alert roster provided by CAP wings in each of the 48 contiguous states and is the central point of contact for CAP participation in SAR missions. The AFRCC also works closely with CAP national headquarters and directly provides input for CAP training in emergency services. Visit http:// www.gocivilairpatrol.com for more information. U.S. Coast Guard Auxiliary.  The USCG Auxiliary is to the USCG what the CAP is to the U.S. Air Force. The auxiliary is made up of citizens who volunteer their time and boats or aircraft to enhance and maintain the safety of boaters. When the Coast Guard “Reserve” was authorized by act of Congress in 1939, the Coast Guard was given a legislative mandate to use civilian volunteers to promote safety on and over the high seas and the nation’s navigable waters. The Coast Guard Reserve was then a nonmilitary service composed of unpaid, volunteer U.S. citizens who owned motorboats or yachts. Two years later, the passage of the Auxiliary and Reserve Act of 1941 designated the Reserve as a military branch of the active service, whereas the civilian volunteers, formerly referred to as the Coast Guard Reserve, became the auxiliary. When America entered World War II, some 50,000 auxiliary members joined the war effort. After the war, their attention returned to recreational boating safety duties in compliance with

the auxiliary’s four cornerstones: vessel examination, education, operations, and fellowship. Following passage of the Coast Guard Authorization Act of 1996, the auxiliary assists the Coast Guard, as authorized by the commandant, in performance of any Coast Guard function, duty, role, mission, or operation authorized by law. Today, as in 1941, auxiliarists are civilian volunteers whose activities are directed by policies established by the commandant of the USCG. Although under the authority of the commandant, the auxiliary is internally autonomous, operating on four organizational levels (smallest to largest): flotilla, division, district regions, and national. When auxiliary resources are engaged under USCG “orders,” they are reimbursed by the USCG for communications expenses, fuel and oil, and a share of vessel and aircraft maintenance expenses. In addition, auxiliary members are covered by the Federal Worker’s Compensation Act in the event of an injury while participating in an authorized mission. Many members of the auxiliary spend their weekends providing free boating safety courses to the public and free courtesy safety inspections to boaters. However, members also respond to minor SAR incidents, and the local USCG station, group, or district RCC coordinates their activities. Some auxiliarists have also become qualified to work in the RCCs or assist regular USCG facilities with regulating and patrolling regattas and other maritime events.45 With its 30,000 members, the auxiliary saves hundreds of lives each year, in addition to assisting thousands of boaters, performing courtesy marine examinations, teaching public and youth classes, and assisting the USCG in both administrative and operational missions.45 The State’s Role in SAR: Coordination and Support All states have passed legislation that provides for direct support to local government entities during emergencies or lifethreatening situations, and most states have a specific agency responsible for overall coordination and support for local SAR problems. This support can take many forms, but most often it is in the area of coordination and “one-stop shopping” for resources. Each state must establish an agency or central location that is familiar with all aspects of emergency management and the resources available to aid in life-threatening situations. Many of these resources belong to the state and can be used to aid local jurisdictions. A number of states, especially in the Northwest, have designated a state agency to be responsible for directing and coordinating air SAR activities. These state agencies develop and maintain aviation SAR response programs with cooperation and support from local and federal agencies. Experience shows that this system usually works better than those in other areas of the country that rely on the federal government to initiate and carry out aircraft SAR activities. If a local emergency manager, sheriff, or fire chief requests outside assistance in the form of specialized teams, search dogs, air support, or enhanced communications, the state agency for emergency services or emergency management can in most cases locate the nearest resources available and coordinate the response. If any federal resources are needed, such as air support or military personnel, the state agency provides a direct link to that resource. For instance, the AFRCC at Tyndall Air Force Base, Florida,42 has working agreements with all states that are updated periodically. Technically, the resources of local and state governments must have been exhausted or be unable to perform a task before federal support can be rendered. However, policy provides for immediate aid when time is critical and in life-or-death situations. Much discretion is given to military installation commanders regarding aid to civilian authorities, as long as the primary (military) mission of the resource is not impaired. In fact, most commanders appreciate the opportunity to fly actual missions. Access to these resources must be gained through the state and AFRCC. Every state’s emergency management agency is responsible for providing support, guidance, training, and coordination to local political subdivisions within that state. As such, it produces a vital behind-the-scenes effort to help local jurisdictions prepare for emergencies, including SAR. The state also promulgates the 693

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relatives, friends, and business associates of the pilot or passengers aboard the missing aircraft, with the hope of establishing the whereabouts of the aircraft or to gather information about the personnel aboard. Through these contacts, the AFRCC determines the pilot’s intentions, flying capabilities, emergency equipment aboard, and other pertinent information that would assist if a search were to become necessary. Through experience, the FAA and AFRCC have learned that most alerts for missing aircraft are due to the pilot failing to either close the flight plan or inform some person or agency of his or her intentions. For this reason, only a small percentage of alerts issued by the FAA result in an actual airborne search for a missing aircraft. All ARTCCs have the capability to recall recorded radar data. The National Track Analysis Program (NTAP) can identify and track targets that are at a sufficient altitude to be tracked by radar regardless of whether they are being controlled by the ARTCC. NTAPs requested by the AFRCC have proved to be a key ingredient in aircraft searches, providing the route of flight and last radar position. With the congressional mandate requiring most aircraft to be equipped with an ELT, the FAA works very closely with the U.S. Mission Control Center (USMCC) and the AFRCC to readily locate the source of ELT signals. All ELT signals reported to FAA facilities are immediately forwarded to the AFRCC and jointly investigated as probable distress signals.50

PART 5  RESCUE AND SURVIVAL

laws and regulations necessary to enhance effective actions for SAR response. Such legislation often indemnifies volunteer SAR teams, provides their medical coverage and insurance, and in some cases replaces personal property lost during SAR work. Although most volunteers work willingly until the job is done, this recognition and coverage by the state often provide additional incentives for volunteer participation.

coordinated and organized. All participants must know their responsibilities, what is expected of them, who is in charge, and to whom they answer. If this knowledge is lacking at any level, the effort can quickly become chaotic, ineffective, and very probably dangerous. Nowhere are these issues more important than in an emergency, when time is a crucial factor.

Local SAR Response The official response to the call for a wilderness SAR situation is usually delegated to a political subdivision within the state. The legal responsibility for SAR is generally vested with the county sheriff or chief law-enforcement officer at the local level, but this varies by region and state. In some cases, it is the responsibility of state police agencies, and in others, it belongs to land management agencies. The SAR response for one jurisdiction may differ greatly from that of another. For instance, many national parks in some areas of the country handle all of their own SAR incidents. Others jointly manage the function, whereas some rely entirely on outside resources. National forest land is managed solely by forest service personnel, but when it comes to SAR, the forest service usually only supports the local responders. In urban and suburban areas, police officers, firefighters, emergency medical technicians, and emergency management organizations maintain some degree of disaster and emergency readiness through daily missions that often involve SAR work. Fire departments have historically been responsible for rescue and response to emergencies within certain geographic or political areas, and volunteers augment many departments. Law enforcement agencies also maintain full-time, efficient response systems designed for their particular SAR requirements. Ambulance and rescue vehicles operated by a variety of private enterprises and volunteer organizations augment existing local government services. Through local emergency response planning and coordination, these services respond to a spectrum of everyday emergencies, including fires, collapsed buildings, hazardous material spills, vehicle extrications, and medical emergencies. County sheriffs, reserve law enforcement, volunteer fire departments, and a variety of volunteer search and rescue units have been established to address local SAR problems. Delivery of SAR aid to rural and wilderness areas often presents many special logistic problems, which may be compounded by distance, terrain, and weather. The demand for wilderness SAR is often seasonal and unpredictable. Volunteer mountain rescue units, Explorer SAR groups, SAR dog teams, CAP squadrons, motorized units, and many types of volunteer composite teams (e.g., teams that have a variety of capabilities) are usually formed locally in response to the type and nature of recurring SAR problems. Regardless of what type of SAR emergencies occur, local resources and effort must be developed because they are closest to the problem. State and federal resources are subject to problems with authority, time lag, distance, weather, logistics, and bureaucracy. The same storm or disaster that incapacitates a local area may also prohibit outside (and sometimes inside) emergency response and resupply. Although official agency responses differ greatly around the country, one major factor remains constant—the dedicated and unfailing willingness of volunteers to respond and work until the job is done. The volunteer effort in SAR nationwide is the backbone of aid to people in distress, as is stated in the rescue service motto: “These Things We Do That Others May Live.” The volunteer response has proved crucial to wilderness-type situations. Volunteer organizations, communications, and special skills cannot be replaced by any “official agency” resources.

INCIDENT COMMAND SYSTEM

Organization of a Search and Rescue Event SAR requires people who take action and meet objectives to achieve a common goal, often with one or more lives in the balance. For any combination of actions to be effective in a particular situation, the enterprise must be systematically 694

The system designed to address the challenges of managing emergency incidents in the United States, including SAR, is called the Incident Command System (ICS). It has been in use in the United States for many years.35 This function-based system was designed to be adaptable to various types and sizes of incidents in a proactive, rather than a reactive, manner. The system groups similar tasks into five functional areas: command, operations, planning, logistics, and finance/administration. Each of these functions is performed at every incident to one degree or another, and all can easily be expanded as the size and complexity of the situation dictate. This expansion, however, is based on the premise that the span of control (the ratio of the subordinates to each supervisor) should never exceed seven to one and should more commonly be five to one. When this is exceeded, another level is added to the hierarchy to maintain an acceptable span of control (Figure 37-1, online). The command section is led by the incident commander and provides overall management of the organization. Within ICS, the command section is responsible for dealing with other agencies (liaison officer), the news media, and other external influences (information officer) and is responsible for the overall safety of the operation and its participants (safety officer). If the incident is too small for these functions to be performed by separate individuals, the incident commander performs them. The operations section is led by the operations section chief, who is responsible for coordinating and performing all tactical operations. This role is commonly performed by the incident commander until the incident becomes sufficiently large and complex that the function must be performed by another individual. When multiple casualties are involved in an incident, their triage, treatment, and transport fall under the purview of the operations section. In such an incident, the operations section is divided into functional groups, often including at least triage, treatment, and transport groups. The person in charge of managing and coordinating the efforts of each group is called the group supervisor. If the operations section is better divided using geography, a division rather than a group is formed. For instance, injured persons at an auto accident might be found on two sides of a road. An east division and a west division might be established to deal with the geographic separation of the resources. In a small organization, the supervisor of each division would answer directly to the operations chief. To respond to specific challenges within an incident, a task force or strike team might be formed. A task force is any combination of single resources assembled for a particular tactical need, with common communications and a leader. For instance, FEMA combines search, rescue, medical, and technical resources to form an urban search and rescue task force. A strike team, on the other hand, is a combination of a designated number of the same kind and type of resources with common communications and a leader. The number of resources used in the team is based on what is needed to perform the function. For instance, four three-person hasty search teams may be combined to form a strike team. These two combinations of resources permit the necessary flexibility when allocating resources. The planning section is led by the planning section chief, who is responsible for collecting, evaluating, and distributing all incident information. As with the other sections, the incident commander performs this function unless the size and complexity of the incident dictate otherwise. In SAR, the planning section is particularly important because it evaluates search evidence and determines, based on what has been learned, what future actions should be taken or how current actions should be modified. Because such interpretation and evaluation often require great technical knowledge, personnel such as hazardous materials specialists, physicians, structural engineers, and other technical

NATIONAL INCIDENT MANAGEMENT SYSTEM In Homeland Security Presidential Directive-5 (HSPD-5), the president of the United States called on the DHS to develop a national incident management system to provide a consistent nationwide approach for federal, state, tribal, and local governments to work together to prepare for, prevent, respond to, and recover from domestic incidents, regardless of cause, size, or complexity. On March 1, 2004, after collaboration with state and local government officials and representatives from a wide range of public safety organizations, DHS issued the NIMS. It incorporated many existing best practices into a comprehensive national approach to domestic incident management, applicable at all jurisdictional levels and across all functional disciplines. Among these best practices, and a key component of the NIMS, is the incident command system, which has been established by the NIMS as the standard organizational structure for the management of all incidents. HSPD-5 also required DHS to establish a mechanism for ongoing coordination to provide strategic direction for and oversight of NIMS. The National Integration Center’s Incident Management Systems Integration Division—formerly the NIMS Integration Center—was established to support both routine maintenance and continuous refinement of NIMS. In 2008, the NIMS document was revised to incorporate a wide range of feedback, best practices, and lessons learned from recent incidents; it clarified concepts and principles and refined processes and terminology throughout the document.46 The NIMS represents a core set of doctrine, principles, terminology, and organizational processes to enable effective, efficient, and collaborative incident management at all levels. To provide the framework for interoperability and compatibility, the NIMS is based on a balance between flexibility and standardization. Incident Management Teams An incident management team (IMT) is a scalable group of trained individuals who work together to augment/assist ongoing operations through the provision of infrastructure support; or, in a large and/or complex incident or event, provide for the command, control, coordination, support, and management of the organization and resources necessary to address the needs of the incident or event. The comprehensive resource that is an IMT may either augment ongoing operations through provision of infrastructure support or when requested, transition to an incident management function to include all components/ functions of a command and general staff.48 The organizational structure an IMT generally would use follows NIMS ICS doctrine and most often looks something like the flow chart illustrated in Figure 37-2, online.

An IMT has the following characteristics: • Includes command and general staff members, unit leaders, and support personnel • May have statutory authority and/or formal response requirements and responsibilities • Has predesignated roles and responsibilities for members (rostered and on-call: identified and able to be contacted for deployment) • Is available 24 hours a day, 7 days a week, 365 days a year • Is scalable, depending on incident/event size and complexity IMTs are designated by “type,” based on capability, the level of training and experience, and reasonably anticipated incident response requirements, with type 1 being the most capable. There are four types of IMTs: • Type 1: National or state team for the largest and most complex incidents of national significance • Type 2: National or state team for incidents of national significance • Type 3: State or regional multiagency/multijurisdictional team for complex or extended incidents • Type 4: Single or multiagency team for expanded incidents Much like search, rescue, and hazardous materials capabilities, incident management capabilities should be based on response requirements that might be reasonably anticipated. According to the DHS,49 every jurisdiction needs to have access to an IMT, but not every jurisdiction needs to have its own IMT. The DHS further recommends the following: • A typical agency needs personnel trained and qualified to fill command and general staff roles at major/complex incidents who will recognize when a more robust level of incident management support is needed (such as a type 3 or 4 IMT). • Larger municipalities or regional areas with several emergency response agencies (those likely to have multiplealarm fires or other major incidents on a regular basis) should have a Type 4 IMT. • Each state and major metropolitan region, as well as other high-risk areas (those likely to have multiday, complex incidents or special events requiring a written Incident Action Plan) should have a multidiscipline, all-hazard (type 3) IMT. If a local incident expands beyond the capability or experience available, a response agency should have the capability to establish a Type 4 IMT on site or they can request a type 3 IMT regionally or through the state. A state type 3 IMT may take 2 to 4 hours to deploy and arrive. If the incident so warrants, and the state does not have a type 2 or type 1 IMT, the state can request, through FEMA or other agreements, a national IMT. However, national teams are expensive (approximately $1 million per day, on average), and they require some type of mobilization order and payment agreement. Depending on the national situation (e.g., during fire season, none may be available), incident type/complexity, and location, the National Interagency Fire Center (http://www.nifc.gov/) may deploy either a type 1 or type 2 IMT if one is requested. However, a state type 3 IMT is definitely more economical, more likely to be available, and provides benefits (e.g., local knowledge, local accountability, improved responsiveness) that national teams may not provide. Upon arrival, the IMT’s incident commander (IC) will meet with the local IC and the agency administrator (e.g., state agency director, county executive, city manager or mayor) to determine what they desire/expect from the IMT and to obtain any necessary delegation of authority. The incoming IC will then brief the rest of the incoming IMT about their roles/ expectations. The IMT will then integrate as requested into the current ICS structure.

Four Phases of a Search and Rescue Event: The Incident Cycle Every SAR event goes through four consecutive phases: locate, access, stabilize, and transport (LAST).6 This sequence, however, could more accurately be described as a continuum that begins 695

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specialists may be required to help the planning section develop and revise the incident action plan. The logistics section is led by the logistics section chief, who is responsible for providing personnel, equipment, and supplies for the entire incident. This awesome task involves ensuring that personnel are available, rested, and fed; that all equipment, including communications equipment, is available and operable; that vehicles are fueled and repaired; and that medical care is provided for all incident personnel. Basically, logistics is charged with seeing that the physical tools required to meet the overall objectives are available, operable, and maintained. If the size and complexity of the incident prevent the incident commander from monitoring finance and administrative issues, the finance/administration section is led by the finance/ administration section chief. This section is responsible for tracking all financial data for the incident, such as personnel hours, resource costs, costs for damage survey, and injury claims and compensation. Because most agencies involved in SAR can usually handle financial issues on their own, and most incidents are small and of short duration, the incident commander usually performs the functions of this section. Only in the largest or most complex incidents is it necessary for the incident commander to assign an individual or staff to perform finance section duties.

PART 5  RESCUE AND SURVIVAL

with planning or preplanning for the incident. Because planning for the next incident should be affected by what happened during the last, the incident cycle is actually continuous and only pauses between incidents. Once first notice of an incident has been received and the locate phase begins, the goal is to progress through the access, stabilize, and transport phases as quickly, safely, and efficiently as possible. Planning between incidents allows decisions to be made in a calm environment without the urgency that often accompanies a SAR operation. Such plans identify who will be in charge, organization of the operation, specific procedures, viable alternatives, and other decisions that are best made before an incident occurs.

LOCATE PHASE The first step in addressing any emergency situation is locating the subject or subjects in need of assistance. This may be as simple as asking for an address or as complex as conducting an extended search for a lost person or persons. If the subject is easily found, rescuers can quickly move into the access phase. However, if locating the subject is difficult, this phase may turn into the crux of the SAR problem. First Notice The first notice of an incident is often conveyed by relatives who report an injury or missing person, by a witness to an incident, by a government agency reporting distress signals (such as an ELT), by bystanders who perceive a problem, or by a 9-1-1 call. Once the initial notice is received, the individual taking the information must know what to do and whom to call next. Planning Data and Their Uses Information gathered at the onset of an incident begins an ongoing investigation. It is used to determine the appropriate response and to help predict how the subject or subjects might react to the situation. This information is called planning data and includes any information that might affect what should be done to resolve the situation. Examples of planning data include name of the subject, situation that caused the problem, last known location of the subject, subject’s physical and mental conditions, subject’s plans (where was he or she going?), available resources, weather information (present and predicted), geographic information, and history of similar incidents in the area. The purpose of collecting all this information is to help decide what to do next while predicting what the subject might do to help or hinder the situation. The investigation and gathering of information continue throughout the incident and are used to modify initial plans. As new information is acquired, an action plan is developed and revised until the end of the incident cycle, when planning for the next incident commences. Once information is gathered, the urgency of the situation is assessed. This assessment ultimately determines the speed, level, and nature of any response and may indicate whether a nonurgent or an emergency response is needed. The specific information used in urgency determination includes the age and condition of the subject, current and predicted weather, and relevant hazards. Figure 37-3 shows an example of an urgency determination form, which can be used by SAR personnel to determine how urgent their response should be.6 Urgency also contributes to allowable risks and thus influences searcher safety—a primary consideration for search managers. Search Tactics During the initial locate phase of the incident, emphasis is on searching for the subject. Exactly how to accomplish this is a priority, especially if this part of the incident cycle is expected to be a problem. SAR managers first initiate techniques that increase the chances of locating the subject in the shortest time. These techniques are generally termed tactics and involve some action performed to find the subject. These actions can be indirect (e.g., not requiring actual field searching) or direct (e.g., requiring deployment of searchers to the field). Examples of indirect tactics include confining the search area to limit movement of the subject and others into and out of the area, 696

identifying and protecting the point last seen (PLS) or the last known position (LKP), and attracting the subject, if he or she is expected to be responsive. Generally, indirect techniques are quicker and easier to apply, so they are started first. As the incident progresses, direct tactics are initiated. In managing an incident, efforts are almost universally made to apply quick-response resources in areas likely to offer early success. The best resources are put in the most likely areas as early as possible. In addition, identifying and protecting the PLS or LKP are crucial indirect techniques that can mean the difference between success and failure of the entire effort.6 Direct techniques include sending teams of searchers into an area to search for clues or the subject. They are categorized by level of thoroughness. For instance, a fast, relatively nonthorough search of high-probability areas is called a hasty search. This type of search would be conducted at campsites, buildings, and other very likely locations where the subject might be found. Loose grid techniques—widely spaced searches of large areas—can be applied when relatively rapid searches of large areas are desired. When using these techniques, thoroughness is greater than with hasty searches, but less than with other slower, more resourceintensive techniques. Loose grid techniques allow some level of effort to be applied to large areas fairly quickly. Alternately, tight grid techniques—slow, highly systematic area searches—are applied only when the absolute highest level of thoroughness is required. Unfortunately, this is almost always at the expense of time and resources. In short, the greater the thoroughness, the more resource intensive and time consuming the technique. Clues and Their Value Clues are discovered during the investigative and tactical phases of a search. Their importance cannot be overemphasized. They may take the form of physical evidence, such as a footprint or discarded item, account by a witness, or information gleaned from the investigation. Clues serve as the rudder that steers the overall search operation. Relevant clues are the basis for all search strategies and can determine or modify nearly all operational actions. Their powerful influence should be obvious; this is why searchers are taught to be “clue conscious” and to seek clues, not just subjects. There are many more clues than there are subjects. People generate clues. A person exudes scent in the form of dead skin cells, crushes or disturbs vegetation, and, when traveling, leaves marks on the ground or other physical evidence of passing. This evidence is often discoverable if the appropriate resource is applied in a coordinated, organized search effort. Searchers must be sophisticated enough to discover this evidence and interpret its meaning before it is destroyed or decays. Because evidence important to a search effort is often easily destroyed once it is discovered, it is important to protect it from damage until it is completely analyzed. Search Resources Resources are defined as all personnel and equipment available, or potentially available, for assignment to support the search effort. Specific types of active tactics are categorized by the resource that performs them, such as dog teams, human trackers, ground search teams, and aircraft. Other common resources include management teams (e.g., overhead teams, public information officers), water-trained responders (e.g., river rescue, divers), cold weather responders (e.g., ice climbers, avalanche experts, ski patrollers), specialized vehicle responders (e.g., snowmobiles, four-wheel-drive trucks, all-terrain vehicles, mountain bikes, horses), and technical experts (e.g., communications experts, interviewers, chemists, rock climbers, physicians, cavers). In addition to these, other less common resources might also be available. These could include attraction devices (such as horns, flags, lights, sirens), mine detectors (military), noise-sensitive equipment (super microphones), infrared devices (forwardlooking infrared [FLIR] on aircraft, night-vision equipment, thermal imagers), thermistors, and even witches, seers, prophets, and diviners. Just about any person or thing imaginable may be available for use in a SAR incident. Their use is limited only by the

Remember: the lower the number, the more urgent the response!!! A.

CHAPTER 37  Search and Rescue

Search Urgency Date Completed: Time Completed: Initials:

SUBJECT PROFILE Age 1

Very Young

1

Very Old Other Medical Condition Known or suspected injury or illness

3

Known fatality

3

1 1-2 3

SUBJECT EXPERIENCE PROFILE Not experienced, not familiar with the area Not experienced, knows the area Experienced, not familiar with the area Experienced, knows the area

E.

1 1-2 2 3

EQUIPMENT PROFILE Inadequate for environment Questionable for environment Adequate for environment

D.

1 2-3

WEATHER PROFILE Existing hazardous weather Predicted hazardous weather (8 hours or less) Predicted hazardous weather (more than 8 hours) No hazardous weather predicted

C.

1-2

Healthy Number of Subjects One alone More than one (unless separation suspected) B.

2-3

1 1-2 2 3

TERRAIN AND HAZARDS PROFILE Known hazardous terrain or other hazards Few or no hazards

1 2-3

TOTAL

If any of the seven categories above are rated as a one (1), regardless of the total, the search could require an emergency response.

•••THE TOTAL SHOULD RANGE FROM 7 TO 21, WITH 7 BEING THE MOST URGENT.••• 8-11 Emergency Respone

12-16 Measured Response

17-21 Evaluate and Investigate

FIGURE 37-3  Urgency determination form. (From Cooper DC, editor: FUNSAR: Fundamentals of search and rescue, Chantilly, Va, 2005, Jones & Bartlett.)

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creativity of those in charge. Here we discuss a few of the most common and useful. Dogs.  Dog teams are a common type of active search resource in the wilderness and are composed of a dog (occasionally more than one) and a human handler. The dog uses scent to search for and follow a subject, while the handler interprets signals from the dog and searches visually for evidence. Three common categories into which dogs fit are tracking, trailing, and air scenting. Tracking dogs follow scent on the ground from a person’s footsteps and usually very closely follow the trail where a person traveled, regardless of the wind. Trailing dogs follow scent that has fallen onto the ground from the subject along the route of travel. Unlike the tracking dog, the trailing dog may follow the scent at some distance from the actual tracks of the subject, and may therefore be more affected by wind. Tracking and trailing dogs are most effective when used in areas that have not been contaminated by humans other than the subject. Also, weather and time tend to destroy scent available to these types of dogs, so the earlier they are used in a search, the better their chances of finding something. Air-scenting dogs work off-lead to follow a subject’s scent to its source. Specifically bred and trained air-scenting dogs can even discriminate between individual humans. They may detect scent from articles of clothing and can often follow it to discover a person buried in rubble or snow or even submerged under water. Wind is very important to this type of dog, as are other environmental forces, such as sun and rain. As long as the source exists, an air-scenting dog can usually detect the scent carried in air currents and follow it to the source. Human Trackers.  Human trackers use their visual senses to search for evidence left by a person’s passing. Human trackers “cut” or look for “sign” or discoverable evidence by examining the area where the subject probably would have passed. This process of looking for the first piece of evidence from which to track is called “sign cutting.” Following the subsequent chain or chronology of sign is called “tracking.”10 In SAR, most trackers use a stride-based approach called the step-by-step method. This simple, methodical approach emphasizes finding every piece of possible evidence left by a subject. However, its most important role is undoubtedly the ability to quickly determine the direction of travel of the subject and thus limit the search area.10 Ground Search Teams.  Hasty Teams.  A hasty team is an initial response team of well-trained, self-sufficient, highly mobile searchers whose primary responsibility is to check out the areas (e.g., trails, roads, road heads, campsites, lakes, clearings) most likely to first produce the subject or clues. Their efficiency and usefulness are based on how quickly they can respond and the accuracy of initial information. Ideally, hasty teams should include two or three individuals who are knowledgeable about tracking. They should be clue oriented, familiar with the local terrain and dangers in the area, and completely self-sufficient. Also necessary are the ability to skillfully interview witnesses and to use navigational skills with pinpoint accuracy. Team members should at least be trained in advanced first aid. Hasty teams usually operate under standard operating procedures, so they do not have to wait for specific instructions. They carry all the equipment they might need to help themselves and the lost subject for at least 24 hours. Grid Teams.  Grid searchers use a more systematic approach to searching. They usually examine a well-defined, usually small segment to discover evidence. The classic approach to grid searching involves several individuals (almost always too many) standing in a line, shoulder to shoulder, walking through an area in search of either evidence or subjects. The distance between searchers can be varied to change thoroughness and efficiency (wide spacing is less thorough and more efficient). However, such resource-intensive approaches to searching are generally less preferred than those that use fewer personnel in a more efficient manner (such as tracking, dogs, or aircraft). In addition, 698

close-spaced grid searching tends to damage evidence and is generally difficult to coordinate. Although grid searching may be an acceptable approach in certain limited circumstances, experience has shown that when the subject of a search is a person, searching in this thorough manner should be used only as a last resort. Experiments involving grid searching have suggested that it is better to place searchers farther apart. This is usually a more efficient use of resources. Aircraft.  Aircraft serve the same purpose as grid searchers, only from a greater distance, at a greater speed, over a larger area, and usually with a lower level of thoroughness. Within a search effort, aircraft can serve both as a tactical tool to look for clues and as transportation for personnel and equipment. They also provide an excellent attraction device for the missing subject as well as witnesses who may have information about the incident. Both fixed- and rotor-wing aircraft have their place in SAR and, like other resources, have their advantages and limitations. Among the most obvious limitations are the expense and complex use requirements. Aircraft not only require specialized personnel and cost a great deal to operate, they also have very strict weather and environmental restrictions. For instance, it would be difficult to search from an aircraft in a snowstorm, and terrain may prevent searching certain areas from the air. However, most of these difficulties can be adequately addressed and minimized in a well-developed preplan. Search Planning Considerations State-of-the-art searching for lost persons has come a long way from the familiar lining up of volunteers shoulder to shoulder and walking in a straight line to search an area. Many new lifesaving concepts have been developed by the national SAR community. By borrowing from psychology, mathematics, business, and analysis of past incidents, search planning and management have evolved into sophisticated sciences. Search effectiveness has also been improved through the study of human behavior, statistics, probabilities, leadership, and the use of good planning and management principles (Figure 37-4). Search planning is guided by two general considerations: where am I going to look for the lost or missing person (strategy), and how am I going to find this missing or lost person (tactics)? To be effective, modern searchers follow several basic principles and techniques that include: 1. Respond urgently—a search is an emergency. 2. Confine the search area. 3. Search for clues. 4. Search at night. 5. Search with a plan and in an organized manner. 6. Grid search (tight grid) as a last resort. Every day, emergency responders receive calls to perform their duties, and they never know what to expect once they arrive. Life-threatening or time-critical situations have engendered what is known today as the “firehouse response.” This means that emergency responders have to assume the worst until proved

FIGURE 37-4  Overlay on topographic map used to manage search. Regions of probability are denoted by letters of the alphabet.

Search Theory.  The mathematic basis for searching and study of search theory had its beginnings during World War II in the work of the U.S. Navy’s Anti-Submarine Warfare Operations Research Group (ASWORG) and was originally based on searching for the wakes of warships as seen by aircraft flying over the ocean.11 The results of this work were collected in a seminal report by B. O. Koopman in 1946,26 but the report was not declassified and generally available until 1958.2 In 1980, Koopman developed a somewhat expanded version of this work.27 Although Koopman’s work is clearly aimed at naval interests, the general theory of search he established is applicable to virtually any type of search problem. Since this early work, search theory has undergone continuous research and development by agencies such as the USCG and U.S. Navy in both the maritime and aeronautic environments, mining and oil businesses in search of mineral and petroleum deposits,14 and even archeologists in search of lost cities, such as Troy.39 The fundamental usefulness of search theory lies in its ability to help determine where and how to search. It accomplishes this by (1) quantifying the likelihood of a missing subject being in a particular area, as well as the likelihood of searchers finding the subject; and (2) offering tools with which one can estimate the chances of success of a particular search. The application of search theory requires appropriate use of probability theory, a branch of mathematics that is used for estimating the likelihood of uncertain events, in planning a search. The chance that the missing person is in the search area is called probability of area (POA). The probability that a search resource will find the missing person or clue if it indeed is in the area being searched is called probability of detection (POD). The product of these two important variables produces a result called probability of success (POS = POA × POD).39 The foremost objective and major challenge for search planners is to deploy the most capable search resources (POD) into segments in which the subject is most likely to be (POA) to produce the most POS in the least amount of time. On the surface this seems to be a straightforward proposition. However, myriad critical factors, such as resource detection capability, environmental influences, search object characteristics, probability density, probability distribution, coverage, and sweep width, conspire to make the most correct search action a complex, unintuitive series of difficult choices. Several initiatives have been undertaken to simplify the process of applying search theory to land search, including standardizing terms7 and developing simplified, yet mathematically correct, approaches to quantifying the variables in less subjective ways.8 Advanced methods have also been developed to optimize the increase in POS over time4,40 and integrate motion and other models into land search problems.51 However, user-friendly computer software will be required for such advances to enjoy widespread use by land search planners. During the past several years, much has been done to improve how scientific search theory is applied to land search. Before 2001, much more research on the topic of search and detection had been conducted in the maritime environment than on land.

In 2001, the NSARC Research and Development Working Group convened a meeting of land search experts.34 After this meeting, several research projects sponsored by NSARC, and supported by several national and international organizations, were developed and funded. The first project produced a model for conducting detection experiments on land.37 In 2004, using the model developed, five detection experiments were conducted across the United States in five different ecoregions.1,24 The results provide tremendous insight into methods of quantifying visual detection on land. In 2004, NSARC, with funding from the Departments of Defense and Homeland Security, published a report that compared published land search procedures with the science of search theory. The full report identified several significant opportunities for improvement in multiple, long-practiced land search procedures and concepts.9 Although software is available to assist in the mathematic decisions, less-than-optimum but historically acceptable results have been achieved when a search planner applies the principles of search theory as an intuitive combination of hard science and sage experience. In the final analysis, search success is based on more than just science. At its finest, it involves the artistic application of science and a high degree of organizational and management skill, sprinkled with intuition and punctuated with a bit of luck. Lost Subject Behavior.  Modern search management is based on the use of what is called a complete “subject profile.” Such a profile identifies as much as is known about the missing subject, including general state of health, past experiences, and state of mind, through the use of a form called the Missing Person Questionnaire. This information is collected and used by search planners to predict how an individual would react in various situations. Analysis of this information from past incidents and understanding how the involved individuals behaved in given circumstances have offered great insight for search managers. It is important to note that most data on abductions, of both children and adults, have been purposefully excluded from SAR research. Although some important work has been done in this area (e.g., Brown and colleagues,3 Hanfland and associates13), the study of abductions and related criminal activity is often more about the perpetrator than the subject of the crime. This is in stark contrast to the study of lost subject behavior, for which the actions of the subject are the focus of the research. One classic land SAR reference suggests that the first rescuerelated statistics were recorded by monks in the early 18th century who, through a system of hostels, guided travelers through the mountains of Europe. This system is best known for the St Bernard dogs that helped monks locate and rescue victims of bad snow storms in the dangerous St Bernard Pass—a route through the Alps between Italy and Switzerland.38 In the many years since, retrospective analysis of historical data from previous incidents has been widely recognized as a key contributor to our understanding of preventing, preparing for, and responding to modern-day searches and rescues. In 1973, Kelley20 published an analysis of 380 incidents from the Montrose (California) Search and Rescue team. Although it included only a limited set of data, it is thought to be the first modern-day research into the behavior of lost persons. Although it is not difficult to appreciate the importance of predicting how a subject might react when lost, the scientific approach to the topic truly began with Syrotuck’s seminal paper41 in 1977. This paper was based on the premise that individuals have similar travel habits when compared with others in the same “category.” The six categories initially identified by Syrotuck included small children (1 to 6 years), children (6 to 12 years), hunters, hikers, older adults (>65 years), and “miscellaneous adults,” such as nature photographers, fruit gatherers, bird watchers, and other outdoor enthusiasts. The author also described two “special categories” (persons with intellectual disabilities and despondents) for which there were very little data. In his study, Syrotuck described the behavioral characteristics of a representative member of each category and computed “probability zones” for each, based on distances traveled. This distance was measured “as the crow flies,” or as a straight-line distance, between the point where the subject was last seen and the location where 699

CHAPTER 37  Search and Rescue

otherwise. They respond with “lights and siren” to most calls just in case the situation is serious. Unfortunately, people who report incidents are often wrong in their initial assessments, and because of this, every call must receive the same urgent response. Essentially, the situation is considered an emergency until proved otherwise. For years, searching has been considered less urgent than other emergencies. Although responders were running with lights and sirens to situations reported as “woman not feeling well” or “dumpster on fire,” reports of a missing/lost child or an overdue hiker were relegated to the “let’s wait and see” category. Through years of experience, search managers now know that a search is as much an emergency as any other call for help. Experience also indicates that an urgent response to a search situation often leads to a faster resolution with less impact on family and to the expenditure of much less effort overall. Any search situation for a lost or missing person should be considered an emergency that justifies an urgent response, high priority, thorough assessment, and immediate action.

PART 5  RESCUE AND SURVIVAL

the subject was eventually found. Realizing that there was likely a substantial difference between how far a lost subject actually traveled and the crow’s-flight distance, the author argued that “it is more important to realize that a known percentage of all lost persons are found within a one- or two-mile radius than it is to know how they got there.” Syrotuck studied 229 cases, most from wooded areas of Washington and New York States, and all involved subjects traveling on foot.41 Beyond identifying categories, Syrotuck41 also documented and described six other factors that were thought to affect the search plan. He suggested that search personnel in possession of the following information could more accurately predict the subject’s location: 1. Circumstances under which the person became lost 2. Terrain 3. Personality 4. Weather 5. Physical condition at time of loss 6. Medical problems He went on to describe how one’s general state of health, past experiences, and physical situation (e.g., hot, cold, altitude) contribute to predicting behavior patterns. How one reacts to being lost, he also suggested, can affect the type and quantity of clues (e.g., disrobing, discarding equipment), survivability (e.g., failure to build a fire), detectability (e.g., bright clothing, bad weather), and tendency to follow travel aids such as rivers, roads, and trails. What Syrotuck produced was the first relatively scientific description of how people might react to being lost and how searchers could use this information to improve operations.41 In 1980, with endorsement from the National Association for Search and Rescue (NASAR), Mitchell29 began collecting SAR case data from various regions across the United States using a standardized incident report form. The author collected and reported on 3511 cases and described a relationship between the behavior of lost subjects and the region of the country in which the incident occurred. In addition to much of what Kelley and Syrotuck reported, Mitchell also reported on how long a subject was mobile after being lost and a number of “survival factors.” Following the theme of lost person behavior and using the crow’s-flight distance, Koester and Stooksbury25 performed a retrospective study of persons who suffered from what they termed at the time dementia of Alzheimer’s type (DAT) and who became the subjects of organized SAR efforts in Virginia. They initially studied 25 cases from the Virginia Department of Emergency Services’ lost-subject database and compared the DAT patients’ behavior with that of lost older adults who possessed normal cognitive abilities. Their findings were of great interest to search managers and planners in that this was the first time research of this type had been conducted for the inland SAR community. The authors also described a “subject profile summary” and suggested specific search techniques for lost DAT patients. Notable in their findings were the facts that none of the subjects in the cases they studied yelled for help and they were usually found 0.8 km (0.5 miles) from the PLS. Since this initial research, Koester21,22 has extended his analysis of the Virginia Department of Emergency Services data. Also using the crow’s-flight distance, Hill16,17 described distances traveled and probability zones for lost persons in Nova Scotia. However, Hill found it useful to modify and add to Syrotuck’s categories of lost persons. For instance, Hill divided young people into four categories: children 1 to 3 years, children 4 to 6 years, children 7 to 12 years, and youths 13 to 15 years of age. He described characteristics for fishermen, skiers, and walkaways (e.g., people who walk away from a constant-care situation) and was the first to report characteristics for those who are despondent. A similar and ongoing study was undertaken in Great Britain in 2001 by the Mountain Rescue Council of England and Wales (now Mountain Rescue–England and Wales) using data collected from mountain rescue incidents in England, Wales, Northern Ireland, and Éire. The latest version of these data was published in 2005 and includes analyses of 708 cases.36 Taking a slightly different approach, Heth and Cornell15 published a study of 162 incidents of persons lost in wilderness areas in southwestern Alberta, Canada. They tabulated crow’s-flight 700

distance traveled and angular dispersion of travel (the angle from a line that connects the PLS with the intended destination) by different categories of wilderness users. They formed 10 categories of outdoor user (Table 37-1) and included only subjects propelled by muscle (no machinery). Interestingly, the authors found a behavioral distinction between “front country” users (i.e., “front” referring to parking lots, groomed trails, frequent signage, along with good, available maps; these areas attracted users with a large range of outdoor experience and skill) and backcountry users (i.e., remote, undeveloped areas; these areas attracted prepared and experienced users). Not unlike Syrotuck and Hill, Heth and Cornell discovered that, with the exception of despondents, there is a similar distribution of distance traveled by persons lost outdoors. However, they went further and suggested that there might be a linear relationship between certain data sets. For instance, their analysis indicated that hikers travel about 2.3 times farther than do campers, and cross-country skiers breaking trail travel about 5.4 times farther than do cross-country skiers using groomed trails. The implication is that if archival data are possessed for one category in one region and are compared with categories of lost subjects similar to those described by Heth and Cornell, a scalar parameter could be applied to extrapolate crow’s-flight distances for other subject categories. Such a possibility is exciting to search managers, who only rarely have access to relevant and reliable archival data.15 The largest and latest attempt to collect data on the behavior of lost subjects began as part of a U.S. Department of Agriculture small business grant in 2001. After years of collecting data for what he termed the International Search and Rescue Database, Koester23 published a book in 2008 that described lost person behavior data from seven countries (91% from the United States), 40 separate sources (including reports from 9 previously published papers), and 16,863 searches. The book describes 34 categories of lost subjects and their interaction with the environment in terms of ecoregions—geographic areas that characterize the effects of local influences such as climate, terrain, and vegetation.1 The specific data reported for each category include distance from the initial planning point (IPP), elevation change from the IPP, mobility hours, dispersion angle (angle established between the direction of travel and the bearing defined by the IPP and where the subject was found), find location (e.g., road, brush, woods, field), scenario causing the subject to be missing, track offset (shortest perpendicular distance from an intended track or where the subject was found), and survivability. With each category description, the author also suggests initial reflex tasking and investigative questions for search managers.23 Tables 37-2 through 37-10 show examples of tabular data from the book

TABLE 37-1  Formal Estimates of Crow’s-Flight

Distance (kilometers) between the Point Last Seen and the Point Found for Persons Lost During Different Wilderness Activities Percentile

Activity Group (N) Campers (18) Cross-country skiers: break trail (5) Cross-country skiers: groomed trail (18) Despondents (6) Hikers (38) Hunters (5) Mountain bikers (18) Scramblers (7) Walkaways (14) Other (13)

25

50

75

90

0.722 4.537 0.842

1.559 9.795 1.819

3.001 18.860 3.501

4.931 30.988 5.753

0.229 1.691 1.222 3.759 1.165 0.701 1.765

0.656 3.650 2.638 8.116 2.515 2.007 3.812

1.793 7.028 5.079 15.626 4.843 5.486 7.339

4.664 11.548 8.345 25.675 7.958 14.274 12.058

From Heth DC, Cornell EH: Characteristics of travel by persons lost in Albertan wilderness areas, J Environ Psychol 18:223, 1998. Note: Estimates for despondents and walkaways were based on a different Wakeby distribution than that used to estimate the percentiles of the other user categories.

TABLE 37-7  Hiker—Find Location (%)

Initial Planning Point (kilometers)

Temperate

N 25% 50% 75% 95%

Dry

Urban

Mountain

Flat

Mountain

Flat

568 1.1 3.1 5.8 18.3

274 0.6 1.8 3.2 9.9

221 1.6 3.2 6.5 19.3

58 1.3 2.1 6.6 13.1

8 2.6

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 184. Used with permission.

From the Initial Planning Point (feet)

% 25% 50% 75% 95%

Uphill

Down

Same

Uphill

Down

32% 182 480 1175 2634

52% 160 400 1166 2175

16%

48% 317 956 1500 3623

52% 500 975 2109 5094

Same

TABLE 37-4  Hiker—Horizontal Change from Initial

Planning Point (miles) for Mountainous Terrain Temperate

Dry

Uphill

Down

Same

Uphill

Down

Same

58 0.5 1.4 2.6 7.2

131 0.7 1.7 4.0 17.4

34 0.0 0.0 1.5 12.8

47 1.8 2.2 4.0 10.7

57 1.0 2.0 5.0 12.3

0

312 13 13 25 12 8 2 3 7 14 4

196 10 17 31 18 9 2 3 6 1 2

17 24 35 18 6 12

6

TABLE 37-8  Hiker—Scenario (%) N Avalanche Criminal Despondent Evading Investigative Lost Medical Drowning Overdue Stranded Trauma

2242

1 1 68 2 16 4 7

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

TABLE 37-9  Hiker—Survivability

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 184. Used with permission.

TABLE 37-5  Hiker—Mobility (hours)

N 25% 50% 75% 95%

Urban

Dry

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 184. Used with permission.

N 25% 50% 75% 95%

Dry

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

TABLE 37-3  Hiker—Elevation (Vertical) Change Temperate

N Structure Road Linear Drainage Water Brush Scrub Woods Field Rock

Temp

Temperate

Dry

232 0 3 6 14

112 4 8 12 26

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

Wilderness

Urban

Uninjured Injured Fatality No trace

78% 16% 6%

59% 24% 12% 6%

Survivability

Alive

n

<24 >24 >48 >72 >96

97% 76% 60% 52% 49%

2460 361 118 51 23

hr hr hr hr hr

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

TABLE 37-6  Hiker—Dispersion Angle (degrees)

N 25% 50% 75% 95%

Temperate

Dry

TABLE 37-10  Hiker—Track Offset (meters)

134 2 23 64 132

28 20 47 124 175

n 25% 50% 75% 95%

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

40 50 100 238 424

Data from Koester RJ: Lost person behavior: A search and rescue guide on where to look—for land, air and water, Charlottesville, Va, 2008, dbS Productions, p 185. Used with permission.

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TABLE 37-2  Hiker—Distance (Horizontal) from the

PART 5  RESCUE AND SURVIVAL

for the category of “Hiker.” For inland searches, the data summarized and reported by the author have been of significant value in planning searches. Search planners have used these behavioral studies and summary reports in a number of valuable ways. By direct analysis and limited extrapolation, search planners have been able to find answers to important planning questions that are helpful in determining where and how to search. Such efforts have also taught search managers the importance of collecting behavioral data on lost persons and the predictive value of such data.

ACCESS PHASE After the subject is located, the search is over. Rescuers must now gain access to the subject to assess and treat injuries, evaluate the situation, and mitigate the problem. Accomplishing these objectives may be as simple as walking up a trail to reach the subject or as complex as reaching a climber on the face of El Capitan in Yosemite National Park. Regardless, planning for this eventuality should be complete and ready to be carried out at the conclusion of the locate phase. Once rescuers reach a subject, the situation and scene must be assessed. In emergency services terminology, this is called the size-up. The size-up consists of identifying hazards to the subject and rescuers, then developing a strategy to deal with the problems. For instance, a subject might be trapped by a winter storm in a high alpine environment. Safety considerations for rescuers entering such a hostile and dangerous environment would certainly influence further actions and may well take precedence over the entire rescue effort. Specialized skills may be required for rescuers to safely gain access to the scene. For instance, rescuers may need to rappel to a patient who has fallen onto a ledge in the Grand Canyon, or they may need to climb sheer rock faces to reach an injured mountaineer on Half Dome in Yosemite National Park. These are examples of how complex the access phase of a rescue may be and point to the importance of thorough and proper planning. If the size-up indicates that the situation or environment is so hazardous that remaining on scene poses an immediate threat to the subject, accelerated rescue techniques may be required. Accelerated rescue techniques are immediate actions required to remove a subject from a dangerous environment without stabilization. They often entail deviations from local standard operating procedures and protocols. Examples of such situations include poisonous gas environments (e.g., in caves), fires, unstable terrain (such as avalanches and rock slides), adverse weather (hurricanes, thunderstorms, severe snowstorms), or any hostile environment that threatens the subject, rescuers, or both.

transportation to a definitive care facility. If medical care is not required, confirming this fact may be all that is necessary at this stage before moving into the transport phase. Emotional stabilization is necessary because an anxious victim is a hazard to rescuers and himself or herself. Again, the goal is to best protect both the rescuers and the victim. Simple, calm communication with the patient, slowly describing what happened and what rescuers are doing, is often enough to calm a nervous subject. Stabilization, like assessment, should continue throughout the transport phase. The overall objective is to prepare the victim for transport to definitive care while maintaining his or her comfort and safety.

TRANSPORT PHASE In the fourth phase of SAR, the subject is moved to definitive care. For this to occur, the stabilized subject must be “packaged” so that he or she can be moved safely and efficiently while stabilization and assessment continue. Transportation will range from foot travel, with the subject walking on his or her own, to evacuation by aircraft. If helicopter extraction is going to be used, the injured person must be briefed thoroughly on what to expect. This should include everything from the effects of the “rotor wash” to movement and noise. The appropriate mode of transportation can be determined by weather, type and severity of injuries, overall urgency, terrain, and available resources, to name just a few. Chapter 39 addresses the numerous considerations that exist when a patient will be packaged and transported from an isolated wilderness area to definitive care.

STABILIZATION PHASE

Rescue Equipment Today’s rescues occur in many remote and unusual environments and often require extremely technical rescue equipment and skills. Responders trained in the appropriate techniques and technologies should be the only personnel to apply them. Much of the gear and many of the techniques have been derived from those first developed by mountaineers, climbers, cavers, and, more recently, white-water enthusiasts. Rescue equipment is generally broken down into three broad categories: personal gear, rescue software, and rescue hardware. Personal equipment includes such items as footwear, gloves, helmets, articles of clothing, eye protection, and other protective apparel. Software is equipment such as rope, webbing, slings, and harnesses that are made of soft, strong synthetic materials specifically designed and manufactured for rescue. Hardware includes equipment such as carabiners, cams, friction devices, pulleys, and litters made of steel and alloys specifically designed and manufactured to endure the rigors of rescue.

The stabilization phase has three primary components: physical, medical, and emotional. Once rescuers have access to the subject, the scene must be quickly evaluated, or sized up, for immediate physical hazards and threats from the environment. Scene safety is an initial priority in the size-up, and risks to everyone must be weighed against the benefits to be gained. An example of physical stabilization would include an occupied automobile teetering on the edge of a cliff. Before the occupant can be medically assessed, the situation (i.e., the automobile) must be stabilized to best protect the rescuers and the patient. Other examples of physical stabilization might include protecting the patient from further injury (i.e., removing him or her from the hazardous environment or applying a helmet) or removing the hazard (i.e., extinguishing the fire, securing the teetering auto). Once the physical environment is stabilized and free from immediate hazards, medical management and stabilization can begin. This process usually follows accepted procedures, starting with primary and secondary physical examinations and progressing through basic and advanced life support. The process should include full-body immobilization, usually in a litter; specific site immobilization of fractures and related injuries; treatment of shock and other hemodynamic compromise; and without exception, some type of protection from the environment. The goal of medical stabilization is usually to prepare the subject for

Personal Equipment.  Rescuers must often wear special equipment to protect them from accidents and hazards. Head, eye, and hand protection is considered mandatory in virtually all rescue environments. Additional personal equipment requirements are dictated by the rescue environment and the specific needs of the situation (Figure 37-5). Special Gear.  In addition to the usual challenges of the rescue environment, certain hazards require specialized equipment. Examples of such equipment include fire-resistant clothing worn by structural and wildland firefighters, personal flotation devices (PFDs) used by rescuers in and around water (Figure 37-6), netting used in outdoor settings when insects become a problem, bulletproof garments used by law-enforcement and military rescue personnel, and chemical protective suits worn when exposure to hazardous materials is possible. No clothing or protective gear meets all of the requirements for involvement in or around a rescue scene. Rescuers study situations so that they understand all hazards before anyone becomes involved. Their conclusions help them identify protective equipment requirements. Gear that may be necessary for one environment can be dangerous in another. A firefighter’s turnout gear may be required in a structure fire but can be deadly in a river rescue situation. Every rescuer is responsible for understanding the rescue environment and how best to prepare for it.

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FIGURE 37-5  Even though the personal equipment necessary is dictated by both the rescue environment and the needs of the specific situation, it usually includes head, hand, foot, and eye protection at a minimum.

Software  Rope.  Rope is by far the most versatile piece of rescue equipment and serves as the universal link in most rescue environments. The material from which the rope is made (e.g., nylon, polyester, polyolefin) and the design (laid, kernmantle, flat) are important in the consideration of the use for which a rope is intended. In most rescue environments, nylon is preferred because of its overall strength, resistance to abrasion, and ability to stretch and absorb energy. Natural fiber ropes such as hemp are no longer considered for use in rescue; synthetic materials are far better. Although design and amount of materials used influence strength, new 13-mm (0.5-inch) diameter nylon rescue rope usually has a tensile strength in excess of 40 kN (9000 lb) (Figure 37-7). The most common design of rescue rope is kernmantle, a term derived from German, meaning “core in sheath.” With this design, a core of material (often parallel fibers) is surrounded by a braided sheath. The sheath protects the inner core, which supplies much of the strength of the overall rope. Other designs, such as laid (twisted) and braided, are also used in rescue rope. Kernmantle rope is either dynamic or static. Dynamic kernmantle stretches more than 4% of its length to absorb the impact of a fall and is used primarily in lead climbing. Static kernmantle stretches less (no more than 4% of its length); it is used in rescues in which a great deal of stretch would be a nuisance or even dangerous. Because of the importance of rope in the rescue chain, frequent inspection, care, and maintenance are important. Rope used in rescue is kept clean, inspected often, and protected from sharp edges, high temperatures, sunlight, chemicals, and abrasion. In addition, a detailed history of rescue ropes is kept so

FIGURE 37-6  Rescuer wearing a personal flotation device and helmet often used for rescue in and around moving water.

FIGURE 37-7  Example of 13-mm (0.5-inch), nylon, static, kernmantle rope of the type commonly used in rescue. Rescue rope should be checked over its entire length for damage before use.

that an educated decision can eventually be made regarding each rope’s removal from rescue service. Webbing.  Flat rope or webbing is another common link in rescue systems. It comes in two common configurations: flat and tubular. Tubular webbing is manufactured as a tube in such a way as to seem flat when in use. In cross section, however, it is obviously tubular and a bit less stiff than true flat webbing. Tubular webbing that is 2.5 cm (1 inch) in diameter can be used in rescues to tie anchor slings and harnesses. It has a tensile strength of about 17.8 kN (4000 lb) when new. Flat webbing is flat in cross section. Its strength is directly proportional to the amount of material used in its manufacture. Automobile seat belts are an example of the material used in rescue harnesses and anchor slings, and where strong, flat software is beneficial (Figure 37-8). Harnesses.  Harnesses come in many sizes and shapes; they are used to attach something (usually a rope) to a person’s body. They may be “full body,” encompassing the thorax and the pelvis (Figure 37-9); “seat,” encompassing only the pelvis; or “chest,” encompassing only the thorax. Each type of harness has its use and associated advantages and disadvantages. Classically, the most common harness for climbing has been the seat harness. However, rescue practitioners have been trying to standardize the full-body harness for rescuer use, with the separate seat and chest harnesses having only limited special use by trained individuals. Webbing can be tied into a large loop (runner) and applied to a person in such a way as to serve as an improvised harness. Although this is not a preferred method of attachment to a rope, it can work if other harnesses are not available. Hardware  Carabiners.  Carabiners are large, safety-pin type of mechanisms used to connect various elements of a rescue system, such as a rope and anchor. They are occasionally called “biners,” “snap links,” or “crabs” and consist of a spring-loaded gate that pivots open, a spine that supports most of the load and lies opposite the gate, a latch, and depending on the specific style, a locking mechanism. Carabiners are most commonly made from either steel or aluminum. Size for size, steel is stronger and heavier, but aluminum is lighter and stronger pound for pound. In rescue, steel is almost always preferred unless weight is a factor, as it is in remote alpine situations. Common shapes of carabiners include oval, D, offset D, pear, and large offset D. The design best suited for any situation is dictated by the specific use. No matter what the shape, carabiners used in rescue usually have a mechanism for locking the gate closed so that opening it takes a specific effort—usually twisting 703

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FIGURE 37-8  A, Tubular webbing with cross section visible. B, Flat webbing used in anchor sling.

A

B

or unscrewing. This design feature not only improves the strength of the device when locked but also reduces the chances that a carabiner will open accidentally at an unexpected time (Figures 37-10 and 37-11). Aluminum, nonlocking, oval-shaped carabiners (see Figure 37-11, B) are common in sport climbing and mountaineering but are generally not recommended for use in rescue situations because of their lack of a locking mechanism and relative weakness when the gate is opened. When available in rescue situations, locking carabiners are usually preferred. When a locking carabiner is not available, two reversed and opposed oval, nonlocking carabiners are sometimes used in its place. One can confirm that the two nonlocking carabiners are configured safely (reversed and opposed) when the open gates form an X (see Figure 37-11, C ). Descending (Friction) Devices.  Many different descending devices exist today, but they all do primarily the same thing: apply friction to the rope to allow controlled lowering of a person or load. The most common descending devices in rescue are the figure-8 plate and the brake bar rack. The figure-8 plate gets the name from its general shape. It has two rings of different sizes. The larger ring produces friction on the rope, whereas the smaller ring is used primarily as an attachment for the load (e.g., the rescuer during rappel). Friction

FIGURE 37-9  An example of a full-body harness. Shown is a CMC ProSeries Harness Combo. Note that this harness encompasses both the pelvis and the thorax. (Copyright CMC Rescue.)

704

is produced by passing a bight of rope through the large ring and around the small ring, then attaching the small ring to either an anchor (for a lowering system) or a rescuer’s harness (for a rappel or abseil) with a locking carabiner (Figure 37-12). The brake bar rack, or simply “the rack,” uses either steel or aluminum bars on a steel rack to produce friction on a rope. When the rope is threaded alternately around the bars and the load or rescuer is attached to the “eye” in the rack, friction is applied. The number of bars applied to the rope and the distance between them can be varied to change the friction. This variable friction allows versatility not available with the figure-8 plate; however, the rack takes a bit more training to use safely (Figures 37-13 and 37-14).

FIGURE 37-10  Various types of carabiners. Top to bottom: (1) RSI Big Hook, steel, screw-locking hinged gate; (2) alloy, offset D, screwlocking hinged gate; (3) RSI Twist Link, steel, screw-locking hinged gate; (4) SMC extra-large, rescue, steel, screw-locking hinged gate;  (5) tri-link, steel, triangular, screw lock; (6) auto-lock, swivel-mount, steel, quarter-twist locking hinged gate (National Fire Protection Association 1983 certified). Note that locking carabiners should always be locked when in use.

A

FIGURE 37-12  Example of figure-8 plate descending device (with “ears”) commonly used in rescue. Shown is a CMC Rescue 8 With Ears; aluminum (left) and steel (right). (Copyright CMC Rescue.)

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B

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CHAPTER 37  Search and Rescue

FIGURE 37-11  A, Close-up view of CMC Rescue aluminum carabiner. Note the locking gate and offset D shape.  B, Close-up view of an oval, nonlocking, aluminum carabiner often used in climbing. This type of carabiner is usually not recommended for rescue applications but is common in climbing due to its light weight and ease of use.  C, Although not generally recommended for rescue applications, two nonlocking carabiners with their gates reversed and opposed—visually confirmed when opening the gates makes an X—are sometimes used when locking carabiners are not available. (A copyright CMC Rescue.)

C

Ascenders.  Ascenders are devices that grip or hold the rope. They have been adapted from climbing and caving equipment, with which they are used to ascend or climb a fixed rope. In rescue, they are used to climb fixed lines when necessary, but they can also be used in hauling systems to grip the rope. In this way, they hold fast when the rope is pulled in one direction and allow the rope to slide easily when it is pulled in the other direction (Figures 37-15 and 37-16). When ascenders are used to climb a rope, one is fixed to the rope and supports the load while the other is moved into position ahead. When this action is alternately repeated, a skilled climber can move up a rope with relative speed and ease. Select rope hitches (e.g., a Prusik hitch) can be used in lieu of an ascender (see Figure 37-15, D). Pulleys.  Pulleys are simple machines that apply a turning wheel to reduce friction on a rope as it rounds a turn. In rescue, these metal devices serve primarily to change the direction of a rope, such as within a mechanical advantage system. The “sheave” is the wheel or pulley, and there may be more than one. The “side plate” or “cheek” is the side of the device that makes contact with the anchor at the “hook,” which is usually the weakest part. The axle or “sheave pin” is what the wheel turns on; it is supported by the side plates. In rescue pulleys, the side plates are movable so that the pulley can be attached to a rope anywhere along its length (Figure 37-17).

C

FIGURE 37-13  A, RSI Rigging Rescue Rack brake bar rack in use. B, SMC National Fire Protection Association brake bar rack with welded eye twisted 90 degrees; configured for use. The top bar has been modified to allow for a secure tie-off. C, Brake bar rack tied off. When the bars are pulled tightly together, the excessive friction prevents movement on the rope.

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forced to choose between wooden backboards, old military stretchers, the wire Navy Stokes basket, or the “scoop” stretcher. Today, strong, lightweight synthetic materials and inventive designs have improved the strength, weight, durability, and comfort of litters. The goals have not changed during evolution of the perfect wilderness transportation device. Rescuers still want a device that is comfortable for a person in pain, serves well as a platform for assessment and medical care during transport, allows for fullbody immobilization, and provides complete security and protection of the occupant from the rescue environment. See Chapter 39 for additional information regarding specific litters, packaging, handling, and evacuation techniques.

Anatomy of a Search and Rescue Incident

FIGURE 37-14  SMC National Fire Protection Association brake bar rack. Straight frame shown; frame also available with eye twisted 90 degrees. The top bar has been modified to allow for a secure tie-off. (Copyright CMC Rescue.)

The larger the diameter of the pulley, the more efficient the device. That is, the bigger the pulley, the more friction (theoretically) is reduced. A rule of thumb often used by rescuers is that a pulley with the largest diameter possible should be used, but never less than four times the diameter of the rope. Therefore, because 13-mm (0.5-inch) rope is commonly used in rescue, a pulley diameter of at least 52 mm (2 inches) should be used. A variation of the pulley is the edge roller. This device uses 10.2- to 15.2-cm (4- to 6-inch) open-face pulleys to reduce both the friction of a rope passing over an edge and any damage to the rope by protecting it from excess abrasion. Single units can protect the rope from 90-degree angles, and multiple units tied together can provide protection for complex projections. Litters.  Litters or stretchers are the conveyances in which victims are transported when they cannot travel under their own power. New high-technology materials and designs have greatly improved the choices available. In past years, rescuers were

A

B

To summarize how all of the previously discussed information fits together, it is convenient to dissect a SAR incident into its component parts and then analyze how all of the parts fit together (Figure 37-18). From the SAR operative’s perspective, an actual callout is merely an interruption of planning for an incident. That is, people involved in SAR are constantly in a state of readiness and are prepared to respond. When a situation occurs, this constant planning stage is suddenly interrupted by the report of an incident. The individual taking the information is charged with conveying it to the appropriate authority. The authority determines the urgency, continues the investigation process, begins to develop an operational strategy, and generates an incident action plan. At the same time, those in charge begin to muster appropriate resources to carry out the action plan. In SAR, this is termed resource callout, or just callout. Once notified of an incident, individual resources are gathered at a collection point and signed in. The sign-in process enhances safety and allows tracking of the types and quantity of resources that are available on scene. Once signed in, resources are given assignments designed to meet the goals of the action plan within a specific operational time frame. This physical implementation of the incident action plan is referred to as tactics. Deployment of resources to the field continues until there is reason to suspend this phase of the operation. If the subject is found, the search is suspended, and the access phase can commence. Once rescuers have access to the subject, the focus turns

C

D

FIGURE 37-15  A, Gibbs ascender applied to rope. When assembled and attached to the rope, and the eye of the cam is pulled, the cam squeezes the rope and holds fast. When the cam is released, the device can be moved along the rope. B, Gibbs ascender dismantled with shell around rope. Note cam (lower left) and pin (upper right). C, Clog-handled ascender. Although used where climbing a fixed rope is required, handled ascenders are rarely used in rescue. D, A three-wrap Prusik hitch can sometimes be used in lieu of a mechanical ascender.

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Search and Rescue Environments Within the Wilderness Setting

FIGURE 37-16  Alternate type of cam ascender specifically designed for rescue. Shown is a Petzl Rescucender for use with 11- or 13-mm (0.45 or 0.5-inch) rope. (Copyright CMC Rescue.)

to stabilization and transportation. If at any point the operation cannot be continued (e.g., the subject was never found, access cannot be gained, transportation is impossible), suspension and demobilization may occur without completion of the entire cycle. The decision to discontinue active search efforts is difficult and involves complex management issues, almost always of the “no-win” variety. When a situation is resolved, mission suspension and demobilization begin. In larger incidents, this may involve structured deactivation of multiple resources, pulling teams out of the field, dismantling facilities, completing documentation, and returning resources to service. Basically everyone finishes what he or she was doing at this incident and gets ready to do it again. All of this takes planning and preparation and should be addressed in the overall preplan long before it is required.

SAR teams throughout the world are frequently called on to solve complex problems in a wide spectrum of environments. Even within the environments addressed in this text, widely diversified subenvironments exist that present unique sets of problems and hazards to SAR personnel. When confronted with the numerous and dangerous environmental conditions found in the wilderness setting, SAR personnel must be prepared to work where others have been unable to cope. An old military motto becomes the SAR credo: “Adapt, improvise, overcome.” It is beyond the scope of this text to discuss in detail how SAR personnel adapt to each of these environments, but it is important to note that adaptation and improvisation are required in nearly all wilderness situations. The particular improvisation depends on the situation, as well as the skill and experience of the individuals involved. Regardless of the type of rescue environment encountered by rescuers, the following general rules should be followed: 1. Use technical personnel for technical rescue. 2. If a missing person is found dead, evacuate only when there is no risk to team members or at least when the hazard has been assessed and the risk justified. 3. Stabilize any injured person before evacuating, and continue stabilization during transport. 4. Find and use the easiest route for evacuation. 5. If a carry-out is required, appoint someone to serve as route finder who has a radio and markers to report potential hazards and problems. 6. Litter teams of six to eight persons per team should be used, with three teams minimum. Normally, there should be no more than 20 minutes per shift. Additional personnel may also be required to carry equipment. 7. Use accepted procedures to care for and protect the victim.

FIGURE 37-17  Two types of pulleys commonly used for rescue. A, Five-centimeter (2-inch) double pulley. B, Fivecentimeter (2-inch) “Prusik-minding.” Note that rescue pulleys are applied to rope by removing the carabiner and swiveling the side plate to allow introduction of the rope.

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After every incident, participants realize that if they had to do it all over again, they would do some things differently. If these thoughts and ideas are not documented, they can be lost, and future responses may be cursed to repeat past mistakes. This is one reason why every incident should contain some type of evaluation of the entire mission, known as the postincident critique. The critique can be formal, involving every participant at a sit-down meeting, or informal, involving just a brief discussion of recent events. The critique documents lessons learned and should provide a basis for revising the preplan. Thus the cycle continues, and lessons learned from one mission influence the next.

PART 5  RESCUE AND SURVIVAL

Incident

Mission suspension

Resource callout

*

First notice of incident

Mission critique

Debriefing

Check-in

Assignment

Briefing

Check-out

Return to service

Preparedness and training FIGURE 37-18  Time progression or the “anatomy” of a search from a searcher’s (operational) perspective. The process is actually a continuous cycle that pauses in the planning and preparation phase until an incident occurs.

8. A radio carrier brings up the rear. 9. If using a helicopter for evacuation, ensure the following: a. The patient is thoroughly briefed. b. The patient is protected. c. Someone goes with the patient who knows what has been done medically. In some cases, because of agency or military service protocols, assisting medical personnel will not be allowed to go with the patient. In these cases, it is imperative that a written log specifying assessment and treatment up to that point accompany the patient.

SPECIAL ENVIRONMENTS IN SEARCH AND RESCUE Specialized SAR environments produce diverse problems and potential complications. Each environment presents its own obstacles to increase the complexity and difficulty of particular rescues. Technical Rock Mountaineering, rock climbing, and casual scrambling have created a need for specialized SAR expertise. Individuals and groups involved in rock rescue have refined and developed techniques for most situations. The hallmark of a technical rock rescuer is the ability to improvise and modify tools or techniques to meet any crisis. He or she must be comfortable using climbing gear and being exposed to heights. Once an individual is located in a rock environment and the situation is surveyed, access to the site is the next step. Often local groups familiar with well-known areas will have already solved this problem. The solution will involve either climbing up or dropping down to the victim. Because any accident during a rescue is almost always catastrophic, safety for all persons involved is of paramount importance. Ascent up rock always requires knowledge of rock-climbing techniques, proper equipment, and familiarity with its designed use and limitations. Local outing clubs or mountaineering stores can be contacted for more detailed assistance. Specialized technical rock rescue teams, such as those sanctioned by the Mountain Rescue Association, routinely practice climbing techniques and solving vertical rescue problems. Caves and Mines (See Chapter 46) Standard obstacles in this environment include poor communications, extreme darkness, difficulty in lighting, small and wet spaces, and often the issue of questionable atmosphere. The various environments included here are collectively termed confined spaces. The levels of moisture in water-containing, or “live,” caves can vary over a considerable range. Some are merely muddy; others have flowing rivers. Caves in the western United States are 708

generally drier than eastern caves; however, humidity, wetness, and cold temperatures create potential for hypothermia in both areas. This is a fact that is greatly underestimated. Flooding can be a lethal problem, and many cavers have died because of inattention to the weather on the outside. During heavy rains, the caves become natural drains for streams. Wind and temperature are other underestimated problems associated with cave and mine emergencies. It is not unusual for strong winds to develop along subterranean passages, which intensifies convective air chilling. Confined passages, low crawls, and squeezes pose unique problems for the rescue of injured cavers. The use of standard items, such as litters, backboards, and splints, may be impossible in such places. Confined passages with varying, or even toxic, constituent gases can lead to difficulties for victims and rescuers alike. Occasionally a self-contained breathing apparatus or surface-supplied air is required. The potential for toxic gases justifies extensive atmospheric monitoring while operating in the underground environment. An essential part of any cave or mine rescue operation is thorough orientation to the hazards associated with a particular underground area. This involves pinpointing the locations of pits, waterfalls, siphons, canyons, and other difficult formations that may pose problems in extrication, search, or safety. Many caves have been mapped by the National Speleological Society and the National Park Service. The real difficulties may begin only after a victim is located. The goal is to move the person rapidly, safely, and comfortably to the surface. Without practice underground, that task will be virtually impossible. Neoprene exposure bags similar to body bags have been used for this purpose and can keep an injured person dry and protected during what may be a very long and slow evacuation. Medical care procedures must be performed under dark, cold, and muddy conditions. Experienced cave rescuers agree that repackaging supplies and equipment for underground use is essential. Streamlining kits, packs, and containers is imperative for unobstructed passage through tight spaces in cold, damp conditions. Team members must carry very specialized equipment, often including a minimum of 24 hours of light in a helmet-mounted lamp; two additional sources of light, with spare bulbs and batteries; and waterproof matches and candles. Depending on the situation, other equipment is also required. This is discussed in Chapter 46. Essential caving skills include all of the capabilities for rock climbing, including vertical rope technique, ascending, rappeling, belaying, and being comfortable working at the end of a rope. All these skills must be practiced until they can be done in the cold and wet without the benefit of light. Team practices are conducted both on the surface and underground, with participants being forced to work in mud, suffocatingly tight squeezes, soaking waterfalls, and complete darkness. This may be a difficult evolution for even the most experienced rescuer to endure, but just another “hang in the hole” for a seasoned caver.

Like river white water, ocean surf can present some very different problems in rescue because there is no “average” beach. There are recurring rescue situations that pose unique problems in the white-water surf environment. Along with the potential for immersion hypothermia, lacerations and contusions can result from being dashed against barnacle-encrusted rocks in the wild and unpredictable ocean surf. Contact with venomous sea life is always a possibility. However, the greatest threat to ocean beach users is the action of the water itself and the possibility of drowning through inattention or unfamiliarity with ocean surf hazards in the forms of runouts, undertows, and rips.

FIGURE 37-19  Common personal river rescue equipment. In the CMC Water Rescue Package shown (clockwise from upper left) is a gear bag, type III/IV personal flotation device, emergency strobe light, glow-inthe-dark Fox 40 whistle, McNett Saturna knife, NRS neoprene paddler’s gloves, Cascade Swiftwater helmet, and a CMC SRT Rescue EZ-Stuff Throwline bag. (Copyright CMC Rescue.)

White-Water River There are dozens of potentially dangerous problems in the river SAR (white-water) situation (see Chapter 45). Log and debris piles at various bends in the river can function as “strainers” for the recreational victim, but they may be death traps for the would-be rescuer. The banks of the stream may be deeply undercut, with treacherous overhanging debris and snags that can catch on clothing, equipment, and skin. Combined with muddy and rapidly rising water, these factors render river rescue difficult and very unpredictable. In fast-moving water, the single greatest problem is that responders underestimate the power and threat of moving water. Foolhardy heroics and excessive enthusiasm frequently lead to further tragedy. Cold-water immersion, coupled with wind and cold temperatures, predisposes everyone to hypothermia. Wet clothing, darkness, and injury add to the insult. The noise of moving water may obviate clear communications and result in poor contact between the victim and rescuers. These same factors could also affect communications between rescuers and lead to additional confusion and danger. All potential responders in this environment must be properly equipped (Figure 37-19) and know how to read the water for capsize points and other dangerous phenomena. The hydraulics of low-head dams, collapsed bridges, and other submerged structures can produce a drowning machine for unsuspecting individuals. Rescue team members must know how to protect themselves in fast-moving water at all times. Mandatory in this environment are good judgment, strong swimming ability, knowledge of all types of technical systems, equipment used in climbing, and a thorough understanding of river dynamics and hydraulic influences.

Runout.  A runout occurs when an offshore sandbar or ledge is built up over a long period. Millions of tons of water flow over the bar during daily tidal changes. Eventually the water may equal or exceed the level outside the bar. Any weak spot in the bar usually gives way, causing a funnel effect (Figure 37-20). Water rushes toward the bar at a terrific rate, sweeping everything with it. This common phenomenon can be easily spotted from the beach. Usually 14 to 46 m (15 to 50 yards) wide, it is characterized by choppy, jumbled-up, little waves. The water often has a dirty, foamy, or debris-laden surface moving seaward. If a bar is visible offshore, definite breaks can be seen where the water pours through. Surfers often seek runout currents for fast transportation out beyond shoreline waves. Swimmers caught in a runout have two options. They may swim parallel to the shoreline out of the strip of current, or if the bar is visible (usually characterized by breaking waves), they may relax and let the current complete its runout. About 23 m (25 yards) beyond the bar, the current dissipates. This is an offshore phenomenon—current force increases near the bar but is often negligible near shore. Rip.  A far worse problem close to the beach is a rip, which can knock children and even adults off their feet and carry them to deep water in seconds. Rips are caused by a slight depression on the beach where wave water rushes after breaking on shore. Water rushing to the depression soon becomes an irresistible seaward flow (Figure 37-21). It may be as narrow as 14 m (15 yards) at its source and usually does not travel as far as a runout. Rips generally dissipate a few yards beyond the breakers. A rip looks like a runout, with a streak of turbulent discolored water or a line of foam leading directly out from shore. A swimmer has the same options as in a runout, either to swim parallel to the beach or to relax and ride the current until it ebbs. A person who swims straight toward the beach will never make it. A beach with several rips moving up and down in unpredictable patterns is very dangerous. An unwary swimmer could panic and drown. Undertow.  On narrow, steep beaches, a type of current known as undertow can be found. It is caused by gravity acting on water thrown up on the beach by wave action. Water retreating back down the steep shore continues under oncoming waves (Figure 37-22). Undertow is usually of very short duration and is ended by the next breaking wave. Wading near shore on a steep beach, an individual could be pulled under in this current and find himself or herself quickly in deep water. If the person resists the

FIGURE 37-20  Runout. A, This phenomenon begins with an offshore sandbar. As waves roll in, the water level builds up behind the bar until a section gives way. B, As the sandbar “dam” gives way, the water develops a very rapid current running seaward. The recommended action is to swim across the current until out of the pull.

A

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White-Water Surf

FIGURE 37-21  Rip. A depression in the beach floor concentrates returning water into a strong current. To escape, a person should ride with the current or swim to the side and out of the pull.

current, the next wave may break directly on the person’s back. In some circumstances, this could cause traumatic injury, especially to the neck and back. A person caught in an undertow should let the current pull until it ceases, then swim to the surface and ride the next wave into shore. Cold, Snow, and Ice Perhaps no other type of SAR environment requires a more broadly based foundation of personal and team skills than do winter snow and ice. These skills include downhill and crosscountry skiing, snowshoeing, technical climbing, winter survival, and a good understanding of snow and ice physics. Unlike rock, snow and ice conditions change on a daily and even minute-tominute basis. The effects of gravity, wind, temperature, slope, heat exchange, load factors, and avalanche continually impose problems for missions under these conditions. Technical and nontechnical SAR problems in snow and ice environments take longer to address and are more taxing, technical, and complex. Combined with shorter days, extremes of weather, and the everpresent threat of hypothermia and localized cold injuries, technical missions of this type are unacceptable for all but the most

FIGURE 37-22  Undertow. This hazard develops on a steep beach where the water returns rapidly seaward after being tossed up by the wave action. A person should never fight this action but should relax and rise to the surface, then ride to shore on the next wave.

experienced SAR personnel. Several chapters in this book address very important issues related to this type of environment: thermoregulation (Chapter 4), accidental hypothermia (Chapter 5), immersion in cold water (Chapter 6), frostbite (Chapter 8), and polar medicine (Chapter 9). Versatility and improvisation are essential components of the overall strategy that must be used in snow and ice. Transportation of the victim is often one of the most difficult problems, but it can usually be resolved through detailed preplanning. Innovations such as covering a litter with a canvas cover or improvising an attachment to cross-country skis are clever solutions to common winter problems. Commercial products, such as the Sked litter (see Chapter 39), have streamlined the laborious task of transporting injured people through snow and ice.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 38 

Technical Rescue, Self-Rescue, and Evacuation  KEN ZAFREN, LOUI H. MCCURLEY, CHARLEY SHIMANSKI, AND WILL SMITH

ACCIDENT ON MT KENYA—1970 On September 5, 1970, two young but experienced Austrian climbers, Gert Judmaier and Oswald Oelz, who were both medical doctors, climbed Mt Kenya (5199 m [17,057 feet]). which is the second highest mountain in Africa. After 6 hours of enjoyable climbing on firm granite, they were enveloped in fog. With some difficulty, they managed to find Shipton’s Notch, which is the key to the last part of the summit ridge. It was snowing when they reached the summit, and snow squalls increased as they descended back to Shipton’s Notch. Gert held onto a boulder while looking at the descent route as his partner, Oswald, prepared a rappel anchor. All of a sudden, the boulder and Gert both fell down the rock face. Oswald was able to catch the unwinding rope in his hands, although he lost skin from his fingers and palms; Gert’s fall was broken momentarily by a rock rib, and he was then able to wrap the rope around his left arm and elbow to stop the fall. 710

When Oswald climbed down, he found that Gert was bleeding profusely from an open tibia fracture. Oswald made a binding to control the bleeding. There seemed to be little or no hope of evacuating the injured climber down the long and complex descent route. It seemed certain that Gert would die from hemorrhagic shock, hypothermia, or fat embolism, but, as long as Gert was alive, Oswald was determined to do what he could. He packed Gert in extra clothes and put him in a bivouac sack, which he anchored to the wall by two pitons. He then left Gert with all of their provisions: a deciliter of whiskey and a box of stewed plums. After a harrowing descent in a snowstorm, Oswald reached the Kalmi Hut, where eight British and American climbers were waiting for favorable weather to attempt the climb. Some of the group descended that night to a lower hut, where they found a radio and medicines. The next day, Oswald and one of the other climbers tried to ascend to his injured partner. The snowfall became heavier.

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the nearest road. They reached the hospital in Nairobi that evening. The surgeon cleaned the wound, and, contrary to expectations, did not perform an amputation. Oswald was proclaimed a hero in Kenya. Gert underwent a series of operations over more than one year. Both Gert Judmaier and Oswald Oelz went on to distinguished medical careers. Twenty years later, they climbed Mt Kenya again, along with some of the rescuers. At the spot of the fall, they thought about the young helicopter pilot, and they fastened a bronze plaque to the rock with the following inscription: “In memoriam, Captain Jim Hastings who lost his life in saving mine. Gert Judmaier 1970-1990.” Adapted with permission from Mit Eispickel and Stethoskop (With Ice Axe and Stethoscope) by Oelz O: Mit eispickel und stethoskop, Zürich, 1999, AS Verlag.

Activities in wild and remote areas can bring great rewards, but they also carry risks of illness, injury, and death. In the wilderness, resources for treating illnesses and injuries are limited. The best plan is to decrease the likelihood of medical problems by taking steps to decrease risks. For example, it is best to ascend slowly to decrease the risk of altitude illness. It is also wise to know how to recognize altitude illness and to know when and how to descend to a lower altitude. In practice, the terms rescue and evacuation have considerable overlap. The processes of rescue or evacuation may include the additional provision of medical care. This chapter is primarily about mountain rescue, but the principles are applicable to rescue in general. The best plan for a rescue in the mountains is to not need one. If someone is stranded, ill, or injured in the mountains, the next best option is self-rescue or rescue by one’s own party. If these plans fail, help from outside resources and agencies will be necessary. The most basic form of rescue is self-rescue that is performed by the patient or by his or her companions. Organized rescue by outside agencies originally evolved from self-rescue. Organized rescue can often offer the use of specialized resources and equipment to accomplish a rescue. This chapter focuses specifically on self-rescue and on the problems of rescue and evacuation in specific situations, especially technical climbing and mountaineering. Medical care in technical settings is not just emergency medical services being provided on a mountain,47,63 nor is it the same as combat casualty care; however, there are similarities to both. Care is usually delayed as compared with most prehospital settings. There is more blunt and less penetrating trauma than in combat casualty care.26 Victims with serious airway problems or severe bleeding are likely to be dead by the time that medical care arrives, although immediately life-threatening bleeding is less likely from blunt trauma than from penetrating trauma. It is challenging to provide medical care in technical environments. In addition to the limitations of wilderness medicine (i.e., the art of the possible), there are dangers for both the rescuer and the patient. Medical providers who plan to work in technical terrain should have adequate skills to ensure that they can function safely under the conditions that they expect to encounter. These skills should be learned by proper instruction and training before traveling in technical terrain and providing medical care in wilderness and remote areas.

Definitions TECHNICAL TERRAIN Technical terrain is terrain in which travel is difficult or dangerous and that may require the use of special equipment (e.g., ropes) for safe travel. Examples include mountainous terrain with cliffs or very steep slopes (i.e., rock, snow, or ice) and glaciers. Operations in technical terrain include mountaineering and climbing, glacier travel, canyoneering (usually called canyoning outside of North America), and caving. 711

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

The other climber had increasing symptoms of acute mountain sickness. They had to turn around, and they reached the hut again after dark. Oswald felt terrible that his friend would now die alone if he wasn’t in fact already dead. Four climbers from the Kenya Mountain Club had arrived with medicines and rescue equipment, but they were also suffering from acute mountain sickness. They had previously discussed the possibility of rescuing someone with a serious injury from Mt Kenya, and they had concluded that it would be impossible; however, they still wanted to try. The following day, Oswald and one of the rescuers reached Gert, 48 hours after Oswald had left him. At first there was no answer when they called, but then Gert pushed the bivouac sack to one side and said, “My God, you’re still alive.” Oswald called into the radio that Gert was alive, but he received no answer. However, more rescuers had arrived and heard the message. Oswald gave Gert an injection of morphine. Gert drank a little and immediately threw up. All three men spent a cold and uncomfortable night on the rock ledge. The next day, September 8, they made a splint for Gert’s leg. The other climber tried to carry Gert on his back, but Gert immediately cried out in pain and fainted. Gert seemed to be dying and he could not swallow fluids, but Oswald did not yet have intravenous (IV) fluids. That night, Gert asked Oswald several times to unclip him from the anchor so that he could roll over the rock ridge and fall to his death. In the morning, the group heard the sound of several airplanes and then a helicopter. Suddenly their hopes rose, but then there was a loud bang followed by silence, and the helicopter sound stopped. Their assumption that the helicopter had crashed later proved to be correct; the pilot had been killed trying to save them. That afternoon, four more rescuers arrived and brought IV fluids. After at least 20 attempts, Oswald got the needle into Gert’s vein, but it slipped out again. Finally, Oswald was able to establish an IV line and to give Gert a liter of fluid. During the night, however, the IV fluids froze. In the morning, Oswald thawed out the bottle with a gas stove. The morning of September 10 was very cold. The five rescuers built a cableway for the difficult traverse to the ascent route. Attempting to use this to transport Gert caused him unbearable pain, so they had to wait for a litter to arrive. Meanwhile, Oswald used up the IV fluids and morphine. Everyone’s morale reached a low point during a heavy afternoon snowstorm. On September 11, Gert had been lying on the small rock projection for 6 days and 6 nights. He was still alive, but he was delirious and had a high fever. At midday, the litter arrived. The rescuers used the cableway to carry the litter on a traverse through technical terrain. By dark, they reached the top of the vertical pitch down which they would have to lower Gert. After a restless night, the group began the descent by rappel, using two ropes at all times to secure the litter and the accompanying rescuers. During a violent snowstorm, they reached the beginning of a traverse over a sharp ridge. There was no way to build a 60-m (197-foot) cableway to the next rock tower with the little remaining rope. It was an impossible problem. At that moment, Werner Heim, a well-known Austrian mountaineer and rescuer, emerged from the fog and the snow squalls. He and six other rescuers from Tyrol, Austria, had heard about the accident 24 hours after it had happened. They had flown to Nairobi on one day’s notice. Two days later, they arrived at the foot of the mountain. Five of them had just returned from the Himalayas and were still acclimatized to high altitude, so they were able to ascend quickly. They had already prepared the entire further rappel route. The remaining lowering was very rapid as a result of the help of these well-trained rescuers, who functioned as a coordinated team. It was midnight when they arrived at the foot of the mountain. Meanwhile, Dr. Raimund Margraiter, a member of the rescue team, had given Gert additional IV infusions. At 4 AM, Dr. Margraiter and Oswald undid the bandages on Gert’s leg. The smell and the sight of the protruding tibia chased away all of the other onlookers. That morning, police porters helped to carry Gert on the stretcher several hours to

PART 5  RESCUE AND SURVIVAL

SELF-RESCUE Self-rescue refers to the removal of ill, injured, or stranded members of a party from a dangerous or unstable situation by members of the same party. In extreme cases, an ill or injured person may have to rescue himself or herself. Examples include the lowering of an injured climber (i.e., “climber pick-off”) by a climbing partner and the extracting of a person from a crevasse on a glacier. This chapter is mainly concerned with self-rescue in technical terrain.

EVACUATION Evacuation is the removal of a person who may be ill or injured from an area in which medical care and other resources (e.g., food, water) are limited to an area in which resources are available or in which a higher level of medical care can be provided.

Epidemiology Wilderness travel is generally quite safe, with the exception of various high-risk activities such as high-altitude mountaineering,30 backcountry skiing in avalanche terrain, and paragliding. There are limited data about the types of illness, injury, and death of wilderness travelers and even less about the types of morbidity and mortality of rescuers. Rescuers should be especially well prepared for the most common causes of injury and illness in victims.

RISKS OF WILDERNESS TRAVEL “No American wilderness that I know of is so dangerous as a city home ‘with all the modern improvements.’ One should go to the wilderness for safety, if for nothing else.” —JOHN MUIR51

In a study of helicopter rescues and deaths among trekkers in Nepal from 1984 to mid 1987, there were 23 deaths and 111 helicopter rescues with a total of 148,000 trekking permits.69 The incidence of helicopter rescue was 75 per 100,000, and the incidence of death was 15 per 100,000. The most common causes of death were trauma (11 persons), illness (8 persons), and altitude illness (3 persons). In a follow-up study of deaths among trekkers in Nepal from mid 1987 to 1991, there were 40 deaths among 275,950 trekkers, for a death rate of 14 per 100,000.68 Trauma was the cause of 12 deaths, and altitude illness caused 10 deaths. There were 4 deaths thought to be caused by heart attacks and 3 deaths from apparent diabetic ketoacidosis above 4000 m (13,100 feet). A small cohort study in one trekking group in Nepal showed that the rates of illness were similar between trekkers and porters.1 In the Alps, an Austrian study estimated the death rate for mountain hiking at 4 per 100,000 hikers annually. About 50% of these deaths were sudden cardiac deaths.10 In North America, there have been several studies in national parks. Some of these are difficult to interpret, because they include both wilderness and nonwilderness activities. In a study of national parks in the state of Washington, the overall injury rate was 22 per million visits. Two-thirds of the injuries occurred during hiking (55%) and mountaineering (12%), but the number of visits related to these activities was not reported.71 A California study that looked only at wilderness activities estimated a mortality rate of 0.26 deaths per 100,000 visits, mostly as a result of heart disease, drowning, and falls.48 The rate of nonfatal events was 9.2 per 100,000 visits. Injuries accounted for more than 70% of all nonfatal events, and these most frequently affected the lower extremities (38%). The risks of climbing in wilderness areas are harder to quantify. In data from mountaineering accidents in North America that included climbing accidents in nonwilderness areas from 1951 to 1995, 80% of the accidents involved a fall or a slip or being hit by a falling object.36 In more recent figures (covering 1951 to 2007 in the United States and 1951 to 2005 in Canada), 71% involved a fall or a slip or being hit by a falling object, 4% involved “exceeding abilities,” and 3% involved illness.84 712

A number of studies have attempted to quantify the mortality rate of various activities in the mountains, including mountaineering. One review claimed that, in the United States, the mortality rate per 100 participants was 0.6 for mountaineering and 0.2 for hang gliding.85 The number for mountaineering is not substantiated by any data or reference, is not credible, and is certainly far too high. A New Zealand study estimated a fatality rate of 1.9 per 1000 climber-days in Mt Cook National Park, with a large variation between high-risk areas (6.5 per 1000 climber days) and low-risk areas (0.3 per 1000 climber-days).43 A study of climbing fatalities on Denali (Mt McKinley) estimated 3 climber deaths per 1000 summit attempts.45 Fatality rates of the world’s highest mountains generally increase with increasing altitude.30 For more information about avalanche risks, please see Chapter 2.

INJURIES AND ILLNESSES IN MOUNTAIN RESCUE VICTIMS There are many published studies of mountain rescue victims. A Scottish study of 622 callouts comprised 333 victims,26 and there were 57 fatalities. Of the living victims, 78% had traumatic injuries, 8% had major trauma, 4% had spinal injuries, 8% had nontraumatic medical problems, and 14% were cold or exhausted. The author concluded that mountain rescuers provide “an advanced level of care” for many victims. Another study, which comprised the entire United Kingdom, showed a preponderance (75%) of rescue casualties due to “hillwalking,” with more than one-half of the injuries affecting the lower extremities.50 A study of mountain search and rescue victims from three national parks in the Canadian Rockies found 317 emergency operations that involved 406 persons over a 4-year period.83 Of these incidents, 44% involved hikers, and 50% were the result of “slips and falls.” About 60% of victims were injured. Injuries to the extremities accounted for 68% of the injuries. There were 40 fatalities; 45% were caused by avalanches, and 28% were caused by slips and falls. A study of wilderness search and rescue in New England looked at 321 incidents that involved 457 victims, 57% of whom were hiking at the time of the incident.19 Injuries were involved in 39% of the rescues, and 40% involved lost and missing persons. The author noted that a rescuer was injured during 2.5% of the rescues. A study of climbers on difficult routes in the Sierra Nevada in California found 215 mountaineering accidents in a 5-year period.46 Acute mountain sickness or hypothermia was noted in 104 patients. There were 17 deaths, most commonly as a result of head injuries. There were 94 injuries involving the ankle and the distal tibia.

Preventive Decision Making RISK REDUCTION Technical rescue, especially technical self-rescue, is often difficult and sometimes dangerous. It may present impossible challenges, with the result that an ill or injured person may not survive. The best strategy is to prevent the need for rescue. Proposed wilderness trips and mountain rescue missions should be examined carefully to ensure that the risks are within tolerable limits. In aviation, this is formalized with the use of rules and especially checklists that cover multiple aspects of a proposed flight. Tolerable limits in commercial aviation are very strictly defined, and the tolerance of risk is extremely low. In mountaineering, there may be a high level of unavoidable risk. The acceptable risk varies with the purpose of the trip or mission. A recreational rock climb has a very low acceptable risk, whereas an expedition to a remote unclimbed peak or a military mission in technical terrain may have a much higher level of acceptable risk. Things to be considered before approving a proposed trip or mission include whether the abilities, training, and experience of the participants are adequate to meet the demands of the proposed operation. Participants should have an adequate level of fitness and technical skills to complete the operation safely.

PLANNING Any climbing trip, expedition, or rescue mission should have a plan of operation that is determined beforehand; this is sometimes called a pre-plan. The pre-plan includes such aspects as a timeline for preparation, travel, and the achieving of objectives as well as the roles of each participant, including leadership and working groups. The plan should also evaluate potential difficulties of travel to remote areas, anticipate risks, and formulate strategies for dealing with problems. Safety culture and standard operating procedures are part of the plan. Planning should also include contingency plans. Medical planning looks at the members of the group to address any preexisting medical conditions and to prepare for known medical risks. Medical risks include infectious diseases, environmental exposures, and preventable conditions. Medical planning also addresses the risk of injury. Planning considers the skill sets of the participants and determines if these match the particular technical environments that are likely to be encountered and if they are commensurate with the acceptable level of risk. If some members of the group lack specific technical or medical skills, they can plan additional training and practice before departure; alternatively, at the start of the trip, members can be added who possess the necessary skills, or the decision can be made to accept a higher level of risk. It is possible to add members in support roles who do not participate fully in the expedition. Examples of supporting members include medical providers who will stay at base camp on a mountaineering expedition and contact persons who are not on the expedition but who can activate an organized rescue if necessary. No expedition or group can include rescue experts and medical providers with the necessary skills and equipment to deal with all potential problems. The organizers will establish a balance among expertise (both technical and medical), available equipment, and level of risk. It is better to do this explicitly rather than after being surprised with problems during the expedition. Equipment that fails or that is lost cannot be replaced during a wilderness trip. Equipment for rescue or medical care must be carried if it is to be available when needed. Planning for a wilderness trip must include decisions about taking backup equipment, rescue equipment, and medical supplies. It is important to recognize that physicians or other medical providers who are participants may not have the level of training and experience necessary to function effectively, especially in austere environments. Potential limitations include problems that are outside of the provider’s specialty area, that require special training that the provider does not possess, or that require special equipment that has not been brought. Even highly trained and well-equipped wilderness medicine experts will not be able to provide the same level of care in the wilderness that they can provide in an ambulance or hospital. The organizers and participants should plan their response to illness, injury, or death. How will rescue or recovery be organized? Will the group stay together or be split? A good pre-plan can organize a group and increase the overall safety of the activity. Beyond self-rescue, the group should consider a plan for coordinating outside rescue if it is needed. With cell phones and satellite phones, no part of the world is completely isolated. Although some individual travelers and groups may prefer the risk of being completely on their own, most groups now have the possibility to communicate the need for outside help. The group can also delegate a support person who is not on the trip to arrange outside help if the group fails to communicate according to a prearranged plan.

LEADERSHIP Leadership is part of the planning process and should be decided beforehand. Although small climbing groups do not necessarily need a leader, most expeditions should have one and also possibly a deputy leader. Larger expeditions may have an overall leader as well as specialized leaders, such as technical climbing leaders and those in charge of transportation, food, medical care, and so on. Organized rescue groups usually have a well-defined leadership structure. In the United States, this generally follows 713

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

Unless there is only one participant (i.e., a solo climb), it is important that participants be able to function as part of a team. This may require special training, ideally with the individuals who will be their teammates on the operation. Interpersonal skills—especially the abilities to communicate and to get along well with others—may be crucial to both prevent and solve problems that occur during the trip. The acceptable level of risk should be decided before the trip or operation begins. All participants should agree regarding this acceptable level. As problems arise, proposed solutions should be examined in the light of acceptable risk. Only in extreme circumstances should the level of acceptable risk be adjusted during the operation. One key to reducing the risk of injury or illness is to establish and adhere to a culture of safety. Aviation operations provide lessons regarding how to establish and maintain a culture of safety. Aviation takes place in a highly technical environment in which one small mistake can be fatal. The high degree of safety in modern aviation, especially commercial aviation, is due in large part to the enforcement of a culture of safety. Every procedure that occurs during activities in technical terrain should be scrutinized to make sure that it does not introduce unnecessary risks. For example, climbers should check the security of each other’s climbing harnesses and tie-ins before climbing or descending, no matter how experienced the climbers. It is best if the team also agrees to standard procedures, such as always tying in to the rope the same way; this makes deviations from safe procedures less likely to occur and easier to spot when they do. The aviation industry depends heavily on the use of checklists. This innovation has allowed commercial aviation, which is an inherently hazardous activity, to achieve low levels of risk to the traveling public. Because flying is a well-characterized activity, the decision process can be successfully characterized. Variables (e.g., weather, aircraft maintenance, flight crew training) and flight crew fitness factors (e.g., rest, prohibition of the use of alcohol and other drugs) can be quantified and acceptable limits established. The decision of whether to launch a flight or not is tightly regulated. Parameters of wilderness operations are not as well characterized or regulated as those of aviation, but many aspects can be characterized. Checklists that address equipment and its use are underused. For example, climbers can use checklists to guide their use of climbing harnesses, rope systems, and other technical aspects of operations. Checklists are commonly used by organized rescue groups to inspect individual systems, such as anchors, knots, the rigging of litters, and communications. Another example from the aviation industry is the use of redundancy and backup systems. No commercial aircraft takes off with a single working altimeter. Although weight restrictions in wilderness operations often make the use of redundancy problematic, it is worth considering what would happen if each piece of equipment were to fail. Trusting one’s life to a single rope or carabiner is often necessary in climbing; however, during an organized rescue, backup systems are usually standard. There are many wilderness areas from which successful evacuation would be extremely difficult or even impossible in the case of injury or if crucial equipment is lost or damaged. Expeditions in these areas require an extra degree of care to avoid the need for evacuation, but members should also be aware of and accept these risks. Soldiers on military operations routinely accept risks that would be unacceptable in civilian life. Many expeditions in the Himalayas are now done “alpine style,” with climbers planning rapid ascents with minimal equipment, rather than in the traditional “expedition style,” with a series of camps and a chain of supplies putting climbers close enough to the summit for a 1-day push to the top. The alpine style is riskier, even with a high level of training and skill, but it can achieve goals that are impossible with expedition style climbs. Increased risk has always been the price for pushing the envelope in wilderness travel. Ernest Shackleton allegedly advertised his famous Antarctic expedition with this unlikely description: “Men wanted for hazardous journey. Small wages, bitter cold, long months of complete darkness, constant danger, safe return doubtful. Honour and recognition in case of success.”81

PART 5  RESCUE AND SURVIVAL

a system known as the Incident Command System.47 Rescue groups also have general plans of operation that can be applied to individual missions.

COMMUNICATIONS To operate effectively, climbing teams and rescue teams should have a standard vocabulary that is used and understood by all members. For example, a rock climber will not start climbing until the person who is using the rope to safeguard his or her progress (i.e., the belayer) has indicated readiness to hold a fall. The technique of “readback” is used to minimize errors. The climber asks, “On belay?” The belayer answers, “Belay on.” The climber then says, “Climbing.” The belayer answers, “Climb” or “Climb on.” Many standard vocabularies have evolved over time to be concise and to limit the potential for confusion. In aviation, each letter has a corresponding word. For example, the letters f and s can be easily confused when spoken, but the corresponding words foxtrot and sierra are quite distinct. Ground-to-air signals (signs and arm signals) and radio language are other examples of standard vocabularies that can be useful for climbers, members of expeditions, and rescue teams. Climbers sometimes find themselves in situations in which communication has been disrupted. It can often be surprisingly hard to communicate by voice with a climber who is at the other end of a rope. Difficulties can be caused by wind, running water, or the fact that one climber has fallen into a crevasse. Radios are generally the best method of communication in such circumstances, but small climbing parties may not have radios, and radios may fail. A redundant form of communication involves using tugs on the rope to communicate. Climbers must know the system of rope signals to be used and practice it with each other in advance to avoid potentially fatal misunderstandings. Many expeditions and most rescue operations will require the use of radio communication among members and often with outside parties. All participants should be able to use standard radio etiquette. Although there are some international variations in vocabulary, the form is relatively standard worldwide. Spare batteries should be available, and preplans should be in place in case radio communications fail. In some areas, the use of cell phones for communication is practical. Expeditions should consider carrying satellite phones in areas that do not have other reliable means of communication with external rescue resources. In case of an emergency, if the usual means of communication are not available or have been disrupted, participants may need to give a distress signal. Special equipment (e.g., headlamps, whistles, flares) may be useful to call for help. A recognized distress signal is any signal in groups of three. The recipient of a distress call should answer with the use of the same means, if possible, so that the victim’s party knows that the distress call has been received. Communications are covered in further detail in Chapter 96.

DECISION MAKING IN SELF-RESCUE After a problem has been recognized, the group will attempt to solve it. Previous planning can help to streamline this process, and it can make the difference between a successful outcome and a tragic one. If there is an ill or injured participant who requires rescue, some or all of the other participants may be required to accomplish the rescue. Outside resources may be available in some circumstances. In some areas, rescue can be as simple as calling a helicopter; however, in most wilderness areas of the world, the initial phases (if not all phases) of rescue will be performed by others in the patient’s party. In technical terrain, it may take only a few people to lower a victim down a steep face or snow slope, because gravity can do some of the work; alternatively, it may take a large group to overcome complex technical problems. On easy terrain, it can take many people to carry a victim who is not ambulatory. Although there should be a general pre-plan, when a rescue is about to be started, the team should agree about a specific plan of action. Time spent discussing this plan is usually time 714

well spent, especially if there are any questions about the best response.

IMPROVISED SEARCHES In organized search and rescue, the first step is often a search for the victim or victims. Searching for avalanche victims is covered in Chapter 2. On a trip with a small team that stays together, searches are not usually necessary. On larger trips and expeditions, if a team fails to arrive at a destination when expected and is unable to communicate with another team, a search will be necessary to find the missing team. This may be the first step in rescue if the missing team is stranded or if it has one or more members who are ill or injured. Search strategy is covered in Chapter 37. Large groups can limit the need for potential searches by frequent radio contact with parties on the move or with passive global positioning system tracking. In areas with cell phone service, most newer cell phones support this application. It is important to be aware that a search is an emergency. The more capable an individual or group, the more likely it is that there is a problem when he or she fails to arrive as expected at a destination. Experienced climbers are likely to know how long it will take them to complete a given itinerary and can overcome many unexpected obstacles. If they are overdue, it is more likely that a serious problem has occurred than when less experienced climbers are late.

Wilderness Medicine Technical Rescue Survival of an injured person may depend on the speed of rescue and the care given during and after the rescue. Any group that is planning to travel in remote, steep, or technical terrain should have specific plans for potential emergencies, assess possible scenarios, and prepare in advance for rescues. The plan for rescue should include clearly defined leadership roles and sufficient technical capabilities. In a perfect world, there would be a plan to ensure that help would be provided promptly to anyone who needed it. Ideally, specific rescue equipment to carry out any foreseeable rescue and a medical kit to deal with any problem should be available. However, the ideal seldom occurs in the wilderness, rescue equipment can be heavy, and no medical kit can deal with all possible illnesses and injuries. Technical rescue equipment is discussed in Chapters 37 and 39. Every technical rescue operation involves some amount of improvisation, because every rescue is different. This variability demands thought and creativity when developing a solution, and it often includes including technical rigging. Most technical rescue operations have a few basic concepts in common: anchors, descent, ascent, raising, and lowering. The ability to apply principles related to all of these concepts in low-angle, high-angle, vertical, and overhanging terrain—whether hanging or with feet planted firmly on the ground—is an essential part of the rescuer’s tool kit.

ANCHORS Anchors for rescue are similar to climbing anchors except that they are implemented with the understanding that they may be subjected to loading by more than a single person (i.e., some combination of rescuers, a patient, and equipment). Rescue anchors need to be stronger than normal climbing anchors. The simplest single-point anchor consists of wrapping a piece of webbing or rope around a “bombproof” anchor point, such as a tree or a rock. In this case, the strength of the anchor will depend on the strength of the anchor point and the connecting components, which may include webbing, rope, and carabiners. Rope is preferred to webbing for use in rescue anchors, because it is more abrasion resistant and usually stronger. One method of anchoring a rope is to use the end of a rope that has been wrapped three or more times around a substantial object such as a tree and clipped back onto itself (Figure 38-1). This

FIGURE 38-1  Tension-less anchor. (Courtesy Loui H. McCurley.)

method, which is known as a tension-less anchor, provides an anchor that is as almost as strong as the rope itself. A single strand of 25-mm (1-inch) nylon webbing (sling) is rated at about 18 kN (4000 lbf), whereas a single strand of 11-mm (0.4-inch) nylon static or low-stretch rope is rated at about 27 kN (6000 lbf). High modulus fibers such as aramid (Kevlar) and ultra-high-molecular-weight polyethylene (Spectra) are even stronger but offer little or no elongation (stretch). Elongation is an important part of rope-based systems: when a shock load occurs, stretch in the ropes and webbing decreases sudden impact on the anchor and on persons who are in the system. High modulus fibers increase the risk of anchor failure and injury

FIGURE 38-2  Webbing basket hitch anchor. (Courtesy Loui H. McCurley.)

caused by shock loading; they should only be used with great caution in rescue work. Webbing used for climbing and mountaineering is often presewn into a continuous loop. Webbing loops may be used in a basket hitch configuration (Figure 38-2) or a girth hitch configuration (Figure 38-3) around an anchor point. When using a girth hitch, care should be taken to align the load properly, as shown in the figures. Some climbers and mountaineers prefer to use a version of 25-mm (1-in) tubular nylon webbing that is not pre-sewn. This allows for greater customization and adaptability, because it may be tied to whatever length is needed for a given situation. Ends of nylon webbing should always be joined with a water knot; this is also known as a ring bend. This and other knots are covered in Chapter 95. Spectra is a very slippery fiber that does not hold knots well, and Spectra webbing should only be used if it is pre-sewn. If Spectra webbing must be tied in an emergency situation, a pre-tensioned triple fisherman’s knot with plenty of excess tail has the best chance of holding. When webbing is tied around an anchor point such as a tree, the most secure method is to wrap the webbing three times around the anchor and then to pull two of the strands out as clip-in points (Figure 38-4). The water knot joining the two ends of the webbing should be positioned so that it is on the back side of the strand that is left tensioned around the anchor point. Because a key premise of any rescue—as of medicine—is to do no harm, placing two anchors rather than one is often desirable. There are many strategies for rigging multipoint anchors. The first decision is whether one anchor will provide “backup”

FIGURE 38-4  “Wrap three, pull two” anchor. When using tied webbing, the knot should be positioned on the back of the anchor. (Courtesy Loui H. McCurley.)

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CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

FIGURE 38-3  Webbing girth hitch anchor. (Courtesy Loui H. McCurley.)

PART 5  RESCUE AND SURVIVAL

difficulty, and be designed so that rescuers can connect to or disconnect from the rope system in an area in which there is no risk of a fall from a height.

DESCENT

FIGURE 38-5  Load-sharing anchor. (Courtesy Loui H. McCurley.)

to the other or if the load will be shared between the two. If rigging is done so that one anchor provides backup to the other, keeping the two anchors in line with one another and the fall line—and pre-tensioning between the two, if necessary—will help prevent catastrophic swing or shock load in the event of a failure. No anchor should ever be used unless it can be reasonably expected not to fail, so in principle this should not be a problem. Because rigging two anchors is desirable, sharing the load between the two anchors from the outset may also be a good plan; this type of anchor system is known as a load-sharing anchor. A load-sharing anchor shares the load between multiple points (Figure 38-5). One concern with a load-sharing anchor is that, unless the fall line is completely consistent, there will be times at which one or the other of the anchor points will bear most or even all of the load. For this reason, a load-sharing anchor should not be used to justify multiple weak anchor points. One method to avoid uneven loading between anchor points is to rig the load-sharing anchor so that it is allowed to selfequalize. This kind of rigging allows the load to remain distributed more consistently by multiple anchor points, even as the load moves across the fall line. The risks of self-equalizing anchors are often debated in climbing and rescue circles. If a sling that is too long is used to connect the anchor points, the failure of one of the points could create an excessive fall distance and a potentially high-impact load. Another useful technique is to use individual anchor slings (e.g., rope) with some forceabsorbing qualities (e.g., elasticity) to extend outward from the anchors to a very short Spectra sling. The slipperiness of Spectra allows for better equalization of the load. In addition, using a short sling helps to prevent a long fall. With any multipoint anchor system, the angle formed by the lines between the two anchors should be as acute as possible. As the angle increases, so does the amount of force placed on each anchor point. Generally, the maximum angle should be 90 degrees. The angle should never exceed 120 degrees. If circumstances demand the use of an angle of more than 90 degrees, increased forces at the anchors, at the anchor line terminations, and on other components in the system should be taken into account. When an anchor is attached to a structure that clearly has more than adequate strength, it is still advisable to anchor each line separately by using two slings or two connectors, even if both slings or connectors go around the same anchor point. Anchors should ideally be unquestionably reliable, be placed so that the rescuer can maintain a working position without 716

The term pickoff refers to rescuing a person who is in technical terrain, usually on a cliff. The person may be an injured climber or a climber who is uninjured but who needs to be removed from a vertical or near vertical setting, usually as a result of his or her inability to self-rescue safely or in a timely fashion. Basic descending techniques provide the foundation for a rescue pickoff. Equipment necessary for descent includes an anchored rope, harness, and descending device. Although using a harness can be avoided in some terrain with the dulfersitz rappel technique, this method of descending is useful for very short descents or in desperate circumstances; it involves wrapping the rope between the legs and around the body to provide friction (Figure 38-6). This technique can be painful to use, even under one’s own weight, and it is certainly not sufficient when carrying another person. Another method, the arm wrap (Figure 38-7), is less uncomfortable, but it is also less effective, and does not provide enough friction to be used in vertical terrain. The Swiss seat harness (Figure 38-8) is a better means of connecting oneself to a rope. It requires about 6 m (21 feet) of webbing, depending on the size of the person. It is much more secure than a simple diaper-style improvisation. Although this method of tying a harness is not easy to remember, the Swiss seat can be mastered with a little practice.

FIGURE 38-6  Dulfersitz rappel. (Courtesy Loui H. McCurley.)

FIGURE 38-7  Arm-wrap rappel. (Courtesy Loui H. McCurley.)

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

FIGURE 38-8  “Swiss” seat harness; a tied harness using webbing. (Courtesy Loui H. McCurley.)

Any descender that provides sufficient friction on the rope may be used. Figure-8 descenders are common, but have the major disadvantages of not providing sufficient friction for a heavy load and of twisting and kinking the rope. Figure-8 descenders can be double wrapped to increase friction (Figure 38-9). Brake racks are commonly used by cavers and rescuers. Manipulating the bars allows for the easy adjustment of the amount of friction; the straight-line design does not twist the

FIGURE 38-11  Climber on rappel. In rescue situations, the climber would either be belayed from above or be using a self-belay. (Courtesy Loui H. McCurley.)

FIGURE 38-9  Double wrapped figure-8 ascender. The double wrap increases friction, thereby enabling control of a rescue load. (Courtesy Loui H. McCurley.)

rope. In Europe, auto-locking devices such as the Prism and the I’D have become popular because they help to prevent catastrophic failure. Some professional rescue teams use the Brake Tube, which facilitates knot passes. Another popular device that allows for the easy adjustment of friction is the Scarab. Most climbing belay devices may also be used as descenders. Although some devices may not provide sufficient friction for lowering a heavy load, additional friction may be gained by “stacking” devices (Figure 38-10) or by adding carabiners to assist with the braking action. The Munter hitch is a good improvised technique that provides a reasonable amount of friction for a single climber and that requires only a rope and a carabiner. Lowering a load may be accomplished either by a rappel-style friction descent (i.e., with the control of the descent occurring by the descending person) at the point of the load or by a lowering system in which the load is controlled by another person from an anchor above the load. One person at a time may descend (Figure 38-11) or be lowered (Figure 38-12), a rescuer may descend with a victim (Figure 38-13), or a rescuer may be

FIGURE 38-10  Stacked figure-8 brake. The two figure-8 brakes can be stacked using a carabiner (as shown) or webbing to provide enough friction to control a rescue load. (Courtesy Loui H. McCurley.)

FIGURE 38-12  Climber being lowered. (Courtesy Loui H. McCurley.)

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Ascending may be accomplished with the use of an ascending device or of soft cams (i.e., slings or ropes that grab the main rope as a result of friction) rigged into a system that ensures that if either ascender should become dislodged, the user will be caught in a seated position by the other ascender. Mechanical ascenders are more efficient than are soft cams. A mechanical descender generally consists of a shell that wraps around the rope and a toothed cam device to grip the rope. Some mechanical ascenders have handles, whereas some are designed to attach to the harness to allow progress only in the forward direction. Some ascenders are more sturdily constructed than others; others have less aggressive teeth for use with heavier loads. Prusiks are the most common type of soft cams, and they may also be used for ascending. A Prusik consists of a pre-tied loop of rope that is at least 2 mm (0.08 inch) smaller in diameter than the main line. When wrapped around the main line, a Prusik grips the rope firmly. If more friction is desired, an additional wrap can be made around the main line. An ascending system may be as simple as Prusiks that are rigged with one as a foot loop to provide a movable “step” and the other at the harness to capture progress. Climbers—including most rescuers—usually choose mechanical ascenders (Figure 38-15). Other systems exist that allow for the use of both legs to ascend longer distances more efficiently; these are especially favored by cavers who often ascend long free-hanging ropes. FIGURE 38-13  Climber on rappel with victim. (Courtesy Loui H. McCurley.)

lowered with a victim (Figure 38-14). Although it may be necessary for the rescuer to rappel with the victim as a result of a lack of manpower or for other reasons, being lowered has the advantage of permitting the rescuer to focus exclusively on the victim.

ASCENT Any person who intends to descend a rope should also be able to ascend—even if only for a few feet—to self-extricate in the event of a mishap. Something as simple as catching a shirtsleeve or not having effectively planned an exit point could become a catastrophic event for a person who is unable to ascend.

FIGURE 38-14  Rescuer being lowered with victim. (Courtesy Loui H. McCurley.)

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HAUL SYSTEMS Ascending is a one-person activity. When the rescuer reaches the victim, it will be difficult or even impossible to ascend with the patient connected to the rescuer’s system. For this situation, the rescuer must know how to create a mechanical advantage system to provide greater lifting force. Haul systems used by rescuers can be complex and technically challenging. However, most of the time such complexity is unnecessary. The same tasks can be accomplished with simple systems.

FIGURE 38-15  Ascending a rope. The climber initially sits in the harness, putting his entire weight on the upper ascender while bending one leg and moving the lower ascender up to just below the upper ascender. He then stands up on one leg, unweighting the upper ascender and allowing him to move it up the rope to capture the upward progress. He then repeats the process as many times as  necessary to reach the top of the rope. (Courtesy Ken Zafren.)

The most common (and generally most useful) haul system configuration is the Z-system, which is also known as a 3:1 advantage system. In a 3 : 1 system, the working end of the haul rope is connected to the load, runs to a pulley at the anchor, and then runs back to another pulley that is connected (by Prusik or rope grab) to the working end of the haul rope. Using some sort of a ratcheting device on the side of the first pulley closest to the working end of the haul rope will help to capture progress and prevent catastrophic failure. Prusiks are often used in this progress-capture position, which is facilitated by use of a Prusikminding pulley (Figure 38-16). Mechanical advantage can be increased further by using additional pulleys (Figures 38-17 and Figure 38-18). A Z-system (or any other haul system) may also be piggybacked onto a main line for the purpose of raising a load. In this case, the ratchet (or progress-capture) device should be placed on the main line, and an attendant should set the ratchet to maintain progress when the system must be reset.

FIGURE 38-18  Five-to-one advantage haul system that shows the litter in the system shown in the previous figure. (Courtesy Ken Zafren.)

descender is especially useful. Once tied off, the rappeller connects an ascender (either mechanical or a Prusik) to the rope above the descender and then continues to rappel until the ascender is under tension and the descender can be removed from the rope. After reattaching the descender below the knot, the rappeller then just needs to remove the tension from the ascender and to reload the descender. This can be accomplished either by attaching another ascender with foot loop to the rope and stepping up (Figure 38-19) or by making a loop with the rope itself and stepping up. Care should be taken to ensure that the rappeller always has a secure attachment from the rope to the harness at waist level. Passing a knot on ascent is much easier. To accomplish this, the climber ascends up to the knot, removes the foot loop ascender from the rope, and then replaces it above the knot. The climber then continues to ascend until the waist ascender is as close as possible to the knot. Next, the spare ascender (which is also attached at the waist) can be placed above the knot, and the rescuer can continue to ascend until the lower waist ascender can be removed from the rope. This technique can also be useful at the top of an ascent, where pulling oneself over an edge can be very difficult.

KNOT PASS The ability to pass a knot while on descent or ascent is a basic skill for any potential rescuer. A spare ascender with a short lanyard connected to the harness at the waist is a useful tool for this purpose. To pass a knot while on descent, the rappeller should stop several inches above the knot and “lock off” high enough so that the descender will not jam into the knot. An auto-locking

FIGURE 38-17  Five-to-one advantage haul system on a glacier. Note the load-sharing anchor. The pulley closest to the rescuer is a directionchange pulley that allows the rescuers to pull parallel to the crevasse from which they plan to raise the victim in a litter. (Courtesy Ken Zafren.)

FIGURE 38-19  Knot pass on rappel. The technique is similar to that used to ascend a rope. (Courtesy Loui H. McCurley.)

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CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

FIGURE 38-16  Prusik minding pulley. The haul system can only move the load a certain distance before it needs to be reset. Before resetting the system, the Prusik is “set” to grip the rope and holds the load, thereby taking tension off the haul system so that it can be reset. The Prusik will also set automatically, thus preventing the load from being dropped if there is a failure in the haul system. (Courtesy Loui H. McCurley.)

PART 5  RESCUE AND SURVIVAL

BELAY/BACKUP SYSTEMS A backup system is any system that is used to prevent a catastrophic fall in the event of a failure of the main line. A secondary braking device or an auto-locking system (e.g., tandem Prusiks) may be used. In a self-rescue situation, using a secondary system for belay or backup purposes may be difficult. However, a backup belay should be considered. There may be a higher probability of failure when working with inexperienced rescuers. A backup system is especially desirable if the rescue system does not incorporate an auto-locking descender.

PERSONAL ESCAPE Any person who is working at height should be capable of emergency escape. Compact rope descent systems that can be carried in a pocket or small bag are now commonly available. Small-diameter nylon or aramid (Kevlar) ropes are often used. Nylon ropes are desirable for shock absorption and reliable performance. Aramid escape lines have become popular because of aramid’s high strength-to-weight ratio and its resistance to high temperatures. Great care should be taken when aramid ropes are used, because they have virtually no shock absorption capability. Aramid is also especially prone to self-destructive internal damage under repeated bending abuse, such as that which might occur over time when the material is stored in a pocket or bag. Smalldiameter ropes used for egress require a descender with extra friction. These may be custom-designed devices, or may resemble small brake racks or figure-8–type devices. Auto-locking devices should be considered when less experienced personnel are involved.

ONE-ON-ONE PICKOFF One-on-one pickoff is a useful skill for extricating a person who is suspended from a rope. Although it is possible to perform this maneuver using only the victim’s rope, it is preferable for the rescuer to reach the victim using a separate rescue rope. If enough rescuers are available and if communications are adequate, the entire operation can be controlled from above. This allows the descending rescuer to have both hands available to manage and care for the patient. A key decision when preparing for a pickoff is whether the rescuer will descend with the victim or remain stationary while lowering the victim to the ground. It is usually better to descend with the victim; this provides added protection and control as well as reassurance. To perform a pickoff that is controlled from above, the descending rescuer ties into the end of the rescue rope using an appropriate end knot (e.g., figure-8 knot, bowline knot). A descender is anchored to a secure anchor at the top of the drop, and an experienced brakeman takes control of the lowering process (Figure 38-20). A secondary system may be used as a belay if resources permit. Communications between the rescuer and the brakeman are critical. All actions are initiated by the rescuer; in other words, the rescuer is in the command role. The exact commands vary by region and training, but it is crucial that the brakeman and the rescuer agree about them in advance. The following is a good example of appropriate communications. Rescuer: On belay? Brakeman: Belay on. Rescuer: Down slow. / Up slow. Brakeman: Down slow. / Up slow. (Repeats rescuer’s command.) Rescuer: Slower. / Faster. Brakeman: Slower. / Faster. (Repeats rescuer’s command.) Rescuer: Off belay. Brakeman: Belay off.

For a pickoff that is controlled from above, the rescuer is lowered to within 1  m (3.3  feet) or so of the victim and asks the brakeman for a “stop” when he or she is just able to reach the victim. The rescuer attaches a lanyard (i.e., a sling or rope) to the rope just above the rescuer’s own connection using a carabiner or an ascender. The ascender can be either a 720

FIGURE 38-20  Friction brake load lowering. The rescuer is using a friction brake to lower a rescue load down a vertical face. (Courtesy Loui H. McCurley.)

mechanical ascender or a tied ascender (e.g., a Prusik). The rescuer then connects the other end of the lanyard to the victim’s harness. If the lanyard is adjustable, slack may be removed by tugging on the tail end of the lanyard. A victim who is attached to his or her own rope by a descender may be removed from that rope by lowering him or her onto the rescuer’s system using the descender. Otherwise, the brakeman at the top will need to build a haul system to raise the victim’s rope until the rescuer can take up enough slack to transition the victim to the rescuer’s rope. Cutting the victim’s rope should only be done as a last resort. This method introduces the potential hazard of shock loading the rescuer’s rope or cutting the wrong rope, thereby creating a catastrophic failure. A one-on-one rescue can also be accomplished with the rescuer using the rescue rope to ascend or rappel to the victim and then accomplishing the rescue from a fixed position on the rope. This method is difficult and should only be attempted by experienced rescuers. It requires rigging systems and using raising and lowering techniques either on a vertical surface or on the rope itself while also trying to manage the victim. In this scenario, the rescuer rappels down or ascends up to the victim using his own rope. Stopping just above but within reach of the victim, the rescuer uses an adjustable lanyard to connect to the victim, with the connection usually being from the victim’s seat harness attachment directly into the carabiner that holds the rescuer’s descender. Attaching the victim to the descender rather than to the rescuer’s harness allows the rescuer more mobility and helps to prevent unsafe cross-loading of the rescuer’s harness. If the victim is suspended by a descender that is attached to his or her rope, the rescuer may simply use the descender to lower the victim onto the rescue system. If the victim does not have a descender in place, the rescuer may need to build a miniature haul system by using the rescuer’s own rope as an anchor and then raising the victim to disengage the victim from the victim’s system. A one-on-one pickoff rescue may be used to lower a victim all the way to the ground or merely to load a victim into a litter mid wall. This method should not be used to lower the victim very far unless the victim is in relatively stable condition and will not be further injured by the lower. A badly injured victim or one who is not fully conscious or alert should be loaded into a pickoff seat or litter before moving occurs.

Belaying involves protecting a climber by means of a rope. In steep terrain, a climber who falls without a belay might fall a long distance and sustain serious injuries, whereas a climber who is belayed is more likely to fall a short distance, if at all, until he or she is caught by the rope. In most organized rescue situations, any rescue system should be belayed, either by a separate rope safeguarding the patient and rescuers or by a double-rope system. This may not be practical in self-rescue. Belay systems require additional time, equipment, personnel, and other resources that may not be available. A useful approach when deciding whether to belay a rescue system is to balance the probability of failure against the likely consequences of failure. The acceptable level of probability of failure is difficult to determine, and is usually best evaluated by an experienced rescue leader. The level of acceptable risk for any given operation depends on many factors, including the resources on hand, available alternatives, victim’s condition, and consequences of failure. The consequences of failure are the likely effects on the rescuers and the victims. If a failure were to occur, would rescuers and victims skin their knees, or would they plunge to their deaths? After the probability and consequences of failure have been evaluated, the leader should consider whether the benefits of a belay outweigh the increased risks caused by the time delay and use of resources necessary to set up and operate the belay system. There are many examples in which the use of a belay may jeopardize the success of an operation. In the case of a critically injured patient, the time required to put necessary resources in place may be a determining factor in the decision to not use a belay. In unstable terrain, a belay may increase the risk of rockfall as a result of the movement of additional personnel and equipment; in that case, belaying might increase rather than decrease the overall risk. On a free-hanging lower, a belay can introduce the potential hazard of tangling lines. Belay systems can be defined as active or passive, based on the actions required for them to function. An active belay requires the participation of a belayer to work effectively. An example might be a bottom belay for a rappeller or a second brakeman behind the primary brakeman on a lowering device. Running a separate belay line with a lowering device operated by a second brakeman is another example of an active belay. Active belays offer disadvantages as well as advantages. The greatest disadvantage is that the probability of human failure is generally higher than the probability of mechanical failure. By including a human action in the chain of required responses to a failure, the probability of failure of the belay can be increased. Alternatively, an active belay can be more effectively adapted to the situation (e.g., when changing from lowering to raising). Passive belays activate automatically in the event of a failure. Advantages of passive belays are that they can sometimes be operated with fewer personnel and that they eliminate the possibility of human failure. However, they often require personnel to operate, and can sometimes engage when they should not do so; this can significantly slow and complicate an operation. Special care must be taken to not overload an automatic belay in a system that consists of more than one person. In any case, it is best to keep rescue loads as light as possible to reduce the potential for failure. Whatever belay is applied must be capable of withstanding the load that might be placed on it. If a belay is introduced into a system, the question sometimes arises regarding which anchor should be stronger: the primary anchor or the belay anchor. The answer is that both anchors must be capable of withstanding any anticipated force, with a degree of safety that is acceptable to rescuers.

HIGHLINES IN RESCUE Highlines are also sometimes referred to as tyroleans, tyrolean traverses, or telphers. All of these terms refer to a rope or cable that is suspended from one point to another along which people, equipment, and other loads can be moved.

FIGURE 38-21  Highline. A special highline pulley can be used to decrease friction. The rescue load (not shown) hangs from the pulley. The lines on either side of the rescue load are tag lines that are used to pull the load along the highline. (Courtesy Loui H. McCurley.)

Highlines may be used to transport rescuers, victims, and equipment across a barrier. Highlines can be used to cross deep canyons or gorges, to avoid hazardous or difficult terrain, or to evacuate persons from a hazardous area in which there is no other practical alternative. Highlines are particularly useful for areas in which there is a lot of loose rock on steep faces, because they can keep ropes, rescuers, and victims out of the line of rockfall. When rigging highlines, consideration should be given to selecting a location with as narrow a span as possible, with sufficient high anchorages, and with room to work on both sides of the span. Horizontal highlines are suspended from two points that are close to the same level, whereas steep-angle highlines are suspended between two points where one is at a much higher level than the other. Highlines may also be suspended from points that result in an intermediate angle. Separate lines (tag lines) are used to pull the load along the highline (Figure 38-21). Special rigging can be added to a highline to make it possible to raise and lower loads from the span. Highlines should be used with great caution. More than any other rope-rescue system, highlines can overstress rope, equipment, and anchors, thereby causing the system to fail. Highlines also require a great deal of teamwork and communications. They are especially problematic for groups that have not frequently practiced together.

ESTABLISHING A MAIN LINE One of the most difficult tasks when rigging a horizontal highline is to get the initial personnel to the far side and to get the rope and equipment across to them. If there is a person on the far side who is at least somewhat mobile, he or she may be enlisted to assist with this process. There are several available linethrowing devices for sending a pilot line across a chasm; these include professional rope guns, throw bags, and softballs fitted with line connectors. When a person on the far side has an end of the pilot line, a rescuer can attach a more substantial rope to the pilot line with a knot and a carabiner and ask the person to pull this across the chasm; this rope will then become the main line. The person on the far side can be asked to wrap this rope two or three times as high as possible around a substantial anchor (e.g., a tree) and then clip the carabiner back to the rope. The main line supports the major portion of the weight of the load in the highline. Although this may be a single line, rigging a double line may be desirable when higher loads are anticipated. Using a static Kernmantle life safety rope as the main line helps rescuers calculate and maintain an appropriate amount of sag in the main line rope to prevent overloading the system. Because of the stresses that are generated in highlines, main line anchors must be extremely reliable. In a horizontal highline, both main line anchors will be subjected to similar stresses. With steep-angle highlines, the upper anchor will be subject to much higher stress, much as an upper anchor would be in a lowering system. The near-side anchor is the anchor to which the main line rope is initially anchored; this is usually the point from which operation of the highline is initiated and controlled, and it is also 721

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BELAYS

PART 5  RESCUE AND SURVIVAL

usually the anchor that is nearest arriving rescue personnel. The far-side anchor is the anchor to which the main line rope is attached at the far side; this anchor must be at least as strong as the near-side anchor. For a steep-angle highline, the far-side anchor will receive less stress while the load remains near the top. As the load approaches the bottom, the far-side anchor will be subjected to greater stress. The load that will be transported by the highline, along with the angle or sag in the system, determines the forces to which the anchors and equipment will be subjected. The load could be one person or a victim attached to a rescuer with a substantial amount of equipment.

TENSIONING THE MAIN LINE One of the most critical activities when rigging a rope for a highline is to include an appropriate amount of sag in the main line. Although a tightly tensioned main line provides an easier path across which to move the load, it is the sag in the line that prevents overloading. A highline system must never be stretched very tight and then loaded; this could cause the rope, equipment, or anchors to become overstressed and fail. There are several theories and complex mathematical equations for working out the appropriate amount of sag. To simplify the calculations, many people use “the 10% rule.” This is a very conservative method of tensioning a highline. According to the 10% rule, for every 100 kg (225 lb) of load and every 30 m (100 feet) of span in the rope, there should be a sag of 3 m (10 feet).44 Other methods may not be sufficiently conservative, especially for ropes with minimal elongation characteristics. Unless a rescuer is incorporating some sort of force measurement system and is thoroughly experienced with rigging, a very conservative approach is recommended. To tension the main line, rescuers rig a haul system to a substantial anchor on the near side and then use this to tension the main line after the main line has been secured on the far side. After a line is established and tensioned, one or more rescuers can cross over to the victim’s side to provide medical care and to continue the rigging. When crossing over water, personal flotation devices should be worn by all rescuers and victims. Additional ropes or rigging gear may be transported across by rescuers to provide a partial belay for the first crossing, a tag line for controlling the load, or another main line.

THE LOAD Rescuers, victims, and equipment may be secured with a harness or in a litter with a spider; this is similar to the spider that is used for vertical evacuation. The moving load may be attached to the main line with a carabiner, but using a pulley will reduce friction and make the trip more efficient. Large pulleys that have been specifically designed for this purpose are available from several manufacturers. When rigging a litter onto a horizontal highline, it should be set to minimize the patient’s exposure to a head-down configuration. Depending on the length of the highline and the intended application, this may mean that the head should go first.

Regardless of the system used, there are several rules of thumb to keep in mind when building rope rescue systems: • Ropes should be protected over all sharp or abrasive edges. • Equipment should be inspected before use to ensure that it is adequate and in good repair. • Appropriate precautions should be taken to prevent damage to equipment both when it is in use and in storage. • Ropes should be rigged to reduce the likelihood of a shock load or a pendulum in the event of a fall. • Ropes should be configured so that users cannot inadvertently descend off the end of the rope. • Slack in the safety line should be avoided to minimize the length of any potential fall. • Using the techniques described in this section, with sufficient training and practice, resourceful rescuers can resolve most rescue situations.

Improvised Methods for Carrying an Ill or Injured Patient Except in organized rescue, the use of special rescue equipment is generally impractical. Even if special rescue equipment is available, it is unlikely to be located at the site of the initial rescue. In remote areas, the supplies that can be used for improvised techniques are more likely to be available where and when they are needed.

THE RUCKSACK STRETCHER Improvised litters are described in Chapters 23 and 39. Although many of the techniques shown have been widely taught in rescue courses, all have severe disadvantages. Most types of improvised litters are difficult to construct or require special materials (e.g., ski poles) that may not be available. None of the commonly taught techniques provides good support for the victim, especially one who may have a spinal injury. An alternative method that is practical and requires only commonly available materials is the rucksack stretcher. The rucksack stretcher gives good support to the victim’s spine, and it can be constructed in minutes.88 A rucksack stretcher is made from three to four rucksacks, preferably with internal stays. The rucksacks should be filled with gear and clothing as if they were going to be carried individually by the rescuers. The optimal number of rucksacks depends on the sizes of the rucksacks and the height of the victim. The rescuers unfasten the shoulder straps of the middle (or middle two) rucksacks; this can usually be done without cutting the security seams at the ends of the straps. The rescuers then run the shoulder straps of each rucksack (except the “top” one) through the shoulder straps of the one above it. They then reattach the shoulder straps in their original positions (Figure 38-22).

TAG LINES AND HAUL LINES An additional non–load-bearing line may be used to connect the load with either side of the highline. A tag line may be used just to maintain contact with the load, or it may double as a belay or haul line. Beyond the center point of a horizontal highline, the load must be pulled upward to overcome the sag in the system. This can be quite an effort and require the use of a mechanical advantage system. Similarly, friction may be needed to control a load on the downward slope of a highline; this can be accomplished by running the tag line through a rescue brake system.

GENERAL PRINCIPLES With a good foundation of knowledge and skills, rescuers can adapt to almost any terrain in almost any environment. 722

FIGURE 38-22  Rucksack stretcher. If the victim has a suitable rucksack, it should be used when constructing the stretcher. (Courtesy Ken Zafren.)

IMPROVISED OVER-SNOW TRANSPORT The high center of gravity of the rucksack stretcher limits its use for sliding on snow. On soft snow, a victim without spinal injuries can be dragged in a sleeping bag that has been placed in a durable bivouac sack, with a sleeping pad under the sleeping bag. If the snow is harder or if the victim has spinal injuries, a rigid litter or vacuum mattress inside a durable bivouac sack can be used as a makeshift sled; however, this method will usually work for short distances only, because snow is generally abrasive on the fabric of any bivouac sack.

Litters and Vacuum Mattresses for Organized Rescue VACUUM MATRESSES Vacuum mattresses may be useful, especially in conjunction with rigid litters. Vacuum mattresses, which are also known as fullbody vacuum splints, are currently the best method for immobilizing patients for transport, especially if transport will be prolonged.21,58 They are more comfortable than backboards,12,16 and less likely to cause decubitus ulcers,66 because they conform to the back and minimize pressure points. Vacuum mattresses are filled with small pellets, like a beanbag. Evacuating the air inside the mattress creates a vacuum so that atmospheric pressure outside the mattress then forces it into a rigid shape. The patient must be lying on the mattress during the evacuation of air so that the shape will conform to the patient. Vacuum mattresses can be carried under some circumstances or used with a flexible litter, but usually they are used inside of a rigid litter. Although vacuum mattresses are state of the art, they have practical and theoretical disadvantages. Their rigidity has the potential to produce large forces on injured areas if the patient is not firmly secured and moves during transport.35 Leaks can occur, but in practice this can be fixed by patching, usually with duct tape. Unlike a rubber raft or other pressurized container in which the patch must withstand the high force of increased pressure in the container, atmospheric pressure works to hold the patch in place on a vacuum mattress. Theoretically, a more uniform padded mattress with a rigid backing would be preferable to a vacuum mattress,28,32 but this solution would have to overcome potential problems such as bulk and weight to be considered a superior solution to the problem of patient transport. If a vacuum mattress is not available, a patient on a backboard or a commercial litter should be placed in or on a sleeping bag with sleeping pads to decrease discomfort and prevent decubitus ulcers from developing. This method of packaging should also be used with improvised rucksack stretchers, if possible.

COMMERCIAL LITTERS Many types of stretchers, which are also known as litters, are marketed for organized rescue teams; these include basket litters

and flexible litters. Many types of litters are presented in detail in Chapter 39. When selecting the type of litter for a given rescue, the first priorities are the safety and protection of the patient. The lightness and compact size of flexible litters make them attractive choices for the initial response in organized rescue, especially for ground teams that must carry all of their own equipment. They can also be convenient solutions in confined spaces, caves, and mines. Flexible litters give little spinal support and are not by themselves well suited to high-angle rope rescue. A flexible litter can be placed inside a larger rigid frame litter after the patient is removed from a confined space for quicker lowering and raising operations without complete repackaging. Rigid frame litters are generally sturdy basket-style stretchers that are designed to connect to a rope system for safety. They can be lowered or negotiated through almost any terrain. They may consist of an open framework (e.g., a Stokes-style litter), or may be of a closed construction of modern composites that provide more protection to the patient. Some closed-construction litters (e.g., Cascade Toboggans Model 200) are designed to slide on snow. Sleds designed to be towed by snowmobiles and specialized sled litters (e.g., the Akja) designed for use by rescuers on skis are also available. Bear in mind that the perfect litter does not exist.29 For prolonged ground evacuation, many litters can be fitted with a wheel. Wheeling a litter over trails and other suitable terrain is often much easier and requires fewer people than carrying. Litters can be rigged for high-angle evacuation in either a horizontal or a vertical configuration. Vertical configurations offer a lower profile for rockfall, but they can be quite disconcerting for the patient. High-angle rescue is usually performed with the litter in a horizontal configuration (Figure 38-23). The litter is supported and connected to the end of the lowering line by means of a spider. These are available in different forms, which range from those with four litter attachment points and a single main line connection to those with six litter attachment points and dual mainlines. A commonly used type is the four-point spider with one litter attendant. Spiders can be ready made, or they can easily be improvised. A bowline on a bight is a knot that results in three loops at the end of a rope. A 15-m (49-foot) rope can be made into two bowlines on bights that are connected in the middle to provide a six-point attachment to the litter for one lowering and one main line or two main lines (Figure 38-24). The patient and rescuers should be attached directly to the lowering line and independently to a belay line, if one is being

FIGURE 38-23  Vertical evacuation in a practice scenario. Note that the rescuer is tied into the lowering ropes and not just the litter. (Courtesy Loui H. McCurley.)

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Without tightening the straps and with the hip belts of the rucksacks open and off to the sides, the rescuers place the victim on the stretcher. The rescuers can use the victim’s clothing as handles to lift the victim onto the stretcher. If the victim will be in a sleeping bag, the sleeping bag can also be used as handles. The victim’s head can be stabilized by the hip belt of the “bottom” rucksack. If the victim has a suspected cervical spine injury, the neck should be stabilized before lifting occurs. An excellent improvised method for cervical spine stabilization is a SAM splint. When the victim is lying on the stretcher, the rescuers fasten the hip belts snugly around the patient, with care taken to not constrict the chest or go directly over the knees. They then tighten the shoulder straps under the victim. One drawback of the rucksack stretcher with a victim lying on it is that it has a high center of gravity. When the rescuers put the stretcher on the ground, they should make sure that it does not roll over with the victim on it.

PART 5  RESCUE AND SURVIVAL FIGURE 38-24  Improvised spider in a practice scenario. (Courtesy Ken Zafren.)

used. There is an advantage to using two rescuers as litter attendants in some situations, especially when lowering over complex rock formations. As the litter is lowered from above, the litter attendants help to provide a smooth ride and to guide the litter away from obstacles. The attendants should wear helmets, and they should also wear their own backpacks to avoid being separated from their gear when they reach the bottom of the descent and also to protect their backs from rockfall. If debris falls from above the litter, attendants should attempt to lean over the litter to protect the patient and to take advantage of the protection provided by their backpacks.

Patient Packaging The first priority is to protect the patient from further injury. Dressings and splints are used to stabilize structures that are injured.21 If cervical spine injury cannot be ruled out, a cervical collar should be used. Clinical clearance of the cervical spine in awake patients may be used by properly trained rescuers to obviate the need for a cervical collar.74,80 Splints and cervical collars can be improvised using various materials or SAM splints; such improvised techniques are discussed in Chapter 23. The patient should be kept warm. Because the patient will be immobile, excessive cooling is possible, even in warm weather. In cold weather, especially in the presence of wind, it can be very challenging to protect the patient from cooling. Special hypothermia bags can be helpful.24 The system should be arranged so that injuries can be reassessed with minimal interruptions during transport. The patient in the litter must have protection from falling or windblown objects, especially during helicopter rescues, and from objects that might protrude and snag the litter during transport, such as rock projections or tree branches. The face and head of a supine patient are particularly vulnerable. The patient should wear a helmet with a face mask, if available, or a litter shield can be used. If a face mask is not available, protective glasses are another means of protecting the eyes. Plexiglas-type litter shields that cover the head, face, and neck can be fashioned for rigid litters; some of these are commercially available. Because tipping or inversion of the litter is always a possibility, the patient should be secured with straps over his or her body. The patient should be prevented from sliding up or down in the litter and prevented from coming out of either end. This can be accomplished with foot loops and shoulder loops in addition to the patient’s climbing harness. All of these devices are secured to the inside of the litter. Commercial litters with foot dividers decrease the potential of the patient shifting toward the foot end, but they do not protect against shifting toward the head end. Straps should not cross the neck and should avoid bony joints, especially the knees. In technical terrain, the patient should always wear a harness that is secured to the main lowering or belay line. 724

Vacuum mattresses conform to the contours of the patient’s back, and they can be secured in the litter. If the patient is secured firmly in the litter with a vacuum mattress, this should decrease the possibility of the patient shifting from side to side or lengthwise.40 Placing padding under the knees can increase patient comfort. Commercially manufactured litters often come with tie-in straps, but improvised straps may still be helpful in protecting certain injured areas and preventing lengthwise sliding. Vacuum mattresses can be placed into most litters, and the patient can be secured along with the vacuum mattress. With rucksack litters, the hip belts can be used as tie-in straps. One hip belt can go around the patient’s forehead, one around the chest, and one around the legs, with care taken to not fasten the chest straps too tightly and not cross the knees with the leg straps. Theoretically, a patient should be transported on one side (i.e., left or right lateral decubitus) in the recovery position so that he or she will not aspirate vomitus. However, there is no accepted method for stabilizing the patient in that position. Because the patient will almost always be transported supine and will be well secured in the litter, close monitoring is crucial. The litter and patient can be turned to one side to protect the airway if vomiting is imminent. Transferring a patient onto a litter or vacuum mattress can be difficult. Patients who are not injured or who have only minor injuries may be able to transfer themselves without assistance. In most technical situations, an efficient method of transferring an injured patient onto a litter is to have two or more rescuers pick up the patient and slide the litter into place underneath from the head or foot end. Extrication devices can be useful to help stabilize the spine during transfer, especially in technical terrain (Figure 38-25). Rescuers can use the patient’s clothes or sleeping bag as handles to lift the patient. Alternatively, if it is easier to load the litter from the side (e.g., when on a narrow ledge), the patient can be turned to rest on one side and then rolled onto the litter. This can be difficult, because the patient must be levered over the edge of the litter.

Fixed-Wing Aircraft in Mountain Rescue In many parts of the world, rescue has become nearly synonymous with the use of helicopters. This is especially true in Western and Central Europe,9 in mountainous terrain near urban areas in other developed countries, and in many national or provincial parks that are popular with climbers. However, fixedwing aircraft (i.e., airplanes) have their uses, especially when distances from bases are more than 160 km (100 mi), which is

FIGURE 38-25  Extrication device in a mass-casualty mountain rescue operation in Alaska. The patient was subsequently placed on the vacuum mattress and then placed in a rigid litter. Bystanders who hiked up to the scene can be excused for not wearing helmets, but professional rescuers who were flown in by helicopter either did not have helmets or removed them, thereby placing them in danger from falling rocks. Only the volunteer rescuer is shown wearing proper head protection. (Courtesy Ken Zafren.)

Helicopter Rescue in the Wilderness Environment (see also Chapter 40) “The sight of a horse makes the strong man lame.” —OLD AFGHAN PROVERB

“The sight of a helicopter makes the strong rescuer lame.” —NEW PROVERB

Few changes in the last few decades have affected search and rescue more than the use of helicopters. In emergency and disaster response, helicopters combine versatility as search and reconnaissance platforms with unparalleled rescue and extrication capabilities (Figure 38-26, online). With rotor tips that turn at more than 250 km/hr (155 mph), this uniquely valuable asset is also potentially very dangerous.67 Helicopters present real hazards to rescuers. In the United States, data from the National Park Service show that rescuers are more likely to die from aviation-related causes—primarily crashes—than from all other causes combined.67

CAPABILITIES OF HELICOPTERS Helicopters are multi-use aircraft that are can perform a variety of missions, including the following: • Searching for or attracting a victim • Evacuating ill or injured victims • Transporting or extricating field members • Short hauling or heli-rappelling to the site of a victim • Aerially surveying topography Although fixed-wing aircraft are generally used for searching large open areas for obvious clues (e.g. ski tracks, tents, downed aircraft), helicopters can be used to search areas such as cliffs, gullies, and cliff bottoms that are more difficult to scan from airplanes. The noise from a helicopter may attract the victim of a search who, in turn, may attempt to attract the attention of those on board the helicopter. Helicopters are often used in rescue situations to transport ill or injured victims to medical care. There are a number of methods that are used by rescue teams to evacuate injured victims; these methods include external loads, including the use of hoist systems and slings. Helicopters can also be used to assist with logistic support by transporting rescuers and their gear. This can be especially helpful for speeding up a rescue and for decreasing rescuer fatigue. Helicopters may allow completion of otherwise impossible missions.

search and rescue teams would be overwhelmed by the number of callouts, and they would be unable to meet the demand. Risk–benefit analysis must take into account the entire rescue environment. Regardless of location and urgency, helicopters should not be used for missions that are beyond the capabilities of the equipment or crew training.

TYPES OF HELICOPTERS Many types of helicopters are capable of responding to search and rescue operations, but not all are suited to the tasks that their crews may be willing to undertake. Search and rescue personnel should maintain a healthy skepticism about the capabilities and safety of any helicopter and crew with which they have not worked in training or on previous missions. Aeromedical Helicopters In North America, most search and rescue teams in developed areas will have access to local aeromedical helicopters, because many rescue missions occur within the proximity of a large town with a hospital trauma center. Flight nurses or paramedics who are specially qualified in critical care medicine usually accompany each flight. Aeromedical helicopters carry one or more supine adult patients, depending on aircraft type and internal configuration. In other areas, such as most of Western Europe, aeromedical helicopters with physicians on board are ubiquitous.9 Emergency medical equipment—including cardiac monitors and defibrillators, airway management equipment, oxygen, and emergency drugs—are standard on most aeromedical helicopters. In effect, the emergency department is carried to the patient for immediate treatment and care. “Air ambulance” services provide rapid response by an emergency medical team to begin stabilizing the patient at the scene and to transport the patient rapidly to an appropriate hospital for definitive care. Search and rescue team members should be aware of how aeromedical helicopters are dispatched. In North America, this will usually be by a local emergency operations manager. Some search and rescue teams may be able to request these helicopters directly. If the description of the rescue indicates that an aeromedical helicopter may be necessary, these specially equipped helicopters should be put on standby before rescuers are on scene. This gives the pilot and flight crew an opportunity to familiarize themselves with the terrain and weather conditions before they are actually dispatched. In Europe, aeromedical helicopters are often equipped for technical rescue and have crews with highly trained rescue personnel who are capable of technical rescue and external load operations42 (Figure 38-27). In the United States, most aeromedical helicopters do not have these capabilities, and the crew is

SAFE USE OF HELICOPTERS To use helicopters safely in any search or rescue operation, the rescue leader must perform a risk–benefit analysis. For example, is it worth the risk for a helicopter to evacuate a healthy search subject to avoid the need for a 1-hour walkout with rescuers in easy terrain? Alternatively, the potential benefit of air rescue is clear when the victim is unconscious and bleeding profusely at the scene. The decision to activate a helicopter depends on a combination of the reason for the rescue and on the flight and safety conditions.25,79 In Western Europe, where the number of mountain accidents dwarfs that of the number within the United States, helicopters are constantly responding to calls for help in the backcountry. Without the assistance of helicopter rescue programs, ground

FIGURE 38-27  Eurocopter EC 135 operated by Austrian Air Rescue shown performing a short-haul operation. This is a fully equipped aeromedical helicopter that is capable of performing mountain  rescue operations, including hoist and short-haul operations. The crew includes an “emergency physician” (Notarzt), who may be an anesthesiologist, an orthopedic surgeon, a general practitioner, or another specialist with additional training for mountain rescue. (Courtesy Ken Zafren.)

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the usual range of helicopters. Some military helicopters are equipped with in-flight refueling capabilities that can greatly extend their useful range. These helicopters depend on fixedwing refueling airplanes for extended-range operations. Airplanes can be adapted with skis for snow landings and with floats for water landings. If they are unable to land, airplanes can often be used to airdrop medical equipment, survival equipment, or supplies. Airplanes are frequently used for technical rescues, especially in remote glaciated areas that are far from helicopter bases. Medical care in airplanes is covered in more detail in Chapter 40.

PART 5  RESCUE AND SURVIVAL

not trained to operate in technical terrain. It is a very dangerous practice to use aeromedical helicopters for technical rescue unless the helicopter is equipped for technical rescue and the crews are specially trained. In some cases, aeromedical helicopters can land in nontechnical terrain to bring rescuers closer to a scene and to receive patients who have been rescued from technical terrain by qualified personnel.25 Law-Enforcement Helicopters In many countries, law-enforcement agencies operate helicopters, especially in the vicinities of large cities. Some lawenforcement helicopters have search and rescue as one of their missions and are capable of rescue operations in technical terrain. Others are of little or no value in the mountains as a result of a lack of training for mountain operations and sometimes also as a result of altitude limitations. Rescue teams should know the limitations of local law-enforcement helicopters and their pilots. Commercial Helicopters Commercial helicopters may be available to rescuers on an occasional basis or on contract. These may be a valuable resource, although there may be a fee for their services. A pre-plan should be made with the rescue authorities and the company that operates the helicopters. The rescuers must be aware of the limitations of helicopters and crews and should not use commercial helicopters for technical rescue unless the helicopters are capable and the crews are properly trained. Media Helicopters Search and rescue teams close to large cities with television stations may be fortunate to have at their disposal one or more media helicopters. Although these helicopters may be an extremely valuable resource for transporting rescuers and gear, they are seldom capable of technical operations. Military Helicopters Civilian rescue teams are sometimes involved in rescues with military helicopters. Many of these helicopters are not suitable for high-altitude terrain and should not be used above their service ceilings (i.e., safe working altitudes). In the United States, military rescue teams operated by the Air National Guard and, in coastal areas, by the Coast Guard may be highly capable in technical terrain, but the helicopters that they use (e.g., Pave Hawk, Jayhawk) have very limited high-altitude capabilities. Specially equipped turbo-Chinook twin-rotor helicopters are operated by the Air Force in the interior of Alaska. These always travel in pairs and, although they may take hours or days to launch, are capable of high-altitude operations of up to 6000 m (19,700 feet) in the Alaska Range. Rescue operations at very high altitudes in the Karakorum Range in Pakistan and in the Himalayas (particularly in Nepal) operate with very little margin for error and are justified only in desperate situations.

and must fly under visual flight rules. Visual flight rules for helicopters mean that there must be flight conditions that are clear of clouds and at an airspeed that enables the pilot to see and avoid collision. No matter what the local or national rules are, visibility minimums are important to rescuers and crews that operate rescue helicopters. A large number of helicopter crashes are caused by pilots flying into adverse weather conditions, which results in uncontrolled flight into terrain. Rescuers must be particularly cautious when weather conditions limit visibility. IFRs apply to aircraft with special navigational instruments that give the pilot greater capability in otherwise difficult flying conditions. IFRs allow for flying in conditions in which electronics provide the pilot with information that is not available with the naked eye. Larger helicopters, such as most of those used in search and rescue operations, can be equipped with instrument flight capability. Still, rescuers should carefully balance the benefits of using a helicopter in a rescue setting with the increased risk of flying the rescue under IFRs. Weather Conditions Turbulence can be a serious problem. Mornings are usually the best time for helicopter flight, because there is less turbulence than during afternoons, which results from heating by the sun later in the day. Cumulus clouds indicate turbulence with strong updrafts and downdrafts. In addition, there are often downdrafts over the middles of valleys. Downdrafts are especially dangerous at high altitudes because of reduced engine power. Updrafts often form directly above or on the sunny sides of ridges; leeward sides of ridges may have severe downdrafts. For areas in which ground-based operations are possible, even if a helicopter is on its way to evacuate a victim, ground personnel should still be dispatched to the scene with equipment that is necessary to transport the victim. The helicopter may not reach the victim as a result of malfunction, changes in weather, or other unexpected complications. One should never assume that a helicopter en route will become a helicopter that is on scene. Fuel Each type of helicopter has a range limited by its fuel supply. In many regions, this is important, because helicopters may be based far from a mountain search and rescue mission. In some areas, a mobile fuel tanker can be stationed at a heliport that can be accessed by road. In more remote areas, fuel caches at a forward heliport can enable a mission to continue with limited interruptions for refueling. Otherwise, the helicopters will have to fly a long distance to refuel, thereby losing valuable time and limiting use of a crucial resource.

SAFETY PRECAUTIONS ON THE GROUND

The advantages of helicopter use during emergency operations must be weighed against the risks involved. Rescuers must be aware of the limitations of helicopters when calling for these resources. Conditions such as altitude, weather, and terrain all affect the usefulness of helicopters in search and rescue operations. All aircraft are limited by their service ceilings, which can change based on temperature and humidity. Rescuers must be prepared to say that the mission is a “no go” when the risk assessment indicates that the risks outweigh the benefits.

Safety training for rescue ground personnel must include items that require special care both in and around helicopters, either on the ground or in the air. Operation of the helicopter should occur during daylight hours; this is usually defined as 30 minutes before sunrise to 30 minutes after sunset, whenever possible. Rescue personnel must be aware of wind velocity and visibility and not dispatch helicopters when the predicted wind velocity exceeds the helicopter’s limitations. Helicopter hand signals should be used whenever possible, but only by personnel who are trained in their use. All personnel should stay at least 30 m (100 feet) away from helicopters, except when loading or unloading.

Visibility Minimums Rules governing visibility minimums in helicopter operations vary widely by country. Although night operation of helicopters for rescue with night-vision goggles is common in countries like Switzerland and Austria, it is illegal in Italy. In the United States, there are specific minimums that have been clearly delineated by the Federal Aviation Administration for day and night helicopter operations for cases in which visibility is limited. Under the Federal Aviation Administration rules, smaller helicopters generally do not have instrument flight rules (IFRs) capability

Landing Zones (Helispots) Contrary to popular belief, helicopters do not normally land “on a dime.” Pilots require—or at least prefer—sizable landing zones, particularly at high elevations. Helicopter pilots generally will not take off or land vertically. Rather, they require a landing zone (often called an LZ or a helispot) that may be more than 100 m (330 feet) long. The ideal helispot is a flat strip that is at least 30 m (100 feet) wide and 90 m (300 feet) long; this is roughly the size of an American football field. Flat ridges and saddles may provide the best helispots in the field. The primary reason

LIMITATIONS OF HELICOPTERS

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Landing Zones in Confined Spaces Helispots should be designed in such a way that the helicopter can land and take off into the wind to increase lift. Only as a last resort should a “hover hole” helispot be chosen. This is a landing zone where, due to size restrictions, the pilot must slow to a hover above the landing area and then descend to the ground. When taking off, the pilot must use all available engine power, which leaves no room for error. Because helicopters can generate rotor wash in excess of 160 km/hr (100 mph) during takeoffs and landings (and significantly more when using very large helicopters such as Chinooks), the helispot should be free of lightweight objects that can blow away. Tall dry grass and shrubs should be avoided to prevent possible damage to the sensitive tail rotor, and tree stumps should be less than 0.3 m (1 foot) high. A snowfield can make a good helispot. Markers such as backpacks and garbage bags filled with rocks or snow should be placed near the helispot to give the pilot a frame of reference for depth perception. Night operations are becoming more common with availability of IFR and night-vision goggles. Because night landings and takeoffs are significantly more dangerous than are the same maneuvers during the day, rescue leaders must consider the risks and benefits of performing night operations. The pilot must be aware of optimal flight paths to avoid hazards such as trees, peaks, ridges, and power lines. Landings and Takeoffs Landings and takeoffs are generally easier in the presence of a light, steady breeze of about 20 km/hr (10 knots or 12 mph) than they are in still air. In addition, pilots may choose not to take off or land in a wind of more than 80 km/hr (45 knots or 50 mph) or with a gust spread of more than 37 km/hr (20 knots or 23 mph). When landing, a pilot will often make a high-level pass over the helispot to observe obstacles and wind indicators and then will come in on a final approach. Despite the tendency to watch during this approach, all personnel who are not in the helispot should look away to avoid injury caused by flying debris kicked up by the rotor wash, especially in the presence of large helicopters. Ground personnel must hold down any loose gear. During final approach, only one ground person should be near the helispot. This person is sometimes referred to as the ground contact or the parking tender. With the helicopter some distance away, the touchdown point is indicated by the ground contact standing upwind with his or her back to the wind and arms facing the desired landing spot. During landings on snow, no rescuers should be in the landing zone at any time. There is always the chance that the helicopter’s weight will cause it to settle in the snow, which could be dangerous for any rescuer in the helispot. The ground contact should be the person most familiar with helicopter operations, including landing zones, ground-to-air communications, and helicopter safety. When the helicopter is within radio range, the ground contact should make radio contact with the pilot. Knowing that a knowledgeable ground contact is available will be helpful for most pilots flying into mountainous terrain. Medical providers at the scene should generally not also be the ground contacts; rather, they should focus on patient care.

or crew chief. No one should approach the helicopter unless he or she is specifically instructed to do so. When approaching, all equipment such as packs, skis, snowshoes, and ice axes should be carried horizontally below waist level and never upright or over the shoulder. Skis are especially dangerous, because mountaineers often carry them upright and over one shoulder. With very few exceptions, rescuers should approach the helicopter only at an angle that is visible to the pilot. There is no reason ever to go back past the skids or the side doors, except in the case of helicopters with rear-entry doors (Figure 38-28, online). Rescuers approaching a helicopter should squat in a low profile to maximize head-to-rotor clearance. Rescuers should bend down, but they should always look at the pilot. Depending on the helispot and other flight factors, the pilot may have to maintain some power. If this is the case, the helicopter may pull off suddenly as a result of precarious positioning or because of ground resonance, which happens when the helicopter begins to vibrate as a result of an harmonic imbalance between landing gear and rotor blades. In either of these cases, the helicopter must become airborne. If the helicopter is going to cool down to a full rotor stop (i.e., “cold” loading and unloading), no rescuer should approach until the rotors have come to a complete stop. It usually takes at least 2 minutes for the engine to cool down. Loading and Unloading Safety Procedures Each of the loading and unloading guidelines listed in this section assumes that the helicopter must maintain rotor power (i.e., “hot” loading and unloading). This markedly increases the hazard as compared with loading and unloading a helicopter in which the rotor is stopped (i.e., “cold” loading and unloading). All loading and unloading must take place on the downhill side of the helicopter, because the rotor blade may be as close as 1.5 m (5 feet) from the ground in many helicopters, even on level ground (Figure 38-29). The tail rotor must be avoided at all times. This rotor may not be visible while turning at high speed. Serious injuries and deaths have resulted from careless personnel coming into contact with the tail rotor. The pilot must see all personnel who are within reach of the tail rotor so as not turn the tail around in their direction. As the rescuer approaches the helicopter, his or her backpack should be carried rather than worn. When he or she is on board, the rescuer should immediately fasten his or her seat belt and secure all equipment. Rescuers should never board an aircraft of any type without their personal packs and survival gear. Sometimes rescuers are encouraged to put packs and other equipment on a second aircraft or on a later flight of the same aircraft to put more rescuers on the first aircraft or first flight. This is a dangerous practice. Rescuers who are given this choice before flying into a mission should refuse to board the aircraft until it is guaranteed that all

LOADING AND UNLOADING Approaching the Helicopter Before approaching a helicopter, rescuers must be sure that the pilot is finished landing. Often the pilot will need to jockey the helicopter around a bit before he or she is comfortable enough to ease off on the power. At this point, there will be a noticeable change in the engine sound. The pilot might give the thumbs-up sign to indicate that it is safe for a rescuer to approach. Only one person should approach a helicopter after it lands, and this person should approach only when signaled by the pilot

FIGURE 38-29  Helicopter unloading. Note the crouched positions of the rescuers who are carrying rather than wearing their packs. (Courtesy Will Smith.)

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helicopters need large landing zones is that a helicopter with engine failure needs extra room to land safely, and engine failure most commonly occurs during takeoff or landing.

PART 5  RESCUE AND SURVIVAL

rescuers will not be separated from their personal packs and survival gear during the flight. Rescuers should also guarantee that they will not be flown out from a mission without their personal packs and survival gear. The second helicopter or second flight may not arrive as a result of changes in weather, changes in plans, or a crash. None of these circumstances can be controlled by the rescuers, so they must never be separated from their personal packs. Helicopter crashes are uncommon, but it is best to be prepared in case of a crash. Rescuers should make every effort to keep their backpacks within reach. Small packs can sometimes be stowed between the feet, and larger packs may sometimes be placed on the laps of the rescuers. It is best to have one’s survival gear, including a handheld radio, nearby in case of a crash. One-Skid Landings Usually a helicopter will be fully on the ground when rescuers enter or exit. However, there are conditions in which the pilot is only able to put one skid down and may be in a semi-hovering state while rescuers board or exit; this situation is called a oneskid landing. One-skid landings occur when only one skid or wheel of a helicopter is placed on the ground and the helicopter maintains a high rotor speed to keep itself level in the air. Extra caution is required for one-skid or hover boarding and exiting. It is best for rescuers to train for these operations with the pilots. At a minimum, the pilot should brief the rescuers about procedures, including hand signals. Helicopters are very sensitive to weight and balance. Stepping in or out of a helicopter that is balancing on one skid should be done very gingerly to avoid sudden weight change on one side of the helicopter. The probability of a downdraft, power settling, or recirculation effect occurring is high during a hover or oneskid landing. In the case of one-skid unloading, communication between the pilot and rescuers is essential. The pilot needs time to adjust the controls for the increased or decreased load coming onto or off of one side of his or her helicopter. The last thing that the pilot wants is for a heavy, clumsy rescuer to jump from the ship. To exit a helicopter that is in a one-skid landing position, the rescuer should not open the door until he or she is told to do so by the pilot. When the door is open, the rescuer puts his or her pack on the ground. It is important for the rescuer to let the pilot know when he or she is about to do this. Shifting weight, especially in a small helicopter, can have a major effect on balance, so the pilot must be prepared. With the headset still on, the rescuer tells the pilot, “On the count of three, I will put my pack down: one, two, three.” Occasionally, the rescuer actually has to drop the pack out. The rescuer then prepares to exit the ship. Again, with the headset still on, the rescuer completes all communications with the pilot. It is pointless to attempt to yell at the pilot without a radio headset. The rescuer tells the pilot, “I will step smoothly from the ship after the count of three. Do you understand?” The pilot will either agree or advise otherwise. At this point, after approval from the pilot, the rescuer removes the headset and then removes the seat belt and refastens it behind himself or herself while staying in the seat. The rescuer then counts to three with his or her fingers in view of the pilot and gently exits the ship. Frequently, the area in which a oneskid landing takes place is in steep and complicated terrain. It may be impossible to move away from the helicopter. After he or she is on the ground, the rescuer stays right next to the helicopter and stays as low to the ground as possible. Alternatively, if instructed to do so by the pilot in advance, the rescuer will move quickly away from the helicopter toward the front and on the downhill side so that the pilot can leave the area as quickly as possible. If there is more than one rescuer off loading via a one-skid landing, the rescuers exit one at a time. Communication is especially critical for any rescuers in the back seat of small helicopters, because the pilot may not be able to see them. Once on the ground, the rescuers should hold their positions and stay crouched as low as possible, or, if instructed to do so by the 728

pilot, they should quickly move away from the helicopter toward the front and on the downhill side so that the pilot can leave the area as quickly as possible. Loading and Unloading Without Moving Toward or Away From the Helicopter In technical terrain, the safest method of unloading is often for the helicopter to land and for the rescuers to disembark but not to move away from the helicopter. This technique can be used with a one-skid landing or a full landing, but it is usually only done when the helicopter will not shut down (i.e., “hot” unloading). In the case of a one-skid landing, the rescuers exit the helicopter on the side of the skid that is on the ground after being cleared to do so by the pilot. Rescuers should still move slowly and gently as they shift positions in the helicopter as well as when putting their packs on the ground and exiting themselves, because each movement changes the weight and balance of the helicopter. It is much easier for the pilot to compensate for gradual changes than for sudden ones. Like all the techniques in this chapter, it is best to practice this in training, before an actual mission occurs. The reverse procedure of the helicopter landing right next to the rescuers may also be the safest method of loading. In the case of reloading in the same place that one has unloaded, the pilot will usually want the rescuers in the same spot in which they unloaded. The unloading procedure is then reversed. The techniques of unloading and loading the helicopter with the rescuers and any victims next to the helicopter and not moving toward it or away from it keeps the rescuers and victims away from the rotors. Like all helicopter operations in technical terrain, these should only be performed by pilots who are trained, experienced, and highly qualified to fly in mountainous terrain. Hover Load and Hover Jump Operations An even more risky loading technique occurs when the helicopter hovers very near the ground but does not touch the ground while rescuers and victims either enter or exit the aircraft. This situation is referred to as a hover load or hover jump. This is a very dangerous operation that should be avoided unless it is deemed absolutely necessary. Center of gravity variations add to the risk of hover operations, because helicopters are very sensitive to changes in weight and balance. Jumping out of a hovering helicopter causes a dramatic shift in the center of gravity and must be coordinated with the pilot. It is preferable to try to find or make a place to land rather than performing one-skid or hover routines. A rescue can be transformed into a tragedy in an instant if the helicopter crashes.

EXTERNAL LOADS In some situations, terrain or other circumstances dictate a technical rescue in which the helicopter is unable to land at the scene or to perform a one-skid or hover operation. Rescuers can be inserted or rescuers and victims can be extracted using external load operations. Such operations include hoist and long-line operations. Hoist Operations Hoist (i.e., winch) operations occur when rescue personnel aboard the helicopter either insert or extract personnel or gear using an electric hoist and cable setup. During a hoist insertion operation, a load consisting of a rescuer, litter, other gear, or some combination thereof is attached by a specialized rescue harness to the end of the hoist cable and then lowered to the ground by a hoist operator on board the helicopter. The hoist operator communicates with the pilot to ensure that the rescuer is placed at a suitable ground location (Figure 38-30, online). Litters being lowered often start to spin, so the insertion point should not be directly above rescuers or victims on the ground if at all possible, and any rescuers on the ground should use extreme caution. Rescuers on the ground should not touch any load hanging from a helicopter until it has touched the ground. Loads may carry a very large static charge that can cause injury to a rescuer if the static is not discharged by ground contact.

FIGURE 38-31  Preparing to hoist. The rescuers are preparing to hoist a litter with a victim into a Pave Hawk helicopter. A tag line was used to prevent the litter from spinning. (Courtesy Ken Zafren.)

A hoist extraction uses the same system. A load—which may be a rescuer, victim, litter, gear, or some combination of these—is attached to the cable at the ground. The hoist operator then raises the load to the aircraft using the hoist. A light rope called a tag line is usually attached to a litter while it is being raised to prevent it from spinning (Figure 38-31). In most cases, the rescuers and victims are hoisted up and brought inside the aircraft. In some cases, however, the hoist operator brings its human cargo only as far as the skid, where these individuals remain until the pilot is able to find a suitable helispot to transfer them on board. A victim who does not require spinal stabilization and who is not already wearing a harness can be placed in an extra harness carried by the rescuers or in an improvised harness for hoisting or for short-haul operations, which are described in the next section. An alternative is a Bauman Screamer Suit or similar device that can be placed quickly on the victim to provide a secure means of suspending the patient during lifting and lowering. Horse-collar–type harnesses are extremely dangerous and should never be used, because they can put pressure on the brachial plexus. Victims and rescuers have fallen out of horse-collar–type harnesses, sometimes with fatal consequences. Short-Haul (or Long-Line) Operations Short-haul operations are similar to hoist operations in that cargo—including people—hangs below the aircraft (Figure 38-32). The difference in a short-haul operation is that the line

Heli-Rappel A final method of external operations in technical terrain involves rescuers rappelling from a helicopter while the aircraft maintains a full-power hover above the scene. A common method of insertion in military operations, a heli-rappel involves significant risks. The helicopter must operate at full power, often in a confined space where there is little margin for error and little room for the pilot to make a controlled landing if there is a problem. Rescuers who are planning to do heli-rappels should be very experienced at free rappels (i.e., rappels in which their feet cannot touch the terrain), should be able to rappel smoothly at a controlled speed, and should be able to remove all connections with the rope rapidly after they have established a safe stance on the ground. Rescuers should not attempt to rappel down a rope that has been tangled by rotor wash, and under no circumstances should they rappel down a rope that is not touching the ground. It is helpful to tie a large knot on the end of the rope to avoid rappelling off the end if the helicopter has to increase altitude during the rappel. Short-haul operations have largely replaced heli-rappels for civilian operations.

PATIENT CARE IN HELICOPTER OPERATIONS Even in well-equipped aeromedical helicopters, patient care can be compromised by noise, vibration, and cramped conditions. Unless there is no other possibility, only the most stable patients should be transported without an attendant who is capable of medical interventions. If there is any question that the patient’s airway may become compromised and if it is possible to secure it, this should be done before transport. Medical care in helicopters is covered in more detail in Chapter 40.

Hazards in Wilderness Travel and Rescue Daring is fine! Reckless impetuosity is stupid! It is therefore wise to discover and learn from the experience of others and to match boldness to mature consideration, ability to good sense. True courage is shown only by one who is fully aware of all the consequences of his actions. —WILHELM PAULCKE55

FIGURE 38-32  Short-haul operation. (Courtesy Will Smith.)

Wilderness travelers, whether in technical or nontechnical terrain, sometimes need to be rescued. The need for rescue may arise from injury, illness, or just being stranded. The problem may be caused by bad decisions, bad luck, or a combination of both. The rescue effort may be a self-rescue, it may be performed by other victims or members of the party, or it may involve external rescue. Rescues often introduce additional risks, especially in technical terrain. Wilderness travelers who understand the possible hazards can minimize the risk of having to be rescued. Experience can be helpful, but it is not a guarantee against future problems. A climber can use the same flawed technique or make the same wrong decision repeatedly without consequences and come to believe that the technique or decision is correct. Rescuers must also be aware of their potential to lose 729

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

that is hanging below the aircraft is not attached to a winch, and the cargo is therefore simply transported while hanging below the aircraft. The term short haul usually refers to live loads, whereas long line is applied to body recovery or other nonlive cargo. Short-haul operations may be the most suitable rescue operation for an injured or uninjured climber who is unable to ascend or descend his or her route. In this case, a rescuer can be inserted into the scene by short haul and then proceed to rescue the subject in a pickoff. Short-haul and hoist operations are both dangerous and difficult on victims. Although rescuers may be familiar and experienced with such operations, victims may become quite anxious when being suspended from a helicopter. The same precautions regarding spinning loads and avoiding contact with charged objects apply to both short-haul and hoist operations.

PART 5  RESCUE AND SURVIVAL

unacclimatized travelers, including rescuers. High altitude is often associated with cold, wind, and storms, thereby further limiting the performance of humans and equipment.31 High-altitude medicine is the subject of Chapter 1.

EXTREMES OF TEMPERATURE AND HUMIDITY

FIGURE 38-33  Plane crash. This fatal plane crash occurred in a remote area of Alaska. Body recovery was considered too dangerous for the rescuers, so the plane and the bodies were left in place. (Courtesy Ken Zafren.)

attention to detail after they have been involved in many search and rescue operations. As compared with many other endeavors, there are real risks for the rescuers. The first priority is the rescuer’s own safety. An injured rescuer is a liability to the team and to the accomplishment of a rescue mission. The rescuer’s second priority is the safety of the rest of the team. The third priority is safety of the victim and successful completion of the mission. Rescuers should be aware that they are not invincible and that one can never eliminate all risk. Although it is critical that rescue groups work to fine-tune their rescue skills, it is equally essential that rescuers—and especially rescue leaders—have a clear understanding of hazard evaluation and risk assessment; these skills should be an integral part of rescue training. Rescue operations are often time critical, and this urgency can lead to “go fever.” No rescue operation should take place until a determination has been made that the operation can be accomplished with a reasonable margin of safety (Figure 38-33). Sometimes the decision has to be made that the operation is a “no go” or that it must be delayed until conditions allow for a greater degree of safety. The remainder of this section will emphasize hazards that are important to consider during wilderness travel, especially in mountainous, glaciated, or other technical terrain. Although these hazards are discussed separately, many “accidents” in the mountains are caused by a combination of hazards. Wilderness travelers and rescuers should be aware that small hazards can compound into larger ones. As conditions change, it is important to reassess the overall effects on safety.

Natural Hazards Wilderness travelers should be aware of natural hazards and how to reduce the risks of exposure. This knowledge is even more important for rescuers, especially when they will be exposed to the same hazards that caused or contributed to the need for rescue.

HIGH ALTITUDE At high altitudes, aircraft performance is impaired; this may result in unacceptably low margins of safety for both fixed-wing and helicopter operations. In addition, human performance and judgment are impaired at high altitude, even in the absence of high-altitude illness. These effects become more important as altitude increases, and they may contribute to injuries.30,46 Highaltitude illness can have serious effects on the performance of 730

Human performance is impaired by cold and wind. Tasks that require dexterity can take a long time in cold and windy conditions. Human performance is impaired by hot conditions, especially in the presence of high humidity. Extremes of temperature and humidity may be limiting factors in wilderness travel and rescue; these topics are addressed in Part 2: Cold and Heat. Performance of equipment (especially electronic equipment) may also be degraded at extremes of temperature and humidity. Cold decreases battery power and increases power requirements, and heat causes overheating. Aircraft tend to perform better in cold conditions as a result of higher air density, but aircraft maintenance is much more difficult in very cold conditions. At very low temperatures, motors may not start. Even properly maintained aircraft with special low-temperature lubricants have temperature limits below which safe operation is not possible.

WEATHER Wilderness travelers should be aware of local weather patterns and general principles of weather prediction. In many parts of the world, weather forecasts are very general, unreliable, or completely nonexistent. While focusing on the actual rescue operation, rescuers and rescue leaders should keep an eye on the sky. Storms can often be predicted in mountainous terrain without the help of forecasts. As clouds get bigger and darker, a storm builds. In temperate and tropical areas with frequent afternoon thunderstorms, rescuers should expect storm activity by midday. Rescue leaders should consider the weather forecast as well as current weather conditions before deciding whether to use airborne resources. It is critical that a helicopter or airplane with a patient on board be able to complete the mission and deliver the patient to a critical care facility or a ground ambulance. In areas with highly developed weather forecasting, rescue leaders might benefit from communicating directly with forecasters, who can give updated forecasts for specific altitudes and locations. Prerecorded weather forecasts, websites, hotlines, and media forecasts may be unreliable. Helicopter and fixed-wing pilots will want to know current weather conditions and weather forecasts when they are dispatched to a rescue scene. They will usually contact aviation weather forecasters for the latest information. Rescue leaders should understand how weather affects the use of aviation support in the mountains. Visibility is a serious problem for helicopter pilots. Fog and rainy conditions can lead to reduced visibility, and a clear sky can be replaced by very hazardous flight conditions within a matter of minutes. Service ceilings can decrease quickly, especially on sunny days. As mentioned in the section about helicopters earlier in this chapter, turbulence is a major potential hazard for helicopter operations. Weather and weather forecasting are covered in Chapter 42.

LIGHTNING Lightning is a hazard in most areas of the world, and it is especially common and dangerous in mountain areas. Even in mountainous terrain, most lightning injuries can be prevented.89 Hikers and mountaineers should avoid summits and ridges not only during ongoing thunderstorms but also during periods that have a high likelihood of lightning activity, such as summer afternoons in temperate and tropical mountains. The interiors of mountain refuges and huts, away from open doors and windows, may be safe, but small open structures offer no protection, and they may in fact increase the risk of side flashes. Tents provide no protection; metal tent poles may act as lightning rods and increase the risk of a lightning strike. Large valleys and large caves are relatively safe, but wet streambeds, small caves, and

CORNICE FAILURES

ROCKFALL

Many mountain areas are glaciated. Glaciers are bodies of ice that move slowly downhill under the influence of gravity and that present unique hazards for travel. Large glaciers may be the equivalent of slowly flowing rivers. The surface of a glacier may be ice, which necessitates the use of crampons, even on gentle slopes. If the glacier is covered with snow, efficient movement may require flotation aids such as skis or snowshoes. On snow-covered glaciers, crevasses may be hidden. Crevasses are cracks in a glacier that form as a result of slow movement of the glacier over underlying terrain features. Ice is very plastic, but crevasses form when ice reaches the limits of its plasticity. The width of crevasses varies from centimeters to tens of meters. A person cannot fall into a very narrow crevasse, but one can easily fall into a crevasse that is a meter or more across. If the surface of the glacier is ice, the crevasses will be visible. However, on snow-covered glaciers, crevasses can be impossible or almost impossible to detect. A crevasse may reveal itself only when a climber falls into it through the snow. Sometimes crevasses can be crossed on snow or ice bridges. However, snow bridges in particular can be prone to fail with the added weight of a climber. Climbers who fall into a crevasse can end up hanging on a rope, sometimes free and away from the edges, or they can land on the bottom of the crevasse, which may be filled with snow or water. There are special techniques for safe travel on glaciers, including roping climbers together, and there are also special rescue techniques for extracting climbers from crevasses.65 On ice-covered glaciers, climbers are usually safer traveling unroped except when overcoming obstacles that require technical climbing skills. When overcoming these obstacles, climbers should be using a safety line or be belayed. When a glacier goes over steep underlying terrain (e.g., a cliff), it may form an icefall. In an icefall, crevasses often run not only across the glacier but also in any other direction. Snowcovered icefalls are particularly dangerous to cross, partly because the crevasses may be oriented in unexpected directions. In larger glaciers, icefalls contain blocks of ice known as seracs, which may be as large as buildings. Seracs can fall over as the glacier moves imperceptibly. In extreme cases, blocks of ice fall over a visible cliff. It is extremely hazardous to be anywhere in a zone in which ice blocks might land.

Rockfall can be a major hazard in technical terrain, and it is particularly dangerous for rescuers who might have to perform a rescue in steep terrain. Rescuers must be alert and aware that they can easily trigger rockfall during technical rescue efforts. It is prudent to limit the number of rescuers in any area in which rockfall may occur. Natural rockfall is common during rainstorms and during freeze–thaw cycles that often occur in the spring. Many fatal rockfall accidents occur when members of a party trigger the event. Rescuers should always wear helmets that are certified by the International Mountaineering and Climbing Federation, and they should equip any rescue victim with a helmet. Litter shields that have been designed to protect the subject’s face from rockfall are essential elements of any mountain rescue. Another risk of rockfall is that ropes may be cut by the impact of rock against rock.

ICEFALL Climbing is often far more hazardous on ice than on rock. Ice is generally less stable than rock, and icefall is a hazard for rescuers as well as for climbers. Rescuers who work in areas that are popular among ice climbers must be aware of the objective and subjective hazards. Use of helmets is mandatory for climbers and rescuers. Helmets can mitigate the impact of falls and protect against small pieces of falling ice, but they offer little protection against the impact of larger ice blocks. Climbers and rescuers on ice use tools that are generally very sharp. Ice axes, crampon points, and ice tools can all cause serious injury in the event of a fall. Ice on the sunny side of a mountain is more prone to decay during certain times of the year. Spring conditions cause increased risk. Warm temperatures cause ice structures to be more hazardous and also more prone to decay. Water runoff on ice routes is a good indication that the hazard of icefall is increasing. Routes with horizontal cracks are showing early signs of collapse.

AVALANCHES Avalanches are covered in detail in Chapter 2.

When snow falls in the mountains, windblown snow can accumulate on the lee sides of ridges to form a vertical or overhanging edge. Because snow has structural integrity up to a point, cornices can be many meters thick and overhang 10 m (30 feet) or more. It is hazardous to climb under a cornice, because it may fail catastrophically as a result of wind or increased loading and fall on the climber, or it may fall on a snow slope and cause an avalanche. It is even more hazardous to climb on a cornice, because the weight of the climber may cause the cornice to fail. Cornices may not be apparent to a climber who is approaching the top of a ridge on the windward side. It is easy to walk on relatively flat snow on top of a ridge without realizing that below the snow is air rather than rock. In areas of heavy snowfall, cornices may overhang 10 m (30 feet) or more. Climbers should avoid walking on the overhanging part of the cornice at all costs. They should attempt to stay several meters back from the overhanging part, because the fracture line formed by cornice failure may not be vertical but rather may veer toward the windward side. Many climbers have been injured or killed by walking on a cornice that collapsed.

TERRAIN FEATURES Many terrain features are potentially hazardous, even in generally nontechnical terrain. These include steep slopes and cliffs as well as rivers and other bodies of water. Even a short stream crossing can be hazardous. These hazards are usually obvious, and technical skills may be necessary for safe travel or rescue when these hazards cannot be avoided.

GLACIER HAZARDS

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areas under overhangs are dangerous locations during lightning activity. The “triangle of safety” near a cliff or wall is a myth. There are no completely safe areas during a lightning storm, only areas of relative safety. It is still best to avoid being the tallest object in an open area. It is also best to stay a short distance away from cliffs and other vertical objects to minimize the risk of ground currents. Sitting or crouching on a dry pack or dry rope may also offer protection from ground currents. Metal objects do not attract lightning, but they are good conductors. They can function as lightning rods, and can cause burns as well as direct lightning injuries. Metal objects such as skis, ski poles, and ice axes should not be carried above shoulder level. Antennae present the same risk and also increase risk of damage to mobile phones and radios. Communications devices should be protected in the center of a rucksack, as should metal objects such as carabiners and crampons. Ropes, especially when wet, can also provide a path for lightning current. A via ferrata is a route on a mountain that would be a technical climb without metal aids such as ladders and cable ropes. Such aids should be avoided during a lightning storm. Anyone who feels his or her skin tingling or hair standing on end is in danger of being struck and should immediately crouch with his or her feet touching each other. Lightning poses special risks for rescuers. If the victim and rescuers are in a relatively safe area, evacuation should be postponed. Otherwise, rapid evacuation to a location with lower risk is probably the best strategy. Helicopters can be struck by lightning while in flight, thereby resulting in crashes. Helicopter operations should be delayed until after lightning danger has passed. Lightning is covered in Chapter 3.

PART 5  RESCUE AND SURVIVAL

Other glacier features that present hazards are known as bergschrunds. These are openings at the top of a glacier that are formed by the movement of glacier ice away from stationary ice that is stuck to the mountain. The sides are composed of ice and snow, and the bottom is made of rock. Another hazard called a randkluft is similar to a bergschrund, but one side is rock and the other side is snow. A randkluft can form at the top or on the sides of a snowfield or glacier. A randkluft is usually quite narrow, and it may also have snow bridging the top that does not fill the opening below. Climbers who fall into a randkluft can easily become wedged into place. Streams running on the surface of ice-covered glaciers may present stream-crossing problems. A feature that is unique to glaciers is a moulin or a glacier mill. This is a depression into which a stream running on a glacier drains, often completely through to the bottom of the glacier. These are attractive nuisances, usually with steep, icy sides. Climbers who fall into a moulin can be injured, drowned, or even carried into the glacier, with predictably fatal results. Moulins are best enjoyed from a safe distance.

EQUIPMENT Even in nontechnical situations, equipment may be important for survival. For example, wilderness travelers, including rescuers, depend on clothing and other equipment to stay warm in cold conditions. Clothing is necessary for protection from cold, wind, rain, and sun. Stoves may be necessary to melt water when it is only available in the form of snow. In technical situations, clothing (including protective clothing such as helmets) and specialized equipment such as crampons, ice axes, ropes, and anchors may be critical for safe travel. In some cases, equipment failure can be fatal. Equipment failure may be caused by improper use, such as a failure to properly secure a harness, or it may be the result of the physical failure of equipment. If a climber or rescuer is hanging free (i.e., not touching the ground at all), the failure of a single rope will cause a fall; this will result in injury or death if the fall is long enough. The use of redundant equipment (in this case, a second rope) can prevent such consequences if the first piece of equipment fails. Personal and group equipment should be in good condition and ready to go before each wilderness trip or rescue mission. For rescue work, the equipment should be checked for damage, inventoried, and repacked at the end of each operation so that it is ready for the next mission. Gear is often packed or organized in modular form: for example, as a rock rescue kit, glacier rescue kit, or medical kit. For an example of the contents of a medical kit for technical rescue, see the appendix at the end of this chapter. A “bash” kit that contains enough equipment to start a rescue can be useful for the first team to go into the field on a rescue. Damaged equipment should be repaired or replaced. Fabrics and fibers have a limited lifespan, and they cannot always be adequately assessed for damage. Ropes and slings should be replaced if there is any known or suspected damage as well as after a certain time span or number of uses. Any helmet that has sustained a significant impact should be retired. Rescue teams should have an equipment manager to oversee the safety and maintenance of equipment. Some equipment, such as radios and avalanche beacons, should be tested just before going into the field.

TRAINING Effective climbing and rescue teams must train to be familiar with the equipment and techniques to be used in technical terrain. Rescue groups should have classroom and field training, including simulated missions. Experienced mountain rescue teams can break each rescue down into small components. The team members who are responsible for each component must be thoroughly familiar with the necessary equipment and techniques. However, this familiarity can only be achieved with regular practice.

Human Factors Human factors for travel or rescue in technical terrain are the same as human factors in all activities in which errors can result 732

in bad outcomes (e.g., driving a car, piloting an airplane, practicing medicine). Physical and mental performance may both be critical to survival. The following discussion in not intended as a complete discussion of human factors; rather, it is intended to highlight areas of particular interest in technical climbing and rescue. Some rescuers think of themselves as invincible because of the “Mountain Rescue” patch on their jackets, but nothing could be further from the truth. Ultimately, the safety of wilderness travel or rescue in technical terrain depends on the judgment of the climbers and rescuers.

PHYSICAL CONDITIONING AND SKILLS Technical climbing and rescues are often very strenuous. Climbers and rescuers should be in excellent physical condition. Rescuers must be careful not to exhaust themselves during their approach to the rescue scene. Rushing to the scene when carrying heavy equipment can result in having no reserve for the actual rescue effort. Experienced rescuers know how to pace themselves. Climbing and mountain rescue require physical skills that must be learned and practiced. Climbers and rescuers must not only understand and be experienced in the use of climbing and rescue systems, they must also possess the physical skills necessary to operate the systems. For example, in a vertical rescue operation, rescuers must know how to maneuver the litter and themselves to move safely past obstacles (e.g., overhangs) while being lowered or raised. Climbers and rescuers should know their limits with regard to both skills and endurance. They should not operate systems with which they are not thoroughly familiar, and should not continue activities (e.g., carrying a litter) beyond the safe limits of their endurance.

FOOD, WATER, AND SLEEP Climbers sometimes go beyond their usual limits of endurance. On long and difficult climbs, climbers may intentionally deprive themselves of food and water to decrease the weight that they have to carry so that they may move more quickly. Speed may increase safety by decreasing time spent exposed to objective hazards, including high altitude. Climbers may also deprive themselves of sleep in an effort to minimize time spent in a hazardous environment or to avoid having to bivouac overnight. Rescuers may also need to move rapidly, but they must consider the increased risks and decreased performance that may result from a lack of adequate food, water, or sleep. Lack of sleep may lead to poor judgment that can jeopardize the safety of a rescue operation. If there are enough rescuers, members can rotate in and out of active roles so that they can eat, drink, and rest. Sleep deprivation is especially dangerous after a rescue has been completed.

HUMAN FACTORS OF VICTIMS It is essential that rescue teams control the victim during technical rescue. Rescue teams should seldom allow the victim to control his or her own ascent or descent, unless the victim is an uninjured stranded climber. Victims in a technical rescue should be placed on systems that are as independent of the subject’s control as possible. Rescuers should monitor and stay with the victim as much as possible. If possible, rescue teams should approach a victim on technical terrain from above or by traversing rather than from below; this reduces the risk of additional rock or debris falling on the rescuers. Victims may cause objects to fall accidentally or sometimes intentionally. Rescue teams approaching from above should attempt to choose a line that does not place the subject in danger of rockfall. The condition of a victim may deteriorate after the arrival of rescuers. The concept of “rescue shock” implies that some victims have succumbed after the arrival of rescuers because they gave up the fight to survive when rescue seemed assured. Although this concept has validity among rescuers, the only evidence seems to be anecdotal and unpublished. However, it is well

EXPERIENCE IN THE ENVIRONMENT Because safety of the rescuers is the first priority during rescue, mountain rescue personnel must be experienced mountaineers and climbers. Experience with mountaineering and climbing comes from repeated trips in the mountains and technical ascents, traditionally with more experienced mountaineers and climbers as mentors. This experience builds confidence as well as the ability to deal with adversity in mountainous terrain. However, experience can also promote a loss of attention to detail and a casual approach to hazards, thus decreasing the perceived risk and increasing the actual likelihood of accidents.

MISSION PLANNING AND RISK ASSESSMENT Mission planning and risk assessment during organized rescue are essentially the same as those during self-rescue. With organized rescue, the plans tend to be more elaborate and the resources greater. However, there are a few considerations that are particular to organized rescue. Rescues in which the victim has died are referred to as body recoveries. If it is known that a mission is a body recovery, the degree of tolerable risk to the rescuers is usually less than that for a mission in which the victim is known or believed to be alive. There should be no time pressure to recover a body; body recoveries can be postponed until conditions are safe. Some body recoveries, because of location, are considered too hazardous for the rescuers ever to attempt, and the mission is cancelled. Examples of such locations are under hanging glaciers and on steep faces of unstable rock. Team Safety Planning and risk assessment in organized rescue are mostly the responsibility of the leaders, but every member of the team should be aware of safety hazards and not assume that the leaders have noticed them. Many accidents—especially in technical rescue—can be prevented if team members look out for potential hazards and communicate their concerns to the leaders. Technical systems should be checked and rechecked by each participant before and during use to make sure an unsafe situation has not developed. Team members should be careful to not act beyond their comfort zones and not perform tasks for which they are not qualified based on training and experience, especially during the operation of technical rescue systems. Aircraft Safety Rescuers on board both fixed-wing aircraft and helicopters should be aware that everyone on board represents an extra set of eyes and ears. Rescuers should never assume that the pilot or crew has seen something that they have seen, such as an obstacle to flight or something out of place in the aircraft. Rescuers should know how to use the intercom system and should point out any hazards they notice. In many helicopter crashes, someone on board saw something that looked wrong but said nothing to the pilot. In one crash, a passenger noticed that the fuel gauge read “empty” but said nothing; the helicopter later crashed as a result of lack of fuel.67

External Influences During organized rescue, external influences can increase risk. Rescue groups sometimes must resist pressure from outside

agencies to deviate from rescue plans. In one spectacular example, the successful rescue of four victims of an airplane crash almost failed when the lead organization on the rescue decided incorrectly that avalanche conditions were too dangerous for the rescuers. It was only through the persistence of the rescuers that the rescue efforts were not prematurely terminated. Government agencies and nongovernmental organizations may have their own agendas that conflict with the objective of rescuing victims in as safe a manner as possible. Family and friends of victims may exert pressure on rescue leaders, and external influences may be amplified by involvement of news media. All of these influences should be managed by rescue leaders and may be turned to the advantage of the rescue efforts. A major problem can be the presence in the wilderness and especially in technical terrain of representatives of government agencies, such as emergency service personnel and lawenforcement officers who are not qualified or suitably equipped to operate in these environments. Other unqualified or unprepared individuals, such as friends and family of the victims and representatives of the news media, may also reach or attempt to reach the rescue site. Whatever their motivation for being on scene, all of these individuals can cause great risk to themselves as well as to the rescuers, and they can interfere with the rescue operation when the rescuers attempt to protect them from harm.36

Planning for Rescue Anyone who ventures into the wilderness should be prepared to assume significant personal responsibility. This is true even for participants in activities that are organized by others. The more remote and inaccessible the destination, the more wilderness travelers must rely on themselves or their own party to provide self-rescue. A certain degree of responsibility is also placed on the organizers to provide care in remote settings. Expeditions and special events (e.g., guided climbing, adventure racing) in remote environments may have both local and traveling guides who provide additional expertise. Guides have the responsibility to lead technical rescue and evacuation of members of their group in case of injury or illness. Local rescue and medical resources may be minimal or entirely lacking. However, if there are local resources available, the expedition should have plans to access them in case they are needed. Organized search and rescue teams have a different purpose than other groups engaged in wilderness activities. They are trained to provide rescue to others, while avoiding the need to rescue their own members. The training includes formal policies and procedures, often involving highly orchestrated responses to specific problems such as rescue from technical climbing routes and avalanche rescue. There are often specific plans for certain high-risk locations, such as individual climbing routes and known avalanche slopes. Rescue teams have access to specialized equipment, and most have a high degree of technical (but often not medical) expertise. There is wide variation in the degree of medical training of mountain rescuers.22 In highly developed areas such as the European Alps, mountain rescue may be fully integrated into an emergency medical services system. Aeromedical helicopters in these areas bring a high level of technical rescue and medical expertise into areas that are otherwise inaccessible, although they may be near major population centers. Most of the helicopters carry a physician and have advanced life support capabilities, including advanced airway equipment and cardiorespiratory monitoring.9 Even with these advantages, the level of care is limited as compared with that offered in a hospital emergency department or an intensive care unit.

TEAM TRAINING Ideally, any organized group that is going to a wilderness location should train together before departure. This applies especially to expeditions and to organized search and rescue teams. For packaged expeditions and adventure races, this may not be possible, because group members often come from disparate geographic areas. Training and practice can occur after the group 733

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

established that the rescuers’ actions can cause deterioration of victims. Movement of hypothermic patients can precipitate ventricular fibrillation. Placing some patients in an upright position rather than a horizontal one can cause decreased venous return to the heart, which can lead to hypotension or cardiac arrest.37,39 Horizontal positioning during rescue is especially important for immersion victims.23,38,41,72,73 Victims may be mentally ill, under the influence of drugs, or agitated as a result of illness (e.g., hypoglycemia) or injury (especially head injury). In all of these cases, there is an increased risk of injury to the rescuers from patients striking out or even throwing rocks. Victims may also have weapons, including knives and guns, although it is rare for this to be an issue during a technical rescue.

PART 5  RESCUE AND SURVIVAL

assembles in a remote location, either in a nonwilderness location before going to the wilderness or during the trip itself before encountering specific technical risks. For organized search and rescue, members are expected to possess standard skill sets based on their roles and responsibilities. Members acquire these skill sets and are usually tested for competency in practice environments before they are involved in actual missions. The actual structure and sponsorship of these organizations vary widely among and often within countries.

ROLE OF THE MEDICAL DIRECTOR Medical oversight of technical rescue is best performed by a medical professional, usually a physician, who is knowledgeable about wilderness medicine and also understands the technical situations in which care will be provided.47 Ideally, the medical director will train with the team. In some situations, the medical director might be at the scene and provide or coordinate medical care59; in others, the medical director may provide consultation remotely. However, because communication problems are inherent in technical rescue, most of the medical direction will be offline in the forms of guidelines and standing orders. The medical director is responsible for quality assurance and improvement. These processes include training and retrospective evaluation of the decisions and care that occurred during rescue. Missions are usually followed by an immediate debriefing and, later, by a formal critique.

Patient Care in Wilderness and Technical Environments PRIORITIES The priorities of wilderness and mountain rescuers are to provide the best possible patient care while limiting risk to themselves and their patients. Often the best possible care will be that which is adequate to stabilize patients and simply treat pain. Rapidly reaching and evacuating patients may also be important, but these should be secondary priorities after safety and adequately stabilizing patients for transport. After they reach the patient, rescuers should assess and treat the patient and plan the evacuation based on the patient’s condition and resources available. Rescuers on scene may have to wait for better weather conditions or for more personnel and equipment before an evacuation can be safely undertaken. Use of a litter or other specialized equipment may be desirable or sometimes mandatory for patient safety and comfort, but these will increase the resources required to evacuate the patient.

LIMITATIONS Participants on wilderness trips should be aware of the risks of wilderness travel and should realize that medical care will be limited. It has often been stated that medical care in the wilderness is the “art of the possible.” Medical providers, no matter how well trained and qualified, will not be able to provide the same level of care in a wilderness environment as they can in less austere settings. This applies even to highly trained rescue physicians on aeromedical helicopters in Europe. Because diagnostic and therapeutic equipment is limited in the wilderness, medical judgment and decision making are more difficult and more crucial than in the usual urban medical settings. Safety concerns may limit treatment. As in all prehospital care, the rescuers may need to remove patients and themselves from a hazardous environment before they can provide even the most urgent medical care. In this way, medical care in the technical environment resembles combat casualty care. Only a few interventions (e.g., opening the airway, stopping extremity bleeding with a tourniquet) may be feasible during the initial rescue.

INITIAL PATIENT ASSESSMENT AND TREATMENT Patient assessment is a critical skill, but in austere technical environments, it must be modified from the usual practice. As in 734

combat casualty care,11 the diagnosis of hypovolemic shock may be based on mental status rather than measurement of blood pressure. The patient should seldom be exposed in technical environments. To remove clothing involves the risk of hypothermia in cold conditions. History and a very limited physical examination are used for diagnosis until the patient is placed on board an aeromedical aircraft or brought to a clinic or hospital. Initial assessment is usually limited to finding problems that require emergency treatment, including airway compromise, breathing problems, external bleeding, and limb-threatening injuries such as fractures and dislocations. Initial treatment is directed at treating these life- and limb-threatening problems. Although advanced life support prioritizes airway, breathing, and circulation in that order, it may occasionally be necessary to stop brisk bleeding during the initial examination before addressing the airway. Direct pressure and tourniquets can both be applied in a few seconds to stop blood loss and thereby increase survival. In practice, this is seldom useful in technical environments, because care is not usually immediate.

RESUSCITATION During mountain rescue, resuscitating patients without apparent vital signs is usually futile, with the exception of hypothermic patients in whom asphyxia did not precede hypothermia.7,8,33,52 Hypothermic patients may have vital signs that are impossible to detect without cardiac monitoring. In the absence of cardiac monitoring, hypothermic patients without apparent vital signs who can receive definitive care within 3 hours should receive ventilatory support and rewarming measures only.15 If definitive care is not expected within 3 hours, aggressive resuscitation measures should be started, assuming that it is safe to do so and that they will not need to be interrupted. Resuscitation efforts should be terminated after 30 minutes if they have not been successful. If cardiac monitoring is available, resuscitation efforts should follow standard advanced life support guidelines.

AIRWAY AND BREATHING Airway management in technical terrain is usually more difficult than in less austere settings. Initial ventilation by bystanders will be by mouth-to-mouth ventilation. This may be all that is necessary to treat patients with respiratory arrest caused by lightning strikes.89 Rescuers can use bag-valve-mask ventilation, but, unless they have sufficient training and regular practice, they will be more effective at using mouth-to-mask ventilation.54 The use of alternative airways such as the Combitube, the King LT, the Laryngeal Tube, and the laryngeal mask airway (e.g., LMA, LMA Supreme) is revolutionizing airway management in emergency medical services,56 and is assuming a greater role in technical environments. Recognition that protection from aspiration may not be significantly different between these airways and the “definitive” endotracheal tube—in combination with the known difficulties and hazards of endotracheal intubation in prehospital settings—may continue to drive the transition away from endotracheal intubation and toward the use of alternative airways.14 At the same time, videolaryngoscopy (e.g., GlideScope) may slow or reverse this trend in aeromedical care.3 There are a number of tricks of the trade for endotracheal intubation using a standard laryngoscope. One trick that can be useful in confined areas (e.g., a rock ledge) is for the rescuer to kneel over the patient’s chest and intubate with the laryngoscope while straddling the patient. This is a common technique in emergency medical services, and it is sometimes referred to as the ice-axe technique or inverse intubation. When intubating on snow, one technique is to put a blanket or another cover over the rescuer’s head and then let the eyes adapt to the relative darkness before intubating.76

CIRCULATION AND CONTROL OF BLEEDING Driven by military experience in Afghanistan and Iraq, the use of tourniquets18 and hemostatic dressings5,90 has become more widespread in civilian prehospital care for controlling external bleeding. Although tourniquets can be improvised, it can be

TREATMENT OF PAIN “Analgesia at the scene of an accident is a human right.” —URS WIGET, PAST PRESIDENT OF THE INTERNATIONAL COMMISSION FOR MOUNTAIN EMERGENCY MEDICINE77

Pain management is an important part of patient care in any environment, including combat casualty care and technical rescue. In addition to providing comfort for the patient, effective pain management may allow a patient who otherwise would not be able to do so to self-rescue. Opiates are the mainstay of pain control.77 In the past, they have been given by the intravenous, intramuscular, and oral routes, but some agents can now be given by other routes. Fentanyl can be given through the oral mucosa (i.e., a “fentanyl lollipop”) or intranasally. Both transmucosal routes offer rapid onset of pain relief. Ketamine can also be used for pain relief or for procedural sedation.4,20 It can be used to produce dissociative anesthesia or at lower doses to allow for a reduction in opiate doses (i.e., opiate sparing). Ketamine can be given intravenously, intramuscularly, or intranasally. The use of regional anesthesia to control pain and facilitate reduction of dislocations in the field is more widespread in Europe than elsewhere. Many “emergency doctors” in Europe are anesthesiologists whose training includes the use of regional blocks. Wider use of regional anesthesia in mountain rescue has the potential to offer greater pain relief than do opiates, with fewer side effects.17 For example, a femoral block could markedly reduce pain from a lower extremity fracture such as a femur or tibia fracture during a prolonged evacuation.

PROLONGED CARE AND TRANSPORT Although it is not unique to technical terrain, prolonged care of seriously ill or injured patients with limited medical resources poses a distinct set of problems and perhaps an increased risk of morbidity and mortality. Even if airway, breathing, and circulation can be stabilized, it may be a challenge to maintain vital

functions. Supplies of oxygen and medications, including medication to relieve pain, may be limited. Injuries that cause ischemia of an extremity (e.g., vascular injuries, compartment syndromes) can cause loss of digits, hands, feet, or an entire limb if they are not corrected within hours. The common advice for life- and limb-threatening problems in wilderness settings is generally to evacuate the patient rapidly to definitive care. However, this is not always possible (Figure 38-34, online). Unconscious patients whose airway is not protected by endotracheal intubation or by alternative airways should be placed in the recovery position (i.e., the lateral decubitus position with the head turned so that vomiting will not result in aspiration). An oral or nasal airway may be helpful to prevent hypoventilation caused by obstructed breathing. Neither endotracheal intubation nor alternative airways completely eliminate the risk of aspiration, but there is evidence that all provide similar degrees of protection.14 For patients who are not breathing spontaneously, it can be a challenge to maintain adequate ventilation. Hypoventilation, hyperventilation, and inadequate oxygenation are all hazards of ventilation, especially if mechanical ventilation and monitoring capabilities are not available. A nasogastric or orogastric tube is helpful and sometimes essential to decompress the stomach; otherwise, ventilation may be severely limited by stomach distension. Bleeding from external sources can be controlled by direct pressure or by using a tourniquet, but hemorrhage from internal organs such as the liver and spleen is not amenable to nonsurgical intervention. Limited volume resuscitation to maintain blood pressure at low but life-sustaining levels has the potential to limit internal bleeding.75 For patients with head injuries, hypotension can be as deleterious as hypoxemia to the outcome of traumatic brain injury. Fluid resuscitation may be essential to prevent hypotension. The use of small-volume intravenous or intraosseous therapy with hypertonic fluids may be beneficial.75 Although the advantages of small-volume therapy remain controversial, limiting the weight of fluids to be carried is an advantage in most wilderness settings. Unconscious head-injured patients should be protected from hypoxemia as well as hypotension and should be maintained as much as possible with the head elevated 30 degrees to maintain cerebral perfusion by decreasing the risk of increased intracranial pressure without decreasing cerebral blood flow. Intravenous and intraosseous fluids are the best options for preventing hypovolemia in unconscious patients. Intravenous lines can be difficult to place, especially in cold conditions. Intraosseous access is an alternative. In desperate situations, fluid can be given and absorbed rectally (i.e., proctoclysis) through any suitable tube.6 Unconscious patients will also require bladder drainage, preferably using an indwelling catheter. For patients without head injuries, permissive hypotension has the potential to limit internal hemorrhage by preventing dislodgment of intravascular thrombi caused by increased hemodynamic pressure. In theory at least, these thrombi may be preventing hemorrhage from an injured vessel. This is a controversial area that has not been well studied, but many case reports suggest a survival benefit.70 If at all possible, fluid administered in wilderness settings should be heated to 40° C (104° F) or at least to body temperature. A number of methods are available to accomplish this in cold wilderness environments.57 Fluid should be given in boluses that have been titrated to effects, especially in the acute setting. Intravenous lines (i.e., maintenance fluids or drips) are difficult to keep warm, although specialized fluid warmers and insulated tubing are available for wilderness use. Even with the best precautions, it is possible for intravenous lines to freeze in cold environments. The best method is to give boluses of warmed fluids and to preserve intravenous or intraosseous access sites between boluses using saline locks. Limb-threatening injuries are addressed by attempting to limit ischemia. Fractured bones should be realigned as well as is possible, and dislocations should be reduced. Patients with open fractures should receive intravenous antibiotics, if available. Compartment syndrome may require fasciotomy despite increased risk of infection. If bleeding cannot be controlled without the use of a tourniquet, there is a risk that the limb will be lost as 735

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

difficult to make an effective tourniquet quickly. Commercially made tourniquets that are approved for military use are small and lightweight, and should be included in all but the most basic medical kits on wilderness trips. Hemostatic agents are less clearly beneficial in civilian practice. However, their use can be considered in certain wilderness situations. The U.S. military evaluates and approves hemostatic agents. Only agents that are currently approved by the U.S. Armed Forces should be used. Internal bleeding is treated surgically, with two important exceptions: pelvic fractures and femur fractures. If the patient is conscious and coherent, cerebral circulation is acceptable. There is no need to check carotid, femoral, or radial pulses to estimate blood pressure. Pelvic fractures should be stabilized by a pelvic wrap.21 When checking for pelvic instability, rescuers should remember that increased bleeding is caused by opening the posterior pelvis (i.e., like an open book). Therefore, it is better to check for instability not by “opening the book” but instead by closing it. Only a single check should be performed to avoid further trauma to the circulation in an unstable pelvis. Femur fractures can be stabilized by traction devices. If the femur fragments are overriding, there is theoretically a globular space into which hemorrhage can occur. If the femur is straightened, this space is converted to a cylinder with a much lower volume. This is thought to tamponade the bleeding and limit further blood loss, but it is not clear if this actually occurs. It is difficult to apply improvised traction in the field. The Kendrick Traction Device is a commercially available lightweight device for providing traction on the femur. Traction devices require an ankle hitch that can cause skin necrosis. There is no convincing evidence that traction devices for femur fractures are better than simple splinting, although they may increase comfort. Many patients with femoral injuries have contraindications to the use of traction devices. If a traction device is not used, patients with femur fractures can be treated using a vacuum mattress or another splint.21

PART 5  RESCUE AND SURVIVAL

a result of ischemia. The time usually quoted for irreversible ischemia is 6 hours, but the limb may remain viable for longer. If the alternatives are fatal hemorrhage or loss of limb, the choice is clearly to maintain the tourniquet for as long as necessary to prevent fatal hemorrhage. Patients with surgical conditions are usually not allowed to eat or drink anything to prepare them for surgery. This can pose problems during prolonged transport, because it can lead to inadequate caloric intake and hypovolemia. If intravenous fluids are available, they can be used to prevent hypovolemia, but will not provide sufficient calories. If there is no contraindication (e.g., bowel perforation), patients may be allowed to eat and drink during prolonged transports. To prevent skin ischemia leading to decubitus ulcers, patients should not be maintained on backboards (even padded ones) for any length of time. The safe parameters are not known, but even 1 hour is almost certainly too long. Unconscious patients who are not being actively transported can be maintained on soft surfaces with frequent turning, which is how they would be managed in an intensive care setting. During active transport, a vacuum mattress is the best solution currently available,58 especially if there is a question of unstable spinal injury. Ill and injured patients who are immobile lose heat rapidly and should be carefully protected from hypothermia. This is especially important for unconscious patients and for those with neurogenic shock. In neurogenic shock, autonomic control is lost in the lower extremities. In addition to hypotension from venodilation, this leads to rapid heat loss. Other details of the care of unconscious patients include eye protection with removal of contact lenses and protection of the cervical spine. Cervical collars can cause localized pressure necrosis of skin if they are maintained for several days.49 During actual transport, a cervical collar may not be necessary if a properly applied vacuum mattress is used. A risk of not using a cervical collar is that cervical spine protection may not be maintained by a receiving hospital when the vacuum mattress is removed. During prolonged waiting, cervical spine protection should be maintained without a rigid cervical collar with the use of padding or an improvised collar that is repositioned on a regular basis. The SAM splint collar is practical for this purpose.

ALTITUDE CONSIDERATIONS DURING RESCUE When technical terrain occurs at high altitude, there is an increased risk to rescue personnel. Both human and helicopter performance is decreased at high altitudes (Figure 38-35). The reduced performance of helicopters may severely limit payloads as compared with sea level and thus limit the ability to carry medical personnel, equipment, and supplies. The service ceilings of helicopters and margins of safety can be improved by

removing unnecessary equipment to decrease payload weight. Unfortunately, “unnecessary” equipment and personnel may be medical equipment and personnel. Many helicopters that are suitable for rescue at low altitudes are dangerous at best at high altitudes, especially when carrying a full complement of crew and equipment. The crash of a Pave Hawk helicopter during a rescue on Mt Hood in 2002 is an example of the danger of using certain helicopters at high altitudes. In addition to human performance being decreased at high altitude,30 there is a risk of high-altitude illness for unacclimatized rescuers.87 It is occasionally necessary to use unacclimatized rescuers at more than 2500 m (8200 feet). In such cases, it is advisable to limit the amount of time spent by unacclimatized rescuers at high altitudes and to have a contingency plan for descent. In most rescue situations, gradual ascent is impractical. For areas in which ground rescues take place at high altitude, rescue personnel should be based at high altitude. In Denali National Park, in which the majority of rescues take place above 4500 m (14,800 feet),27 the rescuers are based at a camp at 4300 m (14,100 feet). However, the helicopter pilots and other crew are based near sea level. The pilots and crew breathe supplemental oxygen when flying higher than 3000 m (9800 feet). The oxygen sets can be removed from the aircraft in case the pilot or another member of the crew needs to leave the helicopter. Rarely, when special technical skills are needed and there is no qualified person at the high camp, short-haul rescues have been carried out by a rescuer who is based at low altitude. In case the helicopter cannot return to low altitude promptly as a result of technical difficulties or weather, there is an “escape plan” for personnel who are based at low altitude; this plan involves the use of oxygen, prophylactic medications, and descent by ground, if possible, during a specified time period.87

SUSPENSION TRAUMA If a climber falls and is held motionless in an upright position by the climbing harness, blood pools in the lower extremities; this can lead to loss of consciousness and death.34,62 This problem is referred to as suspension trauma or harness hang syndrome. Much has been written about this problem but it is based on little research. Climbers who are able to move while suspended in their harnesses can hang upright in a free position (i.e., suspended in air) for an indefinite period without ill effects. Fallen climbers who are suspended vertically have died, presumably from circulatory collapse caused by reduced central venous return.64 An alternative mechanism that involves mechanoelectrical feedback causing a fatal dysrhythmia13,60 has also been proposed; this has reportedly occurred in a matter of minutes in some cases. Prompt rescue is considered essential in cases of suspension trauma.61 This is generally accomplished by lowering the patient to the ground, if possible. Some clinicians have recommended against placing patients in a horizontal position because of the theoretic risk of acute heart failure caused by sudden volume overload or acute cardiac dysrhythmia. There is no evidence that placing a patient in a horizontal position is dangerous.78 On the contrary, in addition to the fact that it is difficult to manage patients in an upright position, some patients may be hypovolemic as a result of internal injuries and require volume resuscitation. Keeping a hypovolemic patient in an upright position would be contraindicated. There is a case report of an industrial worker who was rescued alive after 20 minutes of suspension in a safety harness who reportedly died in the hospital as a result of internal hemorrhage.78

USE OF EXTRICATION DEVICES FOR CREVASSE RESCUE

FIGURE 38-35  Crashed helicopter near Everest Base Camp, Nepal. (Courtesy Ken Zafren.)

736

Glacier travelers are sometimes injured by falling into crevasses. When a patient who has fallen into a crevasse has a suspected spinal injury, the best method of extrication is to immobilize the patient horizontally on a litter using a vacuum mattress and cervical collar.86 Use of cervical collars for distracting cervical injuries (i.e., injuries in which ligamentous disruption allows widening of the intervertebral joints) has recently been questioned.2 When

Afterword There have been joys too great to be described in words, and there have been griefs upon which I have not dared to dwell; and with these in mind I say, Climb if you will, but remember that courage and strength are nought without prudence, and that a momentary negligence may destroy the happiness of a lifetime. Do nothing in haste; look well to each step; and from the beginning think what may be the end. —EDWARD WHYMPER82

APPENDIX 

TECHNICAL RESCUE MEDICAL KIT This kit—used by Will Smith, MD, EMT-P, Medical Director/Team Leader, Teton County Search and Rescue, Jackson, Wyo, USA, who is also one of the authors of this chapter—is presented as an example of a technical rescue medical kit. The contents of a medical kit are matters of personal and institutional preferences. No single set of contents can be appropriate for all providers in all practice settings. This kit is modular. The various components can be quickly sorted and assembled to make an appropriate kit for the anticipated rescue situation. The kit is designed to be carried in a rescue pack, and the entire kit may be used during a helicopter insertion. A long walk in or technical insertion will limit the amount of medical gear that can be carried in addition to personal and technical gear (Figures 38-36 to 38-39, online).

TECHNICAL RESCUE MEDICAL KIT (15 KG [33 LBS]) Medication Bag: 2—Epinephrine 1 : 1000 (1 mg/mL) ampoule 1—Epinephrine 30 mg/30 mL vial 3—Prednisone 20-mg tablets 1—Diphenhydramine 50 mg/mL vial 2—Etomidate 20 mg/10 mL vials intravenous formulation 1—Ketamine 500 mg/5 mL vial 1—Midazolam 50 mg/10 mL vial 1—Succinylcholine 200 mg/10 mL vial (stored in refrigerator) 1—Rocuronium 50 mg/5 mL vial (stored in refrigerator) 2—Vecuronium 10 mg vial 1—Dexamethasone 20 mg/4 mL vial 2—Cefazolin 1 gram 2—Ketorolac 30 mg/mL vial 4—Chewable aspirin 81-mg tablets 2—Hydromorphone 2 mg/mL vial 2—Fentanyl 100 mcg/mL ampoule 1—Naloxone 4 mg/10 mL vial 1—Metoclopramide 10 mg/2 mL vial 1—Promethazine 25 mg/1 mL vial 1—Ondansetron 4 mg/2 mL vial 2—Ondansetron 4-mg sublingual dissolving tablets 2—Albuterol 3 mg/ipratropium 0.5 mg/3 mL for nebulizers 5—10 mL saline flushes 10—Alcohol prep pads

Assorted syringes: 3—1 mL (with needle), 4—3 mL (with needle), 1—10 mL, and 1—20 mL 2—Nasal Mucosal Atomizer Device (MAD) 10—18-gauge needles 10—Syringe caps Intravenous Bag: 1—1000 mL normal saline intravenous solution 1—10 drip intravenous drip tubing 2 each size—Intravenous catheters: 14 gauge, 16 gauge, 18 gauge, and 20 gauge 1—EZ-IO handheld driver and adult needles (15 gauge × 25 mm) 2—Saline lock tubing 2—10-mL normal saline flushes 1—Sharps container 2—Nonlatex intravenous tourniquets 4—Adhesive strips 10—Alcohol prep pads 1—11" tape roll 1—Occlusive dressing for intravenous site 1—Intravenous pressure bag Miscellaneous Bag: 1—Lidocaine 2%, 30-mL vial 1—Lidocaine 2% with epinephrine 1:100,000, 30-mL vial 1—Bupivacaine 0.5%, 50-mL vial 1—Scalpel No. 11 blade 2—11" tape rolls 2—1" Coban nonstick bandages 1—Cavit tube, 7 g (dental) 1—Dental cement kit 1 each size—Steri-Strips: 0.25 and 0.5 inch 1—Stapler with No. 5 staples 1—Burn gel package 1—Rhino Rocket, 7.5 cm for epistaxis 2—18-gauge intravenous catheters 2—OpSite occlusive adhesive bandage 1—Tetracaine eye anesthetic drops 3—10-mL normal saline flushes 5—18-gauge needles 5—27-gauge needles Assorted syringes: 3—10 mL, 3—1 mL, and 2—20 mL Front and Top Pockets: 1—Notepad and pencils, pens, or markers 1—Head lamp 1—Ibuprofen 200-mg tablets (bottle #100) 1—1" tape roll 5—Charcoal hand warmers 2—Bottles of alcohol hand sanitizer 10—pairs of nonsterile gloves (nonlatex) 3—Benzoin swabs 10—Triple antibiotic packets 4—Small, clear, zip-top bags 4—Wooden tongue blades 2—Emesis bags 2—Trauma shears or scissors 1—Pocket mask (Nu Mask) 1—Package of 20 triage tags 1—Package of sanitary wipes Bandaging Side Pocket: 2—4" elastic bandages 2—4" Kerlix bandages 2—10-packs of 4 × 4 gauze 2—5 × 9 absorbable pads 1—Triangle bandage 1—Tourniquet Miscellaneous Side Pocket: 1—Adult blood pressure cuff 1—SAM splint 1—Handheld nebulizer 1—Intravenous pressure bag 1—Strobe light signal device Main Compartment: 1—1000-mL normal saline intravenous bag 1—10-drip intravenous tubing 737

CHAPTER 38  Technical Rescue, Self-Rescue, and Evacuation

horizontal stabilization cannot be accomplished in a narrow crevasse, the patient should be stabilized in a vertical position. The Kendrick Extrication Device has been tested for use in crevasse extrication, and it maintains support of the head, neck, and torso.86 The patient is lifted using a climbing harness rather than with the straps attached to the extrication device. An extra suspension line at the top of the device may reduce pressure on the spine. This line should be attached to the main line with an adjustable system (e.g., ascender, Prusik), and it may need to be adjusted during the extrication process. The patient should be repositioned from an upright to a horizontal position as soon as possible after extrication.

1—Size 4 King LTSD supraglottic airway 1—Asherman Chest Seal 1—16F Foley catheter 1—Foley leg bag 2—Adult diapers 1—Cervical collar (adjustable adult size) 1—Inflatable bag-valve-mask device 1—Adult EZ-IO battery driver with 2—needles (15 gauge × 25 mm) 1—Handheld suction device Airway Bag: 1—Gum elastic bougie 1—Comfit endotracheal tube holder 1—Stethoscope 1—Pocket pulse oximeter with extra batteries 1—Magill forceps (large) 1—Adult endotracheal tube stylet 1 each size—Endotracheal tubes: 5.0, 6.0, 7.0, 7.5, and 8.0 1—Nasogastric tube (18F) 1—End tidal carbon dioxide colorimetric intubation confirmation device 1—Eye protection shield or face mask 1—3-0 silk suture on straight needle (SC-2) 1—Ventilator tubing with one-way valve for remote ventilation 2—14 gauge × 3.25" needles for chest decompression 3—Oropharyngeal airways (assorted adult sizes) 3—Nasopharyngeal airways (30F and 32F) 2—10-mL syringes 1—Laryngoscope handle with AA batteries 1—Macintosh No. 4 stainless steel blade 1—Miller No. 3 stainless steel blade 1—Scalpel No. 11 blade 1—Chloraseptic swab

1—Povidone–iodine swab 1—BAAM whistle device for nasal intubation facilitation 2—Petrolatum vaseline gauze pads, 3 × 9" 2—Heimlich valve and tubing Oxygen Kit (10 kg [22 lbs]): 1—Carbon Fiber DD-lite oxygen tank (up to 3000 psi) 1—Adult nasal cannula 1—Oxymizer nasal cannula 1—Nonrebreather face mask 1—Extension tubing and adapter 1—Pelvic binder 1—Spider straps 2—Oropharyngeal airways (adult sizes) 1—Large charcoal blanket (Ready-Heat) 1—Size 4 King LTSD Supraglottic airway 1—Bag-valve-mask device (traditional) 1—Bag of nitrile gloves (appropriate provider size) 1—Handheld nebulizer 1—SAM splint 1—Kerlix gauze, 4" 1—Triangle bandage 1—Pocket mask 1—Trauma shears or scissors

MOUNTAIN RESCUE RESOURCES International Commission for Alpine Rescue: http://www.ikar-cisa.org International Society of Mountain Medicine: http://ismmed.org Mountain Rescue Association (North America): http://www.mra.org

REFERENCES Further readings and complete references used in this text are available online at www.expertconsult.com.

CHAPTER 39 

Litters and Carries DONALD C. COOPER AND TIMOTHY P. MIER

Every search and rescue event goes through a series of four consecutive phases. These phases are illustrated by the acronym LAST (locate, access, stabilize, and transport). This process ends with the movement of the patient (or patients) from the scene to either a medical facility or an area of comfort and safety (transport)7 (see Chapter 37). In the United States, the term stretcher suggests a flat, unsophisticated frame covered with canvas and used for carrying the sick, injured, and deceased short distances. The term litter can mean the same thing but usually suggests an apparatus specifically designed to immobilize and carry a patient longer distances. Over the years, the subtle differences in the terms have been lost, and users have gravitated to one or the other. In the United States, the term litter is used to describe all manner of rescue conveyance. In Great Britain, however, the preference is to use the term stretcher to describe the same devices. In this chapter, the two terms are used interchangeably.

Size-Up To select the best method for getting a patient to definitive care, the rescuer must make a realistic assessment of several factors. Scene safety is the initial priority. The necessary evaluation, called the size-up (Box 39-1), involves a (usually hasty) determination of whether the victim, rescuer, or both are immediately threatened by either the environment or the situation. Proper 738

immobilization and patient packaging are always preferable, but sometimes the risk for aggravating existing injuries is outweighed by the immediate danger presented by the physical environment. In such a situation, the rescuer has little choice but to immediately move the patient to a place of safety before definitive care is provided or packaging is completed. Evacuation options are limited by three rescuer-related variables: (1) the number of rescuers, (2) their levels of fitness, and (3) their technical abilities. Carrying a victim, even over level ground, is an arduous task. At an altitude where just walking requires great effort, carrying a victim may be impossible. The specific rescue situation or environment encountered may present challenges beyond the capability of the available rescuers. Complex rescue scenarios requiring specially trained personnel and special equipment are called technical rescues and often involve dangerous environments, such as severe terrain, crevasses, avalanche chutes, caves, or swift water. To avoid becoming victims themselves, rescuers must be realistic when evaluating their abilities to perform these types of rescues.

Drags and Carries The most fundamental and expedient method of transporting an ill or injured person is by dragging or carrying him or her. Although these methods of transportation are far less than ideal and may not meet standard care criteria, the urgency of the

For online-only figures, please go to www.expertconsult.com

CHAPTER 39  Litters and Carries

BOX 39-1  Evacuation Size-Up Factors • What are the scope and the magnitude of the overall situation? • Are there immediate life-threatening hazards? • What is the location, and how many victims are there? • What is the patient’s condition? Is the subject able to assist rescuers? • No injury (able to walk unassisted) • Slight injury (able to walk unassisted) • Slight injury (assistance required to walk) • Major injury (requires considerable attention and assistance) • Deceased • Is there a need for technical rescue? • Is the scene readily accessible? • What rescue resources (including rescuers and equipment) are available? • How far must the patient (or patients) be transported? • Are ground or air transport assets available?

situation may outweigh the risks involved. The process can be physically demanding, and rescuers can quickly become fatigued to the point of hazard. Therefore other options often should be considered before a victim is moved, especially a long distance. A drag or carry may be the best option when a person cannot move under his or her own power, injuries will not be aggravated by the transport, resources and time are limited, the need for immediate transport outweighs the desire to apply standard care criteria, the travel distance is short, or the terrain makes the use of multiple rescuers or bulky equipment impractical. A blanket drag (Figure 39-1, A) can be performed on relatively smooth terrain by one or more rescuers rolling the victim onto a blanket, tarp, or even a large coat and pulling it along the ground. This simple technique is especially effective for rapidly moving a person with a spinal injury to safety, because the victim is pulled along the long axis of the body. In extreme circumstances, the fireman’s drag (Figure 39-1, B) can be used. In this type of drag, the rescuer places the bound wrists of the victim around his or her neck, shoulders, or both and crawls to safety.

A

B FIGURE 39-1  A, Blanket drag. B, Fireman’s drag. Both techniques are intended to be used when expeditious transport over a short distance is required. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 5, New York, 2009, Mosby.)

FIGURE 39-2  Classic fireman’s carry: a single rescuer technique for short-distance transport only. The rescuer must use his or her legs for lifting. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 5, New York, 2009, Mosby.)

A carry should be considered only after it is confirmed that the victim cannot assist rescuers or travel on his or her own. Beyond simply lifting a person over one’s shoulder in a fireman’s carry (Figure 39-2) or acting as a human crutch, a more efficient one-person carry can be accomplished by using equipment, such as webbing, backpacks, coils of rope, or commercial harnesses. Equipment-assisted carries are particularly effective when an injured climber or hiker must be evacuated across a short distance over rough terrain or when a person must be quickly removed from a hazardous environment. In the simplest equipment-assisted carry, 4.5 to 6 m (14.8 to 19.7 feet) of webbing is wrapped around the victim, who is then “worn” like a backpack by the rescuer (Figure 39-3). Similarly, a split coil of climbing rope or a backpack (also called a rucksack) can be fashioned into a seat in which the patient sits while carried by the rescuer. A single-rescuer split-coil carry (Figure 39-4) requires only equipment already carried by a climber or mountaineering group and works well for conscious patients without severe injuries. However, the patient’s legs hang close to the ground, especially during downhill carries and when the rescuer is shorter than the patient, and together the rescuer and patient can carry only one rucksack. A similar method, the rucksack carry, simply uses a rucksack as the slinging device (Figure 39-5). The rucksack is placed on the patient with the patient’s legs placed through the shoulder straps and over the waist straps if present. The rescuer then positions the patient on his back (generally with assistance), then the shoulder straps of the pack over his shoulders, and then stands. This method places a victim high relative to the rescuer’s center of gravity; stability of both patient and rescuer can be a factor. This method is particularly useful when used on a patient with a lower limb injury or other situation where he or she is conscious and able to sit up and hold onto the rescuer. It also allows both the rescuer and patient to carry rucksacks. Methods and/or devices that attach a patient in a sitting position to the back of a rescuer are sometimes referred to as Tragsitz (German for “carry seat”) methods and/or devices.13 Although original Tragsitz devices were made from canvas and specifically designed to carry a patient securely and comfortably, they can also be improvised, as in the split-coil and rucksack carries, or commercially produced using modern, stronger, and more robust fabrics (Figure 39-6). For carrying infants and small children, a papoose-style sling works well and can easily be constructed by the rescuer, who ties a rectangular piece of material around his or her waist and neck to form a pouch. The infant or child is then placed inside the pouch, which can be worn on the front or back of the rescuer’s body. 739

PART 5  RESCUE AND SURVIVAL

FIGURE 39-3  Web sling (tied into a loop) used to carry a victim. The rescuer must use his or her legs for lifting.

If two rescuers are available, additional and often superior options for carrying a patient are possible. One option consists of two rescuers forming a seat by joining their hands or arms together. The patient sits on the “platform” and holds on to the rescuers for support (Figure 39-7). It is difficult to cover a long distance or rough terrain when using this technique, and the patient must be conscious and able to sit up and hold on. A coil of climbing or rescue rope can be used to form a tworescuer split-coil seat, with each rescuer slipping a side of the rope coil around his or her outside shoulder (Figure 39-8). The patient then sits on the “seat” formed by the rope. A similar approach involves using padded ski poles or stout limbs tied together and supported by backpacks worn by rescuers. The victim sits on the supported poles with his or her arms around the rescuers’ shoulders. If the poles are properly padded and securely attached to sturdy rescuers, this technique can be quite

FIGURE 39-4  Single-rescuer split-coil carry. Note that the coil can be tied in front of the rescuer, and the wrists of the victim can be bound and wrapped around the rescuer’s neck for more stability.

740

comfortable for both the rescuer and victim. This approach requires gentle terrain without narrow trails. Spine injuries generally prohibit the use of drags or carries because the victim cannot be properly immobilized, but drags or carries may be acceptable when immediate danger outweighs the risk for aggravating existing injuries. Drags are particularly useful for victims who are unconscious or incapacitated and unable to assist their rescuer (or rescuers) but may be uncomfortable for conscious victims. When a drag is used, padding should be placed beneath the victim, especially when long distances are involved. The high fatigue rates of rescuers makes carries less attractive options when long distances are involved.

Litter Improvisation The simplest improvised litter is made from a heavy plastic tarpaulin, tent material, or large polyethylene bag (Figure 39-9). By wrapping the material around a rock, wadded sock, or glove and securing it with rope or twine, the rescuer can fashion handles in the corners and sides to facilitate carrying. The beauty of this device is its simplicity, but it can be fragile, so care must be taken not to exceed the capability of the materials used. As an additional precaution, all improvised litters should be tested with an

FIGURE 39-5  Backpack or rucksack carry.

CHAPTER 39  Litters and Carries

FIGURE 39-6  Manufactured Tragsitz harness in use.

uninjured person before being loaded with a victim. This type of nonrigid, “soft” litter can often be dragged over snow, mud, or flat terrain but should be generously padded, with extra clothing or blankets placed beneath the victim. Three or four filled rucksacks (depending on the size and shape of the patient) can also be laid end-to-end—carrying/strap side up—to serve as an improvised litter. Lay the packs on the ground in a straight line with the tops of all the packs oriented in the same direction, and use the shoulder straps to tie them together. Open the waist straps wide and place the patient flat on his or her back (lifted flat by clothes, neck immobilized if necessary) on the packs before tightening the waist straps. The patient’s head should be placed at the end with the top of the packs. Moving the patient safely in this device takes a coordinated effort, one leader, and at least four rescuers. The full

FIGURE 39-8  Two-rescuer split-coil seat.

rucksacks offer support beyond that which is provided by only the packs and their straps, but their weight when full and added to the patient’s weight can be demanding on rescuers. When stopping to rest, rescuers must be sure not to allow the patient to roll over. This method works well for patients who require transport in a supine position, including those who are unconscious or have femur, pelvis, or spine injuries. It also provides superior stabilization in the body axis compared with most other improvised litter options, and it is unlikely to allow the patient to fall out even if a rescuer slips while carrying. A coil of rope can be fashioned into a litter, called a rope litter or clove hitch stretcher, but a 46- to 61-m (150.9- to Clove hitch

Sport socks, hat, etc.

A

B

FIGURE 39-7  A, Four-hand seat used to carry a person. In this technique, the upper body is not supported. B, Alternative four-hand seat that helps support the victim’s back. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 5, New York, 2009, Mosby.)

FIGURE 39-9  Improvised handled soft stretcher.

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FIGURE 39-11  Laying out the rope for an improvised rope stretcher.

FIGURE 39-10  Tying an improvised rope (nonrigid) stretcher.

200.1-foot) climbing or rescue rope is required (Figure 39-10). The rescuer constructs the litter by laying out 16 to 20 180-degree loops of rope in the middle of the length of rope (8 to 10 on each side of center) across an area the desired width of the finished litter (Figure 39-11). The running ends of the rope are used to tie a clove hitch around each of the loops (Figure 39-12), and then the unused portion of rope is passed through the loops and tied off to form a handhold around the peripheral edge of the resulting device (Figure 39-13). The litter can then be padded with clothing, sleeping pads, or similar material. Lateral stability can be added by tying skis or poles to the finished product. Because of its nonrigid construction, this litter offers virtually no back support, can be uncomfortable for patients, and is best suited for patients with injuries that do not require mechanical stabilization or immobilization. One advantage of this device is that items commonly carried on a wilderness or climbing trip are all that are needed to configure it. However, it can take 30 to 45 minutes to construct and can be difficult to get properly proportioned (length and width) unless rescuers are well practiced. Comfort for the victim is limited at best, and therefore the use of this litter is best suited for carries over a short distance.

A

B

FIGURE 39-12  Tie clove hitches around each loop.

Although the idea of this device may seem initially attractive and relatively easy, in reality it takes quite a long time to construct, is easily tied wrong (taking even longer to re-tie), and is uncomfortable for most patients. A sturdy blanket or tarp can be used in combination with ski poles or stout tree branches. The blanket or tarp is stretched over the top of two poles, which are held about 1 m (3.3 feet) apart; tucked around the far pole; and folded back around the other pole. The remaining material lies over the first layer to complete the litter (Figure 39-14). The weight of the patient holds the blanket in place but the weight of the patient also tends to force the poles together and tightly wrap around the patient. This quickly gets uncomfortable for the patient and is best used only for short periods of time. A similar, and in some ways superior, device can be improvised by passing the poles through the sleeves of two heavy, zipped (closed) parkas.

C

FIGURE 39-13  A to C, The unused portion of rope is passed through the loops and tied off to form a handhold around the peripheral edge of the resulting device.

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CHAPTER 39  Litters and Carries

FIGURE 39-14  Improvising a stretcher from two rigid poles and a blanket or tarp.

It may be necessary to transport victims with certain injuries (i.e., spine injuries; unstable pelvis, knee, or hip dislocations) on a more rigid litter. Ski poles, stout tree limbs, or pack frames can provide a rigid support framework for such a device. For example, three curved backpack frames can be lashed together to form a platform (Figure 39-15). Ski poles or sturdy branches then can be fastened to the frames for use as carrying handles, and the platform can be padded with ground pads, sleeping bags, or a similar material. Combining a rope litter with a rigid litter can provide more strength and versatility. The rescuer fashions this type of litter by first building a platform of poles or limbs, using a blanket as in a rigid litter, and placing the victim in a sleeping bag on the platform. The patient and platform are wrapped and secured with a length of rope. Because a mummy sleeping bag is used to encapsulate the victim, this device is sometimes called a mummy

FIGURE 39-15  Pack frame litter. Note that the sapling poles on the litter can be attached to the rescuer’s pack frames to help support the victim’s weight.

FIGURE 39-16  Mummy litter. (From Auerbach PS: Medicine for the outdoors: The essential guide to emergency medical procedures and first aid, ed 5, New York, 2009, Mosby.)

litter. Although this type of litter offers improved support, strength, and thermal protection, careful thought must be given to the physical and psychological effects such a restrictive enclosure may have on the victim (Figure 39-16). If long distances must be traveled or if pack animals are available, a litter may be constructed so that it can be dragged or slid along the ground like a sled. One such device is known as a sledge (Figure 39-17). This litter is fashioned out of two forked tree limbs, with one side of each fork broken off. The limbs form a pair of sled-like runners that are lashed together with cross members to form a patient platform. The sledge offers a solid platform for victim support and stabilization. If sufficient effort is put into fashioning a smooth, curved leading edge to the runners, a sledge can be dragged easily over smooth ground, mud, ice, or snow. Ropes also can be attached to the front of the platform for hauling and to the rear for use as a brake when traveling downhill.

FIGURE 39-17  A “sledge.”

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A travois is a similar device that is less like a sled and more like a travel trailer (without wheels). A travois is a V-shaped platform constructed out of sturdy limbs or poles that are lashed together with cross members or connected with rope or netting. The open end of the V is dragged along the ground, with the apex lashed to a pack animal or pulled by rescuers. Although the travois can be dragged over rough terrain, the less smooth the ground, the more padding and support necessary for comfort and stabilization. A long pole can be passed through the middle of the platform and used for lifting and stabilization by rescuers when rough terrain is encountered. When victims are transported in improvised litters, especially over rough terrain, they should be kept in a comfortable position, with injured limbs elevated to limit pressure and movement. To splint the chest wall and allow full expansion of the unaffected lung, victims with chest injuries generally should be positioned so that they are lying on the injured side during transport. For a person with a head injury, the head should be elevated slightly, and for persons with dyspnea, pulmonary edema, or myocardial infarction, the upper body should be elevated. Conversely, when the victim is in shock, the legs should be elevated and the knees slightly flexed. Whenever possible, unconscious patients with unprotected airways should be positioned so that they are lying on their side during transport to prevent aspiration.1

Rescue Litters and Stretchers The image most often associated with rescue immobilization and transportation devices in the United States is that of a traditional tubular steel and chicken wire–netted basket, which came to be known as the Stokes basket. Although this apparatus was and still is ubiquitous, many may recall the Thomas, Duff, Mariner, Brancard Piguillem, Perche Barnarde, Neil Robertson, MacInnes, and Bell stretchers for their evolutionary and robust designs. Today there are a variety of devices that meet the following two primary wilderness medical needs: 1. Immobilization and protection of a patient during transportation 2. Safe, comfortable, and stabilized transportation of a patient to definitive care

Desirable Characteristics of a Wilderness Stretcher Peter Bell,4 rescue equipment historian and developer of Bell stretchers in the United Kingdom, has described several specific characteristics of a high-quality, useful rescue stretcher. Bell claims that a good stretcher should have the following characteristics: • Be as strong and robust as possible, with materials compatible with the rescue environment • Be as lightweight as possible • Have smooth edges that will not snag • Be devoid of small spaces that will trap or pinch fingers (rescuers’ and patients’) • Be large enough to provide strength, security, and comfort for the largest of persons when the device is in any position (e.g., horizontal, vertical, on its side, upside down) • Prevent worsening of injuries during use • Provide security for the victim regardless of his or her condition (e.g., slippery, wet, muddy) • Be comforting to the conscious victim • Be easy to use in the dark and in temperature extremes (very hot or cold) • Protect the victim from the environment (e.g., heat, cold, brush, rocks) • Be reliable for many years after many uses in extreme conditions • Be easy to carry and use when carrying a heavy, large person • Be portable (can be carried in a car, boat, plane, helicopter, etc.) • Be impossible to use improperly • Be easy to clean and sterilize 744

Stretchers In the interest of brevity and with some technical latitude, this discussion describes stretchers in five categories: basket-style, flat, wrap-around, mountain rescue, and hybrid.

BASKET-STYLE STRETCHERS The basket-style stretcher derives its name from its shape. The sides curve upward to protect the victim’s sides and to prevent the victim from rolling out. Most basket-style stretchers combine a steel frame (solid, tubular, or both) with a shell of either steel wire netting (i.e., chicken wire) or plastic. Many include wooden slats in the bottom to provide additional protection and support. Most likely, basket-style stretchers initially were adopted by wilderness rescue organizations because they met fundamental needs and were sufficiently robust to endure great abuse in severe terrain. The seminal basket-style stretcher, called the Stokes, first appeared in the late 1800s and likely got its name from the fact that it was designed to be used on naval and commercial ships to remove casualties from the “stokehold,” a room in which the boilers were stoked (Figure 39-18). However, at least one source makes an unsubstantiated claim that the device was invented in 1895 by Charles Stokes.9 The significant influence of this device is reflected in the fact that the Stokes was the first commercially available basket-style stretcher in the United States. The original Stokes design included a leg divider meant to separate and support each leg individually. Many came to consider this configuration counterproductive when the use of long (0.4 × 1.8 m [16 × 72 inch]) backboards and other spinal, fullbody immobilization devices became widespread, especially for early treatment of trauma. Most current designs of the Stokes basket-style stretcher have eliminated the leg divider to allow full immobilization of a patient on a long backboard, which can be inserted into the basket. The Junkin Safety Appliance Company manufactures several Stokes basket-style stretchers, including models that break into two pieces and models with and without wooden slats or leg dividers, that meet the more robust military specifications (MIL-L-37957 and RR-L-1997) (Figure 39-19, online). Although the traditional materials and design (i.e., tubular and flat, welded steel with a steel chicken wire covering) are still in use today, basket-style stretchers are most often constructed from tubular stainless steel, aluminum, and titanium because of the added corrosion resistance, increased strength, and reduced weight. Manufacturers, such as Junkin and Ferno, offer basketstyle devices in full rectangular and tapered rectangular shapes. Both are also available in break-apart versions for easy carrying. Narrower versions (usually 0.5 m [19 inches] wide, instead of 0.6 m [24 inches]) are available for use in confined spaces or caves, although cave rescuers rarely prefer any type of chicken wire litter. Because of the importance of portability in wilderness areas, the break-apart capability is an adaptation to nearly all styles and types of litters. Junkin manufactures a version of the Stokes stretcher completely coated with a plastic material called plastisol, which provides nonsparking, nonconductive, and antistatic properties. Junkin suggests that this coating allows improved purchase (handgrip) on the litter and offers insulation from the temperature of the metal. A collateral benefit of the coating is

FIGURE 39-18  Traditional tapered Stokes litter with leg divider. (Courtesy Junkin Safety Appliance, Inc.)

CHAPTER 39  Litters and Carries FIGURE 39-23  Cascade Toboggan’s Model 200 Advance Series Rescue Litter with optional snow handles. (Courtesy Cascade Toboggan Rescue Equipment Company.)

FIGURE 39-20  Lifesaving Systems Corporation’s Model 404-F Medevac II stainless steel basket litter with optional flotation. (Courtesy Lifesaving Systems Corporation.)

that it extends the life and integrity of the steel chicken wire netting. Lifesaving Systems Corporation of Florida markets the Medevac II series of Stokes-style litters used widely by the U.S. Coast Guard. These devices are made from either a powder-coated stainless steel or titanium, which is 40% lighter (9 kg [20 lb] versus 14.5 kg [32 lb]). It also comes in a break-apart version (Medevac IIA) and is designed to include flotation for use in and around the marine environment (Figure 39-20). In this device, the wood slats used on the original Stokes litter have been replaced with stainless steel reinforcements that run the full length of the litter; smooth, plastic net mesh (with 13-mm [0.5inch] openings) replaces the chicken wire liner. Taking advantage of substantial improvements in polymer research, some manufacturers began producing a stretcher shell composed of rigid plastic instead of steel mesh. Ferno’s Model 71 stretcher has an orange plastic shell wrapped around an aluminum frame and secured with aluminum rivets. Brass grommets in the plastic serve as attachment points for a lifting harness (Figure 39-21). At one-half the weight of a traditional steel Stokes, this device offers protection from snags and obstacle penetration that cannot be provided by the wire netting of the Stokes. In addition, the plastic used is chemical resistant, and the molded underside runners make it slide smoothly over flat ground, ice, and snow. Ferno offers a version with tow handles and a chain brake that is designed specifically for ski patrol applications so that a packaged victim can be “skied” down a slope or pulled along a snow-covered trail. The orange Ferno litter has a load limit of 272.2 kg (600 lb), but its usefulness in a vertical raise configuration depends on the integrity of the aluminum frame and the plastic shell; if one is compromised, both may fail. Because of this limitation and because of the lightweight materials used, bending or twisting the device should be avoided. International Stretcher Systems also builds a basket-style stretcher called the Yellow Jacket. It has a lightweight aluminum frame but uses a different approach for combining the frame with the shell. Its high-density polyethylene shell is similar to the shell in the Ferno Model 71, but it is placed outside a full aluminum

FIGURE 39-21  Ferno Model 71 Stretcher. (Courtesy Ferno.)

skeleton to facilitate sliding over the ground. Inside the stretcher, a spring-suspended victim “bed” that doubles as the victim retention system has been added to protect the victim from the internal frame members. This bed minimizes transport shock and features built-in shoulder straps, pelvic padding, a head and chin immobilizing harness, foot and ankle straps, and a large “doublesecurity” Velcro body restraint flap that wraps around the victim. The stretcher weighs 18.1 kg (40 lb) and has an engineered load rating of 1134 kg (2500 lb) (Figure 39-22, online). The Junkin Model SAF-200B includes parallel stainless steel top rails. The top tube is larger to allow comfortable handgripping and to provide an attachment for lifting bridles, and the smaller solid steel lower rail allows attachment of patient retention straps. The twin rail configuration keeps patient straps and lifting systems from interfering with each other and helps protect the attached materials from abrasion during use. Unlike the International Stretcher Systems device, the stainless steel frame in the Junkin stretcher wraps around the exterior of the basket, which is lined with a smooth-surfaced, permanently padded plastic shell. This design offers comfort for the victim but makes it difficult to slide on the ground because of the external, exposed steel frame members. The unit is heavy (weighing 14.5 kg [32 lb]) but breaks apart for packing and marries well with a litter wheel to allow easier handling. Cascade Toboggan manufactures the Model 200 Advance Series of rescue litters (Figure 39-23). These robust devices— common sights at many recreational ski areas—have a 16-mm (0.6-inch) stainless steel top rail that attaches to a composite basket. It is available in a break-apart version and integrates four 25-mm (1-inch) patient restraint straps into the basket. The device is compatible with both the CMC Rescue Litter Shield and Litter Wheel and weighs less than 8.2 kg (18 lb) for the one-piece version. The two-piece version is just a bit heavier. Cascade Toboggan also developed and manufactures the Litter Skin, an abrasion-resistant shell that can be quickly attached to many types of rescue litters to make sliding across any surface easier (Figure 39-24). Bell Rescue Stretchers offers the Series 2 Ludlow stretcher, which is their strongest flat stretcher with deep basket sides

FIGURE 39-24  Cascade Toboggan’s Professional Series Litter Skin that can be attached to many types of rescue litters for easy sliding across any rough or abusive surface. (Courtesy Cascade Toboggan Rescue Equipment Company.)

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PART 5  RESCUE AND SURVIVAL

added. This strong, stainless steel–framed design has fold-down sides, which simplify access with a backboard. The sides can be completely removed to revert the device back to a flat stretcher. Other available variations on this theme from Bell include versions with shorter sides (the Otterburn), an open foot end (the Newark), and a steel plate welded into the bottom of the stretcher to help protect the victim (the Manchester). The Manchester weighs nearly 22.7 kg (50 lb). The manufacturer claims that the Series 2 models can all accommodate a long spine board and have been “proof tested” to between 500 and 720 kg (1102.3 and 1587.3 lb). The “bed” of Bell’s Series 2 stretchers is made of 14 polypropylene web straps that cross between the steel frame members. This webbing also passes through two movable stainless steel spinal supports (flat steel frame members that run the length of the caudal two-thirds of the litter). Four patient retention straps attached to the outermost rails, a patient shoulder strap, and integral lifting rings are supplied with the device. A slightly smaller, lighter, and less robust version, called the Bell Emergency Stretcher (discussed in the next section), is also available. Peter Bell no longer manufacturers the Bell line of rescue stretchers, but after 35 years of production, many are still in use and are likely to remain so for many years to come.

FLAT STRETCHERS Flat stretchers are generally flat and have very short or no sides. Restraint straps or built-in tie downs serve as the physical means by which the victim is secured in the litter. Although the specific characteristics of these types of stretchers vary greatly (from extremely lightweight to high strength), generally they are used when specific benefit is derived from their low-profile shape. Although this style of stretcher has been modified to allow dragging or sliding (e.g., mountain rescue stretchers), the primary purpose of the flat design is to reduce weight and profile for carrying or for specific applications, such as loading into an aircraft. Although a simple, two-pole canvas litter is fine for use over short distances, uncomplicated terrain, or the battlefield (where haste is paramount), lack of patient protection and immobilization capability limits its usefulness outside of the hospital or battlefield setting. A more modern version of this simple device is made of aluminum, folds for easy storage, and doubles as a long backboard. Another version is hinged at one end so that it can be spread along its long axis and slid under a patient on the ground with little movement or rolling. This “scoop” stretcher was commonly used by emergency medical service providers but has been supplanted by the use of long backboards. In the final analysis, both the military and aluminum iterations of the flat stretcher are intended for carrying a person short distances in an environment with few terrain obstacles or where complete security and immobilization are not required. Several successful varieties of flat stretchers have evolved over the years, including the Brancard Piguillem, the Junkin Air Rescue Stretcher (Figure 39-25, online), and a few of the Bell stretchers that are categorized as flat for the purposes of this discussion. The Brancard Piguillem (Brancard is French for “stretcher,” and Piguillem is a proper name) is a flat, old-style stretcher consisting of a canvas patient bed lashed to a steel and aluminum frame (weighing 13.6 kg [30 lb]), which folds in half for easy carrying by one person. The design, which has evolved over the years in the European and British mountain rescue communities, includes a patient bed with a permanently attached, integral casualty bag lashed to the frame to protect and secure the victim. Full-length runners raise the stretcher a few inches above obstacles and allow for easy bare-handed gripping. This folding, portable design with integral patient protection made the Brancard Piguillem popular with mountain rescuers and served as the impetus for the evolution of several of the current styles of mountain rescue stretchers. An interesting variation on the flat theme is the Rescue Sled Inflatable Rescue Litter manufactured by Switlik and distributed by Life Support International (Figure 39-26). The Rescue Sled is an inflatable, flat litter made of coated ballistic nylon that offers 102 kg (225 lb) of buoyancy and weighs less than 9 kg (20 lb). The device can be lifted, paddled, towed, or slid, both in and 746

FIGURE 39-26  Life Support International’s Rescue Sled (manufactured by Switlik) is a unique, durable, and inflatable device that provides 102 kg (225 lb) of buoyancy and weighs under 9 kg (20 lb). Shown is the Rescue Sled with integral flotation devices inflated (one tube each side). (Courtesy Life Support International Inc.)

out of the water. It may be inflated either manually or by a small carbon dioxide canister. Uninflated, it packs easily into a mediumsized backpack or duffle bag. Integrated head restraints and body straps allow securing a patient, and towing and lifting attachments simplify the process of moving the device when loaded. Although this device may not be best for all situations, its unique buoyancy and design characteristics make it attractive for many ice- and water-related rescues. The Kendall Stretcher, from Bell Rescue Stretchers, has the same features as their Ludlow Stretcher without the basket sides (see the previous section). The Kendall has a stainless steel frame, integral lifting rings, a bed made of polypropylene web straps that cross between the frame members, color-coded patient retention (38-mm [1.5-inch] web) straps, and a detachable foot loop. The Kendall Stretcher can be used with either side up; there is no top or bottom. A slightly less robust version of Bell’s flat stretcher is their Basic Emergency Stretcher. This device is smaller and lighter (weighing 5.2 kg [11.5 lb]) and works well in commercial and industrial settings, where severe terrain is rarely encountered. Although the manufacturer considers this stretcher to be a mountain rescue device, the MacInnes Mark 7 Rescue Stretcher is the latest in a long line of strong, user-friendly stretchers from Hamish MacInnes, the founder of MacInnes Rescue Stretchers and member of the Glencoe (Scotland) Mountain Rescue Team. The designer’s aim was to develop a compact, versatile stretcher made from light, “space-age” materials. The Mark 7 is 10 kg (22 lb) complete, less than 5 cm (2 inches) high (unfolded), constructed of abrasion-resistant titanium and composite materials, and can be folded for easy packing into isolated areas. It also includes a folding foot rest and head protector that double as handles.

MOUNTAIN RESCUE STRETCHERS Mountain rescue stretchers are essentially stronger, more robust flat litters with runners or skis attached to the bottom for easy movement over rugged terrain. Over the years, engineers and litter designers with mountaineering and rescue backgrounds have adapted rescue litter designs to meet specific practical needs of their environment. The result is the strongest and most robust platform available for patient treatment and transportation, but these benefits come at the cost of weight and size. The Thomas Stretcher is an early and beautifully simple example of the mountain rescue device (Figure 39-27). Invented in the United Kingdom in the 1930s by Eustace Thomas (no relation to Hugh Owen Thomas, who invented the Thomas “halfring” splint), it originally included wood (ash) runners, an aluminum alloy frame, a canvas bed, and six or seven patient straps attached to the rails. It also had locking, tubular, retractable handles that stowed in the tubular rails.10 Until recently, the Thomas Stretcher was being manufactured, with some modifications, by Bell Rescue Stretchers in the United Kingdom. However, this manufacturer has since ceased making the devices.5 In the late 1950s, Donald Duff, a pioneer of mountain rescue in Scotland, designed a stretcher with a steel tubular frame and no handles. Channeled steel runners extended along two-thirds

FLEXIBLE, WRAP-AROUND STRETCHERS FIGURE 39-27  Thomas Stretcher as used in the United Kingdom circa 1966. It was made from Duralumin tubing (trade name of one of the earliest types of age-hardenable, aluminum alloys), had telescoping handles, ash or laminated wood skids, and a Teryline (polyester fabric) net bed.10

of the caudal end of the stretcher. It weighed about 13.6 kg (30 lb) and could be fitted with a wheel and undercarriage for easier movement over rocky terrain. Its profile was low and sleek, and the runners could be detached and the remainder folded in two for backpacking.3 Although they have almost completely been replaced by more modern designs, two basket-style mountain rescue stretchers that evolved in Britain and Europe over the first half of this century deserve mention. The Perche Barnarde (Perche is French for “perch” or “pole,” and Barnarde is a proper name) consists of a 2-m (6.6-foot) square section of steel tube from which a canvas casualty bag is suspended. The tube breaks into three pieces for easy carrying. The bag is attached to the tube at each end. Where the patient’s shoulders would fall, a spreader bar is placed to keep the bag open. From each end of the steel tube extend two removable, bicycle type of handlebars fitted with pads so that the handlebars can rest on rescuers’ shoulders. Although this device has been used successfully in many difficult mountain evacuations over the years, its limitations regarding patient comfort, protection, and immobilization are obvious. The Mariner consists of a canvas bed attached to a steel sledlike frame. The bed functionally resembles a reclining chair in that the patient sits flexed at the hips and waist with the lower legs supported by a canvas platform. The frame is rounded from end to end and includes two steel runners to deflect obstacles. Two adjustable handles extend from each end of the frame for carrying. Today, the Mariner is used by several U.K. mountain rescue teams and is noted to have contributed significantly to the evolution of the mountain rescue stretcher. The current British standard for mountain rescue stretchers includes two devices that are incredibly strong, durable, and, unfortunately, heavy. The Mark III Bell Rescue Stretcher (which weighs 24 kg [53 lb]) and the MacInnes Mk 6 Rescue Stretcher (which weighs 22 kg [48.5 lb]) (Figure 39-28) are intended to survive years of use in extreme mountainous environments. Both have break-apart versions for easy packing into isolated areas and incorporate lifting rings, skids, and head guards. The MacInnes Mk 7 Rescue Stretcher (11.3 kg [25 lb]) is the modern and much lighter version of this robust style of stretcher. It is constructed mostly of a light but very strong and radiographopaque composite material. Titanium is used for the shafts and

FIGURE 39-28  MacInnes Mk 6 Mountain Rescue Stretcher. Note the extending handles, folding head guard, and optional twin (solid) tires. (Courtesy MacInnes Rescue Stretchers.)

A focus on improving stretchers for particular environments or situations has led to major developments in a number of litter design areas. It is difficult for a single device to excel in every situation because enhancing one capability or characteristic can be detrimental to another. For instance, it can be difficult to achieve a substantial increase in strength while decreasing overall weight. However, new innovative stretcher designs and materials allow structural flexibility to meet specific needs. Flexible, wrap-around stretchers can be folded, rolled, or otherwise compacted for storage and “wrap around” in that they contain the victim to provide protection, immobilization, and often sufficient support for vertical lifting. The Neil Robertson Stretcher was the impetus for this entire category of device. Adapted from a Japanese design by John Neil Robertson and first produced between 1906 and 1912, this wooden and canvas stretcher was originally made of bamboo and sewn by hand. The “Neil Rob” supplanted the Mansfield military stretcher in the United Kingdom and was first given the name “Hammock for Hoisting Wounded Men from Stokeholds and for Use in Ships whose Hoists are 2 feet, 6 inches in Diameter.”2 The Neil Rob consists of wooden slats that are covered with semirigid canvas and sewn the length of the stretcher. These slats wrap around the patient in mummy fashion, with arms in or out, providing protection without bulk. Full-body immobilization, protection, and a small cross section combine to produce a device well suited for use in small spaces or for situations in which the victim must be moved through a small opening.12 The most basic type of flexible, wrap-around stretcher has long been used by the military under combat conditions to quickly move casualties. London Bridge Trading Company manufactures several versions of a Quick Extraction Litter that integrates web handles and torso straps on an ultralight, coated nylon panel (Figure 39-29). While in use by one person, it may look more like a drag sheet than a litter. By passing litter poles through the web handles, the device, which weighs less than 0.9 kg (2 lb) and can almost be packed in a pocket, works well when spinal immobilization is unnecessary or can be provided separately. The Ferno LifeSaver Stretcher is a modern version of the traditional Neil Robertson Stretcher. It is 152 cm (60 inches) long and uses full-length 5-mm (0.2-inch) ribs interwoven by 1000denier nylon fabric to provide full-body splinting in a very narrow package. Five built-in restraints with forged steel buckles are integrated into the device, and stainless steel rings are used at the foot and head for vertical attachment points (Figure 39-30). For situations requiring full-body protection for the victim without complex restraint systems, the Reeves Sleeve and Ferno Traverse Rescue Stretcher almost totally encapsulate the patient.

FIGURE 39-29  Quick extrication, ultralight, nylon litters; six handle (left) and four handle (right). Designed for rapid movement of casualty by dragging (one person) or lifting and carrying. Note torso straps to secure patient. (Courtesy London Bridge Trading Company, Ltd.)

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some structural elements, a six-point harness can be fitted for lifting/lowering, and a lightweight alloy wheel can be quickly attached. The Mk 7 also folds up completely and can be attached to a pack frame for carrying into the backcountry.11

PART 5  RESCUE AND SURVIVAL FIGURE 39-30  The Ferno LifeSaver Stretcher—a modern version of the Neil Robertson Stretcher. (Courtesy Ferno.)

When used in conjunction with a cervical collar and spinal immobilization, these devices provide environmental and mechanical protection, while allowing the victim to be carried through narrow passages. The Ferno Traverse Rescue Stretcher (TRS) uses heavyweight Cordura nylon to cover a high-density polyethylene sheet that gives the device rigidity when wrapped around the patient (Figure 39-31). This stretcher has an integrated adjustable, fullbody harness to secure the patient in the device, padded straps in the shoulder and groin areas to make for a comfortable fit, and a foot strap that stops the patient from sliding down during vertical lifts. The Reeves Sleeve is a compact immobilizing stretcher suitable for hand-carry situations or vertical environments, but not intended for vertical lifting (Figure 39-32). The device uses a vinyl laminated nylon shell, slides over a full backboard, and depends on the backboard or short spinal immobilizer to provide rigidity. The company now makes a Reeves Sleeve Model 122 that was specifically designed to be lifted both vertically and horizontally. Skedco’s Sked stretcher provides wrap-around protection similar to the Neil Robinson, but a combination of shape and material, rather than integral slats, provides longitudinal rigidity (Figure 39-33). Light and compact when stored in its packable

FIGURE 39-31  Ferno Traverse Rescue Stretcher (TRS) configured for horizontal lift. (Courtesy Ferno.)

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FIGURE 39-32  Reeves Sleeve in use. (Courtesy Reeves Manufacturing, Inc.)

case, the flexible, low-density polyethylene plastic litter wraps around the victim to form a rigid sleeve that is superbly compact for maneuvering in tight quarters. A half-length version is available for moving persons from areas that are too confined for a full-length device, when flexing the victim at the hips might facilitate extrication. The hard and smooth plastic material can be easily dragged over a variety of surfaces and offers substantial protection from penetrating obstacles. Although the Sked stretcher provides spinal protection, the manufacturer recommends using an Oregon Spine Splint (Skedco) or similar device when cervical spine immobilization is necessary. External lift slings are included with the Sked to allow vertical or horizontal lifting, and flotation is available for use in a marine environment. The Brooks-Range Mountaineering Equipment Company Eskimo Rescue Sled (Figure 39-34) is designed as a foolproof, one-piece sled or “drag bag” suitable for ski guides, backcountry skiers, and travelers who need a reliable but minimalist means to transport an injured person out of the backcountry. The Eskimo Sled can also be used with a pair of skis positioned underneath the patient for added immobilization, stability, and protection. A water-resistant, breathable snow guard protects the patient from rope abrasion and snow. The patient can be

FIGURE 39-33  Sked Rescue Stretcher system. (Courtesy Skedco.)

transported in the Eskimo Sled while either prone or sitting. The Eskimo Sled has both front and back tow loops, as well as eight head and side handles to facilitate carrying the patient when needed. The Eskimo Sled is a versatile device that can also be used as a bivouac sack, gear sled, or emergency shelter. It weighs just 850.5 g (30 oz) and is 20.3 × 15.2 × 5 cm (8 × 6 × 2 inches) when packed. Medical Devices International (MDI) makes the Immobile-Vac Full Body Mattress, which is a full-body vacuum splint on which the victim is carried (Figure 39-35). The vinyl-coated, fabric patient bed contains loose polystyrene (Styrofoam) beads similar to those in a beanbag chair. Once the victim is positioned on the mattress, a small hand pump is used to expel air from within it. This process creates a rigid, full-body splint that conforms to the victim’s shape. This “cocoon” immobilizes the spinal column and extremities while providing a comfortable platform. The mattress has integrated web carrying straps that can be used to carry the patient directly, or the mattress can be inserted into a basket-style stretcher for added versatility and strength. The use of a basket stretcher will be necessary for high-angle rescue, because the MDI device is not designed for vertical rescue by itself.

HYBRID DEVICES A hybrid of field improvisation and commercially made sleds and litters, the Rescue Sled line produced by the Brooks-Range Mountaineering Equipment Company (http://www.Brooks-Range.com) offers a lightweight and compact kit of components that can be easily packed into the backcountry. The components of the Brooks system will convert a pair of skis of any length between 135 and 205 cm (53.1 and 80.7 inches) into a secure and durable rescue sled using a pair of stretcher bars, backcountry ski straps, and the sled. The sled component, constructed of lightweight, ripstop nylon fabric, binds the components together and forms a secure cocoon

FIGURE 39-35  The Medical Devices International Immobile-Vac Full Body Mattress is a full-body vacuum splint that can be inserted into other litters. (Courtesy Medical Devices International.)

FIGURE 39-36  The Brooks-Range Mountaineering Equipment Company Ultralite Rescue Sled. The kit is combined with a pair of snow skis and poles to form a stable transport platform suitable for transport of an injured or incapacitated person over snow. (Courtesy BrooksRange Mountaineering Equipment Company.)

FIGURE 39-37  The Brooks-Range Mountaineering Equipment Company Ultralite Rescue Sled with patient. (Courtesy Brooks-Range Mountaineering Equipment Company.)

around the patient. The sled is easily assembled in under 2 minutes and offers 5.1 cm (2 inches) of patient elevation off the surface of the ground or snow.6 The most popular model is the Ultralite Rescue Sled (Figures 39-36 and 39-37). When packed, the kit measures 10.2 × 27.9 × 5 cm (4 × 11 × 2 inches)—not much larger than a 1-L Nalgene bottle—and weighs no more than 705.9 g (24.9 oz). In addition, if a Brooks-Range compact snow shovel is packed on the same trip, the stretcher bars can be omitted from the Rescue Sled kit, because the shaft of the shovel doubles as a set of stretcher bars, thereby reducing the package size of the Rescue Sled to approximately 2.5 × 10.2 × 12.7 cm (1 × 4 × 5 inches) and weight to 246.6 g (8.7 oz).

Transportation Hardware Accessories A number of wheeled devices can be attached to most basketstyle stretchers. These devices take the carrying burden off rescuers in nontechnical evacuations and reduce the load on low-angle haul systems. One example is the CMC Rescue Mule II Litter Wheel (Figure 39-38), which incorporates a large, underinflated all-terrain vehicle tire into a lightweight frame that clamps to the underside of the litter. This single wheel is positioned under the center of gravity, and the rescuers walk alongside, or at each end of, the litter to steady and guide it, with the wheel carrying

FIGURE 39-38  CMC Rescue Mule II Litter Wheel with handles (manufactured by Traverse Rescue). This versatile device allows the wheel to be removed and stored inside the frame and is available without the handles. (Courtesy CMC Rescue, Inc.)

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FIGURE 39-34  The Brooks-Range Mountaineering Equipment Company Eskimo Rescue Sled. This one-piece sled or “drag bag” can also be used with a pair of skis positioned underneath the patient for added immobilization, stability, and protection. (Courtesy BrooksRange Mountaineering Equipment Company.)

PART 5  RESCUE AND SURVIVAL

Most litter manufacturers offer specific packaging or methods for carrying their devices into isolated areas. For instance, London Bridge Trading Company’s Quick Extraction Litter, the Sked, and Ferno’s Traverse Rescue Stretcher can all be compacted and carried in by a single rescuer. Other manufacturers sell special backpacks or integral carrying harnesses for carrying one-half of their break-apart litters because of the greater weight.

Carrying a Loaded Litter FIGURE 39-39  The CMC Rescue Litter Shield protects the victim from falling debris while allowing access to the head and face. It can also be inverted and placed in the litter to save space during storage. (Courtesy CMC Rescue, Inc.)

most of the load. When they encounter large obstructions, such as logs or trenches, rescuers simply lift the litter and continue rolling. One advantage of this device is that it reduces the number of rescuers required to move a litter safely over a long distance. When using this device, only two rescuers (one at each end) are required to control the litter, but more may be used as necessary. To meet a similar need, International Stretcher Systems employs a collapsible steel-frame trailer, the Anchor Man Trailer, with two all-terrain vehicle wheels. With no axle between the wheels, the tires can be set to the outside of the frame for greater side-to-side stability or to the inside and under the frame to negotiate narrow trails or doorways. The drawbar end of the trailer is set up to receive either the T-bar handle, for towing by rescuers on foot, or a hitch adapter, for towing behind motorized vehicles. Skis can also be substituted for the wheels. Junkin markets several useful stretcher accessories, but at least one is notable. Junkin’s Comfo-Pad is designed to fit in all Junkin stretchers and is simply a pad on which the patient lies in the litter. It is made of 13-mm (0.5-inch) foam rubber with a durable, orange nylon cover and is held in place with hook-and-loop type of fasteners. Because comfort is always an issue, this simple accessory can be quite helpful. MacInnes and Bell integrate steel wire head protectors in their mountain rescue stretcher designs. This feature is important where falling rock is a hazard. CMC Rescue markets a similar aftermarket device made of clear polycarbonate under the trademark CMC Rescue Litter Shield (Figure 39-39). It protects the victim’s face from falling debris; allows for easy, rapid airway access; and can be moved out of the way because it hinges on the end of the litter. The shield stores compactly in the litter when not in use. Flotation systems are available for some litters. Ferno, International Stretcher Systems, and Skedco each offer this option to make their devices safer and more versatile in swift- or openwater rescue situations.

A

B

C

An evacuation is defined as high angle or vertical when the weight of the stretcher and tenders (stretcher attendants) is primarily supported by a rope and the angle of the rope is 60 degrees or greater.8 This type of situation is often encountered when a rescue is performed on a cliff or overhang or over the side of a structure and usually requires only one or two tenders. In high-angle rescues, most often the stretcher is used in the horizontal position to allow only one tender and to keep the victim supine and comfortable. However, when the packaged victim and stretcher must be moved through a narrow passage or when falling rock is a danger, the stretcher may be positioned vertically. In a scree or low-angle evacuation, the slope is not as steep (less than 60 degrees), the tenders support more of the weight of the stretcher, and a rope system is still needed to help move the load. In this type of rescue, more tenders (usually four to six) are required, and the rope is attached to the head of the stretcher. The head of the litter is kept uphill during a low-angle rescue. In a nontechnical evacuation, tenders completely support the weight of the stretcher during a carry out. Generally, the terrain dictates the type of evacuation. If the stretcher can be carried without the support of a rope, it is a nontechnical evacuation. If rope is needed to support the load or to move the stretcher, it is either a low- or high-angle evacuation, depending on the angle of the slope. Carrying a litter in the wilderness is difficult and requires many resources. It takes at least six rescuers to carry a person in a litter a short distance (0.4 km [0.2 mile], or less) over relatively flat terrain. With six rescuers, four can carry the litter while the other two clear the area in the direction of travel and assist in any difficult spots. However, depending on the terrain and the weight of the victim, all six rescuers may be needed to safely carry the litter any distance. If the travel distance is longer, many more rescuers are required (Figure 39-40).

Patient Packaging Patients on stretchers must be secured, or “packaged,” before transport. Packaging consists of stabilization, immobilization, and preparation of a patient for transport. Physically strapping a person into a litter is relatively easy, but making it comfortable and effective in terms of splinting can be a challenge. The needs of a person secured and transported in a litter are great and should not be overlooked or underestimated. The rescuer’s goals are to:

D

FIGURE 39-40  Litter-carrying sequence. A, Six rescuers are usually required to carry a litter, but rescuers may need relief over long distances (greater than 0.4 km [0.2 mile]). B, Relief rescuers can rotate into position while the litter is in motion by approaching from the rear. C, As relief rescuers move forward, others progressively move forward. D, Eventually, the rescuers who are farthest forward can release the litter (peel out) and move to the rear. Rescuers in the rear can rotate sides so that they alternate carrying arms. Carrying straps (webbing) also can be used to distribute the load over the rescuers’ shoulders. In most cases, the litter is carried feet first, with a medical attendant at the head monitoring airway, breathing, level of consciousness, and so on.

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• Package the person to avoid causing additional injury. • Ensure the patient’s comfort and warmth. • Immobilize the patient entire body in such a way as to allow continued assessment during transport. • Package the patient neatly so that the litter can be moved easily and safely. • Ensure that the patient is safe during transport by securing him or her within the litter and belaying the litter as necessary. Generally, proper patient packaging must provide for physical protection and psychological comfort. Once packaged in a carrying device, a person feels virtually helpless; thus transport preparation must focus on alleviating anxiety and providing rocksolid security. With this in mind, rescuers must provide for the patient’s ongoing safety, protection, comfort, medical stabilization, and psychological support.7 Splinting and spinal immobilization are usually achieved by using a full or short backboard. The patient is secured to the board, and then the patient (on the board) is placed into the litter. When the immobilized patient is finally placed into the litter, adequate padding (e.g., blankets, towels, bulky clothing, sleeping bags) placed under and around him or her contributes to comfort and stability. During transport, patients like to have something in their hands to grasp, to have pressure applied to the bottom of their feet by a footplate or webbing, and to be able to see what is happening around them.7 Because persons are so vulnerable to falling debris when packaged in a litter, especially in a horizontal high-angle configuration, a cover of some type should always be used to protect the patient. A blanket or tarpaulin works well as a cover to protect most of the body, but a helmet (in the absence of cervical injury) and face shield or goggles are also options to protect the head and face from projectiles. Alternatively, a commercially available litter shield can be used and allows easy access to the airway, head, and neck (see Figure 39-39). Because the head and neck usually require immobilization, the technique and equipment used to protect them should allow this. Remember also that the conscious patient desires an unobstructed view of his or her surroundings. Carrying a person in the wilderness often requires that the litter be tilted, angled, placed on end, or even inverted. In all these situations, the patient must remain effectively immobilized and securely attached to the litter and the immobilizing device within the litter. Any supporting rope must be easily accessible

FIGURE 39-41  One 10-m (32.8-foot) web or rope can be used to secure a person into a litter.

and securely attached. Poor attachment can cause patient shifting, exacerbation of injuries, or even complete failure of the rescue system. Manufacturers have taken several approaches to securing a person within the litter. Most integrate a retention or harness system directly into the litter. However, a few require external straps to secure the patient to the device. Many users suggest that an independent harness be attached directly to the patient to provide a secondary attachment point in case any link in the attachment chain fails. When a harness is not available, tubular webbing, strips of sturdy material, or even rope can be used to secure the patient. One approach uses tubular webbing slings in a figure-8 at the pelvis and shoulders to prevent the patient from sliding lengthwise in the litter. A 10-m (32.8-foot) piece of 5-cm (2-inch) webbing or rescue rope can be used to achieve the same goal (Figure 39-41). The rope or web is laced back and forth between the rails of the litter in a diamond pattern until the patient is entirely covered and secure. Such a technique also easily incorporates a protective cover and support of the patient’s feet. Regardless of the techniques and equipment used, frequently checking vital signs (i.e., distal pulses and capillary refill) during transport can help ensure that strapping does not obstruct circulation.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 40 

  Helicopter Rescue and Aeromedical Transport* ROBERT C. ALLEN AND JIMMY L. COOPER

Rapid provision of appropriate definitive care to acutely ill and injured patients is a major goal of all emergency medical services (EMS) systems. The ability to rapidly transport and initiate treatment of severely ill or traumatized patients is important in decreasing morbidity and mortality. This is particularly germane to wilderness and environmental emergencies, for which medical resources are scarce, transport times to definitive care facilities are often prolonged, and terrain and weather conditions are inherently difficult. Aeromedical transport crews can deliver emergency medical care at the scene, and the time to definitive *The opinions expressed in this chapter are those of the authors and do not necessarily represent the opinions of or endorsement by the Department of Defense, the U.S. Army, or the U.S. Air Force.

care can be greatly decreased. This maximizes the patient’s chance for a successful recovery.

Aeromedical Evolution Rapid evacuation of trauma victims from an injury scene to the location of definitive care is a modern concept with roots in antiquity. The New Testament documented an early instance of prehospital care and transport: “A certain Samaritan … went to him and bound up his wounds, pouring oil and wine, and set him on his own beast and brought him to an inn, and took care of him.”90 The greatest impetuses to the advancement of emergency care and transportation have been epidemics and wars.65 Before the classical Greco-Roman period, injured soldiers were often left on

For online-only figures, please go to www.expertconsult.com

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the battlefield to die. Later, Homer described the use of chariots to evacuate fallen warriors during the Trojan War.48 Napoleon’s forces devised horse-drawn carriages, or ambulances volantes, for the same purpose.55 North American Indians devised the travois, a litter that could be pulled by a person or animal to transport ill or injured persons.63 The U.S. Army began a similar practice during the Seminole War of 1835-1842 and used it again in the Civil War. Major Jonathan Letterman established the process of rapidly clearing wounded soldiers to a point behind the battle line where they could be further triaged to an expectant area for persons with mortal wounds, a local treatment area for the “walking wounded,” or a hospital if definitive care was feasible. The central concept was efficient access to surgery for victims of trauma. These developments were soon followed by invention of flying machines. In France, Richet had predicted the potentials of air transport in 1869.65 This was before the first balloon airlift. The prediction was validated the following year during the Franco-Prussian War, when the first documented aeromedical evacuations took place. During the Prussian siege of Paris, 160 wounded soldiers were evacuated and transported by hot air balloon over enemy lines.92 In the United States, air evacuation took place soon after the Wright brothers flew in 1903.39 Grossman and Rhoades presented their idea of air transport of patients to the War Department in 1910, but the government refused to fund them. It was not until World War I that the U.S. military began to use aircraft to carry injured soldiers, and this occurred only rarely. However, the French transported patients as early as 1912 aboard Dorland ARII fighters converted to carry litters, despite the government’s objection to the concept of aeromedical transport: “Are there not enough dead in France today without killing the wounded in airplanes?”39 The United States began using its first dedicated air ambulances in 1920, using the de Havilland DH-4A, followed by the Cox-Klemin XA-I. World War II saw widespread application of fixed-wing aircraft for evacuation. More than 1.4 million patients were transported from front-line hospitals to tertiary care facilities, with only 46 deaths en route.96 During this time, the concept of medical care during transport was implemented. In November 1942, the War Department began to train flight surgeons and flight nurses and enlisted medical personnel for aeromedical transport.39 Also during 1942, Igor Sikorsky produced a rotarywing aircraft, called a “helicopter,” which the army configured with external litters. It was used in an air evacuation for the first time in 1944 in Burma.36 Helicopters did not enjoy widespread use until more reliable and powerful machines became available. The Sikorsky S-51 and later the Bell 47-B were deployed over the rugged terrain and uncertain roads of Korea with great success to provide wide-scale evacuation of wounded soldiers to Mobile Army Surgical Hospital (MASH) units. Although only 11 dedicated medevac helicopters were used, more than 17,700 casualties were evacuated. For the first time, injury victims could travel directly from the point of injury to definitive surgical care. This set the stage for Army helicopter evacuation (“Dust Off”) operations in Vietnam in 1962. With the Bell UH-1A Iroquois (“Huey”) under the leadership of Major Charles Kelly, the Army’s 57th Medical Detachment became known for the courage and hard work of flight crews, who flew despite darkness, adverse weather, and enemy fire. Later, the Bell model UH-1H was used to evacuate up to nine patients at a time by hoist from above a dense jungle canopy. By 1967, about 94,000 injured men had been evacuated.77 As air evacuation matured, the time from wounding to definitive care declined from 18 hours in World War I to between 1 and 2 hours in Vietnam.98 Although medical advances have contributed to improved survival, battlefield mortality has steadily declined from 18% in World War I to 1.8% in Vietnam, perhaps more because of rapid aeromedical transport to definitive care (Table 40-1). Unfortunately, emergency medical care for civilians greatly lagged behind the developments in the military. In the late 1960s, rescue efforts were more organized, skilled, and rapidly performed for a man shot in the Vietnam conflict than for a civilian 752

TABLE 40-1  Mortality Rates and Evacuation Times

During Major Wars

Conflict World War I World War II Korea Vietnam

Evacuation

Mortality

Time (hr)

Rate (%)

18-30 4-6 2-4 1-2

18.3 3.3 2.4 1.8

From Stewart RD: Prehospital care of trauma, Trauma Q. May: 1, 1985.

injured on a U.S. highway.65 Civilian ambulances were said to be no faster than taxis.89 Civilian transport began to change dramatically in the United States in 1966, when the National Academy of Sciences–National Research Council put forth the white paper “Accidental Death and Disability: The Neglected Disease of Modern Society” (U.S. Department of Health, Education, and Welfare), which outlined the inadequacies of prehospital emergency care, including the observation that “helicopter ambulances have not been adapted to civilian peace-time needs.” This document was the impetus for improving EMS systems through the country, and soon the civilian sector began to emulate the military model. The first U.S. civilian aeromedical program was begun in 1969 as a joint effort between the Maryland State Police and the University of Maryland Center for the Study of Trauma (now the Maryland Institute for Emergency Medical Service Systems). Certain hospitals were designated as trauma centers, and victims of highway and other trauma were flown by police pilot–paramedic teams in a primary response role at the accident scene.94 The 1980s saw rapid growth in helicopter EMS (HEMS) programs, both in terms of the number of services and helicopters (Figure 40-1, online). In 1980, there were only 32 HEMS programs with 39 helicopters flying 17,000 patients. By 1990, this system grew to 174 services with 231 helicopters flying 160,000 patients. In 2009, the Atlas and Database of Air Medical Services (ADAMS) database project identified 307 air medical services providing 867 dedicated rotary-wing aircraft and 309 fixed-wing aircraft. The National Transportation Safety Board (NTSB) estimates nearly 400,000 rotary-wing aircraft transports annually, with an additional 150,000 patients flown by fixed-wing aircraft.32 The distribution of the air medical services programs is graphically depicted by the ADAMS database (Figure 40-2, online). The Commission on Accreditation of Medical Transport Systems (CAMTS; http://www.camts.org) is an independent, nonprofit agency that, since 1991, has established standards for critical care transport systems. CAMTS is made up of representatives from 19 different organizations, including the American College of Emergency Physicians, American College of Surgeons, Aerospace Medical Association, International Association of Flight and Critical Care Paramedics, and Air and Surface Transport Nurses Association. As of July 2009, there were 152 air medical services accredited by CAMTS, which represents approximately 50% of the HEMS programs in the United States. Although CAMTS accreditation is voluntary, several states have adopted CAMTS accreditation as a requirement for licensure of air medical services. Several other states have adopted CAMTS standards as their own standards for air medical service licensure. CAMTS reviews its standards on a routine basis and released the eighth edition of the standards for accreditation on February 25, 2011. The modern-day U.S. Air Force (USAF) aeromedical evacuation system has its origins in the Vietnam War, during which more than 406,000 wounded troops were aeromedically evacuated. Current USAF aeromedical evacuation crews are composed of flight nurses and aeromedical evacuation technicians. Experienced nurses and medical technicians are trained to be aeromedical crews at the USAF School of Aerospace Medicine. This 5-week course includes aircraft configuration, air and ground safety, patient flight physiology, and aeromedical nursing considerations. Aeromedical evacuation crews are trained to move stable patients by fixed-wing aircraft over distances ranging from a few

Types of Aeromedical Transport Programs HOSPITAL-BASED PROGRAMS At one time, the most ubiquitous type of aeromedical transport program was hospital-based. Helicopter service is often provided in primary (to the accident scene) and secondary (to the community hospital emergency department) response roles. In addition, many hospitals provide fixed-wing transport in a secondary response role for long-distance transports or when transport by helicopter is impractical. In a hospital-based transport program, the hospital frequently leases the helicopter from a vendor, who also supplies the pilots, maintenance, and fuel. The hospital has the responsibility for providing the medical crew and determining its configuration. The program directors are responsible for medical control and quality improvement. The hospital may choose to own the aircraft and contract with a vendor for operations or employ its own pilots and mechanics. In most cases, the helicopter resides on a helipad atop or near the hospital, and the crew, which may consist of a specially trained flight nurse, flight paramedic, and physician, is quartered in the hospital, ready for immediate launch (see Flight Crew, later).

NON–HOSPITAL-BASED PROGRAMS Non–hospital-based service is provided by an entity that may be supported by a consortium of hospitals, or it may be an independent corporation, ambulance service, or aviation fixed-base operator. The aircraft may be owned or leased by the entity or by an aviation contractor. This is not a common model for helicopter services in the United States, although many fixed-wing services operate in this manner. Use of the community-based model of HEMS has increased remarkably over the last 10 years and is now commonly seen in the United States. As of early 2009, Air Methods, a large HEMS company, operated a fleet of 335 aircraft at 254 bases in 43 states. About 60% of their operations are hospital based and 40% are community based.76 A corporate airplane with its interior reconfigured may be provided on demand for use in an air ambulance mode, or a dedicated airplane may be provided with a custom-made air ambulance interior configuration, usually under a supplemental type certificate (STC).

PUBLIC SAFETY, POLICE, OR STATE SERVICES The aircraft (usually a helicopter) may be owned and operated by a governmental agency, such as the state highway patrol, and

operated under part 135 of the Federal Aviation Regulations (FAR). As in the Maryland model, flight personnel typically include police pilots and emergency medical technician (EMT)-paramedics.

THE MILITARY ASSISTANCE TO SAFETY AND TRAFFIC PROGRAM The Military Assistance to Safety and Traffic (MAST) program was established to supplement the civilian EMS systems. Under this program, air medical evacuation services are supplied by active-duty military medical units to the extent allowed by their training budgets, provided they can use actual patient transports instead of training exercises. The MAST mission is “secondary”; it is available only when its personnel and equipment are not being used in support of the unit’s primary mission. MAST may be requested by the local EMS or disaster management agency. Typical aircraft include the Bell UH-1 and Sikorsky UH-60 (Black Hawk). The medical crew usually consists of medical corpsmen. The MAST program may not compete with similar civilian services.

OTHER MILITARY RESOURCES The USAF provides aeromedical transport in support of U.S. military operations and some disaster situations. The formal aeromedical evacuation system run by the USAF is the largest in the world, able to move large numbers of stable and critical-stabilized patients over intercontinental distances. In calendar year 2009, the USAF aeromedical evacuation system moved 21,538 patients (4543 of whom had battle injuries); 9-1-1 patients were critically ill and required CCAT team support during flight.99 Other available resources include the Air National Guard and the U.S. Coast Guard. Many states and some counties have organizations (e.g., California Department of Forestry, Los Angeles County Sheriff’s Department) that may be called on to assist in search and rescue (SAR) operations in preparation for aeromedical transport. Many other countries have analogous units. The Israel Air Force, for example, operates a squadron that provides civilian and military rescue and evacuation services.

Patient Mission Types Aeromedical transports have varying mission profiles, with the majority (70%) of flights being interfacility transports and 30% flights from the scene.50

PRIMARY RESPONSE In a primary response role, the aeromedical transport service responds to an accident scene or field location, usually at the request of police, fire, or local EMS personnel, and serves as the initial and sole mechanism of transport to the hospital. In this instance, the aeromedical crew may function as “first responders.” Helicopters are most suited to a primary response role. The required response times must be short (less than 10 minutes from call to takeoff); thus the flight crew must be stationed at or near the launch site 24 hours a day. The service radius (“stage length”) is short (typically less than 50 miles), and crews need to be experienced in techniques for landing in proximity to obstacles, under poor conditions, and on uncertain surfaces. In prehospital situations, patients’ conditions vary widely, and often little or no assessment or stabilization is performed before arrival of the flight crew. Medical personnel must possess a high degree of training and experience and should possess at a minimum EMT skills required for patient extrication and stabilization at the scene. It must be kept in mind that the availability of helicopter transport, particularly for on-scene response, may not affect the outcome of the patient. Several studies have found that helicopter transport does not significantly improve outcomes in areas where ground ambulance transport is readily available.10,17,80,81 The possible benefit to the patient must be measured against the risk to the helicopter crew, especially in poor weather conditions or during the night. 753

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

miles to transoceanic flights. Physicians do not normally accompany aeromedical evacuation flights; patient care and medication are provided by prior physician orders and written protocols. U.S. military operations in Afghanistan and Iraq have led to significant changes in the USAF aeromedical evacuation system. Changes in military doctrine have resulted in the need to move seriously ill but stabilized patients over great distances by air. The requirement has led to development of dedicated critical care air transport (CCAT) teams, which fly with aeromedical evacuation crews to provide care for critical patients. CCAT teams include a critical care physician, critical care nurse, and cardiopulmonary technician. A formal training course in CCAT is given at the USAF School of Aerospace Medicine.11,82 The trend toward formal CCAT teams has been mirrored throughout the world, with countries such as Great Britain, Germany, Japan, Australia, and Colombia developing and fielding CCAT capabilities.11,49,54 With the development of faster and more powerful helicopters, reconfiguration of fixed-wing aircraft for aeromedical needs, enhanced knowledge of aeromedical physiology, and experience accumulated over more than 50 years of transport experience, acceptance, utilization, and success of aeromedical transport are universal. The role of aeromedical transport in the wilderness setting continues to evolve as its importance is recognized in providing rapid emergency medical care and evacuation to sick and injured patients.

PART 5  RESCUE AND SURVIVAL

SECONDARY RESPONSE In the secondary response role, a patient has already been transported by other means to a hospital, where some degree of stabilization may have occurred. The aeromedical service transports the patient in the early stages of care from the emergency department of a hospital to a facility better equipped to offer definitive care. Response times required for this type of mission must be competitive with one-way ground transport times. Stage lengths are short to intermediate (up to 241.4  km [150 miles]). The transport vehicle is typically a helicopter, although in some remote and wilderness areas, fixed-wing services are also suited to this role. Flight crews used in a secondary response vary depending on the needs of the patient (see Medical Mission Types). The responding aeromedical service typically consists of flight nurses, paramedics, and in some cases flight physicians.

TERTIARY RESPONSE In a tertiary response, an inpatient requiring specialized services unavailable at the current facility or requesting relocation is transported to a new facility. Tertiary transports may involve helicopters or fixed-wing aircraft, depending on the level of urgency, stage length, and cost of transport. Commercial entities throughout the world specialize in this type of service.

Medical Mission Types The needs of different patient types may be categorized by medical problem; this in turn dictates the requirements of the aeromedical transport service. In most hospital-based helicopter programs, most patients transported are categorized as adult trauma, cardiac, or medical noncardiac. A number of programs offer or specialize in pediatric, neonatal, perinatal, and organ transplantation services, for which specialized crews and equipment may be required. In addition, aeromedical transport programs that provide SAR operations require specialized equipment and training.

TRAUMA PATIENTS Trauma patients transported in the primary or secondary response modes may account for 20% to 60% of a hospital-based helicopter service’s transport activity, depending on the hospital’s function and capability as a trauma center and the relationship between the aeromedical service and the community EMS and public safety network. A study of one urban setting noted that 20% of helicopter missions were to injury scenes, which were located at a mean distance of 1.6 km (14.4 miles) from the hospital. Of patients transported, 19% had penetrating trauma and 81% blunt trauma (66% from motor vehicle crashes). The most common organ system injuries involved the head (65%), extremities (39%), chest (31%), and abdomen (27%). The overall mortality rate of transported patients was 24%. The most common procedures required at the scene were endotracheal (ET) intubation (41%) and cardiopulmonary resuscitation (CPR) (18.7%). The most common life-threatening conditions were cardiac arrest (18.7%), airway obstruction (5.1%), cardiac tamponade (3.2%), and tension pneumothorax (1.7%).35 A multicenter study of blunt trauma victims transported by helicopter aeromedical services from both urban and rural environments found a mean trauma score of 13 (of 16), mean age of 29 years, and overall mortality rate of 15%.10 A retrospective analysis of 10,314 patients with moderate to severe traumatic brain injury indicated that aeromedical response and transport were associated with better outcomes than was ground transport, even after adjustment for multiple influential factors. Patients with more severe injuries appeared to derive the greatest benefit from aeromedical transport.23 These and other studies indicate the need for skilled crews in the transport of trauma patients.102 Medical personnel must have the ability to assess the patient adequately to detect frequent in-flight complications and to intervene with appropriate procedures, including intravenous (IV) cannulation, ET intubation, 754

BOX 40-1  Trauma Care Aboard Emergency Medical

Services Helicopters

Mechanism of Injury Motor vehicle crash Fall Industrial or agricultural accident Gunshot or stab wound Burn Sporting accident Drowning Hypothermia Procedures Performed by Flight Crew Endotracheal intubation Cardiopulmonary resuscitation Intravenous line placement Central venous access Extrication and splinting Bladder catheterization Nasogastric tube insertion Venous cutdown Tube thoracostomy Cricothyrotomy Pericardiocentesis

CPR, chest decompression, and at times a surgical airway (Box 40-1). In wilderness areas, the flight crew must be skilled at victim extrication and operating in rugged terrain. They must be familiar with standard trauma care and the range of clinical entities most frequently seen in the wilderness setting. In addition, because resources may be limited and backup unavailable, they may be required to function semiautonomously. For this reason, protocols and standing orders are valuable. Most important are training, skill, and judgment.

PATIENTS WITH CARDIAC DISEASE Patients with cardiac disease are most often transported in a secondary or tertiary response role, by either helicopter or fixedwing aircraft. They typically account for 20% to 50% of an aeromedical service’s transport activity. The condition of these patients is often medically complex. Technologically sophisticated treatment modalities may include antiarrhythmics, vasopressors, inotropes, vasodilators, thrombolytic agents, cardiac monitoring, arterial and central venous pressure monitoring, pacemakers, implantable defibrillators, and intra-aortic balloon counterpulsation devices.24,28,37,52 The flight crew must have sophisticated knowledge, expertise, and experience and may include a cardiac critical care nurse and a physician.

PATIENTS WITH MEDICAL, NONCARDIAC CONDITIONS Patients with medical noncardiac conditions, including those with underlying cardiac disease, are most often transported in the secondary or tertiary response mode by either helicopter or fixedwing aircraft. This group consists largely of patients with acute neurologic disease or shock or those who require assisted ventilation.42 The spectrum of potential in-flight challenges includes cardiovascular problems, arrhythmias, hypotension, respiratory difficulties requiring acute airway management, seizures, and alterations in level of consciousness. The flight team must be able to manage an airway and operate a ventilator. Additional considerations relate to the cabin environment and need for pressurization if hypoxemia is present, if barotrauma is likely, or if trapped gas exists, as well as the need to predict the requirement for and manage finite oxygen resources in flight.

Pediatric patients may have traumatic or medical conditions.13,44 In a study of 636 pediatric patients transported by air in the Salt Lake City area, 57.5% were transported by helicopter and 37.5% by fixed-wing aircraft, with a mean stage length of 207 miles (helicopter, 82 miles; fixed-wing, 452 miles). Less than 1% of flights were from the scene. The patient ages ranged from 3 weeks to 16 years, with 45% younger than 1 year. Trauma was the most common diagnosis (15.3% had head injury, 9.3% multiple injuries), followed by neurologic illness (24.2%), respiratory failure or infection (20.1%), gastrointestinal or genitourinary problems (10.2%), metabolic disease (9.2%), cardiovascular disease (6%), and general pediatric surgical problems (5.7%). The overall mortality rate was 7%.64 Many of the considerations for pediatric transport are similar to those for adults, especially with older children. Infants may require an incubator, however, and flight crews must be experienced in caring for infants and children. Specifically, knowledge of pediatric advanced cardiac life support skills, including pediatric drug dosages, airway sizes, and fluid management, is essential.

PERINATAL PATIENTS The need for expedient evaluation, preparation, and transport of the obstetric–gynecologic patient is increasing. Types of problems include ectopic pregnancy, pelvic inflammatory disease, toxic shock syndrome, abnormal fetal presentation, multiple gestation, diabetes in pregnancy, placenta previa, abruptio placentae, disseminated intravascular coagulation, preeclampsia–eclampsia, and preterm labor. The decision to transport patients in advanced preterm labor should be based on such factors as distance between hospitals, time required to cover the distance, personnel available for the transport, gestational age, and speed with which labor has progressed. The flight crew must be knowledgeable about these problems and comfortable with their treatment in order to ensure favorable outcomes for both mother and child.

NEONATES Neonates have unique anatomy and physiology, and the diseases that affect them require specific knowledge and skills by those involved in their transport. Specific issues include newborn assessment, including assignment of an Apgar score, airway clearance, temperature, homeostasis, and familiarity with neonatal resuscitation.4,40 Access to references concerning neonatal emergency drug dosages should be available.3,33 The ability to perform umbilical vein catheterization is an important skill for any member of the transport team involved in neonatal care. In addition, knowledge of fluid, electrolyte, and glucose requirements is essential.49,57 The flight crew involved in the transport of a neonate often includes a neonatal nurse and neonatologist.

are external human load operations in which the rescuer or patient is carried by cable for either insertion or extraction. A hoist uses a cable attached to a harness or basket that can be lowered or raised with the person, whereas a short haul is a fixed length of line attached to the helicopter. The helicopter, equipped with a hoist and winch, is one of the most effective means of providing SAR in the wilderness setting and is essential in mountainous regions. These systems enable extrication and rescue of patients from terrain that may otherwise entail a complex and dangerous ground evacuation. Patients with critical illness may not be able to sustain a long delay between the time of the accident and the call for assistance before adversely affecting patient outcome. The U.S. Air Force routinely uses helicopters and fixed-wing aircraft for long-distance SAR operations. Fixed-wing aircraft often arrive at the scene first and may deploy para-rescue specialists (“PJs”) by parachute. If the rescue site is over water, the aircraft may also deploy an inflatable boat with motor and rescue equipment. The PJs and their survivors are then recovered by surface vessels or by rescue helicopters that have been refueled aerially in order to reach the rescue site (Figure 40-3). This capability permits rapid deployment of rescuers while allowing the most expeditious recovery of survivors and their delivery to definitive care. These services were on alert for all space shuttle launches to provide SAR support in the event of a mishap. In the United Kingdom, the Royal Air Force operates a helicopter SAR service that flew 1490 missions from 1980 to 1989, almost all of which involved vacationers along the coasts or in the mountains.59 The Danish helicopter rescue service was founded in 1966 and uses a Sikorsky (S-61) helicopter. Since 1973, its crew has included a physician trained in aerospace medicine and helicopter transport. From 1973 to 1989, it flew 5733 missions, 2075 of which involved direct medical intervention. The most frequent problems were abdominal trauma and cardiopulmonary diseases.106 In the high Alps, more than 90% (3000 per year) of all rescues are performed using helicopters.5 Of these, 5% are combined rescues; that is, the helicopter carries the rescuers below cloud level, near the site of the accident. Only 5% of mountain rescues are purely ground rescues, mainly necessitated by visibility.88 Currently, a network of SAR systems extends throughout the Alps. In some countries (France, Italy, Germany, Austria, and Spain), air rescues are managed partially or totally by the army or the state. The aircraft most often used for this purpose are the Alouette III, Lama, Ecureuil (French), Bolkow100,117 (German), Agusta AK117 (Italian), and Bell (U.S.). In Switzerland, the rescue system in remote terrain is managed by the Swiss Alpine Club and three air rescue companies, Swiss Air-Rescue (REGA), Air Glaciers, and Air Zermatt. Switzerland may be unique in that its

SEARCH AND RESCUE Wilderness SAR is a unique aspect of aeromedical care and transport that requires significant training and expertise. Most dedicated aeromedical aircraft in the United States are not well suited for SAR operations (see Aircraft for Search and Rescue, later). Most standard aeromedical crews are not trained in SAR techniques. Many aeromedical helicopters and some fixed-wing aircraft become involved in SAR activities, however, and it is important to be familiar with SAR techniques. In addition, outside the United States, persons providing aeromedical transport are frequently involved in SAR activities (see Chapter 37). The keys to a successful SAR operation include proper communications, transport, evacuation, and medical treatment, along with favorable weather conditions and topography. Helicopters are helpful in various SAR activities, including low-altitude search activity, search area evaluation, and movement of supplies and equipment. Fixed-wing aircraft are also useful for search and can provide secondary transport, especially when long distances are involved. A helicopter with hoist or short-haul capability may be the only means of extrication and rescue from the scene. These

FIGURE 40-3  MH-60G Pave Hawk hoisting a para-rescuer during a search and rescue exercise. A variant of the UH-60 Black Hawk, the Pave Hawk is flown by U.S. Air Force rescue squadrons. Modifications include forward-looking infrared equipment, night vision–compatible cockpit lighting, terrain and navigation radar, air-refueling probe, auxiliary fuel tanks, and hoist. (Courtesy U.S. Air Force.)

755

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

PEDIATRIC PATIENTS

PART 5  RESCUE AND SURVIVAL

18 strategically placed helicopter rescue bases allow an aircraft to reach any accident scene within 15 minutes of takeoff. Since the foundation of REGA in 1952, more than 150,000 patients have been transported by either fixed-wing aircraft or helicopter. Up to 8000 patients (5500 from accident scenes) are transported by helicopter every year. Twenty percent of these rescues require a winch, with one-third of all winch operations occurring in accident sites that are difficult to reach.26 More than 75% of all persons rescued by winch were thought to have injuries requiring physician assistance at the scene. Eighty percent of all Swiss air rescue missions are physician assisted, and 20% have a paramedic in charge. All the physicians and rescue crews are physically fit and trained in alpine techniques, because two-thirds of all rescue missions performed from 1990 to 1993 were in topographically remote and difficult terrain (Figure 40-4). Difficult helicopter SAR operations are those that involve low visibility, strong winds, night missions, high-angle rescues, and long-line hoist operations (extension of the hoist cable up to 120 m [394 feet]). In addition, in mountainous regions, power cables and transport cables present considerable risks. In all cases, the risks to the flight crew (as well as to the patient) must be weighed against the degree of injury and risk for further morbidity. The U.S. Air Force, Army, Navy, and Coast Guard equip and train groups to operate in these hostile rescue environments. Helicopters are frequently equipped with precision navigation systems and night vision, forward-looking infrared (FLIR), and thermal imaging equipment. The intense training and specialized equipment permit rescue operations under much more demanding conditions than those encountered by civilian services. Of the military services, only the U.S. Coast Guard has a primary mission of civilian SAR; Army, Navy, or Air Force groups may be requested to assist in civilian rescues in areas in which they are available. An increasing number of people participate in alpine sports, including mountain climbing, downhill skiing, mountain biking, and paragliding.28 A typical representation of the type of mountaineering accidents experienced in the Swiss Alps is shown in Table 40-2. In addition to SAR in mountainous regions, aeromedical rescue presents great challenges to the medical and flight crews involved in rescues from sea and white water, floods, vertical rock faces, and avalanches. Medical treatment of the survivors should begin immediately at the site of the accident unless weather conditions are deteriorating or the scene is inherently unsafe. If a hoist extraction is

TABLE 40-2  Mountaineering Accidents in the Swiss

Alps, 1992 (N = 1844)

Activity Delta gliding Paragliding Off-slope skiing Ski touring Mixed climbing Rock climbing Hiking

756

18 196 35 238 456 178 723

From Dürrer B, Hassler R, Mosimann U: Mountaineering accidents in the Swiss Alps and rescue activities of the Swiss Alpine Club, 1992.

needed, the patient with potential multisystem trauma should be evacuated by a rescue net or basket (Stokes) litter with careful spinal immobilization. A tag line attached to the litter prevents spinning during hoist operations. The tag line should be attached with a weak link so that the tag line will break away if the litter becomes uncontrollable. Persons with minimal or isolated injuries may be hoisted by a jungle penetrator (Figure 40-5), rescue basket, or other dedicated hoist device. If a hoist device is not available, the victim may be hoisted by climbing harnesses or rescue belts.27 The climbing harness or belt should be carefully inspected to make sure that it has not been damaged in the mishap, that it will withstand the strain of the hoist operation, and that it can be safely attached to the hoist cable. The extent of medical treatment rendered on site before extraction depends on many factors, including the victim’s condition, scene safety, medical supplies available, medical skill of the rescuers, weather conditions, aircraft loiter time, and flight time to definitive care. Good communication between the flight crew and the rescue team is essential to the decision-making process. Aeromedical crews involved in mountain rescue need to have a thorough understanding of the unique medical problems frequently found in high-altitude rescue situations.

A

FIGURE 40-4  Helicopter rescue in extremely difficult terrain. (Courtesy P. Bärtsch, MD, and the Swiss Alpine Club.)

Patients Rescued (n)

B

FIGURE 40-5  A, Jungle penetrator used as a hoist device on most military rescue helicopters. The streamlined shape allows it to slip through dense tree canopies to reach the ground. A foam flotation collar can be attached, making the penetrator buoyant. B, Jungle penetrator rigged for hoist. The seats are flipped down, and the safety straps are pulled out from their stowed position and passed over the head and under the arms of the victim, who then straddles one of the seat paddles. Although the penetrator has three seats, usually only one or two persons are hoisted at a time. (Courtesy Robert C. Allen.)

If the helicopter is not able to land at a mishap scene and has a rescue hoist installed, hoist operations may be the only means of evacuating the patient. In most circumstances, a helicopter crew member rides the hoist down to the site to rig the survivor into the rescue device and to oversee the hoist operation, using the following guidelines: • It is critical that personnel on the ground not touch the hoist, rescue device, or cable until after it has touched the ground (or water). Helicopters can build up a very powerful static electricity charge that will be grounded through whatever the hoist touches first. This has been known to knock rescuers and survivors off their feet. • Once the rescue device and cable have touched the ground, put the patient into the rescue device, taking care to keep the hoist cable clear of all personnel. Do not allow the hoist cable to loop around any personnel or around the rescue device, because serious injury is possible when the cable slack is taken up. • Make sure that the patient is properly secured in the rescue device, with all safety straps tightened. • When the patient is secured, move away from the rescue device and signal “up cable.” • If the rescue device is a basket (Stokes) litter, use a tag line with a properly installed weak link to prevent the litter from spinning during the hoist.

International Aeromedical Evacuation A growing segment of aeromedical evacuation is evacuation of international travelers from the point of injury or illness to their home country. This growth is fueled by increasing travel to remote areas of the world, the increase in the age (and concomitant decrease in health) of travelers, and to some extent, risktaking behavior on the part of travelers. The vast majority of international travelers complete their journeys without incident, with fewer than 0.5% of travelers requiring medical evacuation. However, when one considers the huge number of people who travel by air each year (1 to 2 billion per year by some estimates), even this small percentage adds up to thousands of people requiring international aeromedical evacuation.100 There are multiple companies that specialize in fixed-wing movement of patients over medium- to long-range distances. Some operate their own fleet of aircraft and have full-time medical personnel, others charter aircraft as required and fit medical transport equipment and personnel as required for a specific transport. One daunting factor in these evacuations is the large cost associated with international aeromedical transport. It is not unusual for these transports to cost upward of $50,000 to $100,000.100 Frequently this cost is not covered by medical insurance. Several of these companies offer “memberships,” where for a relatively small yearly fee, the member will be provided aeromedical evacuation from just about anywhere on the globe to their home of record. Long-range transport in relatively small aircraft presents some unique challenges, including having adequate space to provide care, oxygen supply, power supply, and the possibility of patient deterioration en route. Unlike the relatively short-range, shortduration flights done by HEMS services, international aeromedical evacuation flights very frequently have aeromedically trained physicians as members of the flight crew.

Flight Crew CREW CONFIGURATION The ideal medical flight crew composition varies with the mission profile. When the aircraft is involved in a primary response to the accident scene, inclusion of an EMT may be beneficial. Transport of patients whose illness or injuries are complex or whose clinical conditions are extremely unstable may benefit from the presence of a physician. Interfacility transport of a

patient on mechanical ventilation may benefit from inclusion of a respiratory therapist as part of the flight crew. All aeromedical transport programs include one or more of the providers below in the transport medical crew. In a 2010 survey of 300 critical care transport programs, none of the responding programs flew either fixed-wing or rotary-wing missions with a single medical crew member.38 The most common crew configuration was a two-person crew, with a nurse and an EMT-paramedic making up the crew 84% of the time in rotary-wing missions and 69% of the time in fixed-wing missions. Two-nurse crews were uncommon (8% rotary-wing and 9% fixed-wing). A respiratory therapist made up the second crew member in relatively few rotary-wing transports (5%); however, they were more common in fixed-wing transport (22%). Nurse–physician crews were relatively uncommon, making up only 3% of the rotary-wing crews and none of the fixed-wing crews. Three-person crews were less common and usually involved adding a respiratory therapist to an RN/EMT–paramedic crew.38

EMERGENCY MEDICAL TECHNICIAN–PARAMEDIC EMTs are increasingly members of the aeromedical flight team. In 1993, 71% of rotary-wing transport programs reported using an EMT–paramedic as a member of the flight team, compared with 44% in 1988.18 EMTs vary in their level of training, depending on the state in which they work, but usually follow Department of Transportation (DOT) guidelines, which include three levels of certification. EMT-basic provides basic ambulance, rescue, and first-aid skills. EMT-intermediate may include IV and intubation skills. The EMT-paramedic level involves such skills as intubation, IV techniques, medication administration, defibrillation, and arrhythmia recognition and treatment. For an aeromedical flight team member, additional training relating to the aeromedical environment is desirable.49,93,103 EMTs can be of particular value in operations that necessitate frequent interaction with ground EMS. In some regions, HEMS service is integrated into the regional primary response network, so that the helicopter and crew arrive at the accident scene before ground units; therefore flight team members experienced in scene assessment and victim extrication are essential. The Association of Air Medical Services (AAMS; http://www.aams.org) has published Guidelines for Air Medical Crew Education, which gives templates for initial training of advanced life support skills for EMT-paramedics, nurses, and respiratory care personnel in advanced techniques that may be required in the aeromedical environment. The International Association of Flight and Critical Care Paramedics (http://www.flightparamedic.org) offers flight paramedic review courses. The Board for Critical Care Transport Paramedic Certification offers an examination for paramedics to become certified flight paramedics (FP-C).

FLIGHT NURSE At least one flight nurse is part of almost all aeromedical transport programs; in 1993, 21% of rotary-wing programs reported using two flight nurses as the sole team members.18 In 2010, 100% of 77 rotary-wing transport programs reported using an RN as part of the flight team. As noted earlier, only 8% used a dual-RN crew.38 Critical care or emergency nursing experience is usually a prerequisite, with additional training that includes patient assessment, advanced cardiac life support, a trauma life support course, and prehospital care skills, including certain procedures such as ET intubation, advanced IV cannulation techniques, and in some cases needle thoracostomy, venous cutdown, cricothyrotomy, and other specialized skills. The flight nurse often is also a certified EMT. The Air and Surface Transport Nurses Association (http://www.astna.org), in association with the Board of Certification for Emergency Nursing, offers a certification in flight nursing, leading to the credential of certified flight registered nurse (CFRN).

FLIGHT PHYSICIAN The experience and training of physicians involved in aeromedical transport depend on their role. Those who function as the 757

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

Hoist Operations

PART 5  RESCUE AND SURVIVAL

online medical control physician communicate via radio or 800-MHz radiotelephone with the flight crew, monitor care, and give necessary orders. In the United States, physicians fly as a component of the flight team in a minority of aeromedical transport programs; in 1993, only 3% of all rotary-wing transport programs reported the routine use of a physician, compared with 10% in 1988.18 As has been noted earlier, very few helicopter EMS flights have physicians as members of the flight crew; this varies, depending on the individual organization. In HEMS operations, an emergency physician or trauma surgeon may be appropriate, whereas with long-range fixed-wing transport of intensive care unit patients, an intensivist may be of value. Physicians functioning in this role must have a current level of skill and expertise sufficient to address a wide range of clinical problems. They must also possess additional training relative to the airborne medical environment, including flight physiology, aircraft operations, and prehospital care (Box 40-2). Most important, they must function in this role with sufficient frequency so as to maintain their skills and remain safe and comfortable within the aeromedical setting. In doing so, they become an asset to the flight team rather than a distraction or liability. The National Association of EMS Physicians has written a position paper on the core training it considers necessary for the flight physician.69 The Air Medical Physician Association has a three-part core curriculum recognized and recommended by CAMTS as background training for the medical director of a critical care transport program applying for accreditation or reaccreditation.

BOX 40-2  Specialized Training for Aeromedical

Transport

Aviation physiology Atmospheric pressure changes with altitude Gas expansion with altitude Changes in partial pressure of oxygen with altitude Effects of motion and acceleration Effects of noise and vibration Changes in temperature and humidity Aircraft safety Aircraft systems and equipment operations In-flight emergency procedures Survival techniques Patient extrication and immobilization Patient loading and handling aboard an aircraft Patient care techniques in the aeromedical environment Respiratory support and ventilation aboard the aircraft Pertinent Federal Aviation Administration regulations and procedures Familiarity with the local emergency medical services system Radio communications skills and techniques Hazardous materials response procedures Record keeping and documentation in aeromedical transport Preflight, in-flight, and postflight procedures Clinical procedures Cardiopulmonary resuscitation aboard the aircraft Defibrillation aboard the aircraft Intravenous cannulation Endotracheal intubation Tube thoracostomy Needle thoracotomy Cricothyrotomy Central vein catheterization Pericardiocentesis Nasogastric tube insertion Bladder catheterization Intraosseous line placement Umbilical vein catheterization

758

Studies during the late 1980s and early 1990s attempted to determine whether a physician crew member has an effect on the outcomes of patients transported by helicopter.8,9 Some studies concluded that a physician crew member had a positive impact on patient outcome, whereas others found no difference in outcome between similar cohorts of patients transported by flight crews with two nurses or a nurse and a paramedic.40,87 The cost of using a physician crew member is substantially higher than that of a nurse–nurse or nurse–paramedic crew configuration. Some argue that this higher cost would be offset by the decrease in hospital stay or lost person-years that would occur if a physician were a standard member of the flight crew. With advanced training in critical procedures and treatment protocols, combined with online medical direction, a nonphysician flight crew usually functions as well as a crew that includes a physician. No objective evidence supports the benefit of a physician as a standard flight crew member in helicopter transports. USAF CCAT teams, U.S. Army burn transport teams, and other military transport teams designed to move critically ill or injured patients over long distances will almost invariably have a specially trained physician (intensivist or burn specialist) as part of the team. Given the long duration of intercontinental missions and the difficulty of diverting transoceanic flights, the presence of a specialist physician onboard is vital to safe transport.11,49,82,86

CREW MEMBER STRESS By its nature, aeromedical transport involves moving a gravely ill patient into an adverse environment with limited resources. Under these conditions, a medical crew of only two or three persons must perform complex tasks, solve difficult problems, and make life-or-death decisions. They must perform in a physically confining space that may be uncomfortable, and they must do so under time pressure and with little or no physical assistance. In some cases, rescuers’ lives may be at risk. This scenario occurs in few other arenas of civilian medical care. The term stress describes an array of adverse physiologic and psychological reactions that occur when a person perceives a threat to existence. Although stress may not diminish performance, it may be responsible for errors, faulty judgment, and uneven manual skill performance. It may also affect the physical and psychological health and satisfaction of the flight crew member.19 When measured during patient flights, the level of anxiety among aeromedical crew members was significantly higher than during a baseline period on the ground.97 Factors that correlate with high in-flight anxiety levels include adverse weather conditions (e.g., low ceilings, high winds), severity of the patient’s medical condition, complexity of illness or injuries, and the crew member’s fatigue. Efforts should be made to minimize stress among crew members. This includes frequent and adequate training; continuing education and feedback; adequate medical backup, including online medical direction, written protocols, and treatment guidelines that can aid in difficult decisions; a supportive rather than an intimidating or critical quality assurance program; adequate rest; and safe weather minimums. Routine mission debriefing and critical incident stress debriefing should be integral parts of all transport programs.67

Appropriate Use of Aeromedical Services Aeromedical transport combines skilled treatment and stabilization capability with rapid access to definitive care, but not without risk, and at high cost. (In 1986, it was estimated that aeromedical transport costs were $1 to $2 million per year for a program, or about $2000 per transported patient, which is about 400% higher than ground transport. This cost has gone up considerably; it is not unusual for an HEMS run to cost over $8000. Long-range international transports can cost upward of $100,000.17,100 However, the comparative risk of aeromedical transport must be placed in perspective against the risk for patient death from nonreferral or from less timely ground transport with limited medical capability en route.

BOX 40-3  Medical Conditions That May Require

Aeromedical Evacuation

Acute neurologic, vascular, surgical, or cardiac emergencies requiring time-sensitive intervention Critical conditions in patients with compromised hemodynamic or respiratory function Critical conditions in obstetric patients whose time of transfer must be minimized to prevent complications in the patient or fetus Critical conditions in neonatal or pediatric patients with compromised hemodynamic or respiratory function, metabolic acidosis more than 2 hours after delivery, or sepsis or meningitis Electrolyte disturbances and toxic exposures requiring immediate lifesaving intervention Organ failure requiring transplantation Conditions requiring treatment in a hyperbaric oxygen unit Burns requiring treatment in a burn treatment center Any injury that is potentially threatening to life or limb, including penetrating eye injuries Data from Teichman PG, Donchin Y, Kot RJ: International aeromedical evacuation, N Engl J Med 356:262, 2007.

of EMS Physicians position paper “Guidelines for Air Medical Dispatch.” These questions can be used to assist in determining appropriate transport modes.70

Dispatch and Communications The dispatch center is the focal point for communications during aeromedical transport operations. Dispatchers receive incoming requests for service; obtain necessary information relative to the launch decision; coordinate the interaction between essential parties; “scramble” the flight crew; assemble and maintain necessary information regarding destination, weather, local telephone numbers, and frequencies; follow the progress of the flight; input data into the system database; and communicate with ground EMS units and hospitals. Communication may occur through a combination of methods: land telephone lines into a dispatch switchboard, hospital–EMS net transceiver, discrete frequency BOX 40-4  Questions That Can Assist in Determining

the Appropriate Transport Mode

• Does the patient’s clinical condition require minimization of time spent out of the hospital environment during the transport? • Does the patient require specific or time-sensitive evaluation or treatment that is not available at the referring facility? • Is the patient located in an area that is inaccessible to ground transport? • What are the current and predicted weather situations along the transport route? • Is the weight of the patient (plus the weight of required equipment and transport personnel) within allowable ranges for air transport? • For interhospital transports, is there a helipad and/or airport near the referring hospital? • Does the patient require critical care life support (e.g., monitoring personnel, specific medications, specific equipment) during transport, which is not available with ground transport options? • Would use of local ground transport leave the local area without adequate emergency medical services coverage? • If local ground transport is not an option, can the needs of the patient (and the system) be met by an available regional ground critical care transport service (i.e., specialized surface transport systems operated by hospitals and/or air medical programs)? From Thompson DP, Thomas SH Position Paper: National Association of EMS Physicians, Guidelines for Air Medical Dispatch, Prehosp Emerg Care 7:265, 2003.

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

Although not proved, advanced provider skill levels during prehospital care are considered beneficial, especially in severely ill or injured patients.51 In rural and wilderness environments, advanced life support services may be made more readily available by EMS helicopters. This is especially true in areas that are difficult or impossible to reach by ground. The speed of access to definitive care is another consideration in choosing the mode of transport. In isolated rural or wilderness locations, a helicopter may be the only means of expedient access. Prolonged victim extrication allows time for a helicopter to arrive at the scene, decreasing total transport time and thereby increasing the advantage of helicopter transport. Patient comfort also must be considered, especially on long transports over rough roads. Although a helicopter moves in three dimensions, fore-and-aft acceleration is usually steady, without the starting and stopping motions present during ground transport. However, helicopters typically travel within 914 m (3000 feet) of the ground’s surface and are more subject to turbulence than are high-flying fixed-wing aircraft. Whether aeromedical transport reduces mortality when compared with ground transport has not been definitively determined. An uncontrolled national multicenter study of trauma patients transported by helicopter showed a 21% reduction in mortality from that expected based on predictions from the trauma revised injury severity score (TRISS) methodology and national normative trauma outcome data.10 A similar study using the TRISS methodology compared actual mortality with helicopter versus ground transport and showed a 52% reduction from expected mortality when patients were transported by air, compared with no reduction in expected mortality when transport occurred by ground.7 Another study using TRISS methodology found a benefit of aeromedical transport only in patients with severe trauma (a probability of survival of less than 90%).15 As has been noted earlier, a retrospective analysis of 10,314 patients with moderate to severe traumatic brain injury indicated that aeromedical response and transport was associated with better outcomes than was ground transport, even after adjustment for multiple influential factors. Patients with more severe injuries appeared to derive the greatest benefit from aeromedical transport.23 In 1990, the AAMS issued a position paper on the appropriate use of emergency air medical services. In 1992, these recommendations were accepted by the California Medicaid provider as reasonable criteria for the use of air medical transport. In a review of 558 consecutive patient transports, 98% had met at least one of the AAMS criteria.80 The aeromedical triage criteria were updated by the National Association of EMS Physicians in the position paper “Guidelines for Air Medical Dispatch” in 2003. These guidelines have been endorsed by the AAMS and Air Medical Physician Association (AMPA).2,70 The risk of aeromedical transport can be placed in perspective if the overall risk for death using ground transport, estimated from the trauma score, is compared with the risk when patients are transported by air. Assuming a reduction in risk of between 21% and 52% when transport is by air, the additional risk for death from crashes (1.18 per 100,000 transports) is negligible in comparison with the benefits. This is probably true, however, only for patients with moderate to severe, but nonmortal, injuries (i.e., trauma scores between 5 and 14). Those having minor injuries, with near 100% likelihood of survival, are unlikely to gain additional benefit; those having mortal injuries, with little hope of survival, are unlikely to be saved by any means attempted or employed. The decision to transport a patient by air requires judgment and a realistic appraisal of the risks. A patient should be transported by air only if he or she is so ill that transport is necessary; if ground transport is unavailable, delayed, or unable to reach the patient; or if aeromedical transport would reduce the risk for death by permitting more rapid access to definitive care, providing greater medical skill en route, or both.81 Box 40-3 gives some of the indications for aeromedical transport. A more detailed list can be found in the AMPA position statement: “Medical Condition List and Appropriate Use of Air Medical Transport.”2 Box 40-4 is from the National Association

PART 5  RESCUE AND SURVIVAL

transceiver (communications with aircraft), or walkie-talkie radios. Familiarity with the EMS system and EMS communications is essential for successful dispatch. Flight following is an important part of aeromedical safety and involves tracking the position of the aircraft during a mission by plotting the location according to reports from the pilot at 10- to 15-minute intervals. If an accident or in-flight emergency occurs, the dispatcher is soon aware and can initiate SAR to a precise location, which enhances the chances of survival.

Pretransport Preparation Once the decision is made to transport a patient by air and the appropriate aeromedical service is contacted, preparations must be made to ensure patient safety and comfort and to aid the flight crew in patient care. A study of the causes of ground delays in a rural interhospital helicopter transport program found that on arrival of the flight team, 31% of patients required minor interventions (insertion of IV line or nasogastric tube, blood transfusion, bladder catheterization, military antishock trousers application) before takeoff, and 33% required major interventions (ET intubation, tube thoracostomy, central venous access).58 When no intervention was required, the mean ground time was 31.2 minutes, compared with 57.4 minutes when one or more major interventions were required. To minimize delays, pretransport preparations should be made for victims of acute trauma (Box 40-5).

Common Aeromedical Transport Problems

attempts should be made to limit sudden pitching of the stretcher. DOT guidelines recommend design of cabin access such that no more than 30 degrees of roll and 45 degrees of pitch may occur to the patient-occupied stretcher during loading.66 The stretcher in turn should be adequately attached to the floor. Motion sickness in the patient may be treated with an antiemetic such as promethazine (25 mg orally). Scopolamine disks are useful for prolonged flight and do not require parenteral or oral administration, although their antiemetic effects are not always uniform and may not occur until 4 to 6 hours after application. They may be best used to decrease motion sickness in the flight crew. A novel approach to prevention of airsickness while not having excessive sedation is to give 25 mg of promethazine orally along with 200 mg of caffeine. A small study in army helicopter passengers showed that this combination produced significant reduction in airsickness symptoms compared with placebo, transdermal scopolamine, meclizine, and acustimulation wristbands. The promethazine–caffeine combination also produced the fewest side effects.29

NOISE Noise can be avoided with hearing protectors, which are devices similar to headphones but without internal speakers. Inexpensive hearing protectors are available as deformable foam ear plugs. In some cases, headphones may be used in an awake patient if the crew wants the patient to communicate on the intercom system.

EYE PROTECTION

Motion, vibration, noise, temperature variations, dry air, changes in atmospheric pressure, confinement to a limited position or backboard, and fear of flying may cause patient discomfort.

When a patient is loaded on or off a helicopter with the rotors turning, the patient’s eyes must be protected. Serious eye injuries can result from debris blown into the air. Lightweight sky diver goggles (“boogie goggles”) are effective and inexpensive. The eyes must be protected even if the patient is unconscious. Taping temporary patches over the eyes is also effective.

PATIENT MOVEMENT

RESPIRATORY DISTRESS

Patient handling and movement can contribute to morbidity and mortality in unstable patients.104 All transported patients should be adequately secured to the stretcher with safety straps to prevent sudden shifting of position or movement of a secured fracture. During transport from the ground to the aircraft cabin,

Patients with respiratory disease or distress should have immediately treatable conditions addressed before takeoff. ET intubation is essential if airway patency is threatened or if adequate oxygenation cannot be maintained with supplemental oxygen. It is better to err on the side of caution when making a decision about a patient’s airway. During flight, it is easier to treat restlessness in an intubated patient than it is to treat airway obstruction or apnea in a nonintubated patient. Nearly all seriously ill patients should receive supplemental oxygen. The fraction of inspired oxygen (FIO2) should be increased with increasing cabin altitude to maintain a stable partial pressure of oxygen (PO2) (Figure 40-6). Small, portable pulse oximeters are readily available and should be used to monitor oxygen saturation while in flight. When oxygen saturation monitoring is unavailable and pretransport arterial oxygen content unknown, 100% oxygen may be administered throughout the flight to ensure adequate oxygenation. Patients with chronic lung disease who are prone to hypercapnia may experience deterioration in condition if the hypoxic drive is eliminated. In these patients, the least oxygen necessary to maintain saturation above 90% is advisable; this amount may be estimated in advance or calculated from the alveolar air equation. Close in-flight monitoring is essential, preferably by continuous pulse oximetry. Finally, altitude changes will affect ET cuff volume, especially on ascent. ET tube cuff pressures on the mucosa must be kept below 30 cm H2O, to avoid mucosal blood flow impairment (lower pressure may be necessary in hypotensive patients).7 Cuff volume changes can be estimated by cabin altitude and appropriately adjusted63; however, an easier and safer alternative may be to use a cuff manometer to check ET tube cuff pressures preflight and again during climb out, cruise, and descent. If any other air-bladder devices (e.g., cuffed tracheostomy tubes, laryngeal mask airways, air splints) are present on the patient, they must also be adjusted during flight to avoid increased volume/ pressure problems.

PATIENT COMFORT

BOX 40-5  Pretransport Preparations Scene Response Airway secured If required, stabilization on a rigid spine board with cervical immobilization device, neck rolls, and tape Two large-bore intravenous (IV) lines in place and carefully secured Landing zone selected and secured Documentation of any on-scene care provided before arrival of aircraft Interhospital Transport Airway secured Stabilization on a rigid spine board with cervical immobilization device, neck rolls, and tape Two large-bore IV lines Tube thoracostomy for pneumothorax or hemothorax Bladder catheterization (if not contraindicated) Nasogastric catheterization (if not contraindicated) Appropriate IV solution hanging Typed and crossmatched blood if available and required Extremity fractures splinted (traction splinting for femur fractures) Copies of all available emergency medical records and laboratory results, including a description of the mechanism of injury

760

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

1 0.9 0.8

FIO2

0.7 0.6 0.5 0.4 0.3 0.2 0

4000

2000

8000

6000

10,000

12,000

Altitude (ft)

FIO2

PB

Altitude (ft) 0

0.21

0.30

0.40

0.50

0.60

0.70

0.80

0.90

1.00

760

2000

0.23

0.32

0.43

0.54

0.65

0.76

0.86

0.97

PP

707

4000

0.25

0.35

0.47

0.59

0.70

0.82

0.94

PP

PP

656

6000

0.27

0.38

0.51

0.63

0.76

0.89

PP

PP

PP

609

8000

0.29

0.41

0.55

0.69

0.83

0.97

PP

PP

PP

564

10,000

0.31

0.45

0.60

0.75

0.90

PP

PP

PP

PP

523

12,000

0.34

0.49

0.65

0.82

0.98

PP

PP

PP

PP

483

A-a:

15

79

150

222

293

364

435

507

578

Calculated from the alveolar air equation under standard temperature and pressure conditions. PP, Positive pressure required; PB, barometric pressure (mm Hg); A-a, alveolar-arterial oxygen gradient (mm Hg). X axis: en route altitude Y axis: FIO2 required to maintain PO2 = 90 mm Hg To calculate the FIO2 necessary to maintain PO2 = 90 mm Hg at a specific altitude, choose the value on the Y axis closest to that necessary to maintain PO2 = 90 mm Hg at sea level (altitude = 0 ft) and follow the corresponding line across to the new altitude (X axis). The proper FiO2 is the Y value corresponding to the new X value.

FIGURE 40-6  Fraction of inspired oxygen (FIO2) required to maintain partial pressure of oxygen (PO2) at 90 mm Hg (varying with altitude).

CARDIOPULMONARY RESUSCITATION AND CARDIAC DEFIBRILLATION

ground.24,105 In the interest of safety, however, it is best to notify the pilot before performing defibrillation.

CPR in an aircraft is difficult at best. The rescuers must perform several tasks simultaneously while ventilating the lungs or compressing the chest, all in a physically confining space. The crew must be familiar with modifications in technique.45 As previously mentioned, there should be no concern with airborne defibrillation if all electronic navigational equipment on the aircraft has a common ground, as mandated by Federal Aviation Administration (FAA) standards. Despite cramped quarters and sensitive electrical equipment, defibrillation can be safely performed in all types of aircraft currently used for emergency transport utilizing standard precautions routinely used during defibrillation on the

PATIENT COMBATIVENESS Patients may be combative to the point that they pose a threat to the safety of the flight and crew. An uncontrollable patient may cause sudden shifts in aircraft balance or may strike a crew member or important flight instruments or equipment. Such patients should be properly restrained in advance. If sedation is necessary, a careful neurologic examination documented beforehand is essential. Useful agents include diazepam or shorter-acting agents, such as midazolam. Paralyzing agents, such as pancuronium, vecuronium, and succinylcholine, have the 761

PART 5  RESCUE AND SURVIVAL

advantage of not altering the sensorium, but they require airway control with ET intubation.99 In addition, it is necessary to sedate a patient who is paralyzed to facilitate intubation and transport.

Danger zone

ENDOTRACHEAL INTUBATION ET intubation may be difficult to perform while airborne, especially in a confining cabin, and should be done before departure if possible. This is especially true in trauma victims with head injuries and in burn victims who have carbonaceous sputum or hoarseness. Special techniques are available to supplement standard methods of intubation. These include lighted stylet, ET tubes with controllable tips, intubating laryngeal mask airways, and digital intubation. Video laryngoscopy has been shown to be effective in the air medical environment.12 U.S. Air Force CCAT teams now carry a small battery-operated video laryngoscope as part of their standard equipment. Sedation or pharmacologic paralysis may be necessary. Of 106 aeromedical transport programs in the United States that report using neuromuscular blocking agents, 39 use them to facilitate intubations, and 67 use them once a patient is intubated to manage combativeness and ensure airway patency.91 Induction of paralysis before intubation in the aeromedical setting is controversial. One study reported a 96.6% success rate using succinylcholine to facilitate intubation, with 3.4% of patients requiring an emergency surgical airway.68 Beside the need for surgical airway if intubation is unsuccessful, concerns exist about cervical spine manipulation during intubation in the paralyzed patient, unrecognized esophageal intubation in a nonbreathing patient, and the relative contraindications to the use of succinylcholine in certain patients. Patients with contraindications to the use of succinylcholine can be treated with vecuronium or rocuronium. As with any critical airway intervention, there must always be a backup plan if endotracheal intubation fails. Blind airway devices such as a laryngeal mask airway or King LT Airway device, or other salvage airway device with which the crew is comfortable should always be available. In some flight programs, nonphysician crew members are taught to perform emergency cricothyrotomy. Although occasionally lifesaving, this procedure can be difficult to perform and should be undertaken only as a final method to secure an emergency airway. Endotracheal tube cuffs are normally filled with air. At one time it was standard operating procedure in USAF aeromedical evacuation to fill the ET tube cuff with sterile water or saline during transport to avoid volume/pressure changes in the cuff associated with changes in cabin pressure. Current procedure is to fill the ET tube cuff with air; however, the CCAT crew is required to check the cuff pressure with a cuff manometer during climb out, cruise, and descent.102 It is good practice to check for overinflation or underinflation of any air-filled devices (e.g., air splints, tracheostomy tubes) at regular intervals during flight.

Prohibited area

Acceptable area Best area Uphill (wrong)

Downhill (right)

FIGURE 40-7  Helicopter safety. A, Safe approach zones. B, The proper way to approach or depart from a helicopter.

passengers. Safety practices vary depending on the type of aircraft but include common guidelines. Approaching the Aircraft Helicopters with turning rotor blades must be approached only from the front and sides and only while under pilot observation (Figure 40-7). The tail rotor must be given wide berth, especially on helicopters with rear doors. It is advisable to station a crew member in a safe position to direct approaching individuals away from the tail rotor. Shutting down the helicopter’s engines completely, when the situation allows, is prudent before patient loading and unloading. Approaching in a crouched position minimizes the risk for contact with the rotor blades should a sudden gust of wind or movement of the aircraft cause them to dip. Loose clothing and debris should be secured (Box 40-6). Fixed-wing aircraft should be approached with similar precautions regarding propellers. This is especially important in aircraft with access doors in front of the wing and engine nacelles.

THROMBOLYSIS Air transport of patients with acute myocardial infarction often involves thrombolytic therapy. Because bleeding is a major adverse effect of thrombolytic agents, one study investigated whether air transport resulted in a higher incidence of bleeding complications compared with a similar cohort of patients given thrombolytic drugs who were transported by ground ambulance. The study concluded that helicopter transport of patients with acute myocardial infarction after initiation of thrombolysis is comparatively safe and without a clinically significant increase in bleeding complications.35

Flight Safety Because aeromedical transport involves medical care delivered in a hostile environment, the patient and crew are at risk for injury or death in the event of a mishap. Flight crew training must emphasize safety. The pilot is ultimately responsible for safety of the aircraft’s occupants and is trained not only to operate the aircraft skillfully and safely but also to provide necessary safety instructions and guidance to crew members and 762

BOX 40-6  Helicopter Safety Do: Approach and depart downhill Use crouched position Approach after visual contact and approval from pilot Await direction of flight crew Approach from the front or the sides Secure area first of people and then of loose debris Don’t: Approach or depart uphill Use tall intravenous poles or other objects Use loose sheets or clothing Smoke within 15.2 m (50 feet) of the aircraft Run near the aircraft Drive a vehicle within 30.5 m (100 feet) of the aircraft Shine headlights or flashlights toward the aircraft

Safety Belt Use The use of safety belts (preferably with shoulder harnesses, especially in helicopters) is an important safety measure. However, certain patient care activities (e.g., ET intubation, CPR) may be impossible to perform with safety belts secured. Design and selection of aircraft and interior configurations should allow maximal access to the patient, with crew members properly restrained. Throughout the flight, crew members and patient should remain restrained as much as possible in smooth air and at all times in rough air. Movement inside the cabin affects aircraft balance. An aircraft loaded near its aft center of gravity (CG) limit may exceed its limits if a crew member moves to a new position within the cabin. Changes in position should be preceded by consultation with the pilot. Light aircraft are sensitive to turbulent air, and appropriate precautions must be taken to avoid being injured from sudden motion. Proper Use of Aircraft Equipment Crew members must be familiar with all aircraft equipment they may be required to operate in flight or in an emergency. This includes aircraft doors, fire extinguisher, communications equipment, oxygen equipment, and electrical outlets. In addition, the crew must be familiar with emergency shutdown procedures. Finally, before takeoff, door security must be confirmed by a crew member familiar with operation of the door. In-Flight Obstacle Reporting An extra pair of eyes can be invaluable to a pilot in a busy airspace or on a scene approach complicated by trees and electrical or phone wires. Primarily important in visual flight rules (VFR) conditions, assistance with obstacle identification can enhance safety of the mission; however, flight should not occur under conditions in which obstacle reporting by a medical crew member is essential to safety, because the person must then divide attention between patient care and obstacle reporting. Ground Coordination and Control Enthusiastic rescue personnel or curious onlookers may approach the aircraft in a hazardous manner. Flight crew members must be able to communicate with ground units during the landing phase to ensure adequate scene preparation; they may be required to perform crowd control while on the ground. This requires directing individuals away from the rotor blades, propellers, or other hazardous equipment at the scene. If loading or unloading the patient while the rotors or propellers are still turning (“hot loading” or “hot off-loading”) is necessary, special precautions must be undertaken for ground crews, the flight crew, and the patient. Emergency Procedures All crew members should memorize and routinely practice emergency procedures. These procedures should address in-flight fires, electrical failures, loss of pressurization, engine failure, emergency landing with and without power, precautionary landing away from an airport, and other in-flight emergencies. Survival An emergency or precautionary landing away from an airport necessitates survival before rescue arrives. Under adverse environmental conditions and with injured victims, survival may depend on specific actions by the crew. The crew should be proficient in emergency egress from the aircraft, including escape after crashes and water landings, especially in helicopters. After water landings, helicopters usually roll inverted and sink rapidly. Helicopter “dunker” training is required for many military helicopter crews. The crews are strapped into a simulated helicopter fuselage and lowered rapidly into a pool, simulating a semicontrolled water landing. The fuselage then rolls inverted and starts to sink; the crew must open emergency exits and egress the simulator. This type of training has been shown to save lives in helicopter water crashes. All crew members should be trained in the use of emergency signaling devices, such as emergency

TABLE 40-3  Swimmer-to-Helicopter and Ground-

to-Air Signals

Intention

Action

Deploy medical kit Situation okay Lower rescue cable with rescue device Lower rescue cable without rescue device Helicopter move in/out Cease operations Deploy litter Personnel secured, hoist rescue device Team recall

Arms above head, wrists crossed Thumbs up Arm extended over head, fist clenched Climbing-rope motion with both hands Wave in/out with both hands Slashing motion across throat Hands cupped, then arms outstretched Vigorously shake hoist cable or thumb up with vigorous up motion with arm Circle arm over head with fingers skyward

locator transmitters (ELTs), flares, signal fires, and ground emergency signals. Survival skills should be taught to all crew members, including advanced first aid, water survival, building emergency shelters, fire starting, and obtaining water and food from the environment. Ground-to-Air Signaling It is best to have radio communication between the ground party and the helicopter crew. This may not be possible, however, and hand signals may be needed to communicate. Standard hand signals are used by military rescue personnel for communication between a deployed rescue swimmer and the helicopter (Table 40-3). These same signals can be used while on land. To acknowledge the signals, the hoist operator gives a “thumbs-up” sign or the pilot flashes the rotating beacon. Landing Zone Operations The ideal helicopter landing zone (HLZ) is a wide, flat, clear area with no obstacles in the approach or departure end. Vertical landings and takeoffs can be done, but it is safer for the helicopter to make a gradual descent while flying forward. Higher altitudes and higher temperatures require larger landing zones (Figures 40-8 and 40-9). The size of the landing zone depends on the weather conditions, type of helicopter involved, altitude, temperature, and types of obstacles in the area. The FAA recommends that the minimum landing zone for a small helicopter (Bell 206 or BK-117 for example) is 18.3 × 18.3 m (60 × 60 foot) square. Medium helicopters such as Bell 212 or 412, or a Sikorsky S-76 require a minimum of 22.9 × 22.9 m (75 × 75 feet), and large helicopters such as the Chinook, Sikorsky H-60 series or the Eurocopter Puma required a minimum of 36.6 × 36.6 m (120 × 120 feet).31 In general, pilots prefer the largest, flattest piece of ground they can find. The condition of the ground (e.g., loose snow,

FIGURE 40-8  Bell 412 emergency medical services helicopter landing on a low bridge in the Texas hill country. Although small, this helicopter landing zone (HLZ) gives good approach and departure paths with minimal obstacles. Traffic over the bridge should be stopped a minimum of 30.5 m (100 feet) away from the HLZ (preferably more) during approach, landing, and takeoff. (Courtesy San Antonio AirLife.)

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

Engine shutdown on the side of entry enhances safety of loading and unloading.

PART 5  RESCUE AND SURVIVAL

Night Operations

FIGURE 40-9  Emergency medical services helicopter landing on a freeway near the Nevada Test Site, 96.6 km (60 miles) north of Las Vegas. Note that traffic in both directions of the freeway has been stopped. (Courtesy Nevada Test Site Fire-Rescue.)

dust, gravel) should be communicated to the pilot before the final approach. Before the helicopter lands, all loose clothing and equipment should be secured. During approach, no personnel or vehicles should move on or near the landing zone. The FAA recommends that no spectators should be within 61 m (200 feet) of the HLZ, and that emergency vehicles should be a minimum of 30.5 m (100 feet) away. If a ground guide is used (see later discussion), that person should be in the HLZ only long enough for the pilot to positively identify the HLZ. The ground guide should then move out of the HLZ in the upwind direction. If at any time an unsafe condition is noted, the ground guide should immediately give a “wave off” signal to the pilot. The FAA recommends that the HLZ be marked at night with a “box and one” configuration (Figure 40-10). Each corner of the HLZ is marked with a light or a flare, with a fifth flare outside the box indicating the direction of the wind.31 Once the helicopter is on the ground, it must be approached only from the front and side, and then only while under direct observation of the pilot. The aft portion of the aircraft and areas around the tail rotor must be avoided at all times. Some helicopters (e.g., BK-117) have rear doors for loading and unloading patients, and ground personnel should wait for directions from the crew before approaching the rear area. If the ground is uneven or is a slope, all personnel should approach and depart from the helicopter on the downslope side. It is safest to load the patient into the helicopter with the engines off and the rotors stopped (“cold load”). If the patient must be loaded with the engines on and blades turning (“hot load”), eye and ear protection should be worn by all personnel approaching the helicopter, including the patient. A safety person should be assigned to prevent anyone from inadvertently walking toward the tail rotor. Once the patient is loaded, all personnel should leave the landing zone, take cover, and stay in place until the helicopter has departed. It is best to be off to the side, not directly in the takeoff path.

Direction of wind

*

*

* Light or road flare

*

*

FIGURE 40-10  A “box and one” temporary helicopter landing zone (HLZ). A light, piece of light clothing, or flare is placed at each corner of the HLZ. A fifth light, flare, or piece of light clothing is placed 5 to 10 m (16.4 to 33.8 feet) outside the square directly upwind, showing the pilot the wind direction. All lights, flares, or clothing should be firmly attached to the ground to prevent them from being blown away by rotor wash.

764

Night helicopter rescue operations are considerably more dangerous than are daylight operations. In most cases, it is best to delay helicopter insertion or extraction operations until daylight. If this is not possible, however, night missions can be done safely with careful planning and coordination between the helicopter and ground party. The same rules of daylight helicopter operations apply to night operations, but with extra care taken to ensure that all personnel understand their roles. In night operations, it is virtually mandatory to have radio communications between the ground and the helicopter. “Nocomm” night operations should be attempted only by personnel specially trained and experienced in these techniques. The landing zone should be clearly marked and the pilot allowed to make the approach. All personnel should stay clear of the landing zone until the pilot has made a safe landing. Personnel approaching the landing zone should have a small light or reflective material attached to their outer clothing so they can be clearly seen. The minimum number of people should approach the helicopter, and a safety observer is mandatory to keep the ground team together and clear of the tail rotor and rotor blades. The landing zone should be as large as possible, preferably at least 50% larger than a daylight landing zone. Any obstacles should be clearly marked with light-colored streamers, small lights, or even light-colored clothing. The FAA Aeronautical Information Manual gives several methods for marking an HLZ at night. One technique is to place a light, strobe, or flare at the four corners of the HLZ and a single light, flare, or strobe outside the HLZ indicating the direction of the wind (the “box and one” configuration noted above; see Figure 40-10). Any small lights, flares, or chemical light sticks should be secured to the ground so they do not blow away in the rotor wash. Another method is to place a vehicle at each corner of the HLZ and aim their low-beam headlights toward the center of the HLZ. Spotlights, hand lights, and vehicle headlights should be pointed at the ground, not into the air; lights pointed at the helicopter during landing and takeoff may distract or momentarily blind the crew. If flashlights are not available, small fires can be used to illuminate the edges of the landing zone, although the helicopter can scatter burning embers for many meters. If crew members are using night vision equipment, lights must never be flashed at the helicopter. Even the amount of white light from a small flashlight may be sufficient to overload the night vision equipment, functionally blinding the crew. Ground Guide If a ground guide for the HLZ is to be used, the person designated to be the ground guide should stand in the middle of the HLZ. Once the helicopter is in sight, the ground guide should hold both arms over his or her head (daytime) or hold two flashlights over his or her head (night operations). Once the pilot has identified the HLZ, the ground guide should move out of the HLZ in the upwind direction. The guide should continue to give the “safe to land” signal from well outside the HLZ until the aircraft has landed. No persons should be in the HLZ or even moving toward the HLZ during landing. If at any time during the approach the ground guide sees any unsafe conditions in the HLZ or surrounding area, he or she should immediately give a “wave off” (Figure 40-11).31 Using a ground guide to “marshal” a helicopter into a tight or crowded HLZ using hand signals is a difficult and dangerous procedure and should only be attempted by personnel specifically trained in this procedure. The pilot also must have been specifically trained in these procedures and must know that the ground guide is competent to guide his or her aircraft to the ground.

Aeromedical Aircraft Many different types of aircraft can be adapted to the air ambulance role. Each type has its strengths and weaknesses. On the other hand, not all aircraft are well suited for SAR in wilderness areas. Matching the physical and flight characteristics of the

LZ unsafe (day)

Land here (night)

LZ unsafe (night)

FIGURE 40-11  Ground guide hand signals. The ground guide should stand in the middle of the helicopter landing zone (HLZ) with arms raised over his or her head (the “safe to land” signal) until the pilot has seen the HLZ. The ground guide should then immediately exit the HLZ heading upwind at least 5 to 10 m (16.4 to 33.8 feet) outside the marked HLZ and maintain the “safe to land” signal. If at any time  the ground guide sees a danger or unsafe condition around the HLZ, he or she should immediately give the wave-off signal and continue this signal until the helicopter has aborted the approach/landing.

aircraft to the needs of the mission is vital. In many circumstances, compromises must be made because of aircraft availability. Rescuers must consider the physical characteristics of the aircraft when caring for a victim in flight.

CABIN SPACE Cabin space should be considered not only in terms of total interior volume in cubic feet, but also with regard to floor space, headroom, and the ergonomics of cabin layout. Ample headroom should be available for the patient to lie comfortably on a secured stretcher and for access to all parts of the body by two crew members. Specifically, access to the head is needed for intubation, the chest for CPR, and the extremities for monitoring perfusion. Some helicopters, such as the Aerospatiale AStar/TwinStar and the MBB BO-105, provide ample upper body access but only limited lower body access while in flight. The relationship of flight crew members when seated (and secured by seat belts) in proximity to the patient is important. The ideal configuration places one medical crew member at the patient’s head for airway management and verbal interaction and one at the patient’s side to monitor vital signs and perform necessary non–airway-related procedures. This arrangement is typified by the MBB BK-117 helicopter (Figure 40-12).

FIGURE 40-12  Stanford Life Flight MBB BK-117. (Courtesy Geralyn Martinez.)

FIGURE 40-13  U.S. Coast Guard HH-60J Jayhawk helicopter in low hover over water, preparing to lower hoist cable to the rescue swimmer. Note the extensive spray under the aircraft. The Jayhawk, a variant of the UH-60 Black Hawk, is a medium-range helicopter used for search and rescue, drug interdiction, and maritime law enforcement. (Courtesy U.S. Coast Guard.)

Although some rotary-wing aircraft, such as the BK, are theoretically capable of transporting two patients, this greatly increases demands on the flight crew and the aircraft and diminishes access to both patients. Policies and procedures regarding two-patient transport in these aircraft should be carefully considered. In some large helicopters, such as the CH-46, CH-47, and CH-53, there is enough room to work on multiple patients. Even on relatively large (by civilian standards) military helicopters, however, such as the Coast Guard HH-60J Jayhawk (Figure 40-13), space for patient care can be at a premium. Cabin space can be more generous in fixed-wing aircraft. Cabin-class airplanes, such as the Beechcraft King Air and Piper Cheyenne III, provide an aisle and capability to carry more than one patient and additional crew or family members. However, even in large military aircraft such as the C-130, carrying multiple patients with equipment and supplies can still result in a remarkably crowded cabin.

ACCESS FOR PATIENT LOADING The cargo door should be wide enough that the patient’s stretcher can be maneuvered into the aircraft without undue tilting, and it should be positioned comfortably near stretcher height to obviate the need for strenuous lifting during ground loading. Standard door configurations on many aircraft do not meet these needs. The “clamshell” doors on an MBB BK-117 helicopter and the oversized cargo door on a Gulfstream Commander 1000 work well for patient loading (Figure 40-14).

FIGURE 40-14  MBB BK-117 with rear clamshell doors open. (Courtesy Susan Lockman, Stanford Life Flight.)

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

Land here (day)

PART 5  RESCUE AND SURVIVAL

Maximum take-off weighta

____________

Less basic empty weightb

– ____________

Less fuel on boardc

– ____________

Less pilot and crew

– ____________

Less medical geard

– ____________

Maximum “patient payload”

= ____________

aMaximum

take-off weight is certificated for each aircraft type and can be found in the operating manual.

bBasic

empty weight includes added avionics, permanent equipment, fluids, and unusable fuel. It is different for each aircraft and is recorded in the aircraft’s operating manual.

cThe quantity of fuel on board depends on the mission needs. Divide round-trip distance by cruise speed to yield time en route. Add time for warm-up, climb, approach, and a 30-minute reserve (VFR) to yield total engine time. Multiply total engine time by rate of fuel consumption to yield total fuel consumed. Fuel weight 6 lb/gal. dMedical

gear includes carry-on and nonpermanent items. FIGURE 40-15  Weight calculation aboard aircraft.

USEFUL LOAD One of the most important considerations for a given patient transport is the aircraft’s useful load. This difference between the maximum takeoff weight and the basic empty weight is a reflection of the load-carrying capability. In most EMS helicopters, the useful load ranges between 680 and 1270 kg (1500 and 2800 lb). On-board avionics, medical equipment, fuel, and crew weights must be subtracted from this value to yield the maximum allowable patient weight (Figure 40-15). Fuel weighs 2.7 kg/3.8 L (6 lb/gal); a twin-engine helicopter may burn 266 L (70 gal) per hour (191 kg [420 lb] per hour), requiring it to carry 286 kg (630 lb) or more fuel for a 30-minute-radius flight (with 30-minute reserve). Thus it becomes evident that a flight crew of three weighing a total of 226.8 kg (500 lb) with a full load of fuel, oxygen, and medical gear may not have the capability to carry even a small patient, especially on a hot day when the helicopter’s performance (lift) is reduced. This consideration can become critical on flights from the accident scene, where terrain obstacles may require vertical takeoff and climb out, demanding maximum helicopter performance. Density altitude (a factor of the air temperature and the pressure at altitude) is critical in the performance of helicopters in mountain regions. High altitude combined with hot weather can seriously degrade the performance of even the most powerful helicopters.

WEIGHT AND BALANCE Not only must the weight of the loaded aircraft remain at or below the maximum allowed takeoff weight for that aircraft, but also the CG must lie within fore and aft limits established by the manufacturer. Each loading configuration places the CG in a unique position, which must be calculated by the pilot before flight, or the flight characteristics may be adversely affected, compromising safety. This consideration may dictate where certain pieces of medical equipment, such as oxygen bottles, may be placed or where heavier crew members must sit. On flights from the accident scene, the patient’s weight is approximated before departure. With pressure to hasten departure, accurate weight and balance calculations are difficult. The aircraft used must have enough margin in the CG envelope that CG limits are not easily exceeded for the given mission profile.

CRUISE SPEED One of the most basic reasons for transporting a patient by air is to take advantage of the greater speed of aircraft compared with ground vehicles. This allows the patient earlier arrival at the 766

destination and minimizes time spent out of the hospital. Not only do aircraft have a speed advantage, but they can also travel in a straight line from origin to destination without the curves and deviations present in surface travel. For an aircraft to compete with a ground vehicle in speed in a primary or secondary response mode, it must be at least twice as fast as an ambulance, because the helicopter must fly round trip (outbound to destination and inbound with patient) in the time that the ambulance would travel one way. This is possible with most EMS helicopters, unless (1) the referral location has no suitable landing area (necessitating a time-consuming transit of crew and stretcher to and from the location), (2) ground “packaging” times for the flight crew with the patient are excessive, or (3) an ambulance has a clear, straight highway as a means of alternative transport. Most EMS helicopters are capable of attaining 193 to 241 km/ hr (120 to 150 mph) over the ground, although a headwind or tailwind may hinder or improve these figures (Table 40-4). Piston twin-engine aircraft have a cruise speed range of 354 to 443 km/ hr (220 to 275 mph), turboprop aircraft a speed range of 483 to 620 km/hr (300 to 385 mph), and jets a speed range of 644 to 861 km/hr (400 to 535 mph) or more.22,78

RANGE Aircraft range is limited by the amount of fuel, which is a function of fuel tank capacity and useful load. In most cases, a tradeoff is made between payload and fuel; the more weight in fuel, the less weight in passengers (or patients). The maximum time aloft can be calculated by dividing usable fuel on board by rate of fuel burn per hour at cruise speed. Multiplying maximum time aloft by cruise speed yields the maximum range. The FAA, under FAR part 91.23, requires that a 45-minute fuel reserve remain at the conclusion of all flights conducted under instrument flight rules (IFR), and a 30-minute reserve under VFR. Most EMS helicopters operate under VFR, whereas most fixed-wing operations are IFR. Because helicopters typically fly to and from a point at which refueling is not available, round-trip fuel must be carried; this effectively limits the customary radius of operation to about half the range (less required reserves). Although it is possible to refuel en route to an airport, this adds to the flight time. Therefore helicopters typically operate within a radius of 241 km (150 miles) or less, unless the transport is one-way outbound or unless refueling at the destination is feasible. Fixed-wing aircraft operate from airport to airport; thus the radius of operation is closer to the maximum range with reserves. Many fixed-wing aircraft are capable of ranges in excess of 1609 km (1000 miles), with some

Helicopter Bell 206L-3 AStar 350D TwinStar 355F1 MBB BO-105 CBS Agusta 109A II Bell 222UT MBB BK-117 Sikorsky S-76 Dauphin 2

Cruise Speed (km/hr [mph]) 209.2 225.3 236.6 233.4 262.3 244.6 257.5 268.8 259.1

(130) (140) (147) (145) (163) (152) (160) (167) (161)

Engine

SHP

Useful Load (kg [lb])

Service Ceiling (m [ft])

Range   (km [mi])*

SE-T SE-T TE-T TE-T TE-T TE-T TE-T TE-T TE-T

650 615 420 420 420 684 650 650 700

884.5 847.3 1084.5 1239.2 1181.6 1531.3 1199.8 2131.9 1867.9

6096 (20,000) 4572 (15,000) 3999 (13,120) 5182 (17,000) 4572 (15,000) 4815.8 (15,800) 5182 (17,000) 4572 (15,000) 4572 (15,000)

523 (325) 609.9 (379) 592.2 (368) 547.5 (334) 577.8 (359) 611.6 (380) 592.2 (368) 885.1 (550) 907.7 (564)

each each each each each each each

(1,950) (1,868) (2,391) (2,732) (2,605) (3,376) (2,645) (4,700) (4,118)

Data from Collins RL, editor: Flying 1985 annual and buyer’s guide, New York, 1985, Ziff-Davis; and 1987 Hospital aviation directory, Hosp Aviat 6:8, 1987. SE-T, Single engine, turbine; SHP, shaft horsepower; TE-T, twin engine, turbine. *Range includes fuel for warm-up, taxi, climb, and 30-minute reserve.

jets able to travel more than 3219 km (2000 miles) without refueling.

PRESSURIZATION The partial pressure of oxygen in the atmosphere declines with increasing altitude so that at 5486 m (18,000 feet) it is one-half that at sea level. Part 91.32 of FAR requires the use of supplemental oxygen for the pilot at flight altitudes above 3810 m (12,500 feet) for longer than 30 minutes.30 Above 4267 m (14,000 feet), supplemental oxygen must be used by the pilot and all minimum required flight crew at all times. Technically a medical flight crew member is not a required minimum crew member for the operation of the aircraft; neither is the co-pilot of an aircraft operated under FAR part 135 and certified for single-pilot operations (as with most aeromedical aircraft). Thus the medical crew member is not required to wear supplemental oxygen, although doing so would be prudent, especially for smokers. At altitudes greater than 4572 m (15,000 feet), in addition to the above requirements, each occupant must be provided with supplemental oxygen (although there is no legal requirement to use it). The effects of hypoxia with increases in altitude are more pronounced in patients with lung disease and preexisting hypoxia; this necessitates supplemental oxygen at much lower altitudes. Supplemental oxygen at night will enhance night vision, even at altitudes below 3810 m (12,500 feet), and should be considered for the flight crew, based on operational requirements. To eliminate the need to provide supplemental oxygen, pressurization is available in many larger, fixed-wing aircraft (Table 40-5). A pressurized aircraft is able to pump air into the cabin to

maintain a pressure differential between the cabin and outside air, generally 4 to 8 lb per square inch (psi). This allows the cabin atmosphere to be maintained at or below the equivalent of a 2438-m (8000-foot) altitude, despite actual altitudes of 9144 m (30,000 feet) or higher.47,66 Pressurization obviates the need for supplemental oxygen for crew members and nonpatient passengers, but passengers with lung disease may still require it. Also, by limiting the drop in cabin pressure that occurs with altitude, changes in trapped gas volumes, such as in ET tube cuffs, air splints, and the gastrointestinal tract, can be decreased or eliminated. Special categories of patients include those with dysbarism. Exposure to increased altitude, with its concomitant decrease in ambient pressure, should be avoided. If possible, sea-level ambient pressure should be maintained when transporting these patients. On the other hand, most helicopters are nonpressurized and generally fly at lower altitudes, where altitude-related hypoxia is unlikely. One exception occurs in mountainous regions where altitudes required to rescue victims or cross mountain passes may exceed 3658 m (12,000 feet). Reasons for transporting patients at higher altitudes include terrain avoidance, the need to surmount adverse weather (which usually occurs within 6096 m [20,000 feet] above ground), and greater speed and fuel efficiency at higher altitudes.

SERVICE CEILING The service ceiling is the maximum altitude at which an aircraft can still maintain a rate of climb of 30.5 m (100 feet) per minute. This ceiling is important in predicting an aircraft’s ability to climb above adverse terrain and weather and in taking advantage of

TABLE 40-5  Fixed-Wing Aircraft Used for Aeromedical Transport Aircraft Seneca III Baron 58TC Cessna 402C Navajo 350 Cessna 414 Cessna 421 Cessna 441 Cheyenne II Cheyenne III MU-2 King Air F90 Commander 1000 Citation I Lear 25D

Cruise Speed (km/hr [mph])

Cabin

Engine

Useful Load (kg [lb])*

Service Ceiling (m [ft])

Range   (km [mi])†

Takeoff   (m [ft])‡

137.3 (221) 172.1 (277) 152.2 (245) 155.3 (250) 160.3 (258) 172.1 (277) 205.1 (330) 182.1 (293) 215.6 (347) 197 (317) 192 (309) 200.7 (323) 254.8 (410) 316.3 (509)

NP NP NP NP P P P P P P P P P P

TE-P TE-P TE-P TE-P TE-P TE-P TE-T TE-T TE-T TE-T TE-T TE-T TE-J TE-J

871.4 (1,921) 1109.9 (2,447) 1258.3 (2,774) 1148.9 (2,533) 1082.3 (2,386) 1273.2 (2,807) 1870.6 (4,124) 1838.4 (4,053) 2017.6 (4,448) 1803 (3,975) 1988.1 (4,383) 1798.5 (3,965) 2368.7 (5,222) 3243.2 (7,150)

7620 (25,000) 7620 (25,000) 8199.1 (26,900) 7315 (24,000) 9387.8 (30,800) 9205 (30,200) 10,668 (35,000) 9448.8 (31,000) 10,668 (35,000) 8321 (27,300) 9448.8 (31,000) 9372.6 (30,750) 12,496.8 (41,000) 15,544.8 (51,000)

1160.4 (721) 1850.7 (1,150) 1873.3 (1,164) 1931.2 (1,200) 2092.1 (1,300) 2449.4 (1,522) 3532.5 (2,195) 2051.9 (1,275) 2879.1 (1,789) 2272.4 (1,412) 2116.3 (1,315) 3458.5 (2,149) 2414 (1,500) 2575 (1,600)

381 (1,250) 823 (2,700) 670.6 (2,200) 670.6 (2,200) 792.5 (2,600) — — 762 (2,500) 975.4 (3,200) — 883.9 (2,900) 914.4 (3,000) 1219.2 (4,000)

Data from Collins RL, editor: Flying 1985 annual and buyer’s guide, New York, 1985, Ziff-Davis; 1987 Hospital aviation directory, Hosp Aviat 6:8, 1987; and McNeil EL: Airborne care of the ill and injured, New York, 1983, Springer-Verlag. NP, Nonpressurized; P, pressurized; TE-P, twin engine, piston; TE-T, twin engine, turboprop; TE-J, twin-engine, turbojet/turbofan. *Useful load excluding avionics, fuel, passengers. † Range estimated at cruise speed, less 45-minute reserve. ‡ Approximate nonbalance-field takeoff length.

767

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

TABLE 40-4  Helicopters Frequently Used for Aeromedical Transport

PART 5  RESCUE AND SURVIVAL

favorable winds aloft to maximize ground speed. In the western United States, mountainous areas require flight at least 610 m (2000 feet) above the highest terrain along the route of flight, which means a 3658- to 4877-m (12,000- to 16,000-foot) service ceiling. These altitudes restrict most helicopters and require use of supplemental oxygen in nonpressurized airplanes. Flight operations that typically require flight at these altitudes should have access to aircraft with sufficiently high service ceilings and pressurization.

RUNWAY LENGTH Although not a factor in helicopter operations, runway length restricts certain fixed-wing aircraft from landing. Most airports in rural areas have runway lengths between 610 and 1219 m (2000 and 4000 feet). Higher-performance airplanes usually have progressively longer runway requirements and may be unable to land and take off safely on these strips. Thus when transport from a rural location with a short runway is requested, it is important to determine the capability of the aircraft being used. Piston twin-engine aircraft can usually operate safely from a 762to 914-m (2500- to 3000-foot) strip but may have difficulty with 610 m (2000 feet); turboprop airplanes require 762 to 1067 m (2500 to 3500 feet); and jets usually require runway lengths of 1219 m (4000 feet) or more.66 The takeoff roll for airplanes increases with increasing temperature and airport altitude; on a hot day, many airplanes may be incapable of taking off from a short runway if heavily loaded. In winter conditions, operating on icy runways may pose a safety hazard for braking. Turboprop airplanes and jets have a reverse thrust mode that can slow the aircraft on rollout without braking.

WEATHER OPERATIONS Adverse weather conditions that may affect a given flight include restrictions in visibility resulting from precipitation, fog, haze, or clouds, as well as airframe icing, turbulence, and wind shear. Flight during instrument meteorologic conditions (IMC) requires adherence to IFR, whereas visual meteorologic conditions (VMC) allow alternative use of VFR. VMC for airplanes are defined as visibility of at least 4.8 km (3 miles) and ceiling of at least 305 m (1000 feet) (departing from an airport in controlled airspace).30 The ability to fly IFR not only improves the likelihood that the mission can be undertaken and completed safely should clouds or adverse weather be present but also enhances ability of the air traffic control center to follow the flight and properly separate aircraft. IFR capability has drawbacks. Sophisticated and expensive equipment and training are required. Many fixed-wing aircraft are capable of IFR operations, but many EMS helicopters are not. IFR operations are usually conducted from airport to airport (where an instrument approach is available), but most helicopters travel to and from nonairport points without an instrument approach. The percentage of actual missions canceled or aborted because of IMC is small in most rotary-wing programs. One study determined that inadvertent excursions into IMC occurred about 1.3 times per pilot per year, and the anticipated percentage of operations that would be conducted IFR, if it were available, was 9.4%.72 For most hospital-based programs, the cost of upgrading to a more expensive IFR-equipped helicopter (especially if a co-pilot is necessary for IFR certification), plus the added expense of maintaining pilot IFR proficiency, would be prohibitive. As a rule, military helicopters fly with a pilot and co-pilot and are usually capable of flying in IFR conditions, although IMC are far from ideal for SAR operations.

PERFORMANCE Closely related to aircraft speed is its ability to climb, expressed in feet per minute (fpm). Known as performance, this ability dictates the type of aircraft used for a given aeromedical transport mission. The greater the performance (a complex function of power, weight, wing, propeller, and air-density characteristics), the better the aircraft’s ability to outclimb adverse weather or to 768

avoid rising terrain or obstacles. Helicopters are unique in their ability to hover above the ground effect, that is, to climb vertically out of the supporting cushion of air produced by the rotor wash. Helicopters perform better when they have a running start, building up forward speed while still in the cushion of ground effect until translational lift is developed. Translational lift results from the forward-to-backward flow of air over the rotor blades. A helicopter’s ability to climb vertically out of ground effect is limited by horsepower and weight. On a hot day at high altitude, performance may be insufficient to take off vertically.46 This must be considered when selecting a landing site away from an airport. If a confined space surrounded by obstacles is selected, a vertical takeoff may be required.21 Fixed-wing aeromedical aircraft are virtually all twin engine, not only for enhanced speed, performance, and cabin space but also for the necessary redundancy of systems required for IFR operations under FAR part 135. If one engine fails, a second is available to allow flight to be maintained; however, if failure occurs during takeoff, single-engine climb performance may not be adequate to provide lift. This fact may be critical if insufficient altitude has been gained to allow a return to the airport before obstructions are encountered. Therefore single-engine climb performance for various types of aircraft must be considered, especially if operating out of high-altitude airports, in hot weather, or in mountainous regions (see Table 40-5). In general, singleengine climb performance is about 200 to 290 fpm in piston twins, 600 to 900 fpm for turboprops, and 1000 to 2000 fpm for jets.66 The airplane with the best single-engine climb performance will provide the greatest margin of safety, but the costs of equipment, pilot training, and adequate runways will be high.

AIRCRAFT FOR SEARCH AND RESCUE SAR is a special type of aeromedical transport that demands aircraft uniquely suited to this role. The aircraft should have good visibility to the sides and below, the ability to fly slowly and to hover, the ability to land away from an airport, and adequate performance in low-density altitude conditions. In addition, certain extrication situations require the capability to hoist victims from rugged or hostile terrain. Helicopters are the aircraft of choice for many SAR missions (Figure 40-16). Few hospital-based EMS helicopters are configured for hoist operations, and hospital flight crews are typically not trained in SAR techniques. The SAR mission differs from other types of medical missions in its requirement for low-level flight over potentially difficult terrain, use of flight crews for visual surveillance for survivors or wreckage, the need for a prolonged hover if hoist operations occur, and the need for flight crew training in wilderness survival principles should there occur a mishap. Experience and training in these activities are essential for safety. In general, military helicopters and their crews are better equipped and trained to carry out SAR operations. For example, U.S. Coast Guard and Air Force helicopters have radio locating equipment to pinpoint ELTs, also known as emergency position-reporting beacons; possess night vision and FLIR cameras to maximize the probability of visually locating a survivor; and have hoists that enable them to extract survivors from areas where landing is not an option. Flight crews on these missions must be specially trained in the use of rescue equipment and must possess appropriate medical qualifications and experience to deal properly with atypical EMS situations. U.S. Navy and Coast Guard rescue swimmers and Air Force PJs are trained to enter the water or proceed on land to aid in recovery of survivors. Navy and Coast Guard rescue swimmers receive basic medical training; USAF PJs are trained to the EMT-paramedic level and are given additional training in long-term care of trauma victims. Special hazards exist in mountainous areas. High-density altitudes may limit an aircraft’s performance, and local weather patterns may be erratic. On the leeward side of mountains or ridges, severe downdrafts may prevent a helicopter from hovering because of ground effect. The landing site selected should be free of terrain obstacles and should allow for a long, shallow approach and departure. Open areas away from the leeward side of mountains or ridges are preferable.

B

FIGURE 40-16  A, U.S. Coast Guard C-130 Hercules aircraft. This long-range aircraft is used for ice patrol, fisheries management, and search and rescue. B, Coast Guard HH-65 Dolphin helicopter. This short-range light-lift helicopter is used for near-shore search and rescue, maritime fisheries enforcement, and law enforcement. (Courtesy U.S. Coast Guard.)

SAR aircraft may not routinely carry the same medical equipment (e.g., ventilators, pacemakers, and defibrillators) as does a typical EMS helicopter. Care should be taken to verify that the medical equipment carried on a SAR aircraft is adequate for the intended mission (see Chapters 37 and 38).

PILOT REQUIREMENTS Helicopter EMS are usually VFR operations, and the FAA has established minimum requirements for pilot experience. FAR part 135.243 specifies that the pilot in command of a helicopter carrying passengers for hire must have at least 500 hours of flight time, including at least 100 hours of cross-country time with 25 hours at night. Fixed-wing services are typically IFR operations, and pilots must have at least 1200 hours of flight time, including 500 cross-country, 100 night, and 75 hours of actual or simulated instrument time. They must also be instrument rated and possess a commercial certificate. Most EMS helicopter pilots have much more experience than the minimum requirements; one survey found 59% had more than 4000 hours, and none fewer than 2000 hours.34 The pilot in command is solely responsible for the safety of all passengers and must decide whether to accept or decline a mission. This decision should be based on the destination, weather conditions, environmental circumstances, and estimated time at the scene, airport, or destination facility. For this reason, the pilot should not be told the nature of the medical mission until a decision to go is made, so that his safety decision is objective. The pilot has the final say on all decisions related to flight safety.

COMMUNICATIONS Helicopter EMS units must have the capability to communicate on very-high-frequency (VHF) air bands assigned for air traffic control, flight service, and local airport Unicom. In addition, the ability to communicate with ground EMS and public safety through VHF and ultrahigh-frequency (UHF) air bands is essential. Air use frequencies are accessible through standard aircraft communications transceivers, but EMS communications require additional radio equipment designed for this purpose. Additional needs include communication with the helicopter’s base station, either on a locally assigned public-use frequency or a Federal Communications Commission (FCC)-assigned discrete frequency in the VHF air band. Another means of communication is aircraft 800-MHz radiotelephones that can access the surface telephone network. Communication over air band frequencies requires strict adherence to FAA communications guidelines and a radiotelephone operator permit from the FCC.25

Medical Equipment and In-Flight Monitoring On-board medical supplies and equipment are typically tailored to the needs of a specific transport program and include medications; airway and ventilation supplies; monitors; ventilators; specialized splints, dressings, and bandages; IV fluids; immobilization devices; and stretchers.84

POWER Most aircraft systems operate from 14 or 28 volts of direct-current (DC) power supplied by an engine-driven alternator or generator. This is not adequate to operate most medical devices, which require 110 to 120 volts of alternate-current (AC) power. Such devices cannot be used without an internal battery of sufficient charge to provide power for the duration of the mission, or unless a 110- to 120-volt AC power source is available from a power inverter, which must be installed under STC. Power inverters are common components of EMS helicopters and dedicated fixed-wing aircraft that have been retrofit with a custom-made air ambulance cabin configuration, but they may not be a standard component in fixed-wing aircraft that support a dual role and use an interchangeable corporate configuration.

STRETCHER The patient stretcher must be secured to the aircraft according to the requirements of FAR part 23.561 or 25.561 for seats: 3.0 g upward (2.0 part 25), 9.0 g forward, and 1.5 g sideways. In this context, g is a measure of force, with 1.0 g being equal to the force generated when an object is subjected to an acceleration equal to the acceleration of gravity, (e.g., 9.8 meters per second). For helicopters, the requirements are 1.5 g upward, 4.0 g forward, and 2.0 g sideways. Special configurations, especially those incorporating oxygen bottles and metal framework, may require an STC. Other guidelines (recommendations only) for stretcher configurations are for clear view and access to the patients with at least 76.2 cm (30 inches) of headroom and at least 30.5 cm (12 inches) of aisle beside the head. The stretcher should be at least 48.3 cm (19 inches) wide by 185.4 cm (73 inches) long.102 If the patient is positioned with head forward, the acceleration that occurs during takeoff of a fixed-wing aircraft may cause venous pooling in the lower extremities and transient hypotension. To prevent this, the patient can be positioned with feet forward.

CLIMATE CONTROL The aircraft must be capable of maintaining a comfortable interior environment; about 24° C (75° F) is recommended. During summer months, the extensive glass area on a helicopter can produce a greenhouse effect, which may necessitate air conditioning for the comfort of both crew and patient.

LIGHTING Lighting should be available to enable the crew to attend to the patient’s needs but not interfere with cockpit operations. Curtains or other physical barriers may satisfy this need.

SUCTION Suction is a requirement for ambulance operations in most states and should be available at all times during aeromedical transport. Integral suction as a custom retrofit system or a portable batterypowered device can be used. 769

CHAPTER 40  Helicopter Rescue and Aeromedical Transport

A

PART 5  RESCUE AND SURVIVAL

TABLE 40-6  Aluminum Oxygen Tank Specifications

and Approximate Endurance

Cylinder Size C D E H

Duration (min)

Empty Weight (kg)

Capacity (L)

At 2 L/min

At 6 L/min

1.7 2.3 3.4 38.7

248* 414* 682* 7506†

124 207 341 3753

41 69 113 1251

From Luxfer Gas Cylinders. http://wwwe.luxfercylinders.com/products. *Fill pressure of 139 bar (2015 psi). † Fill pressure 153 bar (2216 psi).

OXYGEN In general, enough oxygen should be provided for the flight, plus a 45-minute reserve (IFR; 30 minutes VFR). In addition, oxygen should be carried to allow for ground handling time at either end. The amount of oxygen required can be obtained by multiplying the desired flow rate in liters per minute (L/min) by the total duration of transport and patient loading and unloading. Table 40-6 lists the capacities of various types of oxygen tanks and their respective weights. Some portable ventilators have a gas-driven logic circuit that requires additional air or oxygen. Electrically powered ventilators have a lower requirement for oxygen but carry the additional need for a power inverter. Most patients are transported with oxygen supplied by nasal cannulae (1 to 6 L/min). A single E-sized oxygen cylinder is adequate for short flights, although backup cylinders are usually carried. Patients intubated and maintained on 100% oxygen, as well as those ventilated on long flights, will quickly exceed the capacity of an E cylinder; several E cylinders or an H cylinder will be required.

VENTILATORS On short flights, most patients can be bag ventilated manually, with the addition of a positive end-expiratory pressure (PEEP) valve as needed. Manual ventilation has drawbacks. Minute ventilation can rarely be precisely controlled, leading either to respiratory acidosis or more often to alkalosis. The patient’s tidal volume limits may be exceeded, with resultant pulmonary barotrauma. More important, the medical attendant will be completely occupied with ventilation and is thus unavailable to perform other tasks. This takes on added importance if complex infusions are being administered or there occur in-flight complications. The likelihood that manual ventilation will be unsatisfactory increases with the duration of transport, medical complexity of the patient, and severity of underlying lung disease. Compact ventilators are available for use in the aeromedical transport environment.11,16,49 The simplest are pressure ventilators with a timing valve mechanism that will deliver a predicted minute ventilation at a given rate and tidal volume adjustable to patient size. These require that the patient have normal airway compliance. If airway resistance increases, smaller tidal volumes will result, and tidal volumes usually cannot be varied independently from rate. Volume-cycled ventilators are superior and available in configurations in which tidal volume and rate can be varied independently. Oxygen bottles, a 50-psi regulator, high-pressure gas lines, a patient breathing circuit, and source of humidification need to be present. As mentioned, ET tube cuffs need to be appropriately monitored during flight to prevent overinflation or under inflation resulting from changes in ambient pressure.

of power, usually an AC power inverter. With infusions that must be carefully maintained, an infusion pump is preferable. With frequent patient movement and manipulation, tubing can bend and kink, altering resistance to fluid flow. Air trapped in tubing (or in glass IV bottles) can expand with changes in altitude and increase or decrease the infusion pressure. Thus a reliable servocontrolled infusion system provides a margin of safety.

MONITOR-DEFIBRILLATOR AND EXTERNAL PACEMAKER Combination monitor-defibrillators operate from internal batteries when 110 to 120 volts AC is not available. Other monitors capable of pressure monitoring from arterial lines or pulmonary artery catheters may be used, but these may have limited usefulness on flights of short duration, during which vibration and motion (turbulence) can introduce artifact and erroneous readings, as may occur aboard a helicopter. These devices may find a greater role with dedicated fixed-wing aircraft that frequently transport critically ill patients over long distances. Noninvasive blood pressure measurement is reasonably accurate in most patients, although these devices may have insufficient sensitivity.61 Potential hazards of defibrillation while airborne remain a concern, although trials support its safety.24,43 Caution is still advised, and care should be taken to ensure that crew and aircraft systems are isolated from potential electrical contact (see Common Aeromedical Transport Problems, earlier). The pilot should be notified before defibrillation. It is unlikely that defibrillation will cause a problem with the aircraft, but if in a critical phase of flight (e.g., takeoff or landing), the pilot may delay the shock until the critical phase of flight is accomplished. Some external pacemakers have been approved for use in flight; however, care must be taken to ensure that the pacemaker and pads are properly shielded so that they will not interfere with the aircraft systems.

OXIMETRY AND END-TIDAL CARBON DIOXIDE MONITORING Pulse oximetry is often indicated for optimal patient care. Pulse oximeters use a colorimetric method, with placement of a soft probe over a fingertip, a toe, or in a thin skinfold such as an earlobe.1,49,95 They may be extremely useful in aeromedical transport, during which other methods to detect changes in respiratory status are difficult. End-tidal CO2 monitoring is now relatively easy to accomplish, even with transport monitors, and should be used for intubated/ventilated patients whenever possible.

MECHANICAL RESUSCITATORS Cardiac arrest resuscitation while airborne in a small cabin is difficult and physically demanding. In most instances, a standard medical crew of two will be completely occupied in performing chest compressions and ensuring ventilation. Additional tasks may be impossible. Therefore a mechanical resuscitator may be used to prevent fatigue and free crew members for other tasks.71 Mechanical resuscitators are gas-powered devices capable of providing ventilation and chest compressions automatically. Some non–gas powered models provide only chest compressions.

Flight Physiology Aeromedical care is different from ground-based care not only because of special equipment and the space-limited environment, but also because of the hostile physical milieu.

INFUSION DEVICES

HYPOXIA AND ALTITUDE

Several methods of IV infusion delivery are available in the aeromedical setting: gravity-feed microdrip or macrodrip tubing with the drip rate manually adjusted, gravity-feed automatic infusion regulators with a closed-loop drip-monitoring feedback mechanism controlling drip rate, and infusion pumps. If a pump is used over moderate or long transport distances, the internal battery power may be inadequate, necessitating an external source

The earth is blanketed by a sea of air. The troposphere lies in the first 9144 to 18,288 m (30,000 to 60,000 feet) and contains atmospheric moisture. Vertical convection currents, as well as a temperature decline with increasing altitude at a lapse rate of 2° C per 305 m (3.6° F per 1000 feet), occur here. Virtually all atmospheric weather occurs in this layer. Above this level lies the stratosphere, extending from 18,288 to 30,480 m (60,000 to

770

Pressure (mm Hg)

vapor pressure of water (PW, 47 mm Hg) has been subtracted. This is the basis of the alveolar air equation, as follows:

700

PAO2 = FIO2 × (PB – PW) – PCO2/R

600

where PCO2 is the arterial partial pressure of carbon dioxide and R is the respiratory quotient (about 0.8). Arterial partial pressure of oxygen (PaO2) in normal individuals is within 10 to 15 mm Hg of the PAO2. With lung disease characterized by ventilation– perfusion mismatch, intrapulmonic shunting, or severe diffusion defects, the alveolar-arterial (A-a) oxygen gradient is much larger, and higher amounts of inspired oxygen are required to produce sufficient oxygenation of arterial blood. Atmospheric PO2, PAO2, and PaO2 all decline with altitude (see Figure 40-17). To some extent, PaO2 can be maintained through hyperventilation because during this process PCO2 is reduced, but eventually PaO2 will decline below 60% and hemoglobin will begin to greatly desaturate. It is important during aeromedical transport to maintain hemoglobin saturation at or above 90%. Knowledge of the patient’s preflight PaO2 will enable a calculation of the patient’s A-a oxygen gradient, which can then be subtracted from the PAO2 calculated for the anticipated en route altitude (or cabin altitude in a pressurized craft) to yield the expected en route PaO2. Nomograms can be devised for this purpose (Figure 40-18). If the en route expected PaO2 is unacceptably low, supplemental oxygen is required. The FIO2 required to maintain the PAO2 at a given level can be calculated from the alveolar air equation as follows:

500 400 300 200 100 0 0

20

Partial pressure (mm Hg)

A

40

Altitude  1000 feet 100 90 80 70 60 50 40 30 20 10

FIO2 = (PAO2 + PCO2/R)/(PB – PW)

Or, if PCO2 = 40, R = 0.8, and PW = 47 mm Hg, then: FIO2 = (PAO2 + 50)/(PB – 47)

0 2

4

6

8

10

12 14 16

18

20

Altitude  1000 feet

B

PAO2

PaO2

Hyperventilation

FIGURE 40-17  A, Atmospheric pressure versus altitude. B, Alveolar (PAO2) and arterial (PaO2) partial pressure of oxygen versus altitude.

PB = 760 − (23 × Alt ) where Alt is the altitude above sea level in thousands of feet. Transport cabin environments rarely exceed these altitudes because pressurized craft are usually capable of maintaining cabin pressure equal to 2438 m (8000 feet) or below at normal cruising altitudes. Nonpressurized craft must provide supplemental oxygen above 15,000 feet. Even a modest increase in FIO2 is usually enough to maintain oxygenation under these circumstances, unless a severe A-a oxygen gradient exists, in which case 120

Sea level

110

2000

100

4000

90

6000

80

8000

70

10,000 12,000 14,000 16,000 18,000 20,000 22,000 24,000

60 50 40 30 20

TABLE 40-7  Composition of Air

Altitude

100,000 feet), where temperature remains relatively constant and there exists neither moisture nor vertical convection currents. Air exerts pressure on everything it contacts in an amount equal to the weight of the column of air above the point of reference. At sea level, the atmospheric pressure is 14.7 psi or 760 mm Hg. As the person ascends, a progressively smaller air mass remains to exert weight, and the pressure diminishes. At 5486 m (18,000 feet), the atmospheric pressure is one-half of that at sea level, and at 8534 m (28,000 feet), it is one-third as great (Figure 40-17). Similarly, under the weight of air, individual molecules tend to compact, so the density of air is also greatest at the surface and diminishes with increasing altitude. These phenomena underlie most of the important physiologic consequences of flight. Air is composed of several gases, of which oxygen makes up about 21%, an amount that is relatively constant despite increasing altitude28,49,72 (Table 40-7). Henry’s law states that the quantity of gas that goes into solution depends on the partial pressure of that gas (and its solubility characteristics) as exerted at the air–water interface. The alveolar partial pressure of oxygen (PAO2) is determined by multiplying the fractional composition of oxygen in inspired air (FIO2) by the atmospheric pressure (barometric pressure, PB) after the opposing

This allows PAO2 to be determined by inserting the PaO2 desired (the minimum acceptable is 60 mm Hg) to the known A-a oxygen gradient (calculated from the preflight blood gas level). PB can be estimated over the first 4572 m (15,000 feet) of ambient or cabin altitude as follows:

PaO2 at altitude (mm Hg)

0

10

Gas

Percentage

Nitrogen Oxygen Carbon dioxide Other gases Water vapor

78.09 20.95 0.03 0.07 1-5 at sea level

From Del Vecchio RJ: Physiologic aspects of flight, Oakdale, NY, 1977, Dowling College Press.

40 50 60 70 80 90 100 110 120 PaO2 at sea level (mm Hg) FIGURE 40-18  Arterial partial pressure of oxygen (PaO2) at altitude versus PaO2 at sea level. Locate the sea-level PaO2 on the x-axis and intersect with the cruise altitude (on the diagonal). Read across to find the PaO2 at altitude (y-axis).

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

800

PART 5  RESCUE AND SURVIVAL

the addition of continuous positive airway pressure (CPAP) or PEEP may be necessary. The previous equation would predict that a PaO2 of 80 mm Hg at sea level on 40% oxygen and would require that an FIO2 of 50% at 2438 m (8000 feet) be maintained. An oximeter can simplify monitoring of oxygenation; as altitude increases, a fall in oxygen saturation can be treated with increases in FIO2.

EFFECTS OF PRESSURE CHANGES Trapped Gas Boyle’s law states that the volume of a gas varies inversely with pressure. This means that trapped gases expand as an aircraft ascends to higher altitude (and lower pressure) and contract as it descends. The volume change can be determined from the following equation:

A

P1 × V1 = P2 × V2 Clinically this is manifested by such alterations as expansion or contraction of air splints or military antishock trousers, changes in ET tube cuff size, expansion of bowel gas in cases of intestinal obstruction or ileus, expansion of pneumothorax air space, and expansion of air trapped in IV lines (or glass IV bottles) (Table 40-8). Certain precautions must be taken, such as the use of plastic IV bags and frequent monitoring of pressure cuffs. Dysbarism Decompression sickness occurs mainly in scuba divers who ascend too soon after a dive. Too rapid a decrease in ambient pressure allows nitrogen bubbles to form in the microcirculation, which may lead to ischemia and tissue damage (see Chapter 77). Care must be taken during transport of an ill or injured diver to allow a surface interval of at least 12 hours before transport. If an individual must be transported abruptly after submersion, the transport must be conducted at the lowest possible safe altitude in a pressurized aircraft, to reduce the risk for decompression illness. Portable hyperbaric chambers have been developed, and several have been approved for flight in U.S. military aircraft. With one of these chambers, it is possible to transport a diving casualty by air while providing recompression therapy during flight (Figure 40-19). This will usually require a large aircraft and several crew members to monitor the chamber during the flight. Sufficient pressurized breathing gas must be brought along to supply such chambers. Careful planning to ensure sufficient supply is critical.

B FIGURE 40-19  A, Hyperlyte portable hyperbaric chamber being inflated and rigged for a dive on board a U.S. Air Force C-17 aircraft. At the time this photograph was taken, the aircraft was flying at 4572 m (15,000 feet). B, Hyperlyte portable hyperbaric chamber being secured to the deck of a U.S. Air Force C-17 aircraft. Note the gas lines feeding into the near end of the chamber. (Courtesy Robert C. Allen.)

traveling in a turbulent environment without a visual frame of reference. For example, when an aircraft enters a bank to the right, the sensation may be initially correctly interpreted. However, after rollout of the stationary bank to a neutral position, a sensation of rolling into a left bank may be sensed. If uncorrected,

Pitch

MOTION AND ACCELERATION Aircraft not only move through space in a rectilinear fashion, which cannot be detected by human senses in the absence of visual cues, but also rotate around three axes: longitudinal (roll), vertical (yaw), and horizontal (pitch) (Figure 40-20). Motions around these axes are sensed by the semicircular canals located in the inner ear. Sensations from these organs are useful as an adjunct to visual cues. However, they may quickly lead to spatial disorientation, a phenomenon often experienced by individuals

Roll

TABLE 40-8  Clinical Manifestations of Trapped Gas

Expansion

Trapped Gas Location

Clinical Manifestations

Intestinal lumen Pleural space

Abdominal pain, distention Pneumothorax, tension pneumothorax Subcutaneous emphysema Facial pain Ear pain Tooth pain Air embolism, decompression sickness Compartment syndrome, ischemia Flow rate increase Tourniquet effect Air leak, hypoventilation, tissue ischemia

Subcutaneous Paranasal sinuses Middle ear Dental root Blood Air splints, antishock trousers Intravenous bottle and tubing Blood pressure cuff Endotracheal tube cuff

772

Yaw FIGURE 40-20  Axes of movement in aviation.

Severity of Aeromedical Accidents, 1972-1989 Percentages

Major Cause Weather Engine failure Obstacle strike Control loss Other Primary Cause Pilot error Mechanical failure Unknown Accident Severity Fatal Injury Damage only

1972-1985

1987-1988

1989

30 18 18 9 25

30 9 10 20 40

17 0 33 17 33

64 30 6

60 30 10

83 0 17

36 28 36

50 30 20

67 17 17

From Collett HM: 1989 Accident review: Helicopter accidents set second lowest record in decade, J Air Med Transport 9:12, 1990.

apprehension may follow. The best remedy for this effect is to maintain a visual reference to the correct position. Vestibular stimuli, especially in turbulence with limited or no visual frame of reference, may result in motion sickness, manifested most often as nausea or vomiting. Affecting both patients and flight crews, motion sickness can be counteracted with antiemetics such as antihistamines (e.g., dimenhydrinate, 50 mg orally) or phenothiazines (e.g., prochlorperazine, 10 mg orally); however, these may produce sedation and are potentially hazardous in flight. Transdermal scopolamine patches applied behind the ear have been used as effective prophylaxis for nausea and vomiting during flight. As noted before, a combination of promethazine 25 mg and caffeine 200 mg orally has produced good results in a small study conducted on U.S. Army helicopter passengers.29 Also effective for controlling nausea and vomiting are 5-HT3 receptor antagonists, such as ondansetron, but they do not appear to relieve any of the other symptoms of motion sickness. It should be noted that nonsedating antihistamines, such as loratadine, have virtually no effect on motion sickness.

NOISE AND VIBRATION Noise and vibration are components of all aircraft environments, especially helicopters. The most obvious impact of noise is on communications within the cabin, particularly with the patient, who is least likely to have a headset and access to the aircraft’s intercom. In addition, the patient’s breath sounds are difficult if not impossible to hear. Thus other means to identify changes in respiratory status, such as pulse oximetry, must be employed. Headsets are essential for effective communication between flight crew members aboard a helicopter, although they may not be necessary aboard larger fixed-wing aircraft. Noise may lead to permanent defects in auditory acuity if exposure is prolonged or recurrent. Veteran pilots frequently demonstrate 10- to 20-dB reductions in high-frequency auditory acuity. Noise and vibration may also contribute to stress and fatigue.

Aeromedical Accidents Commercial flying is a remarkable safe activity. In fact, most airline passengers are in greater danger driving to the airport than flying across the country. However, air medical and rescue aircraft crashes occur with greater frequency than anyone would like (Table 40-9). Attention continues to focus on HEMS accidents. Statistics from 1986 estimated a rotary-wing accident rate of 17.65, with 5.88 fatalities per 100,000 transports.36 Aviation accident rates are typically reported in relation to flight hours. EMS fatalities therefore amounted to 6.0 per 100,000 flight hours, compared with 3.3 for the helicopter industry in general. The

EMS rate subsequently declined, however, with 3.0 accidents per 100,000 transports reported in 199190,98 (Figure 40-21, online). Since 2003, the rate of HEMS accidents per 100,000 flying hours has steadily decreased to the point where the HEMS accident rate is on a par with non-EMS helicopters and general aviation aircraft. Figure 40-22 shows the helicopter EMS fatality rate per 100,000 flying hours from 2004 to 2009. As can be seen, this has ranged from a high of 1.45 in fiscal year 2005 to a low of 0.17 in 2007. However, as recently as 2008 (an admittedly bad year for HEMS crashes), the occupational risk for HEMS crew members’ being killed in a crash was 164 per 100,000 hours. This is higher than commercial fishing (112 per 100,000 hours) or logging (86 per 100,000 hours). The risk for patients’ dying in an HEMS accident was 0.76 per 100,000 patients.30,72 In 2005, the FAA created a HEMS Task Force to look into HEMS accidents. The analysis of HEMS accidents from 1998 to 2004 indicated three primary safety concerns: inadvertent flight into IMC, night operations, and controlled flight into terrain.30 A retrospective study of all HEMS crashes from 1983 to mid-2005 showed a total of 182 HEMS crashes, with 39% involving fatalities. This study found that the odds of a fatality increased with postcrash fires and with crashes occurring at night and/or in bad weather (Table 40-10).6 The NTSB conducted a safety study of HEMS operations in 1988, evaluating 59 HEMS mishaps. The NTSB determined that HEMS crashes were more common than were non-EMS helicopter crashes, and that HEMS crashes were 3.5 times more likely to be fatal. This study also showed that the most common factor associated with all crashes was reduced visibility.73 The NTSB again addressed the topic of HEMS mishaps in 2006 in a special investigation report that examined both fixed-wing and rotary–wing mishaps. In this report, the NTSB concluded that of the 55 mishaps reviewed, 29 could have been prevented if corrective actions outlined in the special investigation report had been in place. The NTSB made four specific recommendations to the FAA (which has regulatory authority over civil aviation in the United States): (1) All flights with medical personnel on board should be conducted in accordance with FAR part 135 regulations concerning commuter aircraft flights. HEMS aircraft currently fly under FAR part 91 regulations (air taxi regulations) if no patients are on board, and FAR 135 if a patient is being carried. The NTSB would like all HEMS flights, with or without patients, to be under FAR part 135. (2) Develop and evaluate flight-risk evaluation programs. (3) Require formalized dispatch and flight following procedures, including up-to-date weather information. (4) Require installation of terrain awareness and warning systems on aircraft.74 In October 2008, these four recommendations were added to the NTSB’s “Most Wanted Transportation Safety Improvements.” In early 2009, the NTSB held a public hearing into HEMS safety, looking at factors that contributed to HEMS crashes and possible solutions to the problem.75 By February of 2010, the NTSB felt that there had not been sufficient improvement in the HEMS regulatory environment and issued a report stating their “Most Wanted Transportation Safety Improvements.”75 While noting that some improvements had been made, the NTSB again stated their recommendations. These are noted in Box 40-7.

1.6 1.4 1.2 1 0.8 0.6 0.4 0.2 0

1.45

1.26

1.32

1.18 0.56 0.17

FY 2004 FY 2005 FY 2006 FY 2007 FY 2008 FY 2009 FIGURE 40-22  Helicopter emergency medical services fatal accident rate per 100,000 flying hours, 2004 to 2009. FY, Fiscal year.

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

TABLE 40-9  Major and Primary Causes and

PART 5  RESCUE AND SURVIVAL

TABLE 40-10  Percentage of EMS Helicopter

Crashes Resulting In Fatality: United States, 1983 to April 2005

Characteristic Month of Crash March-May June-August September-November December-February Mission* Positioning Going for patient Patient transport Other Number of Occupants 1-3 4-6 Light Condition* Dark Daylight/dusk Instrument Conditions* Yes No Number of Engines* 1 2 Postcrash fire* Yes No

Total   Fatal, N = 182 No.

Fatal, %

Ratio of %   Fatal (95% CI)

43 49 42 48

16 17 13 25

37.2 34.7 31.0 52.1

1 0.9 (0.7-1.1) 0.8 (0.6-1.0) 1.4 (1.1-2.2)

46 51 44 19

18 17 23 6

39.1 33.3 52.3 31.6

1 0.8 (0.6-1.0) 1.3 (1.0-1.6) 0.8 (0.6-1.0)

129 53

45 26

34.8 49.1

1 1.4 (1.2-1.6)

86 95

48 23

55.8 24.2

2.3 (2.0-2.6) 1

30 147

23 45

76.7 30.6

2.5 (2.1-2.9) 1

82 98

34 36

41.5 36.7

1 0.9 (0.8-1.0)

33 141

25 41

75.8 29.1

2.6 (2.2-3.0) 1

*Some missing observations. From: Baker SP, Grabowski JG, Dodd RS, et al: EMS helicopter crashes: What influences fatal outcome? Ann Emerg Med 47:351, 2006.

The FAA has promoted several initiatives to improve HEMS safety. In November 2008, the FAA issued a mandatory change to air ambulance flights, requiring that all air ambulance operators comply with the FAR part 135 weather minimums, including positioning flights with medical crew on board. This change went into effect on February 22, 2009.32 The FAA has fielded an advanced HEMS weather tool through the web-based Aviation Digital Data Service that allows a user to identify gridded weather assessments in 5 × 5 km (3.1 × 3.1 mile) blocks. The purpose of this tool is to enhance weather planning data for VFR flights in order to make better go/no-go BOX 40-7  The National Transportation Safety Board’s

Most Wanted Safety Improvements for Helicopter EMS Operations, February 2010

1. Require all EMS operators to comply with 14 FAR part 135 operations specifications during conduct of all flights with medical personnel on board. 2. Require all EMS operators to develop and implement flight risk evaluation programs that include training all employees involved in the operation, procedures that support the systematic evaluation of flight risks, and consultation with others trained in EMS flight operations if the risks reach a predefined level. 3. Require EMS operators to use formalized dispatch and flight-following procedures that include up-to-date weather information and assistance in flight risk assessment decisions. 4. Require EMS operators to install terrain awareness and warning systems on their aircraft and to provide adequate training to ensure that flight crews are capable of using the systems to safely conduct EMS operations. From National Transportation Safety Board: Most wanted list: Transportation safety improvements, federal issues—aviation: Improve the safety of emergency medical services (EMS) flights, February 2010. http://www.NTSB.gov/Recs/ mostwanted. EMS, Emergency medical services; FAR, Federal Aviation Regulations.

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decisions and help avoid inadvertent flight into instrument weather conditions.30 Controlled flight into terrain can be addressed by multiple methods. A technology-based system, such as a helicopter terrain awareness and warning system, has been advocated for HEMS use. The FAA has not yet required use of this technology (although it does encourage its adoption by the HEMS industry) because of concerns it might not be appropriate for every HEMS operator.76 However, some HEMS operators are installing these systems, even though not required to do so by the FAA. As of June 2010, Air Methods had already installed this technology in 130 of its 305 helicopters. Night vision equipment can be of great help in night flight operations; however, pilots and crews must be specially trained and experienced to fly with this equipment. The FAA has estimated that approximately 30% of all HEMS operators use night vision equipment. The FAA encourages use of night vision equipment in HEMS where appropriate but has not mandated its use, feeling that it is not a “…one size fits all solution.”32 Recommendations for enhancing safety include instituting stringent guidelines to limit flights at night or in adverse weather, increasing pilot proficiency training, and reducing pilot fatigue and workload factors. Decisions on the appropriateness of air transport regarding use and weather should be based on general protocols that are not subject to the emotional turmoil of a medical crisis.14 The trend in the industry has been toward twinengine helicopters for an increased margin of safety from engine failure accidents. In addition, for dedicated EMS helicopter flights, a statistically strong relationship exists between the ability to fly under IFR and a lower accident rate.60 The AAMS considered the question of whether all helicopters should be required to have IFR capability when it published its voluntary standards for rotary- and fixedwing aircraft. This was not mandated because of the tremendous expense and because many programs were unlikely to comply.62 In an effort to decrease internal and external pressures that can accompany air medical flight, the National EMS Pilots Association, in collaboration with other air medical associations, has introduced the No Pressure Initiative. This initiative can provide a significant layer of protection against real or perceived pressures on the pilot and medical crews to initiate and complete an air medical mission. This initiative identifies three areas for intervention, noted in Box 40-8. A detailed explanation of the “No Pressure Environment” is in Figure 40-23. There is no magic bullet that can by itself significantly improve HEMS safety. Like the causes of most aircraft mishaps, the solutions are multifactorial. Adherence to HEMS dispatch guidelines can decrease the number of HEMS calls for responding to persons with conditions that could be transported just as easily by ground transportation. Training of dispatch personnel and flight crews and access to up-to-date weather information can increase flight condition awareness so that inadvertent flight into IFR conditions can be avoided. Helicopter terrain awareness and avoidance systems, night vision equipment systems, and on-board weather radar can increase safety margins at night and in poor weather conditions. However, there is no substitute for a trained, confident crew that knows its aircraft, equipment, and limitations, and that demonstrates the self-confidence and judgment to refuse or cancel a mission if the parameters indicate unacceptable flying conditions. BOX 40-8  The National EMS Pilots Association’s “No

Pressure” Initiative

Culture: Do not apply pressure to yourself or any member of your flight team. Provide positive support and recognition for conservative decisions. Risk assessment: Utilize a robust risk assessment tool prior to every flight. Require outside consultation prior to flight acceptance in mid-to-high risk conditions. En route decision point: Establish airspeed and altitude limitation for cruise flight. Turn around, land or transition to IFR when limit is reached. DO NOT CONTINUE. From National EMS Pilots Association. http://www.nemspa.org. EMS, Emergency medical services; IFR, instrument flight rules.

No Pressure Environment PRESSURE: Attempting to influence any member of a flight team to accept a flight into potentially unsafe conditions, in a potentially unsafe aircraft, or when any flight team member feels they are not able to perform their flight related duties safely due to stress or fatigue.

CULTURE WHY? The National EMS Pilots Association recently conducted an informal survey of more than 250 pilots to determine, in part, the extent to which internal and external pressures may be present within air medical operations. This survey revealed the need for further study and for the reinforcement and enhancement of current safety practices. Further, NEMSPA has developed an additional procedure that can contribute to the pilot's in flight decision making and risk assessment process. It is believed that this procedure along with other current initiatives, combined with a robust operational control structure, and as part of an overall Safety Management System implemented by the aviation operator, can add significant layers of protection against real or perceived pressures on the pilot and medical crews to initiate and complete an air medical mission.

Flight Team (includes Communication Specialists & Controllers): • DO practice good AMRM protocols when discussing flight requests • DO understand and use good ADM techniques to fo rm flight acceptance and flight continuance decisions • DO support and provide positive recognition wh en fellow team members make appropriate decisions • DO NOT allow patient type or condition to influence flight related decisions • DO NOT allow pressure from management and other work related associates to influence flight related decisions Physicians: • DO support and provide positive recognition when associate flight team members make appropriate decisions • DO NOT apply pressure to any flight team member Management: • DO support and reward good decision making • DO NOT allow or tolerate an environment where there is pressure to accept flights • DO NOT emphasize flight volumes or post tracking numbers in flight team areas or quarters All Participants: • DO ask questions during the team or organizational meetings that offer solutions or answers to questions that may arise during the enroute portion of the flight • DO NOT apply pressure either to yourself or any member of a flight team

RISK ASSESSMENT WHY? It is recommended that all EMS flight programs incorporate a RAT (Risk Assessment Tool) as part of the flight team’s preflight decision making process. The RAT should consider the basic risks associated with EMS flight operations, and should be tailored to the specific needs and environment of individual programs or bases. By helping the flight team identify and realize the inherent risks to individual flights, a well designed RAT will significantly reduce pressure on the flight team.

Design: A well designed RAT should account for the following variables: 1. Weather 2. Pilot experience a. EMS operations b. Flight area c. Specific aircraft model 3. Fatigue (preferably Fatigue Risk Assessment Tool) a. Circadian rhythms (ie, Circadian low: 0200-0500, schedules, etc.) 4. Night vs. Day There are numerous methods for accomplishing a RAT. Sample protocols are available in FAA Notice 8000.301.

WHY? The EDP (Enroute Decision Point) protocol has been field proven to be a simple, yet very effective tool that has been designed to minimize the possibility of helicopter CFIT (Controlled Flight Into Terrain) accidents caused by continuing flight into adverse and/or deteriorating weather conditions. NEMSPA believes, and pilots have confirmed, that this protocol can be an effective combatant to both internal and external pressures placed upon pilots to complete flights in marginal weather conditions.

Basic Concept: An EDP is analogous to the decision height on an ILS approach. When a listed limitation is reached the pilot must exercise one of the listed “Decision Options”. Continuing on the present course is not an option. Sample Limitations:

Outside Consultation: Reduced pressure on the flight team is significantly enhanced through the requirement to involve aviation personnel (when possible) outside of the flight team when risks exceed a predetermined level and the flight team believes the flight can be conducted safely. This consultation should not occur (the flight should be cancelled) when the flight team is not comfortable with accepting the flight.

ENROUTE DECISION POINT

The “No Pressure Initiative” is a collaborative effort between IAFP, ASTNA, AAMS, AMPA, NAACS and NEMSPA.

Copyright © 2009 NEMSPA

Airspeed Altitude Altitude

DAY

NIGHT

(Cruise – 30)* 300’ AGL MECA**

(Cruise – 30)* 500’ AGL MECA**

*eg, For 120 KIAS cruise, use 90 KIAS **Minimum Enroute Cruise Altitude – See A021

of blood and blood products, and medications to deal with transfusion reactions must be immediately available.102

BURNS Burn critical care and transport are both very similar and very different from standard critical care and transport. As in any aeromedical evacuation, careful planning is the key to successful transport.41,86 Transport of significant burn victims is best accomplished as early as possible in the course of the burn injury, preferably in the first 24 to 36 hours after injury. If there is any evidence of significant smoke inhalation or thermal injury to the orotracheal area (e.g., carbonaceous sputum, hoarse voice, singed nasal hair), the patient should be endotracheally intubated before flight. Circumferential third-degree burns inhibiting ventilation or circulation may require escharotomy before flight. Burn victims require careful temperature monitoring during flight to avoid hypothermia. Fluid resuscitation algorithms may need to be modified to compensate for increased insensible water losses due to low cabin humidity. Monitoring urine flow hourly is mandatory in burn patients.49,86 The U.S. Army Institute for Surgical Research (ISR) at Brooke Army Medical Center in San Antonio, Texas, houses the only dedicated burn unit in the U.S. military. The ISR has several burn transport teams that specialize in shortand long-range transport of critical burn patients (Figure 40-24). Teams generally include four personnel and about 800 lb of medical equipment. These teams train alongside, and work closely with, USAF CCAT teams and aeromedical evacuation crews. Between March 2003 and February 2007, the ISR transported 380 critical burn patients back to the ISR burn unit using a combination of dedicated burn transport teams and CCAT teams. Of these patients, 181 required mechanical ventilation. No in-flight deaths were reported.86

Note: Aircraft type, terrain, use of NVGs, etc. may influence limitations, which should be tailored to individual program requirements.

Decision Options: When a pilot experiences any of these limitations he or she must 1) Land as soon as practical OR 2) Alter course (turn around) OR 3) Transition to IFR (Instrument Flight Rules) Flight Team Interaction: The medical team, com specs and operational controllers provide an integral part of the flight team, especially in marginal conditions. Individual program AMRM (Air Medical Resource Management) practices should dictate the exact role of these team members under various scenarios. While all team members must support the EDP protocol, their active participation in its implementation should generally be limited to assisting the pilot in making the decision on which option to pursue should EDP limits be reached.

INFECTIOUS DISEASE PATIENTS Transport of infectious patients may be a hazard to the flight crew, medical crew, and other passengers, because everyone on board the aircraft is sealed in an aluminum tube for hours,

FIGURE 40-23  National EMS Pilots Association “No Pressure” initiative. http://www.nemspa.org.

Special Problems in Aeromedical Transport TRAUMA Aeromedical evacuation experiences during operations in Afghanistan and Iraq have shown that large numbers of severely injured patients can be moved long distances by air if proper equipment and personnel are available to carry out the transport. In July 2004, 2121 patients were moved by the USAF; 39 (1.8%) required transport by CCAT teams. In many instances, critical trauma patients are moved after “salvage surgery,” in which initial surgical care is limited to stopping bleeding and limiting contamination, with expectation of further surgery for definitive patient care. Patients have been moved with open abdomens and with intracranial pressure monitors, ventriculostomies, and wound vacuum drainage devices in place.11 In one case, a patient was successfully flown from Hawaii to California while on cardiopulmonary bypass. Transport of severe trauma victims requires careful attention to proper resuscitation, pain control and sedation, fracture stabilization, and temperature control. Abdominal and chest injury patients are frequently flown while on ventilator support; proper attention to sedation, analgesia, antibiotic administration, and neuromuscular paralysis is required. Patients with even a minor pneumothorax must have a chest tube in place before flight.49,102 Blood and blood products can be given in flight; however, careful attention must be given to proper refrigeration of blood and blood products. Blood administration protocols for use in flight should mirror standard practices for administration

A

B FIGURE 40-24  A, Two “burn victims” (actually manikins) being transported by the U.S. Army Burn Transport Team during a training mission on board a U.S. Air Force C-17 aircraft (B). (Courtesy Robert C. Allen.)

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CHAPTER 40  Helicopter Rescue and Aeromedical Transport

3 LAYERS OF PROTECTION

PART 5  RESCUE AND SURVIVAL

sometimes breathing recirculated air. Airflow patterns inside the aircraft cabin may contribute to the problem, wafting fomites downwind of a patient. Several cases of severe acute respiratory syndrome (SARS), influenza, and tuberculosis have been attributed to passenger-to-passenger transmission on commercial aircraft.53,56,79,80 Standard infection control practices, including wearing gloves, masks, and gowns (as required), should be followed with all patients, not just those suspected of being contagious. Handwashing facilities on aircraft are likely to be nonexistent; use of waterless hand cleaners such as alcohol gel is the next best thing.102 Patients in the early stages of some highly infectious diseases may not present with obvious symptoms, or these symptoms may not be recognized by personnel inexperienced in infectious disease or tropical medicine. To help aeromedical evacuation crews evaluate patients before flight, USAF aeromedical evacuation crews are supplied with a checklist of symptoms (Box 40-9). The patients’ clinical signs and symptoms are compared with the list, and if any “yes” answers are found, the aeromedical evacuation crew is required to seek additional guidance from a higher medical authority before allowing the patient on the aircraft. In most cases, patients with contagious diseases can be safely moved by air simply by applying appropriate infection control procedures. Precautions required for transporting an infectious disease patient depend on the pathophysiology and means of contagion. For example, although malaria is an infectious disease, it is not a significant contagion hazard on board an aircraft, whereas pulmonary tuberculosis is a significant contagion hazard. However, this hazard can be mitigated by the patient and medical crew wearing N95 masks, proper hand-washing techniques, and BOX 40-9  Communicable Disease Checklist Rule-Out Checklist (Highly Transmissible Infectious Disease Agents) • Any history of exposure to sewage, body fluids, animals before illness? • Any report of insect bites? • Did progression to severe symptoms and illness occur rapidly (over a period of less than 3 days) once the patient began to feel ill? • Fever (temperature greater than 38.9° C [102.0° F])? • Any bleeding from gums? • Any nosebleed? • Any report of petechiae on the palate, throat, or on examination of the mouth? • Are the patient’s eyes “bloodshot” in appearance? • Any report of tender or painful lymph nodes? • Any report of lymph nodes with a “bruised” or darkened appearance? • Any report of “matted lymph nodes,” “goose-egg” lymph nodes, or lymph nodes draining pus? • Any report of petechiae or purpura on the skin? • Any report of bloody stools, melena, hematochezia, hematemesis? • Any report of a positive “tourniquet test”? (Note: This test is performed by inflating a blood pressure cuff on an extremity. It is considered a positive test if petechiae appear on the skin of the extremity distal to the cuff and is a very good indicator of vasculitis associated with hemorrhagic fever agents.) • Any report of icterus (yellow eyes, skin, or tongue)? • Any report of cough and fever in conjunction with any of the following: • rapid disease progression? • petechiae, purpura? • lymphadenopathy? • Any report of “pox” or “pox-like” skin rash or lesion? Note: Answering “yes” to any one question requires immediate telephone consultation with the theater validating flight surgeon. Data from references 5, 6, 14, 36, 39, 71, 83, 85, 102.

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FIGURE 40-25  Patient Isolation Unit. The unit is self-contained and disposable after a single use. Blowers for filtration and lights can be operated by battery power or multiple voltages/frequencies of electrical power. Both the patient and equipment inside the unit can be manipulated from outside by multiple sets of glove ports set into both sides. Ports allowing monitor leads and intravenous tubing to enter the unit are built in at both ends. (Courtesy Gentex Corporation.)

making sure the patient is seated downwind and well away from other patients or passengers.102,107 Another complication of moving patients with certain confirmed or even suspected infectious disease may be that the destination country may want to quarantine them on arrival. Under an executive order, the Centers for Disease Control and Prevention is authorized to quarantine passengers who are suspected of having any one of nine infectious diseases (Box 40-10).100 Patients suspected of having highly contagious diseases can be moved by specialized transport teams. Until recently, the U.S. Army Medical Research Institute for Infectious Disease at Ft Detrick, Maryland, had a portable biologic level IV patient transport system (Vickers Transport System), capable of moving two patients with a highly contagious disease.20 However, this capability has significantly degraded because of the lack of replacement parts. The British Royal Air Force has a similar system, which it has used to transport patients suspected of having diseases such as Lassa fever. Tsai, Chen, and Chiu101 have reported several cases of moving patients with SARS during the SARS outbreak in Asia using a portable negative-pressure isolation unit equipped with air-purifying respirators. They also report using the same type of system to move four active pulmonary tuberculosis patients. Gentex Corporation has developed a disposable Patient Isolation Unit (PIU) that can be used for biologic isolation of a highly infectious patient. The PIU is designed to fit on a standard NATO litter, has integrated patient restraints, air blower/filtration system, self-supporting canopy, and multiple glove ports and medical ports so that medical care can be continued during transport (Figure 40-25). BOX 40-10  Nine Diseases for Which Patients May Be

Quarantined by Executive Order

1. Influenza viruses that cause pandemics or have pandemic potential 2. Severe acute respiratory syndrome (SARS) 3. Cholera 4. Diphtheria 5. Infectious tuberculosis 6. Plague 7. Smallpox 8. Yellow fever 9. Viral hemorrhagic fevers Data from Teichman PG, Donchin Y, Kot RJ: International aeromedical evacuation, N Engl J Med 356:262, 2007.

However, in most cases, such units are not necessary; standard infection control practices modified for the flying environment should suffice for the majority of infectious disease patients. An outstanding paper on the aeromedical transport of infectious patients was authored by Withers and Christopher.107

Air Medical Services Resources Air Medical Physician Association Air and Surface Transport Nurses Association American College of Emergency Physicians Association of Air Medical Services

http://www.ampa.org http://www.astna.org http://www.acep.org http://www.aams.org

Atlas and Database of Air Medical Services International Association of Flight and Critical Care Paramedics National Association of EMS Physicians National Association of State EMS Officials National EMS Pilots Association

http://www.adamsairmed.org http://www.flightparamedic.org http://www.naemsp.org http://www.nasemso.org http://www.nemspa.org

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 41 



Essentials of Wilderness Survival WARREN D. BOWMAN AND PETER KUMMERFELDT

This chapter discusses the general principles of wilderness survival, particularly in temperate and moderately cold (i.e., nonpolar) environments such as the mountains of the American West. For additional information, especially about other environments, please refer to Chapter 1 for high-altitude medicine, Chapter 9 for polar medicine, Chapter 43 for jungle survival, Chapter 44 for desert survival, Chapter 71 for how to live off the land, Chapter 96 for wilderness navigation techniques, and Chapter 112 for certain aspects of environmental changes (e.g., global warming). According to Webster’s College Dictionary, the word survive means to “continue to function or manage in spite of some adverse circumstance or hardship,” and it implies the presence of conditions that make this more difficult than usual. These conditions may—and frequently do—include a lack of oxygen, food, or water; the presence of rain, snow, high winds, or temperature extremes without shelter; the complicating presence of illnesses or injuries; and the necessity to rely completely on the physical, mental, and material resources that are immediately at hand. Physicians who participate in wilderness recreation or who treat such participants need to be aware of the physical, physiologic, and psychological hazards of environmental stress and how related deleterious effects can be prevented and treated in themselves and their patients. Increased leisure time and growing interest in outdoor activities place more people into settings in which survival situations may develop. The increasing use of all-terrain vehicles and snowmobiles has made it easier to get lost or stranded far from help. In addition, the rise in sedentary lifestyles with inattention to healthy diets, decreased emphasis on physical conditioning, and increasing prevalence of obesity have led to decreased fitness in developed nations, particularly the United States. With modern communications and tactics (e.g., the use of combined helicopter and ground teams), search and rescue operations have become more efficient. At the same time, electronic devices such as cellular and satellite phones, global positioning system (GPS) locators, emergency locater transmitters for aircraft, and personal locator beacons have made it easier to get assistance, but these are accompanied by increased risk taking, a false sense of security, a decrease in a healthy respect for wilderness, a neglect of survival training, a failure to carry survival equipment, and the

less-effective use of simple nonelectronic tools such as maps and compasses. An especially egregious practice is the “Yuppie 911,” when a personal locator beacon that sends a message to a satellite is used for a nonemergency situation. In some cases, carrying such equipment tempts wilderness travelers to take chances that common sense would otherwise prevent. According to the Billings Gazette, in one recent episode, an inexperienced party made three calls in three days from the Grand Canyon, thus “mobilizing helicopters for dangerous, lifesaving rescues inside the steep canyon walls. What was that emergency? The water they had found to quench their thirst ‘tasted salty.’ ” Societal “progress,” then, has made it easier to get assistance when there is trouble, but it is now also easier to get into trouble. This chapter’s main thrust is prevention and successful initial definitive management of such trouble. By paying heed to the recommendations discussed here, the reader will be more apt not only to live through the stress of a survival emergency but also perhaps to do so in relative comfort. A recent episode in Montana illustrates the types of problems that wilderness travelers such as hunters can experience, and emphasizes both the penalties for risk taking and the role of technology in the softening of these penalties. Glenn Eschenko, who was 51 years old, ran a bowling alley and supper club in Big Timber, Montana. A longtime hunter and mule owner, he had returned to the same camp near Anderson Mountain in the Absaroka-Beartooth Wilderness for 20 years. He packed in enough gear to spend a week hunting elk next to the border of Yellowstone National Park. In 2005, he had been hunting for 6 days with four friends. They had harvested a six-point bull elk when the weather started to turn nasty on Saturday, September 17. After four of them had lunch, two of them (Eschenko and Chad Cochran) saddled up to look for the fifth hunter (Courtney Ayers), who had not returned. Eschenko was riding one of his older mule colts when he came around a corner in the rain and saw Ayers up ahead. Ayers was riding down a mountain toward him, wearing a yellow rain slicker. The slicker startled Eschenko’s mule, who whirled and started bucking, throwing his rider after about five jumps. Eschenko was thrown down an embankment, sliding on a skiff of snow on the grass, hitting a rock, and then sliding on his belly farther downhill before crashing into a boulder.

For online-only figures, please go to www.expertconsult.com

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PART 5  RESCUE AND SURVIVAL

Eschenko was able to stagger to his feet, but the wind was knocked out of him, and he could feel loose and moving broken ribs on his left side. His friends loaded him onto another mule and got him back to camp, but he could not move because of his dyspnea. Cochran had a cell phone and called 9-1-1. A helicopter was dispatched from St. Vincent’s Hospital in Billings, about 160 km (100 miles) away, but it was unable to land because of bad weather. Cochran rode to a nearby outfitters camp and asked a nurse for advice. She told him that if Eschenko was still alive when he got back, then the injured hunter would probably survive. The party spent a cold night by a roaring campfire; Eschenko was still alive the next morning. A helicopter from Idaho was set to make a rescue run, but again the weather was too severe. Finally, a helicopter from Mammoth, Wyoming, was dispatched; the camp was found as a result of the pilot’s use of GPS coordinates that the hunters had called in, and the aircraft was able to land at a mountain meadow above camp and drop off two emergency medical technicians. Fearful of getting fogged in, the craft departed down the mountain around 8:30 AM. The emergency medical technicians noted extreme tenderness in Eschenko’s left upper quadrant and felt that his spleen was probably ruptured. Because extreme pain limited Eschenko’s movement and ability to walk, his companions managed to transport him by mule 0.8 km (0.5 miles) to a place where the helicopter could land safely. Eschenko was flown back to Mammoth, where an ambulance was waiting to take him to Livingston Memorial Hospital in Montana. A doctor told Eschenko that he had cheated death because his spleen was “pulverized” although not freely bleeding. Once he was out of the hospital, Eschenko sold the mule that had bucked him. He then planned to show his other mules yellow raincoats to get them used to the sight. He also said that he had acquired an appreciation for cell phones and GPS receivers. The exact type of environmental stress depends on the type, location, and duration of the wilderness experience. Crosscountry skiers, winter mountaineers, and winter campers may be exposed to extremes of cold and storm. Expeditionary mountaineers may explore regions in which winter exists year round and where ambient oxygen is low. Desert or tropical travelers may be exposed to extremes of heat and humidity. Passengers in aircraft, seacraft, or land vehicles may be stranded in almost any type of environment. Requirements for survival, which are discussed in detail later in this chapter, are similar whether the subject becomes lost with few resources during a simple day hike or whether injury occurs or severe environmental conditions develop during a wellplanned wilderness expedition. Although traveling alone in the wilderness is universally condemned, one must always assume that he or she may be alone and possibly injured when in a survival scenario. Therefore, emergency equipment must be familiar, sturdy, uncomplicated, easy to assemble, and—most importantly—available immediately. Necessary skills cannot be learned on the job but must be anticipated, acquired and practiced beforehand so that essential tasks can be accomplished with minimal delay and effort should an emergency arise. Although improvisation and the ability to live off the land are important, anticipation, prevention, and especially preplanning and carrying emergency equipment are vital. Consider examples taken from polar exploration: Roald Amundsen’s style of thorough preparation and the use of familiar equipment should be emulated, whereas Robert Scott’s careless, arbitrary, and stubborn approach should be rejected. Both of these explorers had extensive polar experience, but Scott elected to use European clothing rather than Eskimo furs and unproved motor sledges and ponies rather than Eskimo dogs. He relied excessively on sled hauling by men on foot, rejected the use of skis, failed to establish enough supply depots for his return, and died of cold, exhaustion, and starvation on the way back from the South Pole. Amundsen, who used Eskimo clothing, well-tested Greenland sled dogs, and experienced skiers, won the race to the South Pole and made it back alive. The outcome of an encounter that involves severe environmental stress varies with the stressed person’s resources and the type, magnitude, and duration of the stress. These resources 778

include the state of acclimatization; physical integrity (particularly conditioning and the presence of illness or injury); experience; equipment on hand plus the ability to improvise intelligently; and such intangibles as good judgment and “backcountry common sense.” A common judgment error is to insist on traveling during a storm or other stressful environmental situation, when more prudent persons would stay put in a comfortable bivouac. Excuses for this include wanting to reach a predetermined (but not essential) goal on time so that others will not worry. Recall the old adage, which has been attributed to Will Rogers, that “good judgment comes from experience; experience comes from bad judgment.” To this, we should add, “…provided that you survive the bad judgment.” The most important resource, however, may be the will to survive. This may be inbred in some persons, can be established through training and experience in many, and is impossible to acquire in a few. With a strong will to survive, some persons have withstood incredible hardships. Without such will, the best training and resources may be useless. Although it is based on science, the study and practice of survival is more a craft or learned skill than an exact science. The recommendations in this chapter are based on the opinions of survival experts, research, analysis of actual survival situations, and personal experience. General principles are emphasized, but “tricks of the trade,” which are usually acquired through experience, may hold the key to life or death. Unfortunately, much of the lay literature emphasizes tales of misfortune, hazardous adventures, and mindless bravado in the face of unnecessary hardships that are brought on by the errors of the participants, whereas great deeds go unrecorded or forgotten because the experience and competence of the adventurers kept catastrophic “newsworthy” experiences to a minimum. In the words of Corneille, “To vanquish without risk is to triumph without glory.” Travelers should always plan for the unusual and unexpected. Tools include familiarity with weather forecasts, strategizing worst-case scenarios, carrying emergency items, avoiding solo travel, and leaving notice of the projected route and the expected time of return. With good planning, deteriorating weather or an injury-forced bivouac become more of an inconvenience than a life-threatening ordeal. However, chance always plays a part in survival. Serious but unforeseen or unavoidable hazards can occur, or environmental stresses can become so severe that survival is impossible regardless of preparations. Anyone who ventures into the wilderness must accept the possibility—however remote—of death or serious injury. For survival, the body requires a constant supply of oxygen; a core temperature that is regulated within relatively narrow limits (about 24° to 42° C [75° to 107° F]); water and food; and self-confidence, faith, and the will to live. For comfort and optimum performance, however, the body temperature must be close to normal, and the body must be rested, well nourished, in top physical condition, and free from disease and injury. The most immediate of these latter requirements are the maintenance of body integrity (through accident prevention) and the regulation of body temperature. Dehydration, starvation, and exhaustion make temperature maintenance more difficult and interfere with the rational thought and agility required to prevent accidents. Insufficient oxygen becomes a contributing factor at extreme altitudes or in such mishaps as suffocation caused by avalanche burial or carbon monoxide poisoning from cooking in an unventilated shelter. Abundant food and water are of little value to a hypothermic person with insufficient clothing and shelter or to the victim of heat stroke, although a lack of food and water will eventually weaken and kill an otherwise healthy individual. A lack of self-confidence, faith, and the will to live may cause an attitude of panic and defeatism that prevents a person from taking timely survival actions such as conserving energy, preparing shelter, or lighting a fire. Poor physical conditioning or the presence of illness or injury may interfere with the body’s ability to produce heat by shivering or to lose heat by sweating and increasing skin perfusion; this can hamper wood gathering, shelter building, and other necessary tasks. The most important organ for survival is the human brain, because voluntary actions such as preparedness, regulation of energy expenditure, adjustment of clothing, and provision of

Oxygen As a human ascends from sea level, the body is subjected to increasing cold, decreasing oxygen, increasing solar radiation, and decreasing atmospheric pressure. For every 305 m (1000 feet) of altitude gain, ambient temperature drops by about 2.2° C (4° F), barometric pressure drops by about 20 mm Hg (27 millibars or roughly 0.1 millibar drop per meter of altitude gain), and the amount of ultraviolet radiation increases by about 5%. The percentage of oxygen in the atmosphere remains constant, but partial pressure of oxygen diminishes with altitude so that, at 3077 m (10,000 feet), it is only two-thirds of that at sea level; at 5488 m (18,000 feet), it is only one-half of that at sea level. During acute exposure to high altitude, effects of hypoxia can initially cause fatigue, weakness, headache, anorexia, nausea, vomiting, dyspnea on exertion, insomnia, and Cheyne-Stokes respirations. These symptoms are probably present to some degree in everyone who goes rapidly from sea level to 2462 m (8000 feet) or above. The clinical effects of hypoxia are often difficult to distinguish from those of cold, high winds, dehydration, and exhaustion. Serious degrees of acute mountain sickness are unusual below 3692 to 4308 m (12,000 to 14,000 feet), but they have been reported in trekkers as low as 2308 m (7500 feet). As noted during one author’s experience as a periodic summer physician in Yellowstone National Park, mild acute mountain sickness is occasionally seen in visitors at just over 1829 m (6000 feet) at the north entrance. At any height, oxygen in ambient air may be prevented from reaching the cellular level because of interruption of normal transport pathways, generally by illness or injury. Carbon monoxide poisoning is probably a greater hazard than is generally appreciated. Many famous polar explorers, including Byrd, Andree, and Stefannson, were killed by or had narrow escapes from the toxic effects of stoves operated in tightly enclosed spaces.

Regulation of Body Temperature Humans are considered homeotherms because, as warm-blooded animals, they maintain a body temperature that varies within very narrow limits despite changes in environmental temperature. In poikilotherms, which are cold-blooded animals, body temperature varies with the temperature of the environment. Homeothermy is necessary to support the enzyme systems of the human body, which function best at 37° to 37.5° C (98.6° to 100° F). The human body can be viewed as a heat-generating and heatdissipating machine, where internal temperature is the net result of opposing mechanisms that tend to increase or decrease body heat production, increase or decrease body heat loss, and increase or decrease addition of heat from the outside. With use of these mechanisms, internal body temperature can usually be regulated successfully, despite ambient temperatures that vary by more than 55° C (100° F) from the coldest to the hottest seasons in temperate climates. Wind (mph) Calm 5 10 15 20 25 30 35 40 45 50 55 60

Temperature (° F) 40 36 34 32 30 29 28 28 27 26 26 25 25

35 31 27 25 24 23 22 21 20 19 19 18 17

30 25 21 19 17 16 15 14 13 12 12 11 10

25 19 15 13 11 9 8 7 6 5 4 4 3

20 13 9 6 4 3 1 0 1 2 3 3 4

15 7 3 0 2 4 5 7 8 9 10 11 11

Frost bite in >>

10 1 4 7 9 11 12 14 15 16 17 18 19

5 5 10 13 15 17 19 21 22 23 24 25 26

30 min

0 11 16 19 22 24 26 27 29 30 31 32 33

5 16 22 26 29 31 33 34 36 37 38 39 40

10 min

10 22 28 32 35 37 39 41 43 44 45 46 48

15 28 35 39 42 44 46 48 50 51 52 54 55

20 34 41 45 48 51 53 55 57 58 60 61 62

25 40 47 51 55 58 60 62 64 65 67 68 69

30 46 53 58 61 64 67 69 71 72 74 75 76

35 52 59 64 68 71 73 76 78 79 81 82 84

40 57 66 71 74 78 80 82 84 86 88 89 91

45 63 72 77 81 84 87 89 91 93 95 97 98

5 min

FIGURE 41-1  Windchill chart. (From Bowman WD, Johe DH, American Academy of Orthopaedic Surgeons, National Ski Patrol System [United States]: Outdoor emergency care: Comprehensive prehospital care for nonurban settings, ed 4, Boston, 2003, Jones & Bartlett.)

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CHAPTER 41  Essentials of Wilderness Survival

Basal body heat production is about 50 kcal/m2/hr. This can be increased by muscular activity (both involuntary [shivering] and voluntary), eating, inflammation and infection (fever), and in response to cold exposure. Shivering can increase heat production up to five times the basal rate, and vigorous exercise can increase it up to 10 times. Cold exposure increases hunger; secretion of epinephrine, norepinephrine, and thyroxin; and semiconscious activity, such as foot stamping and dancing in place. Eating provides both needed calories and the temporary increase in basal metabolic rate that occurs during digestion alone; this is specific dynamic action (SDA). The SDA of protein is five to seven times higher than that of fat and carbohydrates, and it lasts longer. However, onset of the SDA is much faster with carbohydrates than with protein or fat. Therefore, the person who is cold inside a sleeping bag at bedtime should eat carbohydrates for quicker warming and protein to stay warm all night. In hot weather, body heat production can be decreased by slowing muscular activity and avoiding foods with a high SDA. In cold weather, heat can be added to the body by exposure to a fire or another heat source (e.g., sunlight) and by ingesting hot food and drink. In hot weather, external heat addition can be decreased by staying in the shade, wearing clothing that blocks the sun’s rays, and avoiding hot objects and hot food and drink. The body loses heat to the environment by conduction, convection, evaporation, radiation, and respiration; it may gain heat from the environment by the same mechanisms (except for evaporation). The relative importance of these mechanisms depends on temperature, humidity, wind velocity, cloud cover, insulation, contact with hot or cold objects, sweating, and muscular exercise. With a resting body in still air at 21° C (70° F), radiation, conduction, and convection account for about 70% of total heat loss; evaporation accounts for about 27%; and urination, defecation, and respiration account for only 3%. During work, however, evaporation may account for up to 85% of heat loss. It is useful to think of the body as being composed of a core (i.e., the heart, lungs, liver, adrenal glands, central nervous system, and other vital organs) and a shell (i.e., the skin, muscles, and extremities). Most of the physiologic adjustments in response to cold or heat exposure occur in the shell. These adjustments are intended to maintain a relatively constant core temperature; in below-freezing weather, these adjustments may predispose parts of the shell to frostbite and other types of localized cold injury. The importance of avoiding travel and seeking shelter during storms and extreme cold cannot be overemphasized. The additive chilling effect of wind when added to cold is impressive. Wind-chill charts (Figure 41-1) show the relationship between actual temperature, wind velocity, and “effective” temperature at the body surface. The term wind chill refers to the rate of cooling; the actual temperature reached is no lower than it would be if wind were absent (unless evaporation of liquid is occurring at the body surface). The increase in heat loss as the wind rises is not linear; rather, it is more proportional to the square root of the wind speed.

shelter are more important than are involuntary mechanisms of adaptation to environmental stress.

PART 5  RESCUE AND SURVIVAL

At moderate ambient temperatures, the body’s core temperature is kept stable by constant small adjustments in metabolic rate, muscular activity, sweating, and skin circulation. When the body is chilled, automatic and semiautomatic mechanisms increase internal heat production by slightly increasing metabolic rate, shivering, and semiconscious activities (e.g., foot stamping), and they reduce heat loss by diminishing sweat production and shell circulation. The person has a strong urge to curl up into a ball, thereby reducing the body’s surface area. At the same time, the brain tells the body to decrease heat loss by adding insulation and wind protection, seeking shelter, and increasing heat gain by increasing muscular activity, building a fire, seeking sunlight, and eating. When the body overheats, these actions are reversed. The body increases heat loss by increasing circulation to the skin and extremities and by increasing sweating. These mechanisms require more water, which stimulates the thirst response. Heat production is decreased as a result of a feeling of sluggishness and languor, which leads to reduction in physical activity and in the amount of heat produced by the muscles. The brain tells the body to decrease heat gain and to increase heat loss by providing shelter from the sun, removing clothing, and fanning itself.

Cold Weather Survival Body temperature in a cold environment is maintained by decreasing body heat loss, increasing internal body heat production, or adding heat from the outside. The most efficient of these methods is the conservation of body heat by decreasing heat loss, generally with the use of clothing and shelter.

DECREASING BODY HEAT LOSS Heat loss from conduction and convection can be prevented by interposing substances of low thermal conductivity, such as clothing made of insulating materials, between the body and the outside air. Clothing creates a microclimate of warmed, still air next to the skin surface. Clothing’s value depends on how well it traps air, the thickness of the air layer, and whether these qualities are reduced by wetting (Table 41-1). Traditional insulating materials are wool, down, foam, and older synthetics such as Orlon, Dacron, and polyester. Wool retains warmth when wet because of a moderately low wicking action and its ability to suspend water vapor within its fibers without affecting its low thermal conductance. It can absorb a considerable amount of water without feeling wet, but is heavier than synthetics, “itchy,” and more difficult to dry. However, its toughness and durability make it a good choice for garments that are subject to hard wear, such as trousers, mittens, and socks. Cotton, particularly denim and corduroy, is a poor insulator. It dries slowly because of its low evaporative ability; high thermal conductance is further increased by wetting. Cotton has no place in the backcountry in cold weather. Orlon, Dacron, acrylic, and polyester were developed to duplicate wool’s properties without wool’s high cost and other perceived drawbacks. They traditionally have been used for hats,

shirts, sweaters, and long underwear. They are almost as warm and not as itchy as wool, and evaporate moisture better. A number of newer fabrics are woven from fibers that have lower thermal conductance, greater insulating ability, and better wicking action than do traditional fibers. Examples include polypropylene and treated polyesters such as Capilene, Thermax, and ThermaStat. Polyester is also made into pile and fleece; these are light, dry easily, trap air well, and stay warm when wet because the fibers do not absorb water. Examples include Polartec, Borglite, Polarplus, and Synchilla. Fibers used as fillers in quilted garments, such as parkas, include hollow synthetics, such as Hollofil II and Quallofil, which were designed on the basis of the principles of reindeer hair. Microfibers that provide good insulating ability with less bulk include Thinsulate, Thermoloft, and Thermolite. One of the newer fibers, Microloft, is supposed to be warmer than down of the same weight. New synthetics come on the market frequently, so one should consult trade journals and “gear” issues of outdoor magazines. The layering principle of clothing is effective for preventing both chilling and overheating. Multiple layers of clothing provide multiple layers of microclimate. Layers are added as necessary to prevent chilling or subtracted to prevent overheating that would cause perspiring. Because water conducts heat 25 to 32 times faster than air at the same temperature, clothing that is wet with perspiration or water may cause rapid heat loss from conduction and evaporation. The need to add or subtract layers should be anticipated before either chilling or heavy perspiring occurs. Clothing should be easily adjustable, sweaters should be closeable from the waist to the neck with a sturdy zipper, and outer layers should be cut full enough to allow for the expansion of inner layers to their full thicknesses. Zippers in the axillary, lateral chest, and lateral thigh areas are useful for ventilation. Loss of heat from convection can be prevented by wearing windproof outer garments. Typical examples include a parka with a hood and a pair of windproof pants (regular or bib style) or ski warm-up pants. Loss of heat from infrared radiation can also be prevented by insulation and emphasizing the proper covering of body parts with a large surface area–to–volume ratio. The uncovered head can dissipate up to 70% of body heat production at an ambient temperature of −16° C (5° F), partly because the body does not reduce blood supply to the head and neck in cold weather as it does to the extremities. High heat loss through radiation during cold nights can be decreased by sleeping in a tent or under a tarpaulin instead of out in the open. Coverage for the head, ears, hands, and feet should not restrict circulation. Developed initially for skiers, a tubular neck gaiter can be pulled up over the back of the head to form a hood or up over the lower face to form a mask. In addition to head and neck protection, this device also blocks some of the heat that would otherwise be lost by the bellows action of clothing that is caused by body motion. Heat loss from the respiratory tract can be diminished by avoiding overexertion and overheating that occur with excessively heavy breathing. When it is extremely cold, inspired air

TABLE 41-1  Fiber Characteristics of Natural and Synthetic Fibers Fabric Wool Cotton Nylon Polyester Acrylic Polypropylene

Specific Gravity* (Ratio to Water)

Thermal Conductance† (cal/m2)

Evaporative Ability‡

Wicking Ability

Moisture Regain§

1.32 1.54 1.14 1.38 1.15 0.91

2.1 6.1 2.4 2.4 2.4 1.2

Low Low High High High High

Moderate High Low Low High High

17 7.9 4 1 1 5

Modified from Davis AK: Nordic skiing: A scientific approach, Minneapolis, Minn, 1980, University of Minnesota. *The lower the specific gravity, the better the insulating ability. † The lower the thermal conductance, the slower the flow of heat from the body. ‡ The higher the evaporative ability, the shorter the amount of time that a fiber will be wet (i.e., in a reduced insulative state). § Moisture regain is the amount of moisture that a fiber can absorb before it feels wet.

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DRESSING FOR COLD WEATHER Anyone who ventures outdoors in cold weather should have enough clothing of the proper kind, either on the body or in the backpack, for the most extreme environmental conditions that are likely to be experienced. Although building fires, carrying emergency shelters, and improvising survival shelters are discussed at length later in this chapter, the process of dressing for cold weather should be approached with the idea that clothing may become the only shelter and endogenous heat production the only heat available. Clothing and other types of insulating materials should be selected with the idea that they need to keep the body warm and dry even during periods of inactivity.

moderate conditions, sturdy leather climbing boots made of fullthickness leather and that are 15 to 20 cm (6 to 8 in) in height, that have rubber lug soles, and that are roomy enough to accommodate the desired numbers of socks are ideal. Boots made of leather and fabric (e.g., Gore-Tex) are lighter and suitable for trail hiking, but they may not be as durable for rough terrain. Boots must be long enough, their toes high enough, and their laces tight enough so that the wearer’s toes do not strike the inside of the front of the boot during downhill walking. Laces should also be tight enough to prevent the heel from moving up and down during walking but not so tight that circulation is restricted and the toes cannot wiggle easily. For colder temperatures, double boots are preferable. These can be all-leather boots, or they can have outer shells of plastic or nylon with inner boots of felt or foam. All-leather versions may be hard to find. The Canadian type of shoe pack with a removable inner felt liner is a good choice for light snowshoeing and other nontechnical outdoor activities in the cold. Special double ski boots are available for ski touring, Telemark skiing, and ski mountaineering, depending on the type of binding selected. Hat.  Hats should be of the stocking variety; made of wool, pile, Orlon, polypropylene, or wool/polypropylene; and large enough to cover the ears. A small bill feature is desirable to shade the eyes. “Bomber” caps with bills and pull-down earflaps and “Andean” caps with ear coverings are preferred by some. Some arrangement should be provided to protect the face from cold wind, as with a balaclava configuration or a separate face mask. A useful combination for very cold and windy weather is a ski hat together with a neck gaiter that can be pulled up to cover most of the lower face; the parka hood can then be pulled over the head from behind.

Pants.  Wool or pile pants are best and should have pockets that are easily accessible for hand warming. Pile pants should have reinforcements at the knees and buttocks and a zipper or Velcro fly for males. Full or partial lateral leg zippers are convenient, especially for removing pants without removing boots.

Third Layer Parka.  The parka can be a standard ski or mountain parka filled with down, Dacron, Quallofil, Thinsulate, or another lofting material. A more versatile combination is two separate garments: a pile jacket plus a water-resistant shell. For snow camping, a pile jacket with a thin outer cover of nylon (i.e., three-season, squall, or warm-up jacket) may be preferred, because, unlike an uncovered pile jacket, it does not collect snow when it is worn without the shell. The shell should have a hood with a drawstring, a two-way zipper with an overlying weather flap closed with full-length Velcro (in case of zipper failure, very cold hands, or upper extremity injury), a cloth flap to protect the chin from the metal zipper pull, armpit or lateral chest zippers for ventilation, and at least four outer pockets plus one or two inside pockets to contain frequently needed items (e.g., gloves, compass, map, sunglasses, neck gaiter). Outer pockets should be located where they can be reached while wearing a backpack with a fastened waist belt. The shell should be fingertip length unless bibs are worn. Zippers should have extra-long tabs added to facilitate closure with cold or mittened hands. Pockets with horizontal openings may close with Velcro, but those with vertical openings should close with zippers. Because the parka is anchored by the shoulders, when using one hand, it is generally easier to pull a vertical zipper down rather than up. In some brands of parkas, vertical zippers are pulled down to close the pockets; in other brands, they are pulled up. The authors prefer the former type: the danger of losing pocket contents as a result of difficulty with closing a zipper is worse than any perceived delay caused by difficulty with opening a zipper. For ventilation, there should be zippered openings at the armpits. These should be large enough so that the parka can be converted into a vest-like garment during warm conditions by inserting the wearer’s arms through the openings and tucking the sleeves inside the parka. Because these zippers usually perform more easily when they are pulled from the distal to the proximal direction, this direction should close them; increasing wind protection is usually more urgent than decreasing it (i.e., freezing is more dangerous than sweating).

Foot gear.  The type of boot chosen depends on the type of activity and the expected environmental temperatures. For

Wind pants.  Wind pants should be light and water repellent; a laminated garment such as Gore-Tex is a good choice. Long and

First Layer Long underwear.  Wool is an excellent choice for long underwear, but it is itchy and expensive, and it may be difficult to find. Merino wool is less itchy. Polypropylene, acrylic, and the newer polyesters may be preferable because of their lower cost, good insulating ability, and outstanding evaporative ability (see Table 41-1). Avoid cotton. Synthetics, more than wool, tend to retain body odor after washing. Socks.  One or two pairs of moderate to heavy wool or wool/ nylon blend socks are excellent, preferably with an additional pair of light polypropylene socks worn underneath next to the skin. Consider carrying at least one spare pair of wool socks. Thin gloves (glove liners).  Light propylene, wool, silk, or fingerless wool or pile gloves are useful for moderately cold conditions or when finger dexterity is required, such as when adjusting ski bindings. Polyester/Lycra gloves provide a tighter but more stretchable fit, which enhances fine finger movements. Second Layer Shirt.  Shirts should be made of light, soft wool or a durable synthetic such as acrylic, and they should have long sleeves. Large breast pockets with buttons or Velcro fasteners are handy to carry such items as sunglasses and a compass. For ventilation, the front of the shirt should open completely (i.e., it should have a button or zipper closure). A turtleneck feature protects the neck, as do neck warmers and mufflers that can be pulled up to protect the lower face.

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CHAPTER 41  Essentials of Wilderness Survival

can be warmed by pulling the parka hood out in front of the face to form a “frost tunnel.” Heat loss from conduction occurs as a result of direct contact with a colder object. Sitting on a pack, a foam pad, a log, or another object of lower heat conductivity is preferable to sitting in the snow or on a cold rock. At low temperatures, bare skin freezes to metal; avoid this by wearing light gloves when handling metal objects. Gasoline and other liquids with freezing points lower than that of water can cause frostbite if they are accidentally poured on the skin at low temperatures. During bivouacs in snow shelters, avoid contact with the snow by sitting on a foam pad or backpack or by improvising a mattress of evergreen boughs, grass, or dry leaves. In cold or windy weather, an injured person needs windproof insulating material under as well as over and around the body. Heat loss from conduction and evaporation can be lessened by avoiding wetting and by changing to dry clothes or drying out quickly when wet. Ideally, outer clothing should be windproof, and it should not collect snow. It should shed water but not be waterproof, because waterproof garments prevent the evaporation of sweat; laminated fabrics such as Gore-Tex and its relatives are designed for this purpose.

PART 5  RESCUE AND SURVIVAL

zippered side openings at the bottoms are useful to permit the donning of pants without removing boots as well as for ventilation and access to inner pants’ pockets. Hand gear.  Mittens and gloves provide hand protection from trauma and cold. Because survival depends to some extent on normal hand dexterity, gloves or mittens should be available to protect the hands from cuts, bruises, blisters, and possible resulting infections. In temperate weather, these can be light and unlined leather gloves. One of the more serious and still unsolved cold weather problems is how to keep fingers warm while leaving them sufficiently unhampered to do work. Mittens are warmer than gloves, because fingers that touch each other warm each other. However, even thin mittens do not allow for delicate finger movements. An important part of the cold-finger solution is to prevent core cooling and compensatory extremity vasoconstriction by addressing core temperature stabilization through exercise, eating, and wearing enough layers on the trunk. A common method is to wear a pair of thin gloves of polypropylene, silk, thin wool, or polyester/Lycra inside a wool or pile mitten covered with a windproof and water-resistant shell. For delicate finger work, the gloved hand is removed from the mitten, the work done as fast as possible, and then the hand returned to the mitten. However, because insulating materials insulate in both directions, when inside a warm mitten, cold fingers wearing gloves will not rewarm as fast as cold, bare fingers. Therefore, another solution is to use bare fingers, which will perform faster than gloved fingers, work as fast as possible, and then return them to warm mittens periodically until the task is done. However, this is not practical when working with metal in very cold weather. Another approach is to keep a pair of gloves warm in a pocket and put them on after removing the hands from mittens. Polyester/Lycra gloves are easier to don than are many other types of thin gloves. Excellent three-layer mitten sets include windproof shells with leather palms and two sets of removable pile mittens, at least one of which is fastened to the inner shell with Velcro. Another good system is a thin glove liner inside a heavy wool mitten (e.g., Dachstein, rag wool, wool/polypropylene) inside a GoreTex shell. An option that provides more finger dexterity in moderately cold conditions is a polypropylene glove liner inside a fingerless wool glove inside a shell. A newer combination is a fingerless wool glove inside a wool mitten that has a horizontal slit in the distal palm (i.e., Cordova’s rag wool convertible gloves). The distal tip of the mitten can be folded backward dorsally and secured with a Velcro patch, thereby allowing the hand that is covered with the fingerless wool glove to be exposed through the slit. However, more layers and increasing complexity mean more difficulty doing delicate hand tasks. Shells should have easily accessible nose warmers of pile or mouton on their backs, they should be long enough to cover the wrists, and they should have palms of soft leather or sticky fabric for securely holding ice axes and ski poles. Gaiters and overboots.  Gaiters, which are long nylon tubes that cover the lower leg and upper part of the boot, are designed to keep snow, sand, and gravel out of boots and socks. They extend upward to just below the knee, open at the side or in front with a zipper or Velcro, have a strap that fits under the boot sole to keep them snug on the boots, and a drawstring at the top to hold them up. Gaiters with a front opening that is closed by a wide Velcro strap are the easiest to put on and take off. Shorter versions that extend to just above the ankle are adequate for summer mountaineering and may be preferable for cross-country skiers who need access for tightening boot buckles before descents. High-altitude mountaineering requires special insulated overboots or lined gaiters. Fourth Layer The previous three layers are usually worn on the body. A fourth layer should be easily available in the pack; this layer should include quilted or pile pants and a jacket or vest. 782

Rain gear.  In moderate climates or in spring conditions, when rain and wet snow may be encountered, outer garments of GoreTex or similar material should be used. For maritime climates and during seasons of heavy rain, it may be better to have two separate sets of outer garments: a light, thin, windproof nylon jacket and pants and a waterproof (i.e., coated nylon) jacket and pants. Vapor barrier systems.  Waterproof garments and sleeping bag liners worn close to the skin are favored by many because they can prevent the wetting of outer clothing by sweat that might result in decreased insulating capacity. There also is claimed to be some reduction in water consumption requirements with such items. These types of vapor barriers seem to work better in very cold weather than at moderate temperatures. A light garment of polypropylene or similar material should be worn next to the skin, with the waterproof garment worn over this. Vapor barrier systems probably should be tried out in the field in nonsurvival conditions before being relied on in severe weather. Persons with hyperhidrosis and those who dislike clammy skin may not feel comfortable with such garments.

Shelter SUMMER EMERGENCY SHELTERS When faced with an unplanned night out, one’s first step should be to locate a place out of the wind. Getting behind a rock, moving to the lee side of a ridge, going down into the tree line, or even turning one’s back to the wind can make a difference. Eliminating windchill allows one to concentrate on dealing with ambient air temperature by using spare clothing and natural insulation and by starting a fire. Look for a space into which you can crawl, such as a rocky overhang or a space under dense evergreens or fallen logs. Experienced and prepared individuals will have some type of waterproof material (e.g., plastic bag, tube tent, tarp) into or under which they can crawl as well. Bright-colored (i.e., orange or red) materials are easier for searchers to spot. Getting out of the wind, rain, or snow quickly and being able to stay as warm and dry as possible are vital. When one is wet and cold, it may be very difficult—and sometimes impossible—to rewarm and dry out.

SPACE BLANKETS AND BAGS Space blankets and bags are lightweight, inexpensive, and compact, but they are of limited value in an emergency. Consider a typical scenario in which it is late in the day; it is cold, rainy, and windy; and the survivor is injured, hypothermic, or both. A space blanket is frequently difficult to get out of its package, to unfold, and to manage in windy conditions. Depending on the brand, space blankets are usually too small to fully encase an adult. When wrapped up, the survivor will find that a space blanket makes a shelter that is so noisy that even an approaching aircraft or ground search party may not be heard. Space blankets also tear easily when they are nicked or punctured. The space bag has the same flaws as does the space blanket except that it is easier to encase an individual and for that person to stay enclosed.

THERMAL BLANKETS Thermal blankets are similar to space blankets, but they are made from much heavier material that is reinforced with fiberglass threads and that has a grommet in each corner. They can be used as body wraps, but again, depending on the size of the person, they are often too small to encase an adult. Some survivors have attempted to use a thermal blanket as a shelter roof by tying lines to each corner and then stretching the blanket between various anchor points. In benign conditions, this may work; however, with any wind or snow loading, the grommets quickly tear or pull out.

Tube tents are usually about 2.4 m (8 feet) long and provide a tubular shelter that is 0.9 to 1.5 m (3 to 5 feet) high, depending on the brand. They can be pulled over the body to provide a quick shelter or pitched as a “pup tent.” To do this, find two anchors (e.g., rocks, trees) that are the proper distance apart, tie a line to one of them, spread the tent out along the length of the line, run the line through it, and then tie off the other end of the line. The height of the line should be such that the tent can be spread out to accommodate the occupant. To avoid ripping, the tent plastic should be 3 to 4 mils thick (1 mil = 0.0251 mm [0.001 inch]). Tube tents can be improvised from two plastic 55-gallon drum liners, which are 3 to 4 mil thick, or from large, heavy-grade, household trash bags by opening up the closed end of one bag, sliding it into the open end of the second bag, and then duct taping the bags together (Figure 41-2).

TARPAULINS Sheets of Visqueen plastic, painters’ drop cloths, large pieces of canvas, or other similar materials can be used to erect a wide variety of effective survival shelters. “Blue crinkly” plastic tarps made of a laminated polyethylene weave are readily available and inexpensive; they can be purchased from most hardware stores, they come in a variety of sizes, and have grommets inserted along the edges. A tarp, no smaller than 2.4 × 3 m (8 × 10 feet), is needed to protect an adult. Tarps of this size weigh about 0.7 kg (26 oz) and roll up into a tube that is 15 cm

FIGURE 41-2  Two large plastic bags can be taped together in tandem and used with a line to form a tube tent. (Courtesy Peter Kummerfeldt.)

(6 inches) in diameter by 30 cm (12 inches) long, which is convenient to carry tied to the outside of a daypack or a fanny pack. To save valuable time in a survival situation, tie 3 m (10 feet) of parachute cord to each corner grommet ahead of time. Tarps can be erected in a number of shelter styles, depending on weather conditions (Figure 41-3). To erect a lean-to shelter, first select a line that is long enough to stretch between two trees that are far enough apart for the tarp to be stretched tight. With the use of a timber hitch, tie off one end of the line to one of the trees at about chest height. Then, rather than passing the line itself through the grommet eyes, insert a small loop of the line

A

B

C

D

E

F

G

FIGURE 41-3  Four types of shelters that can be made from a tarp. A, A simple lean-to. B, An illustration of a method for attaching a line to a tarp. C, A pup-tent type of shelter. D, A lean-to shelter with an eave. E, A triangular tarp shelter. F, Creating a button for attaching a line to a tarp without grommets. G, Attaching a line to the neck of the button with the use of a girth or a clove hitch. (Courtesy Peter Kummerfeldt.)

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PART 5  RESCUE AND SURVIVAL

through the first grommet eye, and secure the loop with a short stick that is thrust through it on the opposite side (Figure 41-3, B). Repeat this process for each grommet, stretching the tarp tight each time. After the tarp is attached to the line, tie off the other end of the line to the second tree, with the line stretched as tightly as possible. The lower edge of the tarp is then pegged to the ground or anchored with large stones or a length of log. When making pegs, select a length of wood that is 3.8 to 5 cm (1.5 to 2 inches) in diameter and that is twice as long as needed. With a saw, make one 45-degree cut at the midpoint of the stick. In this way, one cut produces two pegs, both of which are sharp enough to be driven into the ground by pounding their blunt ends with the back of an ax head or a large rock. Fill in the sides of the lean-to with vegetation. If a fire will be built in front of the lean-to, the front opening should be parallel to the prevailing wind so that the smoke will be carried away from the shelter. If not, the back edge of the lean-to should point to the prevailing wind. To erect a pup-tent type of shelter (Figure 41-3, C), tie a line between two trees, drape the tarp over it, and peg down the sides. Block the ends with vegetation or personal equipment. A lean-to with an eave (Figure 41-3, D) gives more protection from rain and snow than does one without an eave. Instead of attaching the long edge of the tarp to the line between the two trees, drape the tarp over the line so that several feet are on the other side, and then tie the two corners to pegs for a downsloping eave. A triangular tarp shelter can be erected rapidly and provides good protection (Figure 41-3, E). It requires three pegs and an anchor point on a tree.

PLASTIC BAG SHELTERS Large, heavy-grade (3 to 4 mil), orange, plastic, 208-L (55-gal) drum liners make good short-term emergency shelters. Having one to crawl into quickly will speed warming and drying as well as shelter the survivor from further wetness and chilling. However, total enclosure in a plastic bag is both uncomfortable and dangerous as a result of increased wetting from the condensation of water vapor in exhaled air and perspiration plus poor ventilation, with a lack of oxygen and buildup of carbon dioxide. To minimize these problems, cut an opening in the bottom end of the bag that is just large enough for your head, and then pass the bag over your head so that your face is at the opening (Figure 41-4). If you get too warm, you can push your head through the hole. When creating the hole, cut the plastic at 90 degrees to the fold to reduce the likelihood of the bag tearing along the seam.

WINTER AND COLD WEATHER EMERGENCY SHELTERS Everyone who spends time in the winter wilderness should practice the construction of several types of emergency survival

TABLE 41-2  Thermal Conductivity of Various

Substances

Substance Air Down Polyester (hollow) Polyester (solid) Snow (old) Cork Sawdust Wool felt Cardboard Wood Dry sand Water Brick Concrete Ice

Conductivity*

Temperature Measured (° C)

0.006 0.01 0.016 0.019 0.115 0.128 0.14 0.149 0.5 0.8 0.93 1.4 1.5 2.2 5.7

0 20 — — 0 30 30 40 20 20 20 12 20 20 0

*Conductivity is the quantity of heat in gram calories transmitted per second through a plate of material that is 1 cm thick and 1 cm2 in area when the temperature difference between the sides of the plate is 1° C.

shelters before such shelters may be needed. The functions of a shelter are to provide an extension of the microclimate of still, warm air that is furnished by clothing; to contain the heat generated by the body, a fire, or other heat source; and to protect the individual from snow, rain, and wind. A properly designed shelter should allow easy and rapid construction with simple tools and should provide good protection from wind, rain, and snowfall. The type and size of shelter depend on the presence or absence of snow and its depth; on the natural features of the landscape, including the availability of natural building and insulating materials; and on whether firewood or a stove and fuel are available. If external heat cannot be provided, a shelter must be small and windproof to preserve body heat. If possible, a shelter should be constructed in the timber to provide protection from the wind and access to firewood. Generally shelters partway up the side of a ridge are warmer than those in a valley, because cold air tends to collect in valleys and basins during the night. Exposed windy ridges above the timberline are cold. Areas that are exposed to flooding (e.g., drainages, dry riverbeds), rockfalls, cornice falls, or avalanches or that are under dead trees or limbs should be avoided. If open water is available, the camp may be located nearby, although in nonsurvival conditions camps should be at least 61 m (200 feet) from bodies of water. To avoid drifting snow, tents and shelters should be located with the entrance parallel to the prevailing wind. Snow is a good insulator (Table 41-2). Its heat conductivity is 1/10,000 that of copper, and its insulating ability superior to wool felt, so snow shelters may be warmer than other types of constructed shelters as long as the inhabitants remain dry. Contact with the snow or cold ground is avoided by sitting on a foam pad, dry leaves, grass, a backpack, or (in survival conditions only) a bed of evergreen boughs.

NATURAL SHELTERS

FIGURE 41-4  Lean-to shelter. The sides should be closed with brush or snow and a fire built in front.

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Caves and alcoves under overhangs are good shelters and can be improved by building wind walls with rocks, snow blocks, or brush. A fire should be built in such a way that heat reflects onto the occupant. The fire should be 1.5 to 1.8 m (5 to 6 feet) from the back of the shelter, with a reflector wall of logs or stones on the opposite side of the fire; the occupant should sit between the fire and the back of the shelter (Figure 41-5). Adjustments may have to be made to prevent too much smoke from reaching the occupant. In deep snow, large fallen logs and bent-over evergreens frequently have hollows under them that can be used as small caves. Cone-shaped depressions around the trunks of evergreens (i.e., “tree wells”) can be improved by digging them out and roofing them over with evergreen branches or a tarp. A fire that is built to one side of such a shelter will reflect its heat off of

CHAPTER 41  Essentials of Wilderness Survival

A FIGURE 41-5  Example of two large plastic bags used to form a oneperson survival shelter. (Courtesy Peter Kummerfeldt.)

the snow toward the occupant. Ventilation must be adequate, and the fire should not be positioned under snow-laden branches than can extinguish the fire by dumping snow on it.

CONSTRUCTED SHELTERS When no snow is available, shelters can be built of small trees, branches, brush, and boughs. In cold weather with minimal or absent snow cover, the most satisfactory type is a lean-to covered by a tarp, with the two sides closed with brush or piled snow, a fire at the open front, and a wall of logs or stones on the far side of the fire to reflect heat into the interior of the lean-to (Figure 41-6). Walls or a roof of brush, branches, or broad leaves should be thatched (i.e., each layer should overlap the one below it).

SNOW SHELTERS A snow trench is the easiest and quickest survival snow shelter and the one that is least likely to make the diggers wet. It can be dug in most areas that are flat or on slight to moderate inclines as long as the snow is 0.9 m (3 feet) or deeper or can be piled to that depth. A 1.2 × 1.8-m (4 × 6-feet) trench can be dug in 20 minutes, with one end roofed over with a tarp or boughs and a fire built at the opposite end (Figure 41-7). Again, adjustments may need to be made to avoid excessive smoke exposure, which can be prevented to some extent by setting the long axis of the trench at a right angle to the apparent wind direction. If a large (2.4 × 3 m [8 × 10 feet]) tarp and a stove are available, a trench can be dug that is as comfortable as a snow cave;

Overhang

B FIGURE 41-7  Emergency snow trench. A, A pit is dug and overlaid with skis and poles. B, A tarp is placed over the skis and secured with snow and heavy objects.

this will hold two or three people. The object is to keep the maximal amount of snow around and over the trench. The trench is dug as narrow as possible at the surface while still providing sufficient room to shovel; a suitable size for the top is 1.2 m (4 feet) wide by 2.4 m (8 feet) long. It is undercut at the back and sides so that the bottom is 1.8 to 2.1 m (6 to 7 feet) wide by 2.7 to 3 m (9 to 10 feet) long (Figure 41-8). A narrow entrance helps to contain heat and can be closed with a small plastic sheet or a pack. Four or more skis or thick limbs are laid from side to side over the top of the trench, with ski poles or branches interwoven at right angles. A tarp is then laid on top of these and the snow piled around its edges to hold it down. In very cold weather, the entire tarp can be covered by a layer of snow; at least 20 cm (8 inches) is needed for proper insulation. When the entrance is closed, a small stove and the occupants’ body heat will raise the interior temperature to −4° to −1° C (25° to 30° F). Higher temperatures should be avoided so that clothing and bedding will not become wet from melting snow. Above the timberline in deep, wind-packed snow, a similar trench can be roofed with snow blocks that are laid horizontally, set as an A-frame, or laid on skis (Figure 41-9). Chinks between the blocks are caulked with snow.

SNOW CAVES

Reflector Fire

Backpack

FIGURE 41-6  Natural shelter.

Woodpile

Although a small snow cave that is large enough for one person can be dug with a ski or cooking pot, it is much better to have a shovel. Two shovels are best: a medium-sized general-purpose aluminum scoop shovel and a small, straight shovel (i.e., French type) to use while excavating the interior of the cave. The best site is a large snow drift, such as is found on the lee side of a small hill. Areas in avalanche zones or under cornices should be avoided. Because the diggers tend to become wet, water-resistant or waterproof jackets and pants should be worn. In the traditional snow cave, the entrance is dug so that it is just large enough to crawl through, and it is angled upward toward the sleeping chamber (Figure 41-10, A); this arrangement tends to trap warm air inside. It should be large enough for a stove and two occupants who are lying side-by-side. After the entrance is dug with the scoop shovel, the digger crawls inside, lies supine, and uses 785

PART 5  RESCUE AND SURVIVAL

Ski poles

Sides and ends undercut

A1

A2

Skis

Narrow entrance

B1

B2

Tarp

C1

Snow piled along edges

Ventilation hole for cookstove

C2

D FIGURE 41-8  A1 and A2, Three-person snow trench. A narrow entrance and a narrow top with undercut sides are advisable to trap as much warm air as possible. B1 and B2, Skis and ski poles or stout limbs form the roof support. C1 and C2, Finished trench with snow piled along the edges of the tarp to hold it down. Note the ventilation hole for the cook stove. D, Completed trench after a heavy snowfall.

A

B FIGURE 41-9  A, Above-timberline snow trench. B, Completed snow trench the morning after a heavy snowfall.

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C

B

FIGURE 41-10  A, Snow cave entrance. B, Snow cave partly closed with snow blocks. C, Interior of snow cave.

the straight shovel to excavate the chamber until the space is large enough to allow room to use the larger scoop shovel. A long level bench about a foot higher than the floor of the cave is constructed and used for a sleeping area. A ventilation hole as large as a ski pole basket is cut in the roof over the cooking area. Because the traditional cave takes at least 2 hours to dig and gets the diggers quite wet, the alternate “T” method has found favor. This involves excavating a much larger entrance hole, which is shaped like a “T,” so that the digger can stand erect, have plenty of room to dig, and stay drier (see Figure 41-10, B). The crossbar of the “T” is at the level of the sleeping bench; the digger stands in the foot of the “T.” After the cave is finished, the top of the “T” is closed with snow blocks, leaving the foot of the “T” as a small access door hole. Pine branches or other natural materials are used to cover the floor if a sleeping pad is not available.

SNOW DOMES When the ground is flat or the snow cover is shallow, snow can be piled into a large dome that is 1.8 to 2.1 m (6 to 7 feet) high and left to harden for a few hours (Figure 41-11). A low entrance is dug on one side, and, from there, the interior is carved out to make a dome-shaped room that is large enough to sleep three people. A ventilation hole is cut in the roof over the stove. Another method is to make a “form” (i.e., a pile of vegetation or equipment), cover this form with snow, allow the snow to set, and then open one end and remove the form.

IGLOOS Igloos are the most comfortable arctic shelters, but they require experience and engineering skill. They are not recommended for the novice, but they may be worth the effort if the party will be stranded for any length of time. Igloos require one or, ideally, two snow saws and snow of the proper consistency. Wind-blown snow in a treeless area is best; otherwise, a large area of snow can be stamped well and left to harden over several hours. To mark the diameter of the igloo, an individual holds a ski pole by the handle, points it to the side, and then turns his or her body so that the pole basket makes a large circle in the snow that outlines the base of an igloo that is suitable for three people. Cutting some of the snow blocks from inside this circle will lower the floor so that fewer blocks are required for the dome. At least two persons are needed: one to cut and carry the blocks and the other inside the igloo to lay the blocks. The blocks should be about 18 inches wide, 30 inches long, and 8 inches thick. They are laid in a circle that leans in about 20 to 30 degrees toward the center of the igloo, with the sides trimmed for a snug fit. The tops of the first few blocks in the first circle are beveled so that a continuous line of blocks is laid, with the first few blocks of each succeeding circle cocked upward (Figure 41-12, A and B). A common error is to not lean the blocks sufficiently inward, which results in an open tower instead of a dome. Gaps are caulked with snow. The dome should be 1.5 to 1.8 m (5 to 6 ft) high inside and can be closed with a single capstone of snow. The entrance is dug as a tunnel under rather than through the edge of the igloo to prevent warm air from escaping (see Figure 41-12, C ).

TENTS Tents are generally comfortable and dry; however, in very cold weather, they are not as warm as snow shelters. They are preferable to snow shelters at mild temperatures, during damp snow conditions at temperatures above freezing, or when the snow cover is minimal. Because of their weight, they are not usually a component of emergency equipment.

A

B FIGURE 41-11  A, Preparing a snow dome. B, Completed snow dome.

BIVOUAC SACKS AND OTHER SMALL AND PORTABLE EMERGENCY SHELTERS These types of shelters are usually made of thin waterproof or water-resistant fabric or plastic; they do not include an insulating layer, and they hold one or occasionally two persons. Bivouac sacks are carried for emergencies or for sleeping purposes by climbers on long, alpine-style climbs. Their main value is to protect individuals from wind and rain. Many modern packs have extensions so that, when they are used with a cagoule or an anorak (i.e., roomy, knee-length, hooded pullover garments), they form an acceptable bivouac sack. Tube tents and plastic shelters were discussed in the previous section of this chapter. Caution: When spending the night in a snow shelter (e.g., trench, cave, igloo), always have a shovel and flashlight inside the shelter and within easy reach. 787

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A

PART 5  RESCUE AND SURVIVAL

Air vent

Cooking

Sleeping

Entrance

Entrance

C

B

A

E

D

FIGURE 41-12  A to C, Stages of igloo construction. D, Building an igloo on the southeast ridge of Mt Foraker. E, Double igloo for a party of five.

Increasing Body Heat Production Internal body heat production can be increased voluntarily by raising the level of muscular activity and by eating. To obtain maximal heat production from exercise, the body should be well fed and in peak physical condition. This is particularly important for persons with sedentary occupations who participate in vigorous outdoor sports and for rescue personnel who may be subject to severe, unplanned, and prolonged physical stress. A suitable physical conditioning program should develop both aerobic and motor fitness. The goal of aerobic exercise is the efficient extraction of oxygen from alveolar air. This is best developed by rhythmic endurance exercises such as running, cross-country skiing, cycling, swimming, and use of exercise bicycles, treadmills, or Nordic skiing simulators. The most effective activities

A

C

are those that exercise the lower and upper extremities simultaneously. Exercise should be vigorous enough to produce a heart rate of 75% of the age-related maximum (i.e., 0.75 × [220 − the participant’s age]) for at least 15 minutes 4 days a week. Motor fitness, which includes strength, power, balance, agility, and flexibility, is developed by vigorous competitive sports, select calisthenics, and weight-lifting exercises.

Adding Heat From the Outside The ability to build a fire under adverse conditions is an essential skill that should be practiced by all people who engage in outdoor activities (Figure 41-13). Not only does a fire provide warmth that may mean the difference between life and death, but it also cheers the spirit, improves morale, serves as a signal

B

D

E

FIGURE 41-13  Stages of building a fire. A, Select a spot that is out of the wind. Start by placing tinder (i.e., small, dry evergreen twigs) in a lean-to fashion against a larger branch. B, Add a layer of kindling (i.e., larger dry branches and split sticks) over the tinder, and be sure that air can reach each piece. C, Insert a lighted match, a candle, or a cigarette lighter into the base of the lean-to. D and E, Add larger pieces of kindling and fuel (i.e., large sticks and pieces of split wood) as the fire catches well. Keep the fire small so that you can get close to it.

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Heat Sources The devices that are carried to produce the initial source of heat that is needed to start a fire must be easy to use when the hands are cold and have lost their dexterity. These devices must function every time regardless of temperature, altitude, wind, or precipitation; the amount of heat supplied must be great and long lasting. Because survivors are often injured, the devices must function when only one hand can be used. The heat required to ignite tinder traditionally has been provided by matches or cigarette lighters. Metal matches (i.e., ferrocerium rods) are a third and less-commonly used source of fire-starting heat.

Pouring liquid paraffin over matches to waterproof them is a common procedure that sounds good but that in practice complicates a survivor’s ability to get a fire going. The paraffin must be scraped off of the match head before it can be struck. Other people recommend using nail polish and spar varnish to waterproof matches. For the reasons stated previously, this should not be done. In short, waterproof matches should not be included in a survival kit.

MATCHES

WINDPROOF MATCHES

Predecessors of the modern-day match date back to 577 AD and the Northern Qi court in China. Today, a match is a “consumable tool for lighting a fire in a controlled circumstance on demand.” (Wikipedia) Most matches that are currently for sale are not designed for field use but rather for lighting cigarettes or candles and other home uses. Two general categories of matches are safety matches, which can only be ignited by striking the match against a specially prepared surface found on one or two sides of a matchbox, and strike-anywhere matches, which, theoretically, can be struck on any abrasive surface.

Windproof matches have longer and fatter heads than do normal matches; as much as one-half of the matchstick is covered with pyrophoric material. These matches can be difficult to light under benign conditions and almost impossible in adverse weather. Most commonly, the matchstick breaks at the junction of the match head and the stick when pressure is applied. Some windproof matches, once lit, only smolder and have little if any flame (Figure 41-16).

SAFETY MATCHES For a safety match to light, the chemicals (i.e., the pyrophoric material) on the match head must be combined with the chemicals on the striking pad. The chemicals on the match head consist mainly of potassium chlorate (45% to 55%) and a filler material (20% to 40%) that are bound together with glue. The striking surfaces attached to the sides of the box are composed of powdered glass, red phosphorus, black carbon, and a binder. Safety matches can only be ignited by striking the match head on the striking pad on the box from which they were removed; a match taken from one box may not light by striking it on the pad of another matchbox, because the combinations of the chemicals may be different (Figure 41-14, online).

FIGURE 41-15  Waterproof safety match.

STRIKE-ANYWHERE MATCHES Strike-anywhere matches can be identified by their two-tone heads, which are usually blue and white, green and white, pink and white, or red and white. Both chemicals (phosphorus sesquisulfide and potassium chlorate) that are needed to initiate combustion are combined on the match head. The term “strike anywhere” would lead you to believe that they could literally be struck anywhere, but nothing could be further from the truth. These matches must be struck on the striking pad or on another material that is abrasive enough to produce combustion yet that is not so abrasive that the match head is ripped off; it should come as no surprise that such a surface can be difficult to find when the ground is covered in snow. Although some people have developed the ability to ignite strike-anywhere matches by

WATERPROOF MATCHES Commercial waterproof matches have been dipped in a lacquer that “waterproofs” the match head after it dries. To light a waterproof match, the match head must be struck against the striking pad repeatedly until the lacquer is worn away and the chemicals contained in the match head come in contact with the chemicals in the pad. For some matches, this may only take a strike or two, but with others many strikes are required to ignite the match. With every strike, the pad becomes more contaminated with the waterproofing material and eventually a point is reached where there are remaining matches but the pad is so contaminated that it no longer works. Some waterproof matchboxes only have a striking pad on one edge of the box, thus making a bad situation even worse (Figure 41-15).

FIGURE 41-16  Windproof and waterproof safety match.

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to rescuers, and reinforces hopes of rescue and survival. Necessary equipment (which is discussed later in this chapter) includes a knife, a fire starter, and dry matches at a minimum. Most commonly the need for a fire does not arise until a crisis is at hand: for example, the weather has become life threatening, a person has fallen into the river and needs to be rewarmed quickly, or a hunter needs a fire to stay warm when faced with spending a night out far from camp. The need for a fire becomes critical when the survivor’s clothing is inadequate and other shelter is not available. These are not the times to get one’s first practice at building a fire. It is advisable to obtain that practice ahead of time in the backyard when rain or snow is falling and the wind is howling; that is the time to determine the strengths and weakness of fire-starting equipment and the soundness of one’s fire-building skills.

PART 5  RESCUE AND SURVIVAL

FIGURE 41-20  Boy-Scout style match case. FIGURE 41-17  Strike-anywhere match.

rubbing them across the seat of their pants, by flicking the match head with a thumbnail, or even by using their teeth, these methods are not reliable in an emergency. When carrying strikeanywhere matches, always have a piece of the striking pad from the original matchbox in the kit (Figure 41-17).

STORM MATCHES Storm matches are often found in civilian and military survival kits. They differ from other matches by having a “strikeable” tip with as much as one-half of the matchstick coated with a pyrophoric material that continues to burn even in wet and windy conditions. Lifeboat matches, which are a common variety of storm match, should be avoided, because they are particularly difficult to light. The striking pad, which is located on the outside of the lid, is small and wears out very quickly (Figure 41-18, online). All of the matches that are currently available were tested under field conditions, and REI Stormproof Matches were found to be the best. They proved to be the most reliable for starting fires under adverse weather conditions, and they are particularly effective in windy and wet conditions. As long as any match head material remains, the REI matches cannot be blown out, and, if they are extinguished in water, they will relight when they are removed. These matches are propriety and are only sold under the REI brand. Two boxes of matches, each of which contains 25 3-inch long matches, are packaged together in a vinyl pouch. The pouch also contains additional pieces of the striker material that are sealed in a separate waterproof packet (Figure 41-19).

MATCH CONTAINERS The ability to light a match is tied directly to the condition of the matchbox, most of which are made from cardboard or thin wood with striking pads along each side. Neither of these materials is particularly durable, and both tend to disintegrate quickly when wet. For this reason, matches should be protected in a container that is waterproof, easy to open with one hand, and easy to find if dropped. Do not take it for granted that a match case is as waterproof as claimed; be sure to test it.

FIGURE 41-19  REI Stormproof Matches.

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BOY-SCOUT STYLE A Boy-Scout style match container can be very difficult to open when the hands are cold or stiff or have lost both dexterity and strength. Grit or other debris that gets into the threads tends to jam the device in the closed position. Boy-Scout style match cases are almost impossible to open with one hand, especially with a nondominant hand. The “waterproofness” of these containers is questionable, and this style of match container is not recommended (Figure 41-20).

MILITARY STYLE Except for the olive drab green color, the military-style match case meets all of the criteria for a good match container. It is tough, waterproof, and easy to open with one hand. However, these cases can be difficult to find if they are dropped in the grass. Embedded in the base of the case is a small piece of metal match. Many people erroneously believe that a match can be struck on this material and ignited; rather, if this material is scraped with a sharp edge, sparks can be produced with which to ignite tinder (Figures 41-21 and 41-22).

ORANGE MILITARY-STYLE MATCH CASES Orange military-style match cases (Figure 41-23) are available in most sporting goods stores, where they are usually sold under the Coghlins brand name. These versions of the military-style match case are not quite as sturdy as the military versions, but they are much easier to find if dropped. This match case comes in two lengths, with the longer variety just long enough to accommodate the REI matches. If the shorter version is used, the REI matches must be shortened before they are placed in the case. When filling a match case with REI matches, place one-half of the match heads down and one-half with the match heads toward the top; this allows more matches to be carried in the case. Caution: A piece of the striking pad must also be inserted in the

FIGURE 41-21  Military-style match case.

OTHER METHODS OF IGNITING TINDER

FIGURE 41-22  Scrape the metal match material on the base of the match case to produce sparks.

case; be sure that, when you do so, the striking surface is placed toward the plastic wall and away from the match heads.

MULTIPURPOSE MATCH CASE The popular multipurpose match case should be avoided. The device, which includes a whistle, a mirror, a small piece of metal match, a compass, and a match case, combines all of these survival tools into one. On the surface, this sounds like a good idea. However, should the match case become lost or damaged, one loses the ability to build a fire, signal, and navigate successfully. It is better to buy individual pieces of equipment and not to put all of one’s eggs in one basket (Figure 41-24).

Cigarette lighters are frequently carried by inexperienced outdoorsmen, because these people are generally unaware of the shortcomings of lighters with regard to starting a fire. Consider the following: BIC-style lighters are pressure sensitive (i.e., the higher the altitude, the less the fuel will vaporize); they are temperature sensitive (i.e., the colder the temperature, the less the fuel will vaporize); they explode if they are accidentally dropped into a fire, thus sending shrapnel in all directions; and they require good hand dexterity to operate, which is not a problem when it is warm but quickly becomes a problem in cold conditions (Figure 41-25, online). Zippo lighters have a significant advantage over BIC-style lighters in that they will continue to burn until the cover is closed to extinguish the flame; BIC-style lighters continue to burn only as long as the fuel release remains depressed. This difference is put to good effect when, needing a fire, the survivor lights the Zippo, places it on the ground (stabilizing it with dirt), and then places twigs over the flame. One disadvantage of these lighters is that the fuel tends to evaporate rather quickly (Figure 41-26). Piezo ignition-style lighters use an electronic spark to ignite the fuel, which is similar to the spark produce by an outdoor gas grill lighter to ignite the fuel. This system is much easier to use than the BIC style, and it requires far less finger and hand dexterity. If you are going to carry a cigarette lighter, select one with a piezo ignition mechanism and a clear fuel reservoir to see how much fuel remains. When in cold conditions, carry the lighter in an inner pocket where it will stay warm (Figure 41-27, online). Colibri Quantum lighters are more expensive devices that are alleged to be waterproof, shockproof, and windproof, and it is claimed that they will ignite at higher altitudes. However, field testing of these lighters does not show this to always be the case (Figure 41-28). Metal matches are manufactured from a man-made metallic material that, when scraped with a sharp edge, produces a shower of very hot sparks that can be used to ignite tinder. Metal matches have been erroneously called “magnesium matches.” Although there is a small percentage of magnesium in the alloy (4%), the bulk of the mixture is made up of iron (19%), cerium

FIGURE 41-23  Orange military-style match case.

FIGURE 41-24  Multipurpose match container.

FIGURE 41-26  Zippo lighter.

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Regardless of the container used, the matches must be tightly packed in the match case. Loosely packed, the match heads quickly disintegrate. If space allows, a piece of household cotton ball placed in the cap also helps to prolong the life of the matches. It is also wise to replace the matches at least annually to ensure that the matches that are needed in an emergency are fresh and will ignite.

PART 5  RESCUE AND SURVIVAL

FIGURE 41-28  Colibri Quantum lighter.

(38%), and lanthanum (22%), with the remaining balance composed of other rare metals. The metal match material, which is also called ferrocerium or mischmetal, comes in rods of different lengths and thicknesses, and is usually mounted in a plastic, antler, or wooden handle (Figure 41-29). Select a metal match with a wooden handle. Should one find oneself without tinder to light, the wooden handle can be scraped to produce shavings that can be ignited by metal match sparks; the same cannot be said of plastic or antler. Choose a metal match that has a handle that is large enough to hold firmly when the hands are cold. Some metal matches are embedded in either a block or cylinder of magnesium (Figure 41-30). When a fire is needed, the magnesium block is scraped with a knife blade or another sharp edge to produce shavings that can be ignited by the sparks that are created from the metal match. However, several problems will be encountered. First, it takes both hands to produce the shavings. Second, it can be difficult to confine the shavings to one place when trying to start a fire in a windy location, so they may blow away. Third, magnesium shavings burn at a very high temperature (about 2760° C [5000° F]), but the burn time is very brief, which does not allow the survivor much time to capitalize on the heat. The shavings must be scraped into another flammable material that will ignite from the burning magnesium. Metal matches come in styles that require the use of both hands to operate (Figure 41-31) and those that can be operated with one hand (Figure 41-32). When the use of both hands is possible, the user holds the metal match in one hand and a sharp edge in the other. This “sharp edge” could be a knife blade or any other piece of metal that, when scraped down the length of the metal match, produces a shower of hot sparks. Usually the scraper is held between the thumb and index finger of the dominant hand. For a situation in which one only has a single

FIGURE 41-29  Metal match handles. From left to right: plastic, synthetic antler, and wood.

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FIGURE 41-30  Metal match embedded in magnesium.

FIGURE 41-31  Metal match with a hacksaw blade scraper.

functioning arm, it is possible to stabilize the metal match by stepping on it and then using the noninjured hand to produce the sparks. Metal matches that have been specifically designed for one-handed operation are easy to use. With these, the metal match is spring-loaded in a plastic housing that also contains the scraper. The tip of the metal match is placed on a hard surface, and, by pushing against the tip while simultaneously pressing on the scraper, a shower of sparks is created. When planning for a worst-case scenario, having a metal match that can be lit with one hand could mean the difference between a fire and no fire.

FIGURE 41-32  Ultimate Survival Blast Match and Sparkie Fire Starters.

BUILDING FIRES Throughout this description of fires and fire craft, the term build a fire has been used instead of the more commonly used phrase start a fire. This choice is deliberate. Building a fire implies that there is a process involved that, if followed, will result in success. Starting a fire involves only the first step in the fire building process: applying heat to the tinder and then hoping that it catches on fire and ignites other fuel. Many inexperienced people only think through the process as far as “starting the fire” step and forget that there is a lot more to the procedure than that. Consequently, their fire-building efforts are often unsuccessful. When the need for a fire is critical, the tinder must light easily, and the steps used to build the fire must quickly result in a selfsustaining fire, regardless of weather conditions. For a fire to burn, three elements are required. A heat source that is sufficient to ignite the tinder is necessary; oxygen must be available; and good-quality fuel must be on hand. Because it is the flammable gases contained within wood that ignite, the amount of heat provided by the initial heat source must be sufficient to drive off the gases that are contained within the tinder. The heat provided by the burning tinder must, in turn, drive off the flammable gases that are contained within the larger fuel. One of the most common mistakes made by inexperienced fire builders is trying to light fuel that is far too large for the amount of heat that is available to light it; the heat is then insufficient to produce the gases that are needed for combustion. Step number one in fire building is fuel collecting. Too often, people simply pick up sticks from the ground. Although this might work during the heat of summer, this fuel seldom burns well at other times of the year, when rain and snow saturate the wood that is lying on the ground. It is better to collect your fuel, especially that which will be used in the early stages of the fire, by breaking off dead branches that are found on standing trees. The moisture content of this wood is far lower than that in wood that would be collected from the ground. If the wood bends rather than snaps, it is probably green and should not be used. If there are green leaves or needles attached to the branch discard it, because it will not burn. The small, dry, dead branches found under the overhanging branches of evergreen trees, especially fir and spruce, are particularly good for the early stages of a fire (Figure 41-34, online). In some parts of the country (e.g., the Pacific Northwest), even this fuel can be wet, and it is often draped with moss. However, it is only wet and moss-covered on the outside (Figure 41-35); the interior is dry. Scrape off the moss and wet bark with a knife blade. If twigs and smaller sticks are not available, they must be fashioned by splitting large sticks into smaller pieces with the use of a knife and mallet (Figure 41-36). Splitting wood in this manner exposes the dry inner surfaces of the wood, which can be used as fuel when other dry fuel is not available. Gather far more fuel than you expect to need, and then go out and gather more; one can never have too much. Having accumulated a substantial pile of fuel, separate the wood into three piles by size. The first pile should be matchstick size or thinner; the second pile should be sticks up to the thickness of a thumb; and the rest of the pile is the remainder. When collecting fuel, gather it in long lengths. It is easier to carry or drag into the campsite, and the fire will burn the long lengths into shorter pieces, thereby saving the effort of needing to use a saw. It also saves energy if one can break the wood into pieces rather than having to saw it into pieces (Figure 41-37). When the ground is wet, it is advisable to assemble a platform of sticks that is approximately 0.3 m2 (1 foot2) to protect the

FIGURE 41-35  Wet moss and soggy bark can be scraped off to reveal the dry wood underneath.

FIGURE 41-36  A saw and a knife can take the place of an axe.

FIGURE 41-37  Wedge one end of a long branch between two trees to break off pieces.

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CHAPTER 41  Essentials of Wilderness Survival

When faced with choosing the best fire-starting device and comparing the fire-starting potential of a metal match versus a box of matches or a cigarette lighter, the metal match wins hands down. A typical box of matches contains 25 to 32 matches. For most people, who lack good fire-building skills, more than one match—sometimes many more—will be needed to start a fire. A single metal match has the capacity to start more than 500 fires (Figure 41-33, online). Each time a metal match is scraped, some of the material is removed, so eventually the match will have to be replaced.

PART 5  RESCUE AND SURVIVAL

As the twigs begin to burn and flames appear through the first layer of fuel, lay a second handful of twigs at a 90-degree angle over the first layer (Figure 41-41). As the flames appear above this layer, place another handful of slightly larger twigs on the fire, again at a 90-degree angle to the previous layer. (Figure 41-42, online). This process continues until the larger fuel has been added and until the fire will sustain itself without the immediate attention of the person building it. Your firebuilding success with the use of this method is contingent on the use of tinder that produces a lot of heat, that is well ventilated, and that graduates step by step from the smallest twigs to the largest sizes of fuel (Figure 41-43, online).

TOOLS THAT MAKE FIRECRAFTING EASIER FIGURE 41-39  Cotton ball saturated with petroleum jelly being lit with a metal match.

Hand and full-size axes have been the traditional tools carried by outdoorsmen to facilitate the cutting and splitting of large fuel wood (Figure 41-44, online). However, in the hands of an inexperienced person, an axe is an accident looking for a place to happen. Lacking the years of “chopping” practice that men and women a century ago accumulated during the course of their daily lives, men and women today put themselves at risk when using an axe. As compared with saws, axes are inefficient and dangerous tools that can cause wicked injuries. Do not carry an axe unless you are highly skilled in its use.

tinder (Figure 41-38, online). If tinder is placed directly on wet ground, it tends to absorb moisture from soil that may make it more difficult to light. There is no practical way for a survivor to build a fire on top of snow. Lacking a chainsaw with which to cut large logs to build a platform on the snow, the heat from the fire quickly melts the snow beneath a platform that is made from smaller sticks, so the fire is quickly extinguished. Try to locate an area where the snow is shallow enough to scrape it away down to ground level. Wind has a dramatic effect on fire-building efforts. To provide the best chance of having tinder ignite and continue to burn, place a log that is about 25 to 30 cm (10 to 12 inches) long and 10 cm (4 inches) in diameter along the windward side of the platform. Place the tinder in the lee of the log, where it is protected from the wind. When trying to build a fire in rainy conditions or when snow is falling, find a sheltered area that is protected from precipitation, or erect a temporary roof over the fire site to shelter the tinder until the larger fuel is burning. Before lighting the tinder, everything must be ready. The second most common mistake made by inexperienced outdoorsmen and women is igniting tinder and then having to scramble to find kindling to add to the rapidly burning tinder before it burns out. With everything ready to build out the fire, place the tinder on the platform in the lee of the windbreak, and ignite it (Figure 41-39). As soon as the tinder is burning, place a handful of the smallest fuel directly over the flames, with one end of the twig bundle resting on the log brace (Figure 41-40); this will only work well if you have resisted the urge to break the twigs into overly short pieces. The fuel should be broken into lengths that are 25 to 30 cm (10 to 12 inches) long. Resting one end of the twigs on the brace ensures that good airflow is maintained and that the tinder is not smothered when additional fuel is added. If it appears that more oxygen is needed, lift up on one end of the brace to allow more oxygen to flow to the core of the fire.

Linked-style survival saws.  The Ultimate Survival Technologies SaberCut Saw makes use of a flexible linked saw blade that resembles the blade that is found on real chainsaws. Unlike chainsaws, this blade cuts in both directions, and, as with all saws of this type, it requires the use of two hands for proper function. Although it is not designed to be used in this manner, two people could use it, with one pulling on each end. The SaberCut Saw works well but requires significantly more effort to use than does the pocket chainsaw, which is described next (Figure 41-46). Pocket chainsaws have a 56- to 69-cm (22- to 27-inch) flexible blade that looks very similar to the teeth on a conventional carpenter’s saw. This type of saw cuts in both directions. Depending on the model, there are nylon lanyards or metal rings through which a short length of stick can be inserted to serve as handles that are attached to each end of the saw. This is a useful tool that should be considered for a larger survival kit. Although two people could use it, the saw is best used by one person, assuming that the individual has the use of both hands.

FIGURE 41-40  Placing the first handful of twigs over a burning cotton ball.

FIGURE 41-41  Placing a second handful of twigs over a burning cotton ball.

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Saws Wire survival saws.  Wire survival saws can generally be considered a waste of time. However, because they are compact and lightweight, they are commonly found in commercial prepacked survival kits. They require two hands for cutting. With one exception (i.e., a wire saw that comes from Sweden), the cutting teeth are not very aggressive. Consequently, when pressure is applied, the saw binds up and eventually breaks (Figure 41-45).

must be collapsible and then assembled before they are used. However, assembly requires the use of both hands. Bow saws are made up of multiple parts; if any part is lost, the saw becomes nonfunctional. The size of wood that can be cut is in large part determined by the distance between the blade and the arch of the bow. This space is often quite shallow, which requires the user to have to continuously reposition the wood as it is cut. In addition, bow saw blades are notoriously brittle in cold weather (Figure 41-48). FIGURE 41-45  Commercial wire saw.

FIGURE 41-46  Ultimate Survival linked saw, bottom detail.

Folding saws are popular with outdoorsmen and can be effective cutting tools. They are usually lightweight and short enough to be carried in a fanny pack or daypack. To maximize energy expenditure, select a folding saw that cuts in both directions (i.e., some only cut when you pull). Select one that can be locked in the open position to preclude the blade folding back onto the user’s hand. When it comes to cutting wood, the diameter of the wood should be shorter than the length of the blade (Figure 41-47).

Pruning saw style.  The pruning saw style is the most advantageous for persons who need to quickly cut large quantities of wood. Because no assembly is required, this style of saw is particularly useful to a survivor who has an injured arm or hand. The blade length should not be shorter than 46 cm (18 in). This blade length allows for a full extension of one’s arm when sawing, which is efficient and conserves energy. In addition, a blade of this length is ideal for cutting snow blocks for snowblock shelters. Select a saw with a sturdy handle and one that cuts in both directions (Figure 41-49, online). Gardener’s shears are very useful when gathering smallerdiameter wood, such as that found above the tree line. At high altitudes or high latitudes, the only remaining fuel wood available can be obtained from low shrubby bushes. With shears, one can snip out the dead wood quickly and efficiently (Figure 41-50, online). Fire-Starting Aids Commercial fire-starting aids.  Many commercial products that are available in sporting goods stores and other retail outlets cater to persons who recreate or work in the outdoors. Select products carefully, and test them before they must be used in a survival situation (Figure 41-51).

Bow saw style.  There are many varieties of bow saws; some are ridged, and others are collapsible. To be practical, these saws

FIGURE 41-47  Pick a saw that cuts in both directions and that has aggressive teeth.

FIGURE 41-51  Commercial fire starter.

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CHAPTER 41  Essentials of Wilderness Survival

FIGURE 41-48  Wyoming Saw.

PART 5  RESCUE AND SURVIVAL

Petroleum, oil, and lubricant (POL) products are often available from the fuel tanks of vehicles. These are frequently overlooked fire-building expedients. Many people are reluctant to use gasoline to assist with fire starting out of fear that they will be burned in the process. This fear is not without foundation, because many people are injured each year when gasoline is poured on a pile of sticks, a match is lit and thrown into the sticks, and an explosion results. Great care must be exercised when using POL products, because some—red and white gases in particular—vaporize quickly and explode when a spark or another open flame is applied. Red gas and white gas should never be poured over a pile of sticks and then ignited. Other POL products (e.g., aviation gasoline, depending on its octane) are difficult if not impossible to light with a flame or spark and may require the use of a wick to burn. Diesel fuel cannot be ignited with an open flame and requires the use of a wick (Figure 41-52, online). To use gasoline safely, pour about 2.5 to 5 cm (1 to 2 inches) of gasoline into a container (the bottom two inches of a pop can works well), and then place the container on the ground (Figure 41-53). The fuel vapor on the surface can be lit with a match, the sparks from a metal match, or another open flame source without an explosion, and the fuel vapors will burn in a controlled manner (Figure 41-54). When the fuel is burning, small sticks can be placed over the flames, and then gradually larger and larger fuel can be added (Figure 41-55, online). This process works particularly well when the available natural fuels are wet. Caution: Care must be taken not to upset the fuel container during the process of adding wood, because a violent explosion may occur. When larger containers are used with increased quantities of POL, place sand or other soil in the bottom of the container to add to its stability, and then light the fumes that seep to the surface. If you do not have a container, pour fuel directly into a small depression in the ground, and then light the vapor at the surface. In anticipation of having to siphon fuel from a vehicle, it is wise to carry a 1.2-m (4-foot) length of aquarium hose that can be snaked down into the fuel tank. Of all of the expedient heat sources available to a survivor, the best are household cotton balls that are saturated with petroleum jelly. This mixture is easy to make and ignite, it is windproof and waterproof, it burns for a long time, and it is inexpensive (Figure 41-56). Tease out a cotton ball (without tearing it into pieces) until you have a large, thin disc of cotton fibers (Figure 41-57). Use cotton balls that are actually made from cotton as opposed to “puffs,” which are made from synthetic fibers and which do not burn well. Smear large quantities of petroleum into the fibers,

FIGURE 41-54  Burning automobile gasoline.

working the cotton between the fingers until there is no dry cotton (Figure 41-58). Store the material in an airtight and watertight container until needed; a waterproof screw-top match case works well for this. When stored in this manner, the cotton ball and petroleum jelly mixture will last indefinitely. When needed, remove one or more cotton balls from the container. Take the cotton between the thumbs and forefingers of

FIGURE 41-56  A mixture of cotton balls and petroleum jelly makes very good tinder.

FIGURE 41-53  Pouring white gasoline into a container.

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FIGURE 41-57  Creating a cotton ball disc.

FIGURE 41-61  Burning a cotton ball.

FIGURE 41-59  Tearing a cotton ball into two pieces and retaining the feathery edges.

each hand, and pull the cotton into two pieces (Figure 41-59). Being careful to retain the fluffy “fingers” that are produced, then stick the butts together and place the recombined cotton ball on a piece of aluminum foil, a bottle cap, the bottom half inch of a pop can, or another metallic surface (Figure 41-60). In a pinch, a small flat rock with a depression in it will work. If you do not have any of these materials, place the cotton ball on a bed of small sticks or, if necessary, directly on the ground. When the cotton ball is placed on a metallic surface, the oil that is created as the petroleum jelly liquefies from the heat is collected and contributes to burn time. Placing the cotton ball directly on the ground reduces burn time by one-third. A spark from a metal match or from any other heat source will easily ignite the cotton fibers, which in turn causes the petroleum jelly to burn (Figure 41-61). The value of the cotton ball and petroleum jelly mixture is in its windproofness, waterproofness, and burning duration: it will continue to burn in very windy conditions and in wet conditions, and it will burn for 12 to 15 minutes if it is sufficiently large. Before building any fire, careful consideration should be given to ensuring that the fire does not escape. Select a site that is free from materials that could inadvertently ignite and carry flames to other flammable materials. Scrape away any ground cover that might catch fire. Be careful when building a fire under overhanging vegetation that could ignite. During winter months, fires

FIGURE 41-60  Placing the cotton ball on a sheet of aluminum.

built under snow-covered branches will usually result in a cascade of snow into the fire; either shake the snow from the branches before building a fire, or select another site. Building a fire during windy conditions, when sparks could escape the immediate fire site, should be avoided if possible. If it is still necessary to build the fire, select a protected site that is out of the wind. Placing a log on either side of the fire helps to keep a fire from spreading. When it is no longer required, a fire should be completely extinguished. Dousing the fire with large quantities of water is usually the best way to do this, but, when water is not immediately at hand, mixing the coals with Earth until no hot embers remain is the next best method. Survival literature and other media sources are quick to recommend the use of aboriginal fire-making techniques (e.g., bow and drill, hand drill, fire plough) by a survivor who is in trouble (Figure 41-62). What is forgotten are the years of practice that have taken place to develop the proficiency to reliably use these techniques. To believe that a modern person could do the same—simply with the use of a diagram and some text in a survival manual—is ludicrous.

Food Although most persons who are faced with a survival emergency worry more about food than anything else, food is usually less important than shelter or water, because a person can survive for weeks without food, even in cold weather. However, enough water must be available, and energy expenditure must be kept to a minimum. Most wilderness parties carry adequate supplies of food; however, problems arise if food is exhausted, lost, or contaminated. Bare ridges, high mountains above the timberline, and dense evergreen forests are difficult places to find wild food, especially during winter. Success is more likely on river and stream banks, on lake shores, in the margins of forests, and in natural clearings. Because in most cases the amount of wild food

FIGURE 41-62  Bow and drill method of starting a fire.

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CHAPTER 41  Essentials of Wilderness Survival

FIGURE 41-58  Smearing petroleum jelly into a cotton ball disc.

PART 5  RESCUE AND SURVIVAL

found by an untrained individual will not provide enough calories to replenish the energy expended by searching for it, it is important to always carry extra food for emergencies; this is true even for a short afternoon hike. Readers who are interested in the details of obtaining wild food should consult Chapter 71.

Water Water constitutes about 60% of the body weight of an average young adult male; the value for a female is slightly lower. The percentage of water tends to decrease with age. In a sedentary adult, normal daily water losses include about 1400 mL through the urine, 800 mL through the skin and lungs, and 100 mL through the stool, for a total of 2300 mL daily. Because about 800 mL of water per day is contained in food and 300 mL is produced by metabolism, a minimum additional daily intake of 1200 mL is necessary in a temperate climate at sea level to avoid dehydration. In a hot and dry climate, at high altitude, or with exertion, insensible losses and sweating increase considerably, so fluid intake should be increased proportionally. Monitoring urine output determines whether intake is adequate; 1 to 1.5 L of light-colored urine should be excreted per day. Adding fruit flavors and making hot drinks improve the palatability of water. Electrolyte drinks and salt tablets are generally unnecessary in cold or temperate weather, because the electrolytes lost in sweat are easily replaced by a normal diet. When water supplies are limited, avoid overexertion, and try to “ration” your sweat. Almost all surface water should be considered contaminated by animal or human waste, with the possible exception of small streams that descend from untracked snowfields or springs in high and uninhabited areas. At altitudes of less than 5488 m (18,000 feet), simply bringing water to a boil will kill Giardia cysts and most harmful bacteria and viruses. Water can also be disinfected by filtration or by the addition of chemicals (see Chapter 67). At subfreezing temperatures and in locations that are above the snow line, where liquid water is difficult to find, snow or ice must be melted to obtain water. This requires a metal pot (which should be included in every survival kit), fire-starting equipment, and wood for fuel. The time and effort required to obtain water and the decrease in the thirst response in cold weather favor the development of dehydration in cold-weather travelers. In the winter, whenever open water is encountered, individuals should drink their fill of disinfected water, and then top off all canteens. Each evening, enough snow should be melted to provide water for supper plus a full canteen, which is placed in the bottom of the sleeping bag to keep it from freezing and which is then ready for use during the night or for making breakfast in the morning. Before leaving camp in the morning, enough snow should be melted to provide everyone with at least a full canteen for the day. Melting ice or hard snow is more efficient than melting light and powdery snow. To avoid scorching the pot, the snow is melted slowly, or water is heated in the bottom of the pot before snow is added. On warmer, sunny days, snow can be spread on a dark plastic sheet for melting.

Emergency Snow Travel Travel in deep snow is almost impossible without skis or snowshoes. Snowmobilers, pilots, and other mechanized over-snow and above-snow travelers should carry snowshoes for emergencies. Although travel may be unwise for other reasons, wilderness foot travelers in both subarctic and temperate latitudes should know how to improvise snowshoes from natural materials in the event they are stranded by a late- or early-season snowstorm. Emergency snowshoes (Figure 41-63, A) can be made from poles that are 15 cm (6 feet) long, 1.9 to 2.5 cm (0.75 to 1 inch) thick at the base, and 0.6 cm (0.25 inch) thick at the tip and from sticks that are 1.9 cm (0.75 inch) thick and 25 cm (10 inches) long. Twelve long poles and 12 short sticks are needed. For each snowshoe, six long poles are placed side by side on the ground, and the middle point of the poles is marked. One short stick is lashed crosswise to the tail (base) of the poles, and three short sticks are lashed side by side just forward of the midpoint of the poles, where the toe of the boot will rest. Two sticks are lashed 798

A

B FIGURE 41-63  A, Emergency snowshoe. B, Detail of snowshoe binding.

where the heel of the boot will strike the snowshoes. The tips of the six poles are tied together. Each binding (Figure 41-63, B) is made of a continuous length of about 1.8 m (6 feet) of nylon cord (preferably braided, because it will eventually fray). The midpoint of the cord is positioned at the back of the boot and above the bulge of the heel. Each end of the cord is run under the three side-by-side short sticks at the side of the boot and then up and across the boot toe so that it crosses the other end on top of the toe, forming an “X.” At this point, each end is looped around the cord running along the opposite side of the boot, and the ends are brought around the back of the boot heel. The cord is pulled tight around the boot, and the ends are tied together at the lateral side of the heel (see Figure 41-63, B). When walking, the tip of the snowshoe should rise, the boot heel should rise, and the boot sole should remain on the snowshoe. Over-snow travelers should avoid stepping close to trees (because of funnel-shaped tree wells around tree trunks), large rocks (because of weak snow or moats around them), and overhanging stream banks. In snow country, a person who falls into a stream or lake should roll repeatedly in powdery snow to wick water from clothing, brushing off the snow after each roll. A fire completes the drying process.

Survival in Special Instances, Including Natural Catastrophes The general principles of survival in all catastrophes are the same, particularly the need for forethought, planning, and keeping emergency equipment, water, and food on hand. Nevertheless, different types of catastrophes require different approaches, particularly at first. Some common types are discussed in the following sections.

STALLED OR WRECKED AUTOMOBILES Anyone who drives faces the possibility of spending an unplanned night out in a vehicle. Causes include bad weather, breakdown, running out of fuel, and getting stuck. Winter driving is especially hazardous because of the dangers of driving on snow or ice and the threats of frostbite and hypothermia. Accepting the possibility of trouble, carrying communications equipment (e.g., cell phone, satellite phone or radio) and a vehicle survival kit, and giving some thought to survival strategies will help to prevent a night out in a car from deteriorating into a life-threatening experience. Most travelers dress to arrive at a destination and not to survive a night out. A vehicle survival kit (see Appendix C) should include extra clothing, blankets or sleeping bags, food, water, signaling equipment, a quart-sized plastic screw-top bottle to use as a urinal, and communication equipment (e.g., cell

AIRCRAFT ACCIDENTS Aircraft passengers routinely receive short lectures regarding the locations of exits and procedures for emergencies. The safest place to sit is as far back in the tail of the plane as possible. In a crash, this frequently breaks off, and most survivors of crashes were sitting in this area. When a crash is imminent, tighten your seatbelt, link arms with the people on either side of you, bend your head so that your chin is firmly on your chest, and lean forward over a folded coat or blanket. After the aircraft finally stops moving, leave it as instructed by the crew. Assist injured companions to leave, then get everyone away from the immediate area to avoid the hazard of fire. Do not stop to gather personal belongings or luggage. In a remote area crash, after the fire risk is over, revisit the wreckage to salvage food, clothing, water, and other useful items. Remember that aircraft fuselages are poorly insulated. Unless a stove is available, survivors are usually better off constructing a shelter that can be heated with a fire (as described previously) outside of but near the craft. Batteries can be used as fire starters. Oil and gasoline can be used as fuel if they are poured into a container that is full of dirt or sand. Despite the fact that air travel is quite safe (probably safer than ground travel per mile traveled), an argument can be made for wearing comfortable shoes and carrying a coat, cap, and cell phone. It is illegal to carry survival equipment such as matches and a Swiss Army knife.

Unless there is no chance that a search will be mounted to find the aircraft, you should remain close to it rather than trying to go for help; it is much easier for searchers to spot a crash site than to find survivors who are on foot in the wilderness.

FLOODS Flooding in wilderness areas may be caused by thunderstorms, unusual storms such as hurricanes, and the rapid melting of ice and snow during heat waves. Flash floods in canyons can occur both during and after rain, and they can be caused by rain many miles upstream. Submarine earthquakes can cause huge tidal waves (tsunamis) that may drown hundreds of thousands of shore dwellers. Whenever traveling or camping near bodies of water in the wilderness, one should keep in mind what might happen if overflow or rising water should occur. When traveling or camping in box canyons, below dams, close to banks of water channels, and on low ground such as valley bottoms, one should have a well-thought-out exit strategy in case flooding occurs. If you are along the shore and you receive a radio report of an impending tsunami or if you see that the sea has receded and exposed a large expanse of sea bed, flee immediately and seek high ground as far from the shore as possible. Persons who are caught in moving water have no recourse other than attempting to swim to the side or reach floating debris while trying to hang on to emergency supplies. Never attempt to cross an area of moving water unless you are sure that it is no more than knee deep.

THUNDERSTORMS Dangers from thunderstorms include flooding (as discussed previously), lightning strike (see Chapter 3), and exposure, including wetting and hypothermia. Severe thunderstorms may produce hailstones of varying sizes, including stones that are large enough to harm a struck individual. During a thunderstorm, it is wise to seek shelter; this requires getting into raingear and avoiding heavy rain and hailstones by getting into a metal vehicle or a dense grove of trees. If you are on the water, head for shore as soon as threatening weather approaches. If you are in an area in which you are the highest object around, leave immediately, or crouch down on your haunches. Avoid small buildings, electrical wires, metal objects, and rocky overhangs where you may be hit by side flashes from ground currents, solitary trees, and trees that are taller than surrounding trees.

TORNADOS Tornados are funnel-shaped clouds that typically form on a hot spring or summer afternoon in the midwestern United States. They are usually preceded by large cumulonimbus clouds from the bottoms of which a careful observer can occasionally see the formation of the tornado as a dimple that elongates into a typical conical funnel cloud. Persons who witness these phenomena should leave immediately by vehicle in a direction opposite to the tornado’s likely path or seek shelter on the spot. In houses, the best shelters are small interior rooms with non–weightbearing walls, preferably in the basement (but on the ground floor if no basement exists). Ditches and small buildings are not safe. Caves and outdoor root cellars are fairly safe, but vehicles are not.

HURRICANES Hurricanes are severe tropical storms that demonstrate extreme cases of the vortices of wind and rain that frequently form over tropical seas. By definition, they contain winds of 119 kph (74 mph) or stronger. They require ocean temperatures of 25.5° C (78° F) and a spawning area that is at least 10 degrees of latitude from the equator so that the earth’s rotation is strong enough to start them in motion. Deaths that are the result of hurricanes are usually caused by high winds, flooding from heavy rain, or coastal flooding as a result of storm surges. With modern technology, the formation of a tropical cyclone (i.e., tropical low) and its change into a 799

CHAPTER 41  Essentials of Wilderness Survival

phone, satellite phone, citizen’s band radio in remote areas without cell service). It is also generally better to stay with the vehicle, which provides significant protection and is more visible to rescuers than is a person on foot. In cold weather and especially for long-distance travel, drivers should keep their vehicles in the best possible mechanical condition by using winter-grade oil, the proper amount of radiator antifreeze, deicer fluid for the fuel tank, and antifreeze in the windshield-cleaning fluid. Windshield wiper blades that are becoming worn should be replaced. A snow brush and ice scraper should be carried. A can of de-icer is useful for frozen door locks and wiper blades. Snow tires (preferably studded, although these are illegal in some states) are desirable, but chains should be carried as well. All-wheel or four-wheel drive is optimal, and frontwheel drive is superior to rear-wheel drive. The battery should be kept charged, the exhaust system free of leaks, and the gas tank full (i.e., “drive on the upper half of your tank”). The marooned driver should tie a brightly colored piece of cloth (e.g., a length of surveyor’s tape) to the antenna and at night should leave the inside dome light on to be seen by snowplow drivers and rescuers; headlights use too much current. If it is necessary for heat, the standard recommendation is that the motor and heater be run for 2 minutes per hour (after checking to see if the exhaust pipe is free from snow). However, it has been stated that because it takes more gasoline to start a cold engine than a warm one, one should initially turn the heat up all the way and then run the engine until the inside is comfortable. At this point, shut off the engine and wait until it becomes uncomfortably cold, which could be 10 to 30 minutes, depending on the outside temperature. However, the engine will still be warm. Start the engine again, run the heater until the occupants feel warm, and then keep repeating this. Carbon monoxide poisoning is a real threat, so do not go to sleep with the engine running. Keep a downwind window cracked 2.5 to 5 cm (1 to 2 inches). A reusable carbon monoxide detector is a wise addition to the survival kit. One or two large candles (i.e., “fat Christmas candle” size) should be carried to provide heat and light if the gasoline supply runs out; two lit candles can raise the interior temperature well above freezing. However, resources should be used sparingly, because you are never sure how long you will be marooned. Anticipating a possible cold weather survival situation enough to include heavy clothing and blankets or sleeping bags in the cold-weather vehicle survival kit is better than relying excessively on external heat generation. Do not smoke or drink alcohol. If you have to get out of the vehicle, put on additional windproof clothing and snow goggles, and tie a lifeline to yourself and the door handle before moving away from the vehicle. In a blizzard, visibility can be as little as 30 cm (12 inches).

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tropical storm and then a hurricane is predictable and reported in detail by the National Oceanic and Atmospheric Administration. Persons at risk should listen to the radio or watch television so that they will be aware when there is a need for evacuation. Most casualties involve persons who remain in the affected area against advice or who are caught by winds and flooding before they get far enough inland. Persons who live in hurricane-prone areas should have emergency caches of water and nonperishable food, clothing, bedding, a first-aid kit with supplies of any medications that are taken regularly; emergency lights (e.g., candles, matches, flashlights, spare batteries); and a cell phone with a battery or a crank-operated radio. They should also keep the gas tank full in their cars, and should be ready to head inland with these supplies as soon as they are advised to do so. Before they leave, they should board or shutter all of their windows, take inside any yard objects that might be blown away, and shut off electric power and gas.

Navigation (see Chapter 96) Even if they are in familiar territory, backcountry travelers should always carry a compass, map, and altimeter. Prior training and experience with map reading and compass use are necessary. An excellent type of compass for the layperson is the Swedish Silva compass, which was designed to be used during the sport of orienteering. The compass reading is always to be believed, even if it is at odds with one’s gut feelings about direction and location. Topographic maps are available at most outdoor stores in both the 7.5- and 15-minute series, and they can also be ordered from the U.S. Geographic Survey (1-888-ASK-USGS or http://www.USGS.gov). Travelers without a compass should still be able to find rough directions. At night, north can be found by identifying the Big Dipper (in the Northern Hemisphere only) and following the “pointers” (i.e., the farthest stars on the “bowl” of the dipper) to the North Star (Polaris); this is the most distal star in the handle of the Little Dipper, which is located about halfway between the Big Dipper and the W-shaped constellation Cassiopeia. On a sunny day, a nondigital watch set to standard time can be used to find direction. When the hour hand is pointed toward the sun, south will be one-half of the shorter of the two distances between the hour hand and 12 o’clock. The availability of small handheld GPS units has revolutionized wilderness navigation, but has not replaced the need for good map and compass skills.

Backcountry Weather Forecasting (see Chapter 42) Mountain weather is more unpredictable than weather in lower and flatter country. Winds frequently blow up and down mountain valleys, regardless of their orientation, because of the funnel effect of the valleys and the temperature differentials caused by solar radiation. The funnel effect may also cause heavy snowfalls at passes or at the higher ends of valleys. On a sunny day, the sun warms mountaintops and high slopes first, warm air rises, and winds blow up the slope. In the evening, the tops and high slopes cool first, cool air descends, and winds blow down the slope. Glaciers and large snowfields produce significant cool downslope winds. Except on the clearest days, mountaintops may have clouds over them or nearby because of the upslope winds that carry moist air high enough to reach its dew point. In the summer, mountains warm up during the morning and early afternoon, thereby creating cumulus congestus and cumulonimbus clouds that produce thunderstorms, lightning, and hail. Therefore, the standard caution for summer climbers is to arise early and reach the summit well before noon. Lightning usually precedes rain in a thunderstorm and can strike up to 8 km (5 miles) away from the storm. Distance is estimated by counting the seconds between the lightning flash and the first noise of thunder: 5 seconds suggests a distance of 1 mile (i.e., count “one and two and…” at a speaking pace that is slightly faster than normal). 800

Precipitation is frequently on the windward side of large mountain ranges; the leeward sides are usually much drier and, in low areas, may actually be desert. Stationary lens-shaped clouds (i.e., altocumulus lenticularis) are frequently seen near mountaintops in windy weather and signify high winds at the summits. High winds also produce long snow plumes from summits and ridges. The summit wind speed will be about twice the valley wind speed. Winds that are blowing at right angles to a mountain range tend to concentrate at any gaps or passes in the range, thereby creating high winds as a result of the Venturi effect. Warm downslope winds in the winter (i.e., Chinook or foehn winds) are produced when cool, dense air blowing over mountaintops loses its moisture as precipitation on the windward side; the drier air then warms rapidly as it descends on the lee side. These warm winds can melt snow rapidly. Weather is more stable at some times of the year than at others, but the times vary by geographic area. For example, in the northern Rocky Mountains, the best times to hike or climb in the summer traditionally have been the last week of July, all of August, and the first 2 weeks of September. The best time to ski tour or climb in the winter is February. In Alaska, the climbing weather in winter is during February and in spring and summer from April through June. In the Himalayas and the Karakorum, the best climbing weather is immediately before and after the summer monsoon (i.e., the seasonal northward flow of warm, moist air from the Indian Ocean). With global warming, these periods may widen; alternatively, they may narrow as a result of increasing storms. The principal value of understanding weather signs is for predicting severe, life-threatening storms and providing adequate time to seek shelter or the option to stay put rather than try for a summit. Travel in severe weather, especially above the timberline, should never be undertaken casually.

IMPORTANT TIPS FOR BACKCOUNTRY WEATHER FORECASTING 1. A blue sky, a few cirrus or cumulus humilis clouds, cool temperatures, low to medium winds, and a steady or dropping altimeter (i.e., a steady or rising barometer) are predictors of good weather. 2. A lowering cloud pattern (i.e., cirrus followed by cirrostratus, altostratus, and nimbostratus), rising temperatures, wind freshening and shifting to blow from the southeast or south, and an altimeter rise of 152 to 244 m (500 to 800 feet) or a barometer drop of 0.5 to 0.8 Hg (15 to 24 mb) indicate a possibly severe winter storm. 3. Building cumulus congestus clouds changing to cumulonimbus clouds indicate probable thunderstorms with lightning and possible hail. A thunderstorm is frequently preceded by a rush of cold air (i.e., a cold front). 4. Signs that a severe winter storm is abating include clouds thinning, cloud bases rising, temperature falling, altimeter dropping (i.e., barometer rising), and winds shifting to blowing from the north or northwest.

Sanitation Adherence to proper habits of cleanliness and sanitation is as important in the wilderness as at home. Hands should be washed with biodegradable soap after urinating or defecating, before cooking and eating, and before dressing open wounds. If soap is unavailable, snow or the cleanest available plain water is used. Dishes and pots are washed with hot water and biodegradable soap and rinsed well to remove all soap. Waste water is scattered over a wide area of ground and never dumped into a body of water. Bathing and washing clothes should be done at least 60 m (200 feet) from bodies of water with the use of water in a container. Gloves (preferably rubber or vinyl and impermeable) are worn when handling moist animal or human tissues, but be aware of a possible latex allergy. For defecation, dig a “cat hole” that is at least 46 cm (18 inches) deep, 15 cm (6 inches) wide, and downhill and at least 60 m (200 feet) from camp, water sources, or snow that is to be melted

Psychological and Organizational Aspects of Survival Dealing with the psychological aspects of survival is as important as confronting physical and environmental factors. As mentioned previously, the dangerous mindset that keeps a person continuing on a hazardous course—such as completing a climb or reaching a distant campsite despite conditions that would make a more prudent person bivouac or turn back—is a recurring scenario. In a survival emergency, a person with survival training, adequate oxygen, stable body temperature, shelter, water, and food may still die if he or she is unable to withstand the psychological stress. Conversely, persons have survived amazing hardships with little more than a strong determination to live. However, individual reactions cannot be predicted in advance. Groups that are faced with emergencies testify that courage and leadership appear in unexpected places. Still, if persons possess the necessary skills, have at least a minimum of survival equipment (see the appendices to this chapter), and have given some forethought to techniques of wilderness survival, the odds are strongly in their favor. Medical personnel have the advantage of being trained to suppress panic. Fear and surrender are normal reactions that must be opposed by whatever psychological tools are available. In some cases, religious faith or the desire to rejoin loved ones has been credited with survival. Anxieties that paralyze action include fear (of the unknown, being alone, wild animals, darkness, weakness, personal failure, discomfort, suffering, and death) and panic. Panic, which is the uncontrolled urge to run away, interferes with good judgment and results in inappropriate actions, such as abandoning weaker companions, dividing the party, and discarding vital survival equipment. Useless flight saps available energy, leads to exhaustion, and hastens death. Other psychological reactions include apathy and the normal desires to be comfortable and to avoid pain. Apathy involves “giving up”; it is a state of indifference, mental numbness, surrender, and unwillingness to perform necessary tasks. The victim shows resignation, quietness, lack of communication, loss of appetite, fatigue, drowsiness, and withdrawal. Apathy in one’s self is overcome by faith in one’s abilities and equipment and a belief in survival and the possibility of rescue. Apathy in others is combated by communicating plans and positive feelings about resources and outcomes to them and by including all group members in planning and survival activities. Comfort is not essential to survival. Marked discomfort as a result of injuries, illnesses, thirst, hunger, excessive heat or cold, sleep deprivation, and exhaustion is inevitable in a survival situation and must be tolerated so that one may continue to live. There are many accounts of adventurers who have survived many days with severe injuries (e.g., open fractures) because of the will to live, or who, despite multiple injuries, have dragged themselves for miles to find help. Providing an ill or injured party member with psychological support is important. This includes appearing calm, unhurried, and deliberate while trying to encourage optimism, patience, and cooperation. A person with a minor injury or illness should be encouraged to self-evacuate and be accompanied by at least one healthy party member. When a person with a severe injury or illness needs to be evacuated, the party must decide whether to use resources at hand or to send for help. The decision will depend on the weather, size of the party, training, available equipment, distance, type of terrain involved, type of injury or illness, victim’s condition, and availability of local search and rescue groups, helicopters, and other assistance. Unless the weather is excellent, the party strong and well equipped, the

route short and easy, and the victim comfortable and stable, the best course of action generally is to make a comfortable camp and send the strongest party members for help. A written note should include each victim’s name, gender, age, type of injury or illness, current condition, and emergency care given; the party’s resources and location (preferably map or GPS coordinates); and the names, addresses, and telephone numbers of relatives. The victim who must be left alone (e.g., because of a small party size) should have an adequate supply of food, fuel, and water. As soon as you realize that you are lost, stop, sit down in a sheltered place, calmly go over the situation, and make an inventory of survival equipment and other resources. If it is cold or becoming dark, start a fire, and eat if you have food. Take out your map or draw a sketch of your route and location that is based on natural features. Then, unless you know your location and can absolutely reach safety before dark, immediately begin to prepare a shelter for the night. Do not allow yourself to be influenced by a desire to keep others from worrying or the need to be at work or keep an appointment; one’s life is more important than someone else’s peace of mind. If you are alone and unquestionably lost and especially if you are injured, you must decide whether to wait for rescue or attempt to walk out under your own power. If rescue is possible, it is almost always better to use the time to prepare a snug shelter (before dark) and to conserve strength. If you decide to leave, mark the site with a cairn or with bright-colored material such as surveyor’s tape; leave a note at the site with information about your condition, equipment, and direction of travel; and then mark your trail. These actions will help rescuers and enable you to return to the site if necessary. Travel should never be attempted in severe weather, desert daytime heat, or deep snow without snowshoes or skis. If no chance of rescue exists, prepare as best possible, wait for good weather, and then travel in the most logical direction. The best way for a lost or stranded person to help potential rescuers is to do everything possible to draw attention to his or her location. Most modern rescues make use of ground parties, helicopters, and fixed-wing aircraft. When the latter locate victims from the air, they can drop supplies and vector helicopters or ground parties to the site. In addition to radios, cell phones, and other electronic equipment, signaling devices can be either auditory or visual. Three of anything is a universal distress signal (e.g., three whistle blasts, three gunshots, three fires). The most effective auditory device is a whistle. Blowing a whistle is less tiring than shouting, and the distinctive sound can be heard from farther away than a human voice. An effective visual ground-toair signal is a glass signal mirror with a sighting device, which can be seen up to 16 km (10 miles) away but requires sunlight. Special rescue beacons are available and can be carried as emergency equipment; these include strobe lights, laser signal lights, special beacons with both signaling and GPS capability, and personal locator beacons. Smoke is easily seen by day, and a fire or flashlight is seen well by night. On a cloudy day, black smoke is more visible than white; the reverse is true on a sunny day. White smoke stands out well against a green forest background but not against snow. Black smoke can be produced by burning parts of a vehicle, such as rubber or oil, and white smoke can be made by adding green vegetation to a fire. The lost person who anticipates an air search should keep a fire going with large supplies of dry, burnable material (e.g., wood, brush) and have a large pile of cut green vegetation close by. When an aircraft is heard, the dry materials are placed on the fire and allowed to flare, and then armloads of the green vegetation are piled on top; this produces lots of smoke and a hot thermal upward draft to carry it aloft. Ground signals (e.g., “SOS,” “HELP”) should be as large as possible (e.g., at least 0.9 m [3 feet] high and 5.5 m [18 feet] long) and should contain straight lines and square corners that are not found in nature. These types of signals can be tramped out in dirt or on grass, or they can be made from brush or logs. In snow, the depressions can be filled with vegetation to increase contrast. Many pilots do not know the eight traditional international ground-to-air emergency signals. However, these have 801

CHAPTER 41  Essentials of Wilderness Survival

for water. Cover feces completely with dirt or snow. No camp should be within 60 m (200 feet) of a lake or stream, which represents 70 to 80 steps for most adults. Travelers should urinate on rocks or dirt rather than on green plants. To avoid having to go outside, especially at night, when sleeping in a tent or snow shelter, males can use a 500-mL widemouth polyethylene bottle as a urinal. Funnels designed for use with the bottle are available for women.

PART 5  RESCUE AND SURVIVAL

been replaced by the following five simple signals adopted by the International Convention on Civil Aviation. Although in the age of helicopters these are not as important as they once were, they are worth remembering: V: I require assistance. X: I require medical assistance. N: No Y: Yes ↑: Proceeding in this direction Air-to-ground signals include the following: Message received and understood: rock plane from side to side Message received but not understood: make a complete righthand circle When using cell phones, radios, and other electronic devices, persons should move out of valleys and gullies to higher elevations if possible. Operational payphones in campgrounds that are closed for the season or other facilities can be used to call for help. Most will allow 9-1-1 or another emergency number to be dialed without payment, but carrying sufficient coins and memorizing your telephone credit card number are recommended.

Protection From Wild Animals Although persons in a survival situation often worry about wild animal attacks, these are rare. Many wild animals flee when they are confronted by shouting, moving humans. Exceptions include polar bears, grizzly bears, moose, bison, cougars, jaguars, wild pigs, elephants, lions, tigers, water buffalo, leopards, wolverines, females with young (particularly bears, moose, elk, and deer), rabid mammals, and feral dogs and cats (see Chapter 56). Polar bears, some grizzly and black bears, the great cats, and crocodiles may hunt humans as food. Venomous snakes, insects, arachnids (i.e., spiders, scorpions, and ticks) and marine animals are also of concerns (see Chapters 52, 53, 79, 80, and 81). The only effective weapon against large mammals and reptiles is a high-powered firearm, although pepper spray may discourage attacking bears and ungulates. Improvised weapons (e.g., a spear tipped with a hunting knife) are useless. Food should not be kept in a shelter or backpack during the night; all food should be placed in a nylon bag and hung between two trees on a high line. Above the timberline, small rodents such as mice may gnaw holes in expensive tents to reach food that is inside, so all food should be bagged and hung on a line between two high boulders. In warm weather, insect repellent should be carried and used liberally.

Summary of Preparations for a Possible Survival Situation 1. Keep in good physical condition by employing frequent exercise and healthful habits. Avoid tobacco and recreational drugs, and keep alcohol use to a minimum. Maintain current immunizations. 2. Develop the ability to swim well. 3. Learn how to use a map and compass, and know how to find directions without a compass. 4. Be able to build a fire under adverse conditions. 5. Have a working knowledge of local weather patterns, and be able to use an altimeter or a barometer, a thermometer, wind directions, and knowledge of cloud forms to predict storms. Avoid exposure to dangerous meteorologic conditions, such as blizzards and lightning strikes. 6. Be familiar with the special medical problems related to the type of wilderness that is involved. For example, in cold weather and at high altitude, be familiar with prevention, diagnosis, and treatment of hypothermia, frostbite, and altitude illnesses. Safe travel in the desert and tropics requires familiarity with poisonous and edible plants, tropical diseases, snakebite treatment, dangerous animals, tropical skin diseases, and heat illnesses. Understand, basic principles of prehospital emergency care and improvisation of splints, bandages, and stretchers. 802

7. Carry a survival kit that contains equipment appropriate for the topography, climate, and season (see the appendices to this chapter). At a minimum, the kit should include such things as fire-starting, shelter-building, and signaling and navigating equipment plus emergency food, water, spare clothing, and a first-aid kit. 8. Be able to construct appropriate types of survival shelters. 9. Acquire a working knowledge of the characteristics of natural hazards and how to avoid them. These include forest fires, lightning strikes, avalanches, rockfalls, cornice falls, flash floods, whitewater, deadfalls, storms of various kinds, and hazardous animals and plants of the area of travel. 10. Read and analyze accounts of survival experiences (see the Suggested Readings list online at www.expertconsult.com). Remember that more people are killed on simple day hikes than on long wilderness expeditions. 11. Be aware of the psychological aspects of a survival situation and of errors in judgment that can lead to a survival emergency. 12. Know the edible plants and animals of the area of projected travel as well as the poisonous or venomous species. Know how to obtain water. Basic hunting, trapping, and fishing skills are also valuable. 13. Be intimately familiar with the contents of your survival kit and how to use them. Practice and perfect survival activities (e.g., fire building, shelter building) before you need them. 14. Never travel alone. Hunters and other group members who may separate should have a means of communicating with each other, such as small radios with an 8-km (5-mi) range. Products are available that combine a GPS locator with a small radio. 15. Always let at least two responsible persons know your destination, the number of persons in the party, their names, the types of vehicles used and their license plate numbers, and the expected time of return. Add several hours to the latter for “normal” mishaps and miscalculations. To avoid unnecessary rescue attempts, do not fail to notify these persons of your return. Failure to follow these guidelines has led to many unsuccessful searches.

APPENDIX A 

SUGGESTED BASIC CONTENTS OF A TEMPERATE TO COLD-WEATHER SURVIVAL KIT The kit is divided loosely into fire-building, shelter-building, signaling and navigating, and miscellaneous items, all of which will fit into a small-frame backpack with a capacity of 52.4 to 65.5 L (3200 to 4000 inches3). The small items can be carried together in a small net bag for convenience and easy identification. Frequently used items (e.g., knife, map, dark glasses, compass) should be stored in a pocket or a belt pouch. Always remember to replace consumed items—especially first-aid items, repair-kit items, and emergency food—as soon as you return from a trip. Replace stored matches at least every year and first-aid kit medications before they expire.

APPENDIX B 

SUGGESTED ADDITIONS FOR WINTER SURVIVAL KIT (WHEN COLD WEATHER OR SNOW IS PRESENT OR EXPECTED) Basic survival items from Appendix A Spare clothing for severe weather to provide at least four layers total, including spare mittens

Fire-Building Equipment Two waterproof screw-top match containers filled with strike-anywhere matches (If the match container does not include a large, rough match-striking area, a strip of heavy sandpaper should be glued to the top or side of each container.) Candle Fire starter (e.g., cotton impregnated with petroleum jelly) in a waterproof container such as a film canister or an additional match container Metal match Knife: Swiss Army knife (consider a camping model with a saw, file, scissors, and so on; made by Victorinox)   Alternative: Leatherman tool with wire-cutting pliers, file, one serrated and two regular blades, saw, and scissors Shelter-Building Equipment 1 -inch braided nylon cord or parachute cord, 30.48 m (100 feet) 8 Rip-stop waterproof nylon tarp, approximately 2.4 × 3 m (8 × 10 feet) with grommets around the edges   Alternatives:   Tarp (blue and crinkly; laminated polyethylene weave)   or   One or two large, heavy-duty (3- to 4-mil), orange plastic bags, 0.9 × 1.7 m 3 × 5.5 feet Folding saw or small rigid saw (e.g., 18-in Dandy saw) Signaling and Navigating Equipment Headlamp or flashlight with spare bulb and batteries (A good choice is a headlamp with both light-emitting diode and bulb options. The light-emitting diode light uses up much less electricity but is more diffuse and does not cast a long beam. The bulb is brighter and casts a longer beam but uses much more electricity.) Plastic pea-less whistle on a lanyard Small notebook and pencil Small roll of orange surveyor’s tape Glass signaling mirror with sighting device Miscellaneous Metal pot with bale that contains emergency food of choice (e.g., tea, soup mix, power bars, small can of mixed nuts, trail mix) Metal cup with handle (for heating liquid by putting the cup at the edge of a fire) Plastic or Lexan spoon Toilet paper Sunscreen with a sun protection factor of 30 or more Lip balm with a sun protection factor of 30 or more Insect repellent (e.g., N,N-diethyl-meta-toluamide) First-aid kit, one per party (see Appendix D for contents) Canteen (1 to 1.5 L [34 to 50 fl oz] when full; metal or plastic) Sunglasses, preferably polarized, with side shields Light raingear (e.g., laminated [Gore-Tex] pants and jacket with hood) Repair kit that is adapted to the type of travel (e.g., ski, snowshoe, kayak) and that includes the following:   Small needle-nosed pliers with wire-cutting feature (if Leatherman tool not carried)   Small crescent wrench   Small screwdriver with multiple tips   Picture wire   Fiberglass tape, standard roll   Duct tape, small roll   Steel wool for shimming (e.g., ski binding repair)   Assorted nuts, bolts, and screws   Total weight of repair kit Total weight of basic survival equipment (not including shovel, snow saw, backpack, or cold weather fourth layer of clothing; see Appendix B) Other Useful Equipment for Consideration Nondigital watch Altimeter Magnifying glass Two sets of correct coins for pay phone; calling card Light pair of leather gloves (hand protection) Water disinfection equipment: chemicals (e.g., Potable Aqua) or filter Thermometer (plastic alcohol type clipped to the outside of the pack) Spare eyeglasses Electronic communication and navigation equipment:   Cell phone (if service is available in the area)   Global positioning system unit   Personal locator beacon (i.e., person emergency locator transmitter) Pepper spray (to repel bears, moose, and so on) Usual day-trip items to be added:   Small insulated drink cannister of hot or cold drink   Lunch   Binoculars   Camera

Approximate Weight in Grams (Ounces) 57 (2) 43 (1.5) 28 (1) 14 (0.5) 142 (5) 227 (8) 113 (4) 55.3 (19.5) 737 (26) 255-5100 (9-18) 340 (12) 212 (7.5) 14 43 57 57

(0.5) (1.5) (2) (2)

964 (334) 85 (3) 14 (0.5) 43 (1.5) 113 (4) 14 (0.5) 113 (4) 701 (25) 1091-1446 (38.5-51.0) 57 (2) 879 (31) 85 (3) 57 (2) 156 (5.5) 28 (1) 85 (3) 28 (1) 28 (1) 43 (1.5) 510 (18) Approximately 6520 to 7087 g (230 to 250 oz) or 6.5 to 7 kg (14 to 16 lb)

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CHAPTER 41  Essentials of Wilderness Survival

Item

PART 5  RESCUE AND SURVIVAL

Small snow shovel (e.g., a small, collapsible grain-scoop type with a Kevlar blade and detachable handle, with a 680-g [24-oz] capacity) Snow saw (consider this for above-timberline travel and potential igloo building; should have a 227-g [8-oz] capacity)

OPTIONAL ITEMS Three-quarter–length piece of open or closed cell-foam mattress or Therm-a-Rest mattress Sleeping bag Bivouac sac Small stove and fuel Light axe (e.g., Hudson’s Bay type) Small piece of closed-cell foam (0.6 × 0.6 m [2 × 2 feet]) for sitting on snow

MANDATORY FOR AVALANCHE COUNTRY Avalanche probe (folding) or ski poles that join together to form a probe for each party member Avalanche transceiver for each party member Shovels (preferably one for each party member) Inclinometer for measuring slope angles (this is included in some compasses)

APPENDIX C 

VEHICLE COLD-WEATHER SURVIVAL KIT Sleeping bag or two blankets for each occupant Emergency food Metal cup Waterproof matches Long-burning candles, at least two First-aid kit (see Appendix D) Extra doses of personal medications, if any Swiss Army knife or Leatherman Multi-Tool Three 1.4-kg (3-lb) empty coffee cans with lids for melting snow or collecting urine Toilet paper Citizen’s band radio, cell phone, or such other communication device, with charger Portable radio receiver, with extra batteries Battery booster cables Extra quart of oil (place some in a hubcap and burn it for an emergency smoke signal) Tire chains Jack and spare tire Road flares Snow shovel Windshield scraper and brush Tow strap or chain Small sack of sand or cat litter Two plastic gallon water jugs, full Tool kit Gas-line deicer Flagging (e.g., surveyors’ tape, which can be tied to the top of a radio antenna for use as a signal) Duct tape Notebook and pencil Reading material Long rope (e.g., clothesline) to act as a safety rope if you leave the car in a blizzard Carbon monoxide detector Axe Saw Full tank of gas Data from the Montana State Department of Transportation: Montana disaster & emergency survival guide. Available at http:// www.mdt.mt.gov/publications/docs/brochures/winter_maint/ winter_survival.pdf. Accessed May 1, 2011.

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APPENDIX D 

MINIMAL EQUIPMENT FOR SURVIVAL FIRST-AID KIT Because the most common significant medical problems in wilderness emergencies will be injuries, each item is selected on the basis of the likelihood of need, the possibility of multiple use, the urgency of need, the weight-to-usefulness ratio (i.e., the “biggest bang for the buck”), and whether it can be improvised from natural materials. As with the survival kit, the small items can be carried together in a mesh bag for more rapid retrieval.

BASIC ITEMS Small-Bag Items Cardiopulmonary resuscitation mouth shield Surgical gloves, preferably nonlatex 20-mL syringe with needle, catheter, or splash shield for wound irrigation Steel sewing needle (this can be part of a small sewing kit) Clinical thermometer (consider a low-reading thermometer for a cold environment) Small pill boxes that contain the following: Nonprescription analgesic of choice (e.g., acetaminophen, ibuprofen; consider ibuprofen if there is a frostbite risk) Prescription analgesic of choice (e.g., acetaminophen with codeine) Diphenhydramine, 25- or 50-mg caps Small tube of biodegradable soap Splinter forceps Seam ripper Small needle holder (this is useful for retrieving small things out of tight quarters) Small magnifying glass Four large safety pins Other Items One or two cravats Roll of 3-inch Ace or self-adhering roller bandage Roll of 2-inch adhesive tape (waterproof preferred) Small roll of 0.5-inch 3M Transpore tape Small prepackaged bandage strips, 1-inch wide (these can be cut in one-half lengthwise for smaller sizes) Nonadhering sterile gauze pads (Telfa or equivalent), 3 × l4 in Sterile compresses, 4 × 4 inch Alcohol pads for skin cleansing Duct tape or fiberglass strapping tape for improvising litters and splints (this can be carried in a repair kit)

ADDITIONAL ITEMS FOR CONSIDERATION Acetazolamide if there is a risk of acute mountain sickness (i.e., 125 to 250 mg twice daily to speed acclimatization) Plastic oral airways, three sizes Pocket mask instead of mouth shield (This device is easier to use, works better than a mouth shield, and protects the user from the victim’s saliva.) Povidone–iodine swabs for skin preparation 14-gauge intravenous catheter-over-needle for emergency chest decompression (A flutter valve can be improvised by using the finger cut from a rubber glove with its base tied around the base of the catheter and a hole cut in its tip.) Small bandage scissors or paramedic shears (scissors, a Swiss Army knife, or a Leatherman tool can be substituted.) SAM splint Persons who are taking regular medications should carry emergency supplies; anyone who has had an anaphylactic reaction should carry an emergency epinephrine kit (i.e., EpiPen).

SUGGESTED READINGS Suggested readings for this chapter can be found online at www.expertconsult.com.

CHAPTER 42 

Principles of Meteorology and Weather Prediction JOHN MIODUSZEWSKI, D. NELUN FERNANDO, AND DAVID A. ROBINSON

General Circulation and Atmospheric Profile CLIMATE CONTROLS AND RADIATION BALANCE Equatorial regions receive a net surplus and polar regions receive a net deficit of solar radiation because of differences in solar angle and beam dissipation at the poles and the equator. This heat imbalance between the equator and the poles drives the ocean–atmosphere circulation. Heat is transported in the atmosphere primarily through convection, conduction, and advection. Convection and conduction are important in vertical atmospheric heat transport. Latent and sensible heating is the key mechanism by which convective and conductive transport are enacted. Horizontal heat transport is achieved primarily through migration of air masses and through eddy circulation. The average global circulation on a simplified basis consists of three circulation cells. This structure is found in both hemispheres. The cell that straddles the tropics (0 degrees to approximately 30 degrees), known as the Hadley cell, is characterized by rising motion on its ascending limb along the equator and sinking motion on its descending limb at the subtropics (approximately 30 degrees). A second cell, known as the Ferrel cell, has an ascending limb at the midlatitudes and descending limb at the subtropics. The third cell, known as the polar cell, is characterized by rising motion at the midlatitudes and subsidence at the poles. Such a general circulation structure results in a climate with intense convective precipitation in the regions along the rising limb of the Hadley cell. This region is identified as the intertropical convergence zone (ITCZ) because it is a zone where intense heating leads to convective motion and low pressure. Low-level or surface convergence and upper-level divergence result in convective precipitation in this zone. Regions along the descending limb of the Hadley cell—approximately 30 degrees north and 30 degrees south—tend to be warm and dry as subsiding air warms and dries out the air column. It is no coincidence that deserts are found at this latitude. The midlatitudes (40 degrees to 50 degrees)—the rising limb of the Ferrel cell—have cells of low pressure and receive precipitation from storms and frontal systems. Polar regions along the subsiding limb of the polar cell are characterized by cold and dry climates. The three-division structure results in surface wind distribution characterized by winds blowing from the east (easterly) (trade winds) out of the subtropical high-pressure zone to the lowpressure zone at the equator; winds from the west (westerly) out of the subtropical highs to the midlatitude low-pressure zone; and polar easterlies flowing from the polar high-pressure zone to the midlatitude low (Figure 42-1). Such an east–west wind direction, as opposed to a north–south wind direction, prevails because of the Coriolis effect, which acts on the pressure gradient force and deflects winds to the right in the northern hemisphere and to the left in the southern hemisphere. The tricell structure is only a simplified representation of the general atmospheric circulation. In reality, the Ferrel cell does not persist throughout the year, as does the Hadley cell. The pressure gradient at the polar front is so intense that it results in eddies that are instrumental in poleward heat transport,

particularly during the winter, when the equator–pole pressure gradient is at a maximum. The midlatitudes are the regions most influenced by air masses. Eddy circulation is predominant at the boundary— known as the polar front—between the Ferrel cell and the polar cell.

ATMOSPHERIC PROFILE Lapse Rate The temperature generally decreases with altitude in the troposphere, as evidenced by decreasing temperature as one travels up a mountain. The rate at which air cools as it rises depends on the amount of moisture in the air, as well as the dynamics of the atmosphere itself. Moisture Humidity is a measure of the amount of moisture in the air, commonly measured by relative humidity and dew point temperature. Relative humidity is a ratio of the amount of moisture in the air to the amount the air can hold at that temperature. Atmospheric moisture is often given as relative humidity, but this must be accompanied by a temperature to be a valuable indication of the air’s moisture content. Dew point temperature is the temperature to which the air must be cooled to become completely saturated. If air is cooled

FIGURE 42-1  General circulation of the atmosphere. (Courtesy Deborah Mioduszewski.)

805

PART 5  RESCUE AND SURVIVAL

to this temperature at the surface, fog will form. If air is forced to rise and cools to this temperature, clouds will form. Heat capacity is the amount of energy required to increase the temperature of a substance. The importance of this is due to the great difference in heat capacity of land and water. Water heats up and cools down much more slowly than does land, which has important implications for weather in interior continents, compared with coastal areas.

Climatic Regions Controlled by Latitude: Tropics, Midlatitudes, and Poles MIDLATITUDE AND POLAR CLIMATES Most weather systems, such as midlatitude cyclones and thunderstorms, form at the frontal boundaries between air masses of different densities and are steered by upper-level winds, typically to the east in the midlatitudes and west above about 60 degrees. This is in contrast to tropical cyclones, which are not influenced by air masses and only form over the ocean. Midlatitude cyclones are a powerful means by which air can be transported across latitudes. These differing air masses meet at boundaries called fronts. Cold and warm fronts are typically oriented around a cyclone as shown in Figure 42-2. The colder, typically polar air mass advances equatorward behind the cyclone at the cold front, while the warmer air mass advances poleward ahead of it behind the warm front. Typically, the faster-moving cold front catches up to the warm front as the cyclone matures and “occludes,” and the cyclone begins to lose its strength as the temperature differences from which it derives its energy dissipate. Occasionally neither air mass will be able to dislodge the other, and the front will become stationary. Stationary fronts can be conducive to prolonged periods of precipitation. These areas of low pressure have favored storm tracks that shift during the year and as larger-scale atmospheric conditions change. Often atmospheric patterns emerge where cyclones take the same track, moving through the same areas for up to several weeks. Conversely, locations removed from these storm tracks may experience persistent fair weather associated with an accompanying anticyclone. Cyclones often form and move along the polar front, where there is a sharp contrast in temperature and moisture. During winter, the precise track of a cyclone will determine whether rain, snow, or a mixture will fall in a given location, with snow more likely on the north side of the cyclone and rain on the south side. These cyclones bring the most noticeable changes to sensible weather in the mid- and high latitudes. In addition to the precipitation they bring, which ranges from drizzle and fog to severe

Highest probability of severe weather

Advancing cold air

Cold front

Warm, moist air

Warm front

FIGURE 42-2  Midlatitude cyclone model. L, Low pressure. (Courtesy Deborah Mioduszewski.)

806

thunderstorms, temperature and humidity levels vary greatly in different parts of the storm. Warm and moist air is advected in behind the warm front with a shift in the wind, causing extremely uncomfortable weather in the summer and thaws in the winter. Colder, dryer, and commonly breezy or blustery weather accompanies the passage of a cold front as air from higher latitudes is advected in behind a departing cyclone.

SUBTROPICAL AND TROPICAL CLIMATES The subtropics lie north and south of the Hadley cell, roughly at 35 degrees north and 35 degrees south. The subtropics are characterized by warm and dry climates. Tropical climates are found along the rising limb of the Hadley cell. Temperature is high throughout the year, with the average coldest temperature not dropping below 18° C (64.4° F). Convective processes and convective precipitation dominate the climate of the tropics but are not the sole climatic phenomena found there. Monsoons, tropical depressions, and cyclones account for much of the precipitation delivered over the tropics.

MONSOONS The term monsoon refers to the seasonal reversal in atmospheric circulation and associated precipitation in tropical and subtropical regions. Reversal of wind direction takes place with seasonal migration of the ITCZ, which induces a temperature difference between the land surface and ocean. The land–ocean temperature difference induces a land–ocean pressure gradient that drives the monsoonal winds. Regional components of the monsoon include the tropical and subtropical regions of Asia, Australia, Africa, South America, and southwestern North America. The onset of monsoonal rains varies among and within these regions.

TROPICAL CYCLONES Intense convective heating, particularly in the tropics, creates regions of low atmospheric pressure. Such regions of low pressure are characterized by rain-bearing clouds and windy conditions. If low-pressure systems form over warm oceans of the tropics and subtropics at least 5 degrees from the equator, they have the potential to develop into cyclones, which are intense, rotating low-pressure systems. Winds flow counterclockwise in the northern hemisphere and clockwise in the southern hemisphere around cyclones. Cyclones, hurricanes, and typhoons all refer to the same phenomenon. The norm is to use typhoons to identify severe cyclones in East Asia; hurricanes for severe cyclones in North America, and cyclones for severe cyclones that form over the Indian Ocean region. Cyclones form in areas of intense low pressure in the tropics and subtropics. Tropical cyclones are known for their destructive strength—often due to strong winds but also due to storm-surge flooding that occurs along coastal regions. Tropical cyclones form in all the major ocean basins, except in the South Atlantic and the Southeast Pacific. Minimum factors needed for tropical cyclones to develop are sea surface temperatures exceeding 28° C (82.4° F) and a minimal amount of vertical wind shear. Extratropical cyclones form at frontal boundaries. After formation, tropical cyclones tend to move westward and poleward. Some cyclones, particularly in the midlatitudes, recurve and enter the westerlies. Tropical cyclones tend to dissipate on making landfall. Cyclones are classified by their intensity as follows: • Tropical depression: winds up to 64 km/hr (39.8 mph) • Tropical storm: winds of 64 to 118 km/hr (39.8 to 73.3 mph) • Severe tropical cyclone, hurricane, or typhoon: winds greater than 118 km/hr (73.3 mph) These are further categorized using the Saffir-Simpson scale, ranging from category 1 to category 5 (most severe) (Table 42-1).

THUNDERSTORMS Thunderstorms result from atmospheric instability due to intense convective heating processes in the tropics and convergence of air masses of different temperatures in midlatitudes, particularly in continental climates. Cumulonimbus clouds are characteristic

Wind Speed

Storm Surge

Category

Pressure (mb)

km/hr

mph

m

ft

Damage

1 2 3 4 5

≥980 965-979 945-964 920-944 <920

119-154 155-178 179-210 211-250 >250

74-95 96-110 111-130 131-155 >155

1-2 2-3 3-4 4-6 >6

4-5 6-8 9-12 13-18 >18

Minimal Moderate Extensive Extreme Catastrophic

features of thunderstorms, as are electrical activity (lightning and thunder), wind gusts, and heavy rain. Hail may be encountered in some thunderstorms. Heavy thunderstorms in upstream regions of river catchments with sharp elevation gradients may induce flash flooding in downstream regions. One of the major dangers associated with thunderstorms is lightning. Lightning can strike more than 20 miles away from the parent thunderstorm, which may appear far enough away to present the illusion that there is no risk. When a thunderstorm is in the area, it is advisable to seek shelter away from high ground, water, and open spaces. Distance to a lightning strike can be calculated by counting the number of seconds between the flash of lightning and the thunder, keeping in mind that sound can travel a mile in 4.5 seconds. Types of Thunderstorms Severe thunderstorms are storms with wind speeds above 93 km/ hr (57.8 mph). Updrafts and downdrafts associated with severe thunderstorms often reinforce each other and intensify the storm. Mesoscale convective complexes (MCCs) are roughly circular organized storm systems composed of several thunderstorms. MCCs are common occurrences over North America and Canada, where mesoscale (10 to 1000 km in diameter) atmospheric processes provide conditions suitable for reinforcement of thunderstorm complexes. Severe weather in North America and Canada is often associated with MCCs. Frontal/squall-line thunderstorms tend to form parallel to and ahead of cold fronts in the presence of wind shear. They form a linear band of storm cells with a life span of about 0.5 day to 4 days. Supercell storms are violent storms that occur as isolated storms, each with a diameter ranging from 20 to 50 km (12.4 to 31 miles). Supercell storms may give rise to tornadoes. Tornadoes are extremely dangerous weather phenomena characterized by rapidly rotating air that reaches the ground beneath cumulonimbus clouds. They are preceded by a perceived lowering of one part of the cloud base, with rotation of this base (funnel cloud) often visible. All funnel clouds do not produce tornadoes, but all tornadoes are preceded by funnel clouds. Tornadoes most often occur in the interior of continents, particularly North America and Canada. Waterspouts, like tornadoes, are columns of rapidly rotating air that are visible due to condensation of water vapor in the funnel (not water being sucked up). Some are associated with supercells and therefore can be considered tornadoes over water. But most are termed “fair-weather waterspouts” because they generally are not associated with thunderstorms. Instead, they form under large cumulous clouds in light wind conditions. Their life span is typically less than 20 minutes, winds rarely exceed 112.6 km/hr (70 mph), and they are usually found in coastal regions. However, they can still cause considerable damage and injury, and it is advisable to avoid them.

ARID CLIMATES Arid climates are characterized by the presence of very little moisture. These are found most often along subtropical highpressure zones or in the interiors of large continents where the influence of moisture-laden oceanic frontal systems is limited. Deserts are characteristic ecosystems of arid climates. Extreme heat, high diurnal temperature ranges, wind, and often fire danger are important elements of desert climates.

MOUNTAIN CLIMATES The lifting of air because of the presence of mountains is known as orographic lift, which results in cooling of the air. If sufficient moisture is present, condensation takes place. Such convection can induce thunderstorm development on the windward side of the mountain (Figure 42-3). In the presence of steep topography, convective processes may be limited to the windward side because the mountain ridge can form a wet–dry divide. Air flowing over a mountain ridge and downward along the leeward side warms and dries through the process of adiabatic compression. Thus leeward winds are characteristically dry and warm. Such winds are known internationally as foehn winds, and as Chinooks in the United States. The Santa Ana winds that blow into Los Angeles are downslope winds. Wind direction typically reverses twice a day in mountain climates. During the day, wind flows upslope from the valley toward the mountain. At night, winds blow downslope from the mountain toward the valley. Horizontal temperature differences that develop in complex terrain produce diurnal mountain winds. Overnight and into the early morning, cold air accumulates in valleys and causes a temperature inversion. By morning, the valley bottoms are colder than are mountain slopes and a pressure gradient develops that drives upslope winds. Convective heating during the day dissipates the temperature inversion in the valleys. Varied topography in mountain ranges results in a myriad of microclimates. Factors such as exposure to sunshine, slope direction, elevation, and windward or leeward side of major weather systems determine the varied characteristics of microclimates found in mountainous regions.

MARINE/COASTAL CLIMATES The difference in heat capacity between land and ocean initiates a diurnal sea–land breeze circulation. During the day, land heats up much faster than does the ocean, establishing a land–ocean temperature difference that causes a pressure gradient. Wind blows toward the lower pressure over land to equalize the pressure difference. At night, land surfaces cool rapidly compared with adjacent oceans. The cycle is reversed at night, with winds blowing from the land toward the ocean to dispel the ocean–land temperature (and hence pressure) gradient (Figure 42-4). Ocean upwelling (cold) currents, particularly along the west coasts of continents, modify climate in adjacent land areas. Summers and winters in such locations are mild.

WEATHER PHENOMENA Precipitation refers to all liquid and solid forms of water that form in clouds and fall to the ground. Precipitation occurs when rising moist air condenses, which can occur for a variety of reasons. During the cold season in mid- and high latitudes, the type of precipitation that falls often depends on the profile of the atmosphere, which is influenced by factors such as storm track, wind direction, and topography. Snow occurs when the entire atmosphere is below freezing, whereas sleet (ice pellets) and freezing rain occur when there are intrusions of warmer air in the lower atmosphere. This often occurs either as snow is transitioning to rain (or vice versa) or during cold air damming events. These events are most common in the 807

CHAPTER 42  Principles of Meteorology and Weather Prediction

TABLE 42-1  Saffir-Simpson Scale of Tropical Cyclone Intensity

PART 5  RESCUE AND SURVIVAL

Rain ow shad

Prevailing winds

Evaporation

Warm ocean

FIGURE 42-3  Orographic precipitation. (Courtesy Deborah Mioduszewski.)

lee of mountain ranges such as the Appalachians. Hail is formed only in strong thunderstorm updrafts that are able to support ice chunks as the hail nuclei are accreted with more ice before becoming heavy enough to fall to the ground. Virga refers to precipitation that falls from clouds but evaporates or sublimates before reaching the ground. This can sometimes be seen as a rain shaft in the distance, with a veil of rain under the clouds becoming more streaky and disappearing before reaching the ground. Fog is formed when the temperature drops to near its dew point or when moisture is added to the air to saturate it. Radiation fog is typically a shallow layer of fog near the surface caused by rapid cooling of the land. The air just above the land cools to its dew point and condenses, although this type of fog typically dissipates quickly in the morning as the sun rises. Advection fog forms when moist air is transported horizontally (advected) over a cool surface. The surface cools the moist air to its dew point, causing condensation and fog. It is most common on land when warm air advects over a snow pack and the snow cools the air to saturation. It is most common over water when tropical air moves over a cool ocean current, with the same process ensuing. Upslope fog occurs as air is forced to rise. It cools to its dew point, and a cloud forms at the surface.

Human Comfort Wind chill refers to accelerated cooling of the human body that occurs because of atmospheric motion, particularly when temperatures are low—typically around 7° C (44.6° F). Weather forecasts report both absolute and relative (i.e., wind chill) temperatures. Heat index is a metric for describing “how hot it feels” when humidity is combined with actual air temperature. During summer months, particularly across eastern North America where humidity is higher, it is important to heed the forecast heat index values when planning outdoor activities. Table 42-2 provides an indication of the danger levels associated with various values of the heat index. Haze is reduced visibility caused by suspension of particulates in the air. Such particulates may either be aerosols (e.g., carbon particles, salt) or air pollutants (e.g., nitrogen oxides, ozone, and hydrocarbons). Haze generated by atmospheric pollutants is referred to as “photochemical smog.” Air Quality Index (AQI) is a measure of daily air quality in the context of human health. In the United States, the Environmental Protection Agency (EPA) calculates the AQI for five major air pollutants: ground-level ozone, particulate matter, carbon

TABLE 42-2  Categories of Heat Index Category

Heat Index

Extreme danger

130° F or higher (54° C or higher) 105-129° F (41-54° C)

Danger

FIGURE 42-4  Land–sea breeze circulation. H, High pressure; L, low pressure. (Courtesy Deborah Mioduszewski.)

808

Extreme caution

90-105° F (32-41° C)

Caution

80-90° F (27-32° C)

Possible Heat Disorders for People in High-Risk Groups Heatstroke or sunstroke likely Sunstroke, muscle cramps, and/or heat exhaustion likely. Heatstroke possible with prolonged exposure and/or physical activity. Sunstroke, muscle cramps, and/or heat exhaustion possible with prolonged exposure and/or physical activity. Fatigue possible with prolonged exposure and/or physical activity.

From http://www.srh.noaa.gov/ssd/html/heatwv.htm.

Weather Forecasting

Air Quality Index Levels of Health Concern

Numeric Value

OBTAINING DATA AND FORECASTS AND PREDICTING WEATHER IN THE NEAR TERM

Good

0 to 50

Air quality is considered satisfactory, and air pollution poses little or no risk.

Moderate

51 to 100

Air quality is acceptable; however, for some pollutants there may be a moderate health concern for a very small number of people who are unusually sensitive to air pollution.

Unhealthy for Sensitive Groups

101 to 150

Members of sensitive groups may experience health effects. The general public is not likely to be affected.

Unhealthy

151 to 200

Everyone may begin to experience health effects; members of sensitive groups may experience more serious health effects.

Very Unhealthy

201 to 300

Health alert: everyone may experience more serious health effects.

Hazardous

301 to 500

Health warnings of emergency conditions. The entire population is more likely to be affected.

Meaning

From http://www.airnow.gov/index.cfm?action=aqibasics.aqi.

monoxide, sulfur dioxide, and nitrous oxide. The AQI has a range from 0 to 500, with lower values (up to 50) associated with good air quality and higher values (300 and above) associated with levels of air pollution hazardous to health. The EPA uses color-coded categorizations of the AQI to indicate possible health effects associated with different values (Table 42-3). Vector-borne diseases, such as malaria, dengue, and Hantavirus, have been linked to climatic events. For example, in the tropics, dengue outbreaks occur at the onset of rainy seasons, such as the monsoons. Malaria and Hantavirus outbreaks in certain regions of the tropics have been associated with the warm phase of the El Niño Southern Oscillation (ENSO), when increased temperature is conducive to vector breeding. Stratospheric ozone prevents much of the sun’s ultraviolet (UV) radiation from reaching the earth’s surface. UV radiation that passes through the atmosphere is a health concern, primarily to the eyes and skin. The two primary factors in the risk for receiving unhealthy levels of UV radiation are angle of the sun and elevation. Higher levels of UV radiation are more likely at high elevations, where radiation has to pass through less of the atmosphere. The sun angle refers to both its varying angle throughout the day and its differing angles at different latitudes. At low latitudes, the sun angle remains high throughout the year, and therefore the risk for sunburn is always relatively high. At higher latitudes, the risk is especially high in late spring and early summer when the solar angle is highest. In either case, this risk is enhanced during the hours surrounding solar noon. In addition, clouds only scatter solar radiation; they do not block it. This allows UV radiation to reach the surface diffusely, where it is still harmful. Diffuse radiation is radiation that has been scattered, usually by clouds, but still reaches the ground. As a result, protection against the sun should be undertaken even when the sun is blocked by clouds. Stratospheric ozone is not evenly distributed around the world and tends to be thinner at higher latitudes, particularly during the spring. Therefore care should be taken to wear sunscreen and protective clothing and eyewear when engaged in outdoor activity, particularly in springtime in the mid- to high latitudes and at all times of the year in the tropics.

Weather forecasting in the wilderness requires data collection, whether from online sources (ideal) or with what is readily available and observable. Crude forecasts can be made by monitoring clouds and certain basic weather variables, such as temperature, humidity, and wind direction, if that is all that is available. If the Internet is available, reliable short-term forecasts can be obtained for most locations on Earth, typically provided by either private or public weather services. Therefore the primary use of online sources lies in the ability to monitor real-time weather information such as radar, satellite, and observations, in addition to obtaining forecasts. The primary purpose of data collection outdoors should be to make a rough forecast of ensuing weather conditions in the near term through 48 hours.

PORTABLE WEATHER INSTRUMENTS OF USE IN THE WILDERNESS Barometer Barometers are useful for assessing the evolution of weather systems, especially in the midlatitudes. Changes in atmospheric pressure at one location are small in comparison with changes as one moves up or down in elevation. Therefore barometers must be calibrated with changes in elevation if this is not already done automatically. In general the value of the atmospheric pressure is much less significant than its trend over time. A steady drop in pressure indicates the possibility of stormy conditions, whereas rising pressure generally portends fair weather. Thermometer Portable thermometers provide an indication of imminent changes in weather conditions such as those arising from the passage of a frontal system. They could also be consulted to ascertain the probability of freezing conditions and the risk for hypothermia. Because these applications do not require a high degree of precision, there is no need for a costly, high-precision instrument. Lightning Detector Portable lightning detectors are useful for detecting lightning within a 64.4- to 120.7-km (40- to 75-mile) radius, depending on the instrument. They detect the electromagnetic pulses of lightning, so they work best when used out of range of electronic equipment that may interfere with this signal. Lightning detectors operate with varying degrees of accuracy and can be limited in their ability to describe storm position and movement.

TYPES OF FORECASTS Forecasts vary by timescale, ranging from weather forecasts to seasonal climate forecasts. Weather forecasts assess the future state of the atmosphere and its constituent elements in reference to components such as temperature, wind, and precipitation. Weather forecasts are generated using numerical integrations of the equations of motion in the atmosphere. Such forecasts require accurate observations of initial atmospheric states. There are four types of weather forecasts: • Nowcasts: up to 0 to 3 hours, or 6 hours in some locations • Short-range forecasts: up to 48 hours • Medium-range forecasts: 3 to 7 days in advance • Long-range forecasts: greater than 7 days in advance Skill Accuracy of weather forecasts quickly declines with time because of the inherent chaos of the atmosphere. The details of midlatitude cyclones and smaller-scale events are impossible to forecast accurately beyond a few days, even if the pattern that produced them is relatively easy to identify. In the tropics, forecast skill is higher during years when either phase of the ENSO 809

CHAPTER 42  Principles of Meteorology and Weather Prediction

TABLE 42-3  Air Quality Index

PART 5  RESCUE AND SURVIVAL

phenomenon—La Niña or El Niño—is under way, because ENSO is the single most dominant mode of climate variability at the seasonal and interannual timescales.2 Seasonal climate forecasts seek to assess the mean weather of the upcoming season based on the conditions preceding the season by more than a month. They provide a prediction as to whether the coming season will on average be warm, cold, wet, or dry.3 At the seasonal timescale, the importance of initial conditions weakens,2 because detailed “memory” of initial atmospheric conditions is lost.3 Seasonal prediction thus depends on detailed changes in slowly varying boundary conditions.3 Shukla and Kinter4 provide the following list of surface boundary conditions: • Sea surface temperatures govern the convergence of moisture flux and sensible and latent heat fluxes between the ocean and atmosphere. • Soil moisture alters the heat capacity of the land surface and governs latent heat flux between continents and the atmosphere. • Vegetation regulates surface temperature and latent heat flux to the atmosphere from the land surface. • Snow influences the surface radiative balance through effect on surface albedo and latent heat flux by introducing a lag due to the storage of water in solid form in winter that gets melted or evaporated in spring and changes soil wetness. • Sea ice influences the energy balance and inhibits latent heat flux from the ocean. Anomalous boundary conditions can produce statistically significant anomalies in the seasonal mean atmospheric circulation. Such anomalous boundary conditions are more influential in the tropics than in the midlatitudes.4

How to Interpret Forecasts ACCESSING FORECASTS There are many online resources for weather forecasts for a particular location. In any country, the authoritative source for weather forecasts is the National Meteorological and Hydrological Services (NMHS) of that country. Links to the weather forecasts for cities issued by most NMHSs are available through http:// www.worldweather.wmo.int/ on the website of the World Meteorological Organization (WMO). North America In the United States, the National Weather Service (NWS) is responsible for all outlooks, forecasts, and advisories. Some of these responsibilities are handled by specialized centers within the organization. The National Hurricane Center (http:// www.nhc.noaa.gov/) issues all updates on tropical weather in the Atlantic and eastern Pacific Oceans, regardless of the impact on the United States. The Storm Prediction Center (http:// www.spc.noaa.gov/) handles all severe weather, including tornado and severe thunderstorm watches. Local NWS offices are responsible for issuing warnings on such events. Medium- to long-range discussions, outlooks, and forecasts are available from the Climate Prediction Center (http://www.cpc.noaa.gov/), and broader national forecasts and discussions for different regions of the country are available from the Hydrometeorological Prediction Center (http://www.hpc.ncep.noaa.gov/), which also provides guidance on quantitative precipitation forecasts (QPFs) and winter weather. In Canada, Environment Canada (http://www.weatheroffice. gc.ca) is responsible for all outlooks, forecasting, and advisories. These include data and forecasts regarding hurricanes, sea ice, aviation, and air quality. Environment Canada issues watches and warnings, and special weather statements for all of Canada, including its waters. International Forecasts The WMO has a dedicated website for severe weather warnings for various parts of the world. Such forecasts are categorized either by region (e.g., the European Union: http://www.meteoalarm. eu/) or by weather phenomena (e.g., tropical cyclones or thunderstorms: http://severe.worldweather.org/). Forecasts of severe 810

weather in maritime regions are available through the Global Maritime Distress and Safety System (http://weather.gmdss.org/).

FORECAST VARIABLES Seasonal Precipitation Forecasts Seasonal precipitation forecasts are presented as tercile probability forecasts in the United States. Tercile forecasts are based on the assumption that precipitation in a coming season has a 33% probability of falling within one of three possible categories: below-normal, near normal, or above normal. The forecast could be expressed either as the probability of seasonal rainfall being below normal, near normal, or above normal or in terms of expected rainfall anomalies. Temperature Forecasts Temperature forecasts are issued as expected daily minimum and maximum temperatures. In countries outside the United States, the convention is to express the two values in degrees Celsius. However, in most cases, Fahrenheit values will also be provided. Humidity Humidity forecasts are usually issued as expected relative humidity and range from 0% to 100%. Wind Direction and Speed Wind forecasts indicate direction (eight possible directions: N, NE, E, SE, S, SW, W, and NW) and speed (expressed either as kilometers per hour or miles per hour). In maritime environments, the convention is to use knots (1 knot is 1.852 km/hr [1.151 mph]). Precipitation Precipitation is forecast as probability of precipitation (POP) and, if applicable, QPF. POP should be interpreted as the percent of the area expected to receive measurable precipitation, although it is commonly misinterpreted as the chance that precipitation will fall at one specific point. QPF is the total amount of rain (or melted frozen precipitation) expected to fall in a specified period.

Forecast Products UNITED STATES According to the NWS, a warning is issued when a hazardous weather or hydrologic event is occurring, imminent, or likely. A warning means that conditions pose a threat to life or property. An advisory is also issued when such events are occurring, imminent, or likely, but the event is not expected to be as severe. The criteria for advisories and warnings varies among different NWS offices. Events such as heat index and winter weather, including snow, ice, and wind chill, may be perceived differently in different parts of the country. A watch is issued when the risk for a hazardous or hydrologic event is increasing, but its occurrence, location, or timing is still uncertain. As time advances, it could be replaced by an advisory or a warning. A watch is issued when warning-level conditions are anticipated. When a watch is issued, people should proceed with a plan of action for the predicted event and continue to be alert for further information and possible warnings.

INTERNATIONAL Regional Specialized Meteorological Centers (RSMCs) and Tropical Cyclone Warning Centers (TCWCs), established through the WMO, provide warnings on severe weather, particularly cyclones. Figure 42-5 shows the locations of the RSCMs and TCWCs. Tropical storm warnings use the Saffir-Simpson scale. Such warnings are often accompanied by a brief description of the damage likely to occur with the passage of each storm. Box 42-1 provides examples of the narrative used by the Indian Mete­ orological Department, responsible for RSMC-New Delhi, to

20°W

ESCAP/WMO Typhoon Committee

RA IV Hurricane Committee

20°E 40°E 60°E 80°E 100°E 120°E 140°E 160°E 180° 160°W 140°W 120°W 100°W 80°W 60°W 40°W 20°W

0°

60°N

60°N

40°N

RSMC New Delhi IV

20°N EQ

VIII RSMC La Réunion VI

20°S

40°N

RSMC Tokyo

VII

RSMC Nadi

IX Brisbane

Perth

II

III

X

XII

40°S

RSMC Miami

RSMC Honolulu

Port Darwin Moresby

V

60°S 20°W

CHAPTER 42  Principles of Meteorology and Weather Prediction

WMO/ESCAP Panel on Tropical Cyclones

I

20°N EQ

XI

Wellington

20°S 40°S

60°S 20°E 40°E 60°E 80°E 100°E 120°E 140°E 160°E 180° 160°W 140°W 120°W 100°W 80°W 60°W 40°W 20°W

0°

RA I Tropical Cyclone Committee for the Southwest Indian Ocean

RA V Tropical Cyclone Committee for the South Pacific and Southeast Indian Ocean

FIGURE 42-5  Location of the Regional Specialized Meteorological Centers and Tropical Warning Centers. (From http://www.nhc.noaa.gov/gifs/ wmo-tcp2.jpg.)

describe potential damage associated with a “deep depression” (28-33 knots) and a “severe cyclonic storm” (equivalent to a category 4 on the Saffir-Simpson scale).

• Gridded (2° × 2° resolution) monthly precipitation and temperature: http://iridl.ldeo.columbia.edu/SOURCES/. NOAA/.NCEP/.CPC/.CAMS/

How to Obtain Surface Observations

How to Access and Interpret Weather Satellite and Radar Data

UNITED STATES

In the United States, the NWS website has links to real-time radar and weather satellite imagery. The easiest method to track the passage (and associated precipitation) of a storm is to study radar imagery of a system available for different regions of the United States (Figure 42-6). Clicking on the region of interest takes one to a higher resolution image, where relevant warnings (such as thunderstorms) are marked on the imagery (Figure 42-7). The legend on the right enables the user to obtain an idea of the location of the highest intensity of precipitation. Table 42-4 provides an indication of the approximate rainfall intensity, which is associated with the units dBZ (known as “reflected intensities” or “decibels of Z”). Satellite images enable a user to obtain a quick estimation, on a large scale, of where overcast/stormy conditions are located and where clear weather prevails (Figure 42-8).

Surface observations for the United States are available online through the National Climatic Data Center (http://www. ncdc.noaa.gov/oa/climate/climatedata.html). Station-based data are available from hourly to monthly time resolution. The data are available free of charge to e-mail users with domains ending in .edu, .k12, .gov, and .mil; otherwise, fees apply to cover processing expenses. Data are also available from automated stations and volunteer observations through the NWS. Another source of data is the volunteer network of precipitation observers known as Community Collaborative Rain, Hail and Snow; data are available at http://www.cocorahs.org/.

GLOBAL DATA Surface observations from various part of the globe can be accessed through the Global Historical Climatology Network (GHCN). Such observations are available as station-based observations and as gridded products. Precipitation and temperature are the two variables commonly available through the GHCN. The following are links to GHCN data: • Monthly station-based precipitation: http://iridl.ldeo. columbia.edu/SOURCES/.NOAA/.NCDC/.GHCN/.v2beta/ • Daily station-based precipitation and minimum-maximum temperature: http://iridl.ldeo.columbia.edu/SOURCES/. NOAA/.NCDC/.GHCN_Daily/.version1/ • Monthly station-based temperature: http://iridl.ldeo. columbia.edu/SOURCES/.NOAA/.NCDC/.GHCN/.v2/

Weather Prediction in the Wilderness CLOUDS Clouds appear in various shapes and sizes and at different altitudes. Clouds are often classified according to their height and form (Figure 42-9): High clouds: cirrus, cirrostratus, and cirrocumulus Middle clouds: altostratus and altocumulus Low clouds: stratus, stratocumulus, and nimbostratus 811

PART 5  RESCUE AND SURVIVAL

BOX 42-1  Examples of Indian Meteorological

Department Narratives

What is the Damage Potential of a Deep Depression (28-33 knots) and What are the Suggested Actions? Structures: Minor damage to loose/unsecured structures Road/Rail: Some breaches in Kutcha road due to flooding Agriculture: Minor damage to banana trees and near coastal agriculture due to salt spray. Damage to rice paddy crops Marine Interests: Very rough seas. Sea waves about 4-6 m high. Coastal Zone: Minor damage to Kutcha embankments Overall Damage Category: Minor Suggested Actions: Fishermen advised not to venture into sea What is the Damage Potential of a Super Cyclonic Storm (120 knots [222 km/hr]) and Above? What are the Suggested Actions? Structures: Extensive damage to non-concrete residential and industrial buildings. Structural damage to concrete structures. Air full of large projectiles. Communication and power: Uprooting of power and communication poles. Total disruption of communication and power supply. Road/Rail: Extensive damage to Kutcha roads and some damage to poorly repaired pucca roads. Large scale submerging of coastal roads due to flooding and sea water inundation. Total disruption of railway and road traffic due to major damages to bridges, signals and railway tracks. Washing away of rail/road links at several places. Agriculture: Total destruction of standing crops/orchards, uprooting of large trees and blowing away of palm and coconut crowns, stripping of tree barks. Marine Interests: Phenomenal seas with wave heights more than 14 m. All shipping activity unsafe. Coastal Zone: Extensive damage to port installations. Storm surge more than 5 m, Inundation up to 40 km in specific areas and extensive beach erosion. All ships torn from their moorings. Flooding of escape routes. Overall Damage Category: Catastrophic Suggested Actions: Fishermen not to venture into sea. Large scale evacuations needed. Total stoppage of rail and road traffic needed in vulnerable areas. From http://www.imd.gov.in/section/nhac/dynamic/faq/FAQP.htm#q51.

Clouds with extensive vertical development: cumulus and cumulonimbus The frequency of occurrence of the different cloud types differs in the tropics and higher latitudes. Cumulus is the predominant cloud form in the tropics.1

CLOUDS AND WEATHER Clouds are among the best indicators of changing weather in the wilderness. Figure 42-10 shows the typical progression of clouds as a midlatitude cyclone moves through to the left of the observer, whereas a simplified version would apply when it moves to the right. Cirrus are often present 1 to 2 days before a storm and serve as the earliest indication that a cyclone is approaching. They should be noted as a sign that a storm may be on its way, bearing in mind that cirrus can be associated with storms that have no appreciable impact on a location, as well as with other innocuous disturbances. When cirrus begins to transition into a deck of altostratus, it can reasonably be assumed that the clouds are associated with a storm or front that is nearing. Stratus clouds are most commonly associated with warm fronts because they are a good indication that air is being forced to gradually rise over a wedge of cooler air, as is found in a warm front. In general, stratus occur as a warmer air mass is being lifted over a cooler one; the longer this occurs, the more likely the stratus are to be lower and begin precipitating. Therefore, as altostratus lower into a low, gray deck 812

of nimbostratus, it would be a good assumption that a light, steady rain or snow is on the way. Nimbostratus occurs in the vicinity of the warm front and near the center of low pressure where air is being lifted. The location of the low pressure can often be assessed using a simple rule called Buys Ballot’s law. When the observer stands with his or her back to the wind in the northern hemisphere, the low pressure will be to the left. This rule is reversed in the southern hemisphere and works best at higher latitudes. The weather conditions ahead of a warm front typically include winds from the east or southeast with cool conditions and a slowly dropping barometric pressure. After the front passes, the pressure continues to drop and the wind shifts clockwise to the south or southwest, in most regions bringing in warmer and moister air. This region of the cyclone between the cold and warm fronts is associated with the most instability, which allows for increased chances for convection and the highest probability of severe weather (see Figure 42-2). Because there is more instability, cumulous clouds dominate this sector. In the winter, warm air can rapidly be transported into this part of the storm, changing snow and ice to rain. The passage of the cold front is easy to observe because there are several sharp changes in weather conditions. Before passage, wind typically blows from the south or southwest, the dew point and temperature are relatively high, and air pressure is dropping. The strongest atmospheric lift is found near a cold front, so cumulonimbus with associated heavy rain and severe weather can be found at the frontal boundary. Typically, precipitation in the vicinity of a cold front does not fall for as long as it does ahead of a warm front because the slope, and therefore area of uplift, is much steeper and narrower with a cold front. After the front passes, wind typically shifts clockwise to the west or northwest, temperature and dew point slowly drop, and air pressure rises. Strong cold frontal passages can be observed as a deck of low or midlevel clouds sharply giving way to blue sky. Clearing skies are commonly observed relatively quickly after the front has passed, often with gusty winds remaining for a day or more. Dense cumulonimbus clouds in the tropics portend thunder showers and lightning. Altocumulus and altostratus clouds are associated with disturbed weather, such as tropical cyclones or in locations of large-scale orographic lifting.1 Cirrus clouds often form as leftover anvils from cumulonimbus clouds. However, they could also form independently and are usually associated with upper-atmospheric cyclones. Before a tropical cyclone, high cirrus clouds are often observed first, followed by midlevel and low-level stratus clouds. Eventually showery precipitation from cumulous and cumulonimbus arrives and increases in intensity as pressure steadily falls. Tropical cyclones have spiraling bands, often termed “rain bands,” of convective clouds. Intense upward motion and hence the heaviest rainfall occur within these rain bands and in the eye wall. Wind speeds increase toward the center of the cyclone. A dramatic decrease in pressure is observed within the eye of a storm.

BOUNDARY LAYER STABILITY Fronts and cyclones are not always needed for precipitation or severe weather. Strong daytime heating is all that is necessary to induce deep convection, which can occur frequently in more moist parts of the tropics and subtropics, as well as during the summer in midlatitudes. Stability of the boundary layer can be difficult to assess from observation, but it can be useful to determine how much potential there is for thunderstorms to grow. To achieve deep convection, air must be readily able to rise and overcome any resistance. Rising plumes of smoke or steam can give an indication of the stability of the lower atmosphere. If it rises to a certain level before spreading out horizontally, it is safe to assume that the lower atmosphere is at least somewhat stable. If nothing stops it from rising, the lower atmosphere may be quite unstable. In addition, a large amount of haze or pollution in the air is an indication of a stagnant environment where air moves very little, both horizontally and vertically. In arid regions, dust devils are also an indication of an unstable, albeit dry,

CHAPTER 42  Principles of Meteorology and Weather Prediction

FIGURE 42-6  Example of radar imagery over the United States.

FIGURE 42-7  Example of a Doppler radar image.

813

PART 5  RESCUE AND SURVIVAL

GOES WESTERN U.S. SECTOR IR IMAGE

Stormy weather

Fair weather

Western Conus Sector (IR Ch4) FIGURE 42-8  Example of the usefulness of satellite imagery in capturing stormy and clear conditions.

Cirrocumulus

Cirrus

30,000 ft HIGH CLOUDS Cirrostratus

25,000 ft

20,000 ft

Altostratus

15,000 ft

MIDDLE CLOUDS

Altocumulus

Cumolonimbus 10,000 ft

Stratocumulus Cumulus

Nimbostratus

LOW CLOUDS Stratus

FIGURE 42-9  Guide to different cloud types.

814

5000 ft

Cirrus Altostratus Cumulonimbus

Cumulus Nimbostratus

FIGURE 42-10  Progression of a midlatitude cyclone as seen from the ground.

TABLE 42-4  Doppler Radar Scale of Intensity dBZ

Rain Rate (inches/hr)

65 60 55 52 47 41 36 30 20 <20

16+ 8.00 4.00 2.50 1.25 0.50 0.25 0.10 Trace No rain

From http://www.srh.noaa.gov/jetstream/doppler/baserefl.htm#rainrate. dBZ, Decibels of reflectivity (Z).

atmosphere. Clouds themselves can be good indicators of atmospheric stability, namely in their vertical development. Clouds with little vertical development, such as stratus and “fair-weather” cumulus, indicate a stable atmosphere. Rapidly building cumulus clouds are a good indication that the atmosphere is unstable, and showers or thunderstorms should be forecast.

BACKING AND VEERING To aid in assessing current weather conditions, cold and warm air advection can be diagnosed by observing the movement of clouds at different levels. Advection is the horizontal transport of air from one location to another, bringing with it the temperature and humidity characteristics of its source region. Cold air advection, an indication of stability and improving (but colder) weather, often follows passage of low pressure. Wind direction at different levels of the atmosphere differ in this situation; at the surface, the wind may blow from the west or northwest, but much higher in the atmosphere the wind may be out of the southwest or west, respectively. The wind is said to back with height, and this is an indication of cold air advection. Similarly, warm air advected ahead of warm fronts creates an unstable situation, because it is forced to rise over the existing air mass. At the surface, wind out of the southeast is often accompanied by a southwesterly wind at the midlevels of the atmosphere, so the wind is said to veer with height. Two levels of clouds with movement that veers with height is a good indication that a steady rain or snow is on the way.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 43 

Jungle Travel and Survival JOHN WALDEN

Tropical Environment In these forests lies a virtually limitless supply of excitement, joy, and wonder to be encountered in new illuminations on the constructs and workings of life on Earth.32 Tropical rain forests, located between the Tropic of Cancer (23 degrees 27 minutes N latitude) and the Tropic of Capricorn (23 degrees 27 minutes S latitude), are regions with at least 4 inches of precipitation per month and a mean annual monthly temperature exceeding 24° C (75.2° F) without any occurrence of frost. Contrasted with temperate regions, the hours of day and night are about equal throughout the year. Seasons are characterized as “wet” or “dry.” These seasonal designations refer to historical trends and should not be taken as gospel: in some years, the dry season extends for months beyond the usual range; in other

years, the rains may persist for months as a daily drizzle, making it difficult to trek over the spongy terrain. In the Pacific coastal region of the Colombian Chocó and the Cayapas River basin of Ecuador, where annual rainfall can exceed 400 inches, the seasons are said to be “wet” and “wetter.” As the most biologically diverse community of living things on Earth, the tropical rain forest is a realm of superlatives: a single acre of tropical forest may contain more than one-half as many species of trees as occur in all the land mass of temperate North America; 1 square mile of Amazonian forest may be home to double the variety of butterflies that exist in all of the United States and Canada; a single tree in Peru yields as many species of ants as in all of the British Isles. Facts and figures fail to capture the essence of tropical rain forests and their extraordinary biologic diversity. Seen from the air, the forest stretches from horizon 815

PART 5  RESCUE AND SURVIVAL

to horizon in a vast green carpet. In season, the crowns of trees in full blossom dot the landscape with vivid splashes of red, orange, and yellow. Sizable streams may be hidden beneath the emerald canopy. Rivers, usually muddy yellow or black, snake through the forest; early-morning or late-afternoon sun transforms these braided rivers into glistening, mirror-like strands of liquid silver. Observed from the forest floor, the jungle is entrancing. In virgin, deep forest, all is muted and shadowy, save for random shafts of light that spotlight labyrinths of oddly shaped branches and spectacularly colored flowers. Shrubs and herbaceous plants are scarce in forest away from the flood plain, so it is relatively easy to walk undisturbed. The dimness is occasionally disrupted by areas bathed in bright light from larger holes in the canopy caused by a recently fallen tree, sandy beach, or cutting and burning by humans. It is in these sunlit, light-gap areas that the traveler encounters the lush and nearly impenetrable wall of foliage portrayed in adventure films. The tidy textbook division of vegetation into distinct tiers is somewhat arbitrary and not easily confirmed, even by experts.36 Drier, nonflooding, upland forests, known throughout Amazonia as terra firme (“solid ground”), are generally nutrient poor and support a crop yield cycle of only 2 or 3 years by traditional slash-and-burn farming methods. Plots of rich, black soil are encountered throughout many drier forest regions of Amazonia. This soil, commonly referred to as terra preta (“dark Earth”), is thought by many soil scientists and archeologists to be the result of intentional soil enhancement and management techniques developed by ancient farmers in the pre-Colombian era. In contrast to terra firme, terra preta is capable of sustaining crop production over many years. Lowland forests, or várzeas, which remain submerged for several months each year, although making up only a small percentage of forested land, are more fertile than their nonflooding, unimproved, nutrient-poor counterparts.

Trip Preparation Despite environmental differences within the jungle, the basics of travel remain the same.

READING

safety and prompt rescue cannot be assured, a number of group leaders privately note that two individuals who have a sexual relationship may form a team within a team, to the detriment of the expedition as a whole.48

CONDITIONING Indigenous peoples in jungle regions are almost always slender. After trekking with large numbers of nonindigenous men and women in equatorial regions, I have observed that overweight or powerfully built individuals, particularly men, seem to fare the worst, especially with heat-related illness. Achieving an ideal body weight and becoming aerobically fit by walking or jogging for extended periods of time are beneficial before jungle trekking. Although being in good shape is sensible, a person need not be an elite athlete to trek through the jungle and enjoy the experience. Good leg strength, acquired by training 20 to 30 minutes on alternate days with stair-climbing exercise machines, offers appropriate preparation. To keep up with native porters and guides, the prospective expedition member should practice hiking at a fast pace. Once in the jungle, travelers should imitate the energy-saving, fluid rhythm of local inhabitants. Because trekkers frequently encounter single-log bridges, a well-developed sense of balance is desirable (Figure 43-1). Walking on the rails of untrafficked train tracks or on roadway curbs may help in preparation. To adapt to specific situations, trekkers should go to the woodlands and practice walking on logs. Head stability is important. Equilibrium can be enhanced by avoiding brisk head movements and by employing the “gazeanchoring” technique of tightrope walkers. The person fixes the gaze on a spot near the end of the log and does not stare down at the spot just ahead of the feet.3,8 Special cleats (Covell Ice Walker Quick Clip cleats) (Figure 43-2) should be considered for crossing log bridges that are high off the ground, long, and slippery. The cleats can be snapped on quickly before crossing a log bridge and promptly snapped off at the other end. Stability on logs also may be enhanced by turning the feet approximately 20 to 25 degrees to the right or left (whichever seems more natural), rather than walking with the feet in a straight line on the log.

Back issues of National Geographic magazine and the writings of Wilson provide an excellent introduction to people, places, and biodiversity issues.4,50,51 The Smithsonian Atlas of the Amazon,18 the definitive illustrated atlas (150 color maps and 289 photographs) of the region, is highly recommended, as is the Conservation Atlas of Tropical Forests series (Asia and the Pacific,9 Africa,38 the Americas22). The references for this chapter (available online at www.expertconsult.com) offer insights into the complex inner workings of the moist tropical forest.1,35,36 The books by Kritcher26 and Forsyth and colleagues17 are especially helpful. Trips into the rain forest should be scheduled for the dry season because trails are more serviceable for trekking at that time. Information on weather patterns can be obtained from agencies of national governments, anthropologists, and missionaries. Weather Underground (http://www.wunderground.com) provides current, as well as seasonal, weather averages for many cities and towns in tropical regions.

ATTITUDE In selecting participants, experienced expedition leaders look for a sense of humor. The ability to see the bright side in difficult times may be an asset more valuable than physical conditioning. Houston24 and others have discussed the role of humor as a predictor of success. Erb13,14 noted that successful or failed participation in wilderness ventures also is a significant predictor.

RELATIONSHIP CONSIDERATIONS Couples routinely report benefits from the shared experience of wilderness adventure travel, ecotourism, and academic field research. However, in the setting of high-risk expeditions where 816

FIGURE 43-1  A well-developed sense of balance is desirable. (Courtesy John Walden.)

IMMUNIZATIONS Travelers to rain forest regions should protect against the following diseases by vaccination or with prophylactic medications (see Chapter 84): • Diphtheria, tetanus • Hepatitis A, hepatitis B • Influenza (see later) • Measles, mumps, rubella • Polio (where appropriate) • Rabies (see Chapter 60) • Typhoid • Yellow fever (in certain regions of tropical Africa and South America) • Malaria (see Chapter 49) Malaria is prevalent throughout the tropics. Before travel to malarious areas, appropriate prophylaxis is needed. Updated information on the risk for malaria in various regions may be obtained through the Centers for Disease Control and Prevention (http://www.cdc.gov/travel). The Medical Letter on Drugs and Therapeutics (http://www.medicalletter.com) is an excellent source for current recommendations on preventing and treating malaria. Persons traveling into remote regions of Amazonia, where Indian groups live in isolation, should receive yearly influenza vaccinations to reduce the likelihood of inadvertently transmitting disease to these high-risk native inhabitants. Protection against meningococcal disease should be considered where circumstances warrant.

MEDICAL KIT The Wilderness Medical Society points out that it is inappropriate to pack medications and equipment when no team member has the knowledge or experience to use them safely.25 The following items for a basic medical kit (Box 43-1) are adequate for personal use in the rain forest setting: BOX 43-1  Medical Kit for Jungle Travel Bismuth subsalicylate tablets (48) Ciprofloxacin hydrochloride 500-mg tablets (20) Clotrimazole and betamethasone dipropionate cream (60 g) Diphenhydramine hydrochloride, 25- or 50-mg capsules (15) Epinephrine autoinjector (2 adult, 2 child) Ibuprofen, 200-mg tablets (90) Ketorolac, 60-mg single-dose syringe (2) Lidocaine hydrochloride carpules (3) Mupirocin ointment 2% (30 g) Permethrin, 5% cream (60 g) Permethrin, 1% shampoo (2 oz) SAM splint (1) Sulfacetamide sodium ophthalmic solution 10% (15 mL) Sunscreen (4 oz) (2) Tinidazole 500-mg tablets (12) Tramadol hydrochloride, 50-mg tablets (20)

817

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FIGURE 43-2  Covell Ice Walker Quick Clip cleat. (Courtesy Jon Willis.)

• Bismuth subsalicylate (Pepto-Bismol tablets) is an effective over-the-counter preparation for preventing and treating common traveler’s diarrhea. It also is useful for heartburn and indigestion. Pepto-Bismol tends to turn the tongue and stools black. • Diphenhydramine hydrochloride (Benadryl, 50-mg capsules) is safe and effective as an antihistamine, for motion sickness, and as a nighttime sleep aid. • Ciprofloxacin hydrochloride (Cipro, 500-mg tablets) is highly active against the important bacterial causes of enteritis, including diarrheogenic Escherichia coli, Vibrio cholerae, Salmonella species, Shigella species, Campylobacter jejuni, Aeromonas species, and Yersinia enterocolitica. • Clotrimazole and betamethasone dipropionate (Lotrisone) cream combines an antifungal with a steroid for rashes. • Epinephrine autoinjector (EpiPen/EpiPen Jr.) provides for emergency treatment of severe allergic reactions to insect stings, foods, or drugs. • Ibuprofen (600-mg tablets) is a good choice for mild to moderate pain from such problems as menstrual cramps, rheumatoid arthritis, and osteoarthritis. It also lowers elevated body temperature caused by common infectious diseases. • Ketorolac (Toradol, 60 mg for injection) provides good short-term relief for moderate to severe pain. It is preferred over narcotics only because it is less likely to cause problems with customs officers and police. • Lidocaine hydrochloride may be required as a local anesthetic agent for relief of the excruciating pain resulting from stingray envenomation or conga ant and caterpillar stings. It should be infiltrated into and around the wound area using a dental syringe and 25-gauge needle. Lidocaine carpules (used by dentists) are protected and easy to carry and use in the rain forest.19 • Mupirocin (Bactroban) ointment 2% should be immediately applied to burns, abrasions, lacerations, and ruptured blisters, which can rapidly become infected in the tropics. • Permethrin 5% cream and 1% shampoo should be applied to treat scabies and head lice before returning home by travelers who have been in close contact with heavily infested tribal peoples. Many natives, especially in the tropics of Central and South American, are infested with these ectoparasites. Oral ivermectin (200 mcg/kg) can also effectively treat scabies.16 Malathion 0.5% is another good choice for head lice. Marmosets and tamarins are often kept by indigenous peoples of the Americas as pets to aid in grooming for head lice (Figure 43-3). • The SAM splint is lightweight, waterproof, reusable, and not affected by temperature extremes. • Sulfacetamide sodium (Sodium Sulamyd/Bleph-10) ophthalmic solution 10% is excellent for treating conjunctivitis, corneal ulcers, or other superficial ocular infections. • Sunscreen is essential in open areas such as rivers or jungle clearings. Sunscreens designated “waterproof” retain their full sun protection factor (SPF) rating for longer periods during sweating or water immersion than do products designated “water resistant.” Opaque formulations are excellent for the nose, lips, and ears. Visitors to the tropics should wear lightweight, long-sleeved shirts and widebrimmed hats when exposed to the sun for prolonged periods. • Tinidazole is excellent for treating giardiasis (2  g orally [PO] once), acute amebic dysentery (2  g once PO daily for 3 days followed by either iodoquinol or paromomycin), Trichomonas species vaginitis (2  g PO once), and bacterial vaginosis (2  g PO once daily for 2 days). Metronidazole (250-mg tablets) also is appropriate for treating giardiasis, acute amebic dysentery, and Trichomonas species vaginitis. • Tramadol hydrochloride (Ultram, 50-mg tablets) is used for moderate to severe pain. Common sense dictates supplementary items. Women on long trips might add miconazole vaginal suppositories or fluconazole (Diflucan, 150 mg as a single oral dose) to treat yeast infections; older men might take a 16-Fr catheter and sterile lubricating jelly

PART 5  RESCUE AND SURVIVAL

“high-impact” soles should not be worn because they become slippery on wet logs or river rocks. • Quick drying time. Uppers of Cordura nylon and split leather, in addition to resisting abrasion and being aerated, dry rapidly in the sun. Even though hiking shoes usually become soaked within minutes on the trail, it is a psychological boost to start each day with semidry shoes. Because jungle travelers can be in waist-high water while on the trail, waterproof shoes with Gore-Tex liners are not essential. • Snag-proof design. Shoes or boots with “quick-lace” steel hooks should be avoided; vines and weeds become tangled around the metal hooks, causing the wearer to stumble and pulling the laces untied. Shoelaces should always be double knotted. • Lightweight • Well broken in

BOX 43-2  Gear for Jungle Travel

FIGURE 43-3  Tamarins and marmosets are kept as pets to aid in grooming for head lice. (Courtesy John Walden.)

for dealing with urinary retention from prostatic hypertrophy. The fingers may swell rapidly during vigorous activity in the rain forest. To eliminate the possible need for emergency removal, all rings (including toe rings) should be removed before jungle trekking. Body piercings should be removed to eliminate the risk for infection.

GEAR The goal is to travel as “light” as possible. The more gear that is packed, the greater is the likelihood of breakdowns, complications, and misery. The items mentioned in Box 43-2 have withstood the test of time over years of long-distance tropical trekking. Gear must hold up under difficult jungle travel conditions that include heat, wetness, and mud. No line of advertised gear is ideally suited for the traveler in the tropics. Footwear Because feet absorb more punishment than any other part of the body, suitable footwear is the most important item of gear. This is one area in which a person absolutely must not carry inferior equipment. If the feet cannot go, nothing can go. Military “Vietnam-style” jungle boots with leather uppers, steel insole plates, and speed lacing are unsuitable for serious, longdistance trekking. After an hour of hard walking through streams and muddy trails, blisters can form on every surface of the foot, and the skin will peel off in sheets, bringing a jungle trip to a premature end. Furthermore, safely crossing log bridges and mossy, slime-covered river rocks is almost impossible in these boots. Two pairs of shoes are needed: one suitable for the wet, slippery conditions imposed by the trail and another that meets the need for dryness and comfort in camp. Trail Shoes.  The following features are desirable in trail shoes: • Uppers that hit just above or just below the ankles. Some people choose a high-cut design, reasoning that the extra height gives some added snake protection. • Extra protection over the big toe. Rubber or leather toecaps prevent the big toe from being severely battered and bruised. • Moderately deep-tread outsoles. Traction on rugged and muddy terrain is important. Running shoes with hard, 818

Trail shoes (1 pair) Camp boots (1 pair) Covell cleats Socks, lightweight cotton or thin nylon (3 pairs) Hat (1) Pullover garment, polyester (1) Shirts, cotton Long sleeved (2) Short sleeved (2) Nylon or taslan pants, lined with mesh underwear Poncho, nylon (1) Flannel sheet Hammock or Therm-a-Rest Mosquito net Backpack for porter Personal backpack Antifogging solution for eyeglasses Batteries Binoculars Camera equipment and film Campsuds Candles, dripless Cup (Lexan polycarbonate)/plate (melamine) Dry bags Duct tape, 1 small roll Ear plugs Fishing supplies Garbage bags, 13-gal size (2) Headlamp Inflatable cushion Insect repellent Laminated maps Machete (Collins style) Waterproof matches or butane piezo ignition lighter Pen Toilet paper Leatherman pocket survival tool Razor/battery-operated shaver Spoon Sport sponge Sunglasses Umbrella Whistle, plastic Wide-mouth water bottles (2)

Other Options.  The lightweight, comfortable, mesh/neoprene fabric “water” shoes popular for beach and sailboarding activities may have a place on river trips when substantial time will be spent in dugout canoes or rubber rafts. Thongs and open-toe sandals are fine for most towns and cities in the tropics, but in certain jungle regions, such as the Amazon basin, exposed feet invite hordes of biting insects. The jungle traveler must never go barefoot. Plant spines and glass can puncture the feet, and larvae of ubiquitous parasites, such as Ancylostoma duodenale and Necator americanus (the hookworms) and Strongyloides species can enter through the skin. The burrowing jigger flea, Tunga penetrans, is a serious pest and can be avoided by wearing shoes. Socks Cotton or thin synthetic socks should be worn in the jungle to decrease the risk for blisters from wet trail shoes, to reduce insect bites, particularly from no-see-ums (Ceratopogonidae family), and to lessen the risk for lacerations from saw grass (Figure 43-4). Clothing In many countries, military green or camouflage-style clothing is strictly contraindicated. This is particularly true in military dictatorships or in remote border regions. To be mistaken for a guerilla or foreign infiltrator by the military, police, or security (undercover) forces can lead to harassment, detention, or worse. Hat For protection from radiant heat and light objects falling in the forest, the traveler should wear a lightweight, light-colored hat that has a medium or wide brim. It need not be waterproof but should be made of material that can be wadded up. A useful feature is a fastener on each side to snap the brim up for traveling on the trail. A pith helmet, widely regarded as an affectation, is fine for open savanna and river trips, but on the trail, branches make it impractical. Pullover Drenching rain may leave a person feeling chilled and uncomfortable, particularly when traveling mainly by canoe or raft. Chilling generally is not a problem when hiking on the trail as

FIGURE 43-4  Saw grass. (Courtesy V. Ramey, University of Florida, Center for Aquatic and Invasive Plants.)

long as the person keeps moving. A Dacron polyester fleece pullover, such as L.L. Bean’s Polartec pullover, REI’s polyester lightweight MTS long-sleeve crew, or Patagonia’s polyester pullover, will keep a person warm. Wet garments should be wrung out so that they continue to offer thermal protection. Professional white-water boatmen working in tropical regions generally pack a polyester outerwear garment. Shirts Two light-colored, ultra-lightweight, long-sleeved cotton shirts should be taken. At the end of the day, the trail shirt should be washed and rinsed so that it will be ready, although perhaps still damp, the next morning. The second shirt can be used in camp or as a spare for the trail. Expensive synthetic shirts “guaranteed to wick away moisture” are poor jungle trail shirts and make the person sweaty and sticky. In camp, if no-see-ums and mosquitoes are few, a lightweight, short-sleeved cotton shirt is practical. Two should be packed. A four-pocket style called the guayabera, favored by men throughout Latin America and the Caribbean, is ideal. La Casa de Las Guayaberas (Naroca Plaza, 5840 SW 8th St, Miami, FL 33144; 305-266-9683; fax 305-267-1687) has an exceptional selection of short- and long-sleeved guayaberas; be sure to specify 100% cotton. Pants Two pairs of ultra-lightweight, light-colored pants are needed. Although synthetic shirts are unsuitable for trekking in the hot, humid tropics, nylon Supplex or Taslan pants with a built-in mesh brief are ideal. To reiterate: Cotton is preferable above the waist; Supplex or Taslan is preferable below the waist. Pants made of these materials hold up well, are quick drying, and meet the criteria for comfort on the trail. One pair is worn on the trail during the entire trip. The other pair is worn around camp and in towns along the way. Pants with zip-off legs to create instant shorts should be avoided; they will not hold up to strenuous trail conditions. Trail pants should be washed often. Jeans become waterlogged as soon as they become wet and are totally unsuitable for tropical trekking. Undergarments Underpants and sport bras should be made of cotton or polyester mesh. Poncho An ultrathin waterproof poncho is useful on rafting or canoe trips and in villages but is worthless for use on the trail because it will become snagged on twigs and tree spines.

BEDDING Flannel Sheet Tropical rain forests become uncomfortably cold between midnight and sunrise. A cotton sheet does not provide enough warmth, a blanket is too heavy, and a summer-weight sleeping bag retains too much body heat. A flannel sheet sewn together like a mummy bag (40 × 90 inches), but without a taper, provides suitable warmth placed either in a hammock or on a pad. Many inhabitants of the tropical forests sleep with their feet near a fire that is tended throughout the night. They have learned that the chill of damp, cool jungle nights can be lessened as long as the feet stay warm. Disposable “warm packs” (Heat Treat Toe Warmers) can be attached by the adhesive backing to the outside of socks, under the toes. Hammock Soft cloth hammocks are too bulky and heavy for trips and begin to smell after a few days. Fishnet cotton hammocks tend to fall apart within hours or days. So-called camping tent-hammocks or military tent-hammocks are impossible to sling properly, extremely uncomfortable, hot, unstable, and never able to keep the rain out in a heavy tropical downpour. The EZ Sales EZ-199 Marina Double Hammock is available online from multiple sources and has proved nearly ideal for 819

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Camp Boots.  Footwear needs are different in camp, where the trekker wants dry feet. Shoes, although excellent for the trail, are not suited for camp. A noninsulated, pull-on (laceless), open-top boot that comes to midcalf keeps mud off the feet and pants and, when worn with thin nylon socks, allows enough air to circulate to keep the feet cool and dry. Rubber remains an excellent material for keeping water away from the feet. Rubber lug soles provide traction. When rubbersoled boots are worn at an encampment, however, extreme caution is needed when crossing bridges and walking on wet rocks. Camp boots should be lightweight because they must be carried in a pack on the trail. Discount stores usually carry lightweight, lug-soled rubber boots that meet the criteria for jungle camp boots.

PART 5  RESCUE AND SURVIVAL

FIGURE 43-5  Indigenous peoples are accustomed to hauling loads using a tumpline. (Courtesy John Walden.)

jungle travel. It is compact, lightweight, durable, and reasonably comfortable. It cannot rot or absorb odors. For easier handling, the ski rope tie-end lines that are sold with the Double Hammock should be replaced with 1-cm (0.4-inch) nylon double-braided rope available from home improvement retailers or a boating supply source such as West Marine (http://www.westmarine.com). Therm-a-Rest The Therm-a-Rest foam pad is the choice of expedition organizers in temperate and cold climates throughout the world. It combines the insulating qualities of foam and the cushioning of an air mattress, rolls up to a compact size, and inflates on its own when the valve is opened. The traveler who will be sleeping on a pad should pack a 1.4- × 2.3-m (1.5- × 2.5-yard) plastic groundsheet. The sheet should not be placed directly on the jungle floor, where stinging insects and snakes abound. It should be used only in a hut or on an elevated platform. The groundsheet may also be beneficial for temporary rain protection and for keeping bow spray off a person or gear during water travel. For jungle travel, I prefer a hammock over a foam pad. Mosquito Netting A mosquito net designed for use with a hammock is basically a rectangular box that is open at the bottom with sleeves at each end panel for the passage of the ropes by which the hammock is slung. Such nets are difficult to find outside the tropics. Fortunately, a serviceable mosquito net can easily be made from “no-see-um netting.” (No-See-Um mosquito netting is available from U.S. Netting, [email protected].) See later in this chapter for the details of mosquito net construction.

BACKPACKS A sturdy, well-designed backpack should be used to carry gear. Reflective material should be sewn onto the back of each backpack. Iron Horse Safety Specialties (800-323-5889, http://www. fabric.ironhorsesafety.com) sells red-orange reflective material for daytime visibility and reflective silver material for nighttime reflectivity. On serious jungle treks, porters are often present. This frees expedition members to carry much lighter loads. Backpack for Porter An internal-frame backpack with a capacity of 49.2 to 65.6 L (3000 to 4000 inches3) is a good size. It should have external pockets for quick access to liter-sized water bottles. Indigenous peoples are accustomed to carrying packs and hauling loads with a strap, known as a tumpline, slung over the forehead or chest. Many natives, including Amazonian Indians, dislike using the shoulder straps that come as standard equipment on backpacks. Given enough straps, almost any native 820

porter can quickly rig a satisfactory tumpline on a backpack. If you do not have extra straps, tribesmen reared in the tropical forest will strip bark from saplings and fashion an adequate tumpline in minutes (Figure 43-5). Personal Pack A daypack with a capacity of 19.7 to 32.8 L (1200 to 2000 inches3) is useful for carrying a camera, snack food, and other gear that must be kept handy. A waterproof liner will keep perspiration from wicking into the bag and wetting everything inside. The pack should have two outside pockets for quick access to litersized water bottles. Pack for River Trips A durable, waterproof “dry” bag, used by river runners, is worth considering, especially if the trip will involve spending days or weeks at a time in dugout canoes or rubber rafts. Most of these packs, however, cannot stand up to the demands of long-distance overland trekking. The straps tend to be uncomfortable and frequently rip out on the trail.

OTHER USEFUL ITEMS Antifogging Solution for Eyeglasses Antifog solution, available from dive shops, reduces humidityinduced fogging of glasses. Batteries Alkaline batteries should be brought from home. Batteries purchased in Third World nations do not last long and often leak. Binoculars The traveler who is an avid bird-watcher or enjoys watching butterflies or seeking out orchids high on distant limbs will want to pack a pair of binoculars that are lightweight, compact, shockproof, and waterproof or water resistant. Camera Equipment Water-resistant point-and-shoot digital cameras are available, as are rugged, high-performance, water-resistant professional digital cameras such as the Pentax K-7. Because of their proved track record of reliability, older-style film cameras with mechanical shutters are useful in regions of high humidity. Professional film with an ISO of 200 is ideal for use in low-light conditions of the jungle and much preferred over slower film. Camera Case or Bag Hard-bodied Pelican cases are waterproof and virtually indestructible. The silver-gray color cuts down on heat absorption and is preferred in hot climates. The cases are ideal for rafting or canoe

Camp Soap A biodegradable soap should be used. Campsuds soap, in a leak-proof Nalgene bottle, works in hot, cold, fresh, or salt water and cleans dishes, clothing, hair, and skin. Candles Electricity tends to fail at unpredictable times in small towns and even in larger cities in Third World countries. Travelers should carry dripless candles. Spring-loaded candle lanterns should be avoided because they give off an anemic light, gum up, get crushed or broken, and basically waste space in the pack. Cup and Plate A large Lexan polycarbonate cup is unbreakable, does not retain taste or odor, and serves the role of cup, bowl, and plate. Travelers who want an actual plate should buy one made of indestructible Melamine. Duct Tape High-quality duct tape, such as Duck brand, is excellent for protecting existing blisters and for preventing blisters from developing on areas prone to blister formation when applied before trekking. Although a number of products are marketed to prevent blister formation and protect skin once blisters have formed, in my experience nothing beats duct tape. Also, duct tape is useful for removing the urticating hairs of caterpillar envenoming (see Venomous Moths, Butterflies, and Caterpillars, later). Ear Plugs Travel in the tropics often involves flying in incredibly loud helicopters, cargo planes, or short takeoff and landing (STOL) aircraft. Sponge ear plugs that roll up and fit in the ear canal offer inexpensive, effective protection against hearing damage. Be sure to buy these in sealed packets of two per packet and not in bulk. Once the packet is opened, sponge ear plugs quickly absorb moisture in the humid tropics, making them difficult to insert into the ear canal if exposed to ambient humidity for more than a few hours. Fishing Supplies For additional “food insurance” when traveling in extremely isolated regions, the jungle traveler should carry 22.9 m (75 feet) of 20-lb-test fishing line, at least two 30.5-cm (12-inch) steel leaders with swivels, and a few size No. 4 hooks. Travel rods that break down for compact carrying and spin-cast reels should be considered for sport fishing or adding fresh meat to the daily provisions. Throughout the tropics, most species of fish find RatL-Trap lures, particularly the chrome and blue combination, irresistible. The hooks that come standard with Rat-L-Trap lures are not sturdy enough to withstand the hard mouth and powerful bite of tropical freshwater fish. Replace these hooks with 3× or 4× strong, size No. 4, treble hooks. Garbage Bags Two heavy duty 49.2-L (13-gal) capacity plastic garbage bags (or dry bags) can keep dirty boots isolated from clean items in the backpack. Dry Bags Compression dry bags are excellent for storing items that must stay dry, such as bedding and clothes for camp use. Outdoor Research and SealLine dry sacks are high-quality products available from REI. See-through organizer bags help reduce clutter and minimize the risk for misplacing small items. Headlamp Battery-operated headlamps offer hands-free convenience at night for reading or going to the latrine. The Petzl Tikka LED Headlamp weighs a mere 76.5 g (2.7 oz) (with batteries) and has a battery life of 24 hours at 21° C (70° F).

Inflatable Cushion or Pillow A small, self-inflating cushion made with a low-slip polyester fabric top and durable nylon bottom is recommended for sitting in a dugout canoe or aluminum boat. Insect Repellent Insect repellent containing 15% to 30% N,N-diethyl-3-methylbenzamide (DEET) repels mosquitoes, flies, ticks, chiggers, fleas, and gnats, but not no-see-ums. Formulations (often called “jungle juice”) should not contain higher than 30% DEET, because they may pose health hazards (see Chapter 47). Relatively new to the American market, picaridin in the 20% formulation repels mosquitoes, flies, ticks, chiggers, fleas, and offers some protection against annoying no-see-ums. (I have found the 7% formulation of picaridin ineffective in the rain forest setting; it should be avoided.) Picaridin does not damage plastics or synthetic materials, does not have the “wet/sticky” feel of products containing DEET, and can purchased in an odorless formulation. Technique is critical when applying insect repellent. Before dressing, the person should spray the ankles, lower legs, and waist. If clothing has not been pretreated with permethrin (see later), then after the socks are put on, a band of repellent should be sprayed around the top; a band should also be sprayed around both pant legs to midcalf. A light spray to the shirt, front and back, may also help. The hands should be sprayed, rubbed vigorously, and run through the hair. Some repellent should be dabbed on the face, neck, and ears, carefully avoiding the eyes; contact lens wearers should be especially vigilant when applying insect repellent. No-see-ums, which are tiny gnats that abound throughout the tropics of the Americas, are the most common source of insect annoyance in many regions. They are active at sunset and attack humans emerging from jungle streams. No-see-ums cannot bite through even the thinnest cloth and are usually inhibited by Skin So Soft (SSS), which appears to have a slight chemical repellent effect, but more likely works by drowning the tiny gnats in oil. SSS is not effective against ticks, fleas, flies, and chiggers and offers little protection against mosquitoes. SSS should be applied liberally and often to the wrists, knuckles, bare ankles, face, ears, and scalp. Men with full beards seem to be especially troubled by tiny gnats and may benefit by applying small amounts of SSS to the beard area. Picaridin (see above) in the 20% formulation offers some protection against no-see-ums. Permethrin kills or stuns insects that land on clothing that has been impregnated with this product. Permethrin is safe, is highly effective, and persists even after extensive washing of garments (see Chapter 84). It is effective against insects when used on mosquito netting, even when the netting has sizable holes and tears. Laminated Map Accurate maps exist for most regions on Earth. From the best map available, travelers should laminate photocopied portions that are relevant to a particular itinerary (see Rescue Strategies, later). Machete A Collins-style machete (Figure 43-6) is the single essential tool for jungle survival and for the many tasks in camp and on the trail that require steel with a sharp edge. Do not purchase a model with a hand guard. A hand guard serves only for protection against an opponent’s blade when used as a weapon in combat; it does not offer added protection when the machete is used as a cutting implement.23 A newly purchased machete may have a pointed, sharp tip and a cutting edge that extends all the way from tip to handle. To reduce the likelihood of accidental injury, use a metal file to dull the tip of the machete and also to flatten the cutting edge from the handle to approximately 2 inches. It is hazardous to use a machete in the rain or when cutting wet grass, because the weapon may fly out of the hand. Also, when cutting brush, the person often encounters saw grass (see Figure 43-4). The resulting skin lacerations, which are not noticed at first because saw grass is razor sharp, may take a week or two to heal. Because of the risks involved, an experienced individual should 821

CHAPTER 43  Jungle Travel and Survival

trips but bulky for trekking. On the trail, waterproof “dry” bags protect equipment.

PART 5  RESCUE AND SURVIVAL

Toilet Paper American toilet paper is much softer than that purchased in Third World countries. The traveler should never wipe with jungle leaves. Umbrella A collapsible umbrella is useful in tropical cities and in remote villages when walking from hut to hut. It also offers excellent protection from the sun on canoe or raft trips. The umbrella should be reflective silver, not heat-absorbing black. Whistle A high-quality plastic whistle can be used to signal in case someone strays off the path. FIGURE 43-6  Collins-style machete with sheath. (Courtesy John Walden.)

be in charge of transporting and using the machete. For added safety, a machete should be carried in a sheath. Matches or Cigarette Lighter Waterproof, windproof Hurricane Matches light when damp and stay lit for several seconds, even in the strongest wind. Many jungle travelers prefer a butane cigarette lighter with a piezo ignition system. Pen J.L. Darling Corp (2614 Pacific Hwy E, Tacoma, WA 98424-1017; 253-922-5000; http://www.riteintherain.com) sells professional quality outdoor writing products, including Rite in the Rain shirtpocket field notebooks, travel journals, and all-weather pens that write upside down without pumping, underwater, over grease, and in hot and cold temperature extremes. Pocket Tool The Leatherman Super Tool is recommended for jungle travel and survival and features needle-nosed pliers and 12 locking implements. Wide-Mouth Water Bottles Essential gear includes two quart- or liter-sized wide-mouth water bottles. Bisphenol A–free products are now available. Narrowmouth, screw-top 56.7-g (2-oz), heavy-duty bottles come in handy for carrying a salt and pepper mixture to add flavor to boiled plantains and yucca. Nalgene products are legendary; whatever you put in a Nalgene bottle will stay there and not leak into your pack. Razor or Battery-Operated Shaver Both men and women should carry lightweight disposable razors. Most men find that lightweight, AA battery-operated shavers give two shaves a day for up to 2 weeks before requiring a change of batteries. Spoon Knife-spoon-fork sets are unnecessary. A knife blade and a good tablespoon made of either Lexan polycarbonate or stainless steel are sufficient for eating. Sport Sponge A camp towel, made of microporous material, is lightweight, compact, and superabsorbent; it replaces the cotton towel. With the Cascade Designs PackTowel or similar brand, the body and even hair can be dried much more quickly than with a traditional towel. Sunglasses Sunglasses should be polarized with full ultraviolet light protection. Many travelers prefer sunglasses with red-tinted lenses. Because red is the complement of green, these lenses make the jungle foliage stand out intensely and sharply, with enhanced contrast and depth of field. Retainers hold eyeglasses securely during vigorous activity. 822

Coping With the Jungle Environment A visit to the rain forests of the New World tropics can be either a sublime experience or a hellish ordeal.17

WETNESS The superhumid lowland rain forest receives up to 1016 cm (400 inches) of rain a year. In the higher-elevation cloud forest, dense cloud cover throughout the year is accompanied by constant mist or drizzle. In such heat and high humidity, people become mentally fatigued as a result of being constantly wet. Fortunately, travelers can use basic strategies for coping with the physical and psychological burden of wetness. Dryness while trekking or working during the day is not a requirement for physical or mental health. Wetness does not equate with illness, significant discomfort, or dampened spirits. People can tolerate being wet throughout much of the day if they know that they have a dry change of clothes to wear in camp and that they will be dry at night. In addition to the psychological benefits, being dry at night means that maceration is less likely to develop in intertriginous areas. Bedding and clothing can be protected from moisture by careful wrapping in plastic dry-bags. Despite all efforts, however, certain “dry” items eventually become damp or accidentally soaked. Wet articles should be spread out on shrubs and bushes. They will dry within 2 hours in full sun. Myiasis caused by the tumbu fly, Cordylobia anthropophaga, of sub-Saharan Africa can be avoided by hanging clothing to dry in bright sunlight, never on the ground. Clothing dried over a wood fire absorbs smoky odor that does not wash out.

HEALTH ISSUES Health Risks The subject of the tropics causes many people to think about tropical diseases, such as filariasis, and animals, such as the candirú (see later discussion). Malaria, hepatitis, and motor vehicle accidents are the three leading health problems in most tropical regions. Tropical travelers who venture off the path may be exposed to bodily harm and serious diseases, such as leishmaniasis, onchocerciasis, Chagas’ disease (in the Americas), and sleeping sickness (in sub-Saharan Africa). Close contact with many indigenous populations of Amazonia increases the likelihood of infestation with scabies and head lice. Bouts of diarrhea or other annoyances will likely occur, regardless of the extent of precautions taken, but death is unlikely. Duration of Travel and Emotional Response Cashel and colleagues6 examined the mood pattern of participants in eight separate 9-day wilderness expeditions conducted over 4 years and noted a high level of confusion, fatigue, anger, depression, and tension on day 4. After 2 to 3 weeks of travel in remote areas, the general health of expedition participants deteriorates as a result of insect bites, falls, and noxious plants. Inexperienced trekkers may quickly tire

Preventing Heat-Related Illness The following guidelines may help prevent heat-related illness: • Before undertaking long-distance trekking in the tropics, acclimatize by spending at least 5 days in a hot, humid environment and engaging in moderate daily exercise. This acclimatization will be lost within a week if not maintained. • Avoid alcohol and certain drugs. Medications, such as β-blockers, anticholinergics, and diuretics, increase the likelihood of heat-related illness and should be avoided if possible. • Wear ultra-lightweight, light-colored, and loose-fitting cotton clothing and a wide-brimmed hat. As previously noted in this chapter, shirts should always be made of cotton. Pants, however, may be made of synthetic fabrics such as nylon Supplex or Taslan. • Whenever possible, have a native porter carry all gear. • Maintain adequate hydration. Before setting off on the trail, drink a liter of disinfected water. One-half hour later, drink a second liter. One hour after the second liter, drink a third, then consume about 1 L every 2 to 4 hours during strenuous trekking. Heat cramps, often severe, tend to occur when large amounts of water are ingested without adequate salt replacement. Oral rehydration solution (ORS) products, available in premeasured powder form, added to a liter of disinfected water, provide an ideal balance for replacing lost electrolytes. The first liter of disinfected water (noted previously) consumed before trekking should include a packet of ORS. After especially strenuous days, trekkers should drink an additional one-half packet of ORS. The rice-based ORS product CeraLyte has a high absorption rate and reduces ongoing fluid loss in diarrheal illness (see Chapter 68). In the United States, rice-based oral rehydration therapy packets may be obtained from Cera Products (http://www. ceraproductsinc.com) and glucose-based ORS from Jianas Brothers (816-241-2880). To eliminate or reduce the chances of intensely painful leg cramps rousing you from sleep, always perform calf-stretching exercises before falling asleep.

Sport beverages do not contain the ideal concentration of electrolytes found in ORS and are not recommended. Salt tablets are not recommended because they are gastric irritants. Elete Electrolyte Add-In liquid contains concentrated sodium, chloride, magnesium, and potassium for electrolyte supplementation (http://www.eletewater.com).

UNEXPECTED ISOLATION Various factors contribute to unexpected isolation in the jungle. These include inclement weather, mechanical problems, or political turmoil that shuts down public transportation. Many people respond with anger and irritability, which can be devastating to group dynamics. Travelers should accept the situation and use the additional time to appreciate the tropical forest, take photographs, or read paperback books. It helps to shift out of gear mentally and allow the intellectual machinery to idle. Nearly everyone has the experience of driving for hours and arriving at a destination with virtually no recollection of the trip. The same can be accomplished in the village setting, lying around on a hammock. The hours and days pass surprisingly quickly, akin to cruising in a sailboat with no engine. The person learns patience and develops an appreciation that the rhythms of nature are not governed by the ticking of a clock.

CAMP LIFE Shelter Natives rarely spend the night in makeshift shelters. It is usually best to use existing dwellings for a hammock or sleeping pad. Common courtesy governs placement inside the hut of a native. Travelers should ask about taboo spots before bedding down. When huts are not available for use, a tarpaulin provides satisfactory shelter from the rain. Rip-stop polyethylene tarps (2.4 × 3 m [8 × 10 feet]) are lightweight and waterproof. Coated nylon tarps are also acceptable but must be sealed with a product such as Seam Grip. Figure 43-7 illustrates a typical method for erecting a tarp. First, a thick line is run 2.1 to 2.4 m (7 to 8 feet) off the ground between two trees and cinched tight. The long axis of the tarp

Shingled leaves

Tarp

60°

° 72

44°

84°

FIGURE 43-7  Construction of mosquito netting for use with a hammock: Sleeve hole is 2.2 m (88 inches) in circumference; small hole is 0.5 m (18 inches) in circumference; smallest holes (for supporting sticks) are 10.2 cm (4 inches) in circumference.

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CHAPTER 43  Jungle Travel and Survival

of unfamiliar food and miss usual comforts. Experienced leaders therefore prefer to limit expeditions to not more than 3 weeks.

PART 5  RESCUE AND SURVIVAL

1

2

3

4

FIGURE 43-9  Camel hitch.

FIGURE 43-8  Half hitch.

is centered over the rope, and a rope attached to the middle grommet on each end is tied to the tree. The corner grommets are tied to available trees, bushes, or strong clumps of grass; a tie-down in the middle on each side is also helpful. The sides of the roof should be made high enough to enter and exit conveniently, but not so high that driving rain can come in at an angle. Once the tarp is up, the hammock ropes are run through the sleeves of the mosquito net. Then the hammock is slung. The hammock should be suspended high enough that it will not sag to the ground during the night because it naturally sags under an adult’s weight. Next, the mosquito net is suspended. The ropes running from tree to tarp, from tree to mosquito net, and from tree to hammock should be sprayed with DEET-containing insect repellent (or permethrin insecticide) to keep ants and other pests from using the ropes as trails. Finally, a few broad leaves (banana leaves or heliconia) folded at the spine are draped over the bare rope extending from the tarp to the tree and shingled in such a way as to keep rain from running down the hammock ropes onto the hammock itself (see Figure 43-7). Knowledge of two knots is needed for slinging a hammock. These knots always hold and always come undone quickly without jamming. The half hitch is used to tie the hammock to a horizontal beam, as follows (Figure 43-8): 1. Pass the working end of the rope around the object to which it is to be secured. 2. Pass the working end of the rope around again without crossing over itself. 3. Bring the end over and around the standing part and through the loop that has just been created. You have completed a half hitch. 4. Make a second half hitch below the first half hitch. 5. Pull tight. The camel hitch is used to tie the hammock to a vertical post, as follows (Figure 43-9): 1. Make three turns around the vertical pole. 2. Bring the working end up and over the turns. 3. Make a turn at the top and pass the end back under itself. 4. Make a second turn at the top and pass the end back under itself. Weather conditions can change in minutes, and travelers must be prepared with adequate shelter. The use of a tent as shelter in the tropical rain forest is not recommended. Clearing a tent space is time consuming, and the stumps remaining from cutting saplings and bushes invariably perforate the floor. Air does not circulate; after a restless night sweltering in the tent, the traveler emerges tired and irritable. Food Solitary travelers or small groups usually do not need to pack large amounts of food. Edibles are always available in areas 824

inhabited by friendly natives. As a general rule, food is safe to eat if it is peeled, cooked, or boiled. Travelers in the tropics must be open to eating local food. Most creatures are edible, such as boiled caiman (alligator), cooked capybara (a 50-kg [110.2-lb] rodent), or roasted palm grubs (larvae of Rhynchophorus). Raw palm grubs, up to 12.7 cm (5 inches) long, are tasty and a favorite of Amazonian Indians (Figure 43-10). They are eaten by slashing open the thin integument with the thumbnail, extracting and discarding the intestinal tract, placing the opened skin to the mouth, and sucking out the turgid contents. In addition to palm grubs, more than 20 species of edible insects, including ants and termites, are collected year-round by the people of Amazonia.12 Large hairy spiders, Theraphosa leblondi, 25.4 cm (10 inches) in diameter, are often roasted on an open fire. After the barbed hairs are singed off, the spiders are placed in the embers. They have a shrimp-like taste. Indians of the Americas have perfected the art of smoking fish and meat so that they remain safe to eat for long periods. It is common to see huge hunks of tapir meat or slabs of 100-lb catfish resting on racks, coal black from the smoking process. Table 43-1 illustrates the diversity of wild game from 867 day hunts by members of the Waorani tribe of Ecuador.53 The Aguaruna and Huambisa of Peru conceptually recognize and classify as food nearly 500 species of animals.2 The tropics have an abundance of flora as food. The yard-long heart of palm is cool and delicious when eaten in its raw state or may be included in a soup spiced with tropical herbs. Familiar tropical fruits include papaya, mango, pineapple, and passion fruit (genus Passiflora). Many New World fruits have no name in English and generally have not found their way into the world market. These include chirimoya, guanabana, pitahaya, naranjilla, uchuva, tamarillo, zapote, sapodilla, and badea.31,34,49 The boiled fruit of the peach palm, Bactris gasipaes, is nutritious and flavorful.

FIGURE 43-10  The palm grub is a favorite delicacy. (Courtesy John Walden.)

Rank

Common Name

Species Name

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36

White-lipped peccary Wooly monkey Collared peccary Howler monkey Tapir Salvin’s curassow Cuvier’s toucan Capuchin monkey Spix’s guan Blue-throated piping guan Brocket deer Capybara Paca Coati Great tinamou Spider monkey Saki Ivory-billed aracari Red squirrel Gray-winged trumpeter Agouti Golden-collared toucanet Tayra Squirrel monkey Speckled chachalaca Nocturnal curassow Cayman Mealy parrot Red-mantled tamarin Scarlet macaw Douracouli Titi Squirrel Acushi Yellow-ridged toucan

Tayassu pecari Lagothrix lagotricha Tayassu tajacu Alouatta seniculus Tapirus terrestris Mitu salvini Ramphastos cuvieri Cehus albifrons Penelope jacquacu Pipile pipile Mazama americana Hydrochoerus hydrochaeris Agouti paca Nasua nasua Tinamus major Ateles belzebuth Pithecia monachus Pteroglossus flavirostris Sciurus igniventris Psophia crepitans Dasyprocta fuliginosa Selenidera reinwardtii Tayra barbara Saimiri sciurea Ortalis guttata Nothocrax urumutum Caiman sclerops Amazona farinosa Saguinus fuscicollis Ara macao Aotus trivirgatus Callicebus moloch Sciurus cocalis Myoprocta pratti Ramphastos culminatus Miscellaneous small birds (numerous species)

Gross weight

Total Weight (kg [lb])*

Percentage of Gross Weight

4940.1 (10,891.1) 3873.5 (8,539.6) 2740.6 (6,042) 2197.4 (4,844.4) 1314.4 (2,897.8) 610.9 (1,346.8) 414.4 (913.6) 400.8 (883.6) 301.7 (665.1) 261.8 (577.2) 253.4 (558.7) 226.5 (499.3) 194.8 (429.5) 130.6 (287.9) 116.5 (256.8) 110.1 (242.7) 100.0 (220.5) 86.1 (189.8)  82.9 (182.8) 66.5 (146.6)  47.5 (104.7)   30.4 (67) 27.3 (60.2)  23.7 (52.2)  21.6 (47.6)  20.4 (45)  20.0 (44.1)  19.6 (43.2)  18.7 (41.2)  18.2 (40.1) 17.6 (38.8)  17.2 (37.9)   15.4 (34) 11.1 (24.5)  11.0 (24.3)  29.3 (64.6) 

26 21 15 12 7 3 2 2 2 1 1 1 1 1

18,772.1 (41,385.2)

100

5

*Includes only those species whose total weight was more than 10 kg (22 lb).

The banana and its cousin, the plantain, provide a large percentage of the total caloric intake of natives in the American and African tropics. Curiously, in many native villages, it is difficult to find the sweet, finger-length bananas and the common yellow bananas exported from tropical countries. The green plantain features prominently in the daily fare of inhabitants of the tropics. The plantain has little taste and is exceptionally dry. Yucca (manioc or cassava), Manihot esculenta, is a staple source of carbohydrate nutrition throughout the Americas and much of tropical Africa. The two kinds of yucca, “sweet” and “bitter,” are the same species but differ in their distribution and amount of a poisonous constituent, a cyanogenic glycoside, in the root.42 Sweet and bitter yucca cannot be easily distinguished; one must know which variety was planted. Sweet yucca, common in the eastern lowlands of the Andean countries of Colombia, Ecuador, and Peru, is eaten after the bark containing the toxic substance is peeled off and the root boiled. With bitter yucca, the poison is more concentrated and distributed throughout the root, so it must be extracted before consumption. Amerindians use an apparatus called the tipití (Figure 43-11) to express the poisonous juice from the peeled and grated flour of manioc roots. Travelers in a large group should carry dried, packaged foods because the host village might not be able to provide sufficient foodstuffs or travelers might pass through isolated and uninhabited regions. Packaged foods should also be carried by travelers in regions where natives are unfriendly. Dried instant food needs only water to make a meal. A few selections should be tried before a large supply for field use is ordered. It is not necessary to add hot water to all packaged foods; adding disinfected, ambient-temperature water produces acceptable results for most foods. Drawbacks to prepackaged

FIGURE 43-11  The tipití expresses poisonous juice. (Courtesy William H. Crocker, Department of Anthropology, Smithsonian Institution.)

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CHAPTER 43  Jungle Travel and Survival

TABLE 43-1  Rank Order of Species by Total Weight

PART 5  RESCUE AND SURVIVAL

foods include expense, space, and disposing of the empty foil packages. I carry the following supplemental food items for 2- to 3-week treks into remote but inhabited jungle regions: one 56.7-g (2-oz) heavy-duty poly bottle filled with salt and pepper mixed half and half, a few pounds of rice, a tin of long-keeping butter (or oil) for cooking the rice, a few tins of tuna or sardines packed in tropical hot sauce, and several PowerGel energy packets for trail snacks. Potable Water Potable Aqua (tetraglycine hydroperiodide 16.7%) iodine tablets are recommended for disinfecting water because they are easy to use and have proved effective in killing bacteria and many parasite cysts in approximately 30 minutes (see Chapter 67). Potable Aqua iodine tablets are ineffective against Cryptosporidium. (Diarrheal illness due to Cryptosporidium species usually resolves without therapy in 10 to 14 days in immunologically healthy people.) Potable Aqua chlorine dioxide tablets are effective against viruses, bacteria, Giardia, and Cryptosporidium. However, they require a 4-hour treatment time to kill contaminants. Water filters are not recommended for purifying jungle water; they clog with silt and must be cleaned frequently. If a water filter is used, it should be fitted with a good prefilter to catch the excess silt.

JUNGLE HAZARDS The following hazards are common or believed to be common in the wilderness jungle setting. Other chapters provide additional insights and viewpoints, particularly with respect to treatment. Arthropods Ants.  The conga ant, Paraponera clavata, 2.5 to 3.8 cm (1 to 1.5 inches) long, is the terror of the American tropics. The bite of these large black ants can produce intense pain and fever for up to 24 hours, which accounts for the Spanish name, veinte-cuatro (twenty-four). Fortunately they are conspicuous because their large, shiny black bodies tend to stand out against foliage. Special caution is needed when ducking under or climbing over trees, where ants are often found. A conga bite requires strong pain medication and perhaps the injection of lidocaine at the bite site. Travelers should avoid touching trees and bushes. Many plants in the tropics provide a home and food for ants, which provide aggressive defense of the plants. Fire ants are common throughout the tropics and subtropics. Their bite causes discomfort but not excruciating pain. Characteristic sterile pustular lesions in crops often result from fire ant stings. Chiggers.  Chiggers, a form of mite, are a problem throughout equatorial regions. Whereas temperate-climate chiggers may cause mild discomfort for a few days, the tropical chigger sets up an inflammatory and allergic reaction that often persists for weeks. In the South American tropics, chiggers are found in grassy fields, such as jungle airstrips and yards around mission compounds. Walking through chigger-infested areas without protection could leave a person covered with chigger bites. After a few days, the victim begins to itch mildly. As the days pass, the itching intensifies and seems to come in waves. Prevention is the best treatment. Areas known to be infested with chiggers should be avoided when possible. Spraying shoes or boots and lower pant legs with repellent containing DEET or picaridin is highly effective. Pretreatment of clothing with permethrin is recommended. Travelers in the American tropics should never walk through grassy areas in shorts. Jigger Flea.  Tunga penetrans, the jigger flea or chigoe, originally found in South and Central America, has now spread to East and West Africa and India. The fertilized female flea enters the feet through cracks in the soles, between the toes, and around the toenails. The female swells to the size of a pea and may be readily identified as a white papule with a central pit, 826

through which the female extrudes excrement and eggs. When eggs are ripe for release, intense itching causes scratching that helps release large numbers of flea eggs. Incomplete removal of the jigger frequently results in complications caused by secondary infection. A simple extraction technique virtually eliminates complications. Open the skin over the nest of eggs with a surgical blade. Fold back the flaps, remove the easily identified egg sac, and with tweezers, remove the head of the female flea, which can be seen once the egg sac has been removed. Wash the area with hydrogen peroxide.19 Myiasis.  Myiasis (skin infestation by fly larvae) is common in many regions of sub-Saharan Africa (the tumbu fly, Cordylobia anthropophaga) and Central and South America (the human botfly, Dermatobia hominis). The victim finds an itchy swelling that slowly enlarges into a lesion with a single breathing pore from which bubbles emerge or from which drains slightly bloody fluid. Later, movement is felt under the skin as the developing larva wriggles around. Removing the larvae before they emerge on their own is generally advised. Surgical excision, however, should be undertaken with caution because accidental rupture of the larval tegument can lead to secondary infections. Various methods to close off the breathing pore so the larva will emerge on its own include application of bacon fat, meat, chewing gum, or petroleum jelly. Scorpions and Spiders.  Stinging scorpions and venomous spiders are common throughout the tropics and provide another reason to exercise caution before sitting down or placing a hand on logs, bushes, or the ground. The large, aggressive banana spider, Phoneutria nigriventer,48 causes excruciating pain, which may require local anesthetic infiltration of the bite site for relief. Venomous Moths, Butterflies, and Caterpillars.  The larvae and adults of a number of moths (genus Hylesia) and butterflies bear venomous hairs that may cause skin eruptions. A rash may result from direct contact with the adults or larvae or by windblown hairs. Direct contact with certain Amazonian caterpillars can cause disabling pain. In the Amazon tropics, noxious smoke from burning garbage (e.g., plastic wrappers) may cause tree-dwelling caterpillars to loosen their hold on overhead branches and rain down on unwary campers. Treatment of Lepidoptera envenomation may require injection of lidocaine at the site of intense pain and administration of analgesics, antihistamines, and corticosteroids. Moth hairs may be removed with adhesive duct tape or sticky lint removers used upon clothing. Wasp and Bee Stings.  Sudden, intense pain from the sting of certain species of tropical wasps and bees can be so severe that it knocks the victim to the ground as though hit with an electric shock. Perfumes and brightly colored or flower-patterned clothing should be avoided.25 Bird-watchers should not venture too close to the hanging nests of yellow-rumped caciques and oropendolas because wasps are invariably associated with these nests. Fish Stingray.  The stingray, a flattened, cartilaginous cousin of the shark, may be encountered buried just beneath the surface of the bottom ooze in tropical rivers and streams throughout the Amazon basin, Africa, and Indochina. Rays inflict injury by lashing upward with the caudal appendage, driving one or more retroserrated venomous spines deep into the victim’s foot, ankle, or lower leg. This produces agonizing pain, often accompanied by headache, vomiting, and shortness of breath. After the initial phase of envenomation, tissue necrosis may develop. Wearing shoes or boots when wading in water does not always prevent a stingray from jabbing its barb into the foot or leg. Prevention lies in shuffling the feet along the bottom so that the ray will have enough warning to glide away safely. Electric Eel.  The so-called electric eel (actually an eel-shaped fish) is encountered from Guatemala in Central America to the

Candirú.  The candirú is a toothpick-sized parasitic catfish that inhabits Amazonian waters and may invade the urethra of urinating humans. Orifice penetration by the wily candirú can be prevented by wearing a tight bathing suit and not urinating underwater. Native methods of dislodging these fish from the urethra include drinking a tea made from the green fruit of the jagua tree, Genipa americana L.5 Surgery is the recommended treatment. In his exhaustively referenced book entitled Candiru: Life and Legend of the Bloodsucking Catfishes, author Stephen Spotte downplays much of the lore regarding this little fish.43 Piranha.  Although no human deaths have been documented, piranha have nipped off the fingertips of canoeists dangling their hands in the water. Attacks on humans by the speckled or darkbanded piranha, Serrasalmus maculatus, in dammed waters in Brazil have been linked to the fish’s behavior of defending its brood from perceived predators.20 Mammals Bats.  Vampire bats are found throughout Mexico, Central America, and South America, especially in areas that have large cattle ranches. Sleeping humans are unaware of the presence of a feeding bat; the phlebotomy is painless. Both vampire and fruit bats carry rabies. Sleeping under mosquito netting prevents bat bites. The risk for rabies can be reduced by prophylactic human diploid cell rabies vaccine. Dogs.  Most native groups keep dogs for hunting. Populations with a history of recent tribal warfare often keep packs of dogs close by as an early warning system. These semiwild dogs should be treated with caution; threatening them may cause immediate attack because they are not easily intimidated. When approaching huts or villages, the traveler should allow porters to deal with the dogs. Dogs intent on biting often adopt particular behavior patterns. A dog protecting its territory crouches low, straightens its back and tail, emits a deep guttural growl, and stares fixedly at a specific part of the person’s anatomy. Such behavior indicates imminent attack, and a sharp blow to the nose may be necessary. Freezing in place may prevent an attack, and direct eye contact should be avoided. Jaguars.  Jaguar attacks are rare. Recommendations are based on advice for avoiding a cougar attack. Increase your apparent size by raising your arms above the head and waving an object, such as a backpack or stick, or opening a jacket. Yell, shout, whistle, or speak loudly and forcefully in a low, deep tone of voice. Back away slowly; do not turn your back and run.11 Reptiles Snakes.  Snakebites are rare; 450,000 hours of fieldwork at sites in Costa Rican rain forests were documented without a single snakebite10 (see Chapters 54 and 55). Most poisonous snakes tend to blend into their surroundings, and non-natives rarely see them. The most effective protection is putting a jungle-reared guide in front on the trail. Natives almost always spot a poisonous snake and can quickly dispatch it. Snakes are often encountered along the shorelines of rivers and small streams. Particular caution is needed when hiking in such areas or when disembarking from a canoe or rubber raft. In the forest, the hiker should always step onto a log and then step away from it. The log should not be straddled; snakes often are encountered where the log makes contact with the jungle floor. Because many venomous snakes in the tropics are heat seeking and hunt at night, caution is needed.

Anacondas (water boas) feature in the folklore of all native cultures in the regions of Amazonia where these enormous snakes (up to 9  m [29.6 feet] long) live. These nonpoisonous snakes kill by looping coils around prey and then tightening the coils, suffocating the victim. Anecdotal reports of anacondas attacking and swallowing humans, particularly children and women bathing at the edge of jungle streams, are unconfirmed. Alligators and Crocodiles.  Although they appear torpid lying in the sun, alligators and especially crocodiles can move amazingly fast. Humans cannot outswim or outrun a charging crocodile. Bites should be treated with thorough cleaning of the wound, surgical debridement if necessary, tetanus prophylaxis, and an appropriate antibiotic. A study of the oral flora of 10 alligators captured in Louisiana revealed various aerobic and anaerobic organisms responsive to trimethoprim-sulfamethoxazole.15 A fluoroquinolone or third- or fourth-generation cephalosporin should be considered.27 Plants Armed or Spine-Bearing Plants.  Spine-bearing trees abound in forested areas of the tropics. The peach palm (Bactris gasipaes), a tall, slender palm with heart and fruit mesocarp prized by natives, is found from Nicaragua to Bolivia. The trunk of this tree is ringed with needle-sharp spines (Figure 43-12). Peach palms often grow alongside trails. Contact with this palm can result in penetration of spines deep into the flesh. Spines that enter a joint space may require surgical extraction. Secondary infection and inflammation often occur. Chicha.  Throughout much of Latin America, particularly in the Andean countries, a beer-like beverage known as chicha is consumed. Fermentation is initiated by masticating maize, cassava, plantain, or the fruit of the peach palm. Salivary enzymes hydrolyze the starch to sugar, resulting in a beer of 2% to 4% alcohol content. Some traditional populations consume copious amounts of chicha: the average daily intake among men of the Shuar and Achuar tribes of Ecuador and Peru is 7.6 to 11.4 L (2 to 3 gal); for women, 3.8 to 7.6 L (1 to 2 gal). From a health and safety standpoint, and in the social context, there are several aspects to chicha consumption that give pause. In addition to aesthetic considerations arising from its origin by way of human spit, the starchy substrate used for preparing chicha is often kneaded by unwashed hands—a ready source of pathogens transmitted by the fecal–oral route. Although natives accustomed to daily chicha consumption seem to be unaffected with alcohol-related instability on the trail, the non-native jungle traveler will almost certainly experience problems maintaining balance, particularly when crossing single-log bridges, if excess chicha is consumed before or during trekking. Because chicha consumption is such a significant element in the social fabric of many tribes, to refuse to partake of the beverage can be a social gaffe. I have found it acceptable to inform my hosts, in a joking manner that, I cannot trek and drink chicha

FIGURE 43-12  Needle-sharp spines ring the peach palm. (Courtesy John Walden.)

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La Plata River in South America and is especially common in the Amazon region. A person can drown after being stunned by a jolt from this fish. Electric eels are said to prefer deep water. Inhabitants of regions heavily infested with eels report a slight tingling sensation when one is close. No practical way exists to prevent these shocks.

PART 5  RESCUE AND SURVIVAL

throughout the day because “I stagger and fall off logs,” but that I will join in the evening rounds of ritual drinking. Eye contact with a woman who is serving chicha is a cultural signal to initiate a sexual encounter among the Shuar and Achuar. To avoid misunderstanding, hold the chicha bowl in the outstretched hand with the head turned to face slightly to one side or downward; it is not necessary to avert eye contact in a dramatic fashion. Saw Grass.  In many regions of the tropics, saw grass is an everpresent nuisance. The scalpel-like blades of this grass can slice into exposed skin. Even when treated with antibiotic ointment, the lacerations often take 1 to 2 weeks to heal. Hikers should avoid saw grass; special care is needed when working with a machete. Hallucinogenic Plants Hallucinogens permeate nearly every aspect of life in primitive societies. They play roles in health and sickness, peace and war, home life and travel, hunting and agriculture; they affect relations among individuals, villages and tribes. They are believed to influence life before birth and after death.39 To ignore the ubiquitous use of psychoactive drugs among jungle dwelling tribesmen throughout Central and South America is to deny a key element in understanding the rich and complex weave of Amerindian life. Powerful drugs, such as ayahuasca (Banisteriopsis), brugmansia, the Virola snuffs, and yopo (Anadenanthera peregrina), are used by shamans and individuals seeking the truth through visions and a supernatural experience. Ayahuasca.  Also known as caapi, natema, pinde, and yajé, this woody vine (Banisteriopsis caapi) is found throughout western Amazonia in Colombia, Ecuador, Peru, Bolivia, and Brazil. The term ayahuasca derives from the Quechua language and has been translated as “vine of the soul.” The hallucinogenic activity derives primarily from harmine, the major β-carboline alkaloid in the plant. Indigenous peoples use additives (leaves of the shrub Psychotria and a forest liana Diplopterys cabrerana) to prolong and strengthen the intoxication. In addition to experiencing vivid visual hallucinations, users often report a distinct sense of clairvoyance. Adverse effects of ayahuasca ingestion include nausea, dizziness, and vomiting. For some users, the visual hallucinations are intense and disturbing. Brugmansia.  Commonly known as borrachero, floripondio, huacacachu, or toá, the lovely, large bell-shaped flowers of brugmansia are encountered throughout the Andean foothills of western Amazonia. Despite their beauty, these are among the most powerful and dangerous of plant hallucinogens. The leaves and seeds of these bushy plants contain tropane alkaloids, including scopolamine, hyoscyamine, atropine, and secondary alkaloids.41 The effects on the user tend to be highly unpleasant

to the degree that those who partake of brugmansia often must be restrained. Virolas.  Known as epena, nyakwana, and yakee among indigenous populations of northwestern Amazonia, these hallucinogenic snuffs are made from the blood-red resin of the inner bark of trees (Virola species). The narcotic effect is due to tryptamine alkaloids. The drug acts rapidly. The excitement phase is followed by lack of coordination, copious nasal discharge, and vomiting. A curious effect of ingesting Virola snuff is macropsia, in which objects, including hallucinatory spirits (known as hekulas among the Yanomami Indians of Venezuela and Brazil), appear greatly enlarged. Yopo.  Seeds of Anadenanthera peregrina, a South American tree of the bean family Leguminosae, are used to prepare this tryptamine-containing hallucinogenic snuff. Employed by Indians in the Orinoco basin region of Amazonas state, Venezuela, and adjacent regions of northernmost Brazil, yopo is inhaled to communicate with spirits during the phase of intoxication. In preparation, seeds are removed from the distinctive dangling pods and, after being moistened, rolled into a paste that is roasted over a fire and hardened for later use. The dried paste is pulverized and the resulting powder mixed with lime from snail shells or ashes from certain plants. The narcotic is blasted into the nostril through a long tube with the help of an assistant (Figure 43-13). The user experiences immediate effects, including muscular twitching, nausea, profuse nasal secretions, and visual hallucinations.33 As in the case of Virola snuffs, an abnormal exaggeration of the size of objects is common.39 Detailed discussions of additional New World hallucinogens, as well as African and Asian hallucinogens used by jungle dwelling tribesmen, are found in the references listed online at www. expertconsult.com.39-42 Should travelers partake of hallucinogens used by tribesmen? Some argue, with a certain validity, that outsiders cannot possibly acquire insight into the Amerindian’s sense of the cosmos without ingesting their mind-altering drugs and so make the case for limited use by anthropologists and others who plan to live and work closely with tribal populations for prolonged periods. Although none of the hallucinogens discussed in this chapter is known to be addictive, “recreational” use could, in the author’s opinion, have significant adverse consequences for certain individuals, including a lingering blurring of the sense of reality. Therefore I recommend that these powerful intoxicants be avoided.48

MISCELLANEOUS HAZARDS Poison-Dart Frogs Poison-dart frogs are tiny, brilliantly colored species of the genus Dendrobates. They are encountered in Central America and FIGURE 43-13  Hallucinogen is administered through a long tube. (Courtesy John Walden.)

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Streams, particularly narrow ones bounded by vertical banks, can rise 6.1 m (20 feet) in a few hours as a result of intense rains. Camp should not be set up on an island or beach in a small canyon during the rainy season. A cloudburst in the headwaters can send a wall of water rushing downstream, even though it may be a clear, moonlit night at the campsite.

FIGURE 43-14  Poison-dart frog. (Courtesy John Walden.)

northern South America (Figure 43-14). Phyllobates terribilis secretes a toxin from its skin so powerful that a lethal dose could be absorbed if enough secretion entered an open wound. It is wise to avoid all contact with brilliantly colored frogs, caterpillars, and snakes. Falling Trees Tropical trees do not have deep roots and often fall in relatively modest winds. In many regions of the world, risk for snakebite is significantly lower than the risk for injury or death from falling trees. In the forest, hammocks should be slung away from large trees. Travelers setting up camp should always look up at the branches of any trees near camp; although the base of the tree may appear sound, higher areas may be rotted. Fording Rivers The hiker should never attempt to cross a fast-flowing or deep river with a pack on his or her back. Regaining footing in a rapidly moving current can be difficult. Unless experienced in crossing such streams, the traveler should take the hand of a native guide or porter. Canoe Travel Most riverain peoples of the tropics are extraordinarily skilled at hewing felled trees into dugout canoes that perfectly meet their daily needs; the Chachi (Cayapa) Indians of northwest Ecuador construct canoes of such symmetry and visual delight as to qualify for exhibit in any museum of art. These craft are often “tippy” in the extreme and pose a problem for the inexperienced traveler not reared from infancy using these watercraft and therefore lacking the innate sense of balance of the local population. When crossing particularly hazardous stretches of jungle rivers, care must be exercised: It is usually best to sit directly on the floor of the canoe to lower the center of gravity and thus avoid a sudden reflex movement that would tip the canoe over. Log Bridges On frequently used trails, natives generally place a single log across creeks, ravines, and swampy areas. These log bridges may be up to 6.1 m (20 feet) high and 22.9 m (75 feet) long. Good balance is essential. Because a backpack impairs balance, a porter should carry it across. Scooting across a particularly dangerous log bridge on one’s buttocks is always an option. Mercury Contamination Travelers to the Amazon basin should be aware of the serious, widespread contamination of waterways by mercury that gold miners (garimpeiros) use to process their ore. Although most manufacturers of potable water treatment and filtration systems do not specifically claim to remove mercury, any activated carbon system should reduce the risk. Pres 2 Pure makes a line of filters claimed to remove mercury. Travelers should exercise caution in choosing rivulets as a source of potable water in areas where mercury contamination is known or suspected.

Traveling With Children in the Tropics The following guidelines should be considered when trekking with children in the tropical forest: • Do not attempt a daylong hike. Unlike indigenous children, visitors cannot hike all day in the humid tropical forest. Preadolescents should hike only 1 to 2 hours; children ages 12 to 16 years can hike 2 to 3 hours. Do not subject a child to jungle trail conditions unless the child has had extensive experience hiking in temperate climates. • Do not attempt difficult or dangerous trails. • Avoid trekking during the rainy season. • Keep the child well hydrated. • Provide proper footwear (running or hiking sneaker type of shoes or boots with an adequate tread). Avoid leather boots. • Keep the child ahead of you and behind a native guide. Children should not be out of sight on the trail. • When wading across rivers, have an adult native guide hold the child’s hand. • Always have children wear a properly sized life vest while rafting, taking canoe trips, or crossing deep, swift, or wide rivers. • Do not allow a child to carry any equipment in a daypack other than two liter-sized bottles of drinking water. • Ensure that routine vaccinations are up to date. Special vaccinations, such as yellow fever and typhoid, should be considered for certain jungle areas. Hepatitis A vaccine is recommended. Antimalarials are indicated. Any child who plans to visit the tropics should be a strong swimmer. Many natives begin swimming in infancy and are accustomed to deep or rapidly flowing water that would be extremely hazardous to visiting children. Swimming holes are often located in the swift-flowing outer loop of jungle rivers, where depths may reach 1.8 m (6 feet) or more within a yard of the shoreline.

Survival Every year, inexperienced people enter the jungle and become lost. After a person ventures only a mere few yards into the forest, especially jungle that has been cleared and is now a tangle of secondary growth, everything begins to look the same. To avoid becoming lost, travelers should always have an experienced guide when traversing unfamiliar territory. Tribal peoples of the world’s tropical forests have an uncanny ability to find their way and arrive at the desired destination, even after days of travel. They can always find food and water and, if necessary, rapidly construct a shelter or weapon. Occasionally, travelers are left behind on the trail by indigenous guides. Unintentional desertion occurs when trekkers hire natives who have had no experience with neophytes. Realizing that their charges cannot keep up on the trail, the guides run ahead and sit down to rest, not knowing that others cannot navigate the trail alone. Travelers who want to avoid being left behind on the trail should hire a guide who is experienced in traveling with non-natives. Suitable guides and porters can usually be identified with the help of a village leader, local school teacher, village health worker, missionary, or anthropologist.

RESCUE STRATEGIES For individuals in a jungle survival situation, lifesaving items include a large-scale map, Global Positioning System (GPS) unit, some form of electronic voice communication, and a machete. Topographic maps are available from numerous international and national mapping agencies. Satellite images with extraordinary 829

CHAPTER 43  Jungle Travel and Survival

Rising Rivers

PART 5  RESCUE AND SURVIVAL

resolution are available from Space Imaging (800-232-9037; http://www.spaceimaging.com) or the U.S. Geological Survey (Eros Data Center, 47914 252nd St, Sioux Falls, SD 57198-0001; 800-252-4547; http://edcwww.cr.usgs.gov). Small, lightweight GPS units display precise latitude, longitude, and altitude. Such information is extremely useful for navigation and for communicating one’s location to rescue aircraft. Newer units quickly lock onto satellites and are more likely to work under the jungle canopy. Trekkers contemplating an expedition into largely uninhabited and unexplored regions should consider buying a compact personal locator beacon, such as those made by McMurdo Pains Wessex Inc (http://www.mcmurdo.co.uk) or ACR Electronics (http://www.acrelectronics.com). These 406-MHz units offer a reliable method of alerting various rescue services through a global satellite system. These units should be activated only in a true emergency when lives are at risk. Handheld satellite phones are available for worldwide communication. Although currently expensive to purchase and operate, their potential to provide rescuers with precise GPS location makes these lightweight phones worthy of serious consideration for inclusion for wilderness travel, especially on expeditions into areas of extreme isolation. I strongly recommend the inclusion of satellite phones in one’s gear if going off the beaten path. Portable solar panels are lightweight and allow the expeditioner to charge electronics, such as GPS units, satellite phones, or digital cameras. Lightweight, handheld, very-high-frequency (VHF) aircraft transceivers are excellent for emergency communications. Visitors to remote areas should know the radio frequencies used by rescue aircraft. VHF transceivers are line-of-sight instruments and thus are most useful when aircraft are overhead without objects, such as trees or mountains, between the handheld unit and the aircraft. In many regions of the world, the Mission Aviation Fellowship (MAF) provides air service to remote airstrips in small villages. If assistance is needed, a handheld radio transmitter can be used to call an MAF STOL aircraft. Bush pilots appreciate having information on the condition of seldom-used airstrips. A crude but acceptable device can be constructed to measure airstrip hardness (Figure 43-15). Cut a pole exactly 5.1 cm (2 inches) in diameter and about 1.8 m (6 feet) long. Starting exactly 15.2 cm (6 inches) from one end, taper that end to a point. Lash a cross-member on the pole, and have a person weighing about 77 kg (170 lb) stand with assistance on the cross-member. Make a map of the strip, noting the depth to which the pointed end of the pole sinks into the ground at several dozen sites. Communicate this information to the pilot by radio. If the pole goes in only 5.1 cm (2 inches) in most areas, the strip is considered ideal; 5.1 to 10.2 cm (2 to 4 inches) is

A

B

marginal; penetration beyond 10.2 cm (4 inches) indicates that the airstrip is unsuitable for landing and takeoff. If rescue is not feasible, the traveler should continually move downstream at a fast pace. Inhabited areas usually have a trail running alongside a stream. The trail may veer away from the stream where natives have cut a path to connect two villages. Marking the trail every 9.1 m (10 yards) with a machete makes it easier to return to the starting point. To avoid confusion, the traveler should mark trees only on one side of the trail. Recall will be increased by audibly describing the surrounding topography as one hikes down the trail. Where human paths are in frequent use, identifying a trail is fairly easy. Seldom-used trails or any trail traversed during times of optimal plant growth may be extremely difficult for the nonnative to identify and follow. Even under adverse circumstances, however, there are clues to trail identification. Paradoxically, concentrating only on the actual footpath will almost certainly cause a person to lose sight of the trail. Think of the jungle trail not as a track on the ground but as the intestinal lumen of “some gigantic leafy creature,”21 with vertical margins, often an overhead horizontal boundary, and sometimes a visible path beneath the feet. Diagonally sliced saplings or neatly severed branches indicate someone has used a machete. There is a particular reflectivity off the ground where humans have trod; this reflectivity is the best way to follow a trail at night. These trail-finding clues are often so subtle that you may sense the trail rather than see it. Game trails meander and are narrower than human trails. In the jungle setting, navigation with a compass for a distance of more than 182.9 m (200 yards) is fraught with hazard. Travelers should not attempt to cut overland if lost, inexperienced, or on their own, unless a significant landmark is visible or sounds of humans or domesticated animals, indicating a settlement, are clearly heard. A raft may be constructed by lashing logs together with rope or tough, pliable jungle vines. Balsa (Ochroma pyramidale), a tall, fast-growing tree found throughout much of tropical South America as well as Central America into southern Mexico, is ideally suited for the construction of rafts due to the wood’s exceptional light weight, relative strength, and buoyancy. Balsa is often found growing alongside rivers and has the following characteristics: tall, columnar trunk with branches and leaves bunched at the top, which gives the tree a “skinny” look; beige or gray-beige trunk; bark that is smooth but tends to flake, giving it a mottled appearance; and broadly heart shaped, more or less three-lobed leaves. Six logs approximately 3 to 4.6 m (10 to 15 feet) in length and 20.3 to 30.5 cm (8 to 12 inches) in diameter, fresh cut from young balsa trees, are lashed together using rope. Thin, supple bark stripped from local trees handily growing at the river’s edge can be knotted together to form an excellent

C

FIGURE 43-15  A, Young man sharpening a stick to a point. B, Lashing a cross-member to a pole. C, Standing on the pole to take measurements of the depth of penetration into the airstrip. (Courtesy John Walden.)

830

lashing; certain jungle vines (lianas) pretested for suppleness and strength also can be knotted together for lashing (Figure 43-16). For down-river travel, a properly proportioned balsa raft can carry 3 to 4 adult men and adequate gear. Because water will usually wash over the surface of the raft, the buttocks and legs will be wet more often than not. Gear that must remain dry should be suspended from a tripod or tetrapod frame made of strong sticks, sharpened at one end and driven 5 to 7.6 cm (2 to 3 inches) into the balsa raft. Well constructed rafts are surprisingly stable, capable of safely running class II rapids, and will last for days with occasional relashing as the logs begin to shift over time. Subjectively there is a curious sense of tranquility stemming from the giving-motion of floating downstream on such rafts; one has the feeling of running with the river through fast-flowing stretches and small rapids, in contrast to fighting the current in a lurching canoe. Bamboo can also be used to construct a first-class raft. First, cut down 6 stalks of bamboo approximately 3 m (10 feet) long. Next, notch out windows on opposite sides of each section of bamboo near each end. Now, run a sturdy pole through the windows that have been lined up, and lash securely with rope or vines. A raft constructed in this manner should float for several days. Although it is possible to get away with one row of bamboo poles lashed together, better buoyancy is often obtained using two tiers. Because movement of the sections eventually breaks the bindings, it is best to coil up 18.3 m (20 yards) or so of additional vines for use when the original bindings wear out. An easier-to-build version involves a row of 3- to 6-m (10- to 20-foot) long bamboo poles, 6 to 10 stalks wide, with bamboo cross bracings spaced every 0.9 m (3 feet) lashed across the top. A log flotation device may be constructed by tying together two balsa logs or other lightweight wood placed 0.6 m (2 feet) apart44 (Figure 43-17). A “brush” raft may be made by placing buoyant vegetation within clothing or a poncho. Dry leaf litter (“duff”) or plants such as water hyacinth may be used.44

CHAPTER 43  Jungle Travel and Survival

FIGURE 43-16  Balsa raft and four-legged “tetrapod” frame to hold gear above the water.

Edibility Test In a jungle survival situation, the goal is to get out as quickly as possible. In the rare circumstance in which the victim cannot recognize any familiar edible plant; has been unable to capture minnows, crayfish, and insects; and, for whatever reason, is unable to walk out of the jungle or expect prompt rescue, the following abbreviated version of the Universal Edibility Test recommended by the U.S. Army45 and the SAS Survival Guide52 may be used to test an unknown plant: Caveats: • Never eat mushrooms. • Avoid unknown plants that have the following: • Milky or discolored sap • Beans or seeds inside pods hanging from trees • Bitter or soapy taste • Peach or “bitter almond” scent • Tiny barbs on the stems and leaves that could irritate the mouth and digestive tract Choose a plant that is abundant in the area. First, inspect the new plant, then crush a small portion; if it smells of bitter almonds or peaches, discard it. Check for skin irritation by squeezing some juice into the inner portion of the upper arm; if

A

FOOD Food is readily available in inhabited regions. Even abandoned villages yield enough fruit and vegetables on which to survive. Throughout the tropical world, bananas and the large plantain “cooking banana” are ubiquitous. Root crops, such as taro, yams, and yucca, should be sought. Yucca roots should be shredded or pounded and then boiled to release their toxic compounds. As an extra precaution, the wet pulp should be flattened into a “pancake” and cooked on a grate to eliminate any remaining volatile hydrogen cyanide gas. All land crabs, mammals, birds, freshwater fish, turtles, snakes, and lizards are edible, but should be cooked first to eliminate parasites. It is virtually impossible to kill game without firearms. In inexperienced hands, traps and snares are not effective. Much better results are obtained from fishing.

B FIGURE 43-17  Log flotation device. A, Two lightweight logs are tied together. B, Device in action.

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A

Cut vine high

B

Cut vine low

C

Drink

FIGURE 43-18  Water vine: First cut is high (A); second cut is low (B).

discomfort, a rash, or swelling occurs, discard the plant. Next, proceed through the following steps, waiting 15 seconds between each to see if there is any reaction, and discard if discomfort is felt: • Place a small portion on the lips • Place a small portion in the corner of the mouth • Place a small portion on the tip of the tongue • Place a small portion under the tongue • Chew a small portion Swallow a small amount and wait 5 hours. Drink or eat nothing else during this period of waiting. If, after 5 hours have passed, there is no soreness of the mouth, excess belching, nausea, vomiting, or abdominal pains, the plant may be considered safe.

plants), such as bromeliads (Figure 43-20). The water should be strained through a cloth.44 Water may be collected from a banana or plantain plant by cutting the plant about 0.3 m (1 foot) above the ground and scooping out the center of the stump into a bowl shape. The hollow thus formed fills immediately with water. The first two fillings have a bitter taste and should be dipped out. The third and subsequent fillings are drinkable. A banana plant can furnish water in this fashion for several days44 (Figure 43-21). In coastal regions, unripe (green) coconuts provide adequate supplies of refreshing milk. The milk of mature coconuts has a laxative effect and should be avoided.

WATER

Abandoned, temporary shelters previously constructed by natives on hunting expeditions seem to attract particularly aggressive, large biting spiders and stinging ants. Also, venomous snakes

Water may be made safer by boiling or using chemical disinfectants, such as Potable Aqua tablets. Drinkable water may be found in lianas, often called “water vines,” throughout jungle regions. Vines that contain water are fairly easy to identify because they tend to resemble the “grapevines” of North American forests and have rough, scaly bark. These vines may be several inches thick and contain surprising amounts of clear water. Vines that do not contain drinkable water tend to have smoother bark and, when cut, exude sticky, milky liquid. Travelers should not drink from vines that contain milky, latex-like sap; this substance is poisonous. Maximal amounts of water are collected from water-bearing vines if the first cut is high on the vine and the second cut is lower on the vine near the ground (Figure 43-18). When the water stops flowing from the cut section, cutting about 15 cm (6 inches) from the opposite end will start the flow again. Water may be trapped within sections of certain types of green bamboo. Bamboo that contains water makes a sloshing sound when shaken. Water also may be obtained from green bamboo stalks by bending a stalk over, tying it down, and cutting off the top. Water dripping from the severed tip can be collected in a container during the night44 (Figure 43-19). Large amounts of water can be found in the voluminous natural cisterns formed by the cup-like interiors of epiphytes (air 832

SHELTER

FIGURE 43-19  Bamboo can be a source of water.

CHAPTER 43  Jungle Travel and Survival

FIGURE 43-22  Sleeping platform.

frond is separated into halves by grasping it at the distal end, separating the leaves as though parting hair down the middle, and splitting the frond in two with a quick jerk (Figure 43-23). The halves should be overlapped like shingles and secured to the roof framework. It is much easier to construct an adequate shelter using a tarpaulin (see Camp Life, earlier). FIGURE 43-20  Water can be found in the natural cisterns in bromeliads. (Main photo courtesy John Walden; inset photo courtesy Erich Lehenbauer.)

may be attracted to rodents residing in these abandoned shelters. It is often preferable to take the extra time to set up a new camp than to risk encountering venomous insects, arachnids, and snakes. In an emergency, a proper shelter can be constructed using only plant materials. Figure 43-22 illustrates the basics of constructing a sleeping platform and lean-to. A shingled covering can be made quickly and easily from long, broad banana or heliconia leaves. Tropical palms provide a more substantial roof, but require more time and skill in construction. After selecting a suitable ground-hugging species or chopping down a slender tall palm (palm trees with spines often provide the best fronds), each

1 ft. FIGURE 43-21  Water collected from a banana plant.

FIRE In addition to boiling water for drinking and cooking food, fire lifts the spirits, warms the body on uncomfortably cool jungle nights, and can be used to signal rescue aircraft. Tinder and Kindling Small strips 0.3 × 5 × 10.2 cm (0.1 × 2 × 4 inches) of rubber tire carried in a survival kit and a butane lighter are an excellent combination for starting a fire, even in wet conditions. Tampons make a good fire-lighting aid. The silk-cotton or ceiba tree (Ceiba pentandra), found throughout the American, West African, and Southeast Asian tropics, produces balls of cotton-like fibers, known as kapok, which immediately catch fire and make ideal tinder. The cloth-like fibrous material at the base of palm fronds makes excellent tinder. Bamboo Fire Saw If you do not have matches or a butane lighter handy but have access to bamboo, you can make a bamboo fire saw44,48 (Figure 43-24). 1. With your machete, cut a 0.9- to 1.2-m (3- to 4-foot) long section of bamboo. 2. Split the section the long way with the machete. One of the resulting long sections will be the “base board.” 3. Shorten one of the split sections to about 0.3 m (1 foot) in length. This section will be the “running board.” 4. If kapok, palm fiber, or other suitable kindling is not available, with the machete blade, prepare tinder by scraping the outer sheath of a piece of bamboo. You need one large handful of scrapings. 5. Cut a narrow notch at 90 degrees on the outer (convex) side of the running board so that it just breaks through to the inner wall. This will serve as a guide to slide the running board rapidly over the base board. 6. Fill the running board with a fluff ball of tinder. 7. Place a thin strip of wood or a strip of bamboo over the ball of tinder to hold it in place. 8. Anchor the long section of bamboo (base board) with one end in the ground or against a rock or solid log and the other end wedged firmly against your abdomen. The sharp edges of the base board should be facing upward. 9. Holding carefully on to each end of the strip of wood that is keeping the tinder trapped inside the running board, rapidly and vigorously slide the running board up 833

PART 5  RESCUE AND SURVIVAL

FIGURE 43-23  Indian splitting a frond to make a covering for a lean-to (see text). (Courtesy John Walden.)

and down the base board with the groove against the sharp edge of the base board. 10. You will know that you are exerting effort sufficient to generate enough friction to ignite the tinder when you feel nearly exhausted, have worked up a sweat, and begin to entertain thoughts such as, “This just isn’t worth it.” 11. As soon as wisps of smoke begin to billow up from the tinder, gently blow upon the tinder until it bursts into flame. 12. Add small pieces of kindling, and avoid smothering the fire. Using this or any other friction method for making fire is hard work, but it can be done.

cuts at 45 degrees near each end, then run the machete blade between the notches and pop out the “plug.” Support each end of the bamboo pot on stakes or sturdy Y-branched sticks that have been driven into the ground (Figure 43-25).

Bamboo Container Large-diameter bamboo makes a great “pot” for heating water to a sufficient degree to cook items such as crawfish and minnows. To prepare a bamboo cooking pot, take a section of bamboo cut just past each end joint. Notch out an opening by making

PSYCHOLOGY OF SURVIVAL

Palm Spathe Container If bamboo is not available to construct a container, a woody spathe (the durable, canoe-shaped structure that encloses flowers and fruits of palms) can be substituted. Support the spathe at each end over a low fire, and fill the vessel with water. A palm spathe container will stay intact long enough to cook crawfish and minnows (Figure 43-26).

Travelers reared on movies and novels depicting the horrors of the Amazon may have irrational fears of being lost or stranded in the jungle. Visible daytime threats worsen with the onset of darkness, when perception becomes distorted. Travelers incapacitated by fear may throw away survival items or may flee from rescuers. Strategies that can increase travelers’ confidence in survival include the following: • Previous jungle experience. It is helpful to begin tropical excursions in the structured setting of small-group travel. Ecotours, particularly in Costa Rica, Ecuador, and Peru,

Running board Base board FIGURE 43-24  Bamboo fire saw. (Redrawn from Walden JB: Jungle travel and survival, Guilford, Conn, 2001, Lyons Press, p 175.)

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FIGURE 43-25  Bamboo container for heating water. (Redrawn from Walden JB: Jungle travel and survival, Guilford, Conn, 2001, Lyons Press, p 178.)

FIGURE 43-26  Palm spathe container. (Courtesy Jon Willis.)

offer a combination of rain forest trekking and cross-cultural experience. • Survival manuals. Military experts and others provide insights from decades of experience.44,45 • Information on the tropical rain forest. Familiarity with exotic plants and animals lessens the likelihood of fear while increasing awareness of potential usefulness in a survival situation. The anthropologic literature is replete with first-person accounts by anthropologists who have lived under trying circumstances with minimally contacted tribal populations throughout the tropics. • Classic accounts of survival against all odds, such as Alfred Lansing’s Endurance: Shackleton’s Incredible Voyage.28 • Courses in wilderness-oriented skills. The National Outdoor Leadership School (NOLS, 307-332-5300, 800-710-6657, http://www.nols.edu) teaches wilderness-oriented skills and leadership in a core curriculum stressing safety and judgment, leadership and teamwork, outdoor skills, and environmental studies. Wilderness and outdoor safety courses (http://www.outdoorsafe.com) teach both the psychological and physiologic aspects of surviving a wilderness emergency. • Traveling with a Collins-style machete, the one indispensable tool. A map, compass, GPS unit, and windproof lighter are other recommended items. • Taking stock. The traveler facing a wilderness crisis assesses a situation analytically and rationally before planning the course of action. Having survival skills is important; having the will to survive is essential.45

CULTURAL FACTORS Travelers who have the privilege of spending time with jungledwelling populations will find much to admire in the lives of indigenous peoples throughout the world. In some cultures, however, various facets of tribal life lend a discordant note and remind us that all cultures have their unpleasant aspects. Infanticide In a few tribal societies, infanticide is still practiced. Often the first or second of twins (depending on the customs of a particular tribe) and deformed newborns are killed. In some tribes, when the firstborn is a female instead of the more prized male, the decision may be made to kill the child at birth. Intertribal and Intratribal Warfare, Revenge Killings, Homicide Although the rates may be significantly lower or slightly higher on a regional basis, the literature shows that those who observed certain indigenous populations during their first sustained contact with the outside world found a high background level of intertribal warfare, revenge killings, and homicide. Chagnon7

Survival in Hostage Situations The following overview of survival in hostage situations is based on material developed and used by the 2nd Battalion, U.S. Army John F. Kennedy Special Warfare Center and School, and draws heavily from an outline prepared by James Liffrig, MD, U.S. Army.30 Some areas of otherwise pleasant tropical rain forests are in regions of risk for hostage taking by terrorists, guerillas, or criminals whose motivation may be purely mercenary. Individuals traveling to such areas should have insight into the fundamentals of survival in hostage situations.

PREVENTION Since the late 1960s, hostage taking has been on the increase worldwide as a way of setting up a bargaining position to achieve an otherwise unattainable objective. At times, the individual taken is an innocent victim of circumstances who happened to be in the wrong place at the wrong time. Often, however, the individual has been chosen because he or she is an easy target. The home page for the Bureau of Consular Affairs of the U.S. Department of State (http://travel.state.gov) provides current travel warnings worldwide and detailed country-by-country profiles on safety and security matters in Consular Information Sheets.46 The likelihood of becoming a victim of hostage taking or kidnapping can be diminished by avoiding travel to areas of known high risk. If one must travel to an area with a history of recent terrorist attacks or kidnapping, follow commonsense precautions: • Have your affairs at home in order (current will, insurance documents, power of attorney, guardianship arrangements for minor children). • Register with the nearest U.S. embassy or consulate through the State Department’s travel registration website (https:// travelregistration.state.gov/ibrs/).47 • Avoid obvious terrorist targets, such as places where Americans are known to congregate. • Be sensitive to what you discuss with strangers, and that you may be overheard. • Vary routines, including appointments, travel times, and routes. • In a city, walk purposefully as if you know where you are going, even if you are lost. Indecision, hesitancy, and directionless movement attract thieves and kidnappers in the same way that thrashing surface movements attract sharks. • As much as possible, blend in.

CATEGORIES OF HOSTAGE TAKERS Terrorist organizations are often stratified, with educated and dedicated idealists at the top and disillusioned, young, impressionable recruits from colleges or universities lower down in hierarchy. In some organizations, mentally ill persons and sociopaths recruited from prisons make up a nucleus of the more violent members of the group. Political and religious extremist 835

CHAPTER 43  Jungle Travel and Survival

reported warfare-associated male mortality between 20% and 30% among the Yanomamö of Venezuela. Summarizing data for five generations among the Waorani, a linguistic isolate inhabiting the lowlands of eastern Ecuador, Larrick and associates29 concluded that 42% of deaths were attributable to internal spearing raids and 16% were attributable to conflicts with the outside world. Various hypotheses have been advanced by anthropologists and others to explain the high death rates due to violence among Amerindians. If you disregard the theories of squabbling academicians and ask the Indians themselves, you will find preoccupation with warfare and homicide is attributed to revenge killings (vendettas), sexual disputes, and shamanism. Interestingly, after contact with the outside world, most groups rapidly abandon generations of warfare and violence. Influences, including Christian missions, school, and sports, in particular intervillage soccer tournaments, have been credited with transformation to more pacific lifestyles.37

PART 5  RESCUE AND SURVIVAL

hostage takers may represent the most danger to Americans because of the value of Americans as symbolic targets. Paramilitary/guerilla combatants often operate out of remote jungle regions and may cross in and out of one country to another along an unguarded border. Those who trek in such areas may become “targets of opportunity” by chance encounter with these individuals. Guerilla organizations in certain parts of the world engage in drug trafficking in order to obtain money, weapons, and equipment. Such organizations have increasingly turned to hostage taking for ransom as a source of fundraising. Although not a hostage situation in the classic sense, travelers should be aware that in isolated regions inhabited by indigenous peoples, detainment (usually temporary) of uninvited outsiders traversing tribal lands may occur. Detainment usually stems from a misunderstanding of the purpose of travel by outsiders, especially during times of heightened tension such as periods of intratribal or intertribal feuds or when tribes have joined forces to oppose the intrusion of extractive or timbering industries and conclude that the traveler is allied with such interests. It is always best to get advice from individuals with local knowledge, such as missionaries and anthropologists, when entering remote areas, especially areas of known or suspected ethnic unrest. In some countries in South America, particularly Brazil, isolated indigenous peoples can have immunity from prosecution, or receive lenient treatment, in criminal proceedings, including those related to murder.

STRESS MANAGEMENT IN CAPTIVITY

BEHAVIOR AT THE MOMENT OF CAPTURE

The Stockholm syndrome refers to stress-induced alteration of the hostage’s behavior such that the hostage aligns with the hostage taker. This phenomenon is thought to be an automatic, unconscious emotional response to the trauma of becoming a victim. It is not uncommon for hostages to transfer anger from the hostage takers to the society or situation that created the dilemma in which they are now victims. Individuals held in the grip of the Stockholm syndrome have been known to actively participate with the captor group in terrorist activities.

The initial moment of capture is dangerous because the captors are tense and may commit unintentional violence with the slightest provocation. • Do not reach into a coat or purse to produce a document unless so instructed. • Reassure your captors that you are not trying to escape. • If the terrorists use blindfolds, gags, or drugs at the time of abduction, keep in mind the fact that the terrorists want you alive. • If blindfolded, do not remove the blindfold because this could leave the terrorists no alternative but to kill you.

HOSTAGE RULES OF BEHAVIOR Always smile: I had learned that lesson years ago in the Congo, where the penalty for dropping your grin, even for an instant, in the face of nervous soldiers or tribesmen, was slow death with both legs hacked off above the knee with pangas.54 Hostage taking forces the terrorist or criminal into stereotyped responses. The more knowledge and understanding a hostage can have about his or her captors, the better he or she will be able to predict the hostage taker’s behavior and feel some degree of control. The conduct of the hostage can increase or decrease his or her chances for survival. • Smile. Be polite and respectful. • Be aware of the common “Good Guy/Bad Guy” interrogation technique. • Determine the area of particular sensitivity, such as politics or religion, of the hostage taker, and avoid conversation in these subjects. However, if terrorists want to talk about their cause, show an interest. Explain that although you might not agree with your captors, you are interested in their point of view, emphasizing the latter point. • Become an active listener. • Small talk is better than no talk. • Do not argue with captors. • Make brief, casual eye contact during conversation; avoid prolonged eye contact. • Do not refuse to eat unfamiliar local dishes just because they do not look or smell appetizing. It is disrespectful to refuse to eat the food that the captors may themselves be eating. • Adapt to, but do not adopt, the hostage taker’s value system (see Stockholm Syndrome, later.) 836

Long-term captivity often leads to exhaustion, lethargy, and de­ pre­ssion. Oppose these feelings, and try to maintain confidence. • Exercise. • Maintain sleep discipline, and avoid sleeping too much. • Plan a schedule for the day, and attempt to stick to it. • Keep a sense of humor.

ADJUSTING TO CAPTIVITY The hostage must make every effort to adjust to captivity. • Do not focus on mistakes made up to the point of captivity. Focus on the positive. • A positive attitude will help sustain dignity. • Smiles are contagious; the hostage should wear one. • Fight boredom. Engage in creative mental and physical activities. • Avoid setting anticipated release dates or allowing captors to establish these types of milestones. • Remember that the longer a hostage is held in captivity, the greater his or her chances of release or rescue.

STOCKHOLM SYNDROME

ESCAPE Escape planning should begin at the onset of detention because escape may eventually prove to be a viable option. • Escape is considered a last resort but should be considered if conditions deteriorate to the point that the risks associated with escape seem less than the risks of remaining captive: torture, death of fellow detainees, or a credible threat of death. • In group hostage situations, detainees should organize and make every effort to establish and sustain communications with other hostages. • Terrorists often hold hostages in areas where the local population supports their cause. Do not assume locals are friendly, because they may return escapees to their captors.

RESCUE Statistically, most hostages who die are killed during rescue attempts. Hostages should therefore be mentally prepared for rescue attempts. • The first hostage execution, if known by the rescuers, increases the likelihood of a rescue attempt. • The hostage must be especially alert and cautious should he or she suspect that a rescue attempt is imminent or occurring. • At the first sign of an active rescue attempt, the hostage should drop immediately to the floor and avoid any sudden movement, especially with his or her hands. • From the rescuer’s point of view, everyone on the scene is a terrorist until proved otherwise. Therefore, do not attempt to assist the rescue forces because you may be mistaken for a terrorist. • Expect to be tied up or otherwise restrained by rescue forces until you can be positively identified. If you argue, you may be subdued.

RELEASE Statistically the odds favor the hostage being released. • The U.S. government will not negotiate with terrorists. Our government will, however, work closely with the host government from the outset of a hostage-taking incident to encourage that government to exercise its responsibility under international law to protect all persons within its territories and bring about the safe release of hostages. • A number of factors can come into play (including ransom demands met by private efforts) so that the hostage is

released by his or her captors. If an actual release has been arranged, pay close attention to the instructions the captors are giving when the release is taking place. Do not panic or attempt to run.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 44 



Desert Travel and Survival EDWARD J. OTTEN This desert landscape is the indifference to our presence, our absence, our coming, our staying or our going. Whether we live or die is a matter of absolutely no concern to the desert. EDWARD ABBEY, DESERT SOLITAIRE

Deserts are common biomes for travel and can become difficult areas for survival. The key to survival is preparation, and the key to desert survival is water. We can emulate the desert flora and fauna to conserve water. The greatest hazards are dehydration and heat. Clothing, survival equipment, and training can overcome many of the obstacles. Desert travel is inherently dangerous, and special precautions are needed to decrease risk.

The Desert Environment Deserts are land areas that receive less than 25.4 cm (10 inches) of rain, unevenly distributed throughout the year. A number of climatic processes produce desert areas. The most influential are the six cells of cold air currents that descend at the poles and near the Tropic of Cancer and Tropic of Capricorn. These air currents, driven by the sun and rotation of the earth, create areas of relatively warm, dry conditions. Many of the world’s deserts live in a “rain shadow,” an area to the leeward side of a mountain range that prevents the small amount of moisture that is present in the air to move over the mountains. As the air rises, the moisture cools and precipitates in the higher elevations. Therefore the area in the “shadow” of the mountain range receives little moisture. The air that does descend is quite dry and adds to the evaporative effect. The Atlas Mountains shadow the Sahara, the Andes the Patagonian, the Great Dividing Range the Australian, and the Sierra Nevada and Cascades the Great Basin deserts. The amount of rainfall is not an absolute indicator of “dryness” because the rate of evaporation and timing of the rainfall must also be taken into consideration. The amount and type of vegetation, soil composition, altitude, average temperature, wind speed, and solar radiation all contribute to “dryness” and desert formation. Antarctica would be the world’s largest desert by the definition of less than 25.4 cm (10 inches) of rainfall annually, some areas of that continent having had no recorded rain in 30 years. There is a large amount of water present in the form of ice, but it is not available for use by plants. Antarctica has its own special survival problems not associated with precipitation and, for the purposes of desert survival, will not be considered here. In contrast to Antarctica stands the northern coast of Alaska, which receives less than 10.2 cm (4 inches) of rain annually yet is quite wet because evaporation is so low. Deserts are one type of environment on Earth that is increasing in total area, likely because of human as well as geologic factors. Overgrazing, destruction of forests, global warming, and other aspects of increased human population contribute to desertification. Currently about 15% of the land area of the earth

is desert (30% if Antarctica is included) (Figure 44-1; Table 44-1). Most of the earth’s deserts can be found between 30 degrees south and 30 degrees north latitude, making them hot as well as dry. These deserts include the Sahara, Arabian, Kalahari, Australian, Atacama, Thar, Namib, and southwest United States. About 50% of Africa is desert; the Sahara by itself is almost as large as the United States. About 8% of the United States, or 776,996 square kilometers (300,000 square miles), is desert. Most of the U.S. desert areas are adjacent to national parks and forests and are frequently visited, for example, the Grand Canyon, Big Bend, Arches, Zion, Organ Pipe, Joshua Tree, Great Basin, Saguaro, and Capital Reef. Beyond 40 degrees south and north latitude and at elevations over 3048 m (10,000 feet) are the “cold” deserts, which have wide swings in temperature, for example, the Patagonian, Turkestan, Gobi, and Taklamakan. The large temperature variations in desert regions are greater at higher elevations and latitudes but are present in all deserts. Lack of vegetation, cloud cover, and ground-water surface allows 90% of solar radiation to reach the desert surface. By contrast, a forest may reflect 50% to 60% of the solar radiation, and its vegetation disperses the rest. At night, lack of cloud cover and vegetation allows almost 100% of the accumulated heat to escape, as opposed to only 50% from a humid climate. This explains why the desert temperature may reach 48.9° C (120° F) during the day and drop to 4.4° C (40° F) at night. Tropical rain forests may only reach 35° C (95° F) during the day, but at night the temperature only drops to 29.4° C (85° F). It might seem that the extreme desert climate would only allow for sparse life, but that is not the case (Figure 44-2). Death Valley, one of the harshest environments in North America, where air temperatures have been recorded at 56.7° C (134° F), has 600 species of plants, 30 species of mammals, 25 species of reptiles, and 2 species of fishes. Oases are found in most deserts. They are isolated depressions usually fed by a constant source of water. Underground springs and wells supply moisture for plants and animals. Often one must dig to find water at the lowest point of the depression. Many named oases have supported camel caravans, allowing them to move from oasis to oasis and thus cross an otherwise impenetrable desert. Desert way stations and ancient cities have sprung up along these routes. Many ancient oases have wells hundreds of feet deep and because of overuse are gradually drying up. When the water is used up, the oasis disappears, along with its desert life. All desert flora and fauna have one guiding principle for survival, which is to conserve water. The ground surface of the desert has the highest temperature because of the direct effect

For online-only figures, please go to www.expertconsult.com

837

PART 5  RESCUE AND SURVIVAL

Extremely arid Arid

FIGURE 44-1  Desert areas of the world. Many of these areas are growing. TABLE 44-1  Deserts of the World Area (sq km [sq mi])

Name

Continent

Western Sahara Great Erg Tanezrouft Libyan

Africa

266,769 (103,000)

Africa Africa Africa

392,280 (151,460) 149,960 (57,900) 1,199,993 (463,320)

Fezzan Egyptian

Africa Africa

551,165 (212,806) 660,001 (254,828)

Sinai Niger

Africa Africa

60,994 (23,550) 464,307 (179,270)

Darfur Nubian Sahel

Africa Africa Africa

Mauritania Somalia

Africa Africa

440,298 (170,000) 421,650 (162,800) 4,999,972 (1,930,500) 720,017 (278,000) 587,150 (226,700)

Kalahari Namib Andalusian Arabian

Africa Africa Europe Asia

260,009 94,017 265,992 2,299,987

(100,390) (36,300) (102,700) (888,030)

Syrian Negev Taklamakan Thar Gobi

Asia Asia Asia Asia Asia

517,998 11,992 323,749 213,997 1,299,993

(200,000) (4,630) (125,000) (82,625) (501,930)

Karakum

Asia

689,999 (266,410)

Sonoran

N. America

310,799 (120,000)

Death Valley Gran Desierto Mojave Great Basin Chihuahuan Atacama

N. America N. America

14,763 (5,700) 309,996 (119,690)

N. America N. America N. America S. America

64,998 490,000 517,998 199,999

Australia Australia Australia

360,008 (139,000) 299,998 (115,830) 579,277 (223,660)

Great Sandy Simpson Great Victoria

838

(25,096) (189,190) (200,000) (77,220)

Features Dunes, mountains Dunes Rocky, mountains Rocky, dunes, oases Rocky, mountains Basin, plateau, oases Mountains Dunes, mountains, oases Mountains Rocky, dunes Steppe

of solar heat and wind. Therefore, during the hottest times of the day, most animals are either below the surface, in underground burrows, or above the surface in available vegetation, cacti, trees, or shrubs. Most animals forage from dusk until dawn because temperatures are cooler. Some mammals, such as kangaroo rats, never drink but obtain necessary water through plant seeds. Plants have evolved a number of survival skills to maintain water, including stomata that are closed during the day and crassulacean acid metabolism (CAM) photosynthesis. The latter allows for accumulation of carbon compounds at night through the dark reaction. These compounds are converted to carbon dioxide during the day when the stomata are closed. Other adaptations include stem photosynthesis in plants without leaves, thick cuticles, water storage tissues, and widespread shallow root systems. Desert plants also have evolved a variety of defense

Dunes, plateaus Mountains, plateaus Dunes, savannah Dunes, plateaus Rocky, dunes Dunes, mountains Rocky, plateaus Plateaus, rocky Basin, dunes Dunes, cold Plateaus, rocky, cold Basin, plateaus, cold Mountains, alluvial Basin, mountains Basin, mountains Basin, mountains Basin, mountains Basin, mountains Mountains, rocky, cold Basin, dunes Dunes, rocky Dunes, alluvial

FIGURE 44-2  Desert landscape. Note the physical features and abundant flora.

Preparation All things being equal, preparation improves the likelihood of survival. However, things are never equal, so luck is probably the most important, albeit the most uncontrollable, factor. The controllable factors are mental and physical conditioning, clothing, survival kit adequacy, and survival skills. These may allow one to survive even in the most extreme conditions. Mental preparation is key to any survival situation. The “will to survive” has been shown to be the most important factor in the outcome of a number of situations. Knowledge of the terrain features, weather, animal and plant life, and potential hazards should all be studied before travel to a desert area. Not only does this increase one’s chances for survival, but it also enhances enjoyment of the desert environment. Practical experience in finding water and food, navigation, and constructing shelters is more valuable than reading about it. Time spent in attending a course on survival in general or desert survival in particular may be invaluable if one is later in a true survival situation. Physical conditioning and acclimatization are as important for desert travel as for mountaineering. Desert travel is difficult under most circumstances. The terrain is rough and may include sand dunes, sharp loose rock, flash floods, steep grades, and hot surfaces. Lower-body conditioning helps prevent the ankle and knee injuries that can force a survival situation in a harsh climate. Acclimatization may take 10 to 14 days and involves three welldescribed physiologic adaptations. These are increase in sweat volume and number of active sweat glands, decrease in concentration of electrolytes in sweat, and sweating at lower body temperature. These can be induced before arriving in a hot climate by the use of a sauna or vigorous exercise to raise body temperature (see Chapters 10 and 11).

to protect the head, face, neck, and ears. In a survival situation, an expedient head covering can be made from whatever material is at hand (Figure 44-3). A cotton cravat, bandanna, or handkerchief can be used to keep the head and neck cool by soaking the material in water (if plenty of water is available; do not use precious drinking water) and then placing it on the head, followed by a hat. Alternatively, it can be wrapped around the neck and shoulders underneath a shirt. Commercially produced (Cooldanna, Climatech, StaCool) neck wraps and vests, which contain crystals that can be soaked in water and then become cool through a chemical reaction, are also available but probably do not add much in the way of total-body cooling in extreme environments. The cravat can also be used during dust storms to protect the nose and mouth, as a towel, or to absorb moisture from plants when obtaining water. High-top (15.2 cm [6 inches]) boots composed of leather or synthetic materials are necessary to prevent sand, rocks, and burrs from entering the boots, support the ankles on rough terrain, insulate the feet from hot surfaces, and prevent the boots being pulled off in soft ground. Boots should be well broken in before hiking. Military-issue boots with metal spike protection can become extremely hot in desert conditions and should be avoided. Running shoes do not insulate the feet well and may become extremely hot. Socks should not be cotton, because of the risk for blisters and lack of wicking and insulation. Polypropylene or a combination of polypropylene and wool is best for socks because of less friction and thicker material. Foot care is extremely important, especially in a survival situation when walking is the only means of transportation. Feet should be inspected for blisters, foreign bodies, and abrasions on a regular basis while hiking. Socks should be changed frequently, at least twice a day, to allow them to dry out and to remove accumulated

CLOTHING Clothing selection for desert travel is somewhat different than for most other wilderness activities. The less exposed skin, the better. Although cotton is not appropriate for most cold, wet climates, it is useful in the desert. Light-colored clothing reflects sunlight and lowers skin temperature. Ripstop cotton (cotton material with nylon threads latticed within it) is best because it resists rips that are common in the desert. It is light enough to allow heat to escape, does not have a clammy feeling in low humidity, and protects against some ultraviolet rays and blowing sand. If ripstop cotton is not available, any tight-weave cotton is adequate. Long sleeves and long pants are a “must” to protect against spines, thorns, splinters, and insects. More important, they offer some protection against solar radiation that causes sunburn and increased body temperature, and they trap more cool air next to the skin. Sweat that is trapped decreases water loss through evaporation. Trousers can be tucked into the tops of socks to protect from insects; sleeves should be not be rolled up in order to minimize risk for sunburn and heat gain. Gaiters can be worn to protect lower legs and the inside of footwear from sand, rocks, and dust. In a survival situation, puttees (wraps that extend from the tops of the shoes to the knees, either over trousers or bare legs) can be made of strips of cloth, elastic bandages, or stockings to protect the lower legs. They can be incorporated into the socks and wrapped to above the knees in a fashion similar to gaiters. Because of the wide temperature swings, a pile jacket or sweater is necessary at night. Layering, just as in cold climates, is the best means of preserving body warmth. In a survival situation, any insulating material, such as seat cushions, newspapers, or dry grass, can be used to insulate whatever clothing is available. Although wind is more of a problem than is rain, a Gore-Tex jacket is also recommended, especially for “cold” deserts. A wide-brim hat or kepi (a cap with a cloth extending from the back protecting the neck) is necessary

Making a burnoose

T-shirt used as face protection against sand

Facecloth

Neckcloth

FIGURE 44-3  Expedient head coverings.

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CHAPTER 44  Desert Travel and Survival

mechanisms, such as production of toxic compounds that act as herbicides to other plants, and the formation of needles, spines, and thorns that dissuade browsing animals. Obviously humans are not able to evolve these physiologic changes but must rely on behavior, technology, and other adaptations to mimic the methods used by indigenous desert dwellers.

PART 5  RESCUE AND SURVIVAL

BOX 44-1  Desert Survival Kit Swiss Army knife Parachute cord Compass Topographic map First-aid kit Goggles Lip balm Leather gloves Safety pins Mosquito head net Waterproof container Rescue blanket Plastic sheet Plastic tube Metal cup Water container (4.7 L [5 qt]) Hat Sweater or pile jacket Gore-Tex jacket Duct tape Hard candy Plastic bags Matches Metal match Metal mirror Whistle Water filter or iodine Peanut butter Flashlight Sunscreen Insect repellent Cravat

dust and sand. Leather gloves are desirable to protect hands from hot objects, plant spines, thorns and splinters, insects, and blisters. Abrasions and lacerations to the hands can quickly become infected in conditions where hand washing is difficult. Eye protection becomes very important in the desert, especially when traveling. Solar radiation, both direct and reflected, can cause keratitis similar to snow blindness. More commonly, blowing sand, dust, and insects may cause corneal abrasions and conjunctivitis. Contact lenses are difficult to manage in the dry, dusty environment. Tinted goggles are best, just as with mountaineering, but glacier glasses or standard sunglasses can be used. Duct tape, adhesive bandages, or other material can be used to fashion side shields for regular glasses to prevent sand and dust from entering through the sides. Insect head nets can be lifesaving, especially in African, Arabian, and Australian deserts, where insects and insect-borne diseases are particular problems.

matches, metal match, or lighter; first-aid supplies; compass; safety pins; water disinfection tablets; and plastic bags can be stored in a relatively small container that should be kept on one’s person at all times. The first-aid kit should contain bandages, insect repellent, sunscreen, lip balm, antiseptic ointment, aspirin, antihistamines, tape, and any prescription medications. The desert survival kit should include a 1.5 × 1.5 m (5 × 5 foot) piece of plastic, 1.2-m (4-foot) length of plastic tubing, and metal cup (all for making a solar still), emergency blanket (silver on one side, red on the other), extra sunglasses or eye protection, nylon canteen (minimum 4.7 L [5-qt] size), and extra sunblock.

Priorities The “rule of 3s” gives us a priority list for survival. One can live 3 minutes without oxygen, 3 hours without warmth, 3 days without water, and 3 weeks without food.

WATER The key to desert survival is water. Unfortunately, water weighs 3.6 kg/3.8 L (8 lb/gal), and individual needs may be up to 7.6 L (2 gal) per day. Always carry as much water as possible. Collapsible canteens can carry several quarts of water and keep the water cooler (because the surface heat absorption to volume is less) than can hard plastic or metal (Figure 44-4). Drink at every stop. Drink while hiking if using a drinking tube with a reservoir such as a Camelbak or similar water container. Flavoring and cooling water increase palatability and thus consumption. Most hikers do not carry enough water for more than 1 day, so having a method for acquiring water is mandatory. Solar stills, vegetable stills, digging along arroyos and in dry lake beds, wiping dew from plants in the early morning, and extracting water from succulent plants are all methods for obtaining water in a desert survival environment. These alternative methods may not supply enough water for a long-term situation. Although there are a number of methods for obtaining water in the desert, minimizing water loss might be a better strategy for a human with limited water resources. All desert plants and animals have developed adaptive mechanisms for conserving water. Humans, if they are to survive, must develop strategies for conserving their sweat, not their water. Adolph measured water intake, activity, and ambient temperature of World War II soldiers during desert operations. Soldiers who rested in the shade had significantly less water losses than did those who exerted themselves in the heat of the day, and they could extend the length of time they could survive, despite similar water intake. Although it would seem to be intuitive, most desert travelers limit neither their travel to cooler times of the day nor their work activities to the shade. Employing a strategy of resting in the shade from 10:00 AM to 3:00 PM, drinking adequate water based on the appearance of the urine, and keeping as much skin covered as possible has decreased the number of heat casualties in the military during training exercises. Although thirst and amount of sweat on clothing are poor indicators of hydration status, the color and amount of urine produced can roughly

SURVIVAL KIT The survival kit must be carried at all times, have high-quality equipment and supplies, and be protected from the elements. Each item should have multiple uses if possible. There must be items that can be used for shelter, signaling, fire building, first aid, and other uses (Box 44-1). Many items will routinely be carried by most hikers and backpackers, but some specialized items should be added. One’s clothing is the basic survival shelter and, if properly selected, will be the first step in protection from the climate. General-use items include a Swiss Army knife with as many blades as possible. The SwissChamp includes, among many other features, a magnifying glass, which is quite useful for removing cactus spines or starting fires. Parachute cord (eightstrand) has multiple uses, including shelter construction, creation of snares, and fishing nets and lines. A signal mirror; whistle; 840

FIGURE 44-4  Collapsible 5-qt canteen.

CHAPTER 44  Desert Travel and Survival

Water storage tissue Xylem Epidermis

FIGURE 44-5  Desert water hole—currently occupied.

estimate it. The darker in color the urine, the more concentrated it is, indicating a greater degree of dehydration. If potable water is available, it should be consumed; it is better to conserve sweat rather than water. If there is a limited amount of water, food should not be eaten unless the food contains a large amount of water. The metabolism of food, especially protein and fat, and excretion of waste products require potentially unnecessary utilization of body water. Only potable water should be drunk because vomiting and diarrhea caused by contaminated water could quickly become fatal in the desert. Water obtained from lakes, streams, wells, or springs should be considered conta­ minated and must be made potable before drinking. Water holes may attract dangerous animals as well as potential food (Figure 44-5). Desert water may be found by looking for animal signs, such as trails or spore. Some plants, such as cottonwood, sycamore, willow, and cattails, may be indicators of water. Water may sometimes be found by digging at the outside bend of a dry riverbed or stream (arroyo and wadi are terms used to indicate rain run-off channels that may contain water during the rainy season) (Figure 44-6). Rainwater, dew, and water obtained from a solar still or a vegetable still are relatively potable. Urine, seawater, alkaline pools, and brackish water should never be drunk. They contain large amounts of solutes that would require more water to excrete than they provide, thus hastening dehydration and renal failure. However, these sources can be added to a solar still to improve potability as well as increase the still’s output. Liquid from radiators or windshield washer fluid is contaminated with glycols or methanol and should not be drunk or used in solar stills. Many plants, such as barrel cacti and traveler’s tree, and animals, such as the desert tortoise, contain water that can be used in an emergency or added to a solar still to increase output (Figure 44-7). A solar still (Figures 44-8 to 44-10) can be constructed by placing a 1.5 × 1.5 m (5 × 5 foot) piece of clear plastic over a

FIGURE 44-7  Barrel cactus showing pulp that can be a source of water.

hole 0.9 to 1.2 m (3 to 4 feet) in diameter and dug 0.9 to 1.2 m (3 to 4 feet) deep in the ground into which vegetation, urine, or brackish water has been placed. Solar energy causes water to evaporate within the hole and collect on the underside of the plastic. Because it cannot escape, it will drip back into a container placed at the bottom of the hole. A tube can be attached to the inside of the container so that the water can be drunk without dismantling the still. A plug should be put in the drinking end of the tube to prevent clogging. The amount of water produced depends on the amount of moisture in the hole, the amount of sunshine directed at the still, and the size of the plastic sheet. A still dug into a dune or dry sand will not produce much water. Sand or dirt to anchor plastic sheet

Clear plastic sheet Rock Drinking tube

Green foliage moisture producers

Container

Below-ground still using vegetation as a moisture source

Sand or dirt to anchor plastic sheet

Water trough for polluted water

Clear plastic sheet Rock

Drinking tube

Water trough for polluted water Container

Below-ground still for obtaining water from a polluted source FIGURE 44-6  Desert arroyo or wadi.

FIGURE 44-8  Diagram of solar still.

841

PART 5  RESCUE AND SURVIVAL

FIGURE 44-11  Vegetable still. Note drinking tube and water in bottom of plastic.

pulp should not be used, and the pulp should not be eaten. Water can be made potable by boiling, or using filters or chemicals (see Chapter 67).

SHELTER

FIGURE 44-9  Solar still. Note the moisture on the plastic.

Dew, rainwater, and edible animals may fall into the still as a bonus. Moisture can be wiped off plants during the early morning and can be squeezed from the pulp of certain plants, such as yucca or barrel cactus. A vegetable still using a plastic sheet wrapped around a bush or tree branch can trap transpired water from the plant. The plastic should be tied with a piece of cord and a small stone attached to the drinking tube placed in a dependent portion of the plastic so that water can be drunk without dismantling the still (Figure 44-11). Milky, bitter, or sour

FIGURE 44-10  Solar still.

842

Desert shelters are of three main types: natural, well-prepared human-made, and improvised human-made. Natural shelters are caves and rock overhangs. When using natural shelters, one must remember that there may already be other inhabitants that need eviction. Rattlesnakes, tortoises, ground squirrels, lizards, and skunks often use caves and other cool areas during the heat of the day. These animals may be sources of food but are also potentially dangerous to humans. Some reptiles are venomous, and many mammals carry rabies or plague. They can usually be removed by prodding with a long stick or dispatched with a rock. Well-prepared human-made shelters include tents, vehicles, and buildings. Most vehicles become very hot inside, which may hasten heat illness and dehydration. It is better to sit in the shade of an automobile than to be inside it during the heat of the day. Tents and buildings are best if there is adequate ventilation. Improvised shelters are typified by the desert trench shelter, shade shelter, or lean-to. Any structure that provides shade, protects from wind and blowing sand, and decreases heat gain or loss is minimally adequate. The hottest area in a desert climate is at the surface of the ground, so getting above the ground or below the ground decreases exposure to the highest temperatures. Most desert animals take advantage of this fact by their behavior. Birds perch high in trees in the shade of a branch or in some cases inside of a cactus. Most mammals and reptiles burrow into the ground, where just 0.9 m (3 feet) below the surface the temperature may be 30% cooler. Humans can imitate this behavior by constructing a desert trench shelter (Figure 44-12). This is a trench dug in the ground 0.6 to 1.2 m (2 to 4 feet) wide, 0.6 to 0.9 m (2 to 3 feet) deep, and about 1.8 m (6 feet) long. A barrier can be made of any effective material at hand, such as a blanket, sheet, poncho, tarp, or space blanket. This barrier is placed over the trench, about 45.7 cm (18 inches) above the bottom, and its edges are weighted down with rocks or sand. Another similar barrier (the first one can be doubled back on itself if it is large enough) is placed about 30.5 to 45.7 cm (12 to 18 inches) above the first barrier and also weighted down. This construction creates an insulating barrier that traps cooler air in the bottom of the trench and reflects solar radiation from the top. Ideally, a reflective space type of blanket is used for the outer layer, which will increase the amount of heat reflected. Removing the seat from a vehicle and sitting above the ground in the shade of the vehicle or constructing shade with a blanket or tarp and available materials can provide some shelter in the heat of the day until a more adequate shelter can be built (Figure 44-13). At night, when temperatures drop, the shade trench remains warmer because of the heat produced by the inhabitant. The top barrier, with its reflective surface, can be reversed to

Dig trench 18''- 24'' deep

Poncho liner Poncho

CHAPTER 44  Desert Travel and Survival

FIGURE 44-12  Desert shade shelter or trench shelter.

Sand anchor

12''-18'' airspace

reflect heat back into the trench. Any insulating material can be added to the floor of the shelter to decrease heat loss to the ground. Given enough time, a shelter such as a tepee, tent, or lean-to can be constructed using tarps, blankets, parachute panels, or other materials (Figure 44-14). Construction should take place in the cooler times of the 24-hour day to conserve sweat and water. If one has a reliable source of water, such as a desert water hole or “tank” (natural collection of water in nonporous rock), then it is best to stay in that place and try to be rescued rather than attempting to travel large distances without adequate water.

FOOD Food is not as immediate a problem as is water in the desert (see Chapter 71). Most humans have an extra 50,000 to 70,000 calories that they store in the form of fat and can survive for weeks without eating. Food in the form of animals or plants is usually available if water is available. Cactus fruit, such as prickly pear (Figure 44-15), can be eaten when peeled. Legumes, such as acacia, mesquite, and paloverde, produce beans that can be crushed and mixed with water to form tortillas (Figure 44-16). Yucca stems, cattails, agave stems, and prickly pear pads can be cooked and eaten. Avoid plants with milky saps or white berries and other plants that cannot be positively identified as edible. Mushrooms should not be eaten. It is essential to become familiar with the common poisonous and edible plants in any area

through which you will travel. Insects, birds’ eggs, grubs, tortoises, and other slow movers can be captured by hand. Most small animals, such as snakes, lizards, and birds, can be killed with a rock or stick. Jackrabbits, ground squirrels, and rats may be snared or trapped. Large mammals should be avoided because the likelihood of killing one of these without a firearm is small, whereas the likelihood of becoming a casualty is high. All meat should be cooked or dried before ingestion. Animals to avoid as food or in general include caterpillars, spiders, scorpions, centipedes, millipedes, toads, and bats. Although they may be prepared as food, the risk is probably not worth the calories. Many mammals carry plague, tularemia, Hantavirus, leptospirosis, rabies, and other zoonoses.

HAZARDS In addition to heat and dehydration, there are other hazards that one may encounter in the desert. Blowing sand and dust created by vehicle traffic may cause eye, nose, mouth, and skin irritation. Desert winds up to 160.9 km/hr (100 mph) can blow for days, creating immense sandstorms and dust storms that can cover large areas, reducing visibility to near zero (Figure 44-17). In addition to the sand and dust, other objects can be transported with the ferocity of a hurricane. Vehicles, tents, and buildings can be demolished and roads obliterated. Sandstorms blowing for days have caused destruction in large cities, such as Melbourne and Baghdad. Exposed skin must be protected, and

FIGURE 44-13  Expedient shelters.

Shade trench

Shelter for cold deserts

Shade shelter

Double layer of parachute cloth draped from wing

843

PART 5  RESCUE AND SURVIVAL

FIGURE 44-14  Desert tarp shelter.

FIGURE 44-16  Mesquite seedpods.

shelter should be sought within a hard-sided building if possible. The possibility of an individual being buried is remote, but drifting sand can block doors and strand vehicles. Quicksand is another hazard. There are two types of quicksand. The first is a mixture of sand and water found along the shores of lakes, seas, and estuaries of rivers. This type may look solid but is a suspension of fine sand and water that cannot compact. The second type is fine sand deposited by wind in hollow depressions. Depending on the depth of the depression, one could sink 4.6 to 6 m (15 to 20 feet). A person caught in quicksand can usually escape by flattening out and swimming to firm ground because most quicksand areas are small. Animals may panic and struggle, hastening their submersion. A rescuer can usually pull the victim to firm ground using a rope, belt, or strap. Removing one’s pack and throwing it to firm ground allows for easier escape. Animal hazards include venomous snakes and arthropods, carriers of zoonotic illnesses, and large mammals (Figure 44-18, online; Box 44-2). Plant hazards include poisonous varieties that may cause dermatitis or systemic symptoms if ingested. Many types of plants produce spines, hairs, or thorns, which easily penetrate human

skin and may cause infection, especially if the foreign bodies become imbedded. Removal of spines, especially small hair-like spines, can be facilitated using duct tape. Large cactus and yucca spines can penetrate joints and cause serious infections.

FIGURE 44-15  Prickly pear fruit.

FIGURE 44-17  Gigantic desert sandstorm.

844

Travel Even in the best of circumstances, hiking in the desert can be difficult. Most modern travel is performed with high-clearance, four-wheel-drive vehicles. These vehicles should have sand mats (for added traction on soft surfaces) and a winch and cable for self-extracting the vehicle or rescuing another vehicle. Extra water, spare parts (fan belts, hoses, spark plugs, fuses, bulbs), additional fuel and oil, shovel, two jacks, spare battery, spare tires and tire-patching materials, radio, and tool kit are mandatory for desert travel. Traveling in convoys is a must, both for safety and, in some places, for security. Salt flats, mudflats, and soft sand can bog down even four-wheel-drive vehicles. Never attempt to cross arroyos or wadis when they are flooding.

CHAPTER 44  Desert Travel and Survival

BOX 44-2  Dangerous Desert Animals* Arthropods Venomous Spiders, scorpions, assassin bugs, ants, bees, wasps, centipedes, millipedes Zoonotic Disease Vectors Fleas, sand flies, ticks, mites, mosquitoes, kissing bugs, flies Reptiles Venomous Lizards, rattlesnakes, coral snakes, desert vipers, desert black snake, cobras, Australian elapids Nonvenomous but Risk for Attack Crocodiles, monitor lizards Mammals Zoonotic Disease Vectors Dogs, rodents, rabbits, bats, squirrels, cats, primates Mechanical Injuries Camels, carnivores, donkeys, antelope, deer, elephants *See also Part 6.

Many areas offer no access to wheeled vehicles, so travel by camel, donkey, or horse is still common. Camels remain the most efficient desert transportation and can travel for long periods without food or water (Figure 44-19). They also are quite resistant to blowing sand, heat, and temperature changes. Expert assistance is needed for travel by camel. Horses and donkeys are limited to short distances and require more food and water. Current topographic maps and a good compass are essential, whether traveling by vehicle, by animal, or on foot. Local authorities should be consulted concerning water sources; these should be marked on the maps. A copy of the map should be left with someone who knows the travel plans. The route and campsites should be indicated on the map. In that way, if one becomes lost or injured, search and rescue teams will know where to initiate the search. If one becomes lost or injured, it is usually best to stay in one place and signal for help, using a mirror or other reflective object during the day and a fire at night. Cellular telephone, radio, or emergency locator transmitter may aid searchers. Flares and whistles should be used only when searchers are nearby or a search aircraft is moving in your direction. Geometric patterns drawn on the ground, such as “SOS,” “HELP,” or a large “X,” may aid aircraft in identifying the position of a distressed person. Rocks, contrasting soil, plants, or clothing can be used to produce the patterns. It is difficult to see a single human on the ground; therefore it is always best to stay near a vehicle if possible. An automobile can be a good source of signaling equipment.

FIGURE 44-19  Travelers on camel.

The windscreen and windows reflect light, and the mirrors can be removed and used to signal. Oil can be drained, placed in a hubcap, and mixed with sand. When set on fire, it produces dense black smoke. The hubcaps can be used to dig a desert trench shelter, the battery to start a fire, and the seat covers and floor mats for shelter and footwear. If one has adequate water, knows the direction of travel, has good footgear, and decides to try to walk to safety, it is imperative to leave a note outlining plans in a conspicuous place or to draw an arrow on the ground with rocks pointing in the direction of travel. Direction finding can be accomplished without a compass using the sun or stars (see Chapter 96). Before traveling in the desert, it is best to know the locations of key terrain features, such as rivers, highways, mountain ranges, and cities. Power lines, stream beds, and pipelines may also lead to civilization, but it may require days to arrive. It is dangerous to travel through arroyos or wadis because of the danger of flash flooding. Rainfall in mountains several miles away can wash down these formerly dry stream beds, pushing tons of mud, rocks, and water in a lethal torrent. Sand dunes should be avoided because of the amount of energy required to traverse them. Salt marshes may contain soft ground that traps the hiker. One should travel in the cool of the night to conserve water, and use the stars for direction. The dangers at night are that many desert animals are more active, and the chances of falling from a cliff, stepping into a hole, or stumbling into the spines of a cactus are greater.

REFERENCES Suggested readings for this chapter can be found online at www.expertconsult.com.

845

CHAPTER 45 

Whitewater Medicine and Rescue ERIC A. WEISS Rivers have what man most respects and longs for in his own life and thought—a capacity for renewal and replenishment, continual energy, creativity, cleansing. —JOHN M. KAUFFMAN, FLOW EAST

Demographics Rafting, canoeing, and kayaking have become the third largest outdoor recreation industry in the United States.12,54 Participation in canoeing and kayaking (including flat-water paddlers) rose from 16.7 million in 1994-1995 to 22.6 million in 1999.58 According to the Outdoor Foundation, participation in kayaking is increasing at a rate of 23% per year.56 Kayakers are almost 70% male, whereas the male-to-female ratio of rafters is somewhat more reflective of the U.S. population at 55% male and 45% female.55,57,73 Kayaks and rafts are also used by law enforcement officers, park rangers, and game wardens to patrol and manage their territories.45 New equipment designs have opened up more difficult rivers for exploration and commercial recreation.50 The number of river-related accidents and deaths has increased as paddlers with innovative boats and improved skills challenge the boundaries of whitewater rivers. The American Canoe Association reports that about 130 whitewater fatalities occur each year.73 This chapter examines the unique and dynamic hazards associated with rivers and whitewater paddling. Safety equipment, accident prevention, common injuries, environmental hazards, medical management, and swift-water rescue techniques are reviewed.

Historical Perspective Whitewater boating as a recreational activity began in the United States in earnest during the late 19th century, when adventurers attempted to emulate Major Wesley Powell’s Colorado River expedition by rowing boats down many of the West’s large rivers.40 These heavy wooden boats were replaced by inflatable rafts after World War II, when surplus neoprene assault boats and life rafts became available for civilian use.5 In 1956, one of the members of the most affluent business families of America, John D. Rockefeller, built a resort and offered one of the first rafting trips in the country. In the 1960s and 1970s, exclusive whitewater rafting companies were formed, including BeckerCooke Expeditions, Hatch River Expeditions, and Slickrock Adventures. In 1966, fewer than 500 people boated the Colorado River through the Grand Canyon in an entire year. Now, the figure sometimes exceeds 500 per day.40 Rafting did not become popular in the eastern United States until the early 1960s. In 1968, commercially guided raft trips were offered for the first time on the New River in West Virginia.76 The Chattooga River in Georgia attracted many rafters after the movie Deliverance was filmed there in 1971. The Youghiogheny River in Pennsylvania and the South Fork of the American River in northern California have become the two most heavily rafted rivers in the country. The first kayaks were made from wooden frames covered in sealskin and used by the Inuit people in the Arctic regions of Alaska and Canada. They included a small hole in the middle of the craft in which the user could sit and were primarily used for hunting. In the 1950s, fiberglass was introduced, and in the 1970s, Kevlar was added to make kayaks both lighter and stronger. 846

A major innovation in kayaking was development of the plastic kayak, first manufactured in 1972 by the Holloform Company76 (Figure 45-1). The plastic kayak empowered paddlers to run steeper and rockier rivers, because plastic boats were much less likely to break if they impacted rocks. Most recreational whitewater kayaks are now made of molded polyethylene plastic, which does not break apart but has the potential to fold when broached or pinned, trapping the paddler. The hulls, or bottoms, of kayaks have undergone significant changes during the past 5 years. Older-model kayaks had rounded bottoms, or displacement hulls. Most whitewater kayaks today have flat bottoms, or planing hulls. The flat bottom makes the kayak more stable, both on its bottom and its sides. A rounded bottom rocks in the water from side to side, whereas a flat bottom does not. Newer boat technology, combined with shorter kayaks and more advanced paddling skills, allows better maneuverability in tight, steep rapids and is pushing the limits of navigable rivers. Even Niagara Falls has been successfully run by a kayaker. Modern interest in canoeing and kayaking for recreation and sport was brought about by John MacGregor, who designed the “Rob Roy,” a canoe he based on sketches of Inuit canoes and kayaks, in 1845. MacGregor formed the Canoe Club in 1866 with other canoe and kayak enthusiasts, and they brought about competitive canoeing with their first regatta in 1873. Kayaking was first included in the Olympic Games in Munich in 1972. Technological advances have revolutionized whitewater rafting. Electronically welded plastic has largely replaced rubber as the primary material used in raft construction, making the vessels lighter, stronger, and easier to repair. Self-bailing rafts, introduced in 1983, are now ubiquitous and provide greater maneuverability, allowing rafters to run rivers previously considered too difficult and dangerous. Unfortunately, greater mobility has been paralleled by an increase in the number of accidents occurring far from medical care. Rafts come in several different forms. In Europe, the most common is the symmetric raft steered with a paddle at the stern. Other types are the asymmetric, rudder-controlled raft and the symmetric raft with central helm (oars). Rafts are usually propelled with ordinary paddles and typically hold 4 to 12 persons. In Russia, rafts are often handmade and catamaran style, with two inflatable tubes attached to a frame. Pairs of paddlers navigate on these rafts. Catamaran-style rafts have become popular in the western United States, but are typically rowed instead of paddled. The enormous popularity of rafting and kayaking has led to exponential growth of professional guide services. In 1990, 35 million people were taken down U.S. rivers by commercial companies.73 Faced with increased competition, guide services have been leading inexperienced clients with little formal training and few practical skills into difficult and dangerous rivers (Figure 45-2). In the summer of 1988, five U.S. executives died after their raft flipped on the Chilco River in British Columbia. One of the survivors was reported to have said, “We looked at white water as sort of a roller coaster ride.”71

For online-only figures, please go to www.expertconsult.com

1993-1995*

Activity Climbing/hiking Bicycling Snow skiing Swimming Canoeing/kayaking/rafting Horseback riding Boating/water skiing Fishing Hunting

Rank

Fatalities

1 2 3 4 5 6 7 8 9

69 36 32 25 19 18 13 11  6

Data from Colorado Department of Public Health and Environment. *Two hundred fifty-two deaths were the results of recreational activities.

FIGURE 45-1  River rescue. The plastic kayak has revolutionized whitewater sports. (Courtesy Paul Auerbach, MD.)

Morbidity and Mortality Deaths are relatively rare in whitewater sports. In Colorado, fewer people die while engaged in rafting, canoeing, and kayaking than in climbing, bicycling, and skiing. Figures compiled by the Colorado Department of Public Health and Environment showed that during a 3-year period ending in 1995, 69 people died while climbing or hiking, 36 while bicycling, and 32 while snow skiing. Rafting, canoeing, and kayaking incidents, by comparison, resulted in 19 fatalities during that same time period (Table 45-1). A report from American Whitewater (AW) in 2000, based on data from 30 managed rivers from 1994 to 1998, placed the fatality rate of rafters, canoeists, and kayakers at 0.87 per 100,000 user-days.79 The fatality rate for kayakers alone was calculated to be 2.9 per 100,000 participants. The fatality rates of other outdoor sports are listed in Table 45-2. Injury rates for kayaking and rafting are 3 to 6 and 0.26 to 2.1 per 100,000 boating days respectively.26 Acute injuries in kayaking are usually

due to the transferred force of water on the upper extremity, most often the shoulder, or the impact on an object while swimming out of the boat. A retrospective analysis of injury reports submitted by commercial rafting outfitters to the West Virginia Division of Natural Resources from 1995 to 1997 revealed a total of 200 injuries, with a resulting overall injury incidence rate of 0.263 per 1000 rafters. The average age of injured persons was 33.14 years; 53.3% were male, and 59.8% had previous rafting experience.77 Founded in 1954, AW is a national nonprofit organization that maintains the Accident Database, which is a comprehensive compendium and analysis of whitewater accidents and close calls. The analysis provides the foundation for the AW Safety Code, which outlines whitewater safety guidelines applicable to all skill levels.3 The body parts most frequently injured during rafting mishaps are the face (33.3%), including the eye (12.1%), mouth (6.6%), other facial parts (5.1%), nose (4.5%), and teeth (4.0%); followed by the knee (15.3%); arm, wrist, or hand (11.6%); and other parts of the leg, hip, or foot (10.5%). The most common injury types are lacerations (32.5%), sprains or strains (23.2%), fractures (14.9%), contusions or bruises (9.8%), and dislocations (8.2%). Most injuries occur in the raft as a result of collisions among passengers, being struck by a paddle or other equipment, or entanglement of extremities in parts of the raft.77 Because most injuries occur in the raft and involve the face, accident-preventive measures include attaching face protection to paddling helmets and carrying fewer passengers per raft. In the summer and fall of 2000, a survey was distributed to whitewater canoe and kayak paddlers at riverside, through paddle club bulletins, and by the Internet. Three hundred nineteen surveys were returned, reporting 388 acute and chronic injuries. The shoulder, wrist, hand, and elbow were the most common sites of injury. Sprain or strain injuries were the most common (26%), followed by laceration and contusion (17% each). Tendinitis was the most common chronic injury (44%), followed by sprain or strain (27%). Giardia infection was reported in 14%.63 Most injuries occurred while the kayaker was still in the boat (87%). Striking an object was the most common mechanism of injury (44%), followed by traumatic stress and overuse (25% each).27 TABLE 45-2  Fatality Rates of Different Activities

FIGURE 45-2  Class V commercial rafting on the Chattooga River, Georgia. (Courtesy Robert Harrison, Whetstone Photography.)

Activity

Fatality Rate Per 1 Million Participant Days

Kayaking Rafting Trekking Skydiving Scuba diving Alpine skiing Driving

8.7-2.2 4.5-8.7 5-15 8.7 3.1 0.57 152 (1 day of driving is 100 miles)

Modified from Fiore DC: Injuries associated with whitewater rafting and kayaking, Wilderness Environ Med 14:25, 2003.

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CHAPTER 45  Whitewater Medicine and Rescue

TABLE 45-1  Recreational Fatalities in Colorado,

PART 5  RESCUE AND SURVIVAL

Sewn-in chest harness

Lash tabs for knife

Pockets

Belt with quickrelease buckle

Toggle

A

Locking waist tie with buckle

Girth adjustment straps

B

C

FIGURE 45-3  A, Life jacket with built-in rescue harness. B and C, A quick-release buckle allows the wearer to release the tether when necessary. It is essential for swift-water use.

Paddling Equipment The dynamic and unpredictable nature of rivers can turn any mishap into a tragedy. For this reason, the initial mission of whitewater medicine is to emphasize safety and accident prevention. According to the U.S. Coast Guard’s boating accident statistics, the most common factor contributing to whitewater-related deaths is failure to wear a personal flotation device (PFD, or life jacket).73 Exposure to cold river water can stimulate respiratory and cardiovascular reflexes, making it difficult for a swimmer to keep his or her head above water (maintain freeboard).42 The Coast Guard is charged with regulating and testing life jackets and classifies PFDs into five types. Of these, only two types are commonly used in whitewater sports. The type III PFD, a vest-type jacket favored by most paddlers, permits greater mobility and comfort. The Coast Guard requires that type III PFDs have a minimum of 7 kg (15.5 lb) of flotation (lift). Because most adults effectively weigh between 4.5 and 5.4 kg (10 and 12 lb) in the water, this allows at least 1.6 kg (3.5 lb) of effective required buoyancy. Type V PFDs are used by commercial outfitters because they provide greater flotation and are constructed asymmetrically, with more than one-half of the jacket’s flotation distributed in the front. This is supposed to turn an unconscious wearer face up. Although this may be true in calm water, it does not work reliably in swift water. A PFD should fit snugly and not ride up over the head when a person is in the water. Because even a well-fitting life jacket can be pulled off by turbulent water, some manufacturers now include crotch straps as an added safety feature. Testifying before a congressional subcommittee, the president of the National Transportation Safety Association cited the Chilco River accident to support his contention that crotch straps be made mandatory on all whitewater-use life jackets. Several survivors reported that their life jackets rode up over their heads and did not keep their faces above water. Life jackets with built-in rescue harnesses, pioneered by the Europeans, are now widely available in the United States. A typical harness system uses seatbelt webbing threaded through a metal retainer, then run into a plastic cam-lock buckle with a toggle. The toggle allows the user to find the buckle in whitewater. To release the system, the user pulls the toggle, opening the buckle and allowing the webbing to slip through the retainer and release. A D-ring mounted on the back of the jacket provides a point for clipping in a rope (Figure 45-3). This quick-release belt allows the wearer to attempt a strong swimmer rescue and also to get free of the tethering line quickly in an emergency. Beyond flotation, life jackets have other benefits that make them highly useful in wilderness settings. Their insulating properties help prevent hypothermia. The closed-cell foam flotation 848

material acts as thoracic padding during falls on slippery rocks or when swimming in rapids after exiting the craft. Life jackets also make excellent improvised splints; they can be fashioned into cervical collars, cylindric knee braces (Figure 45-4), or padded ankle stirrups. The AW Safety Code recommends the use of helmets at all times in kayaks and canoes, and in rafts and other craft when attempting rapids of class IV or greater difficulty. Surveys have shown that head trauma after capsizing constitutes 10% to 17% of all kayaking accidents.45,75 Whitewater helmets are typically crafted from stiff materials such as carbon fiber and Kevlar; a few manufacturers are also using polycarbonate prototypes. Unfortunately, paddling helmets have not been subjected to testing by any certifying entity, such as the American Society for Testing and Materials (ASTM). The Whitewater Research & Safety Institute, Inc. (WRSI), a nonprofit foundation dedicated to making whitewater recreation a safer sport, initiated the Whitewater Head Impact Protection (WWHIP) Project in 2002 in collaboration with Johns Hopkins University’s Bloomberg School of Public Health (http://www.jhu.edu/news_info/news/home02/may02/ helmet.html). A by-product of WRSI’s work is the creation of a prototype helmet that represents the culmination of their research.78 Placing adequate barriers between the human body and environment is of paramount importance in aquatic sports. Functional, insulated clothing should be considered a mandatory safety item to prevent hypothermia. Cotton is a poor choice for

FIGURE 45-4  A paddler wearing a type III life jacket around his knee as an improvised knee immobilizer to help stabilize a sprained knee.

River Hazards The International Scale of River Difficulty grades rivers and rapids as classes I to VI. An American version of this rating has been adopted by the AWA for most U.S. rivers72 (Box 45-1). Some western rivers use the Grand Canyon System, which rates rapids on a scale from 1 to 10. Neither scale is a truly objective standard; individual and regional variations are common, and the margin of difficulty for a particular rapid may differ significantly for kayaks and rafts. Unfortunately, important safety parameters, such as water temperature, remoteness, and evacuation potential, are not taken into consideration. The difficulty of a river generally increases with the volume and average gradient of flow. The volume of water in a river is usually expressed as a measure of cubic feet per second (cfs). This is the amount of water moving past a certain point during a given period of time. The volume of a river can be determined by multiplying the width by the depth by the speed of the current. For example, a channel 10 feet deep and 20 feet wide moving at a velocity of 5 feet per second (fps) equals a volume of 1000 cfs. As the water level rises, its speed and power increase exponentially, raising the difficulty of most rapids.5 When the speed of the current is doubled, the force of the water against an object in the current is quadrupled; that is, the force of the current increases as the square of its speed. Occasionally, however, a rapid becomes easier as the added water submerges hazardous obstacles. Gradient is the amount of drop between two points and is expressed as feet per mile. The steeper the gradient, the faster the water moves. Not all water flows downstream. The most common upstream flow is an eddy, which is created when water flows around an obstacle. The water piles up higher than the river level on the upstream side of the obstacle, whereas the water on the downstream side is lower. Water flows around the obstacle then back toward it to fill in the low spot. The line between the upstream and downstream current is the eddy line. Eddies are one of the most important features of the river for boat maneuvering and rescue. Exiting the main current by pulling into an eddy allows the paddler to stop the descent and safely scout the next rapid. It also provides a location for a paddler to set up rescue for his or her companion upstream. Hydraulics, also known as holes, reversals, rollers, suck-holes, and pour-overs, are the most common hazards in rivers. A hydraulic is created when water flows over an obstacle, causing a depression that produces a relative vacuum within which the downstream water recirculates (Figure 45-5). The water below a hydraulic is typically very aerated and presents a white, foamy appearance. Rafts and kayaks can be turned upside down by the force of a hydraulic, and if the reversal currents are strong enough, crafts and people can become trapped in the recirculating flow. When proceeding into a rapid that contains a hazardous hydraulic, one of the group should preset a rope below the hole to facilitate rescue. Hydraulics release water downstream from beneath the surface. This may be the only avenue of escape for a swimmer. Escape from a strong hydraulic may require a person to stay submerged and to resist the urge to return immediately to the surface. Surfacing too early can result in recirculation.

BOX 45-1  American Version of the International Scale

of River Difficulty

Class I: Easy Fast-moving water with riffles and small waves. Few obstructions, all obvious and easily avoided with little training. Risk to swimmers is slight; self-rescue is easy. Class II: Novice Straightforward rapids with wide, clear channels evident without scouting. Occasional maneuvering may be required, but rocks and medium-sized waves are easily avoided by trained paddlers. Swimmers are seldom injured, and group assistance, although helpful, is seldom needed. Class III: Intermediate Rapids with moderate, irregular waves that may be difficult to avoid and can swamp an open canoe. Complex maneuvers in fast current and good boat control in tight passages or around ledges are often required; large waves or strainers may be present but are easily avoided. Strong eddies and powerful current effects can be found, particularly on a large-volume river. Scouting is advisable for inexperienced parties. Injuries while swimming are rare; self-rescue is usually easy, but group assistance may be required to avoid long swims. Class IV: Advanced Intense and powerful but predictable rapids requiring precise boat handling in turbulent water. The advanced river may feature large, unavoidable waves and holes or constricted passages that demand fast maneuvers under pressure. A fast, reliable eddy turn may be needed to initiate maneuvers, scout rapids, or rest. Rapids may require “must” moves above dangerous hazards. Scouting is necessary the first time down. Risk for injury to swimmers is moderate to high, and water conditions may make self-rescue difficult. Group assistance for rescue is often essential but requires practiced skills. A strong Eskimo roll is highly recommended. Class V: Expert Extremely long, obstructed, or violent rapids that expose a paddler to above-average danger. Drops may contain large, unavoidable waves and holes or steep, congested chutes with complex, demanding routes. Rapids may continue for long distances between pools, demanding a high level of fitness. Eddies may be small, turbulent, or difficult to reach. At the high end of the scale, several of these factors may be combined. Scouting is mandatory but often difficult. Swims are dangerous and rescue is difficult, even for experts. A very reliable Eskimo roll, proper equipment, extensive experience, and practiced rescue skills are essential for survival. Class VI: Extreme Class VI runs exemplify the extremes of difficulty, unpredictability, and danger. The consequences of errors are severe, and rescue may be impossible. These runs are for teams of experts only, at favorable water levels, after close inspection, and taking all precautions. This class does not represent drops believed to be unrunnable but may include rapids that are only run occasionally. From Safety Code of the American Whitewater Affiliation. http://www. americanwhitewater.org/content/wiki/safety.start?#vi.

Fortunately, most hydraulics eventually release people regardless of what action they take. Novice paddlers often misjudge the force of hydraulics. It is not the height of the drop that generates the recirculating power but rather the shape and angle of the obstruction, combined with water volume and adjacent eddy currents. A “smiling” hydraulic has its outer edges curving downstream, so that the recirculating water feeds out into the main current and is thus easier to escape. In a “frowning” hydraulic, the outer edges curve back upstream into the center of the hydraulic, making escape much more difficult. Low-head dams or weirs form massive hydraulics with enormous recirculating potential. Unlike natural hydraulics, these human-made structures form hydraulics all the way across the river, leaving no escape routes. In the Binghamton Dam disaster 849

CHAPTER 45  Whitewater Medicine and Rescue

river wear; it loses all of its insulating properties when wet and dries slowly. Newer synthetics, such as polypropylene and polyester pile, absorb no more than 1% of their weight in water and maintain thermal insulating qualities when wet.41 When combined with a nylon or Gore-Tex paddling jacket, a synthetic underlayer provides effective protection from cold and wind. Wet suits, previously considered to be optimal garments for paddlers in extreme conditions, are stiff and somewhat constricting.1 The dry suit, with tight-fitting latex seals at the wrist, ankle, and neck, is the new gold standard for cold-water boating. By sealing water out and preventing evaporative heat loss, the dry suit can keep a paddler warm even during winter conditions.31 Overheating is occasionally a problem with dry suits. Recently, a dry suit contributed to profound and unexpected hyperthermia in a kayaker who had suffered a submersion injury in cold water.10

PART 5  RESCUE AND SURVIVAL

Recirculation zone

Escape zone

FIGURE 45-5  Recirculating currents created by a hydraulic. Water and “swimmers” are released downstream beneath the surface.

of 1975, a 4-m (13.5-foot) Boston whaler with a 20-horsepower engine was pulled into a hydraulic while attempting a rescue, resulting in the deaths of three firefighters.69 Undercut rocks are boulders or ledges that have been eroded just beneath the water surface. These usually occur on geologically older rivers. They can be difficult to recognize and pose significant risks for entrapment and drowning, even in class II rapids. The potential for entrapment can also occur when swimmers attempt to stand up and walk in swift-moving currents. A foot can become wedged in an undercut rock or between rocks beneath the surface, causing the victim to lose his or her balance and fall face down into the river (Figure 45-6, A). With the foot entrapped, the victim cannot regain an upright or even face-up position. This type of mishap has caused drownings in water less than 3 feet deep. A swimmer in a rapid should assume a supine position, with feet at the surface and pointed downstream to serve as shock absorbers. This position minimizes the potential for both foot entrapment and head and neck trauma (see Figure 45-6, B). Strainers are obstacles, such as fallen trees, bridge debris, or driftwood, lodged between rocks or jutting out from the shore, that allow water to pass through (sieve effect) while trapping the swimmer or boater. Flooded rivers, a favorite of expert boaters, often develop many new strainers as riverbank debris is washed into the flow. In the summer of 1987, five paddlers drowned when their raft struck a large strainer on Canada’s Ellaho River.71

Negotiating a strainer requires special tactics. The safest option for the swimmer is to swim aggressively into the strainer head first rather than feet first, and then attempt to climb over the debris (Figure 45-7, A). Approaching a strainer feet first may lead to underwater entrapment (Figure 45-7, B). Man-made hazards can also pose a threat to river runners. Bridge pilings, submerged automobiles, dams, and low-hanging power lines can pin or injure boaters. A broach occurs when a boat wraps sideways around an obstacle or when both bow and stern become stuck on separate obstacles simultaneously. Common obstacles include boulders, trees, bridge pilings, and ledges protruding from canyon walls. Drowning can occur if the paddler leans upstream away from the obstacle and flips upside down while still broached or if the boat collapses and entraps the victim (Figure 45-8). A vertical pin happens when a kayaker plunges over a drop and the end of the boat becomes trapped between rocks beneath the surface. The force of the water can fold a plastic kayak over on itself, trapping the occupant upside down beneath the surface (Figure 45-9). A survey of 365 members of AW revealed that 33% of serious kayaking incidents and 41% of open canoeing mishaps involved either pinning or broaching75 (Table 45-3). In a separate survey of 500 paddlers between 1989 and 1993, 42% of kayaking fatalities resulted from vertical pins, broaches, or entrapments in strainers.

A A

B FIGURE 45-6  A, Attempting to stand up in shallow water can produce foot entrapment in an undercut rock. B, Proper way to swim while in a rapid.

850

B FIGURE 45-7  A, Proper approach to a strainer. B, Incorrect approach to a strainer.

Incident Type Vertical pin entrapment Broach entrapment Rock sieve entrapment Undercut rock entrapment Recirculation in hydraulic Long swim Obstacle

FIGURE 45-8  Broach.

Kayak construction can have important safety implications in both broach and pin situations. The force of the current against the deck of the boat or back of the paddler can make it impossible for the victim to extract his or her legs and escape. Boat makers have developed kayaks with larger cockpits that make it easier to raise the knees out and escape the craft. Transverse bulkhead-type foot braces have replaced pedal-type braces to prevent the kayaker from being shoved forward in the boat. This feature ensures the escape potential offered by larger cockpits. One of the compromises of the larger cockpit, however, is that the spray skirt is more likely to come off in turbulent water.

Submersion Accidents Almost all fatalities on rivers result from submersion. Each year, the River Safety Task Force of the American Canoe Association compiles accounts of drownings and other accidents. Every 3 years, it publishes the River Safety Report, which chronicles and analyzes these accidents.69-71,73 Most submersion fatalities occur after paddlers unexpectedly swim from their boats or become trapped in them underwater. The exact cause of drowning often remains unclear and is inexplicably blamed on immersion hypothermia. Although hypothermia induces impaired judgment and coordination and may be an

No. of Incidents

Percentage of Accidents

18 46 16 23 47 42

8 21 7 10 21 19

From Wallace D: Scary numbers and statistics: Results of AWA close calls and serious injuries survey, Am Whitewater: J Am Whitewater Affiliation 37:27, 1992.

important contributing factor, immersion hypothermia is probably never the sole cause of death.77 Studies by Hayward and others have shown that seminude subjects are able to maintain normal core temperatures for 15 to 20 minutes in 10° C (50° F) water.33,34 Continuous immersion for up to 1 hour would be required to produce profound hypothermia.34 Cold-water immersion precipitates drowning by three other mechanisms. Sudden cold-water immersion produces profound cardiovascular and respiratory responses. Reflex sympathetic output can markedly increase blood pressure and heart rate, resulting in lethal arrhythmias.30,42,43 An immediate and involuntary gasp occurs after cold-water immersion. This is followed by hyperventilation.15 Pulmonary ventilation increases up to fivefold because of increased tidal volume and respiratory rate.66 The initial gasp can result in aspiration of water and laryngospasm. Hyperventilation produces respiratory alkalosis with resultant muscle tetany and cerebral hypoperfusion.15 This response can increase the risk for drowning in a person struggling to maintain an airway freeboard in rough water. The respiratory stimulation produced by cold-water immersion significantly decreases breath-holding duration.35 This fact has enormous implications for kayakers, who must hold their breath while attempting to roll up a boat after flipping upside down. This probably accounts for the unexplained swims by expert kayakers who sometimes fail to right themselves after flipping in cold water. Although some maintain that respiratory and cardiovascular reflexes can be abolished by repeated exposure of the face to cold water just before entering a rapid, there are no scientific data to support this theory of acclimatization. Peripheral cold-water–induced vasoconstriction exacerbates rapid cooling of muscles and nerves in the extremities, resulting in loss of strength and coordination.66 Ability to swim, maintain freeboard, avoid obstacles, and climb from the river may be greatly impaired.44 Even when the air temperature is warm, paddlers running cold water rivers should wear sufficiently insulated clothing.

FIGURE 45-9  1, Vertical pin. 2, Pitchpole pin.

1

2

851

CHAPTER 45  Whitewater Medicine and Rescue

TABLE 45-3  Serious Whitewater–Related Incidents

PART 5  RESCUE AND SURVIVAL

The combination of hyperventilation and muscle dysfunction can be lethal for a swimmer in rough water. A PFD helps, but it does not prevent even small waves from submerging a swimmer’s head.29 These dangers make it imperative to preset safety systems in significant rapids and to rescue swimmers first. Safety kayaks with enhanced buoyancy are recommended on commercial raft trips because they provide additional flotation for clients who fall overboard. Unfortunately, paddlers have drowned when their companions chased after equipment, assuming that the swimmer could climb out of the river without assistance.70,72 The main treatment for a submersion incident on a river is immediate and aggressive initiation of ventilation and oxygenation using mouth-to-mouth rescue breathing. A glove can be modified and used as a barrier shield for performing rescue breathing. Cut the middle finger of the glove at its halfway point and insert it into the victim’s mouth. Stretch the glove across the victim’s mouth and nose and blow into the glove as you would to inflate a balloon. After each breath, remove the part of the glove covering the nose to allow the victim to exhale. The slit creates a one-way valve, preventing backflow of the victim’s saliva (Figure 45-10, online). Evidence of trauma should be noted and attention given to cervical spine precautions. Contributing and associating factors such as hypoglycemia, seizures, and hypothermia need to be considered. Because apnea usually precedes cardiac arrest, if ventilation is provided, circulatory resumption may occur spontaneously. Abdominal thrusts are not recommended unless the victim has an obstructed airway and cannot be adequately ventilated.

Trauma A survey of commercial raft clients revealed that the most common significant injury was a sprained or fractured ankle.76 Ironically, these injuries usually occur out of the water when walking on loose, wet, and slippery rocks during scouting and portaging or when entering or leaving the river. Ankle and other lower-extremity injuries also occur on the river when rafters are tossed onto each other in rapids. Kayakers are prone to ankle injuries from forced dorsiflexion or inversion when the bow of the boat hits an obstruction. The feet are held against the narrow horizontal braces while the heels are pushed underneath, or the entire ankle is inverted. Europeanand some American-designed kayaks with bulkhead foot braces have reduced this problem. Management of foot and ankle injuries should begin with ice, elevation, and compression to reduce swelling. Cold river water is usually substituted for ice. Compression wrapping is important after icing to prevent swelling from reflex vasodilation. Splinting is important to reduce pain and edema and to limit exacerbation of the injury during evacuation. Neurovascular integrity must be checked frequently with an air splint. Ankle splints can be improvised from life jackets, kayak float bags, articles of clothing, or a SAM splint. Strains are common in whitewater sports. Researchers at Dalhousie University in Halifax, Nova Scotia, analyzed dynamic electromyographic potentials of the various muscle groups used in kayaking and then correlated them with videotaped sequences.51 Muscles used most often in kayaking that are prone to strain injury are shoulder extensors (latissimus dorsi, teres major, pectoralis major), medial scapula rotators (rhomboideus major and minor, pectoralis minor), lateral scapula rotators (pectoralis minor, serratus anterior), shoulder flexors and horizontal adductors (anterior deltoids, pectoralis major, coracobrachialis), elbow extensors (triceps), and spine erector muscles. Any training program for kayakers needs to emphasize conditioning of these muscle groups. Back strain afflicts rafters, kayakers, and canoeists. In a survey of 2510 rafting guides working in Washington, Oregon, Idaho, Utah, Colorado, and the Grand Canyon during one summer, 77.4% of guides reported back pain while guiding and 20.8% had back pain lasting longer than 1 week.38 Stacking five or more inflated boats for transport was correlated with the presence of pain; loading and unloading rafts were correlated with back pain lasting longer than 1 week. 852

TABLE 45-4  Common Whitewater–Related Injuries,

1980-1991 (N = 85)

Injury Type Shoulder dislocation Near drowning Fractures Head and neck Hypothermia Leg injuries Lacerations Fatalities

No. of Injuries

Percentage of Injuries

14 11 15 6 4 11 9 7

16.5 12.9 17.6 7.0 4.7 12.9 10.5 8.2

From Wallace D: Scary numbers and statistics: Results of AWA close calls and serious injuries survey, Am Whitewater: J Am Whitewater Affiliation 37:27, 1992.

Rafters are also prone to back injuries while portaging, pushing stuck rafts off rocks, and carrying the crafts to and from the river. Raft guides are notorious for suffering back strain when pulling capsized customers, who often weigh more than guides, back into the rafts. Kayakers and canoeists injure their backs lifting water-laden boats and loading their crafts onto automobile roofs. Sitting for prolonged periods with minimal back support and extended legs leads to muscle fatigue in kayakers, compounding the potential for back injury. Repetitive dorsiflexion of the wrist required to operate an offset (feathered) kayak paddle produces tendonitis and synovitis.47 A paddle constructed with a 75- to 80-degree offset instead of the traditional 90 degrees can reduce wrist stress. Aspirin or nonsteroidal antiinflammatory agents ingested 30 minutes before paddling, combined with ice application afterward, may be beneficial. Wrist supports provide limited relief. The injury most often associated with kayaking is the anterior shoulder dislocation. Various surveys have placed its incidence in kayakers at 10% to 16%, making it the second most common whitewater-related injury11,46,75,76 (Table 45-4). The maneuver most notorious for precipitating this injury is the high brace. Often used while supporting the kayaker in a hydraulic, surfing on a wave, or rolling the kayak upright after a flip, the high brace entails abduction of the humerus, with external rotation of the glenohumeral joint (Figure 45-11). If the arm becomes extended behind the midline plane of the body by the force of the current, the triad of abduction, external rotation, and extension of the shoulder can stretch or rupture the glenoid labrum and capsule, resulting in anterior subluxation or dislocation.64 The paddle acts as a lever to increase the force on the glenohumeral joint. To minimize the risk for shoulder dislocation, the preferred method of bracing is the “low brace,” in which the arm is held in internal rotation and close to the body (adduction). Although initially awkward for the novice paddler, this bracing maneuver is inherently stronger and more versatile because it allows backpaddling out of a hydraulic. Exercises that strengthen the rotator cuff and deltoids, triceps, and pectoralis muscles reinforce the glenohumeral joint.

FIGURE 45-11  High brace maneuver.

Thumb pushes inferior point of scapula medially

RIVERSIDE SHOULDER REDUCTION TECHNIQUE On-scene reduction of a shoulder dislocation provides immediate relief of pain, curtailment of ongoing injury, and subsequent ability to function more actively in evacuation. Several techniques have been advocated for reduction.60 The key element is rapid initiation because the longer a shoulder remains dislocated, the more difficult the eventual reduction becomes. Relocation is often delayed because river corridors rarely afford rapid access to a flat and comfortable area upon which to place a victim in the supine or prone position, a requirement for most techniques. For river and other wilderness settings, reduction is facilitated by using a technique in which the victim is standing or sitting (Figure 45-12). For the standing technique, as soon as the diagnosis is made, the victim bends forward at the waist while the rescuer supports the chest with one hand. With the other hand, the rescuer grabs the victim’s wrist and applies steady downward traction and external rotation. While maintaining traction, the rescuer can slowly flex the shoulder by moving it in a cephalad direction until reduction is obtained. If two rescuers are available, one should support the victim at the chest while the other pulls countertraction and flexion at the arm. Scapular manipulation by adducting the inferior tip of the scapula using thumb pressure and stabilizing the superior aspect of the scapula with the cephalad hand may augment reduction52,60 (Figure 45-13).

A

CHAPTER 45  Whitewater Medicine and Rescue

The paddler with a dislocation is usually aware that something has gone wrong and holds the extremity away from the body, unable to bring the arm across the chest.64 The shoulder may appear square because of anterior, medial, and inferior displacement of the humeral head into a subcoracoid position.

Assistant pulls down and forward

FIGURE 45-13  If two rescuers are available, scapular rotation to assist shoulder relocation can be performed while the second rescuer pulls the arm down and forward. The inferior top of the scapula is pushed medially.

Shoulder reduction can also be done while the victim is sitting. Grab the victim’s forearm close to his or her elbow with both hands, and with the elbow bent at 90 degrees, pull steady downward traction on the arm. After about one minute of sustained traction, slowly raise the entire arm upward until reduction is complete. Gingerly rotating the forearm outward while pulling traction may facilitate reduction. If a second rescuer is present, scapular manipulation can be performed simultaneously, as described earlier. Another relocation technique uses the victim’s life jacket to allow one rescuer to apply both controlled traction and countertraction.19 This technique requires that the victim be supine, with room for the rescuer to sit adjacent to the dislocated shoulder. The rescuer then slides his or her foot and leg through the life jacket’s arm opening, under the neck, and out through the jacket’s head opening. The rescuer’s leg functions as a headrest, whereas the foot braced against the opposite shoulder strap of the life jacket provides countertraction. Holding the forearm of the affected side with the elbow bent at 90 degrees, the rescuer slowly leans back to apply traction while the leg exerts countertraction. The life jacket allows countertraction force to be distributed across the victim’s chest. External and internal rotation can be applied to the humerus during traction to facilitate reduction (Figure 45-14). One should always monitor circulation and motor and sensory function to the wrist and hand before and after attempting a shoulder reduction. To prevent a recurrent dislocation, the kayaker’s arm should be splinted across the chest with a sling or swath or by pinning the sleeve of the arm across the chest (Figure 45-15, online). If circumstances preclude exiting the river without further kayaking, the shoulder can be partially stabilized with the use of a functional shoulder immobilizer (shoulder spica wrap). This method allows the victim to kayak while still limiting complete abduction and external rotation of the arm (Figures 45-16 and Figure 45-17).

HEAD, FACIAL, AND DENTAL TRAUMA

B FIGURE 45-12  Technique for shoulder relocation with the victim standing. A, The rescuer supports the victim’s chest with one hand and pulls down and forward (B) with the other hand.

Head, facial, and dental trauma are more common in kayakers and decked canoeists than in rafters because of the potential for flipping upside down while still in the craft. Head and facial trauma can be minimized by wearing a protective helmet and tucking forward, instead of leaning backward, while rolling a kayak. Epistaxis is common following facial trauma, because most paddling helmets do not include face protection. Although most 853

PART 5  RESCUE AND SURVIVAL

FIGURE 45-16  Shoulder dislocation.

FIGURE 45-14  Using a life jacket to assist in countertraction for shoulder relocation.

A

B

C

D FIGURE 45-17  A to D, Shoulder spica wrap.

854

harness

for

support

after

shoulder

SPINE INJURIES Spine fractures have been reported in kayakers and canoers.70,71,73 Cervical spine injuries have occurred in kayakers in conjunction with head trauma sustained after flipping upside down. Vertical compression fractures of the thoracolumbar spine have occurred from axial loading when a kayaker landed flat after paddling over a waterfall. One kayaker was rendered paraplegic after landing on his back on rocks while attempting to negotiate a waterfall.73 Fortunately, his companions recognized the injury and kept him supported on Minicel foam blocks from their kayaks until a backboard could be obtained. Properly modified, the kayak makes an ideal rigid long-board improvised litter. First, remove the seat along with sections of the upper deck if necessary. A serrated river knife (or camp saw) makes this improvisation much easier. Open-deck canoes can be used almost “as is” once the flotation material has been removed. Many rivers have railroad tracks that run parallel to the river canyon. The tracks can be used to slide a canoe by placing the boat perpendicular to the tracks and pulling on both bow and stern lines.

FRACTURES AND IMPROVISED SPLINTING Significant visceral and musculoskeletal injuries can occur when a swimmer is sandwiched between a downstream boulder or obstruction and the upstream craft that has been exited. Swimmers should always stay upstream of their craft. Oar rafts with aluminum and metal frames and containers that flip can produce extremity and pelvic fractures in a hydraulic or large wave. Splint all fractures before the victim is moved unless his or her life is in immediate danger. In general, make sure the splint incorporates the joints above and below the fracture. If possible, the splint should be fashioned on the uninjured extremity and then transferred to the injured one. On river trips, canoe and kayak paddles can be used as improvised splints. Airbags used as flotation for kayaks and canoes can be converted into pneumatic splints for arm and ankle injuries. The Minicel or Ethafoam pillars found in most kayaks can be removed and carved into pieces to provide upper and lower extremity splints. A life jacket can be molded into a cylinder splint for knee immobilization or into a pillow splint for the ankle. Ideally, a splint should immobilize the fractured bone in a functional position. In general, “functional position” means that

the legs should be straight or slightly bent at the knee, the ankle and elbow bent at 90 degrees, the wrists straight, and the fingers flexed in a curve as if the person were attempting to hold a can of soda or a baseball. Splints can be secured in place with strips of clothing, belts, pieces of rope or webbing, pack straps, gauze bandages, or elastic bandage wraps. Pelvic fractures can occur during a raft flip, especially if the raft is outfitted with a rowing frame and heavy oars, or from a fall while portaging crafts around rapids on slippery rocks. Unstable pelvic fractures are associated with a high incidence of morbidity and mortality.8,18,48 In one study, pelvic ring disruption in the trauma patient was associated with a mortality rate of 25%.2 Acute and uncontrolled hemorrhage and its complications are the leading causes of death in these patients.24 Hemorrhage after pelvic injury is from fracture surfaces, venous plexuses, and major arteries, usually branches of the internal iliac artery. Pelvic reduction and stabilization in the early post-traumatic phase are reported to provide the most effective means of controlling venous hemorrhage.7 Pelvic reduction realigns bleeding fracture surfaces and reduces pelvic volume, whereas pelvic stabilization facilitates clot formation by reducing fracture site motion.28 Circumferential wrapping and compression of the pelvic region with a sheet or strap has been studied as a means to stabilize and reduce open-book pelvic fractures.6,8 In a pair of studies from Oregon, circumferential pelvic compression was evaluated with the use of cadaveric models. Circumferential compression was found to result in significant stabilization of open-book pelvic injuries. The optimal placement of compression was at the level of the greater trochanters and the symphysis pubis, and the desired tension was found to be around 180 Newtons (40 pounds).6 Vermeulen reported on the application of a pelvic strap to 19 patients in Switzerland.68 The straps were applied at the accident scene by EMTs upon suspicion of an unstable pelvic fracture. It took only 30 seconds to apply a splint. The benefit was significant reduction in both symphysis diastasis and pelvic inlet area. Routt used a large circumferential sheet pulled tightly around the pelvis.62 The sheet remained in place until further stabilization could be achieved with external fixation. Application of the sheet achieved reduction and stabilization in a safe and time-effective manner and did not interfere with resuscitation efforts. The American College of Surgeons Advanced Trauma Life Support (ATLS) course now includes a protocol for emergency management of pelvic ring disruptions, advising circumferential application of a pelvic sheet. Circumferential compression with a noninvasive pelvic sling should be considered for any patient with a suspected pelvic fracture in the wilderness. The SAM Sling is a commercial device that provides 150 Newtons (34 pounds) of pressure to the pelvis when applied according to the manufacturer. It is equipped with an “autostop” buckle, with spring-loaded prongs that lock the buckle in place when the correct amount of tension is applied. Clothes, sheets, sleeping bags, pads, air mattresses, tents, or tent fly can be used to improvise a very effective pelvic sling in the backcountry. The object should be wide enough so that it does not cut into the victim when tightened. Applying an Improvised Pelvic Sling 1. First, ensure that objects have been removed from the patient’s pockets and that any belt has been removed so that the pressure of the sheet or object does not cause additional pain by pressing items against the pelvis. 2. Very gently slide the improvised sling under the victim’s buttocks and center it under the bony prominences at the outer part of the upper thigh or hips (greater trochanters/ symphysis pubis) (Figure 45-20). Cross the object over the front of the pelvis and tighten the sling by pulling both ends and securing with a knot, clamp, or duct tape. Another tightening technique is to wrap the sling snugly around the pelvis and tie an overhand knot. Place tent poles, a stick, or similar object on the knot and tie another overhand knot. Twist the poles or stick until the sling becomes tight. The sling should be tightened so that it is snug and the pelvis is returned to its normal anatomic position. 855

CHAPTER 45  Whitewater Medicine and Rescue

cases of epistaxis are minor, some present life-threatening emergencies.81 Anterior epistaxis from one side of the nasal cavity occurs in 90% of cases.9 If pinching the nostrils against the septum for a full 10 minutes does not control the bleeding, nasal packing may be needed. Soak a piece of cotton or gauze with a vasoconstrictor, such as oxymetazoline (Afrin) nasal spray, and insert it into the nose, leaving it in place for 5 to 10 minutes. Vaseline-impregnated gauze or strips of a nonadherent dressing can then be packed into the nose so that both ends of the gauze remain outside the nasal cavity (Figure 45-18, online). This prevents the victim from inadvertently aspirating the nasal packing. Complete packing of the nasal cavity of an adult victim requires a minimum of 1 m (3 feet) of packing to fill the nasal cavity and act as a tamponade for the bleeding site.9 Expandable packing material, such as Weimert Epistaxis Packing or the Rhino Rocket, is available commercially. A tampon or balloon tip from a Foley catheter can also be used as improvised packing.81 Anterior nasal packing blocks sinus drainage and predisposes to sinusitis. Prophylactic antibiotics are usually recommended until the pack is removed in 48 hours.81 If the bleeding site is located posteriorly, use a 14- to 16-Fr Foley catheter with a 30-mL (1-oz) balloon to act as a tamponade for the site.14 Prelubricate the catheter with either Vaseline or a water-based lubricant; then insert it through the nasal cavity into the posterior pharynx. Inflate the balloon with 20 to 30 mL (0.7 to 1 oz) of water and gently withdraw it back into the posterior nasopharynx until resistance is met. Secure the catheter firmly to the victim’s forehead with several strips of tape. Pack the anterior nose in front of the catheter balloon as described earlier (Figure 45-19, online).

PART 5  RESCUE AND SURVIVAL

Improvised wound irrigation requires only a container that can be punctured to hold the water, such as a sandwich bag or garbage bag, and a safety pin or 18-gauge needle. Disinfected river water is safe and effective for irrigating wounds.25 Before a wound is closed, remove all foreign material and grossly devitalized tissue. You can accomplish debridement using scissors, knife, or any other sharp object. Close wounds with sutures, staples, tape, pins, or glue. Although suturing is still the most widely used technique, stapling and gluing are ideal methods for closing wounds in the aquatic environment. Clinical studies of the use of staples to close traumatic lacerations have found various advantages of stapling over suturing: wound tensile strength is greater, there is less inflammation, the time required for closure is shorter, and fewer instruments are needed.61 Staples are ideal to use in an aquatic environment, and the cosmetic outcome is not compromised. Staplers are lightweight, presterilized, and easy to use. FIGURE 45-20  Pelvic sling improvised with jacket.

3. If a Therm-a-Rest pad or other inflatable sleeping pad is available, fold it in half so that it approximates the size of the pelvis. Gently slide the pad under the victim’s buttocks and center it under the greater trochanters and symphysis pubis. Secure the pad with duct tape, and then inflate the pad as you normally would, until it produces a snug fit and the pelvis is reduced (Figure 45-21). 4. Place padding between the legs and gently tie the legs together to further stabilize the fracture in a position that is most comfortable for the victim. Wounds are common on river trips. The same principles that govern wound management in the emergency department apply in the wilderness. The main problem faced in the river environment is access to adequate supplies and keeping the wound dry. The primary determinants of infection are bacterial counts and amount of devitalized tissue remaining in the wound.21 Ridding a wound of bacteria and other particulate matter requires more than soaking and gentle washing with a disinfectant.49 Irrigating the wound with a forceful stream is the most effective method of reducing bacterial counts and removing debris and contaminants.53,67 The cleansing capacity of the stream depends on the hydraulic pressure under which the fluid is delivered.20,65 Irrigation is best accomplished by attaching an 18- or 19-gauge catheter to a 35-mL (1.2-oz) syringe or a 22-gauge needle to a 12-mL (0.4-oz) syringe. This creates hydraulic pressure in the range of 7 to 8 lb/in2 and 13 lb/ in2, respectively.65,67 The solution is directed into the wound from a distance of 1 to 2 inches at an angle perpendicular to the wound surface and as close to the wound as possible. The amount of irrigation fluid varies with the size and contamination of the wound, but it should average no less than 250 mL (8.5 oz).

Hair-Tying a Scalp Laceration If you are faced with a bleeding scalp laceration and the injured person has a healthy head of hair, you can tie the wound closed using the victim’s own hair and a piece of suture (0-silk works best), dental floss, sewing thread, or thin string. Take the material and lay it on top of and parallel to the wound. Twirl a few strands of hair on each side of the wound and then cross them over the wound in opposite directions so that the force pulls the wound edges together. Have an assistant tie the strands of hair together with the material while you hold the wound closed with the strands of hair. A square knot works best (Figure 45-22). Repeat this technique as many times as necessary, along the length of the wound, to close the laceration. Dermabond tissue glue is an excellent option for wound closure on river trips because the glue is impervious to water and can be applied without instruments. It also precludes the need for topical anesthesia and is easy to use. When applied to the skin surface, tissue glue provides wound closure for only 2 to 3 days before losing its bond and thus needs to be reapplied on any surface other than the face. Many kayakers suffer abrasions and contusions to the fingers and knuckles while hanging upside down after flipping. Oar frames, oars, paddles, and the metal ammunition boxes used to hold supplies can all inflict injury when rafts are capsized or paddlers are tossed in turbulent water. Blisters on the hands are a frequently reported problem in paddling surveys.76 Kayakers develop them at the metacarpophalangeal (MCP) joint of the thumb along the ulnar aspect. Common sites of blister formation in rafters and canoeists are the proximal palmar surfaces of the MCP joints. Taping and moleskin application reduce the incidence of this potentially incapacitating problem.

Infections Blisters, abrasions, and lacerations are always at increased risk for infection in an aquatic environment. Maceration from prolonged immersion in water and exposure to atypical pathogens are contributing factors. An outbreak of Staphylococcus aureus skin infections among raft guides in Georgia and South Carolina nearly led to the demise of two rafting companies.17 Sharp grommets on the thwarts of the rafts had caused repeated lower extremity abrasions. The causative organism was cultured from rafts up to 48 hours after use. Daily raft disinfection enabled the companies to remain in operation.

FIGURE 45-21  Pelvic sling improvised with inflatable sleeping pad and duct tape.

856

FIGURE 45-22  Square knot.

Otitis externa (swimmer’s ear) is a common problem among paddlers. Water exposure to the ear canal macerates the epithelium and elevates the normally acidic pH of the canal, predisposing the ear to infection.22 The bacteria most commonly cultured are Pseudomonas aeruginosa, Proteus vulgaris, and Staphylococcus species.22,39 Antibiotic eardrops with or without hydrocortisone are widely available and very useful. Irrigation of the canal with commercially available solutions containing acetic acid and alcohol helps prevent infection by lowering pH and drying the canal.39 The drops should be applied after each outing. Recent publicity given to water contamination by Giardia lamblia has been reinforced by statistics from the Centers for Disease Control and Prevention, which report Giardia organisms to be the most common pathogenic intestinal parasite in the United States (see Chapters 67 and 68). Giardia cysts abound in mountain streams and rivers once considered to be sources of pristine water (Figure 45-23). They persist in very cold water and have no detectable taste or smell. Rivers are contaminated by animals that defecate in or near the water. Studies by the Wild Animal Disease Center at Colorado State University, Fort Collins, Colorado, have identified more than 30 animal species as Giardia carriers. Paddlers who travel to foreign countries should seek information on local endemic diseases and relevant prophylactic measures. Whitewater rafting and kayaking in third world countries subject paddlers to unusual aquatic-related infections. This is exemplified by a report of schistosomiasis in rafters returning from Ethiopia.37 Schistosomiasis is endemic in large areas of Africa, South America, and the Caribbean and is transmitted to humans who swim or come into contact with fresh water containing the larval stage. Paddlers who return from endemic regions should be screened with serologic testing because up to 50% of infections are asymptomatic.47 Malaria has been reported in rafters returning from New Guinea, and both leptospirosis and hepatitis have stricken kayakers venturing to Costa Rica.4 In the United States, pulmonary blastomycosis was reported among canoeists in Wisconsin.13

Environmental Hazards Although hypothermia is rarely the cause of death among whitewater paddlers, hypothermia-induced impairment of judgment and coordination is a significant contributing factor in many fatalities and accidents.32,44,69-71,80 The paddling season usually begins in early spring when air temperatures are cool and snow melt–swollen rivers run extremely cold. Paddlers with rusty skills are more prone to frequent swims and the effects of cold-water immersion. Many rivers, especially in the western United States, are controlled by dams that release water from far beneath the surface and thus remain cold year round. Placing adequate barriers between the human body and the environment and carrying adequate food and waterproof matches are of paramount importance.

Swift-Water Rescue RESCUE EQUIPMENT Throw Ropes River throw ropes are usually made of solid-braided polypropylene marine (Spectra) line with a maximum load of about 2000 kg (4500 lb). Throw lines vary in length from 15 to over 23 meters (50 to 75 feet), with 23 meters (75 feet) being optimal because that length of rope can be thrown by most rescuers. Rafters often use shorter lengths in waist-belt systems that can be quickly deployed to recover swimmers who have just fallen out of the raft. The ideal thickness is 9.5 mm (0.375 inch). A breaking strength of 680 kg (1500 lb) is the accepted minimum for river rescue ropes in the United States.74 The vast majority of throwing rescues are made with river rescue throw bags. Throw bags contain throw ropes in which one end of a rope is secured to the bottom of the nylon sack (bag) with a disk of foam to float the bag, while the remainder of the rope is stuffed inside the bag (Figure 45-24). Throw bags

FIGURE 45-24  Example of a throw bag.

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CHAPTER 45  Whitewater Medicine and Rescue

FIGURE 45-23  Giardia lamblia trophozoite seen by methylene blue wet mount staining under oil (1000×). The finding of cysts or trophozoites in a patient with diarrhea is sufficient to make a tentative diagnosis of giardiasis.

Another common environmental affliction suffered by paddlers is dermatitis from poison oak or poison ivy. Most cases occur during spring paddling when the vines are potent but the characteristic leaves have not yet appeared. Barrier creams such as StokoGard Outdoor Cream and Tecnu Ivy Shield can be used by individuals highly sensitive to the plants. After plant contact occurs, the oil may be removed from the skin by washing within 30 minutes.23 A commercial product, Tecnu Oak and Ivy Cleanser, can remove oil from the skin for up to 8 hours after exposure. Any solvent may help remove some of the urushiol oil from the skin. Gasoline, paint thinner, acetone, and rubbing alcohol have all been reported by paddlers to be effective. Unfortunately, these products can also be irritating to the skin or toxic. Treatment of allergic plant dermatitis consists of oral antihistamines and systemic corticosteroids. A 2-week treatment course is needed to prevent recurrence of the rash23 (see Chapter 63). Sunburn and the effects of chronic exposure to solar radiation are compounded by water’s ability to reflect up to 100% of ultraviolet (UV) radiation, depending on the time of day. Sand can reflect up to 17% of harmful UV rays. Most rivers are situated in mountains, where UV rays increase 4% to 5% with each additional 305 m (1000 feet) of altitude.16 Sunscreens must be applied frequently because they are prone to washing off in the water. Zinc oxide and other barrier creams are more resistant to water and are preferable on areas of intense exposure, such as the nose and lips. Paddlers with fair skin should consider using gloves to protect the hands from UV exposure. Eye protection from UV radiation is often overlooked or avoided by paddlers because sunglasses frequently fog while on the river. Application of Dawn dishwashing soap to the lenses prevents fogging for up to 30 minutes. Polarizing lenses reduce glare off the water, but the polarizing feature does not in and of itself filter UV and infrared radiation. Venomous snakes, especially pit vipers, along with scorpions, spiders, and fire ants, are frequently encountered by river enthusiasts and should be considered potential hazards. Paddlers should know appropriate first-aid measures for envenomations. Paddlers commonly consume wild foliage, which may produce severe illness. In one published report, six rafters were poisoned and one of them died after eating water hemlock, Cicuta douglasii.47

PART 5  RESCUE AND SURVIVAL

typically contain 15 to 21 m (50 to 70 feet) of 9.5-mm (0.375-inch) braided polypropylene rope, with tensile strength in the 771 to 907 kg (1700 to 2000 lb) range. The bag can be clipped into a raft, kayak, or canoe with quick release straps or a carabiner and can be rapidly deployed when needed without having to uncoil the rope. The rescuer simply pulls the free end of rope from the top of the bag and then tosses the rope-filled bag to the intended victim. If the victim is moving with the current, the bag should be thrown slightly downstream of the target to account for the velocity of the current and airtime. The most common method of hurling a throw bag is underhand, in which the thrower swings the bag back and forth a few times and then releases it. The release should be at a 45-degree angle to the surface of the water. If the initial throw of the bag misses, a second throw can be executed faster by recoiling the rope into the nonthrowing hand, rather than restuffing the rope into the bag. Starting with the bag end of the rope, make full arm-length coils, laying the coils into the nonthrowing hand, which also holds the bag. Once the rope is coiled, split the coils and make a second throw, allowing the rope to play out while maintaining hold of the bag. Commercial outfitters and large groups of rafters should carry at least one 91.4-m (300-foot) long static rope to be used for Telfar Lowers, Tyroleans, and other rescue situations in which mechanical advantages are needed. Carabiners and Pulleys Although originally designed for climbers, carabiners are often used by paddlers as an alternative to knots to rapidly secure and deploy throw bags and other safety equipment in river crafts. They can also substitute for a pulley in a Z-Drag. Locking type carabiners have the potential to become jammed by sand and dirt encountered along rivers. Pulleys are often used in Z-Drags and other mechanical haul systems to reduce friction and give greater pulling power to the system. As a rule of thumb, a pulley’s diameter should be at least four times that of the rope. Prusik Loops Prusik loops are useful for setting up mechanical advantage hauling systems such as Z-Drags that are used in recovering pinned or broached crafts. Prusik loops are usually composed of 5.5- to 7-mm lines, in which the ends are tied together with a double fisherman’s knot. The Prusik hitch is tied by wrapping the Prusik loop around the rope a number of times (usually 3 to 5 times, depending on the materials) and then back through itself, forming a barrel around the rope with a tail hanging out the middle (see Figure 95-25). When the tail is weighted, the turns tighten and make a bend in the rope. When weight is removed, the loop can be moved along the rope by placing a hand directly on the barrel and pushing. Webbing A loop of webbing, made by tying the ends together with a water knot, can be worn around the waist and secured by a carabiner. The webbing can be used to set up an anchor for hauling systems, as a sit harness, and as a handle or shoulder strap for carrying boats and litters. Knives Because of the potential for rope entanglement, knives can be lifesaving on a river. A knife can also be used to puncture the compartment or floor of a raft to free a pinned or trapped occupant in the event of a broach or flip. Some knives feature a fully serrated edge to cut through a plastic kayak to free a pinned paddler. Molded friction release sheaths have been designed to clip to a belt or the lash tab on a PFD for rapid deployment. It is usually mounted near the shoulder on the PFD. Whistles Whistles should be worn on the life jacket to alert others of an incident, because it can be nearly impossible to hear someone yelling over the noise of a rapid. Choose a whistle that does not have a cork ball in it. The ball often swells when soaked in water, which can reduce effectiveness of the whistle. Fox 40 pealess 858

whistles are louder than traditional whistles and less likely to malfunction.

RAPIDLY DEPLOYED RESCUE TECHNIQUES Time is the most important factor in river rescue and often precludes the use of technical rope-based systems. Experience and understanding river dynamics are essential. The abilities to move around on wet and slippery rocks and maneuver a kayak in swift rapids are more valuable than is knowledge of technical ropebased systems. The most common rescue scenario involves a swimmer who has exited the craft. The victim may be moving downstream at 8.05 to 16.09 km/hr (5 to 10 mph) in the middle of a large river. Because the dynamic nature of swift water does not often allow time for a shore-based rescue system to be established, many whitewater rescues are made from a raft, canoe, or kayak. Rafts should stay close together in rapids to render mutual aid. Throw bags can be used directly from the raft to rescue swimmers, or the victim may often be reached with an outstretched arm and a paddle. A swimmer should be pulled back into the raft by grabbing the shoulder straps on his or her life jacket and then leaning backward into the raft to pull the person in. The swimmer can assist by pulling up on the frame, D-ring, or hand line as he or she is being pulled in. Kayaks can be used to rescue swimmers in midcurrent. The kayak is also an excellent platform to provide additional flotation for a swimmer who is trying to maintain freeboard in rough water. The most common method of rescuing swimmers with kayaks is to have them grab the bow or stern “grab loop” of the boat and then tow them to safety. The loop is usually sized so that it is easy to grab yet will not admit an adult-sized hand. The swimmer can also grab on to the back of the cockpit rim and pull his or her torso onto the back deck. This gets the swimmer out of the cold water, reduces the likelihood of swimmer injury from rocks, and makes it easier for the kayaker to paddle the victim to shore. Body boards and Boogie Boards, originally developed for use in the ocean surf, have been modified for rescue use on rivers. River rescue boards are larger and come with two sets of handles—one for the rescuer and one for the victim. The boards add a substantial amount of flotation to a rescue swimmer and, when used with swim fins, can provide a maneuverable platform for reaching and recovering a victim in the middle of a river. The latest craft to be adapted to swift-water rescue is the personal watercraft, or Jet Ski. Introduced in 1987, these machines have become increasingly popular with professional rescue agencies. Because they lack an exposed propeller, personal watercraft are safe for swimmers and can negotiate shallow rivers. They can be maneuvered upstream in rapids, and can turn within a short radius. Newer versions, adapted for rescue, can tow a backboard or litter device behind them and are quite stable.

WADING AND STRONG SWIMMER RESCUES Rescue from entrapment requires a higher level of skill and often presents greater potential risk to the rescuer. The method used depends on whether the victim can maintain adequate freeboard. If the entrapment site is accessible, direct contact with the victim is quickest and most effective. A rescuer may wade to the entrapment site or reach it by boat if there is a stable site to exit the craft. There are two significant risks involved in wading through swift water: foot entrapment and losing one’s balance, and swimming through a downstream rapid. Before wading, the river downstream should be scouted for hazards, and if possible, a rope thrower should be stationed downstream in the event the rescuer loses his or her footing. There are several techniques that help to stabilize balance and facilitate walking in swift current: (1) Using a paddle for support affords three-point stability and allows rescuers to wade into deeper water. Start by facing upstream, with legs slightly wider than shoulder width. Reach out, turn the paddle blade parallel to the current, and plunge it into the water. Just before the blade hits bottom, turn it sideways to the current. The force of the

CHAPTER 45  Whitewater Medicine and Rescue

Eddy

FIGURE 45-26  Tag line. FIGURE 45-25  Strong swimmer rescue.

on-rushing water will pin it to the bottom. The paddle and two legs form a tripod, which is more stable than the legs alone. Move slowly across the current, facing upstream, moving only one of these three points at a time. As the water deepens, you will have to lean more and more into the current. Although a pole, stick, or tree branch will work, paddle blades are better because, when used correctly, they stay against the bottom more reliably. (2) A group working together as a team can wade into water far deeper and more securely than can a single individual. Group members support one another and, by standing together, also create eddies that provide them protection from the onrushing current. If there are two rescuers, they should face and grab each other by the shoulders of their life jackets, then wade across the current, facing either upstream and downstream or sideways to the current. One person moves at a time; the upstream person goes first, and then the downstream person steps into the eddy created by the upstream individual. The two-person method can also be expanded for more people, with a resultant increase in stability. A strong swimmer rescue is the next-quickest method, but it entails significant risk to the rescuer (Figure 45-25). The rescuer is tethered to a rope, which provides added stability against the force of the current. If a quick-release harness is not available, a loose loop of rope can be passed under the rescuer’s armpits.

TAG LINE RESCUE A tag line rescue should be considered if the victim cannot be reached directly. A tag line is a rope stretched across the river downstream that is then brought upstream to the victim (Figure 45-26). Getting the line across the river sometimes constitutes an insurmountable obstacle. If the river is narrow, it may be possible to throw the line across. Otherwise, it can be ferried across by a boat or team of swimmers. During a ferry, as much of the rope as possible should be kept out of the water to avoid rope drag. There are two types of tag lines. A floating tag line has a life jacket, throwbag, or some other flotation device attached to the middle to keep the rope on the surface, which helps support the victim (Figure 45-27). A snag tag is a weighted line submerged and walked upstream to snare a foot or other body part that has been trapped under the surface. A snag tag can be made by joining together two throw bags filled with rocks (Figure 45-28).

FIGURE 45-27  Two floating throw bags connected with a carabiner to make a tag line.

current will drive the upstream tube under the water. The pressure of the water against the submerged tube and the floor of the boat will then either flip the raft or wrap the boat around the obstacle. When this happens, the crew will usually fall from the raft into the river and may even be trapped under the boat. If there is any possibility that someone may be trapped under the raft, the floor should be cut away carefully with a knife. A wrap can occur when a raft or boat center pins or broaches on a midstream obstacle such as a rock or bridge abutment and then wraps around the obstacle. To release a center pin, determine which end of the boat is under the least pressure and pull on this end until the boat pivots free. Sometimes jumping up and down on the raft is enough to free it. It may be necessary to deflate one of the air chambers in a thwart tube to decrease the effect of the current on that point and reduce the amount of water trapped inside the raft. With a self-bailing raft with a lace-in floor, you can unlace or cut the lacings of the floor to reduce the current’s effect. Avoid pushing or pulling directly against the current, and try to get as much of the pinned craft out of the water, either by lifting it, by dumping the water out of it, or both. If you can reduce the force of the current on the pinned raft at one point by pushing or pulling Rope on surface

Submerged throw bag

RESCUING PINNED BOATS Pinned boats are a common rescue situation in whitewater paddling. Center pins are the most common type of pin. In a center pin, the boat is trapped near its center at right angles to the current across an obstacle. When a raft contacts an obstacle and stops, the pillow formed by the current against the obstacle transfers to the upstream tube of the raft. If the crew fails to highside by transferring all weight to the downstream tube, the

FIGURE 45-28  Submerged snag tag.

859

PART 5  RESCUE AND SURVIVAL

may be pinned inside the boat by the force of the current against his back. Modern kayaks made for steeper runs are shorter and have more rounded ends to mitigate the potential of boat entrapment. Larger cockpits have been created in these boats to facilitate escape if a pin occurs. If the victim can breathe, rescuers should try to stabilize the vertically pinned boat by attaching lines to it so that it cannot shift. A stabilization tag line can be set up to keep the pinned paddler’s head up while other rescue methods are used to extricate him. Once the boat and paddler are stabilized, a shore-based system, like the Z-Drag described earlier, can be set up to extricate the boat and paddler from the pin.

A

B FIGURE 45-29  Vector pull.

APPENDIX A 

the pinned craft to one side, this may be enough to allow the current to push the boat around to the other side of the obstruction.59,74 Most pins can be released by pulling, pushing, or creating a vector pull with ropes and do not require technical mechanical advantage systems. A vector pull can be established by first anchoring a rope between the raft and a fixed object on the shore, such as a tree or large rock. A second rope is then secured to the first rope in a manner that allows the rescuers to pull at right angles to the first rope (Figure 45-29). The vector forces generated by this method greatly amplify the force exerted between the raft and shore anchor. At 10 degrees of deflection, 45.4 kg (100 lb) of pull translates to 227.3 kg (about 500 lb) on the raft.36,74 If greater force is needed to free a pinned craft, a Z-Drag system that offers mechanical advantages can be employed, but this requires more equipment and expertise and is time consuming to set up. With a 3 : 1 Z-Drag, one person pulling on a rope exerts as much force as would three people pulling on the same line. The name comes from the fact that the arrangement of lines is roughly Z-shaped. Besides the mechanical advantage to pulling, it also uses only part of the total length of the rope for the functional part of the system. The Z-Drag configuration uses two single pulleys (or carabiners) and two Prusik knots. The first Prusik knot provides the mechanical advantage. The second Prusik knot is used to hold the position of the rope and is sometimes referred to as a “progress capture device” or brake. It is also advisable to attach a soft object (such as a life vest) to the end of the line near the connection to the object being pulled, because the line is under high tension and could break free and present a dangerous flying hazard (Figure 45-30.)82 Vertical pins occur when the bow or stern of a boat lodges in an undercut rock, obstruction, or at the bottom of a steep drop. If the force of the water is significant, the boat may collapse at the fulcrum created by the obstacle that is trapping the boat and then fold over onto itself. With a kayak, the paddler Pull here Pulley 1 Object Prusik 1

Pulley 2 Prusik 2

Fixed object (tree)

FIGURE 45-30  To set up a Z-Drag, tie one end of the rope to the pinned boat. Tie an anchor around a tree and attach one of the pulleys to the anchor line (if a pulley is not available, a carabiner can be substituted, but this decreases the effectiveness of the mechanical advantage because of increased friction of the rope going through the carabiner, as compared with traveling over a pulley) and run the rope from the pinned boat through it and back toward the boat. Attach another pulley or carabiner (the “traveling” pulley) to the line with a Prusik knot and run the rope through this and back to shore. Rig a brake Prusik knot attached to the anchor.

860

WHITEWATER FIRST-AID KITS The following variables should be considered when designing a whitewater first-aid kit: remoteness and accessibility of the river, difficulty of travel conditions, number of people to be supported by the kit, preexisting medical conditions, and space and weight restrictions. When assembling a kit, the following components are generally recommended for rafting and kayaking:

RAFTING KIT • Waterproof dry bag or Pelican box • Cardiopulmonary resuscitation mouth shield (CPR Microshield) • Hypothermia/hyperthermia thermometer • Bandage scissors • Fine-point tweezers or forceps • Temporary dental filling (Cavit) • Oral glucose gel (Glutose 15) • Irrigation syringe with 18-gauge catheter • Povidone-iodine 10% solution • 3M surgical stapler (each stapler holds 25 staples) • 2-octyl cyanoacrylate tissue glue (Dermabond) • Wound closure strips (Steri-Strips) • Tincture of benzoin • Polysporin ointment • Moleskin • Latex or nonlatex (hypoallergenic) gloves • Antiseptic towelettes • Safety pins • Waterproof matches • Accident report form and pencil • Large garbage bag • 4 × 4-inch sterile dressings • 8 × 10-inch trauma pad or Bloodstopper dressing • Eye pads • Nonadherent dressing (Xeroform or Aquaphor) • Triangular bandage • 3-inch conforming gauze bandage • 3-inch elastic bandage with Velcro closure • 10 yards of 1-inch surgical tape • Duct tape (can be wrapped around the paddle shaft) • Strip and knuckle bandages • Cotton-tipped applicators • Aloe vera gel • Diphenhydramine 25-mg capsules • 1% hydrocortisone cream • Acetaminophen 500-mg tablets • Ibuprofen 200-mg tablets • Prophylactic (against otitis externa) eardrops (mixture of rubbing alcohol and white vinegar) • Neomycin and polymyxin B sulfate and hydrocortisone otic suspension (Cortisporin Otic Suspension) • Epinephrine auto-injector 0.3-mg adult dose (EpiPen) • Ondansetron 4-mg orally disintegrating tablets (Zofran ODT) • Diazepam 5-mg tablets (Valium) • Oxycodone 7.5-mg and acetaminophen 325-mg tablets (Percocet) • Oxymetazoline nasal spray (Afrin)

CHAPTER 45  Whitewater Medicine and Rescue

• Ciprofloxacin 500-mg tablets (Cipro) • Azithromycin 250-mg tablets (Zithromax) • Trimethoprim and sulfamethoxazole tablets (Septra DS) • Sunscreen (sun protection factor [SPF] 15 or higher) • Insect repellent • Iodine tablets or water disinfection device (such as SteriPEN) • Tampons • Tea bags

KAYAKING KIT • Waterproof dry bag or small Pelican box • Cardiopulmonary resuscitation mouth shield • Hypothermia/hyperthermia thermometer • Scissors • Fine-point tweezers or forceps • Small surgical stapler (3M) or Dermabond tissue adhesive (glue) • Wound closure strips • Tincture of benzoin • Polysporin ointment • Latex or nonlatex (hypoallergenic) gloves • Antiseptic towelettes • Safety pins • Waterproof matches • Accident report form and pencil • 3 × 3-inch sterile dressings • Nonadherent dressings • 2-inch conforming gauze bandage • Duct tape • Strip and knuckle bandages • Cotton-tipped applicators • Diphenhydramine 25-mg capsules • Acetaminophen 500-mg tablets • Ibuprofen 200-mg tablets • Epinephrine auto-injector 0.3-mg adult dose (EpiPen) • Ondansetron 4-mg orally disintegrating tablets (Zofran ODT) • Diazepam 5-mg tablets (Valium) • Oxycodone 7.5-mg and acetaminophen 325-mg tablets (Percocet) • Sunscreen • Insect repellent • Iodine tablets or device (e.g., SteriPEN) for water disinfection

APPENDIX B 

UNIVERSAL RIVER SIGNALS Stop: Potential hazard ahead. Wait for “all clear” signal before proceeding. Form a horizontal bar with your outstretched arms. Persons seeing the signal should pass it back to others in the party (Figure 45-31). Help/Emergency: Assist the signaler as quickly as possible. Give three long blasts on a whistle while waving a paddle over your head (Figure 45-32). All Clear: Come ahead (in the absence of other directions, proceed down the center). Form a vertical bar with your paddle or one arm held high above your head. Paddle blade should be turned flat for maximum visibility. To signal

FIGURE 45-32  Help/emergency signal.

FIGURE 45-33  All clear signal.

direction or a preferred course through a rapid around an obstruction, lower the previously vertical “all clear” by 45 degrees toward the side of the river with the preferred route. Never point toward the obstacle you wish to avoid (Figure 45-33).

APPENDIX C 

ORGANIZATIONS American Canoe Association (ACA) 7432 Alban Station Blvd., Suite B-232 Springfield, VA 22150-2311 Internet: http://www.acanet.org Phone: 703-451-0141 Fax: 703-451-2245 E-mail: [email protected] American Whitewater (AW) P.O. Box 1540 Cullowhee, NC 28723 Internet: http://www.americanwhitewater.org Phone: 866-262-8420 E-mail: [email protected] National Organization for Rivers (NORS) 212 West Cheyenne Mountain Blvd. Colorado Springs, CO 80906 Internet: http://www.nationalrivers.org Phone: 719-579-8759 Fax: 719-576-6238 E-mail: [email protected]

REFERENCES FIGURE 45-31  Stop signal.

Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 46 

Caving and Cave Rescue STEPHEN E. HUDSON, LOUI H. MCCURLEY, AND ROGER B. MORTIMER

Caves are among the most awe-inspiring natural wilderness features remaining on Earth. Finding virgin territory within a few miles of major cities worldwide is breathtaking. Unlike the far reaches of space or deep trenches of the oceans, uncharted caves can be explored by any reasonably fit person, without a plethora of fancy equipment. Caves are found on every continent in a wide array of forms. There are limestone caves, lava tubes, ice caves, marble caves, shelter caves, and water-filled caves—the variations are endless. Full of beautiful formations, strikingly odd structures, and mystical allure, caves have intrigued man since prehistoric times. From the practical use of caves as shelter to the sheer exhilaration of sport, the physical challenges of caving and rare environment found in caves set them apart. Cavers are people who thrive on the prospect of exploring deep canyons and pits within the earth. Fascination with the unseen, the thrill of the frontier, the personal challenge of confronting the unknown, and the very darkness itself offer a distinctive aroma of adventure. Caves can contain hostile environments. They present physical challenges such as water obstacles, extreme temperatures, confined spaces, exposure to heights, and hazardous surfaces varying from slippery mud to jagged calcite that can catch or snag on cavers’ clothing. Atmospheres can contain dangerous levels of carbon dioxide, methane, or hydrogen sulfide. Unusual pathogens, such as Histoplasma capsulatum, Leptospira species and rabies virus, are more likely to be found in caves. Well before engaging in underground duties, medical and rescue professionals should become thoroughly familiar with the harsh realities of the cave environment and anticipate unusual diagnoses in patients who frequent caves (Figure 46-1). Underground risks, both physical and medical, can be avoided or mitigated. Even experienced cavers can quickly find themselves in unexpected trouble. Such was the case for Frank and Jim, two experienced cavers who explored a seldom-visited side shaft within an extensive cave in Georgia. It took Frank and Jim 3 hours to

FIGURE 46-1  Litter in tight spot. (Courtesy Kris H. Green.)

walk up the mountain, negotiate the cave entrance, climb down into the cave, traverse several hundred feet of passage, rig and rappel a 38.1-m (125-foot) pit, travel across several hundred feet of additional passage, and then rig a side shaft that ran parallel to the cave’s main 178.6-m (586-foot) pit. Once down the shaft, Frank walked across a large rock slab. It shifted from his weight, and his lower leg was quickly pinned between the slab and the shaft’s wall. Frank’s lower leg was crushed, with pieces of bone sticking through an open wound. Over the next hour, Jim helped free Frank’s leg and did his best to stabilize the injury and make Frank as comfortable as possible. Realizing Frank would be unable to climb the more than 167.6 m (550 feet) of rope back to the surface, much less walk and climb through hundreds of feet of horizontal passage, Jim exited to seek help, leaving Frank alone, injured, and in great pain. With the grim realization that he was now solo-caving and in extreme peril himself, Jim carefully climbed the pits and left the cave as quickly as possible. Once down the mountain, he drove to town and notified local authorities. Fortunately, the incident had occurred in a region of the country where an experienced cave rescue team was available. The team was called out and a response initiated. The first rescuer reached Frank about 7 hours after the accident. It took another 9 hours to get Frank up and across the pits and through the entrance passages using hauls, highlines, and team handcarries. Next came a 30-minute four-wheel–drive trip off the mountain to the waiting ambulance. After a short 15-minute ambulance ride, Frank arrived at the nearest hospital. The rescue involved about 50 people, both inside the cave and above ground; total time was 17 hours from the time of the accident to the emergency department. Rescuers responding to a caving accident must be fully aware of the unique challenges involved. Approaching a rescue situation with the idea that a cave is merely a dark version of a typical wilderness environment is at best naïve and at worst a recipe for disaster. As for any environment, potential cave rescuers should be trained, experienced, and adept in functioning on their own in the cave environment before assuming any sort of active rescue role. The first thought that enters the minds of many newcomers to caving is “claustrophobia.” In fact, claustrophobia is usually less of a problem for cavers (even new cavers) than are such issues as physical agility, route finding, endurance, and maintaining optimum performance levels in cold, wet, and confined surroundings. Learning to cope, indeed to thrive, under such circumstances is a prerequisite for the challenges of cave rescue. Not only must cave rescuers be adept at managing the unique trials of functioning in the cave environment, they must also manage a unique set of rescue problems related to safety, equipment, logistics, access and extrication, and mission support. A cave rescue should be initiated only with the direct and intimate involvement of qualified cave rescuers. Rescuers without cave experience, or cavers without rescue experience, are not sufficient resources with whom to launch a cave rescue. The demands of these two avocations are daunting enough individually; combined, they require physical conditioning and technical skills that are indeed humbling. In addition to experienced ground personnel, the incident commander must be familiar with or seek the advice of someone who is familiar with the unique challenges of the cave environment. The time to learn about caving is not as a medic on a cave rescue. If there is any chance that one will encounter a cave

CHAPTER 46  Caving and Cave Rescue

rescue as part of his or her profession or avocation, time should be spent becoming familiar with caves and caving techniques before the need arises for a rescue.

Environment Any natural opening in the earth large enough to enter is considered a cave. Caves are similar to human-made mines and tunnels only in that they share a subterranean setting. On a practical level, mines and tunnels must be approached with skills, equipment, and training that differ from those for caves. This chapter addresses only natural caves such as may be found in a wilderness environment, not their dissimilar human-made counterparts. Caves take many forms, including sinkholes, cracks, sumps, siphons, springs, pits, and caverns. The precise geology of cave formation is a more complex and diverse topic than can be adequately addressed within the confines of this chapter. Some caves are simply topographic in nature—cracks and fissures that are a natural result of typical geologic features. Included in this category are lava tubes, which form when a volcano erupts and lava flows away from its center. Gases create bubbles in the molten rock, leaving voids as it hardens. Lava tube caves form as flowing lava cools hard on the outside and continues to flow on the inside, leaving a “tube” of passage. Like most caves that are formed as a result of earthen upheaval and movement, lava tubes are unpredictable and may run for long distances or be limited to short passages and isolated rooms. More interesting is the geology of caves that form over long periods of time. An oversimplification of this formation process is that caves—particularly limestone caves, but in truth any cave found in carbonic rock—are most often formed as a result of solution reaction between water, carbon dioxide, and the rock. Known as karst, such topography is formed when carbon dioxide and water combine to form weak “carbonic acid,” which in turn dissolves the carbonic rock. This process is most commonly found in limestone areas. As the limestone dissolves, the acid solution follows the path of least resistance through the earth, and eventually pits are formed, then fissures, and eventually passages. When the calcium carbonate–infused water reaches a large enough opening, the carbon dioxide dissipates and the calcium carbonate is deposited as stalagmites (icicle-like columns protruding from the ground) and stalactites (icicle-like columns hanging from cave ceiling). Sumps, siphons, and springs are all names that describe specific features in water-based cave formations. Springs, which are outflows of water from the earth, are obvious access points between underground passage and the surface, but they can be called a cave only when they are large enough for a person to enter. Springs differ from siphons in that springs outflow water, whereas siphons take in water. Air-filled cave passages that terminate in water-filled passages are known as sumps. Some sumps are only a few feet long before returning to air-filled sections; others can be thousands of feet in length and may never resurface. Sinkholes, cracks, pits, and caverns are terms that describe passages. These may be wet or dry and are differentiated by their shapes and attributes. Sinkholes, also called sinks, are formed when bedrock above a void collapses. Sinks may manifest as a sheer vertical opening into a cave with a well-like or open-air pit entrance, a steep sloping depression with a cave entrance, or a shallow depression of many acres that may not have more than a small, impassable sump to the cave below. Cracks are narrow vertical passages formed as the carbonic acid solution finds its way through the ground. These are usually, but not always, developed along a joint in the rock. The term pit refers to a vertical cave passage. Pits can be found both inside caves and at the surface. Most open-air pits form when the roof of a sinkhole collapses. Pits can also be formed by solution reaction or erosion of passage by flowing water. Solution caves formed in soluble rock are the most common type found on Earth. Depending on local weather conditions and length of time, caves can take up to tens of thousands of years

FIGURE 46-2  Typical large “room.” (Courtesy Kris H. Green.)

to form to the point where humans can enter. Caves are always getting either larger through solution and erosion or smaller by filling in with sand, mud, and fallen rock. These changes usually happen so slowly that they are seldom noticeable. Most cave ceilings and walls are relatively stable. Large breakdown blocks of fallen ceiling and wall rock are often found in caves, but the chances of rock falling precipitously are slim. Breakdown usually occurs suddenly as a result of a major environmental event, such as an earthquake, or very slowly over years as the supporting rock below slowly degrades. Smaller rocks and rock slopes, often the results of ceiling and wall breakdown, are actually the greatest dangers in caves. Because they have not been stabilized by frequent travel, these slopes can shift and slide underfoot. The continuous conduit leading through a cave is known as a passage. Passages can be huge, with room dimensions so large it is difficult to see distant walls (Figure 46-2) even with a light, whereas just around the next corner, the passage can change to tight impenetrable cracks or a dead end (Figure 46-3). Some cave passages wander around in a maze-like pattern that may total many miles in an area as small as a few acres of ground. Other caves may go for miles in the same direction and contain dozens

FIGURE 46-3  Typical tight crack passage. (Courtesy Kris H. Green.)

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PART 5  RESCUE AND SURVIVAL FIGURE 46-4  Wet passages require appropriate clothing. (Courtesy Kris H. Green.)

of miles of passage. Many caves are only a few hundred feet long and have only low, tight, belly-crawl passage. A passage that opens into a wide area is called a room, whereas a tight, narrow passage may be further described as a squeeze or crawl. Caves are formidable, dark, and often dangerous for the unprepared. Considering that running, seeping, or standing water originally formed most caves, it is not surprising that water is a major part of many cave environments. Cavers and rescuers must be prepared to negotiate anything from crawls in water-filled tubes (Figure 46-4) to underground rivers so large that a boat is required. Caves that are no longer hydrologically active are called dry caves or dead caves because they are no longer in their formative state. Some caves are so dry that dust induces respiratory problems in cavers. Visitors to dusty caves should wear appropriate filter masks as a minimum level of protection from dust stirred up by the act of moving through a dry passage. Temperature extremes are another common characteristic of caves. Caves tend to be at the mean ground temperature of the area. For the most part, U.S. continental caves run from cool to cold. Very warm climates, such as in Puerto Rico, sport warm caves, whereas alpine mountain caves in locations such as Montana measure close to freezing temperatures and may even contain ice. Caves found in tropical and desert environments can be so hot that cavers must wear lightweight garments to explore them—even then, these cavers are at risk for heat illness. A common scenario in cave rescue is the concern for hypothermia. Most caves are cool to cold, but temperature differentials can exist within a single cave, depending on exposure, orientation, and water flow. Temperature differentials or pressure differences can result in winds flowing through cave passages. It is not uncommon for a caver to be supine or prone in 4 inches (1.6 cm) of 13° C (55° F) water with his or her back pressed against cold rock, facing a stiff breeze (Figure 46-5).

FIGURE 46-5  Close contact. (Courtesy Kris H. Green.)

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If not prevented, hypothermia will complicate any cave incident. An injured, less mobile person will not generate as much heat as usual in the cold, frequently wet cave environment. Party members and rescuers must work to prevent hypothermia as soon as any injury occurs. Rescuers must also protect themselves from hypothermia. A common scenario is for a rescuer to carry a load of heavy gear rapidly through the cave, then sit in a cold, wet passage to wait for the next assignment. The sweaty rescuer is now subject to evaporative, conductive, and convective heat loss. The wellprepared rescuer dresses in layers, travels light, and adds or removes layers of clothing as needed. Caves can be fragile, often heavily decorated with mineral formations that have developed over thousands of years. Cavers try to protect these formations whenever possible by avoiding walking on or touching delicate areas or otherwise altering the cave. Even natural skin oils deposited by human hands can alter the growth of an active formation. The caver’s motto, “leave nothing but footprints, take nothing but pictures, and kill nothing but time,” extends to rescue operations. Everything brought in must be packed out at the end of the operation. An abandoned flashlight battery can leach its chemicals and poison cave-adapted life forms, ultimately destroying the cave and its environment.

Personal Safety Whether entering a cave for exploration or for rescue purposes, cavers should follow personal gear requirements specifically tailored to caving. Clothing should be appropriate to the environment. Caves can be wet, dry, dusty, cold, warm, or a combination of these. The wind that can exist in passages makes chill factor a significant consideration. Undergarments should provide the necessary thermal layers and be made of a fabric that remains warm when wet. Layering undergarments provides the most versatile system of clothing. Many cavers wear protective suits with a rubberized, vinylcoated, or Cordura outer layer. In very wet caves, it is not unusual to find cavers in wetsuits. Coveralls, or one-piece garments with no exterior straps or accessories, help prevent snagging in crawls or tight passages. Ventilation is an important consideration in accommodating the varying degrees of exertion required in caving. A mountaineering type of helmet, with a nonelastic “threepoint” chin strap that keeps it planted properly on the head, is a must. The helmet protects against impact with the hard and often sharp rock of cave ceilings and walls in tight or low passages and offers protection against falling rock. The helmet is also a convenient mounting platform for the required light source (Figure 46-6). It takes only one episode of trying to navigate in complete darkness underground to understand why every person entering a cave should carry no fewer than three light sources. Rescuers who are underground without functioning lights become additional cavers in need of rescue. Electric lights are preferred, but carbide lamps may also be used. At least two of these lights should be helmet-mountable for hands-free operation, each with

FIGURE 46-6  Typical helmet-mounted light. (Courtesy Kris H. Green.)

Cave Navigation Navigating through the cave environment can be disconcerting, particularly because of the three-dimensional nature of travel. Cave passage moves upward, downward, and side to side through the layers of the earth. Passage may overlap, cross, and twist, all without the benefit of sun, stars, or moss on the north sides of trees to provide directional clues. It is always best for several cavers (or cave rescuers) in a given party to be familiar with the cave and be responsible for navigation. If this is not possible, several options exist. The first, and best, is to use a cave map. Reading a cave map is an acquired skill that every cave rescuer should possess. In a pinch, cavers use navigational skills such as remembering landmarks, leaving temporary route markers (be sure to pick them up on the way out!), and using one wall of the cave as a source of consistency. Route markers are especially useful in cave rescue so that the rescuers can focus on the job at hand.

In an unfamiliar cave, keep track of prominent features so that you can find your way out. Passages often look different on the way out than they did on the way in. A small crawl that enters into a large room can be hard to find hours later when returning across that same room. One trick for finding one’s way out later is to get in the habit of turning around and looking at the passage as you enter into a different room, take a significant turn, or negotiate a climb. Rock cairns, light sticks, and flagging tape can be used as reminders. Another option is to leave pieces of reflective tape to mark the way and then remove them as you leave the cave. During operations in a particularly complex cave, it may be necessary to enlist the help of local cavers to serve as guides for rescuers unfamiliar with the cave. This may be contrary to standard protocols that forbid nonteam members to participate in a search or rescue operation.

Cave Search When the location of the rescue subject is unknown, a search will be required. Searching a cave is a potentially hazardous task and must be done meticulously and under good planning and management.13 A manager of a cave search uses the same basic skills as does an above-ground rescuer. Once the decision is made to begin an in-cave search, teams of cavers will be formed into task forces. Each search task force’s role is to look for, preserve, record, and recover clues that will lead to finding a missing person. The task force should consist of two or three members, one or more of whom should be familiar with basic search techniques, the cave being searched, and cave map reading. Members should be able to perform basic first aid, including patient assessment. In addition to personal caving gear discussed earlier, required equipment includes basic medical supplies, materials to mark passages, pencil and paper, food and liquid for the search subject, hypothermia protection, a map, and a compass. A marking system using colored flagging tape or other means should be established to mark side passages that have already been searched and to differentiate the best route in and out once a subject has been located. Each search task force should obtain a briefing from command and then follow instructions as to where to search, how long to search, the probability of detection, how to preserve and record clues, how to report if a clue is found, and the debriefing procedures on return. If the search subject is found, the task force will assume the functions of an initial response task force. These functions are to determine whether the scene is safe, access the subject, treat the subject, consider possible courses of action (including walking the subject out if conditions allow), and then immediately notify command. The report to command should include a full subject assessment, the task force’s recommendation for course of action, additional medical equipment or personnel needed, type of litter needed, obstacles to evacuation, any rigging that will be needed, and suggestions for action to be taken.

Basic Evacuation On any cave rescue, each person entering the cave must have at least the minimum complement of personal gear, as described in the previous section. Beyond this, the amount of equipment used during a cave rescue is prodigious, particularly in a cave with complex terrain. Equipment and personnel are used nearly as quickly as they can be produced. Dry clothing, food, and water become valuable commodities, and extra supplies not normally used in cave exploration become necessities. This last category, items not normally used in cave exploration, should be sourced, tested, and stored at the ready well in advance of being needed. Communications equipment, such as hard-wired field phones or cave radio systems, can be particularly difficult to find, as can experienced personnel to operate them. Other needs may include generators, warming tents, food services, and a command post. Although most cave evacuations require litter transport, each individual situation should be evaluated carefully to determine whether a litter is really necessary. A properly stabilized “walking 865

CHAPTER 46  Caving and Cave Rescue

sufficient “burn time” capacity or spare batteries to travel into and out of the cave. If carbide lamps are used, care should be taken when working close to patients, because it is easy in tight spots to forget that the light on the head is an open flame that can quickly burn anything with which it comes in contact. For this reason, most cave rescuers prefer electric lights. Many cavers find gloves useful for both thermal insulation and protection against sharp rocks and sticky mud. Neoprene or rubberized gloves are popular choices, and scuba or sailing gloves offer durable protection. If the cave has vertical components, leather-palmed gloves are necessary for rope work. Ideally, a rescuer should carry different pairs of gloves for rope work and for negotiating a muddy passage. Cave mud is slippery and adheres to everything. It makes walking and scrambling through a cave dangerous. Lug-soled boots provide the best traction, and stiff leather uppers help protect feet against sharp rocks. For small passages, or “crawlways,” a set of durable kneepads is a necessity, and many cavers use elbow pads as well. Cavers, as any adventurers in a remote environment, should be self-sufficient and at least able to care for themselves for an extended period. This means being equipped with replacement batteries or carbide, potable water for drinking, food for energy, a basic first-aid kit, and extra insulation, such as thermal layers and a hat that can be worn under the helmet. In many caves, local ethics or regulations also require a “pee-bottle” and material for containing and removing solid waste. Cavers often store a folded trash bag in the suspension of their helmets to be used as an emergency shelter from wind and water, among other possibilities. For the cave rescuer, the concept of self-reliance extends to being capable of caring for oneself, as well as a patient, for an extended period of time. Although the responsibility of patient care may be shared among several people, it takes planning to ensure that enough extra gear exists within the group so that the patient can be appropriately equipped and cared for. Use a small, durable pack to carry extra gear. Because the gear will be alternately carried, pulled, pushed, and dragged through cave passages of different sizes, avoid excessively large packs with extra straps or external attachments because these can impede maneuverability. Not all caves have vertical drops, but for those that do—or when in doubt—a lightweight seat and chest harness, descent device, and a rope-ascending system are essential. A rappelling device must withstand descent down a muddy or gritty rope. A brake bar rack, bobbin-type device, or sturdy figure-8 descender will do. Many devices designed for rock climbing are too lightweight to withstand these conditions repeatedly. In almost all in-cave drops, the caver will have to climb back up the rope. Thus an ascending system is essential. One or two 6-m (20-foot) sections of 25-mm (1-inch) tubular webbing come in handy for an extra step-up or to construct a quick belay or hand line. Vertical caving is a highly specialized sport, and vertical cave rescue is even more specialized. The National Cave Rescue Commission offers courses in cave rescue, recommended for experienced vertical cavers.

PART 5  RESCUE AND SURVIVAL

wounded” caver can be helped out of a cave in a short time and with little manpower. If that same individual is placed in a litter, however, the numbers of rescuers and hours to the hospital increase exponentially. One crisp October day, cave rescuers in Georgia were dispatched to Pettijohn’s Cave on Pigeon Mountain to evacuate a fall victim some 30 minutes from the entrance. Samuel, a fit, experienced caver who was quite familiar with the cave, had taken a fall, experiencing a dislocated shoulder in the process. Pettijohn’s Cave is normally considered a horizontal caving experience, but it also involves scrambling over breakdown block and negotiation of several short vertical drops. Although Samuel and his friends were quite familiar with the cave and he could easily negotiate the passage under normal circumstances, loss of the use of his arm would make it impossible for him to balance or climb on the difficult terrain. The pain of such a dislocation complicated matters greatly, and even a litter evacuation would prove to be a trying ordeal. Terrain in the cave dictated that litter evacuation would require several roped systems, including an initial raise of 4.5 to 6 m (15 to 20 feet), a 30.5-m (100-foot) highline, and one to two more raises to lift the patient through and out the cave entrance. Although Samuel’s location was only an estimated 30-minute walk into the cave, the litter evacuation would easily encompass 6 hours and require numerous riggers and scads of equipment. An experienced paramedic arrived and resolved the evacuation in short order by reducing the dislocation and immobilizing the limb securely to the patient’s body. Instead of requiring litter lowers and highlines, the rescuers were able to rig handlines, and Samuel walked out of the cave under his own power in a fraction of the time that the technical evacuation would have taken. Not all cave rescue scenarios benefit from the fitness and ability of a caver such as Samuel or the presence of a skilled paramedic who can resolve a medical situation. If litter transport is deemed necessary, the next difficult decision is which litter (or litters) to use. On any given evacuation, this selection involves a fine balance of requirements. Maneuvering a bulky litter through narrow cave passages can be a challenging proposition. In larger caves, or where a vertical raise is required, basket litters are the best choice. Plastic-bottomed versions are preferable over steel and mesh versions because plastic allows the option of dragging the litter where necessary (Figure 46-7). In tighter caves,

FIGURE 46-7  Plastic litter offers patient protection and slides easily through passage. (Courtesy Kris H. Green.)

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BOX 46-1  Contents of a Cave Medic Kit Contents for a Basic Cave Medic Kit • Scissors • Adjustable cervical collar • Duct tape • Gauze bandages • SAM Splint or other flexible splint • Elastic wrap • Personal protective equipment • Stethoscope with extension • Blood pressure cuff with extension • Pencil with waterproof paper or acetate • Digital thermometer with extension (indoor/outdoor type) • Antibiotic ointment • Safety pins • Nasal and oral airways Additions for Personnel With Higher Licensing • Oxycodone/acetaminophen pills • Injectable ceftriaxone • Injectable 1% lidocaine syringes and needles appropriate for regional nerve blocks • Povidone-iodine prep pads • Scalpel blades

drag-sheet types of litters, such as the wraparound SKED, provide low profile and relative flexibility, but they are less comfortable or protective for the patient. Occasionally, a cave is so restrictive that even the length of a flexible litter is problematic, and a short board, such as a KED or OSS, is the only alternative. It is not unheard of to begin the carry in a tight section of a cave using an OSS, then add a SKED once the passage opens up a bit, drop the SKED into a full basket litter for ease of carrying in a large walking passage, and then remove package layers all the way back to the OSS to negotiate a tight entrance passage. When choosing a litter and patient packaging, duration of transport and patient comfort should be prime considerations. Natural positioning, pressure points, and temperature are all key concerns. Although rescuers are working up a sweat, the patient lying in the litter is stationary, unable to regulate his or her own comfort, and often extremely cold. Waste elimination may need to be provided for. Thermal layers are a necessity and include a sleeping bag, vapor barrier, and moisture barrier to keep the patient dry. A full-body vacuum mattress works well as padding, immobilizer, and insulator. The patient should also have adequate head and face protection and, if the transport route will become vertical at any point, a harness. A reasonable first-aid kit for a cave rescue operation should contain writing materials for recording patient condition, basic medications, airway management tools, bandages, cervical collars, and splints. Sealing each item in plastic helps keep out cave grit, and the entire kit can be packaged in a large-mouthed bottle or other watertight, durable container. The kit should be able to fit into the caver’s own cave pack because it is much easier to carry one large pack than two smaller ones. The kit should target common injuries. More specialized supplies can be brought in as needed, but a comprehensive kit is not compatible with reasonable movement through the cave. See Box 46-1 for a minimal list of items to include in a cave rescue medic kit. Because of extended times involved in reporting caving accidents and responding to and accessing injured cavers, most patients are either very stable or dead by the time medical help arrives. Advanced life support (ALS) skills and equipment are generally not required. This is fortunate because the effects of cave mud and water are not particularly friendly to medical electronics. Sometimes a cave accident survivor is so badly injured that physicians or paramedics on scene choose serious drug

EQUIPMENT—VERTICAL EVACUATION Ropes used for high-angle underground rescue are usually of the static kernmantle variety. Low stretch, abrasion resistance, and consistency of quality are considered key ingredients. Caves can be harsh and unforgiving, so for this purpose, the tougher the sheath, the better the rope. The toughest-sheathed rope is usually less pliable and forgiving than those more prone to abrasion, so skilled riggers should be used for the task. Rope length may vary, depending on the particular cave and the resources at hand. Ideally, rope lengths should be sufficient to negotiate each drop without tying knots to join ropes. Knot passes can add undesired complexity to the operation. Most cave rescues involve negotiation of difficult passages, as well as raising the patient from below ground to the surface. This may be accomplished in many ways, but pulleys and haul systems are generally basic necessities. Techniques used in high-angle rescue in the cave environment are quite similar to those used above ground, but cave rescue may be complicated by tight spaces, darkness, environmental conditions, and lack of alternative routes. Anchors will seem less available and less obvious to rescuers who are only experienced in rigging above ground. Brake bar racks are most often preferred for lowering operations because of their variable friction advantages. In addition to these, adequate carabiners, anchor materials, and other hardware should be available for rigging. If multiple locations must be rigged for raising, lowering, or traversing, the best possible scenario is to have enough gear to rig each site individually. Having to de-rig a system, sort the gear, carry it past the proceeding litter, and re-rig another system is time consuming and can derail the entire operation. Even a small cave might require multiple sites rigged for safe patient extrication. Prebagged packages of gear for specific common rigging tasks are useful. These include anchor webbing, ample carabiners, pulleys, Prusiks, belay devices, lowering devices, and rope grabs, as required, to set up one site per bag.

LOGISTICS Lack of easy communication, limited access, extended time, and difficulty in obtaining rest and nutrition for teams all contribute to the complexity of cave rescues. Communication is essential to keep rescuers from becoming lost, to issue instructions, and to maintain the tempo of the operation. Various hard-wired field-phone systems are available for use in cave rescue, but generally only well-established teams have access to these. A relatively new development is availability of special low-frequency cave radios that can transmit voice through dense rock and soil. Without such systems, message runners are indispensable. A group of swift, agile, safety-minded, and welltrained cavers with waterproof notepads—and a method for keeping these volunteers rested and nourished—is invaluable. A team of rescuers sent into a known location can take hours or most of a day to reach the patient. It is logistically impractical for these rescuers to carry sleeping bags and food to allow for rest and recovery before starting their work assignment. Keeping rescuers rested, fed, hydrated, and warm as they navigate a challenging cave rescue many hours away requires an incident management team that can predict the needs of the underground workers hours before they themselves realize the need. Whether or not a communication system is available, establishment of a control point at or near the cave entrance is critical.

Entrance control should be established as soon as rescuers arrive at the cave. A record of all personnel and equipment entering or leaving the cave should be documented in a log kept by a team member assigned to maintain entrance control. This log will become invaluable hours later in determining when teams should be replaced, verifying whether someone is still in the cave, and confirming who carried in what piece of missing vital gear. The Incident Command System (see Chapter 36), or a modified version of it, provides the best framework for managing cave rescue personnel by performing required functions while maintaining a reasonable span of control. Generally, the functions required during a cave rescue are similar to those required during any other rescue, although the specific means of accomplishing those functions will vary. There should always be one person in command of an operation. This is the foundation of creating accountability and organization, which are the keys to efficiency and safety. The incident commander assesses the incident, activates resources, determines the strategy, and approves the plan for the operation. This may be particularly challenging in jurisdictions in which the cave rescue experts are not the same individuals as the emergency response experts. Preplanning and relationships developed in advance are the best solutions for preventing problems in this area. Other functions vital to success are planning, operations, logistics, and finance. The incident commander may have one or more assistants, or the commander may be responsible for several of these functions. Someone must plan strategies, supervise the operation, take care of the physical needs of the rescuers and required equipment, and track the resources used.

CAVE ACCESS Gaining access to the patient is a matter of overcoming an array of obstructions inherent in the cave. Merely to move a few hundred feet through a cave might require rappelling, crawling on one’s belly, squeezing through cracks in the rocks, climbing over large rocks, swimming, and slithering through mud. Each of these is a more challenging experience when undertaken during a rescue while dragging a vast amount of equipment. The total darkness of a cave imposes limits on any operation and its effect can be debilitating to some individuals. Even this simple matter can quickly become a major obstacle, particularly if noncavers are called on to assist in medical or other aspects of the operation. Psychological inhibitions, such as fear of the dark or confined spaces, can cause panic and severe dysfunctional behavior. In no case should a would-be rescuer ever be pushed beyond his or her comfort level. Other factors inherent to the cave rescue operation include temperature variables, wetness, and restrictive cave passages. Certain large or weak people or bulky and heavy equipment might be physically incapable of passing through these tight spaces. These considerations exemplify why it is best for any medical or other rescue person who may eventually become involved in a cave rescue to gain knowledge and experience in advance. If the cave rescue requires raising or lowering a patient or traversing the patient over horizontal rope lines, people skilled in cave rigging should be responsible for building the systems. Rigging in caves is an art because of anchoring difficulties, directional changes, tight squeezes, and minimal working surface. Details on cave rigging and professional training can be acquired through the National Cave Rescue Commission, a nonprofit organization that teaches courses in cave rescue techniques and management. Many vertical drops in caves are overhung at the top, preventing the rescuer access to a wall while descending and ascending the rope or moving the patient. In cases in which the roped drop has the rope running against a wall, it can be advantageous to place anchors at points throughout the length of the drop. This “re-belay” method allows multiple people to ascend or descend simultaneously, lessens rope wear points, and provides the added safety of having a shorter rope length for each anchor to protect. Practice at crossing re-belays is essential before attempting to enter a cave thus rigged. The caver must be able to 867

CHAPTER 46  Caving and Cave Rescue

intervention. At these times, electronic tools for monitoring vital signs can be extraordinarily valuable, but great care must be taken because the cave environment is ill-suited to the use of such devices. Even simple interventions such as intravenous (IV) infusions are problematic during cave rescues. In most cases, hanging a gravity-operated IV line is not an option, and positivepressure infusion methods must be used. Furthermore, consideration must be given to methods for keeping the skin insertion point clean and care taken not to interrupt IV fluid flow while negotiating tight passageways.

PART 5  RESCUE AND SURVIVAL

effectively transfer from one free-hanging rope to another while hanging in midair. This is easy to do with the correct equipment setup and practice, but not so easy when the technique is tried for the first time underground on the way to a medical emergency. Usually, single-rope techniques are used, especially where a long free-hanging drop is involved. This means that just one rope is put over the side for the rescuer to ascend or descend. The use of an additional belay line not only requires additional people but also might prove more hazardous if the two lines become entangled. The moving belay line also has the potential to dislodge rocks onto the caver below. In the United States, the most common cave-ascending systems are the frog system, Mitchell system, and various renditions of the ropewalker system. These are all efficient means of ascending and can easily be mastered with practice. The frog system requires more climbing effort but is easier to use when ascending past re-belays in the system. It is imperative that an ascending system be fitted to the user. Some rigs work best for tall, lean frames, and others work best for heavier body types. All rescue team members entering a vertical cave should have their own personally fitted rope-climbing system and must have practiced climbing in that system in a safe practice area. Large holes or boulder slopes inside the cave may best be negotiated by using a highline traverse. Proper setup of highlines can be a time- and equipment-intensive process, but it can shave away hours of litter movement time by passing above difficult cave terrain that otherwise would present many challenges for a litter carried by hand. Use of a highline is most practical when it is known in advance that there will be sufficient time for rigging. The decision to take the time to rig a highline traverse should be made based on three factors: the time it will take to move the patient to the obstacle you want to traverse, the time necessary to rig the highline, and the time that will be saved by using the highline to move the patient over the obstacle.

ENVIRONMENTAL HAZARDS One often-overlooked hazard to cavers is the ambient atmosphere. Most caves in the United States breathe naturally, either from changes in barometric pressure or from the chimney effect of multiple entrances. When this airflow is interrupted, limited, or polluted in some way, the resulting air can become hazardous to entrants. The most basic type of atmospheric hazard is lack of oxygen. Some caves have small rooms with so little airflow that a few cavers can quickly consume most of the oxygen. While frightening, this type of atmospheric hazard is usually quickly recognized as open flame headlamps sputter or cavers become short of breath. Once recognized, the hazard can be mitigated by avoiding panic, controlling air consumption, and relocating to a friendlier part of the cave. Another type of atmospheric hazard involves buildup of gases such as carbon monoxide, carbon dioxide, methane, and hydrogen sulfide. This can happen as a result of natural metabolism of organic material or through external influences. Instances of gasoline seeping into caves from underground storage tanks have been recorded. If poor air quality is suspected, use of an airmonitoring device is essential. It is possible to enter a cave containing high levels of unhealthy gases, but only with appropriate caution. In such cases, it is advisable to solicit participation of the local hazardous materials emergency response team. With the assistance of a hazardous materials or confined space rescue team, “bad air” in caves can be mitigated in several ways. One way is to release compressed air into the cave, forcing good air in and bad air out. Success of this method is limited, and because of the massive amounts of air in a cave, this approach is slow at best. If this method is used, entrants should carry an air monitor because pockets of bad air may remain trapped in parts of the cave. The concept of simply releasing oxygen into the cave is a nice idea, but impractical in all but the smallest of spaces. Exhaust fans offer a reasonable method, although care must be taken to prevent generator exhaust from entering the cave. 868

FIGURE 46-8  Recreational caver in wet pit. (Courtesy Kris H. Green.)

If necessary, rescuers can be equipped for entry with surfacesupplied air with bailout bottles, self-contained breathing apparatus, or rebreathers. Each of these has advantages and disadvantages, but all are difficult to manage in the cave environment and thus should be avoided if possible. Pre-event training and practice in the safe use of any of this equipment are imperative before entering an atmosphere that is hazardous for breathing. In any rescue situation, atmospheric hazards should be considered before entering a cave. If such hazards are suspected, no rescuer should enter the environment without an appropriate filter mask and other personal protective equipment. Other environmental hazards posed by caves may be more readily recognized and should also be considered before any rescue. As discussed earlier, water and caves are usually closely associated. Created by water, caves are a natural deposit for overflow or drainage from a variety of sources. This makes caves particularly prone to flooding with little or no warning. A recreational caver (Figure 46-8) or rescuer caught in a flooding cave is in mortal danger. Flooding is usually associated with heavy rains, which can cause diffuse seepage over a large area of the cave or a high flow into sinkholes. Occasionally, sinking streams can carry floodwater. In some parts of the world, entire rivers disappear underground, flow through caves, and resurface miles away. A flood crest from many miles upstream can pass through these caves without warning. Flood-prone caves are generally identifiable by their makeup. Cave walls coated with thick mud can be an indication that flooding is not unusual in that section of the cave, and extra caution is warranted. Bedrock cave walls with gravel deposits at key points in the cave and debris lodged in the ceiling can also be warning signs. Becoming trapped in a flooding cave is not desirable, but it can be survivable. If possible, find a high point in a wide passage, downstream of any major constriction, and wait out the flood. It is also possible, with enough advance warning, to remove a sediment dam downstream that may otherwise cause water to back up into your “safety zone.” It is seldom wise to attempt to swim, either upstream or down. For a rescuer called to assist cavers trapped in a flooded cave, entering the torrent is not wise. If the location of the trapped persons is known, it may be possible to use (or make) another entrance from which to evacuate them. Knowledgeable local cavers can be extremely valuable in this instance. If entry into a flooded cave through the main entrance is absolutely necessary, it is imperative that the water level be controlled before entry. Methods of accomplishing this goal vary depending on the situation. Often, it may be enough to simply wait out the flood and let the water level subside naturally. If the water level is still on the rise, however, or if the source remains constant, additional measures may be warranted. Keep in mind that water is a powerful force, and any plan should be engineered by professionals.

MEDICAL HAZARDS The most common cave-acquired disease is histoplasmosis, which is caused by Histoplasma capsulatum, a dimorphic fungus present worldwide but especially prevalent in the Ohio and Mississippi River valleys of the United States.1 It is associated with bird, and especially bat, guano (Figure 46-9).12 At a national caving convention in 1994, at least 18 people contracted symptomatic histoplasmosis, with an attack rate of greater than 70% for attendees going into two local caves.1 A follow-up skin test survey found that 60% of one group of cavers showed evidence of Histoplasma capsulatum exposure.1 Cavers get histoplasmosis by breathing dust from affected parts of the cave. Incubation is 2 to 3 weeks. Most primary cases are not even recognized, because they resemble a flulike illness

with fevers, headaches, and cough.21 Persons with significant illness demonstrate patchy lung infiltrates, which may calcify, and hilar lymphadenopathy. Some cases progress to cavitation or dissemination. Detection of urinary antigen is the mainstay of diagnosis. In most cases treatment is not necessary. If symptoms last longer than a month, treatment is indicated with itraconazole or other azole drugs or, in cases of dissemination, amphotericin B. Patients may require 3 to 6 months of treatment.9 Leptospirosis has been reported on caving expeditions to tropical climes but is probably a risk in temperate regions as well.5,6,17,22 Transmission occurs when water contaminated by urine from infected animals comes into contact with mucous membranes, the conjunctivae, or abraded skin.18 Cavers often crawl through small passages in the rock to explore what lies beyond, sometimes greatly abrading the skin, especially in hot humid caves where protective clothing may be minimal. Immersion may increase the risk.4 Water that has percolated through carbonate rocks in which most caves form will have a higher pH, which favors survival of leptospires.11 Leptospirosis manifests with fevers, chills, myalgias, and headache after a 1- to 4-week incubation.16 More specific findings are conjunctivitis, proteinuria, and hematuria. It is most commonly diagnosed with serum microscopic agglutination titers (MAT). The diagnosis is confirmed by a fourfold rise in MAT, but is suggested by a titer of 1 : 800 with appropriate exposure and symptoms. Treatment is IV penicillin or ceftriaxone for severe cases and oral doxycycline for mild cases. It can be prevented with 200 mg of weekly doxycycline.23 The Centers for Disease Control and Prevention recommend rabies vaccination for “spelunkers.” This dates from a concern about two cases of rabies in cavers that were attributed to aerosol transmission. These two people separately visited Frio Cave in Texas, where millions of bats congregate, and developed rabies soon thereafter. Subsequent research demonstrated the presence of rabies virus in the air of Frio Cave, presumably from bat respiratory secretions.2,24 Transmission to animals exposed only to airborne virus has since been demonstrated in the laboratory and in Frio Cave.7,8 Therefore in the context of massive bat maternity colonies, aerosol transmission of rabies appears possible. Still, the matter is not so simple. In both cases, there was a more probable cause for rabies than aerosol transmission.10 In the first case, the caver was employed in a rabies laboratory and worked inoculating bats with rabies virus.14 The second patient denied being bitten by a bat, but was noted to have a bleeding lesion on the face while exiting Frio Cave.10,15 So what are cavers to do? Certainly, anyone doing bat research needs to be vaccinated against rabies and to check titers routinely. Anyone working in caves like Frio needs appropriate masks to filter the hazardous atmosphere, of which rabies is just one component. It is questionable whether the sport caver really has any business at all roaming in a bat maternity colony.3 Decades of exposure have not resulted in further documented cases of cavers contracting rabies. Although some persons have called for vaccination of all cave explorers, the opinion is not unanimous.3 Each caver needs to decide on the level of risk and act accordingly.

PATIENT CARE

FIGURE 46-9  Caver in guano. (Courtesy Peter Febbroriello.)

As with many remote accidents, the time it takes to report, respond to, and access a caving accident usually means that the person, if alive, is relatively stable. Although this generalization has exceptions, the treatment issues faced by most rescuers are related to extended transportation times. Data compiled for American Caving Accidents indicate that the leading cause of caving injury is falls, and that hypothermia, fractures, and head injuries top the list of complaints.19,20 Unfortunately, with significant falls, spinal injury must be contemplated, which compounds the transportation challenge. The approach to medical care should be similar to any other medical situation, with a notable difference: the patient has suffered an acute injury but will be confined for an extended period. Care, then, will be a combination of acute emergency responses adapted for a patient who is, for all practical purposes, bedridden. 869

CHAPTER 46  Caving and Cave Rescue

One of the simplest diversion methods is to broaden the flood crest so that less of it flows into the cave. Water can be diverted using sandbags, hay bales, or dirt or by digging channels. If this is not possible or feasible, one may be able to lower the water level by digging through debris downstream, thereby expediting the exit. Pumping is also an option, although the hazards inherent in this method should be evaluated closely beforehand. Pumps run on fuel or electricity. Fumes from fuel-driven pumps and generators have entered caves and poisoned the air of the cavers waiting for rescue. Electrical power in a flooded cave situation adds a high risk for electrocution to the operation. Failure of the pumps after rescuers enter a cave can trap additional people if the water rises again. Entering a flooded cave with scuba equipment is a dangerous, last-resort method that should be attempted only by certified cave divers. A scuba entry may be justified if cavers are known to have been entrapped for an extended period of time, if there is a known medical emergency, or if the cave is completely flooded. In these cases, it may be advisable for certified cave divers to enter and assess the condition of entrapped people, transport survival supplies, or provide medical assistance. Even certified cave divers require additional skills and equipment to enter a recently flooded or sumped cave passage, compared with the typical sport cave dive. A flooded cave may have little to no visibility, currents, and debris blocking the passage. Only in the most dire circumstances is it justified to attempt to transport a patient through a flooded passage. At a minimum, a scuba entry requires two to three divers, as well as a backup diver. Diving is gear intensive and requires an air compressor, extra tanks, 110-volt electricity to charge dive lights, underwater communications equipment, waterproof bags, full face masks for subjects, water rescue suits, underwater lights, transport cases, and surface personnel to assist with transporting equipment.

PART 5  RESCUE AND SURVIVAL

The Caving Expedition

FIGURE 46-10  Monitoring patient as litter moves. (Courtesy Kris H. Green.)

Once the patient has been stabilized and packaged, the assessment process should continue throughout the evacuation. It is best if one medical person stays with and monitors the patient throughout the evacuation (Figure 46-10). The ideal medic is a strong caver with good single-rope technique skills and at least paramedic training. By constantly staying with the patient, the medic is best placed to observe changes. The medic will need to know the complete patient history and clinical evolution while en route in order to make decisions that affect the extrication effort, such as needs for urgency and patient orientation. Although other evacuation personnel may cycle through the rescue, the constant presence of the medic is reassuring to the patient. Because the medic may need to spend many hours with the patient, he or she should not take part in the strenuous activity of litter handling. Hypovolemia is a common complaint in caving injuries, so establishing an IV line early in the intervention can be useful, even if it is often times difficult to maintain. Take measures to ensure that rescuers will be able to maintain IV access and manage the supplies throughout the evacuation, and infuse only fluids not contraindicated for head or other injury. If the patient is alert and oriented, oral fluids may be appropriate. The patient is unlikely to be at a hospital soon, so it is not necessary to automatically keep the stomach empty, as one might mandate in an urban rescue. Fluid administration increases the need to urinate. A Foley catheter might be necessary, or a diaper might suffice. During extremely long rescues, the patient may be assisted to leave the litter in order to attend to personal needs. As much as possible, maintain communication with the patient, encouraging him or her to flex muscles to maintain good circulation. Allow the patient to assist in care when possible. Availability of ALS and drug therapy is useful on extended transports, so it is helpful to have a strong rapport with local medical authorities should complex treatment become necessary.

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All of the issues that make a caving rescue difficult in the United States become magnified during expeditions abroad. In some locations, there may be no organized rescue team at all, let alone one qualified to do cave rescue. Freight costs for personal gear and expedition gear make additional costs for litters and first aid supplies seem prohibitive. When the purpose of the expedition is to chart virgin caves, there will be no map to share with rescuers, other than an improvised sketch. First aid and other medical supplies may be limited to very general, multipurpose items. Specialized gear may be days away. Expedition leaders must prepare for accidents. All members must have had appropriate vaccinations and be on appropriate prophylaxis for the area, guided by recommendations available at the travel section of the CDC website. Someone on the trip should have a medical background and be responsible for medical supplies. Most expeditions have sufficient rope and carabiners to construct appropriate systems to extract an injured patient, although this equipment may be spread out in the caves. An extra set of gear dedicated to rescue, such as pulleys and Prusik loops, should be kept with the medical supplies. A portable, all-purpose litter such as the SKED should be kept in camp or staged appropriately. Medical supplies should be multipurpose and capable of being packaged to survive a trip into the cave. As an expedition starts or when new cavers arrive, the expedition leaders should orient cavers to the rescue gear, make them aware of its location and how to use it, and explain procedures for a rescue should an accident occur.

Closing Comments Never underestimate a cave rescue. Caves are unique environments, and entry should not be attempted without appropriate technical training and preparation. The advantage to any rescue group of establishing a good working relationship with local cave rescue resources, as well as local recreational cavers, cannot be overemphasized. These are the people with the best knowledge of the caves; with the training, equipment, and experience to handle the obstacles and the environment; and who already feel at ease underground. They could prove to be the most valuable resource for a successful cave rescue. Many cavers have taken extensive training in cave rescue techniques and are members of organized cave and cliff rescue teams. The first step to finding cavers is to contact a local chapter, or “grotto,” of the National Speleological Society, the largest cave exploration, education, and science-oriented organization in the United States. National Speleological Society 2813 Cave Avenue Huntsville, AL 35810 [email protected] http://www.caves.org/ People interested in enhancing cave rescue training should contact the National Cave Rescue Commission (NCRC). The NCRC conducts week-long cave rescue seminars and weekend orientations across the United States. It can be reached at the address above as the National Cave Rescue Commission of the National Speleological Society or online at http://www.caves.org/ io/ncrc/.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 47 

Protection From Blood-Feeding Arthropods MARK S. FRADIN AND SCOT T P. CARROLL

Of all the hazards, large and small, that may befall the outdoor enthusiast, perhaps the most vexatious come from the smallest perils—blood-feeding arthropods. Mosquitoes, flies, fleas, mites, midges, chiggers, and ticks all readily bite humans. The bites are, at best, a minor annoyance; at worst, arthropod bites transmit to humans multiple bacterial, viral, protozoan, parasitic, and rickettsial infections (Box 47-1). Mosquito-transmitted diseases alone will be responsible for the deaths of 1 out of every 17 people currently alive.160 This chapter reviews the arthropod species that bite humans, suggests ways to avoid them, and discusses various options for personal protection against these nefarious organisms.

Mosquitoes (Family Culicidae) Mosquitoes are responsible for more arthropod bites than any other blood-feeding organism. They occur in all major terrestrial regions except Antarctica. These two-winged insects belong to the order Diptera, the flies. There are 170 species of mosquitoes in North America, and more than 3000 species worldwide. Anopheline, or malaria-transmitting, mosquitoes can be distinguished by their resting position on the skin—their bodies are characteristically raised high, as if they are standing on their heads. Most other species, in contrast, alight with their backs parallel to the skin surface (Figure 47-1, A). Mosquitoes vector more diseases to humans than any other blood-feeding arthropod. They transmit malaria to 300 to 500 million people each year, resulting in as many as 3 million deaths per year.148 In addition, about 30,000 international travelers visiting malaria-endemic countries contract the disease yearly.74 Mosquitoes vector multiple arboviruses to humans, including several forms of encephalitis, epidemic polyarthritis, yellow fever, and dengue fever (see Chapter 48). Mosquitoes also transmit the larval form of the nematode that causes lymphatic filariasis. Only female mosquitoes bite, requiring a blood-protein meal for egg production. Male mosquitoes feed solely on plant juices and flower nectar. Mosquitoes feed every 3 to 4 days, consuming up to their own weight in blood with each feeding. Certain species of mosquitoes prefer to feed at twilight or nighttime; others (such as the now-widespread Asian tiger mosquito, Aedes albopictus) bite mostly during the day. Some mosquito species are zoophilic (preferring to feed on animals, including birds, reptiles, various mammals, and amphibians), whereas others are anthropophilic (preferring human blood). Members of the genera Anopheles, Culex, and Aedes are the most common biters of humans. In some mosquitoes, seasonal switching of hosts provides a mechanism for transmitting disease from animal to human. Mosquitoes rely on visual, thermal, and olfactory stimuli to help them locate a blood meal.* For mosquitoes that feed during the daytime, host movement and dark-colored clothing may initiate orientation toward an individual. Visual stimuli appear to be important for in-flight orientation, particularly over long ranges, whereas olfactory stimuli become more important as a mosquito nears its host. Carbon dioxide and lactic acid are the best-studied attractants. Carbon dioxide serves as a long-range attractant,

*References 15, 17, 29, 35, 58, 80.

872

luring mosquitoes at distances of up to 36 m (118.1 feet).56,57,152At close range, skin warmth and moisture serve as attractants.15,29 Volatile compounds, derived from sebum, eccrine and apocrine sweat, and/or the cutaneous microflora bacterial action on these secretions, may also act as chemoattractants.65,87,103,143,170 Floral fragrances found in perfumes, lotions, soaps, and hair-care pro­ ducts can also lure mosquitoes.48 One study has shown that alcohol ingestion increases the likelihood of being bitten by mosquitoes.149 Mosquitoes are more attracted to individuals infected with transmittable malaria than to uninfected people or to treated individuals who are no longer infected.89 There can be significant variability in the attractiveness of different individuals to the same or different species of mosquitoes22,32,81—a point that travelers should keep in mind when visiting new areas. In some studies, men have been bitten more than women, and adults more than children.81,113 Other studies have shown that repellents based on N,N-diethyl-3methylbenzamide (DEET) (previously called N,N-diethyl-mtoluamide) may protect women more poorly than they do men.60 Heavyset people are more likely to attract mosquitoes, perhaps due to their greater relative heat or carbon dioxide output.128 Of note is that some studies have failed to confirm these findings.22 Mosquito bites commonly produce small local wheal reactions and associated itching. More dramatic reactions, including generalized urticaria, angioedema, and anaphylaxis have been reported in highly sensitive individuals. Rare “skeeter syndrome” has been documented in five young children who had dramatic localized redness, swelling, warmth and induration develop within hours of a mosquito bite. This entity mimics cellulitis but resolves spontaneously and is associated with significantly elevated serum levels of IgE and IgG to mosquito salivary gland antigens.151 Antihistamines may be useful when taken prophylactically to reduce the intensity of mosquito bite reactions: Compared with placebo, levocetirizine was shown in one study to reduce the size of the 24-hour bite papules by 71% and the accompanying pruritus by 56%.75 During the day, many mosquito species tend to rest in cool, dark areas, such as on dense vegetation, or in hollow tree stumps, animal burrows, and caves. To complete their life cycle, mosquitoes also require standing water, which may be found in tree holes, woodland pools, marshes, drainage ditches, or puddles. To minimize the chances of being bitten by mosquitoes, campsites should ideally be situated as far away from these sites as possible.

Blackflies (Family Simuliidae) At 2 to 5 mm (0.1 to 0.2 inch) in length, blackflies20,39,59,79,104 (Figure 47-1, B) are smaller than mosquitoes. They have short antennae, stout humpbacked bodies, and broad wings. Blackflies are found globally wherever there are fast-running, clear rivers or streams, which they require for larval development. In temperate regions, adults are most prevalent in late spring and early summer and are most likely encountered near larval habitats, where they are difficult to avoid. However, unlike most mosquitoes, blackflies tend to bite during the daytime. They primarily use visual cues to locate a host. Dark moving objects are particularly attractive, but carbon dioxide and body warmth also serve as attractants. Only the female bites, taking up to 5 minutes to

blackflies are vectors of the parasite Onchocerca volvulus, which causes the disease river blindness.

Mosquitoes Eastern equine encephalitis* Western equine encephalitis* St Louis encephalitis* La Crosse encephalitis* Russian spring–summer encephalitis West Nile virus* Japanese encephalitis Venezuelan equine encephalitis Malaria Yellow fever Dengue fever Lymphatic filariasis Epidemic polyarthritis (Ross River virus) Chikungunya fever Rift Valley fever

Biting Midges (Family Ceratopogonidae)

Biting Arthropods

Ticks Lyme disease* Rocky Mountain spotted fever* Colorado tick fever* Relapsing fever* Ehrlichiosis* Babesiosis* Tularemia* Tick paralysis* Rickettsialpox* Southern tick-associated rash illness (STARI)* Tick typhus Taiga encephalitis Flies (Nonmosquito) Tularemia* Leishmaniasis* African trypanosomiasis (sleeping sickness) Onchocerciasis Bartonellosis Loiasis Chigger Mites Scrub typhus (tsutsugamushi fever) Rickettsialpox* Fleas Plague* Murine (endemic) typhus Lice Epidemic typhus Relapsing fever Kissing Bugs American trypanosomiasis (Chagas’ disease) *May be found in the United States.

feed. Blackflies may be present at high densities, inflicting numerous bites on their victims. Blackflies are particularly attracted to the eyes, nostrils, and ears of their hosts. They often crawl under clothing or into the hair to feed. The insect’s mouthparts tear the skin surface, producing a pool of blood from which the fly feeds. Blood loss from the bite site often continues after the blackfly has departed. The resulting intensely pruritic, painful, and edematous papules are typically slow to heal. Rare systemic reactions, including fever, urticaria, anaphylaxis, and even death have been reported following blackfly bites. Although these flies are not known to transmit disease to humans in North America, in the tropics,

Also known as no-see-ums, sand gnats, sand fleas, and sand flies, biting midges20,39,59,79,104 are small, slender flies (<2 mm [0.1 inch] body length) with narrow wings (Figure 47-1, C ). Their small size makes them difficult to see, and they can pass readily through common window screens. Biting midges occur from low to high latitudes worldwide. They breed most commonly in salt marshes, but larvae also develop in moist organic matter associated with freshwater wetlands and irrigated pastures. Despite their inconspicuous size, female midges are aggressive biters, frequently attacking in swarms and inflicting multiple painful and pruritic bites within minutes. Midges often crawl into the hair before biting. Depending on the species, midges may bite during the day or at nighttime. Their activity is greatest during calm weather, declining as wind speed increases. They may be avoided by moving to open areas with greater airflow or into shelters with no-see-um netting. Biting midges are not known to transmit diseases to humans in temperate regions but vector filarial and microbial parasites in tropical regions.

Tabanids (Family Tabanidae) The family Tabanidae (Figure 47-1, D) includes horseflies, deerflies, greenheads, and yellow flies.20,39,59,79,104 These insects are relatively large (10 to 20 mm [0.4 to 0.8 inch]) robust fliers, with numerous species worldwide. Tabanids breed in aquatic or semiaquatic environments, with a life cycle of over 1 year. They are able to fly for miles and rely primarily on vision to locate a host by movement. Dark-colored clothing may increase the likelihood of being bitten. These flies are most active on warm, overcast days. Only the females bite, using scissor-like mouthparts to create within the skin a bleeding slash, which is slow to heal. Despite their size, these flies usually bite painlessly, but the resulting reaction can include intense itching, secondary infection, and, rarely, systemic reactions, such as urticaria or anaphylaxis. Because the adult fly usually lives only about 1 month, and only one generation emerges per year, the potential season for being bitten is relatively short in higher latitudes and altitudes. In the United States, deerflies have been shown to be capable of transmitting tularemia to humans; in Africa, the deerfly may vector the filarial parasitic worm, Loa loa.

Sand Flies (Family Psychodidae) Sand flies* are tiny (2 to 3 mm [0.1 inch]), hairy, and long-legged flies, with multisegmented antennae and a characteristic V-shape to the wings when at rest. (Figure 47-1, E ). Only female sand flies are blood feeders, feeding mostly during calm, windless nights and resting during the day in animal burrows, tree holes, or caves, which should be avoided. Larvae develop in moist organic matter within such habitats. Most sand fly bites occur on the face and neck, but all exposed skin may be attacked. In tropical and subtropical climates, sand flies have been shown to vector multiple cutaneous, mucocutaneous, and systemic diseases, including bartonellosis and three forms of leishmaniasis. Visceral leishmaniasis is endemic in the tropical and subtropical regions of Central and South America, Africa, Asia, the Mediterranean, and Southern Europe. The only sand fly– transmitted disease in the United States has been cutaneous leishmaniasis, reported in Texas and Oklahoma.

Tsetse Flies (Family Glossinidae) Tsetse flies20,39,59,79,104 are found only in tropical Africa. They are 7 to 14 mm (0.3 to 0.6 inch) long, yellowish-brown, with wings that fold over their backs, giving them the appearance of *References 20, 39, 43, 59, 79, 104.

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CHAPTER 47  Protection From Blood-Feeding Arthropods

BOX 47-1  Diseases Transmitted to Humans by

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A1

A2

B

C

D

E

F

G

H

I

J

K

L

FIGURE 47-1  Biting arthropods. A1, Anopheles mosquito. A2, Culex mosquito. B, Blackfly. C, Biting midge. D, Tabanid fly. E, Phlebotamine sand fly. F, Tsetse fly. G, Stable fly. H, Chagas bug. I, Flea. J, Chigger mite. K, Hard tick. L, Soft tick. (A1 from http://commons.wikimedia.org/ wiki/File:Anopheles_albimanus_mosquito; A2 from http://commons.wikimedia.org/wiki/File:CulexNil; B from http://www.flickr.com/photos/rich_ parker/3686158791/courtesy Richard Parker; C from http://www.ars.usda.gov/is/graphics/photos/jul99/k8488-1.htm; D from http://commons. wikimedia.org/wiki/File:Nied_fg02; E from http://commons.wikimedia.org/wiki/File:Phlebotomus_pappatasi_bloodmeal_begin; F courtesy David Bygott; G from http://commons.wikimedia.org/wiki/File:Fly_November_2007-14; H from http://en.wikipedia.org/wiki/File:Rhodnius_prolixus 70-300; I courtesy Rui Andrade, http://www.flickr.com/photos/ruiamandrade/2734079506/; J courtesy Anthony Gould, http://www.flickr.com/ photos/8463947@N08/765513406/; K from http://phil.cdc.gov/phil/details.asp, search: 7663; L from http://pathmicro.med.sc.edu/parasitology/ soft%20tick.)

874

Stable Flies (Family Muscidae) Stable flies59,79 resemble common houseflies, and are most often encountered in coastal areas. Unlike a housefly, which rests with its body parallel to the surface, a stable fly rests with its head held higher than its posterior (Figure 47-1, G). Both male and female stable flies are vicious daytime biters, requiring a blood meal every 48 hours in order to survive. If disturbed, they will attempt to feed multiple times, preferring to bite the lower extremities. Horses and cattle are the preferred hosts, but hungry stable flies readily bite humans. These flies have knife-like mouthparts that they use to puncture flesh before pumping up the blood. Stable flies breed in decaying vegetation (e.g., wet hay bales, beach seaweed) and herbivore manure and are frequently found congregated on sunny walls. Moving away from these breeding habitats will reduce the likelihood of being bitten. Stable fly bites are generally self-limited. They are not known to transmit disease to humans.

Kissing Bugs (Family Reduviidae) Kissing or Chagas bugs* (triatomine or assassin bugs) are large (10 to 30 mm [0.4 to 1.2 inches] adult length) insects with coneshaped heads, overlapping wings, and an alternating pattern of dull orange and dark brown stripes on the lateral abdomen (Figure 47-1, H ). Kissing bugs get their name from a tendency to bite around the human mouth, but they also bite other parts of the body. Both male and female kissing bugs bite, requiring a blood meal in order to mature through each of five nymphal growth stages. They are nocturnal feeders, attracted to their hosts by warmth, carbon dioxide, and odor. During the day, they rest in trees or indoors in crevices of house walls and ceilings. Kissing bug bites are initially painless, but frequent exposure to the bites can produce erythema, edema, and pruritus at the bite sites. Kissing bugs are the vector for Trypanosoma cruzi, the causative agent of Chagas’ disease, which has been reported in Central and South America, as well as in the southwestern United States. Chagas’ disease symptoms are more severe with long-term repeated inoculations and are also more harmful in South America than farther north. Kissing bugs often feed on rodents that may live within thatch roofing material. Avoiding sleeping under thatch roofing in Chagas-endemic areas may reduce the pro­ bability of infection.

these reddish-yellow insects are readily encountered in damp, grassy, and wooded areas, especially along the margins of forests, where they may number in the thousands. Only the tiny (less than 0.2 mm [0.1 inch]) larval stages are parasitic, feeding on mammals, birds, reptiles, and amphibians. Chiggers are most active in the summer and early autumn. They usually infest humans by crawling up the shoes and legs, preferring to attach to skin at areas where the clothing fits tightly, such as at the tops of socks or around the elastic edges of underwear. Chiggers do not burrow into the skin or actively suck blood. Rather, they pierce skin with their mouthparts and secrete a proteolytic salivary fluid that dissolves host tissue, which they in turn suck up. If undisturbed, chiggers may feed for several days, before dropping off. In humans, this rarely occurs, because the larvae usually cause enough irritation that they are dislodged by scratching. The host response to chigger bites is brisk, often leading to intensely pruritic, bright-red 1- to 2-cm (0.4- to 0.8-inch) nodules. Chiggers are especially abundant in warm, moist temperate climates (e.g., the southeastern United States) and tropical areas of high mammal density, including livestock pastures and natural parks and reserves, where moist grassy or understory areas can be found. These areas may seem like attractive camping areas but should be avoided. In Asia, chiggers may serve as vectors of scrub typhus. Rickettsialpox is also transmitted by a mite bite.

Ticks (Families Ixodidae and Argasidae)

Trombiculid mites20,39,59,79,104 (Figure 47-1, J ) may be found worldwide. Commonly known as chiggers, redbugs, or harvest mites,

(See Chapter 51.) Ticks,* like mites, are arachnids rather than insects. There are hard ticks (family Ixodidae) and soft ticks (family Argasidae) (Figure 47-1, K and L). Hard ticks are so named because of the presence of a sclerotized plate, or scutum, that covers part of the body. Both types of ticks may be found worldwide, but hard ticks are more commonly encountered in North America. Hard ticks are usually found in weedy or shrubby areas, along trails, and at forest boundaries, where mammalian hosts, such as deer, are plentiful. Soft ticks are more resistant to desiccation than are hard ticks. Soft ticks thrive in hot and dry climates and are commonly found in animal burrows or caves. After hatching, both genders of ticks pass through three developmental stages—larval, nymph, and adult—all of which bloodfeed. Ticks are unable to fly or jump. Soft ticks are nocturnal and feed rapidly, in just a few minutes. Hard ticks most commonly “quest” for hosts during the day, often climbing vegetation and waiting still for hours or days, forelegs outstretched, until they detect the vibration or carbon dioxide plume of a passing host. When they encounter fur or skin, they climb onto the host and then crawl in search of an appropriate location on which to attach and feed. The attachment bite is usually painless. Hard ticks may remain and feed on a single host for days. People in suspected tick habitats should check clothing frequently for the presence of ticks. If multiple ticks are seen on clothing, they are most easily removed by permanently trapping them on a piece of cellophane duct tape or by rolling a sticky tape type of lint remover across them; hundreds of small ticks can be easily removed by this method. Tape can be stuck onto the inner thigh area of pants for storage between episodes of tick removal. Laundering infested garments cannot be relied on to kill nymphs, unless the clothing is subjected to the hot cycle of the dryer.21 Attached ticks are more difficult to remove. Tick mouthparts are barbed, and some species of tick also secrete a cement that firmly anchors the tick into the skin. Erythema, pruritus, and edema are commonly seen at the site of a tick bite. Improper partial removal of the mouthparts may initiate a long-lasting foreign body reaction, leading to secondarily infected lesions that are slow to heal, or granuloma formation that may persist for months. (For a discussion of the best method for tick removal, see Chapter 51.)

*References 20, 39, 44, 59, 79, 104.

*References 20, 39, 59, 79, 104, 155.

Fleas (Family Pulicidae) Adult fleas20,39,59,79,104 are small (2 to 6 mm [0.1 to 0.2 inch]), wingless insects with powerful legs that enable adults to jump distances of up to 30 cm (11.9 inches) (Figure 47-1, I ). Hungry adult fleas of both sexes feed on humans and other warm-blooded mammals and birds. Different flea species are associated with specific hosts, and they may be especially abundant around rodent and bird nests, which serve as both adult and larval habitats and should be avoided. Fleas usually move actively on the host, probing and biting several times, resulting in grouped lesions of pruritic papules. Fleas are capable of transmitting sylvatic plague and murine typhus.

Chigger Mites (Family Trombiculidae)

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CHAPTER 47  Protection From Blood-Feeding Arthropods

honeybees at rest (Figure 47-1, F ). Both sexes bite, feeding in daytime on a wide variety of mammals, including humans. Lightcolored, thickly-woven, loose-fitting clothing may deter biting. Tsetse flies seem to rely primarily on vision and movement to identify their hosts. Their bites are painful and may cause petechiae or pruritic wheals. Tsetse flies vector African trypanosomiasis (sleeping sickness).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

After the tick is removed, the bite site should be cleansed with soap and water, or an antiseptic, and hands should be washed. It may be prudent to save the tick, in case later identification becomes necessary. Laboratory studies of Borrelia burgdorferi (Lyme disease)–infected ticks show that duration of attachment is directly correlated with the risk for transmission of the spirochete.* Prompt removal of attached ticks (ideally within 24 hours of attachment) will greatly reduce the likelihood of disease transmission.125 In the United States, soft ticks of the single genus Ornithodoros are capable of transmitting to humans the Borrelia spirochete that causes relapsing fever. Three genera of hard ticks transmit disease to man: Ixodes (which vectors Lyme disease, babe­siosis, tick paralysis, and Russian spring–summer encephalitis), Dermacentor (vectors tularemia, Rocky Mountain spotted fever, ehrlichiosis, Colorado tick fever, and tick paralysis), and Amblyomma (vectors tularemia, ehrlichiosis, and tick paralysis).107,155 Larval, nymph, and adult ticks may all transmit disease during feeding. Transovarial transmission also enables female ticks to directly infect their offspring.

Personal Protection Personal protection against bites may be achieved in three ways: avoiding infested habitats, using protective clothing and/or shelters, and applying insect repellents.

HABITAT AVOIDANCE As discussed in the sections above, knowing where to find biting arthropods’ breeding and resting places can help reduce exposure and the chance of being bitten. Mosquitoes and other nocturnal bloodsuckers are particularly active at dusk, making this a good time to be indoors. To avoid the usual resting places of biting arthropods, campsites should ideally be situated in areas that are high, dry, and open, devoid of rodent burrows and nests, and as free from vegetation as possible. Areas with standing or stagnant water should be avoided, because these are ideal breeding grounds for mosquitoes. Attempts should be made to avoid unnecessary use of lights, which attract multiple insects.

PHYSICAL PROTECTION Physical barriers can be extremely effective in preventing insect bites, by blocking arthropods’ access to the skin. Long-sleeved shirts, socks, long pants, and a hat will protect all but the face, neck, and hands. Tucking pants into the socks or boots makes it much more difficult for ticks or chigger mites to gain access to the skin. Rubber boots are commonly worn, particularly in tropical areas, to reduce chigger and tick contact while walking and hiking. Light-colored clothing is preferable, because it makes it easier to spot ticks and is less attractive to mosquitoes and biting flies. Ticks will find it more difficult to cling to smooth, closely woven fabrics (e.g., nylon).146 Loose-fitting clothing, made out of tightly woven fabric, with a tucked-in T-shirt undergarment is particularly effective at reducing bites on the upper body. A light-colored, full-brimmed hat will protect the head and neck. Deerflies tend to land on the hat instead of the head; blackflies and biting midges are less likely to crawl to the shaded skin beneath a hat brim. Mesh overgarments, or garments made of tightly woven material, are available to protect against insect bites. Head nets, hooded jackets, pants, and mittens are available from a number of manufacturers, in a wide range of sizes and styles (Box 47-2). Mesh garments are usually made of either polyester or nylon and, depending on the manufacturer, are available in either white or dark colors. With a mesh size of less than 0.3 mm (0.01 inch), many of these garments are woven tightly enough to exclude even biting midges and immature ticks. As with any clothing, bending or crouching may still pull the garments close enough to the skin surface to enable insects to bite through. Shannon Outdoors addresses this potential problem with a double-layered *References 10, 123, 124, 126, 127, 154, 155.

876

BOX 47-2  Manufacturers of Protective Clothing,

Protective Shelters, and Insect Nets

PROTECTIVE CLOTHING (Includes Hooded Jackets, Pants, Head Nets, Ankle Guards, Gaiters, and Mittens) Bug Baffler, Inc PO Box 444 Goffstown, NH 03045 800-662-8411 http://www.bugbaffler.com The Original Bug Shirt Company 60 Industrial Parkway, #467 Cheektowago, NY 14227 800-998-9096 http://www.bugshirt.com Outdoor Research 2203 1st Avenue South Seattle, WA 98134-1424 http://www.outdoorresearch.com Shannon Outdoors’ Bug Tamer PO Box 444 Louisville, GA 30434 800-852-8058 http://www.bugtamer.com Protective Shelters and Insect Nets Long Road Travel Supplies 111 Avenida Drive Berkeley, CA 94708 800-359-6040 http://www.longroad.com Travel Medicine, Inc 369 Pleasant Street Northampton, MA 01060 800-872-8633 http://www.travmed.com Wisconsin Pharmacal Company 1 Repel Road Jackson, WI 53037 800-558-6614 http://www.pharmacalway.com

mesh that reportedly prevents mosquito penetration. Similarly, Outdoor Research manufactures head nets with a lightweight spring-steel hoop positioned to prevent the netting from collapsing against the face. Although mesh garments are effective barriers against insects, some people may find them uncomfortable during vigorous activity or in hot weather. Lightweight insect nets and mesh shelters are available to protect travelers, sleeping indoors or in the wilderness (Figure 47-2). The effectiveness of insect nets or shelters may be enhanced by treating them with a permethrin-based contact insecticide (discussed below), which can provide weeks of efficacy following a single application.

REPELLENTS For many people, applying a topical insect repellent may be the most effective and easiest way to prevent arthropod bites. The quest to develop the “perfect” insect repellent has been an ongoing scientific goal for years and has yet to be achieved. The ideal agent would repel multiple species of biting arthropods, remain effective for at least 8 hours, cause no irritation to skin or mucous membranes, possess no systemic toxicity, be resistant to abrasion and washing off, and be greaseless and odorless. No presently available insect repellent meets all of these criteria. Efforts to find such a compound have been hampered by the

B

C

D

CHAPTER 47  Protection From Blood-Feeding Arthropods

A

FIGURE 47-2  A to C, Protective shelters. D, Bed net.

Chemical Repellents DEET.  DEET has been the gold standard of insect repellents for many decades. Only in the past 5 years have other repellents come to market that show comparable broad-spectrum efficacy (discussed later). DEET has been registered for use by the general

public since 1957. It is effective against many species of crawling and flying insects, including mosquitoes, biting flies, midges, chiggers, fleas, and ticks. The U.S. Environmental Protection Agency (EPA) estimates that about 30% of the U.S. population uses a DEET-based product every year; worldwide use exceeds 200 million people annually.167,168 Decades of empirical testing of more than 20,000 other compounds has not yet led to the release of a clearly superior repellent.* The mechanism of action of DEET is only partially understood. One recent study demonstrated that DEET blocks a specific olfactory sensory neuron in mosquitoes, effectively masking odors that would normally attract the mosquito to a host.40 Another study, in contrast, found that a single olfactory neuron in mosquitoes responds to DEET and induces avoidance behaviors.159 DEET may be applied directly to skin, clothing, mesh insect nets or shelters, window screens, tents, or sleeping bags. Care should be taken to avoid inadvertent contact with plastics (such as watch crystals, glasses frames or lenses, other optics, equipment, and fishing line), rayon, spandex, leather, or painted and varnished surfaces, because DEET may damage these. DEET does not damage natural fibers like wool and cotton. In the United States, DEET is sold in concentrations from 5% to 100%, in various formulations, including lotions, solutions, sprays, and impregnated wipes (Table 47-1). As a general rule, higher concentrations of DEET will provide longer-lasting protection. Duration of efficacy of DEET increases only slowly above 35% concentrations, and the longest-lasting (extended duration) formulations all use concentrations no higher than 35%. Higherconcentration and extended-duration DEET formulations are probably best reserved for circumstances in which the wearer will be in an environment with a very high density of insects (e.g., tundra in early summer, or salt marsh), where there is a high risk for disease transmission from insect bites, or under circumstances where there may be rapid loss of repellent from

*References 55, 81, 83, 101, 102, 132, 137.

*References 34, 72, 85, 130, 139, 164.

multiplicity of variables that affect the inherent repellency of any chemical. Repellents do not all share a single mode of action, and different species of insects may react differently to the same repellent.133 Many chemicals that are effective repellents evaporate or absorb into the skin too quickly to be of great usefulness. To be effective as an insect repellent, a chemical must be volatile enough to maintain an effective repellent vapor concentration at the skin surface but not evaporate so rapidly that it quickly loses its effectiveness. Multiple factors play a role in effectiveness, including concentration, frequency and uniformity of application, the user’s activity level and overall attractiveness to blood-sucking arthropods, interaction between the individual user and the repellent formulation, and the number and species of the organisms trying to bite. The effectiveness of any repellent is reduced by abrasion from clothing; evaporation and absorption from the skin surface; being washed off by sweat, rain, or water; physical activity; and a windy environment.* Each 10° C (18° F) increase in ambient temperature can lead to as much as 50% reduction in protection time.83 Recent formulation developments improve the duration of effectiveness and the cosmetic properties of repellent active ingredients, such that a well-formulated mediocre active ingredient may outperform a poorly formulated stronger active ingredient. Insect repellents do not “cloak” the user in a chemical veil of protection; any untreated exposed skin can be readily bitten.102 Individuals not wearing insect repellent may be bitten with increased frequency when standing next to someone who is wearing insect repellent.111

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 47-1  DEET-Containing Insect Repellents Manufacturer

Product Name

Forms

Sawyer Products Saftey Harbor, Fla 800-940-4664 S.C. Johnson Racine, Wisc 800-558-5566

Sawyer Controlled Release Sawyer Ultra 30 Insect Repellent Sawyer Maxi-DEET OFF! Family Care OFF! Family Care Unscented OFF! Family Care OFF! Active OFF! Active Deep Woods OFF! Deep Woods OFF! Sportsmen Deep Woods OFF! Sportsmen Deep Woods OFF! Sportsmen Ben’s Tick and Insect Repellent Ben’s Tick and Insect Repellent

Lotion Lotion Pump spray Wipes Pump spray Aerosol spray Aerosol spray Pump spray Aerosol, pump spray, wipes Pump spray Aerosol spray Pump spray Aerosol, pump spray, wipes Pump spray

20% 30% 100% 5.6% 7% 15% 15% 25% 25% 25% 30% 98% 30% 100%

Cutter All Family Insect Repellent

Aerosol, pump spray, wipes Pump spray

7%

Tender Corp Littleton, NH 800-258-4696 Spectrum Brands Alpharetta, Ga 800-336-1372

Cutter Skinsations Insect Repellent Cutter Unscented Cutter Backwoods Cutter Max Repel Sun and Bug Stuff (SPF 15) Repel Family Formula Repel Sportsmen Formula Repel Sportsmen Formula Repel Sportsmen Formula Repel Sportsmen Formula Repel Sportsmen Max Repel 100 Insect Repellent

3M St Paul, Minn 888-364-3577

Ultrathon Ultrathon Ultrathon

the skin surface, such as under conditions of high temperature and humidity or rain. Under these circumstances, reapplication of the repellent will likely be necessary to maintain its effectiveness. For most uses, however, there is no need to use the highest concentrations of DEET. Most manufacturers, responding to consumer demand, offer a large variety of low-concentration DEET products. Persons averse to applying DEET directly to their skin may get long-lasting repellency by applying DEET only to their clothing. DEET-treated garments, stored in a plastic bag between wearings, maintain their repellency for several weeks.32 Sequential application of a DEET-based repellent and a sunscreen can reduce the efficacy of the sunscreen. In a study of 14 patients who applied a 33% DEET repellent, followed by a sun protection factor (SPF) 15 sunscreen, the sunscreen’s SPF was decreased by a mean of 33%.109 One study showed that the efficacy of a polymer-based DEET repellent was not decreased by the subsequent application of sunscreen 5 minutes later.115 Another study, however, showed that reapplication of sunscreen 2 hours after DEET repellent was applied significantly decreased the protection time of the DEET repellent.172 There has been some concern that DEET and the sunscreen oxybenzone act synergistically to enhance the percutaneous absorption of the other chemical.77 Combination sunscreen-DEET products are available and will deliver the SPF as stated on the label. However, these products are generally not the best choice, because it is rare that the need for reapplication of sunscreen and repellent is exactly the same. For these reasons, in 2000 Health Canada decided to discontinue approval of combination sunscreen and insect repellent products, pending further safety data. Likewise, the EPA in 2007 also issued a request for information regarding proper regulation of combination products, given the conflicting issues regarding proper application frequency.165 3M and Sawyer Products currently manufacturer extendedrelease formulations of DEET that make it possible to deliver 878

Aerosol spray Aerosol, pump spray, wipes Pump spray Lotion Aerosol spray, lotion Lotion Pump spray Aerosol spray Wipes Aerosol spray, lotion Pump spray Pump spray Aerosol Lotion

% DEET

7% 10% 23% 100% 20% 23% 20% 25% 29% 30% 40% 100% 19% 25% 35%

long-lasting protection without relying on high concentrations of DEET. 3M’s product, Ultrathon, was originally developed for the U.S. military but is also available to the general public. This acrylate polymer 35% DEET formulation, when tested under multiple different environmental/climatic field conditions, was as effective as 75% DEET in ethanol, providing up to 12 hours of greater than 95% protection against mosquito bites.* Sawyer Products’ controlled-release 20% DEET lotion traps the chemical in a protein particle that slowly releases it to the skin surface, providing repellency equivalent to a standard 50% DEET pre­ paration, lasting about 5 hours.46 Sixty percent less of this encapsulated DEET is absorbed when compared with a 20% ethanol-based preparation of DEET.45 In vitro experiments confirm that microencapsulation of DEET can reduce its cutaneous absorption.78 Sawyer Products also markets a controlledrelease 30% DEET lotion in which the chemical is slowly released from a lipid sphere (liposome). This nongreasy formulation has low odor and can provide more than 10 hours of protection. Liposomal preparations of DEET can help to retain potency of the repellent on the skin surface, while minimizing percutaneous absorption.134 Given its use by millions of people worldwide for 50 years, DEET continues to show a remarkable safety profile. In 1980, as part of the EPA registration standard for DEET,168 over 30 additional animal studies were conducted to assess acute, chronic, and subchronic toxicities; mutagenicity; oncogenicity; and developmental, reproductive, and neurologic toxicities. The results of these studies neither led to any product changes to comply with current EPA safety standards nor indicated any new toxicities under normal usage. The EPA’s reregistration eligibility decision,167 released in 1998, confirmed that the agency believes that

*References 2, 63, 86, 108, 142, 144.

Picaridin.  The piperidine derivative, Picaridin (also known as KBR 3023 and Icaridin), is the newest repellent active ingredient to become available in the United States. Picaridin-based repellents have been sold in Europe since 1998, under the brand names Autan and Bayrepel. Picaridin is a synthetic repellent developed by the Bayer Corporation using molecular modeling techniques. From more than 800 screened substances, KBR 3023 showed the best repellent efficacy against a variety of arthropods,16 along with a very favorable safety profile, low percutaneous absorption, and good aesthetic qualities.135 In 2005, the first picaridin-based repellent was brought to the market in the United States. It is currently available in concentrations ranging from 5% to 20% (Table 47-2). This nearly odorless, nongreasy repellent is effective against mosquitoes, biting flies, and ticks. The 7% repellent provides protection against mosquito bites for up to 4 hours. At 20%, picaridin repellents offers comparable efficacy with DEET against mosquitoes, giving up to 8 *References 18, 38, 42, 50, 66, 69, 70, 91, 99, 117, 118, 177.

BOX 47-3  Guidelines for Safe and Effective Use of

DEET Insect Repellents

• When only short-term protection is needed, repellents with 10% DEET or less may provide adequate protection. • Use just enough repellent to lightly cover the exposed skin; do not saturate the skin. • Repellents should be applied only to exposed skin and clothing. Do not use under clothing. • To apply to the face, dispense into palms, rub hands together, and then apply thin layer to face. • Young children should not apply repellents themselves. • Avoid contact with eyes and mouth. Do not apply to children’s hands, to prevent possible subsequent contact with mucous membranes. • After applying, wipe repellent from the palmar surfaces to prevent inadvertent contact with eyes, mouth, and genitals. • Never use repellents over cuts, wounds, or inflamed, irritated, or eczematous skin. • Do not inhale aerosol formulations or get them in eyes. Do not apply when near food. • Frequent reapplication is rarely necessary, unless the repellent seems to have lost its effectiveness. Reapplication may be necessary in very hot, wet environments because of rapid loss of repellent from the skin surface. • Once inside, wash treated areas with soap and water. Washing the repellent from the skin surface is particularly important when a repellent is likely to be applied for several consecutive days. • If you suspect you are having a reaction to an insect repellent, discontinue its use, wash the treated skin, and consult a physician. Modified from U.S. Environmental Protection Agency, Office of Pesticide Programs, Prevention, Pesticides and Toxic Substances Division: Reregistration Eligibility Decision (RED): DEET, (EPA-738-F-95-010), Washington, DC, 1998, EPA.

or more hours of protection.* Picaridin is superior to DEET as a tick repellent.12 The chemical is aesthetically pleasant and, unlike DEET, shows no detrimental effects on contact with plastics. The EPA found picaridin to have a very low toxicity risk, with low dermal absorption. In 2005, the Centers for Disease Control and Prevention (CDC) released a statement adding picaridin to the list of approved repellents that could be used effectively to prevent mosquito-borne diseases. IR3535 (ethyl-butylacetylaminoproprionate).  IR3535 is an analog of the amino acid β-alanine and has been sold in Europe as an insect repellent for 20 years. In the United States, this compound is classified by the EPA as a biopesticide, effective against mosquitoes, ticks, and flies. IR3535 was brought to the U.S. market in 1999 and is sold by Avon Products, Inc and Sawyer Products in concentrations from 7.5% to 20%, with and without sunscreen (see Table 47-2). Depending on the species of mosquito and the testing methodology, this repellent has demonstrated widely variable effectiveness, with complete protection times ranging from 23 minutes to over 10 hours.6,7,23,27,51 IR3535 can provide up to 12 hours of protection against black-legged ticks.23 Higher concentrations of IR3535 give longer protection times. In general, IR3535 does not match the efficacy of high-concentration DEET.6,7,51,52 IR3535 is most effective at 20% concentrations. It is nongreasy, nearly odorless, will not dissolve plastics, and has a very good safety profile. In 2008, the CDC released a statement adding IR3535 to the list of approved repellents that could be used effectively to prevent mosquito-borne diseases. Botanical Repellents Thousands of plants have been tested as sources of insect repellents. Although none of the plant-derived chemicals tested to *References 4, 30, 36, 37, 53, 153.

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CHAPTER 47  Protection From Blood-Feeding Arthropods

“normal use of DEET does not present a health concern to the general U.S. population.” Case reports of potential DEET toxicity have been extensively reviewed.8,50,119,157,169 Fewer than 50 cases of significant toxicity from DEET exposure have been documented in the medical literature over the last four decades; over three-quarters of these resolved without sequelae. Many of these cases involved longterm, excessive, or inappropriate use of DEET repellents; the details of exposure were frequently poorly documented, making causal relationships difficult to establish. These cases have not shown a correlation between concentration of the DEET product used and the risk for toxicity. The reports of DEET toxicity that raise the greatest concern involve 18 cases of encephalopathy, 14 in children under age 8 years.* Three of these children died, one of whom had ornithine carbamoyl transferase deficiency, which might have predisposed her to DEET-induced toxicity.69,70 The 11 surviving children recovered without sequelae. The EPA’s analyses of these cases concluded that they “do not support a direct link between exposure to DEET and seizure incidence.”167 Animal studies in rats and mice show that DEET is not a selective neurotoxin.117,136,168 Even if a link between DEET use and seizures does exist, the observed risk, based on DEET use patterns, would be less than 1 per 100 million users.167 Other studies have confirmed that children are not at greater risk for developing adverse effects from DEET when compared with older individuals.3,8,88,169 A review of adverse events reported to the DEET Registry from 1995 to 2001 concluded that individuals with underlying neurologic disorders were not predisposed to a greater risk for DEET toxicity. There was no evidence that using higher concentrations of DEET increases the risk for adverse events.119 Very limited studies have investigated DEET safety during pregnancy. One followed 450 Thai women who used 20% DEET daily during the second and third trimesters of pregnancy to reduce the risk for contracting malaria.106 Of these women, 4% had detectable levels of DEET in umbilical cord blood at the time of delivery. However, no differences in survival, growth, or neurologic development could be detected in the infants born to mothers who used DEET when compared with an equal number of mothers treated with a daily placebo cream during their pregnancies. The EPA has issued guidelines to ensure safe use of DEETbased repellents167 (Box 47-3). Careful product choice and common-sense application will greatly reduce the possibility of toxicity. Current recommendations of the American Academy of Pediatrics are that children over the age of 2 months can safely use up to 30% DEET.173 When required, reapplication of a lowstrength repellent can compensate for their inherent shorter duration of protection. Questions regarding the safety of DEET may be addressed to the EPA-sponsored National Pesticide Information Center, available every day from 6:30 AM to 4:30 PM PST at 800-858-7378 or via their website at http://npic.orst.edu/.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 47-2  Biopesticide Repellents Manufacturer

Product Name

Form(s)

Active Ingredients

S.C. Johnson Racine, Wisc 800-558-5566 Spectrum Brands Alpharetta, Ga 800-336-1372 Tender Corp Littleton, NH 800-258-4696 Sawyer Products Saftey Harbor, Fla 800-940-4664 Avon Products, Inc New York, NY 800-367-2866 Sawyer Products Tampa, Fla 800-940-4664

OFF! Family Care Insect Repellent II Clean Feel

Spray pump

Picaridin 5%

Cutter Advanced Cutter Advanced Sport Cutter Skinsations Ultra Light Natrapel

Spray pump, wipes Aerosol spray Aerosol spray Pump spray, aerosol spray, wipes

Picaridin Picaridin Picaridin Picaridin

Picaridin Insect Repellent

Pump spray

Picaridin 20%

Bug Guard Plus IR3535 SPF 30 Skin So Soft Bug Guard Plus Picaridin Bug Guard Plus IR3535 Expedition Sunblock Insect Repellent IR3535 (SPF 30)

Lotion Aerosol spray, pump spray, towelettes Pump spray, aerosol spray Pump spray

IR3535 7.5% Picaridin 10% IR3535 20% IR3535 20%

date demonstrates the broad effectiveness and duration of DEET, many show repellent activity and some may be superior against certain important vectors such as anopheline mosquitoes. Plants with essential oils that have been reported to possess repellent activity include citronella, eucalyptus, neem, cedar, verbena, pennyroyal, geranium, catnip, lavender, pine, cajeput, cinnamon, vanilla, rosemary, basil, thyme, allspice, garlic, and peppermint.* Unlike DEET-based repellents, botanical repellents have been relatively poorly studied. When tested, most of these essential oils tended to show short-lasting protection, lasting minutes to 2 hours, after which insufficient material remains on the skin to be repellent. A summary of readily available plant-derived insect repellents is shown in Table 47-3. Citronella.  Oil of citronella was initially registered as an insect repellent by the EPA in 1948. It is the most common active ingredient found in “natural” or “herbal” insect repellents marketed in the United States. Originally extracted from the grass plant Cymbopogon nardus, oil of citronella has a lemony scent. Conflicting data exist on the efficacy of citronella-based products, varying greatly depending on the study methodology, location, and species of biting insect tested. One citronella-based repellent was found to provide no repellency when tested in the laboratory against Aedes aegypti mosquitoes.26 Another study of the same product, however, conducted in the field, showed an average 88% repellency over a 2-hour exposure. The product’s effectiveness was greatest within the first 40 minutes after *References 5, 19, 33, 41, 62, 82, 85, 122, 129, 161, 162.

5.75% 15% 15% 20%

application and then decreased with time over the remainder of the test period.158 All Terrain Company produces citronella-based lotion in which the essential oil has been encapsulated into a beeswax matrix, which slowly releases it to the skin surface, prolonging its efficacy. In laboratory testing against A. aegypti, this product provided complete protection for the first 2 hours and 77% protection 4 hours after application.67 Many citronella repellents on the market incorporate geranium oil and/or soybean oil to increase the repellent effect of the product. In general, studies show that citronella-based repellents are less effective than DEET repellents. Citronella provides a shorter protection time, which may be partially overcome by frequent reapplication of the repellent. In 1997, after analyzing available data on the repellent effect of citronella, the EPA concluded that citronella-based insect repellents must contain the following statement on their labels: “for maximum repellent effectiveness of this product, repeat applications at one-hour intervals.”166 Citronella candles have been promoted as an effective way to repel mosquitoes from one’s local environment. One study compared the efficacy of commercially available 3% citronella candles, 5% citronella incense, and plain candles to prevent bites by Aedes species mosquitoes under field conditions.97 Subjects near the citronella candles had 42% fewer bites than did controls who had no protection (a statistically significant difference). However, burning ordinary candles reduced the number of bites by 23%. There was no difference in efficacy between citronella incense and plain candles. The ability of plain candles to decrease biting may be due to their serving as a “decoy” source of warmth and carbon dioxide. In contrast, in a field study, candles with 5%

TABLE 47-3  Botanical Insect Repellents Manufacturer

Product Name

Form(s)

Active Ingredients

HOMS, LLC Pittsboro, NC 800-270-5721 All Terrain Co Sunapee, NH 800-246-7328

BiteBlocker Xtreme Sportsman BiteBlocker BioUD BiteBlocker Herbal Herbal Armor Herbal Armor SPF15 Kids Herbal Armor Kids Herbal Armor SPF 15 Buzz Away Extreme

Lotion, pump spray Lotion, pump spray Pump spray Pump spray and lotion Lotion Pump spray Lotion Pump spray, wipes

Soybean oil 3%, geranium oil 6%, castor oil 8% 2-Undecanone 7.75% Soybean oil 2%, geranium oil 5% Citronella oil 10%, soybean oil 5.6%, peppermint oil 2%, cedar oil 1.5%, lemongrass oil 1%, geranium oil 0.05%, in a slow-release encapsulated formula

Cutter Lemon Eucalyptus Repel Lemon Eucalyptus

Pump spray Pump spray

Quantum, Inc Eugene, Ore 800-448-1448 Spectrum Brands Alpharetta, Ga 800-336-1372

880

Soybean oil 3%, geranium oil 6%, castor oil 8%, cedarwood oil 1.5%, citronella 1% Oil of lemon eucalyptus 40% Oil of lemon eucalyptus 40%

BiteBlocker.  BiteBlocker is a “natural” repellent that was released to the United States market in 1997, after being sold in Europe for several years.163 BiteBlocker’s present formulation combines derivatives of soybean oil, geranium oil, and castor oil. Studies conducted at the University of Guelph showed that this product was capable of providing over 97% protection against Aedes species mosquitoes under field conditions, even 3.5 hours after application. During the same time period, a 6.65% DEETbased spray afforded 86% protection, whereas Avon’s Skin-SoSoft citronella-based repellent gave only 40% protection.94 A second study showed that BiteBlocker provided a mean of 200 ± 30 (SD) minutes of complete protection from mosquito bites.95 A laboratory study using three different species of mosquitoes showed that BiteBlocker provided an average protection time of about 7 hours.7 Another study showed that BiteBlocker could give about 10 hours of protection against biting black flies; in the same test, 20% DEET only protected for about 6.5 hours.96 BioUD (2-Undecanone).  HOMS is the sole distributor in the United States of another repellent, BioUD (2-Undecanone). This repellent was derived from the wild tomato plant and registered by the EPA in 2007 as a biopesticide for use against mosquitoes and ticks. In field studies against mosquitoes, 7.75% BioUD provided repellency comparable with 25% DEET.13 BioUD repelled the American dog tick Dermacentor variabilis from human skin for over 2.5 hours and was still effective 8 days after application to cotton fabric.13 Laboratory testing demonstrated that BioUD was two to four times more effective than 98% DEET at repelling Amblyomma americanum, D. variabilis, and Ixodes scapularis.11 BioUD was significantly better than either IR3535 or PMD (see below) at repelling A. americanum.14 Lemon Eucalyptus.  A derivative (p-menthane-3,8-diol, or PMD) isolated from oil of the lemon eucalyptus (or pine) plant has a strong lemony scent and has shown promise as an effective “natural” repellent.33 PMD evaporates more slowly from the skin surface than do molecularly similar botanical insect repellents like citronella, and it offers longer-lasting protection. PMD has been very popular in China for years and is currently sold in Europe as Mosi-Guard and in the United States as Repel Lemon Eucalyptus Insect Repellent and Cutter Lemon Eucalyptus Insect Repellent. Tests of this repellent have shown mean complete protection times ranging from 4 to 8 hours, depending on the mosquito species and testing methodology used.* Several studies suggest that PMD-based repellents are superior to DEET against malaria-vectoring Anopheles mosquitoes.22 PMD-based repellents can cause significant ocular irritation, so care must be taken to keep them away from the eyes and that they are not used in children younger than 3 years. In 2005, the CDC added this repellent to the approved list of products that can be effectively used to prevent mosquito-borne disease. Efficacy of DEET Versus Botanical Repellents Limited data are available from studies that directly compare plant-derived repellents with DEET-based products. Available data proving the efficacy of “natural” repellents are often sparse, and there is no uniformly accepted standard for testing repellent products. As a result, different studies often yield varied results, depending on how and where the tests were conducted. *References 7, 16, 22, 24, 61, 110, 112.

Studies comparing “natural” repellents to low-strength DEET products, conducted under carefully controlled laboratory conditions with caged mosquitoes, typically demonstrate dramatic differences in effectiveness between currently marketed insect repellents.7,51 Citronella-based insect repellents usually provide the shortest-duration protection, often lasting only a few minutes. Low-concentration DEET lotions (under 7%) typically prove to be more effective than citronella-based repellents in their ability to prevent mosquito bites and can generally be expected to provide about 1.5 to 2 hours of complete protection.51,68 Reapplication of these low-concentration DEET products can compensate for their shorter durations of action. Because DEET repellents show a clear dose–response relationship, higher concentrations of DEET can be used to provide proportionately longer complete protection times—up to 6 to 8 hours after a single application. BiteBlocker and oil of eucalyptus repellents offer the best protection of the “botanical” repellents, but some consumers may object to their odor; the aesthetic qualities of IR3535 and picaridin may be better choices for those sensitive individuals. BioUD also shows promise as an effective alternative to DEET in repelling both mosquitoes and ticks. Alternative Repellents There has always been great interest in finding an oral insect repellent. Oral repellents would be convenient and would eliminate the need to apply creams to the skin or put on protective clothing. Unfortunately, no effective oral repellent has been discovered. For decades, lay literature has made the claim that Vitamin B1 (thiamine) works as a systemic mosquito repellent. When subjected to scientific scrutiny, however, thiamine has unanimously been found not to have a repellent effect on mosquitoes.84,174 The U.S. Food and Drug Administration (FDA), prompted by misleading consumer advertising, issued the following statement in 1983: “There is a lack of adequate data to establish the effectiveness of thiamine or any other ingredient for OTC [over the counter] internal use as an insect repellent. Labeling claims for OTC orally administered insect repellent drug products are either false, misleading, or unsupported by scientific data.”47 Tests of over 100 ingested drugs, including other vitamins, failed to reveal any that worked well against mosquitoes.156 Ingested garlic has also never proved to be an effective insect deterrent.131

INSECTICIDES Permethrin Pyrethrum is a powerful, rapidly acting insecticide, originally derived from the crushed dried flowers of the daisy Chrysanthemum cinerariifolium.25 Permethrin is a synthetic pyrethroid. It does not repel insects but instead works as a contact insecticide, causing nervous system toxicity, leading to death, or “knockdown,” of the insect. The chemical is effective against mosquitoes, flies, ticks, fleas, lice, and chiggers. Permethrin has low mammalian toxicity, is poorly absorbed by the skin, and is rapidly metabolized by skin and blood esterases.71,176 Permethrin should be applied directly to clothing or to other fabrics (tent walls138 or mosquito nets98), not to skin. Permethrins are nonstaining, nearly odorless, and resistant to degradation by heat or sun, and they will maintain their effectiveness for at least 2 weeks, through several launderings.140,145 The combination of permethrin-treated clothing and skin application of a DEET-based repellent creates a formidable barrier against biting insects.64,86,150 In an Alaskan field trial against mosquitoes, subjects wearing permethrin-treated uniforms and a polymer-based 35% DEET product had greater than 99.9% protection (one bite per hour) over 8 hours; unprotected subjects sustained an average of 1188 bites per hour.93 Permethrin-sprayed clothing also proved very effective against ticks.12 One hundred percent of Dermacentor occidentalis ticks (which carry Rocky Mountain spotted fever) died within 3 hours of touching permethrin-treated cloth.90 Permethrin-sprayed pants and jackets also provided 100% protection from all three life stages of Ixodes dammini ticks, the vector of Lyme disease.146 In contrast, DEET alone (applied to the skin), provided 85% repellency at the time of application; this protection deteriorated to 55% repellency at 6 hours, when tested against the lone star tick 881

CHAPTER 47  Protection From Blood-Feeding Arthropods

geraniol placed 1 m from volunteers reduced the mosquito biting pressure by an average of 56% and the sand fly pressure by 62%, compared with paraffin control candles.114 These efficacies are, unfortunately, far too low to offer useful protection from mosquito-borne diseases. The citrosa plant (Pelargonium citrosum “Van Leenii”) has been marketed as being able to repel mosquitoes through the continuous release of citronella oils. Unfortunately, when tested, these plants offer no protection against bites.28,105 In experimental hut trials in Africa, potted live plants of Ocimum americanum, Lantana camara, and Lippia uckambensis repelled an average of 40%, 32%, and 33% of mosquitoes, respectively.147

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 47-4  Permethrin Insecticides Manufacturer

Product Name

Form(s)

Active Ingredient

Coulston Products Easton, Penn 610-253-0167 Sawyer Products Saftey Harbor, Fla 800-940-4464 Spectrum Brands Alpharetta, Ga 800-336-1372 3M St Paul, Minn 888-364-3577

Duranon Odorless Perma-Kill

Aerosol spray Liquid concentrate

Permethrin 0.5% Permethrin 13.3%

Permethrin Clothing Insect Repellent

Aerosol and pump sprays

Permethrin 0.5%

Repel Permanone Clothing and Gear Insect Repellent

Aerosol spray

Permethrin 0.5%

Clothing and Gear Insect Repellent

Aerosol spray

Permethrin 0.5%

A. americanum.153 Ixodes scapularis ticks, which may transmit Lyme disease, also seem to be less sensitive to the repellent effect of DEET.141 Permethrin-based insecticides available in the United States are listed in Table 47-4. To apply to clothing, spray each side of the fabric (outdoors) for 30 to 45 seconds, just enough to moisten it. Allow to dry for 2 to 4 hours before wearing it. Permethrin solution is also available for soak-treating large items, such as mesh bed nets, or for treating multiple garments simultaneously.

REDUCING LOCAL MOSQUITO POPULATIONS Consumers may still find advertisements for small ultrasonic electronic devices that are meant to be carried on the body and claim to repulse mosquitoes by emitting “repellent” sounds, such as that of a dragonfly (claimed to be the “natural enemy” of the mosquito), male mosquito, or bat. Multiple studies, conducted both in the field and laboratory, show that these devices do not work.9,31,49,73,92 Although most studies have shown that DEETimpregnated wristbands offered no protection against mosquito bites,51,73 in one study wearing impregnated anklets, wristbands, shoulder strips, and pocket strips provided up to 5 hours of complete protection.76 Likewise, mass-marketed backyard bug “zappers,” which use ultraviolet light to lure and electrocute insects, are also ineffective: mosquitoes continue to be more attracted to humans than to the devices.116 One backyard study showed that of the insects killed by these devices, only 0.13% were female (biting) mosquitoes.54An estimated 71 to 350 billion beneficial insects may be killed annually in the United States by these devices.54 Newer technology, using more specific bait, such as a warm, moist plume of carbon dioxide, as well as other known chemical attractants (e.g., octenol), may prove to be a more successful way to lure and selectively kill biting insects. Although the manufacturers of these machines accurately claim that these machines can lure and kill thousands of mosquitoes, it remains to be proven that an individual unit can actually kill enough mosquitoes to reduce the local biting pressures. Pyrethrin-containing “yard foggers” set off before an outdoor event can temporarily reduce the number of biting arthropods in a local environment. These products should be applied before any food is brought outside and should be kept away from animals or fish ponds. Burning coils that contain natural pyrethrins or synthetic pyrethroids (such as D-allethrin or D-trans allethrin) can also temporarily reduce local populations of biting insects.73,100,175 Concerns have been raised about the long-term cumulative safety of using these coils in an indoor environment.1,121 Wood smoke from campfires can also reduce the likelihood of being bitten by mosquitoes. The smoke’s ability to repel insects may vary depending on the type of wood or vegetation burned.120,171

in the world and which species of insects may be attacking. Maximum protection is best achieved through avoiding infested habitats and using protective clothing, topical insect repellents, and permethrin-treated garments. When appropriate, mesh bed nets or tents should be used to prevent nocturnal insect bites. DEET-containing insect repellents are the most effective products currently on the U.S. market, providing broad-spectrum, long-lasting repellency against multiple arthropod species. Based on strong scientific support for their efficacy and safety, the CDC has now approved picaridin, IR3535, and oil of lemon eucalyptus as alternative repellents that can be used to reduce the likelihood of contracting insect-borne disease. Insect repellents alone, however, should not be relied on to provide complete protection. Mosquitoes, for example, can find and bite any untreated skin and may even bite through thin clothing. Deerflies, biting midges, and some blackflies prefer to bite around the head and will readily crawl into the hair to bite where there is no protection. Wearing protective clothing, including a hat, will reduce the chances of being bitten. Treating one’s clothes and hat with permethrin will maximize their effectiveness, by causing “knockdown” of any insect that crawls or lands on the treated clothing. To prevent chiggers or ticks from crawling up the legs, tuck pants into the boots or stockings; rubber boots are especially protective. The U.S. military relies on an integrated approach to protect troops deployed in areas where arthropods constitute either a significant nuisance or medical risk. The Department of Defense’s Insect Repellent System consists of DEET applied to exposed areas of skin and permethrin-treated uniforms, worn with the pant legs tucked into boots and the undershirt tucked into the pant’s waistband. This system has been proved to dramatically reduce the likelihood of being bitten by insects, although troop compliance with DEET-use mandates is poor. Persons traveling to parts of the world where insect-borne disease is a potential threat will be best able to protect themselves if they learn about indigenous insects and the diseases they might transmit. Protective clothing, mesh insect tents or bedding, insect repellent, and permethrin spray should be carried. Travelers should check the most current CDC recommendations about traveling to countries where immunizations (e.g., against yellow fever) or antibiotic prophylaxis (e.g., against malaria) should be undertaken before departure. The CDC maintains these recommendations on its website at http://www.cdc.gov/ travel/index.htm, or by telephone at 888-232-3228. An excellent summary of information on issues relating to travel health can also be found at http://www.tripprep.com. This website culls its information daily from the CDC, the Morbidity and Mortality Weekly Report, World Health Organization, and the U.S. State Department.

INTEGRATED APPROACH TO PERSONAL PROTECTION

REFERENCES

An integrated approach to personal protection is the most effective way to prevent arthropod bites, regardless of where one is

Complete references used in this text are available online at www.expertconsult.com.

882

CHAPTER 48 

Mosquitoes and Mosquito-Borne Diseases HEMAL K. KANZARIA AND RENEE Y. HSIA

Mosquitoes are in the biologic phylum Arthropoda, class Insecta, order Diptera, family Culicidae. There are approximately 35 genera, which include Anopheles, Culex, Psorophora, Ochlerota­ tus, Aedes, Sabethes, Wyeomyia, Culiseta, and Haemagogus. Worldwide there are more than 3000 species and subspecies, and in the United States alone, there are an estimated 200 different species of mosquitoes that vary in habitat and behavior.179 In addition to transmitting the parasitic disease of malaria to 300 to 500 million people per year and thereby killing up to 2.7 million people per year,13 mosquitoes also serve as vectors for arboviruses that cause significant morbidity and mortality to humans worldwide. In addition, mosquitoes are responsible for transmission of the larval nematode that leads to lymphatic filariasis.

Mosquitoes Mosquitoes (the word is derived from the 16th-century Spanish or Portuguese word for little fly) have been in existence for an estimated 170 million years. They are characterized by scaled wings, long legs, and a slender body. The size varies but rarely exceeds 15 mm (0.6 inch) in length. They weigh approximately 2 to 2.5 mg and can fly at about 1.4 to 2.6 km/hr (0.9 to 1.6 mph).

MOSQUITO ANATOMY Mosquito anatomy (Figure 48-1) includes a slender body with two wings (rather than the four possessed by flies) and six long, delicate legs. The wings are covered with scales. The body is divided into three parts: head, thorax, and abdomen. The head has two large compound eyes with many lenses angled in different directions, and two antennae. The mouth, or proboscis, looks like a funnel extending downward, and is used to pierce skin and suck blood (for females) or sip nectar (for males). The thin and short neck connects the head to the thorax, which is triangular and holds the wings in place. The thorax also has two pairs of spiracles, which are tubes through which the mosquito can breathe. The shape of the abdomen can be pointed or rounded, depending on the species, and it has eight pairs of spiracles. The legs are divided into the coxa, femur, tibia, and tarsus. The spiracles form the basis of the mosquito’s tracheal system, which is finely branched so that the cells of the body are directly oxygenated. Mosquitoes have a dorsal blood vessel that extends directly from the eighth abdominal segment into the head. The heart is the portion of the blood vessel located within the thorax and although it is not innervated, it pulses automatically at a rate of 85 beats/min.161 The mouthparts of the mosquito include the labrum and the labium, which can be understood as the upper and lower lips of the mosquito, respectively. The mandible and maxilla are anterior and posterior structures that compose a jaw-like configuration. The maxillary palps are small, antenna-like sensory structures that detect chemicals from animals, and sensory hairs (setae) on the antennae sense vibration and motion from potential prey and other organisms.

MOSQUITO LIFE CYCLE The life cycle of most species of mosquitoes is defined by four stages: egg, larva, pupa, and adult. The time a mosquito spends

in each stage depends on the species and temperature. Culex tarsalis, for example, has a 14-day life cycle at 20° C (68° F), and 10-day life cycle at 25° C (77° F). The life cycle varies from 4 days to 1 month, but averages around 2 weeks, which means that several generations can arise within a single year.179 Most mosquitoes that do not have habitats in the tropics lie dormant as eggs, although some, such as the genus Culex, overwinter as larvae or adults. The female mosquito usually mates once in her lifetime and stores sperm in her body. She fertilizes her eggs when she lays them, which is generally on the surface of the water—often in the form of egg rafts, shown in Figure 48-2—or sometimes in groups in empty containers or jars, shown in Figure 48-3. Eggs can survive winter and hatch in the spring. They hatch into larvae (also known as wrigglers), about 1 to 2 cm (0.4 to 0.8 inch) long, that feed on microscopic animals, plant life, and, in some cases, other mosquito larvae. Except for the genus Anopheles, the larvae must come to the surface to employ their air tubes, or siphons, which supplement their gills (Figure 48-4). After molting several times, they develop into pupae (Figure 48-5), floating on the surface of the water and breathing through an air tube, now called a trumpet. While encased in the hard pupal case, they transform into adult mosquitoes. Enough pressure is created to burst the case, and when their wings harden, they can fly and live on land.161

MECHANISM OF MOSQUITO BITES Mosquitoes technically do not sting, because there is no stinger; they simply pierce the skin and suck blood. Only the females of most species have sucking mouth parts that can pierce skin and thus transmit disease (Figure 48-6). The blood protein is required because the normal mosquito diet of nectar and fruit juices does not contain enough protein for egg development. (One genus, Toxorhynchites, does not suck blood, and its larvae prey on other mosquito larvae). Mosquitoes generally identify victims by scent, as well as by the carbon dioxide of exhaled breath and some chemicals found in sweat. Mosquitoes have been shown to have odorant-binding proteins on their antennae that bind humanspecific odorants, stimulating their olfactory neurons and allowing them to locate their human prey.154 Other risk factors for getting bitten include male gender, heavier weight, and type O blood.61 When mosquitoes pierce human skin, all six legs are usually positioned on the skin surface, along with the labella (part of the proboscis). The female proboscis is made up of six shafts, four of which cut and pierce skin. One serves as a conduit for blood into the mosquito, and another transports mosquito saliva into the skin. The mosquito lays the labella on the skin, which allows the maxillae of the fascicle (a bundle of feeding stylets, contained within the proboscis) to saw into the skin in an oscillatory cutting fashion. Blood is drawn up into the fascicle, which collects into the labrum held between the mandibles of the mosquito. The female mosquito usually requires about 50 seconds to insert the fascicle into the skin, and approximately 2 minutes to finish feeding. She can withdraw her fascicle in 5 seconds.60,69 Mosquito saliva contains a wide array of antihemostatic molecules that allow feeding upon blood. These molecules include vasodilators, such as amines and prostaglandins; platelet aggregation inhibitors, such as nitric oxide; prostaglandins; 883

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Anopheles mosquito (Adult female) Head

Thorax

Abdomen Tibia

Femur

Antenna Maxillary palps

Tarsus

Banded abdomen 2 compound eyes

3 pairs of legs

Proboscis

FIGURE 48-4  Culex larvae suspended diagonally, with siphons at the surface of the water.

FIGURE 48-1  Anatomy of a mosquito.

11 m m FIGURE 48-5  Pupae, where the eyes, legs, and wings are visible.

Individuals vary in their responses to mosquito bites. Almost all experience local irritation caused by a type I immunoglobulin E (IgE)-mediated response of a soft, pale, pruritic wheal or plaque (Figure 48-7). The subsequent effects reveal which immune response a person has to the bite. Type I IgE responses can also

create immediate hive-like skin lesions (rare), whereas type IV cell-mediated immunity causes delayed pruritic papules or vesicles within 48 hours of the bite. Other type IV reactions caused by mosquito bites include blisters, bullae, and erythema multiforme or purpura, but these are rare. One common type IV hypersensitivity response is papular urticaria, which describes an eruption of pruritic papules measuring 3 to 10 mm (0.1 to 0.4 inch) in diameter that may be surrounded by vesicles grouped in irregular clusters (Figure 48-8). Because repeated exposures may lead to desensitization in adults, these lesions are more common in children. They begin as an erythematous wheal, lasting from 2 to 10 days, and may lead to temporary hyperpigmentation. Children who suffer this hypersensitivity may develop a firm, light-brown papule, whereas most adults have only a transient wheal without formation of a persistent papule. The dermatopathology of the epidermis in papular urticaria shows spongiosis with exocytosis and vesicle formation. The upper dermal layer reveals a localized perivascular infiltrate with lymphocytes, histiocytes, eosinophils, and mast

FIGURE 48-3  Eggs of Aedes aegypti mosquito, which transmits dengue virus.

FIGURE 48-6  A female Aedes albopictus mosquito (a vector of the West Nile virus) becoming engorged with blood while feeding on a human.

FIGURE 48-2  A Culex mosquito “egg raft,” measuring 11 mm (0.4 inch) in length and composed of 200 to 300 eggs.

apyrase; molecules that sequester adenosine diphosphate (ADPsequestering molecules), and peptides and proteins specifically targeted to integrin receptors; and anticoagulants, such as thrombin and factor Xa inhibitors. The saliva and its accompanying proteins (specifically, the 33-kilodalton F-1 protein found in mosquito saliva) that remain in human skin after feeding serve as antigens that evoke an immune response.43

PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS OF MOSQUITO BITES

884

Diseases

FIGURE 48-7  Urticarial plaque.

cells, and a spattering of eosinophils and mast cells in the mid-dermis.168 The pathophysiology behind the phenomenon of itching is complex. There are abundant theories on the neurophysiologic basis of itch. The most traditional is that the local reaction induces production of histamine, which stimulates C nerve fibers that travel to the brain and induce the sensation of itching.195 Histamine, however, is only one of many pruritogenic substances that stimulate a subset of specialized skin C fibers. Other mediators of itch include proteases, opioids, lipid peroxidation metabolites (such as leukotrienes and prostaglandins), neuropeptides (e.g., substance P), cytokines, and growth factors (e.g., nerve growth factor). Pruritus is now seen as an interdisciplinary issue that reaches into the fields of neurophysiology, neuroimmunology, neuropharmacology, protease research, internal medicine, and dermatology. In general, mosquitoes confer disease on humans by carrying and harboring viruses from animal reservoirs. Different viruses have different transmission patterns, some with avian reservoirs and others with nonhuman primate reservoirs (and sometimes even humans). The geographic distribution of mosquitoes and changes in their habitats affect the distribution of disease as well. Although mosquitoes are often thought of as living only in temperate and tropical areas, their geographic distribution extends

FIGURE 48-8  Mosquito bite demonstrating papular urticaria.

The effects of mosquitoes on human life are far reaching. Every year, they are responsible for transmitting a wide spectrum of diseases, such as malaria, dengue fever, yellow fever, and encephalitis to millions of people. This chapter discusses the main diseases transmitted by mosquitoes, other than malaria (see Chapter 49). Table 48-1 summarizes the viruses discussed in this chapter.

DENGUE Dengue was first identified as being caused by a virus in the 1940s, although its existence was probably present much earlier, as reports of dengue fever epidemics occurred as early as 1779. Like West Nile virus (WNV), dengue viruses belong to the family Flaviviridae, genus Flavivirus, and have four distinct but closely related serotypes (DEN-1, DEN-2, DEN-3, and DEN-4), all of which cause infection. Dengue has become a major public health issue over recent decades, as the incidences of cases and dengue hemorrhagic fever (DHF) epidemics have dramatically increased. Currently, it is estimated that 50 to 100 million people in more than 100 countries are infected yearly with dengue viruses.76,189 Epidemiology and Transmission Aedes mosquitoes are responsible for transmission of dengue viruses via a human-mosquito-human cycle: having picked up the virus, the infected female mosquito carries it for the rest of her life and can transmit the disease to many susceptible individuals. Several species of Aedes can transmit dengue, but the most important is Aedes aegypti, which is found in temperate zones from latitude 45 degrees north to 35 degrees south. Certain factors make Aedes mosquitoes a particularly effective vector. Specifically, the mosquito itself is quite susceptible to dengue virus; they feed preferentially on human blood; they inhabit highly populated areas and breed inside or close to houses; and their bite is often unnoticed by humans. Moreover, because they feed many times in a breeding cycle, numerous people living in one household can be infected by the same mosquito. Aedes albopictus has a larger geographic distribution than does A. aegypti and can also transmit the virus, but it is less often the culprit responsible for dengue transmission because these mosquitoes breed farther from households and bite humans less frequently.67,76 Dengue virus transmission is classified as epidemic dengue when a single virus strain is introduced into a region with a large number of hosts and mosquitoes, or as hyperendemic when there is uninterrupted circulation of numerous dengue serotypes in one area. Epidemic dengue is the usual transmission pattern for many smaller islands in South America, Africa, and Asia, where several years pass between epidemics and then the disease reemerges. For travelers, this means that the risk for acquiring the infection is high during epidemics, but it is very low between those periods. Generally the frequency of DHF during epidemics seems to be lower than that in areas where the transmission pattern is hyperendemic. In hyperendemic areas, competent mosquito vectors are present throughout the year, and the population of uninfected individuals is sufficiently large to sustain the disease. This latter pattern of transmission accounts for the preponderance of global dengue virus infections.74 As shown in Figure 48-9, dengue virus has been found in Southeast Asia and the western Pacific islands (with 885

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

to climatic extremes and ranges north of the Arctic Circle, where they have adapted to conditions by spending their larval stage frozen in the ice. Disease patterns differ depending on the geographic distribution of the species. Malaria, for example, is mostly found in sub-Saharan Africa, India, Bangladesh, Southeast Asia, Central and South America, and some parts of the Middle East; dengue fever is found in Southeast Asia, Central America, the Caribbean, the southwestern Pacific, and recently in the United States; Japanese encephalitis (JE) spans the bottom half of India in a northeastern direction up to Japan, covering eastern China and Southeast Asia. Geographic distributions and transmission patterns are discussed in the remainder of this chapter.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 48-1  Characteristics of Mosquito-Borne Viral Diseases

Virus

Family

Geographic Distribution

Encephalitis West Nile virus

Flaviviridae

Africa, West Asia, Middle East, Europe, United States Central, western, southern United States

St Louis encephalitis <5000 cases (1964present) Japanese encephalitis 50,000 cases yearly Murray Valley encephalitis (Australian) Eastern equine encephalitis 257 cases (1964-2008) Jamestown Canyon virus

Flaviviridae Flaviviridae Flaviviridae Togaviridae Bunyaviridae

Japan, China, Southeast Asia, India Australia, Papua New Guinea Eastern and Gulf coasts of United States, southern United States, South America United States (including Alaska) and Canada Central and eastern United States

La Crosse virus (California) Bunyaviridae 80-100 cases yearly in the United States Dengue Fever, Dengue Hemorrhagic Fever, Dengue Shock Syndrome Dengue fever virus Flaviviridae Central and South America, 50-100 million cases Africa, Asia, southeastern yearly United States Liver and Renal Failure, Encephalopathy, Coagulopathy, Shock Yellow fever virus Flaviviridae Africa and South America 200,000 cases yearly Polyarthritis, Polyarthralgias Ross River virus Togaviridae Australia, Papua New Guinea, South Pacific

Main Age-Group Affected

Mortality (%)

Specific Treatment?

Human Vaccine Available?

Adults

3-15

No

No

Adults

3-30

No

No

Children and adults

30

No

Yes

Children and adults

30

No

No

Children and adults

33

No

No

Children and adults

Unknown

No

No

Children

<1

No

No

Adults

DHF: 5 DSS: >40

No

No

Men ages 15-45

20

No

Yes

Children and adults

Rare

No

No

DHF, Dengue hemorrhagic fever; DSS, dengue shock syndrome.

hyperendemic transmission of all four serotypes present in Thailand, Vietnam, Indonesia, Malaysia, and the Philippines). Hyperendemic dengue fever (DF) is also found in India, Pakistan, and Sri Lanka. A. aegypti mosquitoes are also distributed across much of sub-Saharan Africa and the Middle East. In the Americas, A. aegypti exists in the southeastern United States, Mexico, Central America, South America, and the Caribbean.76 Reports of DF and DHF are increasing. In fact, before 1970, only nine countries had suffered DHF epidemics; by 1995, this number had expanded more than fourfold. In the past, DF was considered a relatively benign and nonfatal disease. However, since World War II, during which time Aedes mosquitoes were transported around the world in cargo, there has been expansion of the disease not only in frequency and geographic distribution but also in morbidity and mortality. The 1980s and 1990s saw a rise in DHF (specifically, serotype DEN-3) in southern Asia, and in the 1980s, there was a rise in epidemic DF/ DHF (specifically serotype DEN-2) in Taiwan and the People’s Republic of China. Africa has also seen large increases in DF incidence since 1980.72 Dengue has also been emerging much more rapidly in the Americas, with the first major outbreak in Cuba in 1981 and continuing outbreaks in other Central and South American countries since then.145 The World Health Organization (WHO) reports that in 2007 alone, nearly 900,000 cases of dengue were reported in the Americas, with 26,000 cases of DHF. Countries such as Venezuela reported devastating epidemics in the same year, with more than 80,000 cases of DF and more than 6000 cases of DHF.189 Demographic changes, such as population growth and increased human density, contribute to transmission and also to emergence of DHF. Moreover, unplanned urbanization resulting in substandard housing situations and poor water and sanitation systems leads to the same outcome. The situation seems to be potentiated by deterioration of mosquito control programs and of health systems in general in dengue-endemic countries, where the disease cannot be well controlled.110 Climate change alters the interaction between infective mosquitoes and humans. Increased rainfall during certain seasons in tropical areas causes an increased density of mosquitoes. Not only do warmer 886

temperatures decrease the incubation period of the virus inside the mosquito so that the virus can be transmitted earlier, but they may also allow greater mosquito population growth and raise the number of susceptible humans, who perpetuate the disease.79 Clinical Presentation The clinical presentation of dengue virus can range from asymptomatic infection to self-limited mild febrile illness to lifethreatening shock syndrome. Risk factors influence disease severity and development of DHF or dengue shock syndrome (DSS), as opposed to simply dengue fever. These factors include serotype, prior exposure, age, malnutrition, and genetic factors such as human leukocyte antigen (HLA) type. All four serotypes can cause DHF, but DEN-2 appears to be most virulent. The four serotypes do not provide cross-protective immunity, so it is possible for one individual to sustain four separate dengue infections over a lifetime. Although previous infection provides homologous immunity to one serotype, individuals who experience secondary infection by another serotype are at higher risk for more severe forms of disease. This theory supports the observation that infants less than 1 year of age with passively acquired maternal antibodies have a higher rate of DHF/DSS. This phenomenon, known as immune enhancement or antibodydependent enhancement, is thought to occur because the Fc receptors of monocytes by dengue viruses complexed to IgG antibodies are more accessible to infectious immune complexes and result in a higher number of cells being infected with this different serotype.75,114,123 In terms of age distribution, DHF in the past was seen as a disease of children (especially in Asia, where the disease was previously more predominant). This distribution, however, is slightly different in the Americas, and epidemics have shown increasing numbers of adult patients. Moreover, some epidemiologic studies have demonstrated that most children less than 15 years infected with dengue virus tend to be asymptomatic or have a mild fever. Malnourished children, compared with well-nourished children, seem less inclined to develop DHF/DSS than other diseases, perhaps secondary to immunosuppression. Whites have a higher frequency of developing severe disease than do blacks.114

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

Atlantic Ocean

Pacific Ocean

A

Dengue risk areas No known dengue risk

Pacific Ocean

Indian Ocean Atlantic Ocean

B

Dengue risk areas No known dengue risk

FIGURE 48-9  A, Distribution of dengue, western hemisphere. B, Distribution of dengue, eastern hemisphere. (From http://wwwnc.cdc.gov/travel/ yellowbook/2010/chapter-5/dengue-fever-denguehemorrhagic-fever.aspx.)

The incubation period for the virus in the mosquito is 8 to 12 days before it is transmissible, and in humans there is a 4- to 6-day incubation period from bite to clinical infection. Pathogenesis of the virus is hypothesized to be a result of endothelial cell dysfunction, activation of cytokines and complement, and suppression of the reticuloendothelial system.76 At autopsy, the virus is commonly found in the liver, spleen, thymus, lymph nodes, and lung cells.187 WHO currently classifies symptomatic dengue infections into three categories for surveillance purposes. These include undifferentiated fever, classic dengue fever, and DHF. Although this classification system remains controversial,51 the clinical characteristics of DF, DHF, and DSS are discussed here. The majority of children infected with dengue viruses are asymptomatic or present with mild self-limited fever. Typically, older children and adults with DF present with high fever (greater than 39° C [102.2° F]), myalgias, headache, arthralgias, and rash.187 Patients may also describe retro-orbital pain, and suffer gastrointestinal (nausea, vomiting, and diarrhea) and respiratory (cough,

sore throat, and nasal congestion) symptoms.49 A particular characteristic of dengue infection is central nervous system (CNS) involvement in both DF and DHF. Patients present with symptoms that range from irritability and depression to encephalitis with seizures and death, with the more severe symptoms noted in DHF. Despite these complications, the prognosis for patients with DF is generally good, with an acute phase of 1 week and up to 2 weeks of convalescence with general malaise and anorexia. Case fatality rates for dengue fever are less than 1%.33 The main characteristic that differentiates DHF from DF is development of increased vascular permeability resulting in plasma leakage. After 2 to 7 days of high fever, patients with DHF have bleeding (ranging from petechiae, ecchymoses, epistaxis, and mucosal bleeding, to more severe gastrointestinal bleeding and hematuria), thrombocytopenia (<100,000/mm3), and, paradoxically, hemoconcentration and hepatomegaly in some settings.114 Symptoms include severe abdominal pain, nausea and vomiting, and restlessness or lethargy. Plasma leakage may cause pleural effusion, ascites, and hypoproteinemia. This may lead to 887

PART 6  ANIMALS, INSECTS, AND ZOONOSES

circulatory failure, resulting in DSS with hypotension, cool extremities, and altered mental status. Encephalopathy is possible in DHF and can result from cerebral anoxia, edema, or intracranial hemorrhage.165 It is still currently unknown whether dengue viruses infiltrate the CNS directly or if neurologic manifestations are nonspecific complications. Case fatality rates for DHF are approximately 5%38; in DSS they can be greater than 40%.33 Diagnosis Dengue is typically diagnosed clinically, because laboratory confirmation is typically only available in specialized reference laboratories in the developed world. Clinical characteristics are as discussed above; however, it may remain difficult to differentiate dengue from other febrile illnesses. One recent systematic review evaluating 15 studies conducted between 1990 and 2007 attempted to identify clinical criteria to help differentiate such disease processes. In this review, thrombocytopenia, leukopenia, neutropenia, transaminitis, and petechiae were all associated with dengue across multiple studies.147 Another study of 1200 patients from Vietnam and Singapore with acute febrile illness demonstrated a decision algorithm using clinical and hematologic parameters (platelet count, white blood cell count, neutrophil and lymphocyte counts, hematocrit, and body temperature), which accurately identified 84.7% of the dengue cases in their study population. This algorithm had a 71.2% sensitivity and 90.1% specificity for predicting the diagnosis of dengue but has not been externally validated.171 Such studies use both clinical and laboratory findings to identify patients with DF. The tourniquet test (Figure 48-10) for capillary fragility, which describes the appearance of 20 or more petechiae over a square-inch patch on the forearm after deflation of the blood pressure cuff (held for 5 minutes between systolic and diastolic pressures), may also be positive. Although WHO typically uses a positive tourniquet test to help distinguish DHF from DF, the test has been shown to be positive in both disease states.184 Patients may have neutropenia with subsequent lymphocytosis marked by atypical lymphocytes, hyponatremia, hypoproteinemia, and mild elevation of liver enzymes. Other findings include albuminuria and occult blood in the stool. In patients with DHF, either thrombocytopenia (defined by WHO as less than 100,000/mm3) or hemoconcentration (elevation of hematocrit 20% or greater than the average for age, gender, and population) is used by WHO to reach a provisional diagnosis of DHF if certain clinical observations (e.g., acute onset of high fever, hemorrhagic manifestations, hepatomegaly, shock) are made. In cases with extensive liver involvement, vitamin K–dependent prothrombin factors, such as II, VII, IX, and X, may be reduced, and assays of coagulation factors may reveal reduced fibrinogen, prothrombin, factors VIII and XII, or antithrombin III. About one-third to one-half of patients with DHF have increased partial thromboplastin and prothrombin times. Chest radiographs may show a unilateral (usually right-sided) pleural effusion in more severe disease.187 Definitive diagnosis of dengue can be made by isolating the virus or detecting specific antibodies. Immunofluorescence assay of serum or cerebrospinal fluid (CSF) with serotype-specific

FIGURE 48-10  Positive tourniquet test.

888

monoclonal antibodies (IgM enzyme-linked immunosorbent assay [ELISA]) is the test of choice to confirm diagnosis. Although the IgM immunoassay has a sensitivity of 90% to 97%,76 samples collected within the first 4 to 5 days of illness may lead to false negative results.184 Serologic diagnosis of DF then com­ monly depends on demonstration of a fourfold or greater increase in IgM or IgG antibody titer between acute-phase and convalescent-phase serum samples by hemagglutination inhibition or enzyme immunoassay (and less commonly complement fixation and neutralization test). Other methods for laboratory detection include detection of DF genomic sequences from autopsy tissue, serum, or CSF with polymerase chain reaction (PCR).187 Several protocols have been written for PCR detection of DF, because this technology can aid in detection of the virus within 1 to 2 days.46,47,52,95 However, this method is not widely available, and thus its use is limited to detecting dengue viruses in pathologic tissue, cell cultures, and mosquito specimens.76 Unfortunately, attempts to develop rapid bedside tests using immunochromatographic or immunoblot technologies remain relatively unsuccessful.11 Virus identification can also be confirmed by inoculation of serum into mosquitoes or certain mosquito cell lines (most commonly A. albopictus [C6-36] and Aedes pseudoscutellaris [AP61], but with better sensitivity when mosquitoes in the genus Toxorhynchites are used), but these methods are not commonly available. The recommendation of the Centers for Disease Control and Prevention (CDC) is that, for testing and reporting, both acutephase and convalescent-phase (6 days after the onset of symptoms) serum samples be sent to the state health department, which will forward them to the CDC for testing. The acute-phase specimen should be stored on dry ice (or unfrozen at 4° C [39.2° F] if sent within a week), and the convalescent-phase specimen should be shipped on ice (or in a rigid container without ice if next-day delivery is possible).33 Despite all this, however, dengue infections are often diagnosed clinically because laboratory-based diagnosis is often unavailable and has limitations as well.184 That said, dengue should be considered only after other common tropical infections such as malaria are ruled out.184 History is of utmost importance; symptoms in a traveler or immigrant that begin 2 weeks after departure from an endemic area cannot be attributed to dengue, because the incubation period is less than 2 weeks.158 Treatment and Prevention Treatment includes supportive therapy, including aggressive fluid and electrolyte resuscitation. Early recognition is important, because the acute increase in vascular permeability may cause extreme amounts of plasma to be lost from vascular compartments for 24 to 48 hours. Fever should be treated with antipyretics (especially in children to avoid febrile seizures), and WHO recommends treatment with acetaminophen (paracetamol) if the temperature is greater than 39° C (102.2° F), with dosing as follows: for infants less than 1 year of age, 60 mg per dose; 1 to 3 years of age, 60 to 120 mg per dose; 3 to 6 years of age, 120 mg per dose; and 6 to 12 years of age, 240 mg per dose. WHO recommends no more than six doses in a 24-hour time period, and advises against salicylates to prevent bleeding complications and Reye-like syndrome in children.187 Volume expanders can include normal saline, Ringer’s lactate, or 5% glucose diluted in half-normal or normal saline administered in 10 to 20 mL/kg boluses initially, and then continued with maintenance therapy as needed. One recent double-blind randomized study suggests that Ringer’s lactate at 25 mg/kg over 2 hours should be given for initial resuscitation in children with moderately severe DSS, and that 6% hydroxyethyl starch (also in the amount of 25 mg/kg) may be preferable in children with severe shock.185 Corticosteroids have also been attempted in DSS for their antiinflammatory properties. However, one recent Cochrane meta-analysis of 284 patients demonstrated no reductions in mortality, length of hospital stay, DSS-related complications, or need for blood transfusions when comparing patients who received corticosteroids with those those who received placebo.138 Because of plasma loss, the hematocrit may initially increase, but blood transfusion should be given if there is a clinical indication of internal bleeding. WHO recommends

YELLOW FEVER The first epidemic caused by the yellow fever virus is thought to have been in the Yucatan Peninsula in 1648. This singlestranded RNA flavivirus causes infection in up to 200,000 persons per year, with an estimated 30,000 deaths annually, mainly in Africa (90% of cases) and South America (10% of cases).8,182 Epidemiology and Transmission It is thought that the yellow fever virus evolved about 3000 years ago from other arthropod viruses in Africa and was carried to the Americas by Dutch slave traders in the 17th century. During the late 17th century, epidemics and outbreaks occurred in the Yucatan Peninsula, several places on the East Coast of the United States, and the Caribbean islands. While the English, Spanish, and French were colonizing the Americas, yellow fever played

Western Sahara

Cape Verde

Mali

Mauritania

Senegal

Guinea-Bissau

Oman

Eritrea

Chad Sudan

Benin

Yemen

Burkina Faso

Guinea

Sierra Leone

Saudi Arabia

Egypt

Libya

Algeria

Niger Gambia

a prominent role by decimating populations of sailors, troops, and citizens, especially near port cities. Unfortunately, factors such as increased urbanization and waning yellow fever immunization programs have contributed to resurgence of the disease since the 1980s.8,150 Accurate data regarding the burden of disease are difficult to obtain because of underreporting (especially in remote areas), lack of diagnostic facilities, and delayed recognition of outbreaks. Nevertheless, of particular concern are the increasing incidence of yellow fever in West Africa (which includes multiple countries suffering humanitarian crises that hinder effective immunization campaigns) and the high (>50%) case fatality rate in South America. Given such concerns, the Yellow Fever Initiative was launched in 2006 as a collaborative effort toward improved yellow fever surveillance and prevention through mass vaccination campaigns.193,194 Figures 48-11 and 48-12 show the most recent endemic areas in Africa and the Americas. Yellow fever in travelers to South America and Africa has been very rare, likely due to routine vaccination. Between 1970 and 2002, only 10 cases of yellow fever were reported, 9 of which occurred in unvaccinated individuals.38 The mosquito species A. aegypti was hypothesized as early as 1881 to be the vector, and it is indeed one of the main mosquitoes that transmit yellow fever in urban settings. There are three patterns of yellow fever transmission: urban, intermediate, and sylvatic (jungle). In urban yellow fever, no monkeys are involved in transmission, and domestic mosquitoes, such as A. aegypti, carry the virus from person to person. In intermediate yellow fever, mosquitoes of the genus Haemagogus, or other forest-canopy species, are known to transmit this disease to both monkeys and humans; this is the most common type of transmission in recent outbreaks in Africa. Finally, in sylvatic yellow fever, nonhuman primates, such as monkeys, are the zoonotic focus, and wild mosquitoes can become infected by the monkeys and pass the disease to humans.38,190 Interestingly, there is also vertical transmission of the virus within mosquitoes; a female mosquito can pass the virus to her offspring. Thus mosquitoes serve as additional reservoirs and vectors of the virus, which ensures endemicity of the disease.182 Peak transmission in Central and South America is during the rainy season between January and March, whereas in Africa it is highest through the end of the rainy season into the early dry season (July through October).38

Nigeria

Somalia

Ivory Coast Ghana

Liberia

Togo

Cameroon

Ethiopia

Central African Republic

Equatorial Guinea Sao Tome and Principe

Uganda Democratic Republic of the Congo

Gabon

Republic of the Congo

Kenya

Indian Ocean

Rwanda Burundi Tanzania

Atlantic Ocean

Madagascar

Malawi Angola Zambia

Areas of no risk Areas at risk for yellow fever transmission

Namibia

Zimbabwe

Mozambique

Botswana

FIGURE 48-11  Yellow fever–endemic zones in Africa, 2009. (From http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-2/yellow-fever.aspx#668.)

889

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

fresh-frozen plasma and concentrated platelets only if there is massive risk for bleeding from coagulopathy. At the same time, because of the volume resuscitation, a drop in hematocrit does not automatically indicate internal hemorrhage, because reabsorption of extravasated plasma may occur when shock ceases. Continued overzealous administration of fluids at this point can lead to pulmonary edema or heart failure. All these measures must be based on clinical judgment, in turn based on indicators such as vital signs, urine output, and hematocrit.187 Despite ongoing vaccine initiatives, there is not yet a licensed vaccine against dengue viruses. As discussed above, a primary infection with one serotype induces long-term protective immunity to reinfection with the homologous serotype but not the heterotypic serotypes. In addition, infection of any serotype can lead to DHF, and sequential exposure to DF may predispose a person to DHF. Thus a successful vaccine must induce longlasting neutralizing antibodies to all four dengue serotypes. Tetravalent vaccines that enable immunity to all four serotypes are in development and have shown promising results in preliminary clinical testing.58,129 However, vaccine development remains difficult, because administration of four live viruses can result in competition between serotypes and incomplete stimulation of neutralizing antibodies. At this point, vector control through environmental, biologic, and chemical means remains a mainstay of prevention (see information regarding vector control in Global Programs, later).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

sign (bradycardia occurring at the height of the fever), conjunctival injection, and a coated tongue with pink edges. The infection stage may resolve rapidly within 3 to 4 days and be followed by up to 48 hours of remission.8,128,182 The intoxication period occurs in an estimated 15% or more of individuals infected with this virus, manifesting with liver and renal failure (jaundice, azotemia, and oliguria), myocardial involvement, encephalopathy, and shock. Viral-induced thrombocytopenia and acquired coagulopathy can cause severe hemorrhage, ranging from epistaxis, metrorrhagia, and gastrointestinal bleeding (the reason Spanish-speaking peoples called the disease vomito negro, or black vomit, before the disease was officially named).16 Severe illness has a case fatality rate of about 20%, which may approach 50% in some outbreaks.117

Atlantic Ocean Panama

Panama Canal Zone

Caracas

Trinidad and Tobago Guyana Suriname Venezuela French Guiana Colombia Maturin

Panama

Ecuador

Puyo

Quito Riobamba

Chachapoyas

Fortaleza

Manaus

Iquitos

Recife

Peru

Brazil

Huánuco Lima

Bolivia Cuzco

La Paz Sucre

Brasilia

Chile

Belo Horizonte

Santa Cruz

Paraguay

Tarija

Pacific Ocean

Aracaju Salvador

Asuncion Salta Resistencia

Sao Paulo Rio de Janeiro

Iguassu Falls Posadas

Argentina Uruguay Atlantic Ocean

Areas of no risk Areas at risk for yellow fever transmission Falkland Islands

FIGURE 48-12  Yellow fever–endemic zones in the Americas, 2009. (From http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-2/ yellow-fever.aspx#668.)

The female mosquito inoculates about 1000 virus particles (the 50% lethal dose for monkeys is less than one particle) intradermally during one human feeding, and viral replication occurs at that site. It is believed that the virus spreads through lymphatic channels and has preference for replication in lymphoid cells, after which it spreads hematogenously. During this viremia, uninfected mosquitoes can become infected if they bite infected humans. Clinical Presentation The main risk factor for disease is exposure, as evidenced by the fact that a large portion of cases are in men of ages 15 to 45 years who have occupational exposure in mosquito-infested areas. Unvaccinated individuals (such as persons too young to have been immunized) in epidemics are also at higher risk, as are individuals in areas with poor health care.182 There are three phases in the classic description of yellow fever: infection, remission, and intoxication. After an incubation period of 3 to 6 days, the infection stage consists of sudden onset of fever, headache, photophobia, malaise, back and epigastric pain, anorexia, and vomiting. Helpful clinical signs include Faget 890

Diagnosis Preliminary diagnosis is based on clinical presentation and travel history. However, given the clinical overlap with several other disease processes (e.g., leptospirosis, louse-borne relapsing fever, DHF, viral hepatitis), virus detection or serologic examination is required for definitive diagnosis. Laboratory findings may also be supportive in making the diagnosis. They may include leukopenia with relative neutropenia; thrombocytopenia with reduction of all liver-produced clotting factors; elevation of liver enzymes (but usually a normal alkaline phosphatase); elevated blood urea nitrogen (BUN) and creatinine levels; and albuminuria.128 Definitive diagnosis is typically obtained by IgM ELISA and is best done with paired acute and convalescent sera. The acute sample should be drawn within several days of symptom onset, and the convalescent sample should be drawn about 14 days later. A neutralization test, which is done by showing loss of infectivity through reaction of the virus with a specific antibody, can also be done to confirm the diagnosis of yellow fever. Given cross-reactivity between antibodies from other flaviviruses, such confirmatory tests are especially important in Africa, where multiple flaviviruses coexist. The virus can be isolated from serum specimens or liver tissue after death, via inoculation of mice, mosquitoes, or cell cultures, but these techniques are most effective in the preicteric state. Once the intoxication period begins, the viral RNA is usually undetectable and thus such methods are generally not used for diagnosis. Other methods, including PCR for viral genome identification and liver biopsy for demonstration of characteristic midzonal necrosis, have been discussed but are not used for diagnosis.7,38,128,182 Treatment and Prevention Although there is no treatment other than supportive care, there is a vaccine against yellow fever (17D-204 strain YF-VAX); 0.5 mL of the reconstituted vaccine is administered subcutaneously.42 This vaccine is a live, attenuated vaccine that is generally considered very effective and safe. Seroconversion rates exceed 95%, and side effects are usually limited to injection site pain, mild headaches, myalgias, or low-grade fevers for several days.9,65,128,131 As more travelers enter endemic areas without receiving the vaccine, the number of yellow fever cases imported into the United States and Europe has increased.117 The CDC roughly estimates the risk for acquiring yellow fever for an unvaccinated traveler going to endemic areas of West Africa and South America to be 50 per 100,000 and 5 per 100,000, respectively.38 The CDC and the Advisory Committee on Immunization Practices recommend that travelers (older than 9 months) to certain areas in Africa and South America be vaccinated. Some countries (not the United States) require vaccination before allowing travelers to enter from endemic areas. Vaccination guidelines (and authorized centers for vaccination) can be found on the CDC Yellow Book website at http://wwwnc.cdc.gov/travel/yellowbook/2010/ chapter-2/yellow-fever.aspx. International travelers must receive yellow fever vaccines approved by WHO and administered at an approved yellow fever vaccination center and then obtain an international certificate of vaccination. Although the International Health Regulations require boosters every 10 years, many studies suggest that vaccine immunity endures for over 30 years and possibly for life.190 Immediate hypersensitivity reactions in people with allergies to eggs or other substances are thought to occur in 1 per 131,000

American countries, with much credit owed to the Pan American Health Organization. However, vigilance must be maintained, because A. aegypti has reestablished itself in many of these areas. Much work must be done in Africa, where the mosquito has never been eradicated.117

JAPANESE ENCEPHALITIS The Japanese encephalitis (JE) virus, a member of the Flavivirus genus, is the major cause of viral encephalitis in Asia, with as many as 50,000 cases reported every year. Although JE virus is a leading cause of viral encephalitis in Asia, there is less than one case per year in U.S. civilians and military personnel living in or traveling to Asia, with rare outbreaks in U.S. territories in the western Pacific. There has been more recent expansion of JE into northern Australia (Figure 48-13).39,40,81,135 Epidemiology and Transmission Culex mosquitoes (usually Culex tritaeniorhynchus, C. vishnui, and C. pseudovishnui) are the vectors for this virus, and vertebrate hosts such as pigs and birds sustain the virus. Because humans are not necessary for transmission, the virus can still be maintained in an enzootic cycle even where JE immunity is high (either in endemic regions or through vaccinations) and human cases do not occur. The mosquitoes breed in flooded fields associated with rice production. Because these settings contain factors that enhance the JE transmission cycle (e.g., large numbers of pigs and birds to serve as reservoirs for infection), JE infection rates may be as high as 3% in these areas.117

RUSSIA

KAZAKHSTAN MONGOLIA

NORTH KOREA

KYRGYZSTAN TAJIKISTAN

SOUTH KOREA

JAPAN

CHINA AFGHANISTAN

PAKISTAN

NEP AL

BHUTAN Saipan

INDIA

Myanmar (Burma) BANGLADESH

TAIWAN LAOS

Guam

THAILAND

Saipan

VIETNAM PHILIPPINES

SRI LANKA

Guam

CAMBODIA MALAYSIA SINGAPORE

INDONESIA

Risk areas for Japanese encephalitis

PAPUA NEW GUINEA

INDONESIA

AUSTRALIA

FIGURE 48-13  Geographic distribution of Japanese encephalitis.

891

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

vaccinations, whereas anaphylaxis is reported to occur in 1.8 per 100,000 doses administered. Additional significant adverse reactions to the yellow fever vaccine typically occur in first-time vaccinees and are categorized as yellow fever vaccine–associated neurotropic disease (YEL-AND) and yellow fever vaccine– associated viscerotropic disease (YEL-AVD). YEL-AND is typically due to neuroinvasion by the 17D virus and represents multiple different clinical syndromes, including Guillain-Barré syndrome and meningoencephalitis. Historically the vaccine was associated with encephalitis in children, but standardization of the virus vaccine has decreased the incidence in the United States to 0.8 case per 100,000 doses administered. Although the incidence is thought to be higher in the older adult population, the case fatality rate remains low.9,38 YEL-AVD is a severe illness resembling wild-type disease, in which vaccine virus replication often leads to multisystem organ failure and death. The incidence in the United States is 0.4 cases per 100,000 doses administered, but host factors such as increased age, history of thymus disease, and male gender are thought to increase the risk. The case fatality rate remains a staggering 53%.9,38 Caution is advised in infants less than 9 months old; in individuals with a history of hypersensitivity to vaccine products, thymus disease, or human immunodeficiency virus (HIV); and in individuals who are pregnant, nursing, immunocompromised, older adults, or receiving other vaccines simultaneously.9,38,42 The CDC encourages health care providers to report febrile illness thought to be caused by the yellow fever vaccination to the CDC/FDA Vaccine Adverse Events Reporting System (VAERS) at http://vaers.hhs.gov/esub/index. Eradication of A. aegypti via well-executed control campaigns in the 1970s has been successful in many Central and South

PART 6  ANIMALS, INSECTS, AND ZOONOSES

JE has two main transmission patterns in Asia. Seasonal transmission occurs in the more temperate northern regions (e.g., Japan, People’s Republic of China, Taiwan, northern India) and can cause large epidemics. The second pattern of yearround transmission presents in tropical southern regions (e.g., southern Thailand, southern Vietnam, southern India, Indonesia, Malaysia, Philippines, Sri Lanka) and is usually more endemic or sporadic.54,117,159 Clinical Presentation Persons at increased risk include individuals (residents, active duty military, or expatriates) living in endemic areas. Travelers have a low risk for acquiring the disease, estimated to be less than one in a million American travelers going to endemic areas.19 Most residents of endemic areas are infected during childhood or early adulthood,86 with about 10% of the susceptible population infected yearly. The disease appears to affect mainly children less than 15 years of age, although there also seems to be a secondary increase of disease in older adults, posited to be caused by waning immunity.19 The incubation period is from 5 to 15 days. Most infections with JE are subclinical. Early symptoms include sudden onset of fever, headache, nausea and vomiting, and abdominal pain. JE may also manifest with coryza, diarrhea, and rigors. In some individuals, abnormal behavior is the only clinical manifestation, so JE has been misidentified as mental illness.163 In the Korean conflict, for example, American military personnel with JE were sometimes diagnosed with “war neurosis.”113 After several days, JE may develop into aseptic meningitis with or without encephalopathy, or into encephalitis (less than 1% of infected individuals) presenting with delirium and abnormal motor movement. Children in particular seem to have more convulsions than do adults infected with the virus.56,107,126,164 In fact, 98.7% of children hospitalized for JE during a recent epidemic in India presented with seizures.109 Seizures are more often generalized tonic–clonic than focal.126 Abrupt onset of flaccid paralysis in one or more limbs has also been reported.166 The case fatality rate of JE is approximately 30%, and almost 50% of survivors have severe neurologic sequelae, including motor deficits, upper and lower motor neuron weakness, and cerebellar or extrapyramidal signs.40,163,164 Diagnosis Laboratory analysis demonstrates that patients can have peripheral leukocytosis. Patients may also have hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fifty percent of patients have high CSF opening pressure on lumbar puncture, and analysis of CSF may show pleocytosis (predominantly lymphocytic) of 10 to 100 cells/ mm3, with normal glucose and slightly elevated protein. With early disease, however, there may be no CSF pleocytosis, and leukocytes are predominantly neutrophilic.109,174 Definitive diagnosis is achieved by demonstration of IgM antibody by enzyme immunoassay antibody captured in CSF or serum; by a fourfold or greater rise in serum antibody titers against JE virus; or by isolation of virus from or demonstration of viral antigen or genomic sequence in tissue, blood, CSF, or other body fluid.174 Of note, it can be difficult to isolate JE virus from blood because of the low viral burden. The most common method of diagnosing JE in the past was with a serologic hemagglutination inhibition test. Since the 1980s, however, IgM-capture ELISA has been used, and confirmation is recommended with another assay for IgG antibody. One recent study looked at anti-JE virus IgM levels in both serum and CSF of 155 confirmed JE cases in Thailand between 2002 and 2004. Specific IgM was detected in nearly all serum samples (23/26) collected at least 9 days after symptom onset, and in all but one CSF sample collected at least 7 days after symptom onset. In fact, in most JE cases, anti-JE virus IgM was detectable in CSF as early as day 1 after symptom onset.45 Both noncontrast and contrast computed tomography (CT) and magnetic resonance imaging (MRI) may show nonenhancing low-density areas in the thalamus, basal ganglia, midbrain, pons, or medulla, and an electroencephalogram may show theta and delta coma, burst suppression, and epileptiform activity.97,125,127,160 892

Treatment and Prevention There is no specific treatment for JE beyond supportive care. Other modalities, such as reducing intracerebral pressure with mannitol and providing seizure prophylaxis, have been suggested by some experts, but there have been no studies on agents to use and whether these interventions are beneficial in JE.117,174 Therapies such as corticosteroids, interferon-α, and ribavarin have all been studied in randomized, double-blind, placebocontrolled trials. JE patients do not seem to benefit from any of these treatment measures.87,108 Vaccination is an important method of disease control and has nearly eliminated the disease in some parts of the world. In Asia (e.g., the People’s Republic of China, Japan, Korea, Taiwan), more than 500 million doses of JE vaccine have been administered since the 1970s. There are a number of vaccines currently available. In March 2009, a new inactivated Vero cell culture–derived vaccine (Ixiaro) was approved for use in the United States for individuals 17 years and older.34,172 This vaccine has not been studied in children. It produces a 97% seroconversion rate after two doses administered 28 days apart. In a multicenter, multinational randomized clinical phase III trial comparing Ixiaro with JE-Vax, the vaccines were shown to have equal clinical efficacy and safety profiles.172 Historically the most widely available JE vaccination has been an inactivated mouse brain–derived vaccine ( JE-Vax) typically prepared using the Nakayama or Beijing-1 strain of JE virus. This was the only vaccine available to international travelers (adults and children older than 1 year of age) from nonendemic countries. For adult travelers, the recommendation for primary immunization is a series of three subcutaneous vaccinations of 1.0 mL each (0.5 mL for children 1 to 3 years of age), on days 0, 7, and 30 (an abbreviated schedule of days 0, 7, and 14 is used if the longer schedule is not feasible). Although the literature regarding this vaccine’s dose-dependent efficacy is somewhat conflicting, one recent retrospective study evaluated over 30 years of JE-Vax use in Taiwan. They estimated that the vaccine’s long-term efficacy was 87% for even a single dose, whereas it was 98% effective for the three-dose series.192 The last dose should be given at least 10 days before the actual date of travel to allow a sufficient immune response. There have been no studies on administering this vaccine to infants younger than 1 year of age.18 JE-Vax has a low rate of side effects.18 It is associated with a moderate frequency of local adverse effects, as well as mild systemic effects (e.g., fever, headache, malaise, rash), in 10% to 20% of vaccinated individuals. More serious events, including angioedema, can appear up to 2 weeks after administration and sometimes after the second or third dose when the first was received without complications. There have also been concerns about vaccine-related neurologic events, including encephalitis, seizures, and even death.146,162,92 WHO estimates that the rates of such severe adverse reactions are in the range of 18 to 64 per 10,000 vaccinated individuals.92 However, since the 1990s, the reported rate for all adverse events for this inactivated vaccine is 2.8 per 100,000 in Japan and 15 per 100,000 in the United States.117 The usefulness of this vaccine is further limited due to high production costs and the need for serial doses in addition to booster doses. At this time, JE-Vax is no longer being produced and given a shortage of supplies, the CDC recommends that this vaccine now be used only in children 1 to 16 years old.40 A live, attenuated vaccine based on the strain SA14-14-2 is also available. This vaccine has been used in China for over 20 years and has recently been licensed in Nepal, Sri Lanka, South Korea, and India. Numerous large field studies and case-control studies have shown efficacy of over 95% following two doses given 1 year apart. WHO estimates that this vaccine was helpful in reducing the burden of JE in China from 2.5 per 100,000 in 1990 to less than 0.5 per 100,000 in 2004.140,153,162,92 It is difficult to assess which travelers should receive the vaccine. The low rate of human disease must be balanced against the severe effects of JE infection. Furthermore, the JE infection rate in travelers is low, and there are legitimate concerns regarding the side effects of vaccination. The vaccine should not be given to all travelers to Asia; according to the CDC, it should be

WEST NILE VIRUS First identified in 1937 from the blood of a febrile woman in the West Nile province of Uganda, WNV is a flavivirus that before 1999 was found only in Africa, West Asia, and the Middle East. WNV has received significant press in North America because of its intrusion into the United States, with the first report in the summer of 1999 in New York.5,137 The most accurate epidemiologic trend data include neuroinvasive disease (meningitis/ encephalitis), because most patients with West Nile fever (WNF) are asymptomatic and do not seek care. Through 2007, more than 11,000 cases of WNV neuroinvasive disease have been reported, and it is estimated that 1.5 to 3 million individuals have been infected in the United States alone. Since 1999, cases of human disease have been found in all 50 of the United States except Hawaii, Alaska, and Maine.37,142 Epidemiology and Transmission WNV is a single-stranded RNA virus that is part of the family Flaviviridae, genus Flavivirus. All flaviviruses have a size of approximately 40 to 60 nm (Figure 48-14), are enveloped with icosahedral nucleocapsids, and have single-stranded RNA of about 10,000 to 11,000 bases.37 Mosquitoes are the vectors for this virus, and birds are the most common reservoir. The most commonly named vector is the Culex mosquito species, but WNV has recently been identified in more than 64 different mosquito species in North America, which contributes to its permanent establishment and wide distribution in the United States (Figure 48-15). The different species of mosquitoes have varying host preferences and behavior, and frequent transmission to migrating birds extends the reach of the

FIGURE 48-14  Electron microscopy of the West Nile virus.

virus.70 Newly infected birds sustain viremia for about 1 to 4 days (after which they develop lifelong immunity), and during that time, mosquitoes can contract the virus. Humans and other mammals such as horses are considered incidental or “dead-end” hosts, because they often do not sustain viremia long enough to serve as reservoirs for the virus. The effects on nonhuman life can be significant; the 2002 WNV epidemic and epizootic in the United States, for example, reported 16,471 dead birds and 14,751 equine cases. In horses, as in humans, WNV crosses the blood– brain barrier and interferes with CNS functioning, ultimately leading to possible death.26 Another recent study conservatively estimated the American crow population to have declined 45% since WNV arrival, and only two of the seven avian species documented to have been impacted returned to pre-WNV levels by 2005.111 Other, rarer methods of transmission include organ transplantation,28,89 blood transfusion,24,25,141 transplacental infection,22 and

Indicates human disease case(s) Avian, animal or mosquito infections WA 36 OR 7

ID 37

NV 12 CA 103

MT 5

VT

ND 1

WY 12

MN 4

SD 21

AZ 18

CO 101

KS 10 OK 8

NM 8 TX 104

NH MI

IA 5

NE 51 UT

WI 1

NY 6 PA

MO 3

IL 4

LA 20

AK

OH 2

IN 4

WV

VA NC

TN 7 MS 52

AL

GA 4

MA RI CT NJ

KY 3

AR 4

ME

SC 3

2

DE MD 2 DC

FL 3 HI

Puerto Rico

FIGURE 48-15  2009 West Nile virus activity in the United States. (From http://www.cdc.gov/ncidod/dvbid/westnile/Mapsactivity/surv&control 09Maps.htm.)

893

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

offered to those persons older than 9 months staying a prolonged amount of time (>1 month) in endemic areas during transmission season, and if travel includes rural areas. Persons staying less than 1 month but with specific risk factors for exposure (e.g., extensive amount of time spent outdoors during seasons of peak transmission) may also consider vaccination.18

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 48-2  Criteria for Clinical and Definite Diagnoses of West Nile Neuroinvasive Disease Possible Clinical Diagnosis of West Nile Neuroinvasive Disease (before serology results available)   Requirements: 1, 2, 3 (A, B, or C), 5 with 4 supportive New onset of: 1. Fever >38° C or subjective fever by patient when temperature never taken 2. Acute systemic symptoms (>1 lasting > 48 hours) Headache Nausea or vomiting Myalgias Transient erythematous maculopapular rash 3. Acute neurological signs and symptoms (A, B, or C required) A. Altered mental status for >48 hours (>1 below are required) Marked lethargy that often incapacitates the individual Delirium or agitation Marked disorientation or confusion that often incapacitates the individual Profound sleepiness (sleeping all day for >2 days) Stupor or coma B. Brainstem or spinal cord signs that persist >48 hours (>1 below are required) Cranial nerve palsies Myelitis i. New focal weakness in one or more limbs that is not due to arthritis or limb pains lasting > 48 hours ii. Respiratory failure requiring intubation that is not solely due to pneumonia iii. Electromyographic evidence of recent denervation in more than one nerve root C. Cerebrospinal fluid (CSF) (all required if examined): Pleocytosis (rarely may be absent if lumbar puncture performed within first 2 days of central nervous system symptoms) Cerebrospinal fluid IgM antibody for West Nile virus Negative cultures for bacteria and negative Gram stain (if mycobacterial, fungal, or viral cultures were done, they should be negative) 4. Supportive criteria A. Focal neurological signs of acute onset (≥1 desired but not required) Hemiparesis Visual field loss or chorioretinitis Hyperactive deep-tendon reflexes or Babinski's sign Seizure Tremor or myoclonus Bradykinesia, spasticity, or rigidity Photophobia Severe generalized weakness and fatigue that keeps patient in bed B. Mosquitoes as vector (1 desired unless patient received transfusion or transplant organ): Positive West Nile virus (WNV) mosquito pools or infected horses in region within past 3 weeks or Recent cases of acute WNV infection in region or Travel within past 3 weeks to region with positive WNV mosquito pools or cases of WNV infection 5. Exclusion criteria (required) Underlying dementia, congestive heart failure, or chronic obstructive pulmonary disease that could cause altered mental status and no known other neurological disease that could cause the neurological signs Definite or Confirmed Diagnosis of West Nile Neuroinvasive Disease   Above criteria plus WNV serology/virology (A and B plus/or C or D) A. Demonstration of WNV IgM antibody in serum without vaccination with yellow fever or Japanese B viral vaccine in past 5 years or recent infection with other flavivirus, such as St Louis encephalitis virus. Note: If WNV has occurred in region in prior years, criterion B is needed because previously infected individuals may have prolonged persistence of IgM in serum. B. Fourfold or greater increase in serum WNV IgG or IgM antibody titer between acute and convalescent samples taken 10 to 28 days apart. C. Demonstration of WNV IgM antibody in CSF D. Identification of WNV in CSF by viral culture or of WNV nucleic acid by polymerase chain reaction From Davis LE, DeBiasi R, Goade DE, et al: West Nile virus neuroinvasive disease, Annals of Neurology 60:294, 2006.

possibly human breast milk.23 Because transmission from blood transfusions reached 2.7 cases per 10,000 units during the peak of the 1999 outbreak in New York, and because there were confirmed cases of WNV transmission to organ transplant recipients, routine screening of blood donors for WNV RNA began in the summer of 2003. In 2003 and 2004, 519 donors were identified by this method, resulting in removal of more than 1000 potentially infectious units of blood products from the Red Cross supply. All donated blood continues to be screened for WNV with nucleic acid amplification tests, either on individual samples or on “minipools” of up to 16 donations.169 A recent study of targeted nucleic acid amplification testing of individual donations in high-prevalence regions suggests that this approach may be cost-effective, because units with low levels of viremia may not be detected in minipools of blood donations.17 Despite reduction in transfusion-related transmission with universal screening of blood, this limitation has prevented eradication and cases are still reported.31 894

Clinical Presentation The virus has an incubation period of 3 to 14 days.143 Disease usually occurs in temperate zones either in late summer or early fall, or year-round in milder climates. Clinical syndromes caused by WNV include asymptomatic infection, WNF, and West Nile neuroinvasive disease (WNND). Most WNV infections in humans are asymptomatic. Of the 20% of symptomatic cases, the majority of patients develop WNF, which usually involves a mild influenzalike illness with malaise, headache, nausea, vomiting, anorexia, lymphadenopathy, and rash. In a case-series review of 98 community-dwelling patients with laboratory evidence of WNV infection but no evidence of neuroinvasive disease, fatigue was present in 96% of patients, fever in 81%, headache in 71%, and difficulty concentrating in 53%.181 Even in cases of WNF, the impact on quality of life can be severe. Of the 98 patients, 39% reported ongoing symptoms at 5 month follow-up, 82% reported limitations in household activities, and there was a median of

Diagnosis For public health and surveillance purposes, the CDC uses specific criteria for arboviral infections and includes disease caused by California serogroup viruses, eastern and western equine encephalitis viruses, Powassan virus, St Louis encephalitis virus, and WNV. This was most recently revised in 2004 (Box 48-1).35 Typical findings for severe disease usually include normal or slightly elevated leukocyte counts in peripheral blood, possible hyponatremia in individuals with WNV encephalitis, pleocytosis and increased protein in the CSF, and no findings on CT scans of the brain.37,143 Although MRI may yield abnormal results in 25% to 35% of cases, findings may be nonspecific.37,196 For definitive diagnosis, serum is ideally collected within 8 to 14 days of symptom onset, and CSF is collected within 8 days to give the highest diagnostic sensitivity. Serum or CSF should show IgM antibodies to WNV by IgM-capture ELISA (MAC-ELISA). There is, however, a chance that persistent IgM antibodies can be found in people years after living in places where WNV is epidemic. The diagnosis can be further confounded by the fact that these IgM ELISA tests have a cross-reactivity of up to 44% with other flaviviruses during acute infection.37,70 The most specific test for arthropod-borne flaviviruses is the plaque-reduction neutralization test (PRNT). It can be used both to negate the false-positive results sometimes seen in MAC-ELISA or other assays and to facilitate discrimination among the flaviviruses.37 Efforts have been made to develop more specific and rapid serologic assays. Promising candidates include a microsphere immunoassay that discriminates among different flavivirus infections, as well as an immunofluorescence assay that has less cross-reactivity among WNV IgM antibodies and closely related flaviviruses. PCR (as used for screening blood products in the United States) or viral culture can also isolate the virus, but sensitivity is not high because of the transient and low levels of viremia, because the virus quickly disappears from the periphery into the CNS in severe disease.37,143 However, one recent study showed that the combination of serologic assay and nucleic acid testing allowed for more accurate identification of WNV cases

BOX 48-1  2004 CDC Case Definition for Neuroinvasive

and Non-Neuroinvasive Domestic Arboviral Diseases

Clinical Criteria for Diagnosis Neuroinvasive disease requires the presence of fever and at least one of the following, as documented by a physician and in the absence of a more likely clinical explanation: • Acutely altered mental status (e.g., disorientation, obtundation, stupor, or coma), or • Other acute signs of central or peripheral neurologic dysfunction (e.g., paresis or paralysis, nerve palsies, sensory deficits, abnormal reflexes, generalized convulsions, or abnormal movements), or • Pleocytosis (increased white blood cell concentration in cerebrospinal fluid [CSF]) associated with illness clinically compatible with meningitis (e.g., headache or stiff neck). Non-neuroinvasive disease requires, at minimum, the presence of documented fever, as measured by the patient or clinician, the absence of neuroinvasive disease (above), and the absence of a more likely clinical explanation for the illness. Involvement of non-neurologic organs (e.g., heart, pancreas, liver) should be documented using standard clinical and laboratory criteria. Laboratory Criteria for Diagnosis Cases of arboviral disease are also classified as either confirmed or probable, according to the following laboratory criteria: Confirmed Case • Fourfold or greater change in virus-specific serum antibody titer, or • Isolation of virus from or demonstration of specific viral antigen or genomic sequences in tissue, blood, CSF, or other body fluid, or • Virus-specific immunoglobulin M (IgM) antibodies demonstrated in CSF by antibody-capture enzyme immunoassay (EIA), or • Virus-specific IgM antibodies demonstrated in serum by antibody-capture EIA and confirmed by demonstration of virus-specific serum immunoglobulin G (IgG) antibodies in the same or a later specimen by another serologic assay (e.g., neutralization or hemagglutination inhibition). Probable Case • Stable (less than or equal to a twofold change) but elevated titer of virus-specific serum antibodies, or • Virus-specific serum IgM antibodies detected by antibodycapture EIA but with no available results of a confirmatory test for virus-specific serum IgG antibodies in the same or a later specimen. Case Definition • A case must meet one or more of the above clinical criteria and one or more of the above laboratory criteria. From Centers for Disease Control and Prevention. http://www.cdc.gov/ncphi/ disss/nndss/casedef/arboviral_current.htm. CDC, Centers for Disease Control and Prevention.

compared with either approach alone.173 Such studies have recommended that these measures be used as an adjunct to serologic testing. Treatment and Prevention Currently there is no specific treatment for WNV, and supportive care remains the mainstay of therapy.66 Certain antivirals, antibodies, and drugs altering the inflammation process (e.g., interferon) are being tested. Nucleoside analogs have been studied in vitro,2,134 but the most advanced testing in vivo has been with ribavirin, with no reduction in disease88 or viremia116 shown. In a retrospective, uncontrolled, nonblinded study of 233 human WNV cases, ribavirin was associated with poorer outcome in bivariate analysis. Although this effect was not seen in multivariate analysis, ribavirin was ineffective.48 Similarly, there have been promising in vitro studies and human case reports evaluating the usefulness of interferon-α2,96,133 and intravenous immunoglobulin,1,10 but these treatment options remain controversial. Currently 895

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

10 days of missed school or work.181 In another follow-up study done in a population-based cohort of 656 nonfatal cases, 91% of patients reported limitations in routine daily activities secondary to WNV infection. Moreover, in cases of WNF alone, there was a median number of 16 school or work days missed, and 53% of this subset of patients reported symptoms of at least 30 days’ duration. The impact was even more significant in patients with WNND.139 West Nile neuroinvasive disease occurs in less than 1% of individuals infected with WNV and includes encephalitis, meningitis, meningoencephalitis, and acute flaccid paralysis/poliomyelitis.50 Older adult and immunocompromised patients are at increased risk for severe neurologic disease from WNV. In a retrospective medical chart review of 221 hospitalized WNV patients, 16% of those with meningitis and 32% of those with encephalitis had autoimmune disease, were immuno­suppressed, or were organ transplant recipients. Age over 50 years, alcohol abuse, and diabetes were also found to be associated with WNND.12 Clinical criteria for WNND are listed in Table 48-2. Although the clinical presentation of meningitis and encephalitis in WNV is nonspecific, one particular feature of WNV encephalitis is that it may manifest with parkinsonian features or other movement disorders, such as myoclonus or intention tremor. In a small prospective case-series, 94% of WNV-seropositive patients experienced dyskinesias compared with 13% in the control group.156 Another clinical syndrome associated with severe WNV disease is acute flaccid paralysis, which can rapidly progress to paralysis of one or up to all four limbs. It may also manifest as severe, asymmetric weakness, usually with sensation preserved. Affected limbs show decreased or completely absent deep tendon reflexes, most likely from anterior horn cell involvement similar to that seen in poliomyelitis.50,70,155,156 Other clinical findings may include ocular complications (e.g., optic neuritis, chorioretinitis, retinal hemorrhage, uveitis, conjunctivitis),44,102,191 bladder dysfunction,70 myocarditis, pancreatitis, and fulminant hepatitis.143

PART 6  ANIMALS, INSECTS, AND ZOONOSES

there are two randomized, double-blind, placebo-controlled studies being conducted to evaluate the potential therapeutic effect of interferon and a monoclonal antibody. Information regarding these trials can be found at http://www.nyhq. org/posting/rahal.html and http://clinicaltrials.gov/ct2/show/ NCT00927953, respectively. For prevention of disease, general control measures such as blood donor screening and precautions against mosquitoes can be taken, but so far there is no specific way to prevent WNV. Although vaccines have proved efficacious in multiple animal species, unfortunately no human vaccine exists. Theoretically there is potential for an inactivated virus to induce long-term immunity, because such a vaccine exists for JE and other flavivirus diseases. Multiple candidate vaccines against WNV are being evaluated, a couple of which have shown promise in small human studies. These include a chimeric virus (ChimeriVax-WN) based on the live, attenuated yellow fever 17D vaccine virus containing the premembrane and envelope proteins of WNV, and a single-plasmid recombinant DNA vaccine. ChimeriVax-WN was evaluated in a randomized, double-blind placebo-controlled study of 45 healthy adults. The vaccine was well tolerated, and within 21 days of receiving a single inoculation dose, all study subjects developed high titers of WN-specific neutralizing antibodies. In addition, 43 of 45 participants developed a WNVspecific T-cell response.130 The DNA vaccine was recently evaluated in an open-label phase 1 trial of 15 healthy adults. The vaccine was well tolerated, and in the 12 participants that completed the three-dose vaccination schedule, all developed WNVspecific neutralizing antibodies.120 Other WNV vaccines under development include a candidate live-attenuated chimeric WN vaccine that uses an infectious dengue virus type 4 cDNA clone as a backbone and a recombinant subunit WN vaccine.188 Surveillance and Reporting Reporting requirements for suspected WNV infections vary across local and state health departments, but WNV encephalitis is on the list of designated nationally notifiable conditions. The CDC may use results from commercial laboratories but may also request samples for diagnosis in its own laboratory. Information on how to send specimens can be found at http://www.cdc.gov/ ncidod/dvbid/misc/arboviral_shipping.htm. For ecologic surveillance, the CDC and other federal agencies have established specific guidelines and protocols to track avian, equine, and mosquito epizootics.

ST LOUIS ENCEPHALITIS The St Louis encephalitis (StLE) virus is a flavivirus related to Japanese encephalitis and West Nile virus that is also transmitted by mosquitoes.

occupations, and older age. Patients with symptomatic StLE present with high fever and headache, aseptic meningitis and encephalitis. Infants in particular may have occasional convulsions and spastic paralysis. Of recognized cases, 95% are hospitalized for CNS involvement. The case fatality rate is 3% overall and up to 30% in older adults.30 Diagnosis As with other arboviral diseases, clinical and epidemiologic features must be taken into account to make a presumptive diagnosis. However, StLE may be difficult to differentiate on clinical features alone. Thus definitive diagnosis is typically obtained by testing serum or CSF for serotype-specific monoclonal antibodies (IgM ELISA). Further confirmatory tests, such as demonstrating at least a fourfold increase in antivirus antibody titer between acute and convalescent period, may be done.30 Antigenic crossreactivity with other flaviviruses is a known problem, encour­ aging some facilities to use PRNT or develop discriminatory algorithms to differentiate infections.119 A potential additional option for diagnosis includes a newly developed rapid microsphere-based IgM assay that would shorten the test processing time to less than 5 hours.93,94 Treatment and Prevention As is the case for many viral illnesses, treatment is supportive care, because there are neither specific antiviral therapies nor vaccines. One interventional pilot study of 15 patients with meningoencephalitis due to StLE showed that treatment with interferon-α2b reduced severity and length of complications. Given the small number of participants and the nonrandomized nature of the study, further investigation must be conducted.148

EASTERN EQUINE ENCEPHALITIS First discovered in the brain of a horse with encephalitis in 1933 in New Jersey, eastern equine encephalitis (EEE) is a serious mosquito-borne disease that appears in the eastern half of the United States with a high case fatality rate. The virus is a member of the family Togaviridae, genus Alphavirus, and it is related to western and Venezuelan equine encephalitis viruses.118 Epidemiology and Transmission The transmission cycle involves birds and several species of mosquitoes, predominantly Culiseta melanura (Figure 48-16). Other possible mosquito vectors include species in the genera Aedes and Coquillettidia.118 Humans and horses are considered hosts with incidental infections that can progress to severe disease. EEE occurs mainly along the eastern and Gulf coasts of the United States, but cases have been documented in Canada as

Epidemiology and Transmission The Culex mosquito is the main species that transmits StLE virus, with birds as a reservoir and humans as another host. The viremia, however, does not cause illness in birds or mosquitoes. Around the Gulf Coast, Ohio and Mississippi River Valleys, the culprit mosquitoes are Culex pipiens and C. quinquefasciatus; in Florida, C. nigripalpus; and in the western states, C. tarsalis.30 StLE virus is found throughout much of the Americas. In temperate parts of the United States, disease usually occurs in late summer or early fall, but it can occur year-round in the southern United States. Outbreaks can occur almost anywhere in the United States, though epidemics have occurred mainly in the Midwest and Southeast. Between 1964 and 2008, less than 5000 human cases of StLE were reported in the United States.32,30 In some areas, it appears that WNV is displacing previously endemic StLE because of cross-protective avian herd immunity and differences in transmission efficiency.149 Historically few cases were reported from Central and South America, although there have been recent large outbreaks in both Argentina and Brazil.55,132,167 Clinical Presentation StLE has an incubation period of approximately 5 to 15 days, with a 300 : 1 ratio of asymptomatic to symptomatic cases. Risk factors for infection include low socioeconomic status, outdoor 896

FIGURE 48-16  Micrograph of eastern equine encephalitis virus.

Clinical Presentation Individuals who live (or visit) endemic areas and those who spend significant time outdoors are at risk for developing EEE, and individuals older than 50 years and younger than 15 years have a greater chance of developing severe disease. Clinical presentation can be within the spectrum from mild influenza-like illness to encephalitis, coma, and death. One study collecting the 36 cases from 1988 to 1994 in the United States showed that clinical signs included fever (83%), headache (75%), nausea and vomiting (61%), confusion (4%), myalgias and arthralgias (36%), chills (25%), seizures (25%), focal weakness (23%), abdominal pain (22%), respiratory symptoms (11%), and cranial nerve palsies (8%).53 The case fatality rate for EEE is 33%, making it the most severe of the arboviral encephalitides. Moreover, 50% of individuals who survive are left with mild to severe neurologic deficits.41,53 Diagnosis Peripheral blood may show leukocytosis, and analysis of CSF may reveal elevated protein with red and white cells in the range of 600 to 2000/mm3 (white cells being predominantly lymphocytes). Preliminary diagnosis may be completed by demonstration of IgM antibodies by capture ELISA. Definitive diagnosis lies in serologic evidence based on paired sera (acute and convalescent samples) in hemagglutinin-inhibition assays or in neutralization assays. Acute samples should be obtained within 10 days of symptom onset, and convalescent samples about 2 or 3 weeks after the symptom onset. It is possible to isolate the virus directly from the serum in acute infection, but this method is used less commonly.20,35,118 Other helpful diagnostic modalities include MRI, which may show focal changes, particularly in the basal ganglia, thalamus, and brainstem.53,68 Treatment and Prevention No specific treatment is available. There has been one case report of a child being treated with corticosteroids and intravenous immunoglobulin,68 but this has not been further studied. No human vaccine is available, but there are equine vaccines that should be employed in endemic areas. Surveillance and Reporting EEE is a nationally notifiable disease.

AUSTRALIAN ENCEPHALITIS (MURRAY VALLEY ENCEPHALITIS) Epidemiology and Transmission Occurring mainly in Australia and New Guinea, Murray Valley encephalitis (MVE) virus is from the family Flaviviridae, genus Flavivirus, and is transmitted via a bird-mosquito-bird cycle with Culex annulirostris. Because humans do not have high levels of viremia, they are seen as dead-end hosts. Clinical Presentation Most infections are asymptomatic, and only 1 in 1000 to 2000 infections actually develops into clinical illness.115 The clinical course is similar to that of JE, with headache, fever, myalgias, nausea and vomiting, and anorexia. The neurologic involvement can involve lethargy, irritability, confusion, or meningismus, as well as seizures, spastic paresis, and coma. Individuals who

succumb to progressive MVE infection have a poor prognosis; more than 30% die and 30% to 50% suffer neurologic sequelae, with a bimodal risk for children and older adults.57 Diagnosis As is true for many other viral illnesses, definitive diagnosis of MVE is by identifying IgM antibody via immunoassay of the CSF or a fourfold rise in serum antibody titers. Direct viral isolation or PCR can also prove the infection in tissue, blood, or CSF. However, these tests can be obscured by cross-reactive antibodies to Kunjin, JE, Edge Hill, Alfuy, Sepik, dengue, and other flaviviruses.177 Two-thirds of patients have normal CT scans. If the scans are abnormal, they may show nonspecific signs of encephalitis, including mild hydrocephalus and cerebral edema.103 Treatment and Prevention There is no specific treatment or vaccine for MVE. Prevention depends on adequate mosquito control and avoidance of mosquito bites.

CALIFORNIA (LA CROSSE) ENCEPHALITIS La Crosse (LAC) virus is a California serogroup bunyavirus that can cause encephalitis (usually in children) in the central and eastern United States. La Crosse encephalitis constitutes 8% to 30% of all cases of encephalitis in the United States, and is one of the major causes of arboviral illness.152 In fact, its incidence in endemic areas (20 to 30 cases per 100,000 population per year) exceeds that of bacterial meningitis.124 Epidemiology and Transmission Aedes triseriatus, the eastern tree hole mosquito, is the main vector, although A. albopictus, or Asian tiger mosquito, may be emerging as another significant species. Vertebrate hosts include chipmunks, tree squirrels, and foxes. The annual incidence in the United States is about 80 to 100 cases.27 Most infections are asymptomatic and occur from late summer to early fall in the central and eastern United States.21,27,59 Clinical Presentation The majority of cases are children less than 15 years of age.27,78,122 For 80% to 90% of infected persons, the clinical course is mild, with only headache, fever, and vomiting after an incubation period of 3 to 7 days. Approximately 10% to 20% of infected individuals develop a severe form of the disease within the first 8 to 24 hours of symptom onset.123 In one pediatric study of 127 hospitalized children, it was noted that 70% of patients presented with headache, fever, and vomiting. Of children, 46% had seizures (generally focal seizures, with some progression to status epilepticus), and 20% had focal neurologic findings. Encephalitis does not always occur, because aseptic meningitis was also found. Although all patients survived, over 10% had neurologic deficits at time of hospital discharge, and preliminary analysis suggested patients may suffer long-term cognitive and behavioral deficits as well.122 Only one case report has mentioned California encephalitis causing infarction of the basal ganglia, leaving a child with acute hemiparesis.112 The CDC recently described a case of possible congenital infection after identification of IgM antibodies in umbilical cord serum. The mother declined collection of infant serum to document seroconversion, but fortunately the infant remained asymptomatic and development was normal at 6-month follow-up. The CDC reports the case fatality rate to be less than 1%, although recent studies have found this to be an underestimate.36,77,78 Diagnosis Laboratory findings may reveal leukocytosis with polymorphonuclear leukocyte predominance and pleocytosis in the CSF (either neutrophilic or lymphocytic predominance), although studies of laboratory values for LAC and non-LAC cases show no statistically significant differences.82 More than one-half of patients have abnormal electroencephalographic findings. A CT scan may show nonspecific cerebral edema, if there are any findings at all, and MRI may reveal gadolinium enhancement in cortical areas.122 897

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

well as Central and South America. It occurs mainly in the summertime. Between 1964 and 2008, there were approximately 257 confirmed cases in the United States, with an average of 5 cases per year. Most of the cases have been in Florida, Georgia, Massachusetts, and New Jersey, near coastal areas and freshwater swamps. The real incidence is probably higher because of underreporting and underrecognition. In fact, in 2005, 21 cases were reported to the CDC, compared with an average of 8.2 cases per year from 2000 to 2004. This included an outbreak of 7 cases in New Hampshire, a state which was previously not known to have locally acquired EEE.32,29,41

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Definitive diagnosis is made with IgM antibody by capture immunoassay of CSF, a fourfold rise in serum antibody titers against LAC virus, or isolation of virus from or demonstration of viral antigen or genomic sequences in tissue, blood, or CSF.20 As in almost all other viral infections discussed in this chapter, IgM antibody capture with ELISA is the most common method, with the recommendation to confirm IgG antibody with another serologic assay such as a neutralization test. Treatment and Prevention No specific treatment is available beside general measures to control cerebral edema and seizures. Certain studies have looked at ribavirin,123 but there is no strong evidence to recommend its use. No vaccine is available against this virus.

EPIDEMIC POLYARTHRITIS (ROSS RIVER VIRUS) A mosquito-borne alphavirus in the family Togaviridae, Ross River virus (RRV) is a single-stranded, enveloped RNA virus in the same family as chikungunya, Sindbis, and eastern and western equine encephalitis. The virus is endemic and enzootic in Australia and Papua New Guinea and causes epidemic polyarthritis.84 It is the most common human arboviral disease in Australia, causing approximately 5000 reported cases a year.175 In the late 1970s, RRV spread to the South Pacific islands, but it disappeared after the end of an epidemic in which 500,000 people were infected; recent reports, however, show that there are new cases reappearing in Fiji.104 Epidemiology and Transmission The main vectors are Culex and Aedes (particularly Aedes vigilax) mosquitoes, and marsupials such as kangaroos and wallabies are important as vertebrate-amplifying hosts.151 Vertical transmission is possible from mosquito to offspring, and human-mosquitohuman transmission is also thought to occur. Tropical coastal regions with salt marsh habitats are the primary habitats for the mosquito vector species, and infections are most common in the spring, after summer rains, or after inundation of salt marshes by rain or tides.104 Clinical Presentation After inoculation, the virus is thought to replicate within macrophages. It causes local cell-mediated immune responses that appear to be the cause of arthritis. After an incubation of 3 to 9 days (or as long as 21 days), patients can present either with acute febrile illness with arthritis and rash; with acute fever, rash, or arthritis alone; with polyarthralgia; or with arthritis.63 The joints involved are usually symmetric and include the wrists, knees, ankles, and metacarpophalangeal and interphalangeal joints of the hands, with true arthritis present in 40% of infected individuals.170 About 50% have fever and a sparse maculopapular rash on the limbs and trunk that may occur before or after the arthritis. Whereas fever may resolve within several days, rash may persist for several months. Joint symptoms and fatigue, on the other hand, have been reported to last years, even after fever and rash have subsided.118 However, recent literature suggests that patients with chronic symptoms may have additional underlying comorbidities, such as rheumatic disease or depression.85,136,170 Diagnosis There are no laboratory findings specific for RRV infection. Patients often have normal leukocyte counts (although mild neutrophilia or atypical lymphocytes can be found) and possibly elevation in the nonspecific erythrocyte sedimentation rate. Joint aspiration may reveal viscous fluid with predominantly mononuclear cells and points to viral arthritis.63 Serum can be screened for IgM antibody against Ross River virus IgM, which can then be confirmed by PRNT. These tests are available at only a few reference laboratories, including the CDC.104 Viral culture and PCR are not commonly used for diagnosis of RRV infection. Treatment and Prevention There is no specific treatment. Management of arthralgias and myalgias is with standard analgesic and nonsteroidal 898

antiinflammatory drugs. There does not seem to be any direct association of mortality with RRV. As with other arboviral diseases, prevention depends on adequate mosquito control and avoidance of mosquito bites. One recent prospective case-control study showed that protective measures such as mosquito coils, repellants, and citronella candles decreased this risk for RRV infection twofold with a dose response for the number of protective measures used. In addition, light-colored clothing decreased risk threefold, whereas camping in the 3 weeks before symptom onset increased the risk eightfold.83 There has been additional research on understanding the environmental, anthropogenic, and social factors responsible for disease outbreaks. Some believe factors such as climate variability can affect virus replication, vector demographics, and even human behavior, each of which can be modeled to predict onset and severity of RRV epidemics. Early warning systems could potentially enable improved disease control measures.*

JAMESTOWN CANYON VIRUS Jamestown Canyon virus is a California serogroup bunyavirus widely distributed throughout the United States and Canada. White-tailed deer, Odocoileus virginianus, are the principal vertebrate host and boreal Aedes and Ochlerotatus mosquitoes are the primary vectors.3,4,64 Documented human infections are scant, but the virus usually causes a mild febrile illness, and rarely meningitis and encephalitis. There is a case report of Jamestown Canyon virus–induced encephalitis in an 8-year-old girl in rural southwestern Michigan, who presented with symptoms of headache and fever that quickly progressed to seizures and coma.71 The infection is difficult to distinguish from other California serogroup bunyaviruses, such as California encephalitis, snowshoe hare, Keystone, and trivittatus viruses, because of crossreactivity in the more common serologic tests and difficulty in isolating the actual virus.178 The virus has been posited as a possible emerging infectious disease,71,121 but there have been few identified cases and the literature on this subject is scant.

Mosquito Control GENERAL GUIDELINES FOR INDIVIDUAL PROTECTION For personal protection and prevention, individuals can take precautions such as avoiding mosquitoes at their most active time (from dusk to dawn) and wearing loose-fitting cotton clothing covering their arms and legs (see Chapter 47). Individuals may also apply repellents to exposed areas of skin. The most effective preparations contain N,N-diethyl-3-methylbenzamide (DEET),144 and generally concentrations need not exceed 20% to 35%.62 DEET is safe in children older than 2 months of age and pregnant women.37,106 However, it can rarely cause neurologic toxicity. Thus it should be kept away from mucous membranes and used sparingly to avoid systemic absorption. Studies have shown that a single application of a product containing 24% DEET confers an average of 5 hours (and up to 12) of protection against A. aegypti mosquitoes. Compared with DEET, newer formulations containing the compound IR3535 fared poorly.62 Picaridin (KBR 3023), a shorter-acting plant-derived repellent, is thought to be as effective as DEET and better tolerated.6,98 Agents such as p-menthane-3,8-diol (PMD) and BioUD have not been evaluated as well but are thought to be less effective compared with DEET. Permethrin-containing compounds and other residual insecticides that kill rather than simply repel mosquitoes may be applied to clothing and netting. Other strategies include using mosquito coils and sprays containing pyrethroids in sleeping areas. Citronella has been also shown to be mildly effective in reducing the number of bites, but it requires frequent applications if used topically (as opposed to the candle form).61 Current research in insect repellents involves sophisticated appreciation of the olfactory senses of mosquitoes and creating proteins to inactivate human-specific odorants.98,154 *References 90, 91, 100, 101, 175, 176, 186.

Aedes aegypti

17

In general, global eradication programs for all infectious diseases, including mosquito vector surveillance and control, have declined dramatically in the past few decades. Because of the success of control programs in the 1970s and the resultant decreased public health threat, less attention has been paid and fewer resources have been allocated to maintaining good control. One result is fewer trained personnel, because training programs are less well funded. The effect has been detrimental, with a reversal of previous gains. In Central and South America, for example, dengue fever was largely eliminated with eradication in the 1950s and 1960s of the A. aegypti mosquito, the main vector for the disease. However, because these programs were largely dismantled in the 1970s, the mosquito species has reinfested most of these tropical regions.73 Vector control has three arms: environmental management, biologic control, and chemical control.105 Environmental management consists of monitoring and intervening to reduce the vector population, as well as transmission factors that sustain the human-vector-pathogen contact. For example, simply removing old tires, covering water storage containers with tight lids, keeping floor drains cleaned and covered, and chlorinating ornamental pools and fountains (or populating them with larvivorous fish) can help prevent the breeding of mosquitoes. Biologic control includes using organisms that naturally prey on the vector. For example, larvivorous fish and Bacillus thuringi­ ensis H-14 (BTI) are commonly used against larvae. Biologic control, however, requires expense and time to raise these organisms, and the organisms may have limited success when the environment in which they are placed does not sustain their existence. Furthermore, even if they are effective in reducing the number of larvae, there is not conclusive evidence to show that this decreases transmission of disease, because a lower density of larvae in a certain area may mean healthier and stronger adult mosquitoes if food is limited. Chemical control is the most well-known vector control. It consists of using products such as pyrethrins (e.g., deltamethrin, resmethrin, permethrin) or organophosphate insecticides (e.g., fenthion, malathion, fenitrothion, temephos). These can be applied in several forms: larvicidal application, perifocal treatment, or space spraying. Larvicidal application is focal treatment to domestic water supplies that cannot be eliminated (e.g., for A. aegypti, either 1% temephos or methoprene can be used to regulate larvicidal growth, or BTI can be used to safely treat drinking water). Insecticides such as fenthion, malathion, and fenitrothion can be used as perifocal treatment for nonpotable sources of water to eliminate larvae and adult mosquitoes. Finally, space spraying can be used against adult mosquitoes, often in emergency situations. The chemicals mentioned here can be used as aerosols or mists applied by portable machines, vehicle-mounted generators, or aircraft. Parameters for use (e.g., grams of active ingredient per hectare, wind conditions that may limit effectiveness) depend on the type of chemical, equipment, and target vector. Table 48-3 shows selected insecticides and dosages for cold-spray control of A. aegypti. Precautions must be taken seriously when using these products, such as following instructions on labels, using physical protection such as gloves and masks, and correctly disposing of chemicals.187 Integrated vector control programs that incorporate all three methods, along with public education and campaigns, are the most effective ways to control disease.183 One recent study demonstrated success of a low-technology strategy for vector control involving community education and participation, as well as biologic control of mosquito larvae using Mesocyclops copepods. Although A. aegypti and dengue transmission were eliminated in 32 rural Vietnamese communities, it remains unclear and unlikely that such a strategy would be as effective in more urban or westernized areas.80,99 Nevertheless, such integrated initiatives should also encourage vaccination, not only of humans, but of the animal reservoirs for which vaccines are available. This includes, for example, equine vaccinations against West Nile virus. Recently, leading health organizations have been trying to reinstate vector and disease control, as can be seen by a short

Insecticide Organophosphates Malathion Fenitrothion Naled Pirimiphos-methyl Pyrethroids Deltamethrin Resmethrin Bioresmethrin Permethrin Cypermethrin Lambda-cyhalothrin

Dosage (Grams of Active Ingredient per Hectare) 112-693 250-300 56-280 230-330 0.5-1 2-4 5 5 1-3 1

From World Health Organization: Dengue haemorrhagic fever: Diagnosis, treatment, prevention and control, ed 2, Geneva, 1997, World Health Organization.

history of their efforts. In the 1950s, WHO embarked on a mission to eradicate malaria. Despite some early success, by the mid1970s, it was increasingly difficult to achieve the eradication goal for a number of reasons, including resistance to DDT and other insecticides. However, in 1998, WHO, the United Nations Development Programme, the World Bank, and UNICEF established the Roll Back Malaria initiative with a special focus on Africa. One arm of the campaign is to encourage widespread use of antimalarial drugs in clinics and health centers with a simple diagnosis. The other objectives are to plan and implement sustainable vector control. Experience has shown that pyrethroidimpregnated bed nets may be a better global strategy for eradicating disease, because this approach is less expensive than repeated spraying of household walls, reduces infections (and thus the human reservoir for infection in malaria), and is more effective in terms of horizontal implementation than top-down, or vertical, programming.14 Although source reduction through environmental management has been shown to be effective in some places,180 it is generally very difficult and may not be feasible everywhere.157 Resistance to insecticides is a very real problem. However, it is often a local phenomenon, so certain chemicals and insecticides should not be completely abandoned once reports of resistance are raised. For example, sampling sites only a few kilometers apart in Guatemala showed a large difference in resistance for Anopheles albimanus mosquitoes. Similarly, in the United States, resistance of Culex species to organophosphates is high in areas where vector control is well implemented, but is lower in rural areas.73 WHO has developed bioassays to determine resistance and keeps a database of resistance. This database, however, can be misleading because it is based on a single dataset from a single point in time that may be several years, or even decades, old and no longer relevant.73 There are newer diagnostic methods to test resistance, including genetic linkage and physical maps, that may elucidate factors in vector competence.15 A further step is to detect and contain epidemics through epidemiologic surveillance and then to train personnel and build local capacity to sustain these efforts. Vector surveillance is of primary importance, not only to learn the geographic distribution and density of mosquito vectors and to evaluate control programs but also to predict and intervene to stop the advance of preventable diseases. For mosquitoes, indices have been created to study immature and adult populations (e.g., the “house index” [percentage of houses infected with larvae or pupae], and an index of adult mosquitoes’ landing or biting rates per person-hour). Surveillance also includes verification of control measures, which includes periodically testing the vector’s susceptibility to certain insecticides. Ongoing inspection of areas free of disease and taking measures to prevent reinfestation by vectors (e.g., removing standing water sources and environmental habitats, such as tires and cemetery vases) should be instituted.189 A list of references the WHO currently uses toward the goal of integrated 899

CHAPTER 48  Mosquitoes and Mosquito-Borne Diseases

TABLE 48-3  Insecticides and Cold-Spray Control of

GLOBAL PROGRAMS

vector management can be found at http://www.who.int/malaria/ publications/vector-management/en/index.html. Many countries are committed to the idea of vector and disease surveillance (particularly aided by the work of bodies such as the Pan American Health Organization, the CDC, and WHO), but hundreds still fall short of pursuing these initiatives and are thus ill prepared to effectively control disease. Concerted

international efforts to collect accurate information and relay it in a timely fashion is the next herculean, but worthwhile, task.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 49 

Malaria SHERAL S. PATEL

Malaria is a major international health problem. As global travel increases, malaria is found with increasing frequency in areas in which malaria is not endemic. Human malaria is typically caused by four species of parasitic protozoa—Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae—that are transmitted by mosquitoes. Prevention of malaria infection through counseling, chemoprophylaxis, and personal protective measures can significantly reduce the risk of malaria morbidity in travelers. Because malaria infection can be life threatening, awareness of rapid diagnosis and management of this disease by health care providers are essential.

TABLE 49-1  Risk of Malaria by Region Risk

Region

High

Sub-Saharan Africa, Papua New Guinea, the Solomon Islands, and Vanuatu Indian subcontinent and Haiti Southeast Asia, Central America, and South America

Intermediate Low (but significant)

From the American Academy of Pediatrics: Malaria. In Pickering LK, Baker CJ, Long SS, et al, editors: Red Book: 2006 report of the Committee on Infectious Diseases, ed 27, Elk Grove Village, Ill, 2006, American Academy of Pediatrics, pp 435-441.

Epidemiology Malaria is endemic throughout tropical areas of the world and is usually transmitted to humans through the bite of a female Anopheles mosquito (Figure 49-1, online). Nearly 48% of the world’s population live in malaria-endemic areas.25 According to the World Health Organization (WHO), there were an estimated 243 million cases (5th to 95th percentiles, 190 to 311 million cases) of malaria worldwide in 2008, which resulted in an estimated 863,000 deaths (5th to 95th percentiles, 708 to 1.3 million deaths).64 The majority of the cases occurred in the African region (89%).64 Most malaria-related deaths occur among infants and young children. In Africa, malaria accounts for 20% of all childhood deaths. P. falciparum and P. malariae are found throughout malaria-endemic areas of the world, including Latin America, sub-Saharan Africa, Asia, and the South Pacific. P. vivax is endemic in Latin America, Asia, and the South Pacific, but uncommon in areas of sub-Saharan Africa. Both P. falciparum and P. vivax were historically endemic in temperate areas such as North America and Europe, and transmission still occurs rarely in these areas.38 Specifically, in the United States, anopheline mosquitoes are present (at least seasonally) in all states except Hawaii. Low frequencies of P. ovale infection are prevalent in most malaria-endemic areas, especially in West Africa. The risk of acquiring malaria is highest for travelers to subSaharan Africa and Oceania (i.e., Papua New Guinea, Vanuatu, and the Solomon Islands), intermediate in the Indian subcontinent and Haiti, and lowest (but still significant) in Southeast Asia and the Americas (Table 49-1).7 There can be variability in transmission within endemic areas based on season, altitude, and type of travel. For example, the risk of acquiring malaria is lower for a business traveler to a Southeast Asian city staying in an air-conditioned hotel than for a backpacker hiking and sleeping in tents in East Africa. Rates of malaria among U.S. civilians have been rising as travel to malaria-endemic areas increases.32 In 2009, there were 1484 cases of malaria in the United States reported to the Centers for Disease Control and Prevention (CDC).32 The majority were imported from malariaendemic areas of Africa (73%) and Asia (14%) and caused by 900

P. falciparum (46%).32 In addition, cases of malaria have been acquired in the United States, which indicates that transmission is possible in temperate areas where Anopheles mosquitoes are present.16,32 Parasite resistance to antimalarials has been increasing (Table 49-2).56 In addition, P. falciparum is becoming resistant to other antimalarials, such as mefloquine, pyrimethamine–sulfadoxine, and halofantrine (Figure 49-2).7 Pyrimethamine–sulfadoxine resistance is common throughout Africa. Mefloquine resistance has been demonstrated in Burma (Myanmar), Thailand, Cambodia, Vietnam, and China.7 In Southeast Asia, partial resistance of P. falciparum to quinine or quinidine has also been reported. Areas with reports of chloroquine-resistant P. vivax include Indonesia, Papua New Guinea, the Solomon Islands, Vanuatu, Myanmar, India, Brazil, and Guyana.3 Chloroquine-resistant P. malariae has been described in Sumatra.31 Many genetic changes in human red blood cells occur in areas where malaria is or was historically endemic, which suggests that these polymorphisms have arisen to protect individuals from malaria. Sickle cell disease, thalassemia, glucose6-phosphate dehydrogenase (G6PD) deficiency, and Southeast TABLE 49-2  Antimalarial Drug Resistance in

Malarial Parasites

Plasmodium Species P. falciparum

P. vivax P. ovale P. malariae

Drugs for Which Resistance is Established Chloroquine, mefloquine, pyrimethamine– sulfadoxine, and halofantrine; partial resistance to quinine and quinidine; resistance to multiple drugs Chloroquine, pyrimethamine–sulfadoxine, and primaquine None established None established

For online-only figures, please go to www.expertconsult.com

CHAPTER 49  Malaria

FIGURE 49-2  Geographic distribution of mefloquineresistant malaria. (From the Centers for Disease Control and Prevention: CDC health information for international travel 2012: The yellow book, New York, 2010, Oxford University Press. From Map 3-11, http://wwwnc.cdc.gov/ travel/pdf/yellowbook-2012-map3-11-distribution-mefloquine-resistant-malaria.pdf.)

India China

Vietnam

Burma Laos

Gulf of Tonkin

Thailand

Cambodia

Andaman Sea

Gulf of Thailand

Mefloquine-Resistant Malaria

Indonesia

Asian ovalocytosis (including Gerbich negativity) have all been suggested to confer protection from falciparum malaria mortality.42,55 In sub-Saharan Africa, nearly 100% of the population is negative for the Duffy blood group and has absolute protection against P. vivax, which depends on the Duffy antigen as a receptor for invasion.35

Malaria Parasite ETIOLOGY The malaria parasite is an intra-erythrocytic protozoan that is part of the Plasmodium genus. Plasmodium species infect mammals, birds, and reptiles. The four species that typically infect humans include P. falciparum, P. vivax, P. ovale, and P. malariae. The simian parasite P. knowlesi has been documented as a cause of severe infections and fatalities in Southeast Asia.17

MOSQUITO VECTOR The female Anopheline mosquito is the arthropod vector for the malaria parasite (Figure 49-3). Of almost 430 Anopheles species, only 30 to 40 transmit malaria (Figure 49-4). These include Anopheles gambiae, Anopheles funestus, and Anopheles arabiensis in Africa; the Anopheles punctulatus group in Papua New Guinea; Anopheles culicifacies in India; Anopheles darlingi in

Malaysia

South America; and Anopheles quadrimaculatus in North America.29 The female mosquito’s proboscis pierces the skin of a person to obtain the blood meal necessary for her to produce eggs. Distinguishing features of Anopheles mosquitoes include sensory palps that are as long as the proboscis and discrete blocks of black and white scales on the wings.5 Both male and female Anopheles mosquitoes rest with their abdomens sticking up in the air as opposed to parallel to the surface on which they are resting.6

LIFE CYCLE The life cycle of the malaria parasite involves both vertebrate and arthropod hosts (Figure 49-5). The asexual haploid form of the malaria parasite in the mosquito is the sporozoite. Transmission of 8 to 12 sporozoites usually occurs through the bite of a nocturnal-feeding female Anopheles mosquito (see Figure 49-3). Sporozoites then rapidly migrate through the bloodstream to the liver, where they mature and produce 10,000 to 30,000 merozoites per sporozoite. The merozoites are released into the bloodstream 8 to 25 days later to invade circulating erythrocytes (see Figure 49-5).21 A subset of P. vivax and P. ovale parasites may remain dormant as hypnozoites in the liver and emerge as merozoites months to years after the initial inoculation to establish blood-stage infection. Merozoites enter red blood cells rapidly through specific erythrocyte receptors, many of which are 901

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 49-3  Female Anopheles gambiae mosquito feeding. Distinguishing features include sensory palps that are as long as the proboscis and discrete blocks of black and white scales on the wings. Both male and female Anopheles mosquitoes rest with their abdomens sticking up in the air. (From the Centers for Disease Control and Prevention: Public Health Image Library. http://phil.cdc.gov/phil/home.asp. Left, image no. 1665; right, image no. 1664. Courtesy Dr. Jim Gathany and the Centers for Disease Control and Prevention.)

yet undefined. P. falciparum has several invasion pathways, including glycophorins A and C, whereas P. vivax depends solely on the Duffy antigen for erythrocyte invasion.65 In the red blood cell, the asexual parasites consume hemoglobin and enlarge from the ring forms to become trophozoites and then schizonts. As the schizonts mature through multiple nuclear divisions, the red blood cell bursts and releases 6 to 24 merozoites to invade additional circulating erythrocytes.4 The blood-stage cycle takes place over 48 to 72 hours. Some parasites

develop into gametocytes (the sexual stage), which can infect mosquitoes when taken up during a feeding. After being ingested by an Anopheles mosquito, diploid zygotes are formed. Zygotes mature into ookinetes in the mosquito midgut.47 The resulting oocyst expands through meiotic reduction division within 7 to 10 days and releases sporozoites that localize through the hemolymph to the salivary gland of the mosquito.4 The sporozoites are subsequently transmitted to another human host during the next blood meal.

Messeae Atroparvus Superpictus Sinensis Pulcherrimus Sacharovi Quadrimaculatus Fluviatilis Anthropophagus Sergentii Multicolor Pharoahensis Funestus, arabiensis Minimus Funestus and Stephensi and gambiae s.s. Albimanus arabiensis Culicifacies Sundaicus Melas Nunez-tovari Arabiensis Funestus and Dirus gambiae s.s. Annularis Punctulatus group Aquasalis Maculatus Gambiae s.s. Flavirostris Gambiae s.s. and funestus Darlingi Pseudopunctipennis Barbirostris Farauti

Freeborni

Labranchiae

Arabiensis and funestus

No vector Albimanus Annularis Anthropophagus Aquasalis Arabiensis Arabiensis and funestus Atroparvus

Barbirostris Culicifacies Darlingi Dirus Farauti Flavirostris Fluviatilis Freeborni

Funestus and arabiensis Funestus, arabiensis, and gambiae s.s. Funestus and gambiae s.s. Gambiae s.s. Gambiae s.s. and funestus Labranchiae Maculatus Marajoara

Melas Messeae Minimus Multicolor Nunez-tovari Pharoahensis Pseudopunctipennis Pulcherrimus

Punctulatus group Quadrimaculatus Sacharovi Sergentii Sinensis Stephensi Sundaicus Superpictus

FIGURE 49-4  Global distribution of malaria vectors. (From Kiszewski A, Mellinger A, Spielman A, et al: A global index representing the stability of malaria transmission, Am J Trop Med Hyg 70:486, 2004.)

902

A

MAJOR CLINICAL FINDINGS B

C

E D

F

FIGURE 49-5  Malarial parasite life cycle. During the malarial parasite life cycle, sporozoites are transmitted through the bite of a nocturnalfeeding female Anopheles mosquito (A). Sporozoites then migrate to the liver (B) and mature to merozoites (C). A subset of P. vivax and P. ovale parasites remains dormant as hypnozoites emerging months to years after the initial infection to cause disease. Eight to 25 days after the initial infection, 10,000 to 30,000 merozoites are released to invade erythrocytes (D). Asexual parasites mature in 48 to 72 hours, each releasing 6 to 24 merozoites to invade more erythrocytes (E). Some parasites develop into gametocytes (sexual stages), which are taken up during a mosquito blood meal. Diploid zygotes form ookinetes and develop into haploid sporozoites (F). The sporozoites migrate to the mosquito salivary gland and continue the life cycle in humans with the next blood meal. (Courtesy Sheral S. Patel, with permission.)

RECURRENT AND PERSISTENT INFECTIONS Recurrent malaria infection can occur in several ways. First, relapses from P. vivax or P. ovale can occur when dormant hypnozoites mature and release merozoites, thus producing blood-stage infections. Second, incomplete treatment or a partially effective host immune response can lead to low-concentration parasitemia and may lead to recrudescence of blood-stage infections. Relapse and recrudescence are caused by the same parasite clone that was responsible for the initial infection. Although recrudescence can occur with any malarial species, it is most common with P. falciparum because of antimalarial resistance. Finally, in areas of intense transmission, simultaneous infection or reinfection with multiple parasite species or strains can occur. P. malariae is frequently associated with persistent infections that can remain in the bloodstream at undetectable levels for up to 20 or 30 years.

TRANSMISSION Natural transmission of malaria occurs through the bite of a female Anopheles mosquito. Blood-stage infection can also be established by transfusions of blood or blood products, by organ transplantation, or by sharing contaminated needles or syringes.32,45 Occasionally congenital malaria occurs when mothers of newborns are infected.32,54 It may be difficult to distinguish congenital malaria from natural mosquito-borne transmission when the diagnosis is made in neonates 2 to 3 weeks after birth.

Clinical symptoms of malaria can develop as soon as 7 days to as late as several months after exposure in an area with endemic malaria. The majority of individuals who are diagnosed in the United States experience the onset of signs of symptoms after they return to the United States. A febrile illness in a traveler who has returned from a malaria-endemic area within the previous 3 months should be evaluated urgently. Red blood cell lysis and the release of merozoites at the end of a period of intraerythrocytic asexual reproduction result in the classic presentation of a malarial paroxysm, which is characterized by high fevers, chills, rigors, sweats, and headache (Table 49-3). Without appropriate therapy, paroxysms can recur in a cyclic pattern (i.e., every 48 hours with P. vivax and P. ovale and every 72 hours with P. malariae). Although P. falciparum has a 48-hour asexual erythrocytic cycle, fever and chills typically occur without any periodicity, because erythrocyte lysis is not synchronized. Patients with malaria infection may also present with gen­ eralized weakness, backache, myalgias, vomiting, diarrhea, and pallor. If an appropriate travel history is not obtained, malaria infection can be mistaken for a viral syndrome or acute gas­ troenteritis. In addition, severe malaria can mimic other diseases (e.g., meningitis, typhoid fever, dengue, hepatitis) that are common in malaria-endemic countries. Partially immune individuals who have recently arrived from endemic areas (e.g., immigrants, refugees) may be asymptomatic or have jaundice or signs of hepatosplenomegaly. Laboratory studies may reveal anemia and thrombocytopenia. Perinatal transmission of malaria is usually caused by P. falciparum and P. vivax. Clinical manifestations of congenital malaria can mimic neonatal sepsis and include fever, poor appetite, irritability, and lethargy.

COMPLICATIONS OF P. FALCIPARUM Infection with P. falciparum has a greater risk for complications and death than infection with the other three human malarial species. First, P. falciparum can invade erythrocytes of all ages TABLE 49-3  Clinical Manifestations and

Complications of Human   Plasmodium Infection

Plasmodium Species All species

P. falciparum

Clinical Manifestations and Pathogenesis SUSCEPTIBLE POPULATIONS Patients with malaria present with variable and nonspecific signs and symptoms ranging from asymptomatic parasitemia to severe disease and death. Individuals living in malaria-endemic areas develop partial immunity through repeated infections with malaria parasites and rarely experience serious complications after childhood. Nonimmune individuals—such as travelers and immigrants from nonendemic areas, children from the age of 6

P. vivax and P. ovale P. malariae

Manifestations and Complications Fever, chills, rigors, sweats, and headaches Weakness Myalgias Vomiting Diarrhea Hepatomegaly Splenomegaly Jaundice Anemia Thrombocytopenia Hyperparasitemia Cerebral malaria: seizures, obtundation, and coma Severe anemia Hypoglycemia Acidosis Renal failure Pulmonary edema (noncardiogenic) Vascular collapse Splenic rupture Relapse months to years after primary infection because of latent hepatic stages Low-grade fever and fatigue Chronic asymptomatic parasitemia Immune complex glomerulonephritis

903

CHAPTER 49  Malaria

months to 5 years who are living in endemic areas, and pregnant women—are at risk for severe disease and complications, especially with P. falciparum infection.2

PART 6  ANIMALS, INSECTS, AND ZOONOSES

and thus produce overwhelming parasitemia. Second, red blood cells that are infected with P. falciparum adhere to endothelial cells, leading to microvascular pathology not observed with other malarial species.34 Third, P. falciparum is frequently resistant to antimalarials (see Figures 49-1 and 49-2; Figure 49-1, online). Travelers from nonendemic areas, children, and pregnant women are at greatest risk for developing complications from malaria infection. A person is considered to have complicated malaria when the manifesting signs include altered mental status, seizures, profound anemia, respiratory distress, gross hematuria, shock, or severe laboratory abnormalities, including hypoglycemia, acidosis, signs of disseminated intravascular coagulation, and hyperparasitemia (see Table 49-3). These are summarized as follows: • Cerebral malaria: Acute neurologic events, such as seizures, obtundation, and coma, are associated with cerebral malaria. Cerebrospinal fluid examination is typically unremarkable, thus differentiating cerebral malaria from bacterial meningitis. Pathogenesis is a result of microvascular obstruction by parasitized erythrocytes, but neurologic impairment can result from multiple factors, including hypoglycemia, acidosis, impaired cerebral oxygenation from anemia, and pulmonary edema.37,50 The mortality rate can be as high as 15% to 30% in endemic areas, and higher in nonimmune adults (e.g., travelers). Children surviving episodes of cerebral malaria often have subtle cognitive and motor deficits.28 • Severe anemia: Overwhelming parasitemia (i.e., >106 parasitized red blood cells/µL or >20% parasitized circulating red blood cells) can develop rapidly in nonimmune individuals, resulting in severe anemia (i.e., hemoglobin level of <5 to 7 g/dL). The degree of parasitemia is always proportional to the degree of anemia. Moderate to low-grade parasitemia as well as persistent or recurrent infections in semi-immune individuals can lead to slow development of severe anemia. Factors contributing to development of anemia include red blood cell lysis and release of mature schizonts, suppression of erythropoietin by cytokines, and peripheral destruction of erythrocytes by the spleen.34 • Metabolic complications: Nonimmune individuals are at risk for hypoglycemia and acidosis. Hypoglycemia can result from decreased oral intake, depletion of liver glycogen, parasite consumption of glucose, insulin release from the pancreas by quinine or quinidine, and inhibition of gluconeogenesis.33,44,52 • Renal failure: The pathogenesis of renal failure may be multifactorial. These individuals have sequestration of parasitized erythrocytes in the cortex and findings consistent with acute tubular necrosis in the medulla. Other factors contributing to renal failure include hypotension, microvascular obstruction by P. falciparum–parasitized red blood cells, and free malarial pigment or heme.52 Renal failure is rare among children who are younger than 8 years old. Nonimmune individuals receiving treatment with quinine or quinidine may develop renal failure from massive hemolysis, resulting from overwhelming parasitemia and leading to free hemoglobin in the urine (i.e., blackwater fever).51 • Pulmonary edema: Late during the course of severe malaria, individuals can develop pulmonary edema with normal intrapulmonary and intracardiac pressures consistent with a capillary leak syndrome.33,52 Sequestration of parasitized red blood cells is uncommon, and pulmonary edema is a rare complication among children. • Diarrhea: Children living in malaria-endemic areas often present with watery diarrhea as a result of P. falciparum infection. This is thought to be secondary to sequestration of parasitized erythrocytes in the intestinal microvasculature. The precise mechanism is not known, but cytokines may also contribute to secretory diarrhea via tumor necrosis factor, prostaglandins, and cyclic adenosine monophosphate. • Vascular collapse and shock: Individuals with severe malaria can develop vascular collapse and shock, which are often associated with adrenal insufficiency and hypothermia. 904

TABLE 49-4  Indicators of a Poor Prognosis with

Severe Malaria

Indicator

Factor

Clinical

Age <3 Impaired consciousness Seizures (≥3 in 24 hr) Absent corneal reflexes Papilledema Decerebrate or decorticate rigidity Opisthotonus Respiratory distress Shock Hypoglycemia Acidosis

Biochemical

Hyperlactatemia Renal impairment Elevated aminotransferases Hyperbilirubinemia Hematologic

Hyperparasitemia

Anemia Visible malarial pigment

Comments

Glucose <40 mg/dL Plasma bicarbonate <15 mmol/L Lactate >45 mg/dL Serum creatinine >3 mg/dL; BUN >60 mg/dL >3 times normal Serum total bilirubin >2.5 mg/dL >500,000 parasites/mL or >10,000 mature trophozoites and schizonts/mL Hemoglobin <5 g/dL; packed cell volume <15% >5% neutrophils with malarial pigment

BUN, Blood urea nitrogen.

Asplenic individuals are at increased risk for more severe disease and death. Factors indicating a poor prognosis for persons with severe malaria include clinical, biochemical, and hematologic features (Table 49-4).24,43,58 Poor clinical prognostic indicators include impaired consciousness, repeated convulsions, respiratory distress, bleeding, and shock. Biochemical indicators include renal impairment, acidosis, jaundice, hyperlactatemia, hypoglycemia, and elevated aminotransferases. Finally, hematologic features indicative of a poor prognosis include a hemoglobin level of less than 5 g/dL, parasitemia of more than 500,000 parasites per milliliter, greater than 10,000 mature trophozoites and schizonts per milliliter, or malaria pigment in at least 5% of neutrophils. A video clip of an African child with severe malaria can be accessed at http://video.who.int/streaming/malaria/severemalaria.wmv.63

COMPLICATIONS OF P. VIVAX AND P. OVALE Individuals with P. vivax infection typically present with fevers, chills, headaches, and myalgias, whereas individuals with P. ovale infection do not usually present with a toxic appearance. Anemia can result from acute P. vivax or P. ovale parasitemia. Anemia and splenomegaly are common among persons chronically infected with either P. vivax or P. ovale, and splenic rupture is an important late complication (see Table 49-3).27 Because both P. vivax and P. ovale have a hepatic hypnozoite stage, symptoms may manifest months to years after the initial infection. P. vivax invades reticulocytes, resulting in lower levels of parasitemia than those seen with P. falciparum infection. Cytoadherence does not occur with P. vivax or P. ovale. Thus, all stages of the parasite circulate in the peripheral blood, and microvascular changes associated with sequestration in deep vascular beds are not observed. Individuals lacking expression of the Duffy blood group antigen (e.g., many Africans) are protected from P. vivax infection, because this antigen is used as a receptor for erythrocyte invasion by the P. vivax parasite.36

Because P. malariae produces persistent low-level parasitemia, it usually manifests with mild symptoms such as weakness, lowgrade fever, and fatigue. Individuals can have chronic asymptomatic parasitemia for years. This can be associated with an immune complex glomerulonephritis, where complement-fixing antibodies are directed against P. malariae antigens.18

Diagnosis HISTORY The most important factor for early and prompt diagnosis of malaria, particularly in nonendemic areas, is for the health care provider to consider it in the differential diagnosis of a febrile patient with appropriate travel history. Most imported malaria cases in the United States occur among travelers who have visited friends or relatives in malaria-endemic areas.32 Because of the risk of complications and death, fever in the returned traveler should be taken seriously. A thorough travel history must be obtained, including travel dates, destinations, and any chemoprophylaxis taken.30,57 As a result of drug resistance and the possibility of inadequate adherence to medication schedules, a history of chemoprophylaxis use in a returned traveler does not exclude a diagnosis of malaria. The patient may not have the typical malarial paroxysms of fever and chills. Nonspecific symptoms such as fatigue, diarrhea, headache, myalgias, and sore throat may lead to another diagnosis. Fever and persistent malaise may occur among semi-immune individuals.

BLOOD SMEARS The thin and thick blood smears are the gold standard for the clinical diagnosis of malaria (Figure 49-6).10,46 Blood smears should be interpreted by skilled microscopists trained in malaria diagnosis. Blood Smear Preparation Thin smears are used to identify the parasite species as well as the degree of parasitemia. A drop of blood is placed at one end of a slide and drawn across the slide with the edge of another slide (see Figure 49-6, B).10,46 Individuals with low parasitemia may have false-negative thin blood smears because the number of red blood cells examined in the thin smear is insufficient to detect the parasites. In these cases, thick smears are useful for establishing a diagnosis of malaria, because they allow for concentration of blood to find parasites that may be present in small numbers. Thick smears are made by placing a drop of blood on a smear, spreading it in a circle, and allowing it to dry (see Figure 49-6, B).10,46 The red blood cells are lysed by staining without methanol fixation. Thus, the degree of parasitemia can be ascertained, but the size and morphology of parasitized red blood cells cannot. Giemsa is the preferred stain for malaria smears, because details such as Schüffner dots are often missed with Wright staining. However, Wright staining is generally more available than Giemsa staining in areas that are not malaria endemic, and it usually allows one to determine the presence of parasites. Both thin and thick blood smears should be repeated every 12 to 24 hours if the initial smear is negative and the diagnosis of Plasmodium species infection remains a consideration. Blood Smear Examination Oil immersion (×100) is used to examine thick and thin blood smears (Table 49-5 and Figures 49-7 and 49-8).12,59 Examination of the thin smear should begin at the thin edge of the blood smear, farthest away from where the drop of blood was placed (see Figures 49-7 and 49-8). P. falciparum ring stages have a delicate cytoplasm with one to two small chromatin dots and occasional appliqué forms.11,13 P. falciparum trophozoites and schizonts are rarely seen in peripheral blood, and gametocytes have a crescent or sausage shape. Red blood cells infected with more than one parasite are more common with P. falciparum

than with the other species. P. vivax ring stages have a large cytoplasm with occasional pseudopods and a large chromatin dot.11,13 Occasional Schüffner dots are seen in the red blood cell. P. vivax trophozoites are large with an amoeboid cytoplasm; schizonts contain 12 to 24 merozoites. Gametocytes of P. vivax are round to oval in shape. Ring stages of P. ovale have a large chromatin dot. P. ovale –infected red blood cells occasionally have Schüffner dots and are fimbriated.11,13 P. ovale trophozoites are compact with large chromatin, and the schizonts contain 6 to 14 merozoites with large nuclei. The gametocytes of P. ovale are round to oval in shape. P. malariae rings also have large chromatin.11,13 P. malariae trophozoites have a compact cytoplasm with an occasional band form. Schizonts contain 6 to 12 merozoites with large nuclei, and the gametocytes are round to oval. Parasite Density Parasite density is usually calculated on the thick smear by counting the number of parasites per 200 white blood cells. The actual number of parasites per microliter of blood is then calculated based on an average of 8000 white blood cells per microliter or on the actual white blood cell count if it is available.11,13 False-positive blood smears are common when inexperienced microscopists mistake platelets or stain debris for parasites. Most false-negative blood smears result from low parasitemia (often with the semi-immune state) or altered parasite morphology related to chemoprophylaxis, partial treatment, or drug-resistant parasites. If the initial blood smears are negative for Plasmodium species but malaria is still a leading diagnosis, the smear should be repeated every 12 to 24 hours during a 72-hour period.

OTHER DIAGNOSTIC METHODS Most of the alternative nonmicroscopic methods of malaria diagnosis are more applicable to areas in which malaria is not endemic, because reagent and processing costs are much greater. The sensitivity of many of these tests is equal to or greater than that of the blood smear for the diagnosis of malaria.39 However, most alternative diagnostic methods require microscopy to be performed in parallel for parasite species identification or quantification. These tests include the following: (1) fluorescence microscopy; (2) DNA probes for parasite-specific sequences; and (3) rapid diagnostic tests (RDTs) that incorporate imm­ unologic detection of Plasmodium histidine-rich protein 2 or parasite lactate dehydrogenase.14,62 Commercially available kits are available for the enzyme-linked immunosorbent assay of histidine-rich protein 2 or parasite lactate dehydrogenase, and can be completed in 10 min.40,62 These kits have a sensitivity of 49% to 99% for the detection of Plasmodium infection, and are useful for areas in which experienced microscopists may not be available.39 The U.S. Food and Drug Administration approved BinaxNOW Malaria for use by hospital and commercial laboratories in 2007.40 The test can detect P. falciparum; however, it cannot distinguish among P. vivax, P. ovale, and P. malariae or determine mixed-species infections.40 All malaria RDTs should be followed by malaria microscopy. A positive malaria RDT can inform the health care worker to initiate malaria treatment urgently; however, a negative RDT does not exclude the diagnosis of malaria. Furthermore, the RDT result is qualitative, so microscopy must be used to quantify infection and response to therapy.

Prevention Prevention of malaria infection requires appropriate counseling, chemoprophylaxis, and personal protective measures (Table 49-6).7,26 The most current recommendations for travelers can be obtained from the CDC (http://www.cdc.gov/malaria). The Malaria Map application by the CDC is an interactive map that provides information about malaria endemicity throughout the world, and it is found at http://www.cdc.gov/malaria/map/index. html.8 Similar information can be found through the WHO International Travel and Health Interactive Map at http://apps. who.int/tools/geoserver/www/ith/index.html.61 905

CHAPTER 49  Malaria

COMPLICATIONS OF P. MALARIAE

PART 6  ANIMALS, INSECTS, AND ZOONOSES

COUNSELING The risk of malaria and the importance of malaria chemoprophylaxis and personal protective measures must be emphasized with each traveler.7,20,26 Medication adherence should be emphasized, and the importance of taking chemoprophylactic medication on

the same day each week or at the same time each day should be stressed. Potential side effects of any drugs prescribed for malaria prophylaxis as well as the signs and symptoms of malaria should be discussed. Because treatment is most effective early during the course of disease, a delay in appropriate therapy can have potentially serious or fatal consequences. A plan for where

A FIGURE 49-6  A, Blood collection method for blood smear preparation. (From the Centers for Disease Control and Prevention: Update: Influenza activity: United States, January 11-17, 2004, MMWR Morb Mortal Wkly Rep 53:35, 2004. http://www.dpd.cdc.gov/dpdx/HTML/PDF.Files/Malaria_ procedures_benchaid.pdf.)

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CHAPTER 49  Malaria

B FIGURE 49-6, cont'd B, Preparation of thin and thick blood smears. (From the Centers for Disease Control and Prevention: Update: Influenza activity: United States, January 11-17, 2004, MMWR Morb Mortal Wkly Rep 53:35, 2004. http://www.dpd.cdc.gov/dpdx/HTML/PDF.Files/Malaria_ procedures_benchaid.pdf.)

907

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 49-5  Characteristics of Plasmodium Species on Human Blood Smear Infected Red Blood Cells Plasmodium Species

Size

Shape

Schüffner Dots?

P. falciparum

Normal

Crescent (gametocyte)

No

P. vivax P. ovale

Enlarged Enlarged

P. malariae

Normal

Ameboid Fimbriated, elongated, and oval —

Parasites

Rings

Trophozoites

Schizonts (Mature)

Gametocytes

—

8-24 (rare)

Crescent

Yes Yes

Numerous delicate rings only (occasional gametocytes); multiple infected red blood cells; and numerous appliqué forms Thick Thick

Ameboid Compact

12-24 6-14

Round Round

No

Thick

Compact, band form

6-12, rosettes

Round

to obtain urgent medical care should be in place before traveling to any malaria-endemic area.

CHEMOPROPHYLAXIS Chemoprophylaxis is a strategy used for preventing malaria by administering medications.7,20,26 Primary prophylaxis uses medications before, during, and after travel to prevent disease caused by the initial infection (i.e., by inhibiting the replication of asexual parasites that have emerged from the liver), whereas terminal prophylaxis uses medications toward the end of the exposure period to prevent relapse or delayed onset of disease caused by the Plasmodium liver stages, including hypnozoites of P. vivax and P. ovale.7 Except for pregnant women, routine chemoprophylaxis is not recommended for residents of malaria-endemic areas because of the emergence of parasite resistance and potential suppression of the development of immunity that protects against severe disease after 3 to 5 years of age. Chemoprophylaxis should be prescribed for nonimmune individuals, including children, traveling to malaria-endemic areas.7,19,49 In 2009, only 25% of the U.S. civilians with imported malaria had taken malaria chemoprophylaxis,32 and 10% of these individuals had not taken a CDC-recommended chemoprophylactic regimen for the area visited.32 The health care provider must consider several factors when choosing an appropriate chemoprophylactic regimen for the traveler. These include destinationspecific malaria risk and resistance patterns, age, underlying medical conditions, allergies, tolerability, and length of stay.7 Pediatric dosages are based on weight and should never exceed adult dosages. A summary of available medications and recommendations for malaria chemoprophylaxis can be found in Tables 49-7 and 49-8.9

The most current information about malaria risk, resistance patterns, and recommendations for travelers is available through the CDC and the WHO (see Resources, later).7 Most areas of the world have chloroquine-resistant P. falciparum, with the exception of the Caribbean, Central America west of the former Panama Canal Zone, Egypt, and some countries in the Middle East. In addition, mefloquine-resistant P. falciparum has been documented on the borders of Thailand with Burma and Cambodia, in the western provinces of Cambodia, the eastern states of Burma, on the border between Burma and China, and along the borders of Laos and Burma and southern Vietnam (see Figure 49-2). In general, primary chemoprophylaxis should be started 1 to 2 weeks (chloroquine or mefloquine) or 1 to 2 days (doxycycline or atovaquone–proguanil) before travel to allow the antimalarials to achieve adequate serum concentrations before exposure. If there are concerns about tolerance or adverse effects, chemoprophylaxis can be started earlier to allow for the discovery of potential adverse events. Most adverse events occur during the first three doses of the medication. Chemoprophylaxis should be continued during travel in the malaria-endemic area and for 4 weeks (chloroquine, mefloquine, and doxycycline) or 7 days (atovaquone–proguanil) after leaving the malaria-endemic area. Travelers to Areas with Chloroquine-Sensitive P. falciparum, P. vivax, P. ovale, and P. malariae Chloroquine is the drug of choice for primary prophylaxis for travelers to areas with chloroquine-sensitive malaria. The drug should be started 1 to 2 weeks before travel to a malaria-endemic area, continued once a week on the same day of the week during travel, and for 4 weeks after leaving the malaria-endemic area. Hydroxychloroquine is an alternative that may be better tolerated FIGURE 49-7  Representative malaria blood smears. (Courtesy Royal Perth Hospital, Perth, Western Australia. http://www.rph.wa.gov.au/malaria/teach.html.)

908

2

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10µ

A

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CHAPTER 49  Malaria

0

1

2

7

11

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3

8

10µ

0

Plasmodium falciparum

6

10µ

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Plasmodium vivax

B

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Plasmodium ovale

0

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10µ

Plasmodium malariae

FIGURE 49-8  A, Thin smears, Plasmodium falciparum. B, Thin smears, Plasmodium vivax. C, Thin smears, Plasmodium ovale. D, Thin smears, Plasmodium malariae. (A to D from Coatney GR, Collins WE, Warren M, et al: The primate malarias, Bethesda, Md, 1971, U.S. Department of Health, Education, and Welfare. All images from http://www.dpd.cdc.gov/dpdx/HTML/ImageLibrary/Malaria_il.htm.) Continued

909

PART 6  ANIMALS, INSECTS, AND ZOONOSES

7.

6.

3.

4.

1.

1.

8.

5.

6. 8.

2.

6.

1.

5.

1.

1.

5.

7.

3.

1. 4. 2.

E

Plasmodium falciparum Blood stage parasites, thick blood smears

Plasmodium vivax Blood stage parasites, thick blood smears

1: Small trophozoites 2: Gametocytes — normal 3: Slightly distorted gametocyte 4: “Rounded-up” gametocyte 5: Disintegrated gametocyte 6: Nucleus of leukocyte 7: Blood platelets 8: Cellular remains of young erythrocyte

1: Ameboid trophozoites 2: Schizont — two divisions of chromatin 3: Mature schizont 4: Microgametocyte 5: Blood platelets 6: Nucleus of neutrophil 7: Eosinophil 8: Blood platelet associated with cellular remains of young erythrocytes

F

8.

3. 4.

7. 5.

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1. 5.

7.

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G

Plasmodium ovale Blood stage parasites, thick blood smears

Plasmodium malariae Blood stage parasites, thick blood smears

1: Small trophozoites 2: Growing trophozoites 3: Mature trophozoites 4: Schizonts 5: Gametocytes 6: Nucleus of leukocyte 7: Blood platelets

1: Small trophozoites 2: Growing trophozoites 3: Mature trophozoites 4, 5, 6: Immature schizonts with varying numbers of divisions of the chromatin 7: Mature schizonts 8: Nucleus of leukocyte 9: Blood platelets 10: Cellular remains of young erythrocytes

H

FIGURE 49-8, cont'd  E, Thick smears, Plasmodium falciparum. F, Thick smears, Plasmodium vivax. G, Thick smears, Plasmodium ovale. H, Thick smears, Plasmodium malariae. ( E to H from Wilcox A: Manual for the microscopical diagnosis of malaria in man, Washington, DC, 1960, U.S. Department of Health, Education, and Welfare. All images from http://www.dpd.cdc.gov/dpdx/HTML/ImageLibrary/Malaria_il.htm.)

910

in Travelers

Counseling

Chemoprophylaxis

Personal protective measures

Importance of chemoprophylaxis Potential adverse reactions or side effects from chemoprophylaxis Clinical manifestations of malaria Plan for urgent medical care Assess malaria risk Determine malaria resistance patterns Consider the following:   Age   Underlying medical conditions   Allergies   Tolerability   Length of stay   Advise when to start medication and how long to continue after return Determine whether medication should be prescribed for presumptive self-treatment Minimize outdoor activity at dusk, nighttime Wear long sleeves, long pants, and hats at dusk, nighttime Use insect repellent:   10% to 35% N,N-diethyl-3methylbenzamide for exposed skin   Permethrin for clothes, shoes, mosquito nets, tents, and other gear Insecticide-treated bed nets Mosquito coils and candles

by some people. Side effects of chloroquine and hydroxychloroquine are generally mild and include gastrointestinal disturbance, headache, dizziness, blurred vision, pruritus, and insomnia. If the traveler is unable to take chloroquine or hydroxychloroquine, other medications that are effective against chloroquine-sensitive Plasmodium include atovaquone–proguanil, doxycycline, and mefloquine. Travelers to Areas with Chloroquine-Resistant P. falciparum Three efficacious chemoprophylaxis options for travelers to areas in which there is chloroquine-resistant P. falciparum are atovaquone–proguanil, doxycycline, and mefloquine.7,9,20 In special situations, primaquine can be used as primary prophylaxis as well. Travelers to areas with mefloquine-resistant strains of P. falciparum (i.e., the borders of Thailand with Burma and Cambodia, in the western provinces of Cambodia, and in the eastern states of Burma [see Figure 49-2]) can use either atovaquone–proguanil or doxycycline for malaria prophylaxis.7,9 The following medications (given in alphabetical order) are used for prophylaxis in areas with chloroquine-resistant falciparum malaria: Atovaquone–Proguanil. Atovaquone–proguanil is a fixed combination drug. Primary prophylaxis should begin 1 to 2 days before travel to malaria-endemic areas, and continued once a day at the same time each day during travel and daily for 7 days after leaving the malaria-endemic area. Common adverse effects associated with atovaquone– proguanil prophylaxis include abdominal pain, nausea, vomiting, and headache. Atovaquone–proguanil should not be used in pregnant women, women who are breastfeeding infants weighing less than 5 kg, or individuals with severe renal impairment (i.e., creatinine clearance of <30 mL/min).7,9,19,49 Atovaquone–proguanil should be used with caution in individuals taking warfarin (Coumadin). A pediatric formulation of atovaquone–proguanil is available in the United States. The CDC states that atovaquone– proguanil may be used for children weighing at least 5 kg; however, providers should note that prophylactic dosing for children who weigh less than 11 kg is considered an off-label use in the United States.7 Doxycycline. Doxycycline primary prophylaxis should be started 1 to 2 days before travel to malarious areas,

continued once a day at the same time each day during travel, and continued daily for 4 weeks after the traveler leaves the malaria-endemic area. Doxycycline can cause photosensitivity, which usually manifests as increased sunburn reaction; this can be minimized by avoiding direct sun exposure and using sunscreens. It is also associated with an increased frequency of Candida vaginitis. In addition, doxycycline may decrease the effectiveness of oral contraceptives among women of childbearing age. Gastrointestinal disturbances such as nausea and vomiting can be decreased if the medication is taken on a full stomach. Doxycycline should not be used for children younger than 8 years old or for pregnant women because of the risk of dental staining. For travelers requiring oral typhoid vaccine (Ty21a), doxycycline should be stopped 24 hours before vaccine administration.7 Mefloquine. Mefloquine prophylaxis should be started 2 weeks before traveling to a malaria-endemic area and continued once a week on the same day of the week during travel and for 4 weeks after leaving the malaria-endemic area. Rare serious adverse reactions with prophylactic doses of mefloquine that have been reported include psychoses and seizures.7,9 In addition, neuropsychiatric side effects occasionally reported include sensory and motor neuropathies (e.g., paresthesia, tremor, ataxia), agitation, mood changes, panic attacks, forgetfulness, confusion, hallucinations, aggression, paranoia, and encephalopathy. These reactions are seen more frequently at the higher doses used for treatment. Other side effects include gastrointestinal disturbances, headaches, insomnia, vivid dreams, visual disturbances, depression, anxiety disorders, and dizziness.7,9 Mefloquine is contraindicated in people with seizures, active depression, a recent history of depression, generalized anxiety disorder, and a history of psychosis or other major psychiatric disorders. Mefloquine is not recommended for use by people with cardiac conduction abnormalities.7,9 However, mefloquine may be used by persons taking β-blockers if they have no underlying arrhythmia.7,9 Individuals taking mefloquine should use caution when performing tasks requiring fine motor coordination and spatial discrimination. Mefloquine is not approved for use in children who weigh less than 5 kg or are younger than 6 months old. A copy of the U.S. Food and Drug Administration Medication Guide should be provided to any traveler receiving a prescription for mefloquine (http://www.fda.gov/ downloads/Drugs/DrugSafety/ucm088616.pdf). Primaquine. Primaquine is rarely used—and then only after consultation with malaria experts—for primary prophylaxis for travelers who are unable to take any of the other recommended chemoprophylaxis regimens for areas with or without chloroquine-resistant P. falciparum7,9 (see Resources, later). Primary primaquine prophylaxis should begin 1 to 2 days before travel to the malaria-endemic area and continued once a day at the same time each day during travel and daily for 7 days after the traveler leaves the malaria-endemic area. Before receiving a prescription for primaquine, the traveler must have a G6PD level in the normal range, because primaquine can cause oxidantinduced hemolytic anemia and methemoglobinemia in G6PD-deficient persons. The most common adverse event among individuals with normal G6PD levels is gastrointestinal upset, which can be minimized by taking the medication with food. Travelers to Areas with Predominant P. vivax The U.S. Centers for Disease Control and Prevention recommends primaquine for primary prophylaxis in areas where P. vivax predominates. It should be used in conjunction with personal protective measures for travelers who are not G6PD-deficient. Health care workers should know that the use of primaquine for this indication is considered off-label in the United States. For travelers unable to take primaquine, other medications can be used based on resistance patterns. Please refer to resources listed 911

CHAPTER 49  Malaria

TABLE 49-6  Checklist for Malaria Prevention

912

OR:

Doxycycline

Chloroquine-Resistant Areas Drug of Atovaquone– choice: proguanil

Vibramycin, Vibra-Tabs, Doryx, Periostat, and others; generic

Malarone

Plaquenil

Alternative:

Hydroxychloroquine sulfate

Aralen, generic

Trade Names

Chloroquine-Sensitive Areas Drug of Chloroquine choice: phosphate

Drug

100 mg orally, daily

4 wk

How Long to Continue

1-2 d

When to Start

≥8 yr: 2.2 mg/kg up to adult dose of 100 mg/d

7d

4 wk

4 wk

How Long to Continue After Return

1-2 d

1-2 wk

1-2 wk

When to Start Before Travel

5-8 kg: 12 pediatric tab¶ daily >8-10 kg: 3 4 pediatric tab¶ daily >10-20 kg: 1 pediatric tab¶ daily >20-30 kg: 2 pediatric tabs¶ daily >30-40 kg: 3 pediatric tabs¶ daily ≥40 kg: 1 adult tab‡ daily

5 mg/kg base (6.5 mg/kg salt) orally, once/wk, up to maximum adult dose of 310 mg base

310 mg base (400 mg salt) orally, once/wk

1 adult tab‡ orally, daily

5 mg/kg base (8.3 mg/kg salt) orally, once/wk, up to maximum adult dose of 300 mg base

Pediatric Dose†

300 mg base (500 mg salt) orally, once/wk

Adult Dose

TABLE 49-7  Medications Used for the Prevention of Malaria*

Gastrointestinal upset, vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis

Headache, nausea, vomiting, abdominal pain, diarrhea, increased transaminase levels, and seizures

Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia

Adverse Effects

Take with food or milk. Contraindicated in persons with severe renal impairment (i.e., creatine clearance of <30 mL/ min). Not recommended for children <5 kg, pregnant women, and women breastfeeding infants <5 kg. Partial tab doses should be prepared and dispensed by a pharmacist. For children weighing 5 to <11 kg, off-label use is recommended by the Centers for Disease Control and Prevention. Take with food. Contraindicated in children <8 yr and pregnant women.

Has been used extensively and safely during pregnancy. May exacerbate psoriasis.

Has been used extensively and safely during pregnancy. May exacerbate psoriasis.

Comments

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Primaquine

Alternative:

—

Lariam, Mephaquin, generic

Trade Names ≤9 kg: 4.6 mg/kg base (5 mg/kg salt) orally, once/wk >9-19 kg: 14 tab once/wk >19-30 kg: 12 tab once/wk >30-45 kg: 3 4 tab once/wk ≥45 kg: 1 tab, once/wk

0.5 mg/kg base (0.8 mg/ kg salt) up to adult dose, orally, daily

30 mg base (52.6 mg salt) orally, daily

Pediatric Dose†

228 mg base (250 mg salt) orally, once/wk

Adult Dose

G6PD, Glucose-6-phosphate dehydrogenase. *Caused by Plasmodium falciparum, P. ovale, P. vivax, and P. malariae. † Should never exceed adult dose. ‡ Adult tabs contain 250 mg atovaquone and 100 mg proguanil hydrochloride. ¶ Pediatric tabs contain 62.5 mg atovaquone and 25 mg proguanil hydrochloride.

Mefloquine

OR:

Drug

1-2 d

2 wk

Before Travel

7d

4 wk

After Return

Nausea, abdominal pain, and hemolytic anemia (especially in patients with G6PD deficiency)

Gastrointestinal disturbances, headache, insomnia, vivid dreams, visual disturbances, depression, anxiety disorder, and dizziness

Adverse Effects Contraindicated in persons with active depression or a history of depression, generalized anxiety disorder, psychosis, schizophrenia, other major psychiatric disorders, or seizures. Not recommended for persons with cardiac conduction abnormalities. Use with caution in travelers involved in tasks requiring fine motor coordination and spatial discrimination. In the U.S., 250-mg tab of mefloquine contains 228-mg mefloquine base. Outside the U.S., 275-mg mefloquine tab contains 250-mg mefloquine base. For children weighing <5 kg, off-label use is recommended by the Centers for Disease Control and Prevention. An option for primary prophylaxis in special circumstances and in consultation with malaria experts. Take with food. All persons taking primaquine should have a documented normal G6PD level before beginning the medication. Contraindicated in persons with G6PD deficiency and during pregnancy and breastfeeding, unless the infant being breastfed has a documented normal G6PD level.

Comments

CHAPTER 49  Malaria

913

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 49-8  Reliable Supply Regimens for the Treatment of Malaria* Drug

Adult Dose

Atovaquone-proguanil The adult tab contains 250 mg atovaquone and 100 mg proguanil. The pediatric tab contains 62.5 mg atovaquone and 25 mg proguanil.

4 adult tabs, orally as a single daily dose for 3 consecutive days

Artemether-lumefantrine One tab contains 20 mg artemether and 120 mg lumefantrine.

Pediatric Dose

Daily dose to be taken for 3 consecutive days: 5-8 kg: 2 pediatric tabs 9-10 kg: 3 pediatric tabs 11-20 kg: 1 adult tab 21-30 kg: 2 adult tabs 31-40 kg: 3 adult tabs >41 kg: 4 adult tabs A 3-day treatment schedule with a total of 6 oral doses is recommended for both adult and pediatric patients based on weight. The patient should receive the initial dose, followed by the second dose 8 hr later, then 1 dose twice per day for the following 2 days. 5-<15 kg: 1 tab per dose 15-<25 kg: 2 tabs per dose 25-<35 kg: 3 tabs per dose ≥35 kg: 4 tabs per dose

Comments Contraindicated in people with severe renal impairment (creatinine clearance <30 mL/min) Not recommended for people on atovaquone-proguanil prophylaxis Not recommended for children weighing <5 kg, pregnant women, and women breastfeeding infants weighing <5 kg Not for people on mefloquine prophylaxis Not recommended for children weighing <5 kg, pregnant women, and women breastfeeding infants weighing <5 kg

*If used for presumptive self-treatment, medical care should be sought as soon as possible.

at the end of the chapter for additional prescribing information. These are new guidelines from the 2012 Centers for Disease Control Yellow Book.7

PREVENTION OF RELAPSES WITH P. VIVAX AND P. OVALE Terminal prophylaxis with primaquine decreases the risk of relapse by acting against the liver stages of P. vivax and P. ovale. Individuals, such as missionaries, Peace Corps volunteers, and military personnel, with prolonged exposure to malaria returning to nonendemic areas should generally be given terminal prophylaxis.7 Primaquine is given for 14 days after returning from malariaendemic areas (Table 49-9). If chloroquine, doxycycline, or mefloquine is used for primary prophylaxis, primaquine can be given during the last 2 weeks of postexposure prophylaxis. If atovaquoneproguanil is used for primary prophylaxis, primaquine can be given during the last 7 days of atovaquone-proguanil prophylaxis plus an additional 7 days, or for 14 days after atovaquone-proguanil is completed. Individuals should have a normal G6PD level documented before primaquine is prescribed.

CHEMOPROPHYLAXIS FOR INFANTS, CHILDREN, AND ADOLESCENTS Because infants, children, and adolescents are at increased risk for developing complications from malaria infection, antimalarial drugs should be prescribed for them when traveling to malariaendemic areas.7,9,19,49 Drug dosages should be calculated on the basis of body weight and should never exceed adult dosages (see Table 49-7).7,9,19,49 Depending on P. falciparum suscep­tibility, chloroquine and mefloquine can be used for children of nearly all ages and weights. Doxycycline can be used for children 8 years of age and older. Atovaquone–proguanil is available in pediatric tablets and can be used for infants and children weighing at least 5 kg. Use of atovaquone–proguanil for malaria prophylaxis in children who weigh less than 11 kg constitutes off-label use in the United States.7 Overdoses of antimalarials can be fatal, so medications should be stored in childproof containers and kept out of reach of infants and children. Many antimalarials have a very bitter taste and are available only as tablets. Pharmacists can pulverize tablets and put them in gelatin capsules, which the parents can then break and mix with small amounts of sweetener such as applesauce, chocolate syrup, or jelly. To ensure adequate antimalarial blood levels, the caregiver should make sure the child takes the entire dose at one time. Gastrointestinal upset and vomiting can be minimized by giving the antimalarial dose on a full stomach. 914

CHEMOPROPHYLAXIS DURING PREGNANCY Pregnant women are at increased risk for severe malarial disease and adverse pregnancy outcomes, including prematurity, abortion, and stillbirth. If possible, women who are pregnant, or are likely to become pregnant, should be advised to not travel to malaria-endemic areas, if possible. If travel cannot be avoided, an effective chemoprophylactic regimen in conjunction with personal protective measures should be recommended. Malaria prophylaxis with chloroquine phosphate or hydroxychloroquine sulfate is safe and effective for pregnant women traveling to areas with chloroquine-susceptible P. falciparum and P. vivax.7 For pregnant women traveling to areas with chloroquine-resistant P. falciparum, mefloquine is the drug of choice. Limited data show that mefloquine used at prophylactic dosages during the second and third trimesters is not associated with adverse fetal or pregnancy outcomes.7 There are insufficient data to recommend the use of atovaquone–proguanil for prevention of malaria during pregnancy. Doxycycline is contraindicated in pregnant women, because it may be associated with discoloration and dysplasia of teeth and inhibition of bone growth in the fetus. Primaquine should not be prescribed to pregnant women, because the fetus may have G6PD deficiency and develop hemolytic anemia in utero. Health care providers who require assistance with the management of pregnant travelers should consult malaria experts at the CDC (see Resources, later).

CHEMOPROPHYLAXIS WHILE BREASTFEEDING Both the mother and the breastfeeding infant should receive chemoprophylaxis, because most antimalarial drugs are not secreted in sufficient amounts in breast milk to protect the infant from malaria. The very small amounts of chloroquine and mefloquine excreted in breast milk are not harmful to the infant, but are at insufficient levels to provide protection against malaria. Infants who require malaria chemoprophylaxis should receive the recommended dosages.7 There are limited data about the use of doxycycline in lactating women, but most experts believe the risk of adverse events in the breastfeeding infant to be remote. No data are available regarding the amount of primaquine excreted in breast milk. Therefore, an infant should be tested for G6PD deficiency before primaquine is given to a woman who is breastfeeding. It is not known whether atovaquone is excreted in human milk, but proguanil is excreted in quantities that are insufficient to provide protection to the infant. Because data are not yet available regarding the safety and efficacy of atovaquone– proguanil for infants who weigh less than 5 kg, this drug is not currently recommended for the prevention of malaria among women who are breastfeeding infants of this size.7 Text continued on page 922

Trade Names Adult Dose

Pediatric Dose†

Has been used extensively and safely during pregnancy. May exacerbate psoriasis.

Take with food or milk. Contraindicated for persons with severe renal impairment (i.e., creatine clearance of <30 mL/min). Not recommended for children <5 kg, pregnant women, women breastfeeding infants <5 kg, and persons who received atovaquone–proguanil prophylaxis.

Take with food. Contraindicated during the first trimester of pregnancy. Safety during second and third trimesters of pregnancy is unknown. Contraindicated for persons taking medications that prolong the QT interval or are metabolized by CYP2D6. Should not be used in patients with cardiac arrhythmias, bradycardia, severe cardiac disease, or a prolonged QT interval.

Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia

Headache, nausea, vomiting, abdominal pain, diarrhea, increased transaminase levels, and seizures

Headache, anorexia, dizziness, asthenia, arthralgia, and myalgia

Continued

Has been used extensively and safely during pregnancy. May exacerbate psoriasis.

Comments

Pruritus, nausea, headache, skin eruptions, dizziness, blurred vision, and insomnia

Adverse Effects

BID, Twice a day; G6PD, glucose-6-phosphate dehydrogenase; IV, intravenously; qd, every day; QID, four times a day;TID, three times a day. *Caused by Plasmodium falciparum, P. ovale, P. vivax, and P. malariae in the United States. † Should never exceed the adult dose. ‡ Pediatric tabs contain 62.5 mg atovaquone and 25 mg proguanil hydrochloride. ¶ Adult tabs contain 250 mg atovaquone and 100 mg proguanil hydrochloride.

Oral Treatment: Chloroquine-Sensitive P. falciparum, P. vivax, P. ovale, and P. malariae Aralen, 600 mg base (1000 mg salt) 10 mg base/kg Drug of Chloroquine generic choice: phosphate‡ po immediately, followed (max. 600 mg by 300 mg base (500 mg base) po immediately, salt) po at 6, 24, and 48 hr followed by 5 mg Total dose: 1500 mg base base/kg po at 6, 24, and 48 hr (2500 mg salt) Total dose: 25 mg base/kg OR: Hydroxychloroquine Plaquenil 620 mg base (800 mg salt) po 10 mg base/kg po sulfate immediately, followed by immediately, 310 mg base (400 mg salt) followed by 5 mg po at 6, 24, and 48 hr base/kg po at 6, 24, and 48 hr Total dose: 1550 mg base (2000 mg salt) Total dose: 25 mg base/kg Oral Treatment: Chloroquine-Resistant P. falciparum Drug of Atovaquone– Malarone 4 adult tabs¶ (1 g <5 kg: not choice proguanil atovaquone/400 mg indicated proguanil) qd x 3 d 5-8 kg: 2 pediatric tabs‡/d x 3 d 9-10 kg: 3 pediatric tabs‡/d x 3 d 11-20 kg: 1 adult tab¶/d x 3 d 21-30 kg: 2 adult tabs¶/d x 3 d 31-40 kg: 3 adult tabs¶/d x 3 d >40 kg: 4 adult tabs¶ qd x 3 d OR: Artemether– Coartem, 1 tab (20 mg artemether and 1 tab (20 mg lumefantrine Riamet 120 mg lumefantrine); six artemether doses over 3 d (0, 8, 24, 36, and 120 mg 48, and 60 hr) lumefantrine). Six doses over 3 d (0, 8, 24, 36, 48 and 60 hr) 4 tabs/dose 5-<15 kg: 1 tab/ dose 15-<25 kg: 2 tabs/ dose 25-<35 kg: 3 tabs/ dose ≥35 kg: 4 tabs/dose

Drug

TABLE 49-9  Medications Used for the Treatment of Malaria*

CHAPTER 49  Malaria

915

916

Doxycycline

Tetracycline

Clindamycin

PLUS:

OR PLUS:

OR PLUS:

Alternative: Mefloquine

Quinine sulfate

OR:

Drug

20 mg base/kg/d divided TID x 7 d

250 mg QID x 7 d

100 mg BID x 7 d

542 mg base (650 mg salt) q 8 hr x 3 or 7 d

Lariam, 648 mg base (750 mg salt) Mephaquin, initial dose, followed by generic 456 mg base (500 mg salt) 6-12 hr later Total dose: 1250 mg salt

Cleocin and others

Achromycin, Sumycin, Panmycin, and others

Vibramycin, Vibra-Tabs, Doryx, Periostat, and others; generic

—

Trade Names Adult Dose

TABLE 49-9  Medications Used for the Treatment of Malaria—cont'd Adverse Effects

8.3 mg base/kg Cinchonism, hypoglycemia, sinus (10 mg salt/kg) arrhythmias, po TID x 3 or 7 d atrioventricular block, prolonged QT interval, ventricular tachycardia, and ventricular fibrillation Gastrointestinal upset, >8 yr: 2.2 mg/kg vaginal candidiasis, q 12 hr x 7 d photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Gastrointestinal upset, >8 yr: 6.25 mg/kg vaginal candidiasis, QID x 7 d photosensitivity, (25 mg/kg/d) allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis 20 mg base/kg/d Diarrhea, nausea, divided TID x 7 d vomiting, abdominal pain, rash, pruritus, jaundice, and urticaria 13.7 mg base/kg Gastrointestinal disturbances, (15 mg salt/kg) headaches, insomnia, initial dose, vivid dreams, visual followed by disturbances, 9.1 mg base/kg depression, anxiety (10 mg salt/kg) disorders, and 6-12 hr later dizziness. Total dose: 25 mg salt/kg

Pediatric Dose†

Take with food. Contraindicated in individuals with a history of antibiotic-associated colitis or ulcerative colitis. Use with caution in individuals with hepatic or renal impairment. Contraindicated in persons with active depression or a history of depression, generalized anxiety disorder, psychosis, schizophrenia, other major psychiatric disorders, or seizures. Contraindicated for treatment during pregnancy. Not recommended for persons with cardiac conduction abnormalities. Use with caution in travelers involved in tasks that require fine motor coordination and spatial discrimination. In the U.S., 250-mg tab of mefloquine contains 228-mg mefloquine base. Outside the U.S., 275-mg mefloquine tab contains 250-mg mefloquine base. Do not give with quinine, quinidine, or halofantrine. Mefloquine resistance has been reported in areas of Thailand and Southern Vietnam as well as border areas of Thailand-Burma (Myanmar), Thailand-Cambodia, Burma-China, and Burma-Laos.

Take with food. Contraindicated in children <8 yr and pregnant women.

Take with food. Contraindicated in children <8 yr and pregnant women.

In Southeast Asia, continue treatment for 7 d because of increased relative resistance to quinine. Continue treatment for 3 d for infections acquired in Africa or South America. Contraindicated in patients with a history of blackwater fever, thrombocytopenic purpura, cardiac conduction defects and arrhythmias, myasthenia gravis or optic neuritis.

Comments

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Artesunate

Atovaquone– proguanil

Doxycycline

Clindamycin

Mefloquine

OR:

PLUS:

OR PLUS:

OR PLUS:

OR PLUS:

Drug

20 mg base/kg/d divided TID x 7 d

100 mg BID x 7 d

4 adult tabs¶ (1 g atovaquone/400 mg proguanil) qd x 3 d

4 mg/kg/d x 3 d

Lariam, 648 mg base (750 mg salt) Mephaquin; initial dose, followed by generic 456 mg base (500 mg salt) 6-12 hr later Total dose: 1250 mg salt

Cleocin and others

Vibramycin, Vibra-Tabs, Doryx, Periostat, and others; generic

Malarone

—

Trade Names Adult Dose

Adverse Effects

Comments

4 mg/kg/d x 3 d

Continued

Available in the U.S. through an investigational new drug Gastrointestinal upset, protocol from the Centers for Disease Control and bradycardia, rash, and Prevention (see Resources). For use in patients with fever severe disease who do not have timely access or who cannot tolerate or fail to respond to IV quinidine. Information regarding use in pregnant women is limited. Use with caution in individuals with renal or hepatic impairment. Take with food or milk. Contraindicated in persons with Headache, nausea, <5 kg: not severe renal impairment (i.e., creatine clearance of vomiting, abdominal indicated <30 mL/min). Not recommended for children <5 kg, pain, diarrhea, 5-8 kg: 2 pediatric ‡ increased pregnant women, women who are breastfeeding infants tabs /d x 3 d transaminase levels, <5 kg, and persons who received atovaquone–proguanil 9-10 kg: 3 pediatric and seizures prophylaxis. tabs‡/d x 3 d 11-20 kg: 1 adult tab¶/d x 3 d 21-30 kg: 2 adult tabs¶/d x 3 d 31-40 kg: 3 adult tabs¶/d x 3 d >40 kg: 4 adult tabs¶ qd x 3 d Gastrointestinal upset, Take with food. Contraindicated in children <8 yr and >8 yr: 2.2 mg/kg vaginal candidiasis, pregnant women. q 12 hr x 7 d photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Take with food. Contraindicated in individuals with a history 20 mg base/kg/d Diarrhea, nausea, of antibiotic-associated colitis or ulcerative colitis. Use divided TID x 7 d vomiting, abdominal with caution in individuals with hepatic or renal pain, rash, pruritus, impairment. jaundice, and urticaria Contraindicated in persons with active depression or a 13.7 mg base/kg Gastrointestinal history of depression, generalized anxiety disorder, disturbances, (15 mg salt/kg) psychosis, schizophrenia, other major psychiatric headaches, insomnia, initial dose disorders, or seizures. Contraindicated for treatment vivid dreams, visual followed by during pregnancy. Not recommended for persons with disturbances, 9.1 mg base/kg cardiac conduction abnormalities. Use with caution in depression, anxiety (10 mg salt/kg) travelers involved in tasks requiring fine motor disorders, and 6-12 hr later coordination and spatial discrimination. In the U.S., dizziness Total dose: 250-mg tab of mefloquine contains 228-mg mefloquine 25 mg salt/kg base. Outside of the U.S., 275-mg mefloquine tab contains 250-mg mefloquine base. Do not give with quinine, quinidine, or halofantrine. Mefloquine resistance has been reported in areas of Thailand and Southern Vietnam as well as border areas of Thailand-Burma (Myanmar), Thailand-Cambodia, Burma-China, and Burma-Laos.

Pediatric Dose†

CHAPTER 49  Malaria

917

918

Tetracycline

Atovaquone– proguanil

Mefloquine

OR PLUS:

OR:

OR:

>8 yr: 6.25 mg/kg QID x 7 d (25 mg/kg/d)

>8 yr: 2.2 mg/kg q 12 hr x 7 d

25 mg/kg/d in 3 doses x 3-7 d

Pediatric Dose†

13.7 mg base/kg (15 mg salt/kg) initial dose, followed by 9.1 mg base/kg (10 mg salt/kg) 6-12 hr later Total dose: 25 mg salt/kg

Treatment as per chloroquine- Treatment as per resistant P. falciparum chloroquineresistant P. falciparum

Lariam, 648 mg base (750 mg salt) Mephaquin; initial dose, followed by generic 456 mg base (500 mg salt) 6-12 hr later Total dose: 1250 mg salt

Malarone

Achromycin, Sumycin, Panmycin, and others 250 mg QID x 7 d

100 mg BID x 7 d

Doxycycline

PLUS:

Vibramycin, Vibra-Tabs, Doryx, Periostat, and others; generic

650 mg q 8 hr x 3-7 d

Trade Names Adult Dose

Oral Treatment: Chloroquine-Resistant P. vivax Drug of Quinine sulfate — choice:

Drug

TABLE 49-9  Medications Used for the Treatment of Malaria—cont'd

Cinchonism, hypoglycemia, sinus arrhythmias, atrioventricular block, prolonged QT interval, ventricular tachycardia, and ventricular fibrillation Gastrointestinal upset, vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Gastrointestinal upset, vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Headache, nausea, vomiting, abdominal pain, diarrhea, increased transaminase levels, and seizures Gastrointestinal disturbances, headaches, insomnia, vivid dreams, visual disturbances, depression, anxiety disorders, and dizziness

Adverse Effects

Take with food or milk. Contraindicated in persons with severe renal impairment (i.e., creatine clearance of <30 mL/min). Not recommended for children <5 kg, pregnant women, women who are breastfeeding infants <5 kg, and persons who received atovaquone–proguanil prophylaxis. Contraindicated in persons with active depression or a history of depression, generalized anxiety disorder, psychosis, schizophrenia, other major psychiatric disorders, or seizures. Contraindicated for treatment during pregnancy. Not recommended for persons with cardiac conduction abnormalities. Use with caution in travelers involved in tasks requiring fine motor coordination and spatial discrimination. In the U.S., 250-mg tab of mefloquine contains 228-mg mefloquine base. Outside the U.S., 275-mg mefloquine tab contains 250-mg mefloquine base. Do not give with quinine, quinidine, or halofantrine. Mefloquine resistance has been reported in areas of Thailand and Southern Vietnam as well as border areas of Thailand-Burma (Myanmar), Thailand-Cambodia, Burma-China, and Burma-Laos.

Take with food. Contraindicated in children <8 yr and pregnant women.

Take with food. Contraindicated in children <8 yr and pregnant women.

In Southeast Asia, continue treatment for 7 d because of increased relative resistance to quinine. Continue treatment for 3 d for infections acquired in Africa or South America. Contraindicated in people with a history of blackwater fever, thrombocytopenic purpura, cardiac conduction defects and arrhythmias, myasthenia gravis, and optic neuritis.

Comments

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Primaquine phosphate

—

OR:

Quinine — dihydrochloride (IV)

Adverse Effects

Nausea, abdominal 0.5 mg/kg base pain, and hemolytic (0.8 mg/kg salt) anemia, especially in up to adult dose, patients with G6PD orally, daily for deficiency 14 d after departure from the malarious area

Pediatric Dose†

6.25 mg base (10 mg salt)/kg Same as adult dose Cinchonism, tachycardia, loading dose IV (maximum prolonged QRS and of 600 mg salt) in normal QTc intervals, saline slowly over 1-2 hr, flattened T-wave, followed by continuous ventricular infusion of 0.0125 mg base arrhythmias, (0.02 mg salt)/kg/min until hypotension, and oral therapy can be started hypoglycemia or parasitemia is <1% Alternative regimen: 15 mg base/kg (24 mg salt/kg) loading dose IV infused over 4 hr, followed by 7.5 mg base/kg (12 mg salt/kg) infused over 4 hr every 8 hr, starting 8 hr after the loading dose (see package insert). Same as adult dose Cinchonism, 20 mg/kg loading dose IV in tachycardia, 5% dextrose over 4 hr, prolonged QRS and followed by 10 mg/kg QTc intervals, over 2-4 hr q 8 hr (max flattened T-wave, 1800 mg/d) until oral ventricular therapy can be started or arrhythmias, parasitemia is <1% hypotension, and hypoglycemia

30 mg base (52.6 mg salt) orally, daily for 14 d after departure from the malarious area

Trade Names Adult Dose

Parenteral Treatment: All Plasmodium Drug of Quinidine gluconate — choice: (IV)

PLUS:

Drug

Continued

In Southeast Asia, continue treatment for 7 d because of increased relative resistance to quinine. Continue treatment for 3 d for infections acquired in Africa or South America. Not available in the United States. Continuous electrocardiography, blood pressure, and glucose monitoring are recommended, especially for pregnant women and children. The loading dose should be decreased or omitted for patients who have received quinine or mefloquine. If >48 hr of parenteral therapy are required, the quinine or quinidine dose should be decreased by 13 to 12 . Contraindicated in people with a history of blackwater fever, thrombocytopenic purpura, cardiac conduction defects and arrhythmias, myasthenia gravis, and optic neuritis.

In Southeast Asia, continue treatment for 7 d because of increased relative resistance to quinine. Continue treatment for 3 d for infections acquired in Africa or South America. Continuous electrocardiography, blood pressure, and glucose monitoring are recommended, especially for pregnant women and children. The loading dose should be decreased or omitted for patients who have received quinine or mefloquine. For problems with quinidine availability, call the manufacturer (Eli Lilly, 800-821-0538) or the Malaria Hotline at the Centers for Disease Control and Prevention (770-488-7788). If >48 hr of parenteral therapy is required, the quinine or quinidine dose should be decreased by 13 to 12 . Contraindicated in people with a history of blackwater fever, thrombocytopenic purpura, cardiac conduction defects and arrhythmias, myasthenia gravis, and optic neuritis.

Use with any of the above drug regimens to prevent relapse of P. vivax. Take with food. All persons taking primaquine should have a documented normal G6PD level before beginning the medication. Contraindicated in persons with G6PD deficiency and during pregnancy and breast-feeding unless the infant being breastfed has a documented normal G6PD level. Primaquine-tolerant P. vivax strains are found throughout the world. Relapses of primaquine-resistant strains should be retreated with a 30-d course of 30-mg base/d.

Comments

CHAPTER 49  Malaria

919

920

Doxycycline

Tetracycline

Clindamycin

Artesunate

Atovaquone– proguanil

PLUS:

OR PLUS:

OR PLUS:

OR:

Followed by

Drug

Malarone

—

Cleocin and others

Achromycin, Sumycin, Panmycin, and others

Vibramycin, Vibra-Tabs, Doryx, Periostat and others; generic Gastrointestinal upset, vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis

>8 yr: 2.2 mg/kg q 12 hr x 7 d

Take with food. Contraindicated in children <8 yr and pregnant women.

Comments

Treatment as per chloroquine- Treatment as per resistant P. falciparum chloroquineresistant P. falciparum

Available in the U.S. through an investigational new drug Gastrointestinal upset, protocol from the Centers for Disease Control and bradycardia, rash, and Prevention (see Resources). For use in patients with fever severe disease who do not have timely access or who cannot tolerate or fail to respond to IV quinidine. Information regarding use in pregnant women is limited. Use with caution for individuals with renal or hepatic impairment. Take with food or milk. Contraindicated in persons with Headache, nausea, severe renal impairment (i.e., creatine clearance of vomiting, abdominal <30 mL/min). Not recommended for children <5 kg, pain, diarrhea, increased pregnant women, women who are breastfeeding infants transaminase levels, <5 kg, and persons who received atovaquone–proguanil and seizures prophylaxis.

Take with food. Contraindicated in children who are Gastrointestinal upset, <8 yr and pregnant women. vaginal candidiasis, photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Take with food. Contraindicated in individuals with a history 20 mg base/kg/d Diarrhea, nausea, of antibiotic-associated colitis or ulcerative colitis. Use divided TID x 7 d vomiting, abdominal with caution in individuals with heptic or renal pain, rash, pruritus, impairment. jaundice, and urticaria

>8 yr: 6.25 mg/kg QID x 7 d (25 mg/kg/d)

Adverse Effects

Pediatric Dose†

20 mg base/kg/d divided TID x 7 d If unable to take po medication, give 100 mg IV q 12 hr and then switch to oral doxycycline (see earlier) as soon as patient can take oral medication. 4 mg/kg/d x 3 d 4 mg/kg/d x 3 d

100 mg BID x 7 d If unable to take po medication, give 10 mg base/kg loading dose IV followed by 5 mg base/kg IV every 8 hr. Switch to oral clindamycin (see earlier) when patient can take oral medication. 250 mg QID x 7 d

Trade Names Adult Dose

TABLE 49-9  Medications Used for the Treatment of Malaria—cont'd

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Clindamycin

Mefloquine

OR:

OR:

20 mg base/kg/d divided TID x 7 d

100 mg BID x 7 d

Lariam, 648 mg base (750 mg salt) Mephaquin; initial dose, followed by generic 456 mg base (500 mg salt) 6-12 hr later Total dose: 1250 mg salt

Cleocin and others

Vibramycin, Vibra-Tabs, Doryx, Periostat and others; generic

Trade Names Adult Dose

G6PD, Glucose-6-phosphate dehydrogenase; IV, intravenously. *Caused by Plasmodium falciparum, P. ovale, P. vivax, and P. malariae in the United States. † Should never exceed the adult dose. ‡ Pediatric tabs contain 62.5 mg atovaquone and 25 mg proguanil hydrochloride. ¶ Adult tabs contain 250 mg atovaquone and 100 mg proguanil hydrochloride.

Prevention of Relapses: P. vivax and P. ovale Only Drug of Primaquine — 30 mg base (52.6 mg salt) choice: phosphate orally, daily for 14 d after departure from the malarious area

Doxycycline

OR:

Drug

Adverse Effects

Nausea, abdominal 0.5 mg/kg base pain, and hemolytic (0.8 mg/kg salt) anemia, especially in up to adult dose, patients with G6PD orally, daily for deficiency 14 d after departure from the malarious area

>8 yr: 2.2 mg/kg q 12 hr x 7 d

Comments

Take with food. All persons taking primaquine should have a documented normal G6PD level before beginning the medication. Contraindicated in persons with G6PD deficiency and during pregnancy and breastfeeding unless the infant being breastfed has a documented normal G6PD level. Primaquine-tolerant P. vivax strains are found throughout the world. Relapses of primaquineresistant strains should be retreated with a 30-d course of 30 mg base/d.

Gastrointestinal upset, Take with food. Contraindicated in children <8 yr and vaginal candidiasis, pregnant women. photosensitivity, allergic reactions, blood dyscrasias, azotemia in renal diseases, and hepatitis Take with food. Contraindicated in individuals with a history 20 mg base/kg/d Diarrhea, nausea, of antibiotic-associated colitis or ulcerative colitis. Use divided TID x 7 d vomiting, abdominal with caution in individuals with hepatic or renal pain, rash, pruritus, impairment. jaundice, and urticaria Contraindicated in persons with active depression or a 13.7 mg base/kg Gastrointestinal history of depression, generalized anxiety disorder, disturbances, (15 mg salt/kg) psychosis, schizophrenia, other major psychiatric headaches, insomnia, initial dose, disorders, or seizures. Contraindicated for treatment vivid dreams, visual followed by during pregnancy. Not recommended for persons with disturbances, 9.1 mg base/kg cardiac conduction abnormalities. Use with caution in depression, anxiety (10 mg salt/kg) travelers involved in tasks requiring fine motor disorders, and 6-12 hr later coordination and spatial discrimination. In the U.S., dizziness Total dose: 25 mg 250-mg tab of mefloquine contains 228-mg mefloquine salt/kg base. Outside the U.S., 275-mg mefloquine tab contains 250-mg mefloquine base. Do not give with quinine, quinidine, or halofantrine. Mefloquine resistance has been reported in areas of Thailand and Southern Vietnam as well as border areas of Thailand-Burma (Myanmar), Thailand-Cambodia, Burma-China, and Burma-Laos.

Pediatric Dose†

CHAPTER 49  Malaria

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

Atovaquone–proguanil can be used for the treatment of malaria in a breastfeeding woman when potential benefit to the mother’s life outweighs the potential risk to the infant.7

CHANGING MEDICATIONS DURING CHEMOPROPHYLAXIS BECAUSE OF SIDE EFFECTS Travelers should consult with a health care professional if they must change medications during chemoprophylaxis as a result of side effects. There may be special considerations, because medications recommended for prophylaxis against malaria have different modes of action that affect the parasite at different stages of its life cycle. For example, if a traveler starts with chloroquine, mefloquine, or doxycycline and then changes to atovaquone– proguanil, the standard duration of atovaquone–proguanil therapy would be insufficient. Atovaquone–proguanil would have to be continued for 4 weeks after the switch or 1 week after returning from the malaria endemic area, whichever is longer.7 Health care providers who require assistance in the management of travelers requiring a chemoprophylactic regimen switch are encouraged to consult malaria experts at the CDC (see Resources, later).

MEDICATIONS ACQUIRED OVERSEAS Antimalarials are widely available outside the United States. Travelers should be cautioned against purchasing medications overseas, because not all countries have manufacturing controls and approval procedures similar to those in the United States.7,53 Medications available overseas may not have undergone rigorous testing and review to verify their identity, potency, purity, and stability. Furthermore, medications purchased overseas may be ineffective, dangerous, counterfeit, or contaminated. Additional information regarding counterfeit and substandard antimalarial drugs can be found at http://www.cdc.gov/malaria/travelers/ counterfeit_drugs.html and http://www.usp.org/worldwide/.

PERSONAL PROTECTIVE MEASURES Preventing bites from infected Anopheles mosquitoes (see Chapter 41) is an important adjunct to chemoprophylaxis for malaria prevention in travelers (see Table 49-6). Anopheles mosquitoes are nocturnal feeders, so outdoor activity should be minimized from dusk to dawn, when they are most active. If outdoor exposure is unavoidable during these times, individuals should wear dark-colored long-sleeved shirts, pants, and hats. Mosquito repellent such as N,N-diethyl-3-methylbenzamide (DEET) should be applied to exposed skin.7,26 DEET is safe and effective, when used appropriately, both for children and infants who are older than 2 months. DEET formulations of 20% to 50% provide protection for at least 4 hours; lower percentages provide a shorter duration of action.26 Permethrin or deltamethrin is a long-acting insecticide that can be applied to clothes, shoes, mosquito nets, tents, and other gear. When applied properly, permethrin-treated clothes repel mosquitoes for up to 25 launderings. In addition, an insecticide-treated (i.e., permethrin) bed net tucked underneath a mattress provides protection during peak mosquito feeding times, particularly when accommodations are not adequately air conditioned or enclosed by screens. Finally, travelers can use mosquito coils or candles to help repel mosquitoes when outdoors. Picaridin is a synthetic repellent that has been shown to be comparable with DEET in clinical trials; however, the 7% formulation available in the United States is a lower concentration than was used in most studies.26

Treatment Malaria treatment consists of rapid and appropriate antimalarial therapy as well as supportive care. Whereas uncomplicated malaria can be treated with antimalarials and antipyretics, severe falciparum malaria is a medical emergency and requires immediate assessment and treatment. In general, drugs used for the treatment of malaria should be different from those the patient was using for malaria chemoprophylaxis. Individuals living in 922

areas with perennial malaria transmission develop immunity against severe malarial disease. These semi-immune individuals are often asymptomatic and have a lower risk of serious complications and death. Malaria in nonimmune and at-risk populations (e.g., infants, children, pregnant women) should be considered a medical emergency, because falciparum malaria can progress rapidly and be lethal. When initiating medical therapy, the health care provider should consider the infecting Plasmodium species, resistance patterns, parasite density, and the patient’s clinical status.1,7,9,23,48 If the diagnosis of malaria is suspected but cannot be confirmed, antimalarial treatment that is effective against P. falciparum should be initiated. Health care workers requiring assistance with the diagnosis and treatment of malaria should consult physicians specializing in tropical medicine or infectious diseases or the CDC (see Resources, later). An algorithm that addresses treatment of malaria in the United States is available from the CDC (Figure 49-9).9

RELIABLE SUPPLY REGIMENS FOR PRESUMPTIVE SELF-TREATMENT Travelers with signs or symptoms of malaria should be counseled to seek urgent medical evaluation, which includes obtaining thick and thin blood smears. A reliable supply regimen for antimalarial medications for self-treatment may be prescribed for individuals who plan on living in remote areas, where prompt access to medical care will be difficult (see Table 49-8). Presumptive selftreatment should be taken immediately if the traveler develops an influenza-like illness with fever and chills and professional medical care is not available within 24 hours. It is imperative that the traveler seek medical care promptly after taking medication for presumptive malaria. Atovaquone–proguanil can be used for presumptive malaria self-treatment in the traveler if it is not being used for malaria chemoprophylaxis.7 Alternatively, artemetherlumefantrine can be used if the traveler was not taking mefloquine prophylaxis. Medical providers should consult with malaria experts or call the Malaria Hotline at the CDC (770-488-7788) for recommendations on reliable supply regimens for travelers who are unable to take atovaquone–proguanil or artemetherlumefantrine (see Resources, later). The CDC recommends presumptive treatment for P. falciparum malaria for refugees living in malaria-endemic areas of sub-Saharan Africa before immigration to the United States.15 The most recent guidelines for presumptive predeparture treatment of asymptomatic malaria and directed treatment for special populations with asymptomatic malaria are available on the CDC website.15 Medications recommended for use in this population include artemether–lumefantrine, artesunate–amodiaquine, and oral quinine.

TREATMENT OF MALARIA CAUSED BY CHLOROQUINE-SENSITIVE P. FALCIPARUM, P. VIVAX, P. OVALE, AND P. MALARIAE Chloroquine and hydroxychloroquine are the drugs of choice for infections with chloroquine-susceptible malarial parasites.1,9 These drugs have excellent oral absorption and can be administered via nasogastric tube in patients with impaired consciousness. Parenteral quinidine or quinine is recommended (see Table 49-9) for patients unable to take oral chloroquine. Drug administration, blood pressure, cardiac rhythms, and blood glucose levels should be monitored closely during intravenous administration of quinidine or quinine.9 Individuals infected by P. malariae or P. knowlesi can be treated with chloroquine or hydroxychloroquine.9 For patients with P. vivax or P. ovale infection, treatment should be followed by a course of primaquine.

TREATMENT OF CHLOROQUINE-RESISTANT P. FALCIPARUM Medications that can be used for the treatment of chloroquineresistant P. falciparum infection include atovaquone– proguanil as well as quinine or quinidine in conjunction with doxycycline, tetracycline, or clindamycin (see Table 49-9).1,9,23,48

CHAPTER 49  Malaria

History of travel to malaria-endemic area or clinical suspicion of malaria

Perform thick and thin blood films and read within a few hours

Blood film positive? No

Yes

Repeat blood films every 12-24 hr for a total of 3 sets

Blood film positive?

Calculate parasitemia

Yes

No Evaluate clinical status and disease severity

Consider alternate diagnoses

Uncomplicated malaria

Severe malaria and/or patient unable to take oral medication

Determine species

Plasmodium falciparum or species not yet identified

Non-falciparum species

P. malariae

Chloroquine or hydroxychloroquine

P. ovale or P. vivax acquired outside Papua New Guinea or Indonesia

P. vivax acquired in Papua New Guinea or Indonesia

Chloroquine or hydroxychloroquine

Atovaquone– proguanil or quinine plus tetracycline or doxycycline or mefloquine

P. knowlesi

Acquired in chloroquinesensitive area

Acquired in chloroquineresistant area

Atovaquone– proguanil or artemetherlumefantrine or quinine plus tetracycline or doxycycline or clindamycin

Plus

Atovaquone– proguanil or artemetherlumefantrine or quinine plus tetracycline or doxycycline or clindamycin or mefloquine

Primaquine if not G6PD deficient

Admit to hospital to monitor for progression of disease severity

Repeat blood films if symptoms recur

Chloroquine or hydroxychloroquine

Acquired in mefloquineresistant area

Intravenous quinidine plus tetracycline, or doxycycline, or clindamycin If quinidine is unavailable, contact CDC malaria hotline for artesunate. Admit to intensive care unit for continuous cardiac monitoring. Prevent and treat complications. Consider exchange transfusion if parasitemia is ≥10% or if patient has an altered mental status, ARDS, or renal failure. Switch to oral medicines to complete the treatment regimen after appropriate clinical response.

FIGURE 49-9  Algorithm for treatment of malaria in the United States. (From the Centers for Disease Control and Prevention: Guidelines for the treatment of malaria in the United States, 2009. http://www.cdc.gov/malaria/pdf/treatmenttable.pdf.)

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

Artemether–lumefantrine or mefloquine can also be used for treatment of chloroquine-resistant P. falciparum.1,9 Health care workers should not treat malaria with the same medication used for malaria prophylaxis. In addition, mefloquine should not be used to treat malaria infection acquired in areas of reported mefloquine resistance.7 Artesunate is used widely overseas for the treatment of malaria, and is available in the United States under an investigational new drug protocol by contacting the CDC (see Resources, later).41 In the United States, parenteral quinidine is preferred over quinine for the following reasons: (1) it is more active than quinine; (2) blood levels can be followed; and (3) parenteral quinine is no longer available in the United States. Quinidine should be used in conjunction with doxycycline, tetracycline, or clindamycin. If malaria treatment is being given outside the United States, artemisinin derivatives should be considered, because they clear parasitemia and end coma more rapidly than quinine or quinidine, particularly when the level of parasitemia is very high. To prevent recrudescence with artemisinin derivatives, additional drugs are often given; these include atovaquone– proguanil, doxycycline, clindamycin, and mefloquine. For infections acquired in Africa or South America, quinidine or quinine treatment should be continued for 3 days, whereas the treatment of infection acquired in Southeast Asia should be continued for 7 days because of increased relative resistance. Mefloquine should not be used to treat malaria infections acquired in Southeast Asia as a result of drug resistance.9

TREATMENT OF CHLOROQUINE-RESISTANT P. VIVAX Chloroquine-resistant P. vivax can be treated with mefloquine or atovaquone/proguanil. Quinine or quinidine in conjunction with doxycycline is a recommended therapy (see Table 49-9).1,9 Mefloquine should only be used for treatment if the individual did not use mefloquine for malaria chemoprophylaxis. Treatment of P. vivax should be followed by a course of primaquine.

ERADICATION OF P. VIVAX AND P. OVALE HYPNOZOITES To prevent relapse, primaquine can be used to eradicate the hypnozoites in individuals with P. vivax or P. ovale infection. A normal G6PD level should be documented because of the risk of hemolytic anemia and methemoglobinemia. Primaquinetolerant P. vivax has been documented in malaria-endemic areas throughout the world1,9 (see Table 49-9).

SUPPORTIVE CARE FOR SEVERE MALARIA Severe malaria is considered a medical emergency. Rapid clinical assessment, confirmation of diagnosis, and initiation of parenteral therapy are the fundamentals of good clinical outcomes.1,9,23,60 Nonimmune individuals diagnosed with malaria should be hospitalized until a response to treatment has been seen and complications from severe disease are unlikely (i.e., 24 hours after a negative blood smear and when afebrile). Individuals with partial immunity (e.g., those residing in malaria-holoendemic areas) and uncomplicated P. falciparum infection, as well as some nonimmune individuals with P. vivax, P. ovale, or P. malariae infection, may be treated as outpatients if reliable follow-up treatment is anticipated. Patients with severe complicated malaria require aggressive supportive care.1,9,23,48,60 In addition to rapid clinical assessment and initiation of antimalarial chemotherapy, dehydration, hypoglycemia, and acidosis should be corrected. Admission to the intensive care unit is often required to manage complications such as seizures, severe anemia, hypoglycemia, acidosis, renal failure, pulmonary edema, hypoxemia, and hypovolemia.* A patient receiving quinine derivatives should be placed on a cardiac monitor in the intensive care unit and undergo frequent blood pressure measurements. Quinine or quinidine derivatives are typically given with a continuous infusion of 5% to 10% *References 1, 9, 23, 33, 48, 60.

924

dextrose. Blood glucose measurements should be monitored every 4 to 6 hours. Some drug dosages should be adjusted for patients who are experiencing renal failure. For example, individuals receiving quinine derivatives should have the standard loading dose, but maintenance doses should be decreased 30% to 50% to prevent accumulation of the drug as a result of decreased renal excretion if more than 48 hours of parenteral treatment are required.* Total plasma concentrations of 8 to 15 mg/mL for quinine and 3 to 8 mg/mL for quinidine are effective for the treatment of severe malaria without causing toxicity.* Dose reductions for renal failure are not necessary with chloroquine or artemisinin derivatives. Anticonvulsants (e.g., benzodiazepines) should be used for treatment of seizures. Antibiotics that treat bacterial meningitis should be initiated until a lumbar puncture can be performed to exclude the diagnosis. Exchange transfusion may be beneficial, because there is rapid reduction of parasitemia and toxic byproducts. However, guidelines for when to use exchange transfusions for treatment of malaria remain controversial. Exchange transfusion may be beneficial for severely ill patients with parasitemia of more than 10% or with signs of a poor prognosis, such as cerebral malaria, nonvolume overload pulmonary edema, or renal failure (see Table 49-4).23,33,60 Various adjunctive therapies that have no proved benefit or are harmful include dexamethasone for cerebral malaria, heparin for thrombocytopenia, iron chelators to reduce parasite clearance time, pentoxifylline for tumor necrosis factor synthesis inhibition, and dichloroacetate for metabolic acidosis.33,60 Therapeutic efficacy can be monitored by checking multiple sequential blood smears (i.e., at least every 6 to 12 hours for 2 days). If high levels of parasitemia persist or clinical improvement is not evident, there may be primary drug resistance, and therapy should be changed immediately. Management of severe malaria should preferably be carried out in consultation with a tropical medicine or infectious diseases physician or with the assistance of the CDC (see Resources, later).

Research and Vaccine Development The human host responds to malaria infection by several mechanisms. After repeated exposure to different parasite strains over years, individuals develop protection from high-level parasitemia and severe disease but not from Plasmodia infection. The malarial parasite has developed multiple mechanisms by which to evade human immune responses. Progress toward an effective vaccine against malaria, especially P. falciparum, is hindered by the diversity of human populations infected with malaria as well as by the diversity of parasite strains that infect humans. Three strategies for vaccine development are being developed simultaneously. The first strategy is to prevent infection caused by sporozoites by using a pre-erythrocytic vaccine, thus preventing development of merozoites in the liver as well as the asexual parasitemia responsible for clinical disease.22 This vaccine would be ideal for travelers, because any form of clinical disease would be prevented. The second strategy of vaccine development is the asexual blood stage erythrocytic vaccine, which would limit parasite erythrocyte invasion and multiplication.22 This vaccine would contribute to reduction in burden of disease in malariaendemic countries. The third vaccine strategy consists of preventing spread of the parasite by using a transmission-blocking vaccine that inhibits sexual development of the parasite.22 An effective vaccine may require a combination of these strategies. Because most deaths from malaria occur in children with severe malaria disease, a vaccine may be effective if it can prevent severe disease rather than asymptomatic asexual parasitemia. Although there are many vaccines in clinical trials, there is no vaccine currently licensed for the prevention of malaria infection or disease.22

Resources Several resources are available to help health care providers with prevention, diagnosis, and treatment of malaria. Comprehensive websites include the CDC (http://www.cdc.gov/malaria and *References 1, 9, 23, 33, 48, 60.

http://www.cdc.gov/travel), the WHO (http://www.who.int/ topics/malaria/en), and the Malaria Foundation (http://www. malaria.org).26 Updated detailed information about malaria prophylaxis can be obtained through the CDC’s Traveler’s Health information website, http://www.cdc.gov/travel. Information about the diagnosis of malaria is available through the CDC’s Laboratory Identification of Parasites of Public Health Concern diagnostic website, http://www.dpd.cdc.gov/dpdx. Health care professionals requiring assistance with diagnosis and treatment of suspected or confirmed cases of malaria should refer to the CDC website http://www.cdc.gov/malaria/ diagnosis_treatment/treatment.htm or call the CDC’s Malaria Hotline (770-488-7788, or toll free 855-856-4713, from 9:00 AM to 5:00 PM Eastern Standard Time, Monday through Friday) or the Emergency Operations Center during evenings, weekends, and holidays (770-488-7100, ask to page the malaria clinician on-call). Additional websites that may be useful to health care workers who are treating patients with confirmed or suspected malaria include the following: • CDC • Treatment: Guidelines for Clinicians including reporting, evaluation, diagnosis, and approach to treatment of severe and uncomplicated malaria can be found at http:// www.cdc.gov/malaria/resources/pdf/clinicalguidance. pdf. The treatment guidelines table, with medications listed in tabular form, can be found at http://www.cdc. gov/malaria/resources/pdf/treatmenttable.pdf.9 • Laboratory Identification of Parasites of Public Health Concern: http://www.dpd.cdc.gov/dpdx/Default.htm. This site provides free Internet-based laboratory

diagnostic assistance to laboratorians and pathologists who are investigating suspected parasitic diseases. • Malaria Map Application: http://www.cdc.gov/malaria/ map/index.html.8 This interactive map provides information about malaria endemicity throughout the world. The map displays assessments of the presence of malaria in most countries at the national and provincial level. • WHO • International Travel and Health (Green Book, online edition): http://www.who.int/ith/en/. This site provides information for health risks, including malaria, to travelers. • Guidelines for the Treatment of Malaria, second edition: http://whqlibdoc.who.int/publications/2010/97892415 47925_eng.pdf 60 Global, evidence-based guidelines are provided for the diagnosis and treatment of malaria. • International Travel and Health Interactive Map: http:// apps.who.int/tools/geoserver/www/ith/index.html. This interactive tool provides information regarding malaria risk to travelers. • Training Materials: http://www.who.int/malaria/publica tions/training/en/index.html. This link provides a list of several free electronic resources for training including microscopy, entomolgy, and prevention and control programs.

REFERENCES For additional websites and video clips, as well as the references for this chapter, please go to www.expertconsult.com.

CHAPTER 50 

Arthropod Envenomation and Parasitism TIMOTHY B. ERICKSON AND ARMANDO MÁRQUEZ, JR.

The phylum Arthropoda contains about four-fifths of the known animals of the world, and insects are the largest group of arthropods. Insects are an important part of the biota of all terrestrial and freshwater environments that support life. More species of insects exist than of any other form of multicellular life, and they may well exceed all other land animals in biomass. Insects can use most animal and plant substances as food, and their feeding plays a vital role in recycling organic compounds. They compete with other organisms for the world’s food supplies but are themselves a major food source for many forms of life. They are essential for the pollination of many plants. Insect life cycles are diverse and often complex, involving developmental and sexual stages that are widely different in morphology and ways of life. Although sexual reproduction is the rule, parthenogenesis (unisexual reproduction) and pedogenesis (sexual development in the larval stage) occur. Some groups, such as ants, bees, and termites, have developed a high degree of social organization. During at least part of its life cycle, an insect’s body is divided into three distinct regions (head, thorax, and abdomen), with three pairs of legs attached to the thorax. Except for a few primitive or parasitic groups, most adult insects have wings. The greatest direct medical importance of insects is associated with their feeding on human blood and tissue fluids. In doing so, they often inject salivary secretions. This is a highly effective method of transmitting pathogenic microorganisms; moreover,

the secretions are often allergenic and sometimes toxic. Other insects may carry human pathogens passively on their feet or mouthparts or in their digestive tracts. Venoms have evolved in several insect groups, and venomous insects may attack humans, sometimes with lethal results. Skin, hair, and secretions of insects may be irritant or allergenic, producing cutaneous and respiratory syndromes. Finally, insects can be highly annoying.

Hymenoptera (Bees, Wasps, and Ants) By far the most important venomous insects are members of the order Hymenoptera, including bees, wasps, and ants (Figure 50-1). They vary in size from minute to large (up to 60 mm [2.4 inches] in body length). The abdomen and thorax are connected by a slender pedicle that may be quite long in certain wasps and ants. Bees and most wasps are winged as adults; ants are wingless, except for sexually mature adults during part of the life cycle. Mouthparts are adapted for chewing but in some species are modified for sucking. The life cycle includes egg, larval, and pupal stages before emergence of adults. Immature stages may be protected and provided with food by the adult. Both animal and plant foods are used. Many species are parasitic on other

For online-only figures, please go to www.expertconsult.com

925

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

B

C

D

E

F

FIGURE 50-1  Representative venomous Hymenoptera. A, Hornet (Vespula maculata). B, Wasp (Chlorion ichneumerea). C, Yellowjacket (Vespula maculiforma). D, Honeybee (Apis mellifera). E, Fire ant (Solenopsis invicta). F, Bumblebee (Bombus species).

arthropods. All ants and many species of bees and wasps are social insects. Colonies range in size from a few dozen individuals to many thousands. In cold climates, most individuals die in autumn, leaving the fertilized females to winter over and found new colonies in the spring. Bees The honeybee (Apis mellifera) is one of the few domesticated insects and is maintained in hives in many countries (Figures 50-2 and 50-3). Numerous geographic races of the honeybee exist; the Italian bee (Apis mellifera ligustica), a common domestic strain of Europe, is also widely distributed in the United States. Feral honeybee colonies usually nest in hollow trees or crevices in rocks but may nest in the walls of occupied buildings. An event of considerable health and economic significance in the Americas was the introduction of an African race of the honeybee (Apis mellifera scutellata, also referred to as Apis mellifera adansoni). This race was introduced from Africa into Brazil because it was thought to be a more efficient honey producer in the tropics. It is characterized by large populations (one queen may lay tens of thousands of eggs), frequent swarming (6 to 12 swarms a year), nonstop flights of at least 20 km (12.4 miles), and a tendency toward mass attacks on humans after minimal provocation. As a result, these Africanized honeybees, also known as killer bees, are much more aggressive than are the typical Western Hymenoptera. They attack in swarms of

FIGURE 50-2  Worker honeybee, Apis mellifera.

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hundreds and chase their victims much greater distances from the hive than does any other species.155,187 The first escapes from hives occurred in the state of São Paulo in 1957, and the “Brazilian killer bees,” or “Africanized bees,” have spread widely. These bees are actually hybrids between A. scutellata and European honeybee races.373 Cold climate seems to have stopped their southern spread in Argentina, but they have moved steadily northward at 322 to 482 km (200 to 300 miles) per year and in October 1990 reached the southern border of the United States.374 By mid-1991, 103 swarms had been captured in southern Texas. Populations are established in Arizona, New Mexico, and California.322 The expanded distribution of Africanized honeybees from South America to the southwest United Sates in less than 50 years is considered one of the most spectacular biologic invasions yet documented.284,319 The resulting feral honeybee population of south Texas is now viewed as a hydrid swarm. Future populations may eventually be distributed as far east as North Carolina.371 Several human deaths have occurred from multiple stings. Unless the bees acquire greater resistance to winter conditions, their range will be confined to the southern one-third of the United States

FIGURE 50-3  Stinger of a honeybee.

FIGURE 50-6  Early yellowjacket nest.

and may also be restricted by scarcity of suitable flowers in the arid Southwest. Periods of the year characterized by high temperatures and low rainfall are conducive to the greatest activity of Africanized bees and a larger number of swarms, thus giving rise to increased contact with human populations.86 The greatest impact of Africanized bees in the United States will probably be economic, related to decreased honey production and less effective pollination of crops. The bees also present a threat to human health. Africanized bee colonies are extremely sensitive to disturbance, respond faster in greater numbers, and are up to 10 times more active in stinging than are European bees. The quantity of venom per sting is slightly less in African bees; however, there is no significant biochemical or allergenic difference between the venoms.237,252,324 Africanized honeybees can overwhelm and kill even healthy nonallergic victims.32 About 50 simultaneous stings can cause systemic envenomation, and an estimated 500 are necessary to cause death by direct toxicity.179 As few as 30 to 50 stings have proved fatal in small children.39 About 350 fatal attacks have been documented worldwide, of which at least 70 occurred in Venezuela during 1977 and 1978. More than 300 bee attacks occurred in Mexico between 1987 and 1992, with 49 fatalities.249 A more recent account puts the fatalities at 190, with future estimates of 60 deaths per year.322 Because Mexico and the southern United States have many feral and domestic honeybee populations, researchers thought that the aggressiveness of the African bees could be dampened by hybridization. Large numbers of male European bees were released to facilitate this, and African queens were replaced by European stock when possible. However, recent studies indicate that European bee populations are becoming rapidly Africanized with little reciprocal gene flow, as African females take over European hives.156,207,336,375 Bumblebees (Bombus and related genera) are a largely holarctic group often found in quite cold environments. Increasing reactions to stings in Alaska may be related to the recent changing trends in climate.85 Small colonies usually nest just under the surface of the ground, often in mammal burrows. Some species are aggressive if disturbed, although most have mild dispositions.208

Wasps Social wasps occur throughout most of the world but are recognized as a medical problem, chiefly in the United States and Europe. They often establish colonies close to human dwellings. Yellowjackets (Vespula species) may be more important than honeybees as a cause of human stings in the northern United States286 (Figure 50-5). They make underground nests (Figure 50-6) in rotted-out tree stumps, cavities under stones, and mammal burrows. They are strongly attracted to garbage. Paper wasps (Polistes species) (Figure 50-7) suspend their nests in shaded places, often in shrubbery near houses or below eaves, gutters, or window frames. Old World hornets (Vespa species) and white-faced hornets (Dolchiovespula maculata) create large paper nests that may be plastered to buildings, but more typically hang from tree branches (Figures 50-8 and 50-9). Solitary wasps are predators, feeding largely on other insects and spiders. Adults often carry the prey alive and paralyzed to the nest as food for the larvae. Some wasps excavate burrows, whereas others make mud nests that may be plastered on shaded walls of buildings or under bridges. Although many nests may be grouped together, the adult wasps have no social organization and make little effort to defend them. The cicada killers (Sphecius speciosus) (Figure 50-10) and tarantula hawks (Pepsis species) (Figure 50-11) are among the largest North American wasps. Velvet ants (family Mutillidae) are female wingless wasps that are nest parasites of other Hymenoptera (Figure 50-12). They are found in deserts and other dry and open habitats and can inflict a painful sting.

FIGURE 50-5  Yellowjacket, Vespula maculiforma.

FIGURE 50-7  Paper wasp, Polistes species.

Sweat bees (family Halictidae) are small bees of cosmopolitan distribution (Figure 50-4). They are attracted to sweaty skin and ingest perspiration. They nest in burrows, often in clay banks. Females sting if squeezed or trapped under clothing. The sting is not very painful, but anaphylactic reactions have been reported. The allergens are immunologically unrelated to those in other bee and wasp venoms.277

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FIGURE 50-4  Sweat bee, family Halictidae. (From http://www.encarta. msn.com.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 50-8  White-faced hornet, Dolchiovespula maculata, largest of the common social wasps in the United States. FIGURE 50-10  Cicada killer wasp, Sphecius speciosus. (From http:// www.ento.okstate.edu.)

Two species, Vespula orientalis and Vespula vulgaris, have recently been introduced into Australia, where they have become significant problems.63 Paper wasps of the genus Polistes are plentiful in tropical America and Australia (Figure 50-13). Another Australian paper wasp, Ropalidia revolutionalis, constructs nests that resemble belts of bullets and hangs them from shrubs and fences. Fire wasps (Polybia) are found from Mexico to northern South America. The common species are black with yellow markings. They construct globular, cylindric, or cone-shaped paper nests up to 70 cm (28 inches) long that are hung usually from trees and sometimes under bridges. They may defend these nests with great vigor.

FIGURE 50-9  Typical nest of the white-faced hornet.

Internationally, hymenopteran insects are worldwide in distribution and often constitute a major part of a region’s insect fauna. Honeybees are exploited for their honey throughout the world; even the aggressive A. m. scutellata is used for honey production in Africa. Honeybees in southern Asia attach huge nests to limbs of forest trees. The giant bee Apis dorsata of Southeast Asia has a reputation for savagery, and deaths from multiple stings have occurred. Yellowjackets and hornets are common in Europe and the Middle East, where their medical importance is similar to that in the United States. The genera Vespula, Vespa, and Dolichovespula are found all over Europe.82 The genus Polistes, present throughout central Europe, is not found in the United Kingdom and represents a larger clinical problem in areas surrounding the Mediterranean Sea. Amino acid sequencing of the venom allergens of the different species of Polistes in Europe shows them to be very similar, but the similarities to American strains are less pronounced.118

Ants Ants are social insects, worldwide in distribution over a wide range of habitats. Many ants sting, and others have repugnant secretions. The ant species of greatest medical significance in the United States is the imported fire ant Solenopsis invicta (see Figure 50-1, E).183 It was apparently introduced from South America into Mobile, Alabama, in 1939 and has subsequently spread throughout the southern states from southeastern Virginia to central Texas and Oklahoma, largely eliminating another introduced fire ant (Solenopsis richteri) and two native species. Mound nests are usually found in open grass settings, often in urban areas (Figure 50-14). Other states that harbor fire ants include Arizona, California, New Mexico, Oregon, and Washington, as well as Puerto Rico. As many as 600 mounds per acre have been reported. Worker colonies may reach a maximum size of 500,000 ants in 2 years and rapidly give rise to satellite colonies.341 S. invicta are extremely irritable insects. They are usually easy to identify, as they do not fly away but instead grasp their victims with their mandibles and inflict multiple painful stings.193 Species other than imported fire ants can cause severe reactions.192 Harvester ants (Pogonomyrmex species) of the southwestern United States and Mexico are of medical importance.

FIGURE 50-11  Tarantula hawk, Pepsis species. (Courtesy Mary Beth Stowe, McAllen, Tex.)

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CHAPTER 50  Arthropod Envenomation and Parasitism

FIGURE 50-12  Velvet ant, family Mutillidae.

A

B FIGURE 50-13  Wasp colony (Courtesy Wikimedia Commons.)

Entrances to the underground nests are usually surrounded by clear zones and sometimes by rings of soil. Some species react aggressively to disturbance of the nest. The stings are painful and may be accompanied by systemic symptoms; anaphylaxis has been reported. There are numerous stinging species of ants in the tropics. Although native to South America, fire ants do not seem to be a major medical problem there, perhaps because of native competitors, predators, and parasites. Two fire ant species are important in areas outside the United States. Solenopsis geminata has been introduced into Okinawa and Guam and is widespread in Central America, Mexico, and some Caribbean islands. Solenopsis xyloni is common in Mexico and also occurs in California and Texas. Anaphylaxis caused by imported fire ants has also been described in Australia.338 Severe human urticaria produced by the ant Odontomachus bauri has been reported in Venezuela.307 Amino acid sequences of all fire ant venoms are very similar.168 Therefore, all fire ant stings can be managed medically in the same manner.

FIGURE 50-14  Fire ant mound.

FIGURE 50-15  A, Red bull ant. B, Australian jumper jack ant. (Courtesy Wikimedia Commons.)

The samsum ant, Pachycondyla sennaarensis, is an ecologic counterpart of the fire ant that is widely distributed in the African tropics and the Arabian Peninsula. It nests in the ground but does not make a conspicuous mound. In the United Arab Emirates, it is plentiful in urban areas and may cause multiple stings.6,96 Australian bull ants (Myrmecia species), such as the “jumper jack,” are large insects (about 20 mm [0.8 inches] or the size of a medium cockroach) with prominent jaws (Figure 50-15, A and B).298 They are ground dwelling and common in suburban areas in southeastern Australia. Many neotropical stinging ants live in trees. The giant black ants (16 to 22 mm [0.7 to 0.9 inches]) of the genus Paraponera are found from Nicaragua to the Amazon basin. Although they nest in the ground, workers forage in trees from almost ground level to high in the forest canopy. They are most active at night. The green tree ant of northeastern Australia makes a leaf nest in trees. It has no true sting but ejects formic acid into wounds made by its jaws.

HYMENOPTERA STINGING PATTERNS Multiple stings often result from disturbance of a nest, as the first insects encountered release alarm pheromones that incite aggressive behavior in other members of the colony. With large species such as the white-faced hornet, 40 to 50 stings may create a lifethreatening injury.369 The lethal dose of honeybee venom has been estimated at 500 to 1500 stings.330 However, most of the 40 to 50 deaths per year in North America from Hymenoptera stings are the result of anaphylaxis occurring in victims with prior stings who developed specific immunoglobulin E (IgE) antibodies.132 In the United States and other Western nations, the incidence of serious insect stings is higher in adults than in children, and higher in males than in females. Most persons are stung while engaged in outdoor work or recreation. Beekeeping is a high-risk occupation; however, many beekeepers develop considerable immunity as a result of frequent stings.250 Other relatively highrisk occupations include farmers, house painters, carpenters, highway workers, bulldozer operators, and emergency personnel

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during flooding disaster relief.94 Wasps and bees are sometimes swept into the interior of a moving automobile, exposing the occupants to risk of both a sting and a highway accident. Many foods, particularly meats, ripe fruit, or fruit syrups, attract yellowjackets, which often swarm around picnic areas and recycling bins. Syrups, flowers, sweat, and some perfumes attract bees. In such aggregations, the insects are not particularly aggressive but may become trapped in clothing or hair. A recent source documented that Africanized bees were more aggressive after exposure to 20% ethanol than to standard sucrose solutions placed in front of their hives.2 In temperate zones, the incidence of hymenopteran stings is highest in late summer and early fall, when insect populations are highest. Fire ants may invade houses during periods of heavy rain and in hot, dry weather as they seek food and water.91 There have been increasing incidents of fire ant attacks on patients in health care facilities, such as nursing homes, where frail elderly patients are incapable of fleeing for protection.88,141,302,349 In one report, one patient experienced a severe anaphylactic reaction and four patients died within 1 week. The presence of fire ants around immobilized, often cognitively impaired patients seems to be a primary risk for massive fire ant attacks.90 Fatal anaphylaxis to indoor native fire ant stings has been described in infants.243

VENOM AND VENOM APPARATUS Venom is present in many hymenopteran species and is used for both defense and subjugation of prey. The venom apparatus is located at the posterior end of the abdomen and consists of venom glands, a reservoir, and structures for piercing the integument and injecting venom. Venoms of most medically important Hymenoptera are mixtures of protein or polypeptide toxins, enzymes, and pharmacologically active, low-molecular-weight compounds such as histamine, serotonin, acetylcholine, and dopamine. Melittin, a strongly basic peptide, is the principal component of honeybee venom, making up 50% of the dry venom weight. It damages cell membranes through detergentlike action, with liberation of potassium and biogenic amines.70 Peptides with similar activity occur in bumblebee venom. Histamine release by bee venom appears to be largely mediated by mast cell degranulating (MCD) peptide. A third peptide, apamin, is a neurotoxin that acts principally on the spinal cord. Adolapin, a recently described bee venom peptide, has antiinflammatory activity, which may explain the effectiveness of bee venom in treating some forms of arthritis. The chief enzymes of bee venom are phospholipase A and hyaluronidase. The former is believed to be one of the major venom allergens and, with melittin, to account for much of the acute lethality. Histamine makes up about 3% of the dry weight of bee venom. The intravenous (IV) median lethal dose (LD50) of honeybee venom for mice is 6 mg/ kg. An average sting injects about 0.50 mL of venom containing approximately 0.05 mg of solids. Intense pain after stings by hornets and other social wasps is largely caused by serotonin and acetylcholine, which constitute 1% to 5% of dry venom weight. Wasp kinins (peptides) contribute to pain production and have strong, brief hypotensive effects. Mastoparans are similar in action to MCD peptide but are weaker. Phospholipase A, phospholipase B, and hyaluronidase are present in relatively large amounts. Unidentified proteins, some of which appear to be major allergens, are also present. A lethal protein in Vespa basalis venom releases serotonin from tissue cells and has hemolytic and phospholipase A activity.166 The IV LD50 of different hornet venoms for mice ranges from 1.6 to 4.1 mg/kg. Less is known of venoms of solitary wasps. The venom of Sceliphron caementarium, a mud dauber (Figure 50-16), is comparatively low in protein and contains no acetylcholine, histamine, serotonin, or kinins but does contain several unidentified low-molecular-weight compounds. Its proteins are immunologically different from those of honeybee, yellowjacket, and paper wasp venoms. Philanthotoxin (molecular weight 435) from venom of the beewolf (Philanthus triangulum) acts at the insect’s myoneural junction and has potential value as an insecticide. Ant venoms show great variation. In the life of the fire ant (S. invicta), venom plays several important roles, including prey

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FIGURE 50-16  Solitary mud dauber wasp.

capture, defense, and antimicrobial action. The synthesis of fire ant venom is limited to early life, and the injected venom dose appears to be carefully modulated. Older ant workers (foragers) deliver less venom per sting than do middle-age workers (reserves), and the volume from nest defenders is 50% higher than from their counterparts, particularly in the spring.154 Venoms of more primitive ants (subfamilies Ponerinae, Myrmicinae, and Dorylinae) resemble venoms of social wasps, containing kininlike peptides, enzymes, and unidentified proteins. In more highly evolved ants (subfamilies Dolichoderinae and Formicinae), a variety of low-molecular-weight compounds (terpenes, ketones, and organic acids) make up the bulk of the secretion, which may be sprayed rather than injected. Venoms of fire ants (Solenopsis species) are composed largely of piperidine alkaloids, which cause histamine release and necrosis in human skin. Proteins make up only 0.1% of the dry weight of fire ant venoms, but they are highly allergenic.131,132 Hyaluronidase and phospholipase activities have been demonstrated.

CLINICAL ASPECTS Hymenoptera stings are most often inflicted on the head and neck, followed by the foot, leg, hand, and arm. Stings in the mouth, pharynx, and esophagus may occur when bees or yellowjackets in soft drink, iced tea, or beer containers are accidentally ingested.257,326 A single wasp, bee, or ant sting in an unsensitized individual usually causes instant pain, followed by a wheal and flare reaction, with variable edema. Fire ants typically grasp the skin with their mouthparts and inflict multiple stings. These produce vesicles that subsequently become sterile pustules (Figure 50-17). Multiple Hymenoptera stings may cause vomiting, diarrhea, generalized edema, dyspnea, hypotension, tachycardia, and collapse. Ocular stings with corneal involvement and bilateral ptosis have been described.7,261,334,335 Widespread necrosis of skeletal muscle with hyperkalemia, rhabdomyolysis,

FIGURE 50-17  Fire ant lesions.

*References 53, 59, 72, 113, 205, 295, 348, 366.

50% cross-sensitization occurs between Polistes and other social wasp venoms, and nearly 100% between yellow jacket and hornet venoms. Positive radioallergosorbent test (RAST) reactions to imported fire ant venom were seen in 51% of patients allergic to bee and wasp venoms but without exposure to fire ants. The allergen appears to be identical to antigen 5 of wasp venoms.167 Examination of the sera of hypersensitive individuals for IgE and IgG antibodies against purified venom proteins indicates that phospholipase A, hyaluronidase, and acid phosphatase are important in honeybee venom, whereas phospholipase A, antigen 5, and hyaluronidase are important in wasp venoms. Antigen 5, a nontoxic protein of unknown activity, is reported to have sequence similarity to mammalian testis, human brain tumor, and certain plant leaf proteins. This may explain anaphylactic reactions to first insect stings.190,367 Despite the small amount of protein in fire ant venoms, about 12% of persons treated for fire ant stings show systemic allergic reactions, and at least 32 anaphylactic deaths have been confirmed. Four antigens in S. invicta venom have been reported to be allergenic.52 Allergic sting reactions occur remote from the sting site and include flushing, pruritus, papular urticaria,342 hives, and angioedema. In life-threatening reactions, marked respiratory distress with airway edema, hypotension, loss of consciousness, and cardiac arrhythmias may be seen. At least one-half the severe reactions occur within 10 minutes after a sting, and virtually all occur within 5 hours. Most fatalities occur within 1 hour. The interval between the first known sting and the reaction-producing sting is usually less than 3 years, but may be as long as 48 years. In a group of 3236 Hymenoptera-allergic individuals, 61.5% were male and 32.3% had a history of atopy. The mean age was 30.5 years. No correlation existed between systemic reactions and number of stings in the past or number of stings per incident and severity of a systemic reaction. In a series of 138 adults with a history of insect sting anaphylactic reactions, 99 had no anaphylactic reactions to later stings, 17 had more severe reactions, and 22 had mild to moderate reactions.361 In another series of 90 adults with previous anaphylactic reactions, 60 had similar reactions when restung, and 23 had more severe reactions.293 In children age 10 years and younger, life-threatening reactions occur less often than in adults, and repeated sting episodes usually are not increasingly severe. However, 17% of children with a history of systemic bee or wasp sting reactions developed a systemic reaction after a sting challenge test, as did 5% of children who sustained a sting in the field.159 Children were once thought to outgrow the allergy to insect stings, but there are no reports accurately documenting this theoretical maturation process.144,151 Fatalities that occur within the first hour after a sting result from airway obstruction, hypotension, or both. In 69% of fatal cases, obstruction of the respiratory tree by edema or secretions was the principal finding at autopsy; in 12%, vascular pathology was the principal finding; and 7% of the victims had primary central nervous system involvement such as petechial hemorrhages, infarction, and cerebral edema.20 Hemostatic defects, including reduction of all clotting factors and release of a thrombin inhibitor, may be seen with insect sting anaphylaxis. Severe fetal brain damage, presumably associated with hypoxia, has been reported. Delayed (3 to 14 days) atypical reactions after hymenopteran stings include serum sickness and Arthus reaction, which are caused by systemic and local effects of antigen– antibody complexes; nephrotic syndrome; thrombocytopenic purpura; grand mal and focal motor seizures; transient cerebral ischemic attacks; Guillain-Barré syndrome; and progressive demyelinating neurologic disease.315 Most appear to be immunologically mediated. In one series, elevated IgE to bee or yellowjacket venom was observed in 6 of 13 such patients.206,236 Identification of the individual with potentially dangerous allergy to hymenopteran sting is not always possible. Skin testing with hymenopteran venoms is the most sensitive method; RAST for IgE antibody to venoms is less sensitive, but an important complementary test.143,196 Serum tryptase and basophil responsiveness to venom allergens are also sensitive indicators and should be analyzed in patients with a history of severe sting reaction.30,312,319 A small but significant number of individuals with 931

CHAPTER 50  Arthropod Envenomation and Parasitism

acute tubular necrosis with renal failure, and hepatorenal syndrome with hemolysis have been reported.62,188,210 Acute renal failure may result from toxic ischemic mechanisms, with hypovolemia or anaphylactic shock, myoglobinuria, or acute tubular necrosis.39 Hemolytic anemia and acute renal failure requiring dialysis have also been described following massive attacks by 600 to 1500 Africanized bees, as well as following wasp stings in children.73,74,359 Acute pancreatitis, disseminated intravascular coagulation, and multiorgan dysfunction are also well documented.75,89,122,129,369 Myocardial infarction, atrial flutter, and atrial fibrillation in previously healthy individuals may follow multiple hymenopteran stings.* In one case, a 67-year-old man with acute ST-segment elevation myocardial infarction required fibrinolytic therapy.216 Possible pathogenic mechanisms include severe hypotension due to hypovolemic shock, and prolonged coronary spasm with subsequent thrombosis of coronary vessels due to release of vasoactive, inflammatory, and thrombogenic substances contained in Hymenoptera venom.53 Cerebral infarction, descending aortic thrombosis, and coagulation abnormalities are also reported.67,217,300,352 Dermatologically, large local reactions spreading more than 15 cm (6 inches) beyond the sting site and persisting for more than 24 hours are relatively common. Formation of large bullae may also occur.210 This represents a cell-mediated (type IV) immunologic reaction, although more than one-half of these patients also have IgE antibody against venom or show a positive skin test. Later stings in these individuals usually result in another large local reaction; systemic reactions are rare.378 Allergy is the most serious aspect of hymenopteran stings. Anaphylaxis and related syndromes from this source are relatively common outdoor wilderness emergencies. An estimated 0.4% of the U.S. population shows some degree of clinical allergy to insect venoms, and 40 to 50 deaths are reported annually.294 This number may be underestimated, because not all anaphylactic episodes are recognized or reported. Fatal anaphylaxis due to fire ant stings has also been reported.288 Asymptomatic sensitization, as shown by positive venom skin test, was observed in 15% of 269 randomly selected subjects with no history of an allergic sting reaction.146 Sensitization is transient but may persist for years. These individuals are at higher risk of systemic allergic reactions than are those with negative skin tests.147 Recent studies have reported a high prevalence of hypersensitivity symptoms after intake of wine. Wine contains many contaminants. Some of them come from Hymenoptera insects that fall into the wine when grapes are collected and pressed. Patients with allergic symptoms related to wine consumption may have been sensitized to Hymenoptera venom without previous stings.11 Sudden death from insect sting may not always be recognized. One-half of individuals with fatal sting reactions had no documented history of previous systemic reaction.29 Unexplained deaths at poolsides, golf courses, or any recreational area may be caused by unrecognized Hymenoptera envenomations.99 Of 142 sera obtained after sudden, unexpected death, 23% contained elevated levels of IgE to at least one insect venom. In contrast, 6% of sera from 92 blood donors contained comparable IgE levels. In eight fatal cases of Hymenoptera sting anaphylaxis, IgE to the putative venom source was elevated in all, although levels were not higher than those of some healthy individuals in the same population.326 Allergy-specific IgE antibodies to imported fire ants is nearly twice as common in adults living in endemic areas, making these individuals more susceptible to severe anaphylaxis.55 Anti–fire ant IgE and elevated serum tryptase were detected in a case of fatal fire ant sting.250 Elevated levels of venom-specific IgE were detected in two fatal cases of wasp sting.357 However, the level of specific IgE antibodies against venoms is not predictive of the severity of anaphylactic reaction, as documented by recent studies conducted to determine the reliability of postmortem specific IgE antibody testing in venominduced anaphylactic deaths.169 Wasp and bee venoms contain 9 to 13 antigens, some of which are potent allergens. Available evidence indicates little cross-sensitization between honeybee and wasp venoms. About

PART 6  ANIMALS, INSECTS, AND ZOONOSES

no history of sting reactions have IgE antibody specific for hymenopteran venoms; prevalence of this antibody is higher in summer.385 These methods do not identify all at risk, and antibody levels do not correlate with severity of sting reactions. In a significant number of individuals, particularly children, clinical sensitivity disappears and IgE levels fall virtually to zero 3 to 18 months after a reaction-producing sting. In about 40% of cases, sensitivity may disappear within 3 years.204 Venom antibody (both IgE and IgG) may be found in healthy individuals (40% of beekeepers, 12% of blood donors) with no history of systemic reaction to insect stings. No unique features distinguish Hymenoptera envenomations in other parts of the world from those in North America. Venoms of the various groups show little geographic variation. This is also true of groups at risk, with the possible exception of a few honey-gathering Asian tribes. The incidence of Hymenoptera sting allergy may be slightly higher in western Europe than in the United States, and fatal allergic reactions may be slightly more common.65 Anaphylactic reactions to bee venom are more prevalent in the rural populations closer to the Mediterranean than in western Europe, where urban populations predominate.240 Paraponera ant stings are intensely painful for several hours and may be accompanied by fever and lymphadenitis. Systemic anaphylactic reactions to stings of Australian bull or jumper jack ants, as well as samsum ants, are increasing, with reports of fatalities.46,228 Acute renal failure has also been described.1 Patients with a history of systemic reactions to samsum ant stings have IgE and positive skin test reactions to fire ant venom.96

TREATMENT AND PREVENTION Treatment of anaphylaxis is conventional. Aqueous epinephrine 1 : 1000 should be administered subcutaneously in the prehospital setting at the first indication of serious hypersensitivity. The dose for adults is 0.3 to 0.5 mL, and for children under age 12 years it is 0.01 mL/kg, not to exceed 0.3 mL. Compared with methylprednisolone alone, early combination of epinephrine helps to further inhibit the diffusion of allergy and inflammation cytokines, and therefore reduce the severity of injury.380 When symptoms are predominantly respiratory, epinephrine by inhalation (10 to 20 puffs for an adult; 2 to 4 puffs per 10 kg [22 lb] of body weight for a child) may provide more rapid relief.246 In the presence of profound hypotension, the patient may be in shock and not adequately perfusing the skin. In this scenario, 2 to 5 mL of a 1 : 10,000 epinephrine solution may be given by slow IV push, or an infusion may be initiated by mixing 1 mg in 250 mL and infusing at a rate of 0.25 to 1 mL/min. If an IV line is delayed or cannot be established, epinephrine may be given intramuscularly, intralingually, or via an endotracheal tube.14 Two cases of Hymenoptera-induced anaphylactic shock with profound hypotension were successfully resuscitated using 40 IU of IV vasopressin followed by a rapid fluid bolus.189 Selective inhaled (nebulized) β2-adrenergic agents, such as albuterol, can also be effective in relieving bronchospasm at doses of 2.5 mg/3 mL of a 0.08% solution. Aminophylline, 5 mg/kg as a loading dose followed by 0.9 mg/kg/hour as an infusion, may relieve bronchospasm not relieved by epinephrine or albuterol. In the presence of hypotension, IV crystalloid solutions should be infused; pressor agents such as dopamine or norepinephrine may be required. Oxygen, intubation, and mechanical ventilation may be needed to correct airway obstruction. Antihistamines can alleviate symptoms of anaphylaxis but should be used only in addition to epinephrine, not as a substitute.14 Corticosteroids are also indicated in acute anaphylactic reactions, although the time of onset with corticosteroids is delayed. Propranolol is contraindicated because of the β-adrenergic blockade effect on the bronchioles. Persons taking β-adrenergic blockers may respond poorly to epinephrine. In these cases, administration of glucagon to counteract the beta blockade effect may prove beneficial.303 Persons with insect sting anaphylaxis require close observation, preferably in the hospital, over a period of 24 hours.246 For mild hymenopteran stings, ice packs often provide relief. Honeybees frequently and yellowjackets occasionally leave a stinger in the wound. Although recommendations were that stingers should be scraped or brushed off with a sharp edge and 932

not removed with forceps, which might squeeze the attached venom sac and worsen the injury, this has been refuted.304,364 Advice to victims on the immediate treatment of bee stings now emphasizes rapid removal of the stinger by any method.364 Wheal size and degree of envenomation increased as the time from stinging to stinger removal increased, even for a few seconds. The response was the same whether stings were scraped or pinched off after 2 seconds. Home remedies, such as baking soda paste or meat tenderizer applied locally to stings, are of dubious value, although the latter is often regarded as effective. Topical anesthetics in commercial “sting sticks” are also of little value. Topical aspirin paste is not effective in reducing the duration of swelling or pain in bee and wasp stings and may actually increase the duration of redness.18 Local application of antihistamine lotions or creams, such as tripelennamine, may be helpful. An oral antihistamine, such as diphenhydramine, 25 to 50 mg for adults and 1 mg/kg for children, every 6 hours is often effective. All fire ant stings can be managed medically in the same manner. No therapy is effective against local effects of fire ant stings, although oral antihistamines and corticosteroids may provide some relief in severe cases. Because infection is common, topical antimicrobials (e.g., mupirocin) and prophylactic oral antibiotics are recommended. Breaking fire ant blisters should be avoided.69,89 Corticosteroids, such as methylprednisolone, 24 mg/day initial dose tapered off over 4 to 5 days, often help resolve extensive local reactions to bee and wasp stings. This may be combined with cold packs and oral antihistamines. Chronic facial edema caused by multiple bee stings has been effectively treated with plastic surgery and liposuction.4 Envenomation from multiple hymenopteran stings may require more aggressive therapy. IV calcium gluconate (5 to 10 mL of 10% solution) with a parenteral antihistamine and corticosteroid may be helpful in relieving pain, swelling, nausea, and vomiting. Development of a hyperimmune bee venom antiserum is under investigation.323 Hypovolemic shock is managed conventionally. Plasmapheresis was used successfully to treat a person who sustained about 2000 honeybee stings.95 Patients should be observed for 12 to 24 hours for coagulopathy and evidence of renal and neurologic damage. Urine output is monitored and urine tested for hemoglobin and myoglobin. Serum potassium, creatine kinase, and lactate dehydrogenase levels should be monitored. Oliguria with myoglobinuria, azotemia, and hyperkalemia are indications for hemodialysis.

IMMUNOTHERAPY It is suggested that at least one-half of sting fatalities in patients with a previous history of severe systemic reactions could have been avoided through the timely administration of specific immunotherapy.28 Venom immunotherapy is 75% to 98% effective in preventing sting anaphylaxis.143 Immunotherapy should be offered to patients with a history of anaphylaxis after a sting, mastocytosis, and specific IgE antibodies to the agent confirmed by positive skin testing or in vitro assays.132,209 In addition, venom immunotherapy significantly reduces the size and duration of large local reactions.145,329 Desensitization with purified venoms produces an excellent blocking antibody response and prevents anaphylaxis in more than 95% of patients. A protective antiidiotypic antibody to honeybee venom has been identified.186 Venoms for desensitization generally available in the United States are honeybee, yellowjacket, wasp (Polistes), and mixed vespid. More than one venom can be given concurrently, but this requires multiple injections. Commercial preparations consisting of a mixture of yellowjacket, white-faced hornet, and yellow hornet venoms are available.132 A whole-body extract of fire ant containing at least three venom antigens has also been developed.368 Children under 16 years with only cutaneous or mild systemic allergic reactions and persons with a history of only large local reactions do not need immunotherapy.254 Evaluation of anaphylaxis risk is recommended in children using wasp venom extract challenges.321 As mentioned previously, children were once thought to “outgrow” their allergies to insect stings, but this has

ANTIVENOM THERAPY AND FUTURE INTERVENTIONS A group in the United Kingdom has developed ovine Fabbased antivenom as a potential treatment for mass bee stings. Sera from sheep immunized against the venom of A. m. scutellata contained high levels of specific antibodies, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and chromatography. Although effective experimentally in a mouse model, no human administration of the antivenom has been documented.179 Another approach based on genetic engineering is the use of non-IgE binding peptide fragments of the insect allergen with preserved T-cell epitopes for advanced immunotherapy. Such preparations of bee venom phospholipase A2 have been used successfully in pilot studies. Additionally, DNA vaccination with phospholipase A2 sequence plasmids has been proved effective in a mouse model.244 Patients who experience severe anaphylaxis to venom immunotherapy can now be treated with the anti-immunoglobulin (Ig) E monoclonal antibody, omalizumab.135

PREPAREDNESS AND PREVENTIVE MEASURES Persons with a history of allergic reactions to insect stings (including large local reactions) should carry an emergency kit con­ taining epinephrine autoinjectors and should wear medical identification tags.132 Kits should be available in work and recreation areas where the risk of insect sting is high. Two kits widely available in the United States are EpiPen and Ana-Kit. EpiPen and EpiPen Jr. are autoinjectors that deliver 0.3 mg or 0.15 mg of epinephrine, respectively (Figure 50-18, online). They are quick and easy to use; however, patients should be cautioned against injecting the material into fingers or buttocks or directly over veins. Ana-Kit contains two doses of 0.3 mg of epinephrine in a single conventional syringe, plus chewable antihistamine tablets and a tourniquet. It is more versatile but requires more instructions for the user. Twinject is another product that may be used to inject two doses of epinephrine. Frequent cleaning of garbage cans and disposal of decaying fruit makes premises less attractive to bees and wasps. Hymenopterans are highly susceptible to many insecticides, and their control around dwellings and other inhabited buildings is rarely difficult. Spraying the nests after dark is safer because these insects are less active at night. Many hymenopterans are economically valuable as pollinators of plants or predators on other insects, so their control on a wide scale is rarely desirable. The fire ant in the southern United States has been the target of massive but marginally effective control campaigns that adversely affected local ecosystems. A new approach uses grain baits containing synthetic insect growth hormones that are carried into the nests, where they disrupt ant caste differentiation and inhibit egg production. Arrays of thousands of hormone-baited traps placed in select areas of Mexico, however, failed to stop the northward spread of Africanized bees. For controlling populations of Africanized bees, care should be taken that items such as boxes and empty oil drum containers are not left outdoors. Ceilings and walls should be sealed off as potential nesting sites for colonies and swarms.80

Lepidoptera VENOMOUS SPECIES AND VENOMS Next to flies, lepidopterans are the most abundant arthropods, with more than 165,000 species worldwide, with most species posing no human threats. However, caterpillar species from approximately 12 families of moths or butterflies can inflict serious human injury.93 Insects of the order Lepidoptera may cause human envenomation that is generally less serious than that with hymenopterans. Injury usually follows contact with caterpillars and is less frequent with the cocoon or adult stage. The larval lepidopteran (caterpillar) is usually free living, is moderately active, and feeds on plants, although a few are parasites of insect nests or eat food of animal origin. The pupal stage may be free or encased in a silk cocoon. Wintering over in cold climates is usually in the pupal stage. Adults (butterflies and moths) have wings with microscopic chitinous scales. They feed primarily on nectar and other plant juices, but some eat semiliquid mammalian feces and urine. The adult provides no care or protection of immature stages. No social organization exists, although larvae and adults of some species assemble in large aggregations. Many venomous caterpillars are broad, flat, and sluggish. Some have the dorsal surface densely covered with long hairs. Others are spiny and may have bright, conspicuous colors and markings. Some are highly camouflaged. Venoms in Lepidoptera are purely defensive. The venom apparatus consists of spines that are simple or branched and frequently barbed. They may be scattered widely over the surface of the insect or arranged in clumps and often are intermixed with nonveniferous hairs or spines. In the most venomous caterpillars, the spines are hollow and brittle with venom glands at the bases. Muscles surrounding the glands may help in expelling venom. In other Lepidoptera, the spines are solid and function primarily as mechanical irritants or contain surface toxicants. Little is known of the chemistry of caterpillar venoms. Some are heat 933

CHAPTER 50  Arthropod Envenomation and Parasitism

never been proved. In fact, a clinically important number of children retain their allergic reactions to Hymenoptera venom. Immunotherapy in children leads to a significantly lower risk of systemic reaction to stings, even 10 to 20 years after treatment is completed. This prolonged benefit is greater than that observed when the immunotherapy is given to adults.144,151 Persons receiving β2-adrenergic blockers should be shifted to other appropriate medications if possible. Regimens for desensitization attempt to achieve tolerance to venom doses of about 100  mcg. It requires about 95 days to achieve a maintenance level of immunity. Rapid or “rush” programs requiring 3 to 7 days for initial immunization appear to be effective in high-risk patients.24,104,180,344,371 A recent study suggests that an ultra-rush sublingual immunotherapy may be as efficacious and better tolerated than traditional subcutaneous immunotherapy.274 Some programs make use of both active and passive immunotherapies.245 In a series of 1410 patients, 12% had systemic reactions during treatment, but no fatalities were reported.213,214 A report of 26 women with 43 pregnancies does not suggest significantly increased risk from venom immunotherapy during pregnancy.325 Maintenance doses are required at intervals after basic immunization. Neither skin testing nor determination of IgG and IgE antibody levels against venom will reliably indicate success of immunization, although the majority of persons will be protected by a specific IgG antibody level of 400 RAST units/mL of serum. Actual sting challenge is the most reliable test for determining immunotherapy candidates and desensitization,362 but this is not widely used in the United States. It must be done in the hospital with careful monitoring and consideration of economic, ethical, and safety factors.311 If the skin test is negative after 3 years of immunotherapy, patients may be placed on immunologic surveillance. Few patients require more than 5 years of immunotherapy.294 According to some authorities, if a sting challenge or field sting is tolerated during the period of immunotherapy, treatment can be terminated after 3 to 5 years.289 For unknown reasons, desensitization to wasp venoms is achieved more quickly than to honeybee venom.36 Although the low mortality and morbidity associated with patients who suffer subsequent stings following immunotherapy has led some to conclude that many patients are being treated unnecessarily, this conclusion is refuted by the fact that venom immunotherapy improves the quality of life and health of the vast majority of patients receiving this intervention.268,269 Patients should be warned that the efficacy of venom immunotherapy might be less than optimal and they should continue to carry adrenaline auto injectors.256 Like bee venom immunotherapy, purified Myrmecia ant venom immunotherapy has been established and shown to be highly effective for Australian bull or jumper ant and imported fire ant anaphylaxis.40,43,44,160,228

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 50-22  Saddleback caterpillar, Sibine stimulea. FIGURE 50-19  Puss caterpillar, Megalopyge opercularis.

FIGURE 50-23  Gypsy moth, Lymantria dispar. (From Wikimedia Commons.) FIGURE 50-20  Flannel moth caterpillar, Megalopyge crispata.

labile and contain proteins. Histamine and serotonin have been found in caterpillar venoms but are not common. Hairs of the brown-tailed moth (Euproctis chrysorrhea) contain enzymes with esterase and phospholipase activity. Probably the most important venomous caterpillar in the United States is the puss caterpillar.139,328 It is also known as the asp caterpillar106 or woolly slug (Megalopyge opercularis) (Figure 50-19). This caterpillar is distributed throughout most of Texas, Louisiana, Florida, and north to Maryland and Missouri. The hairy, flat, and ovoid caterpillar reaches a length of 30 to 35 mm (1.2 to 1.4 inches) and feeds on shade trees, including elm, oak, and sycamore. Some years it may be plentiful enough to be a nuisance. In southeast Texas in 1958, 2130 persons were treated for stings, and eight were hospitalized. A related species, the flannel moth caterpillar (Megalopyge crispata) (Figure 50-20), occurs in the eastern states north to New England. Its sting is

less severe than that of M. opercularis. The large, spiny caterpillar of the io moth (Automeris io)117 is pale green with red and white lateral stripes (Figure 50-21). It is widely distributed in the eastern United States, but rarely plentiful. The saddleback caterpillar111 (Sibine stimulea) (Figure 50-22) and oak slug (Euclea delphinii) are flat and almost rectangular; both can deliver a painful injury. The gypsy moth (Lymantria dispar) (Figure 50-23) feeds on a variety of plants and has caused thousands of cases of dermatitis in the northeastern United States. These caterpillars have also been imported to Europe across the Atlantic Ocean on exported house or garden plants.68 Other common nettling caterpillars are E. chrysorrhea, which also occurs in Europe, and the tussock or toothbrush caterpillar (Hemerocampa leucostigma), with its conspicuous red head and four tufts of bristles. Another tussock caterpillar, Oryia pseudotsuga, causes numerous cases of dermatitis and conjunctivitis among lumberworkers and foresters in the northwestern states. The hickory tussock caterpillar (Lophocampa caryae) can cause skin irritation and urticaria with dermal contact, or drooling if ingested (Figure 50-24).200,285 The eastern tent

FIGURE 50-21  Caterpillar of the io moth, Automeris io. Widespread in the eastern United States, this species can inflict a painful sting.

FIGURE 50-24  Hickory tussock moth caterpillar, Lophocampa caryae. (Courtesy EDUPIC Graphical Resource.)

934

caterpillar, Malacosoma americanum (Figure 50-25), is native to North America. Populations fluctuate from year to year, with outbreaks occurring every several years. Defoliation of trees, building of unsightly silken nests in trees, and wandering caterpillars crawling over plants, walkways, and roads cause this insect to be considered a pest in the late spring and early summer. Eastern tent caterpillar nests are commonly found on wild cherry, apple, and crabapple trees, but may be discovered on other various fruit trees.

STINGING PATTERNS Lepidoptera are uncommonly recognized causes of localized stings, eczematous or popular dermatitis, and urticaria.172 Caterpillar envenomation usually occurs when living insects are touched as they cling to vegetation or drop onto bare skin. Persons cutting branches, picking fruit, or climbing trees are likely to be stung. However, the largest outbreaks have been associated with spines detached from live or dead caterpillars and cocoons. These may be airborne or deposited on bedding or laundry hung outdoors. In temperate regions, caterpillar stings are most common from August to early November. Heavy caterpillar infestations seem to occur during exceptionally favorable weather and with decreases in populations of parasites and predators that serve as natural controls.

TREATMENT AND PREVENTION Treatment of lepidopteran envenomations is symptomatic. Prompt application and stripping off of adhesive tape or a commercial facial peel at the site of the sting may remove many spines and serve as a diagnostic procedure, as the spines can then be identified by microscopy (Figure 50-28). Patients with local symptoms usually obtain relief from group I corticosteroid creams, oral antihistamines, and ointments.171 Over-the-counter

CLINICAL ASPECTS Two general syndromes are associated with lepidopteran envenomations. In the cases of caterpillars with hollow spines and basal venom glands (e.g., Automeris, Megalopyge, and Dirphia), direct contact with the live insect causes instant nettling pain, followed by redness and swelling (Figure 50-26). Puss caterpillar stings show a characteristic gridiron pattern of hemorrhagic

FIGURE 50-26  Nettle rash from unidentified caterpillar.

A

B

C

D

FIGURE 50-27  Lepidopterism. A, Toxic irritative caterpillar dermatitis. B, Silken nest on the trunk of an infested oak tree with living larvae. C, Sixth larval instar of Thaumetopoea processionea L. D, Setae (×200). (From Spiegel W, Maier H, Maier M: A non-infectious airborne disease, Lancet 363:1438, 2004.)

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CHAPTER 50  Arthropod Envenomation and Parasitism

FIGURE 50-25  Eastern tent caterpillar, Malacosoma americanum. (Courtesy Richard Seaman. http://www.richard-seaman.com.)

pinpoint papules. In typical cases, no systemic manifestations occur, and symptoms usually subside within 24 hours. However, pain may be intense with central radiation, accompanied by urticaria, nausea, headache, fever, vomiting, muscle spasms, paresthesias, and lymphadenopathy. Hypotension, shock, dyspnea, abdominal tenderness, and convulsions have been reported with more severe cases of puss caterpillar stings.117,137,139,170,328 The second syndrome is associated with caterpillars with a less highly developed venom apparatus (e.g., Lymantria, Euproctis, Thaumetopoea). Contact with the living insect is not necessary; detached spines are often involved. Little or no immediate discomfort is experienced. An itching, erythematous, papular, or urticarial rash develops within a few hours to 2 days and persists for up to a week (Figure 50-27). Rarely, the lesions may be bullous. Conjunctivitis, upper respiratory tract irritation, and rare asthma-like symptoms may be seen with or without dermatitis. Ophthalmia serious enough to require enucleation may be caused by detached spines lodged in the eye. Acute anaphylactic reactions have not been reported to follow lepidopteran stings. Patch testing has demonstrated both immediate and delayed hypersensitivity. A pediatric case series reported 10 patients who ingested various caterpillar species. Adverse effects ranged from mild (drooling and refusal to drink) to diffuse urticaria. Five of the patients underwent direct laryngoscopy and endoscopy to assess for pharyngeal and esophageal injuries. None had adverse outcomes.194 The pine processionary caterpillar has been reported to cause significant local reaction and airway compromise mimicking an allergic event in children with oral ingestions.175

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 50-30  Moth of Lonomia achelous, which has no venomous spines.

FIGURE 50-28  Microscopic view of Lepidoptera spines. (From http:// www.microscope.mbl.edu.)

preparations containing corticosteroids and antihistamines are not significantly better than simpler preparations such as calamine lotion with phenol. Oral antihistamines such as fexofenadine (60 mg, twice a day) or antiinflammatory drugs such as tolmetin sodium (400 mg, three times a day) are often effective in more severe cases. Occasionally, codeine (30 to 50 mg) or oxymorphone (1.5 mg) in combination with an antiemetic may be needed to control pain and vomiting. Intravenous calcium gluconate has been used successfully in severe puss caterpillar envenomation to control muscle spasms.255,283 Trees on which caterpillars feed may be sprayed with appropriate insecticides to control species such as the puss caterpillar. Screens on windows and doors protect against moths with toxic spines. Internationally, Lepidoptera show high diversity in the tropics with correspondingly greater medical importance, particularly in Latin America. Caterpillars of the genus Lonomia, native to northern South America, especially Venezuela and the southern region of Brazil, can inflict life-threatening stings56 (Figures 50-29 and 50-30). These caterpillars are 50 to 70 mm (2 to 3 inches) long and have numerous branched dorsal spines. They live in primary tropical forests in groups of up to 50 individuals. Disturbance of their habitat has resulted in an increasing number of envenomations. Stings cause intense pain but not much local reaction. Venom of Lonomia is a protein that activates prothrombin and is stimulated by factor V and calcium ions.152 Signs of coagulop­ athy, such as ecchymoses, bleeding gums, hematuria, and melena, may develop in a few hours or be delayed for several days. The venom-induced hemolysis or hemorrhagic syndrome results from prothrombin and factor X and promotes fibrinogenolytic activity and massive fibrinolysis.173,222 Fibrinogen, factor V, factor XII, and plasminogen are decreased, fibrin degradation products are

FIGURE 50-29  Caterpillar of Lonomia achelous, which can inflict injuries characterized by potentially fatal coagulopathy.

936

increased, and platelets usually are normal. Acute renal failure,34,47 cerebral hemorrhage, and pulmonary hemorrhage may occur. Coagulopathy may last 2 to 5 weeks. In one series of 33 cases, four were fatal.12,47,103 Treatment with prednisone, plasma, and whole blood is ineffective. An antivenom has been developed, and preliminary reports indicate possible clinical efficacy.76,79 Neotropical caterpillars of the genera Dirphia, Megalopyge, and Automeris are large, stout, spiny, and sometimes covered with hair. Most are forest species but can adapt to areas of cultivation. Agricultural workers are most often stung and the incidence of stings is higher in the rainy season. Intense, centrally radiating pain with local edema, erythema, and lymphadenop­ athy is typical. Systemic symptoms include nausea, headache, malaise, chills, and fever. Hypotension, shock, and convulsions have been reported. An Automeris caterpillar bite reported from French Guyana produced syncopal pain and edematous infiltration of the thigh lasting several days.71 Symptoms usually subside within 24 hours. Treatment is symptomatic. Oral antihistamines are often effective if given within an hour after the sting. Opioid agents are occasionally needed to control pain. A chronic granuloma known as pararama occurs on the hands of Brazilian rubber tappers after contact with Premolis semirufa caterpillars. Permanent extremity disability may result.280 Moths of the genus Hylesia are found from southern Mexico to Argentina. The caterpillars have venomous spines, but the greatest problem is created by the moths, which have a coating of spines on their abdomen. The spines or setae are hollow and pointed, contain a toxin of unknown nature, and are freely shed into the air. The moths are attracted to lights in enormous numbers, and their airborne spines can cause great discomfort. Their activity has created serious problems at airports, shipping docks, and tourist resorts. Within a few minutes to a few hours after contact with the spines, victims develop a pruritic, erythematous rash that progresses to urticaria and excoriation. Any portion of exposed skin may be involved, but palms and soles are often spared. Irritation of eyes and mucous membranes is unusual. Symptoms subside in about a week if there is no further exposure. Topical and systemic treatments have had little benefit.97 In Korea, outbreaks of dermatitis, presumably caused by setae of the yellow moth Euproctis flava, are well known. In the summer of 1980, hundreds of U.S. soldiers were affected.23 The caterpillars feed on hardwood trees, and great numbers of moths appear in summer and are attracted to lights. Dermatitis usually involves direct contact with moths or their cocoons or with clothing contaminated with setae. The lesions are similar to those described for Hylesia and are equally refractory to treatment. Other outbreaks of dermatitis ascribed to Euproctis moths and caterpillars have been reported in Japan and China. One outbreak in Shanghai in 1972 affected about 500,000 individuals. Outside Shanghai, where chemical insecticides would have been harmful to silkworm culture, Euproctis caterpillars (Figure 50-31) have been controlled by spraying with an insect virus. Cases of Euproctis dermatitis and ophthalmia have also been reported in Australia and Great Britain. Sensitization with elevated IgE levels may occur.280,339

FIGURE 50-32  Centipede, Scolopendra heros.

In the Mediterranean region and the Middle East, the pine processionary caterpillars Thaumetopoea pityocampa and Thaumetopoea wilkinsoni are plentiful and make silk nests in trees. The setae from these caterpillars can cause a maculopapular rash accompanied by urticaria, bronchitis, and conjunctivitis. A non–IgE-mediated release by Thaumetopoea results in a type I hypersensitivity foreign-body reaction, resulting in dyspnea and bronchospasm.340 Outbreaks typically occur when groups of tourists or military personnel camp in pine groves. The rash usually results from contact with detached setae rather than with caterpillars. The adult moth stage apparently does not have irritating spines. Systemic reactions manifesting as abdominal pain and hypertension have been reported.198 Moths of the genus Calyptera, native to Southeast Asia, have a serrate proboscis and feed on mammalian blood, including that of humans. Tropical species of several moth genera feed on human ocular secretions. Their medical importance is unknown. In Australia, five families of caterpillars that inflict lesions resulting in local pain and urticaria have been described (Arctiidae, Limacodidae, Anthelidea, Lymantriidae, and Spingidae). All dermal reactions were responsive to ice packs and antihistamines. Ingestions resulted in no adverse side effects.16 Contact dermatitis or erucism has been described in New Zealand from exposure to gum leaf skeletoniser (Uraba lugens) caterpillars in the Auckland region.87

a large centipede from that of a snake.109,211 Contrary to popular folklore, centipedes do not inject venom with their feet or caudal appendages. The jaws inject a neurotoxic venom through venom ducts. Centipede bites have been reported from numerous tropical and subtropical regions but never as a serious medical problem. Most bites have been ascribed to species of Scolopendra, which has a wide distribution with several species in the southern United States (Figures 50-32 and 50-33). Fatalities are almost unknown; however, a death in the United States was recently mentioned, but the locality and other details were not given.203 Burning pain, local swelling, erythema, lymphangitis, and lymphadenopathy are common manifestations of a centipede bite. Some theorize that there is a close relation between centipede allergy and bee or hymenoptera venom allergy.158 Swelling and tenderness may persist for as long as 3 weeks or may disappear and recur. Severe and prolonged symptoms have been described in patients with sickle cell disease.310 Superficial necrosis may occur at the site of fang punctures. Few bites result in cellulitis, necrotizing fasciitis and serious systemic reactions.358 In one case ascribed to Scolopendra heros in the southwestern United States, a woman had massive edema of the leg, necrosis of the peroneal muscles, loss of motor function in the foot, myoglobinuria, and azotemia.215 An Israeli patient bitten on the neck complained of inability to turn her head, probably because of muscle spasm.241 Other cases have been characterized by dizziness, nausea, collapse, and pyrexia.247 An infant who ingested a centipede identified as Scutigera morpha developed hypotonia, vomiting, and lethargy, presumably from being bitten in the mouth or pharynx. The child recovered spontaneously after about 48 hours.21 Centipede envenomation in a newborn inflicted by Scolopendra gigantean was reported in Venezuela and caused crying, irritability, and localized wound edema.306 Cryptops and Otostigmus genera are responsible for most cases of centipede stings.231 Acute coronary ischemia associated with myocardial infarction with electrocardiographic changes and elevated cardiac troponin has been described after envenomation from an unidentified centipede in Turkey.270,381 Although some centipede bites may be excruciatingly painful, they are not fatal and seldom require more than supportive care. Treatment of centipede envenomation is symptomatic. Ice packs, hot water immersion, and analgesics all can improve pain from centipede envenomation.54 Infiltration of the bitten area

Centipedes and Millipedes Centipedes are elongate, flattened arthropods with one pair of legs for each of the typical body segments, which may number from 15 to more than 100. The first segment bears a pair of curved hollow fangs with venom glands at the bases. The last segment bears a pair of filamentous to forceps-like caudal appendages not associated with the venom apparatus.34 The largest species reach lengths of about 30 cm (12 inches). Most centipedes live in crevices or beneath objects on the ground. Some are burrowers and others are climbers. Many are nocturnal. Scutigera coleoptrata, with a body length of 25 mm (1 inch) and long thin legs, is a common house arthropod in much of the United States. Lithobius is a cosmopolitan ground-dwelling genus. A species common in eastern U.S. gardens is orange and 30 to 50 mm (1.2 to 2 inches) long. Envenomations by imported varieties of the Vietnamese centipede have been reported in Long Island, New York.227 Centipedes prey chiefly on invertebrates, but larger species occasionally eat small vertebrates. Female centipedes of some species curl around their egg clusters and newly hatched young, and may actively defend them. Centipedes use venom primarily to kill prey and only secondarily for defense. Venom may also have a digestive function. Enzymes, including acid and alkaline phosphatase and amino acid naphthylamidase, lipoproteins, histamine, and serotonin, are variably present.241 Venom of Scolopendra subspinipes produces hypotension followed by hypertension. The major lethal toxin is an acidic protein with a molecular weight of 60,000 daltons. It produces vasoconstriction, increased capillary permeability, and cardiotoxicity.148,149 Like spiders, any centipede whose fangs can penetrate human skin can cause local envenomation. Centipede bites are typically pointed in shape, a feature that can help differentiate the bite of

FIGURE 50-33  Centipede fangs.

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CHAPTER 50  Arthropod Envenomation and Parasitism

FIGURE 50-31  Euproctis caterpillar. (Courtesy Walwyn.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Hemiptera (Sucking Bugs)

Millipedes Millipedes differ from centipedes in having two pairs of legs per body segment and in lacking apparatus for injecting venom. Several large species of the genus Spirobolus are common in the southern United States (Figure 50-34). Some species are broad and short and roll into a ball when disturbed (Figure 50-35). The millipede species Illacme plenipes found in California comes the closest to having its namesake’s mythical 1000 legs—individuals can bear up to 750 legs.223 Millipedes are generally ground dwelling and secretive. Occasionally, they aggregate in enormous numbers. They generally feed on decaying vegetation. Millipedes are exceptionally well endowed with defensive chemical secretions that include hydrogen cyanide, organic acids, phenol, cresols, benzoquinones, and hydroquinones. These effectively deter most predators. Some large species can eject secretions for distances up to 80 cm (32 inches). Human injury from millipede secretions has been reported from a number of tropical regions.162 The most common injury is dermatitis that begins with a brown-stained area, which burns and may blister and exfoliate.224 Millipede burns have been described in unusual sites with pediatric cases mimicking child abuse.78 Millipede secretion in the eye causes immediate pain, lacrimation, and blepharospasm. This may be followed by chemosis, periorbital edema, and corneal ulceration. Blindness has been reported.157 Individuals exposed to large millipede aggregations may complain of nausea and irritation of the nose and eyes. No specific treatment is available. Prompt irrigation with water or saline should be followed by analgesics, anti­ microbials, and other measures appropriate for superficial che­ mical burns. Ophthalmologic evaluation is mandatory for eye injuries. Infestation of the human intestines by the millipede Nopoiulus kochii has been described in Turkey. Antiparasitic drugs (niclosamide and albendazole) may not be effective in eradicating the problem.114

Hemiptera is a large order of insects characterized by sucking mouthparts, generally in the form of a beak, and a life cycle with no well-demarcated larval and pupal stages but a gradual transition from the hatchling nymph to adult. Most hemipterans are winged as adults, with the anterior wings generally divided into chitinized and membranous sections. Most feed on plant juices, but several families are predators, and two feed on the blood of humans and other vertebrates. Hematophagous bugs are able to exploit the temperature differences observed over the skin surface to locate blood vessels. These bugs generally bite into the warmest temperature regardless of the target or background temperature.119 The assassin bugs (family Reduviidae) are generally recognized by their long and narrow head, a stout and three-jointed beak, long antennae, and typical hemipteran wings (Figure 50-36). Most are of a dark color; a few are brightly marked or have a checkerboard pattern along the posterior edge of the abdomen. Some species attach fragments of their prey, sand grains, or other debris to their backs. Reduviidae occur on all continents. They have a variety of habitats and are often nocturnal. The triatomids (e.g., kissing bugs, flying bedbugs, Mexican bedbugs, barberos) are a subfamily of the Reduviidae adapted for feeding on blood. They feed on a wide range of mammals and often live in the nests or burrows of their hosts. Armadillos, dogs, opossums, and pack rats are common hosts in the southern United States and Mexico. Some triatomids adapt readily to life in human dwellings, particularly those of adobe construction. Triatomids are primarily a neotropical group, with species ranging northward in the United States to Utah and southern Indiana. Triatoma protracta and Triatoma sanguisuga are among the better-known species. The family Cimicidae, or bedbugs, are flat, ovoid, and reddish brown insects whose wings are reduced to a pair of functionless pads. Lack of large terminal claws distinguishes them from lice. Bedbugs are cosmopolitan in distribution and have increased dramatically in the United States and in the United Kingdom.353 This recent resurgence is attributed to increased travel and resistance to insecticides.195 Two species, Cimex lectularius and Cimex hemipterus, feed primarily on humans and live in dwellings, where they hide in bedding, under wallpaper, behind baseboards, and in window frames. Homes of poorer persons are more likely to be heavily infested, but the insects may be carried into well-kept residences, hospitals, and hotels. Homeless persons are more prone to exposure when residing in large shelters.42 Other species of Cimex, normally parasitic on bats and swallows, occasionally attack humans. Venomous aquatic hemipterans include the giant water bugs (family Belostomatidae) (Figure 50-37), back swimmers (family Notonectidae) (Figure 50-38), and water scorpions (family Nepidae). Water bugs are distinguished from aquatic beetles by their beak and hemipteran wings; back swimmers have greatly elongated hind legs; and water scorpions have a slender body with long, terminal breathing tubes. These insects are widely distributed in freshwater habitats.

FIGURE 50-35  Giant Madagascar millipede.

FIGURE 50-36  Wheel bug, Arilus cristatus, a large assassin bug common in the eastern United States.

FIGURE 50-34  Spirobolus millipede.

with lidocaine or another anesthetic promptly relieves pain. Antihistamines and corticosteroids have been suggested for more severe reactions. Tetanus prophylaxis is advisable.51,242 Hot water immersion has proved beneficial in Australia from bites of centipedes from the genera Scolopendra, Cormocephalus, and Ethmostigmus.17

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The hemipteran venom apparatus consists of two or three pairs of glands in the thorax. Secretions are ejected through onehalf of a double tube formed by the interlocking of the elongated maxillae and mandibles, which have distal tips modified for piercing. Few hemipteran venoms have been studied. Venoms of two reduviids, Platymeris rhadamanthus of Africa and Holotrichus innesi of the Middle East, contain several enzymes and nonenzymatic proteins.107,383 Sialidase, an enzyme unusual in invertebrates, is found in Triatoma venom; it has anticoagulant activity.8 Venom serves primarily for subjugation and probably digestion of prey, but the insects may defend themselves by biting. Salivary secretions of blood-sucking hemipterans also contain potent allergens.

CLINICAL ASPECTS Triatomids usually bite at night on exposed parts of the body. Feeding may last from 3 to 30 minutes. Bites are painless. On initial exposure there is usually no reaction. Repeated bites are followed by reddish, itching papules that may persist for up to a week. Bites are often grouped in a cluster or line (Figure 50-39) and may be accompanied by giant urticarial wheals, lymphadenopathy, hemorrhagic bullae, fever, and lymphocytosis. Systemic anaphylactoid reactions with respiratory or gastrointestinal manifestations may occur.174,219 Entomologists and small children are most frequently bitten by assassin bugs, as handling induces the insect to bite. Bites of several U.S. species, such as the wheel bug (Arilus cristatus), black corsair (Melanolestes picipes), and masked bedbug hunter (Reduvius personatus), are described as being as painful as the sting of a hornet and accompanied by local swelling lasting several hours. Bedbug bites usually raise a pruritic wheal with a central hemorrhagic punctum, followed by a reddish papule that persists for several days. Bullae, generalized urticaria, arthralgia, asthma, and anaphylactic shock are rare

FIGURE 50-38  Back swimmer bugs have greatly elongated hind legs. (Courtesy Gari Weinraub.)

FIGURE 50-39  Triatomid feeding pattern.

sequelae of bedbug bites. Bites by aquatic hemipterans are similar to those of assassin bugs, but few cases have been described in detail.

TREATMENT AND PREVENTION Treatment is symptomatic and not particularly effective. Various antipruritic preparations are helpful in mild cases. Topical or intralesional steroids have generally been ineffective. Immobilization, elevation, and local heat are helpful in severe limb bites. Desensitization with triatomid salivary gland extract has been used in a small series of patients with history of life-threatening anaphylactic reactions.308 Triatomids and bedbugs are more difficult to eradicate with insecticides than are many other household insects. A wide range of empirical treatments, including antibiotics, antihistamines, topical and oral corticosteroids, and epinephrine, have been used for bite reactions with varying results. No evidence-based interventions to eradicate bedbugs or prevent bites have been identified.142 Benzene hexachloride has been effective against triatomids in Latin America.

Beetles and Other Insects Beetles (order Coleoptera) are the largest group of insects, with at least 250,000 species. The prothorax of beetles is generally very distinct, whereas the two posterior thoracic segments are more or less fused to the abdomen (Figure 50-40). In most beetles, the anterior wings are heavily chitinized, acting as covers for the posterior membranous wings used in flight. Mouthparts are of the chewing type. The life cycle involves larval and pupal stages before emergence of the adult. Many beetles feed on plants throughout their life cycle, many are predators or scavengers, and a few are parasitic. No beetles have a bite or sting venomous to humans, but several families have toxic secretions

FIGURE 50-40  Beetles (order Coleoptera) represent the largest group of insects.

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CHAPTER 50  Arthropod Envenomation and Parasitism

FIGURE 50-37  Giant water bug, Benacus griseus, a large insect common in aquatic habitats in the eastern United States.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 50-41  Spanish fly, Cantharis vesicatoria. (Courtesy Wikimedia Commons.)

that may be deposited on the skin. The blister beetles (family Meloidae) are a cosmopolitan group with numerous representatives in deserts and semiarid regions. A species may suddenly appear by the thousands, especially after rains, persist for a few days, and be replaced by another. The majority are of medium size (about 15 mm [0.5 inch]) and have soft, leathery forewings (elytra). Some are brilliantly colored. They are plentiful on vegetation, and some species are attracted to lights. A low-molecularweight toxin, cantharidin, is present in the hemolymph and most of the insect’s tissues. It is exuded from multiple sites if the beetle is gently pressed or otherwise disturbed. Cantharidin content of African meloid blister beetles were measured at values more than 6 mg per beetle, pointing to the high risk of severe and even fatal poisoning when ingesting these insects.230 In the eastern United States, blister beetle dermatitis is usually caused by Epicauta species, which reside on many garden plants. Contact with the beetle is painless and seldom remembered by the victim. Blisters appear 2 to 5 hours after contact and may be single or multiple, usually 5 to 50 mm (0.2 to 2 inches) in diameter and thin walled. Although not naturally found in the United States, the most well known blister beetle is the Spanish fly (Cantharis vesicatoria catoria) (Figure 50-41). Unless broken and rubbed, the blisters are not painful. Cantharidin dermatitis and nephritis have been reported after unusually heavy vesication but more frequently result from using a cantharidin preparation as an aphrodisiac. Darkling ground beetles are moderately large, dark, and heavily chitinized insects that assume a characteristic posture with head down and tail up when disturbed. They are found worldwide in arid regions, where they live under stones and other cover and crawl about at night. Most species can spray irritant secretions, mostly benzoquinones, from the tip of the abdomen to a distance of 30 to 40 cm (12 to 16 inches). These secretions are generally harmless to humans, but blistering of the skin has been reported, and eye injury is possible. No special treatment for beetle vesication is available. The injuries are best treated as superficial chemical burns. Local

A

preparations containing corticosteroids or antihistamines are not particularly effective. An outbreak of a blistering disease was reported in a military unit training in the Arizona desert during an unusual heavy rainfall and flooding. Staphylinid (rove) beetles (genus Paederus, family Staphylinidae) (Figure 50-42) were collected at the site. These beetles have been responsible for vesicular dermatitis in other parts of the world but before this series were never reported in the United States.66 Internationally, small rove beetles of the genus Paederus are troublesome in many tropical and subtropical regions. The whiplash beetle or Finch Hatton bug (Paederus australis) caused evacuation of an entire aboriginal community in northern Australia,250 and several cases of blistering dermatitis were reported in central Queensland.19 A large suburban hospital in Sri Lanka had 108 cases of painful dermatitis among members of its staff on night duty.197 More than 200 cases were reported in Turkey, resulting in lesions similar to bullous impetigo or infectious herpes zoster.360 The furniture beetle (Anobium punctatum) of France can give an unusual pruritic dermatitis associated with a specific clinical finding called the “comet sign,” likely secondary to the parasite Pyemotes ventricosus within the beetle.83 Pustular dermatitis epidemics from other staphylinid (rove) beetles related to the paederids have been reported in Nigeria in 1990, Egypt in 1994, Kenya in 1998 after sudden floods,66 and most recently in Pakistan among deployed U.S. military personnel.105 These beetles are slender with elongate abdomens and very short rectangular elytra. They frequent damp habitats and may be plentiful in irrigated crop fields. They usually fly after dark in hot, humid weather and are attracted to lights. Their vesicant secretion is an alkaloid present in greatest concentration in hemolymph; it is usually deposited on human skin when the beetles are pressed or crushed, but it may occasionally be spontaneously secreted. There is no immediate reaction to the secretion, but after 12 to 24 hours, painful erythematous lesions develop and soon become vesicular. The vesicles last 3 to 7 days and are followed by crusting and pigmentation. Conjunctivitis results if the secretion is rubbed into the eyes. This condition is known in parts of the world as “Nairobi eye” or “Christmas eye.”66 Some persons with extensive skin involvement may show generalized symptoms. Treatment is symptomatic and not very effective. Prompt soap-and-water washing after insect contact is recommended. Screening of sleeping and working quarters is the best prevention. Lady beetles (ladybugs, family Coccinellidae) are widely distributed and highly beneficial as predators on aphids and scale insects. Species in the eastern United States often overwinter in houses and do no harm. However, an Australian lady beetle, Diomus notescens, is reported to bite, causing papules with small necrotic centers.287 Two cases of human ear invasion by a predaceous beetle, Crasydactylus punctatus, or the carabid beetle, have been reported from Oman. One victim had a severe otologic injury caused by biting and chewing on the external auditory canal and tympanic membrane.26 Other types of insect envenomation are sporadic. Many insects that normally feed on plant juices occasionally inflict annoying bites. This behavior may be initiated by dehydration of the insect or by unknown factors. Small predatory insects, such as lacewing

B

FIGURE 50-42  Rove beetles, genus Paederus, family Staphylinidae. (A courtesy Trevor Jinks, Gold Coast, Australia; B from Wikimedia Commons.)

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FIGURE 50-44  Tsetse fly, Glossina species. (Courtesy David Bowles and Mark Pomerinke, U.S. Air Force.)

larvae, anthocorids, and Sclerodermus species, occasionally attack humans instead of their normal arthropod prey. Thrips may bite and produce itching macules.248 A small hemipteran, Leptodemus minutus, caused numerous cases of dermatitis in Kuwait.327 The stick insect, Anisomorpha buprestoides (Figure 50-43), a common species in Florida and adjacent states, ejects a noxious fluid from its thoracic region that deters birds and other predators. According to regional folklore, this fluid can be directed toward human eyes with painful consequences.

Most of these insects are cosmopolitan in distribution, except tsetse flies, which are restricted to Africa, and tropical and subtropical sand flies. Some species of mosquitoes and blackflies are adapted to cold temperate, sub-Arctic, and alpine environments, where their numbers may make areas uninhabitable during peak activity. Other mosquitoes and biting midges are equally abundant and annoying in some coastal areas and on islands. Two groups of biting flies and several species involved in human myiasis are largely confined to the tropics (see Table 50-1). Tsetse flies (Glossina species) are of great importance as vectors of human and animal trypanosomiasis in sub-Saharan Africa (Figure 50-44). Although not closely related to deerflies and other tabanids, they are similar in appearance and habits. Their life history is peculiar in that a single large larva develops in the uterus of the female and is expelled shortly before pupation, which takes place in the soil. Tsetse fly bites produce comparatively little local reaction other than brief pain and itching. Human African trypanosomiasis, also known as sleeping sickness, continues to pose major threat to 60 million people in 36 countries in sub-Saharan Africa. Transmitted by the bite of the tsetse fly, the disease is caused by the protozoan parasites of the genus Trypanosoma.184 Symptoms of sleeping sickness include abnormal sleep patterns, fever, body malaise, headache, and lymph node enlargement.191 Most patients can be treated successfully with melarsoprol.333

Diptera (Two-Winged Flies) Insects of the order Diptera are characterized by one pair of wings. What would have been a second pair is usually modified to form a pair of drumstick-like structures known as halteres. A typical life cycle consists of eggs, limbless larvae, pupae, and winged adults, but numerous variations exist. Mouthparts are of the sucking type. Females of many species, although free-living, take blood or other tissue fluids from vertebrates, injecting salivary secretions that are not intrinsically toxic but are potent sensitizing agents for most humans. Larvae of some Diptera are human parasites. Other adult Diptera feed indiscriminately on feces and human foodstuffs. These habits make them by far the most important arthropod vectors of human disease (Table 50-1).

TABLE 50-1  Major Groups of Biting Dipterans Insect

Recognition Features of Adult

Larval and Pupal Stages

Mosquitoes (Culicidae, subfamily Culicinae)

Prominent proboscis; wings with scales; palps of female much shorter than proboscis; usually rests with body parallel to substrate Prominent proboscis; wings with scales and often with dark mottling; palps of females about as long as proboscis; usually rests with head down and body held at an angle to substrate Stout; humpbacked; short antennae; wings broad, with most veins faint; body length >2.5 mm (0.12 inch) Small (usually >2 mm [0.1 inch] body length); hairy; wings with straight, prominent veins Small (>2 mm [0.1 inch] body length); wings often mottled; most wing veins faint

Aquatic in great variety of habitats; both larval and pupal stages motile

Mosquitoes (subfamily Anophelinae) Blackflies, buffalo gnats (family Simuliidae) Sand flies (family Psychodidae) Biting midges, sand flies, no-see-ums (family Ceratopogonidae) Horseflies, deerflies (family Tabanidae) Stable flies (family Muscidae) Tsetse flies (family Glossinidae) Snipe flies (family Rhagionidae)

Large (body length 5-25 mm [0.2-1 inch]) with large eyes; usually brilliantly colored; body stout; wings with prominent veins Similar to housefly in size and general appearance; sharp-pointed proboscis projects downward and backward Large (6-14 mm [0.25-0.5 inch]); proboscis projects forward; wings fold scissor-like over back Long legs; relatively slender body; large eyes; wings with prominent veins

Same as above Sessile in flowing water; usually attached to rocks and logs, sometimes to crustaceans In damp crevices, animal burrows, leaf litter In mud, wet sand, rotting vegetation; larvae very motile In mud or shallow water In decaying vegetable matter or urine-soaked straw Larvae complete most of development in female; pupate in soil a few hours after birth Aquatic; in moist soil or rotten wood

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CHAPTER 50  Arthropod Envenomation and Parasitism

FIGURE 50-43  Stick insect, Anisomorpha buprestoides, ejects a noxious fluid from its thoracic region that deters birds and other predators. (From http://www.penvalehouse.org.uk.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Mosquitoes (see Chapter 48) are characterized by a fringe of setae along the posterior margin of the wings and delicate scales along the wing veins. Only the females feed on blood. The prominent beak contains a kit of piercing and sucking tools. Most mosquitoes have body lengths of 3 to 4 mm (0.1 to 0.2 inches), but some large species may be about twice this size (see Table 50-1). The estimated 3000 species of mosquitoes are cosmopolitan in distribution. Carbon dioxide, body heat, and sweat gland secretions, especially apocrine, are attractants for mosquitoes; certain skin lipids are repellent.185 Children under 1 year of age rarely show a skin reaction to mosquito bites, but by age 5 nearly all are reactors. Both immediate and delayed types of hypersensitivity are induced. Typically, immediate pruritic wheals are followed by red, swollen, and pruritic lesions in 12 to 24 hours. These lesions are associated with both IgE and IgG antibody complexes and a lymphocyte response.278,297 All the classic types of immunologic injuries have been reported after mosquito bites, including injury from circulating immune complexes, asthma, and Arthus reaction.138,164 Seasonal bullous eruptions in a coastal area of Britain were ascribed to Aedes detritus. Most of those affected were women with varicose veins or deep vein thromboses. Intense skin reactions accompanied by fever, lymphadenopathy, and hepatosplenomegaly have been described and are associated with infiltration of skin lesions by natural killer lymphocytes.229 Nodular skin lesions lasting up to a month have been reported after mosquito bites in patients with acquired immunodeficiency syndrome (AIDS) receiving zidovudine.100 Papulovesicular lesions with eosinophil infiltration were reported following insect (including mosquito) bites in patients with lymphocytic leukemia.69 Among 21 Japanese patients with severe local and constitutional reactions to mosquito bites, seven died of malignant histiocytosis before age 28. Nine others retained hypersensitivity; three lost the reaction.164 Treatment of mosquito bites consists of local application of antipruritic lotions or creams. Antihistamines relieve the itching of early lesions but have no effect on later ones.296 Group I corticosteroid creams and ointments may be helpful. Desensitization with insect whole-body extract is difficult but occasionally successful.226 Prolonged heavy exposure to mosquito bites causes some individuals to lose sensitivity, occasionally in less than 1 year. Delayed hypersensitivity is lost more readily than is immediate hypersensitivity, with decreases in both IgE and IgG.279

BITING MIDGES (CULICOIDES) Biting midges are very small flies that have a bite out of proportion to their size. Only females feed on blood. The wormlike aquatic larvae usually develop in water-saturated soil; mangrove swamps are a common habitat. Larvae of some species use axils of banana and similar plants. The genus is cosmopolitan but presents the greatest problem in subtropical and tropical coastal regions. Activity is often seasonal. The flies bite most intensely in still air and reduced light. Bites are immediately painful and result in raised, red, and pruritic lesions that persist from a few hours to a week or more. Some victims develop vesicles, pustules, and superficial ulcers, particularly if bitten by the genus Leptoconops. Hypersensitivity is involved, although some persons seem to develop intense reactions on first exposure to the insects. Treatment of bites is symptomatic and similar to that for mosquito bites. Artificial hyposensitization has not been successful; however, spontaneous decrease in skin reactivity may occur in some individuals.

BLACKFLIES (SIMULIIDAE) Blackflies are small, stocky flies that have a characteristic humpbacked appearance. Adults prefer open and sunny areas and are good fliers. Not all species are anthropophilic. The sessile larvae and pupae are found in flowing water, from large rivers to small brooks. Blackflies are cosmopolitan, but their abundance and medical significance vary widely. They range well into the Arctic and constitute a major problem for both humans and domestic animals in parts of Europe, Canada, and the northern United 942

States. In the tropics they tend to be more localized, often remaining close to streams. Blackflies bite more commonly on the upper half of the body. They snip the skin and suck the pooled blood, leaving relatively large punctures that may bleed, a symptom rarely seen with bites of other small flies. The local pain, swelling, and redness that follow blackfly bites are unusually intense and persistent. Vesicles and weeping, crusted lesions may last for weeks. Systemic symptoms such as malaise, fever, and leukocytosis may occur. Enlarged indurated lymphatics, particularly in the posterior cervical region, are common in Canadian children living where blackflies are abundant. Blackfly bites can infrequently cause severe hyper­ sensitivity reactions and localized cellulitis, similar to those seen with Hymenoptera stings.264 Hemorrhagic symptoms have been reported in Brazil. Generalized urticaria, bleeding, angioedema, cough, wheezing, toxemia, and even death may occur.176,201,376 No specific treatment for blackfly bites is available. Hyposensitization has been attempted with little success. Neither repellents nor ordinary clothes provide satisfactory protection against blackflies when they are present in large numbers. Avoidance of heavily infested areas during fly season is often the most practical solution. Control measures have not proved highly effective. Onchocerciasis, also known as river blindness, is the world’s second leading infectious cause of blindness. It is caused by Onchocerca volvulus, a nematode that can live for up to 15 years in the human body. It is transmitted to humans through the bite of a Simulium blackfly. The worms spread throughout the body and when they die cause intense itching and a strong immune system response that can destroy nearby tissue, such as the eye. Treatment with ivermectin is recommended.5 Blackfly population control in Africa has evolved over the years. In the 1960s, DDT was used. In the 1970s and 1980s, water flow manipulation was instituted for better environmental preservation. In the 1990s and currently in Africa, the organophosphate temephos and toxins produced by the bacterium Bacillus thuringiensis have been tested and shown to be effective.251 Temephos is a nonsystemic organophosphorus insecticide used to control mosquito, midge, and blackfly larvae. It is used in lakes, ponds, and wetlands. It also may be used to control fleas on dogs and cats and to control lice on humans.

HORSEFLIES AND DEERFLIES (TABANIDAE) Horseflies and deerflies are medium to large (10 to 25 mm [0.4 to 1.0 inch] body length) stocky flies whose large eyes often are brightly colored. They are strong fliers and prefer open and sunny habitats. The tabanids attack a variety of large mammals, including humans. The predacious maggot-like larvae live in water-soaked soil or shallow water. Bites from these large flies, especially the deerfly (Chrysops species), are painful and may cause both external and subcutaneous bleeding. An itching wheal up to 1 inch in diameter develops but usually does not last long. In some victims, severe and prolonged swelling of the face or an extremity develops. About 30 cases of systemic anaphylactoid reactions have been reported. Patients with a history of systemic reactions to wasp stings had a similar reaction to a horsefly bite, commonly referred to as the wasp-horsefly syndrome.134,161,290 As with other fly bites, treatment is symptomatic. Hyposensitization has been attempted in a few cases, with some success.

OTHER BITING DIPTERA Sand flies (Lutzomyia vexator) are very small biting flies and the vectors for leishmaniasis, a protozoal disease of humans and dogs in regions of Asia, Africa, and South America. Recently, cases of visceral leishmaniasis have been reported in upstate New York with outbreaks in dog kennels.267 Leishmaniasis has also been described in Washington County, Texas.229 Sand flies are widely distributed in tropical and subtropical regions. They live in damp, shaded places such as mammal burrows, rock crevices, and cracks in walls of houses and other structures. Favorite habitats in Central America are gambas, which are deep clefts between the buttresses of large forest trees. Larval and pupal stages are found in moist detritus in holes and crevices. The adults usually emerge at night when air is still and temperatures are above

MYIASIS

A

B FIGURE 50-45  A, Stable fly life cycle. B, Stable house fly, Stomoxys calcitrans, dorsal view. (A and B courtesy Jim Kalisch, University of Nebraska-Lincoln Entomology Department.)

13° C (55° F). They are poor fliers. Sand fly human biting activity is typically highest between midnight and 3 AM.316 In addition to leishmaniasis, these flies are vectors of Bartonella bacilliformis in Peru and Brazilian Amazonia.84,262 Although the cutaneous form of the disease is often self-limited, it results in significant scarring and can spread to more invasive, mucocutaneous disease.272 Sand fly populations can be controlled with pyrethroid insecticide sprayed into the mounds and burrows. Spraying a 100-m (328-foot) wide barrier zone around a campsite can reduce sand fly numbers for an extended period.108 Other preventive measures include impregnated bed netting and clothing, specialized dog collars, and spraying residential dwellings and animal shelters. Glucantime has been shown to be effective against Old World cutaneous leishmaniasis when used in doses recommended by the World Health Organization (20 mg/kg/day for 20 days).121 A recent source describes vaccine development for prevention of sand fly fever.98 Snipe flies (Rhagionidae) prey primarily on insects, but some species, such as Symphoromyia, feed on the blood of mammals. Their habits and life history are similar to those of tabanids. Reactions to snipe fly bites range from pain to anaphylaxis. A person who reacts severely may be bedridden for days. The stable fly (Stomoxys calcitrans) (Figure 50-45) is related to the housefly, which it closely resembles. It is plentiful throughout most of the United States, particularly in agricultural districts. Eggs are deposited in piles of decaying vegetation, where the larvae develop. Thunderstorms seem to stimulate fly activity, which accounts for the widespread belief that houseflies bite just before a storm. Bites cause a sharp, stinging sensation, but dermal lesions are uncommon. Itching is transient. Louse flies (Hippoboscidae) are peculiar Diptera that may lack wings entirely or have them for only part of their adult life. The wingless forms are flat, leathery insects that resemble lice or ticks. They are ectoparasites of birds and mammals. Larvae are carried in the uterus until development is almost complete; the pupal stage may be spent in the soil or on the host. The sheep ked (Melophagus ovinus) is a common species in the United States and sometimes bites sheep shearers and handlers. The related deer ked (Lipoptena cervi) is a seasonal pest in wooded

The term myiasis for parasitism by fly larvae was introduced into the medical literature in 1840, although the condition has been observed since antiquity. More than one hundred species of Diptera have been reported to cause human myiasis.239 Some are obligate parasites, for which humans are one of several hosts; some are opportunistic invaders that find parasitism an alternative to feeding on decaying tissue or its products. Nevertheless, humans are not a particularly good host for most species of fly larvae, and many infections terminate prematurely. Sensitization of host tissues to fly larvae does not occur as readily as with many other arthropod and helminth parasites. Myiasis may be classified by clinical manifestations or etiologic agents. This chapter discusses only dermal and wound myiasis.260 Myiases that involve primarily the gastrointestinal tract, urinary tract, eye, and nasopharynx are not covered. Furuncular Myiasis.  In furuncular myiasis, the fly larva penetrates the skin but remains sedentary, producing a boil-like lesion that usually has a central opening. Here the larva completes its development but typically emerges to pupate outside the host. As a human problem, this form of myiasis is largely confined to the tropics, although imported cases are being recognized in increasing numbers in other regions of the world, particularly in North Americans who travel to more southern tropical regions.221 A German travel clinic reported 13 cases in travelers returning from tropical countries during a 3-year period.178 Tourists and divers recreating in tropical regions of Mexico, South and Central America, and Trinidad are also at risk.18 The classic agent of furuncular myiasis is the so-called human botfly, Dermatobia hominis (Figure 50-46). Humans, however, are only one of many mammals that serve as suitable hosts for the obligately parasitic larvae of this fly. It is widely distributed in the American tropics and is an important parasite of domestic cattle in many places. The adult fly resembles a bumblebee (body length, about 15 mm [0.6 inch]). It does not feed and is infrequently seen. The life cycle of this fly is unique in that the female attaches her eggs to the body of another arthropod for transfer to the host. Large mosquitoes of the genus Psorophora are often used (8% were found bearing Dermatobia eggs in one study), but about 40 other species of insects and ticks have been reported to be egg carriers. When the carrier alights on a mammal, the eggs hatch immediately, and the larvae enter the skin through the bite of the carrier or some other small trauma. Small larvae are fusiform and later become pyriform to ovoid as they reach full development at lengths of 15 to 20 mm (0.6 to 0.8 inch). They are encircled by several rings of spines. The larval stage

FIGURE 50-46  Dermatobia larva.

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sections of northern Europe, causing hundreds of cases of dermatitis annually. The pigeon fly (Pseudolynchia canariensis) is an avian parasite that sometimes infests buildings and bites the occupants. Lesions from hippoboscid bites appear 1 to 24 hours after the bites as reddish itching papules that may persist for up to 3 months. Topical corticosteroids may afford symptomatic relief and hasten resolution of the lesions. Repellents are reported to be ineffective against these insects.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

lasts 6 to 7 weeks, after which the larva emerges from the skin and drops to the ground, where pupation occurs. Infection is fairly common among rural people of Central America. Cases in returned tourists and visitors from Latin America have been diagnosed in many parts of the United States. Six cases occurred in one group of tourists visiting archaeologic sites in Guatemala.46,173,199,271,347 Lesions may be on any part of the body exposed to insect bites and may be single or multiple. An initial pruritic papule becomes a furuncle, with a characteristic opening from which serosanguineous fluid exudes. Pain often accompanies movements of the older larvae, but the lesion is not particularly tender to palpation. Lymphadenopathy, fever, and secondary infection with systemic inflammation are less common.363 This form of myiasis should be suspected in patients with furuncular lesions and a history of residence or travel in endemic areas. It must be differentiated from leishmaniasis and onchocerciasis, which have a different prognosis and treatment. The sensation of movement within the lesion, accompanied by pain but little tenderness or inflammation, suggests myiasis. The tip of the larva may protrude from the central opening, or bubbles produced by its respiration may be seen. Often, simple pressure will extrude the organism, particularly if it is small.263 Occlusion of the breathing hole may cause the larva to emerge sufficiently for it to be grasped and withdrawn.81 An effective folk remedy is binding a piece of fat, such as bacon, over the opening.40 This often causes the larva to leave its burrow. Another technique is injection of about 2 mL of a local anesthetic into the base of the lesion, thus extruding the larva by fluid pressure. If these methods are unsuccessful, surgical excision under local anesthesia is indicated (Figure 50-47). Whatever method is used, care should be taken not to break or rupture the larva. This may cause a strong inflammatory reaction, often followed by secondary infection. Repeated infections tend to confer some immunity that may abort larval development. Screens, protective clothing, and use of insect repellents are helpful in preventing infestation. Furuncular myiasis in tropical Africa is caused by the tumbu fly, Cordylobia anthropophaga (Figure 50-48). The larval stage

FIGURE 50-48  Furuncular myiasis. (Courtesy Capt. Randall L. Goodman, USAF,MC: Anterior orbital myiasis caused by human botfly [Photo Essay], Arch Ophthalmol 118:1002, 2000.)

of this fly is an obligate parasite of many mammals, but rats and dogs are the most important epidemiologically. The adult is about the size of a housefly, but stockier. It prefers shade and is most active in early morning and afternoon. Females lay eggs on dry sandy soil or on clothing. They are attracted by the odor of urine. The eggs hatch in 1 to 3 days, and hatchling larvae can survive up to 2 weeks waiting for contact with skin of a suitable host. They can penetrate unbroken skin. They become fusiform to ovoid and reach a length of 13 to 15 mm (0.5 to 0.6 inch). The larval stage is completed in 9 to 14 days. Human infections occur in most nations of sub-Saharan Africa. Transmission increases during the rainy season. Among indigenous peoples, infection is most frequent in children, as adults evidently acquire some immunity. Infections among Americans and Europeans visiting Africa are reported regularly.177,178,318 Lesions may be on any part of the body but are more common on the legs and buttocks. The furuncles are discrete, elevated, and nontender and have a central opening. The number of lesions, up to about 50, is greater than with Dermatobia. Infections in children have been mistaken for chickenpox,258 but the course of the infection is much shorter. An exceptionally heavy infection (about 150 larvae) was caused by Cordylobia rodhaini, normally a parasite of forest mammals. It was accompanied by lymphadenopathy, leukocytosis, and elevated IgA. Clothing left to dry on the ground was the presumed source of the parasites.273 Principles of diagnosis and treatment are much the same as for Dermatobia. Avoidance of skin contact with potentially contaminated soil and ironing of clothing and bedding after open-air drying are preventive measures that often are difficult to achieve. FIGURE 50-47  Multiple images of botfly larva being removed from a child’s eye.

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Hematophagous Myiasis.  The sole cause of hematophagous myiasis is the Congo floor maggot, Auchmeromyia luteola. It is dark, distinctly segmented, ovoid, and 15 to 18 mm

Migratory Myiasis.  One type of migratory myiasis is caused by flies of the genus Hypoderma. Adult flies are large and hairy, resembling bumblebees. Normal hosts for the parasitic larvae are cattle, deer, and horses. The flies attach their eggs to hairs. Hatchling larvae penetrate the skin and wander extensively through the subcutaneous tissues, eventually locating under the skin of the back, where they produce furuncular lesions. The condition has veterinary importance. Humans are abnormal hosts in which the parasite is unable to complete its development. Human infections usually occur in rural areas where cattle and horses are raised and are more common in winter. Larvae migrate rapidly (as much as 1 cm/hr [0.4 inch/hr]) and erratically through subcutaneous tissues, producing intermittent, painful swellings over months. The person often senses larval movement. Larvae respond negatively to gravity, so the last lesions are usually on the head or shoulders. Eosinophilia (up to 35% eosinophils on white blood cell differential) and angioedema may be seen. Larvae may emerge spontaneously from furuncles or may die in the tissues. In rare cases, larvae were seen to have invaded the pharyngeal region, orbit, and spinal canal. Another form of migratory myiasis is caused by larvae of Gastrophilus, which normally are gastrointestinal or nasal parasites of horses (Figure 50-49). In human infections, which are reported more frequently from Europe than from the United States, the young larvae burrow in the skin, producing narrow,

FIGURE 50-49  Larvae of the botfly Gastrophilus haemorrhoidalis from a horse’s stomach.

CHAPTER 50  Arthropod Envenomation and Parasitism

(0.6 to 0.7 inch) long, and it assumes the larval stage of a moderate-size yellowish fly. It is widely distributed in subSaharan Africa and is essentially a human parasite. It is unique among parasitic fly larvae in living apart from its host in the earthen floor of native dwellings. It seeks persons lying or sitting on the floor or on mats and feeds intermittently on blood, usually at night. The bites are trivial but may interfere with sleep. Sensitization appears to be uncommon. Autochthonous furuncular myiasis may occur in the United States, usually in children. Most cases are caused by larvae of botflies of the genus Cuterebra, whose normal hosts are small rodents and rabbits. The fly eggs are attached to low vegetation and hatch on contact with skin of the host. Adult human skin seems impervious to them, but that of children may be penetrated. There is usually a history of outdoor play in weeds or grass or with a pet rabbit. In one case, eggs were apparently deposited directly on the skin.140 Lesions typically develop on the head, neck, or chest in 1 to 2 weeks. Once recognized, the larvae can often be removed by simple pressure.130,332 The syndrome may also be caused by larvae of Wohlfahrtia vigil, a large fly native to Canada and the northern United States. Its normal hosts are newborn mammals, particularly mink, dog, and fox. The fly deposits larvae on the skin, which penetrate in about an hour. Human infections are typically in infants under 9 months, and the furuncular lesions are usually on the face. Fever, irritability, and loss of appetite are common. Larvae can usually be expressed from the lesion; surgery rarely is necessary. Netting over the crib or pram when outdoors usually affords protection.

A

B FIGURE 50-50  A, American (New World) screw-worm fly, Cochliomyia. B, Asian-African (Old World) screw-worm fly, Chrysomyia.

tortuous, reddish, and linear lesions with intense itching. Lesions usually advance 1.5 cm/day (0.6 inches/day), but more rapid progress has been reported. Death of the larvae terminates the infection in 1 to 2 weeks without sequelae. This infection is clinically similar to creeping eruption, an invasion of the skin by larvae of the hookworms Ancylostoma braziliense and Ancylostoma caninum. The helminthic parasitosis occurs more often in warm, moist regions, including the southern United States, and is associated with dogs and cats. The myiasis is seen more frequently in cooler regions and is associated with horses. Definitive diagnosis can be made only by removal of the parasite from its burrow and microscopic examination. Removal of the larvae by surgery or expression is the usual treatment for migratory myiasis, although local freezing of cutaneous burrows is sometimes successful. Ivermectin given to a patient with Hypoderma myiasis resulted in expulsion of the larva.178 The most effective prevention is control of the infections in domestic animals. Wound Myiasis.  About 85% to 90% of cases of wound myiasis are caused by larvae of flies of the family Calliphoridae, which includes both obligate parasites and opportunists. The most dangerous type of myiasis may be caused by larvae of the screwworm flies—Cochliomyia americana (formerly Callitroga hominivorax) (Figure 50-50, A) in the Americas and Chrysomyia bessiana (Figure 50-50, B) in Asia and Africa. The adults are rather stocky flies, 8 to 12 mm (0.3 to 0.5 inch) in body length, and metallic blue-green to purplish black. The parasitic larvae are pinkish, fusiform (providing the common name), and strongly segmented. Length at maturity is 12 to 15 mm (0.5 to 0.6 inch). They are obligate parasites whose chief hosts are cattle, sheep, and goats. They are a major cause of economic loss among livestock. Enzootic areas are mostly in the tropics and subtropics; in the past, summer infections have occurred as far north as Colorado and Nebraska. Female flies deposit eggs near any break in the skin or around the nose, mouth, or ears if a discharge is present. Larvae invade healthy 945

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 50-51  Scalp myiasis appearing as pediculosis capitis. (From http://www.spc.int/rash/munual/images.)

tissue, often causing considerable damage. The larval stage lasts 4 to 8 days, and the entire cycle is 15 to 20 days in enzootic areas. Screw-worm has been eradicated in the southern United States and some other areas primarily through the release of large numbers of laboratory-bred male flies sterilized by gamma irradiation. Females mate only once, so mating with a sterile male nullifies the female’s reproductive effort, greatly reducing the population. Flies may be dispersed by prevailing winds. Infection is often acquired while resting outside during the day or may result from trauma.233 Lesions may appear on any exposed parts of the body. Lesions on the scalp may be associated with pediculosis capitis (Figure 50-51). Typical dermal lesions are ulcers or sinuses that may contain up to 200 larvae. These are surrounded by a zone of induration (Figure 50-52). Pain is variable. Secondary bacterial infection is common. Tissue destruction may be extensive and mortality is associated with nasopharyngeal invasion. Irrigation of the wound and mechanical removal of larvae are generally sufficient for treatment. Topical application of 5% chloroform in olive oil followed by irrigation and manual removal of larvae is often adequate in dermal infections. Deeper nasopharyngeal and orbital infections require surgery. Antimicrobial therapy as dictated by culture and sensitivity tests is often necessary. The most effective prevention is elimination of the disease in domestic animals. Opportunistic invasion of wounds by fly larvae is often seen during war and natural disasters, when injured persons are exposed to flies and medical facilities are inadequate to cope with the emergency. Wound myiasis may also be seen sporadically in nursing homes and hospitals and often is not reported for cultural and medicolegal reasons.48 Six of 14 cases in one series were acquired in the hospital. Eleven patients were older than age 63 years, and nearly all had underlying problems, such

FIGURE 50-52  Wound myiasis. (From http://www.icb.usp.br.)

as diabetes or peripheral vascular disease. Most of the infected lesions were on the feet or ankles.99 In another series of 16 cases, most victims were debilitated and older than age 65. Men were affected more often than women. Seven species of flies were involved.237 Fifty Lucilia larvae were removed from the nose, mouth, paranasal sinuses, and enucleated eye socket of a hospitalized patient left in a room with an open window.77 The most common fly species involved are Lucilia (green-bottle flies) (Figure 50-53), Calliphora species (blue-bottle flies), Phormia regina (black blowfly), Sarcophaga haemorrhoidalis (flesh fly), and Musca domestica (housefly). The flies, whose larvae normally feed on decaying animal tissues, often deposit eggs or larvae in wounds or around body orifices if a malodorous discharge is present. The larvae feed on necrotic tissue, and damage to healthy tissues and secondary infection are uncommon. They actually may debride wounds, and “maggot therapy” with aseptically bred larvae was briefly used in the 1930s. More recently, laboratory-bred fly larvae were used to debride venous stasis ulcers and other superficial necrotic areas when antibiotic therapy and surgical debridement were unsuccessful.331,343 Maggots serendipitously present have been used to debride lesions.291,238 Diagnosis is usually obvious on inspection of the wound. Species identification often requires the larvae to reach maturity. If this is not feasible, examination of the spiracular plates on the last segment of the larva and the chitinized oral structures usually permits adequate identification.

FIGURE 50-53  Green-bottle fly, Lucilia. (From Wikimedia commons.)

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SPECIES, LIFE CYCLE, AND DISTRIBUTION Lice are small wingless insects that are ectoparasites of mammals. They are mostly host specific, and two species are human parasites: Pthirus pubis (pubic louse)136 and Pediculus humanus, the latter with two varieties, Pediculus humanus capitis (head louse) and Pediculus humanus corporis (body louse).194 They are obligatory parasites, subsisting on blood from the host, and have mouthparts modified for piercing and sucking. The mouthparts are drawn into the head of the louse when not in use. The number of head lice infestations occurring annually in the United States is estimated at 6 to 12 million.372 The adult head louse is about 2 to 4 mm (0.1 to 0.2 inch) long with an elongated body that is flattened dorsoventrally (Figure 50-54).305 The head is only slightly narrower than the thorax. The three pairs of legs are about equal in length and possess delicate hooks at the distal extremities. The entire life is spent on the host’s body. The eggs (nits) are deposited on hair shafts, generally one nit to a shaft (Figure 50-55). The nits hatch in about 1 week, and the freshly hatched larvae, which must feed within 24 hours of hatching or die, mature in about 15 to 16 days. The adult female lives for approximately 1 month and may deposit more than 100 eggs during her reproductive life. Body lice are slightly larger than head lice but are similar in appearance with a similar life cycle, although the nits are deposited on fibers of clothing. Head lice and body lice interbreed. Pubic lice maintain a worldwide parasitic population infesting 2% to 10% of human populations.9 Adult pubic lice are about 1 to 2 mm (0.04 to 0.07 inch) long, the head is much smaller than the thorax, and the broadly oval body is flattened dorsoventrally (Figure 50-56). The anterior legs are much shorter than the second and third pairs, and the insect resembles a miniature crab. Nits are deposited on hair shafts, often several per shaft, and the egg-to-egg life cycle is approximately 1 month.

A

FIGURE 50-55  Unhatched nit of the head louse, Pediculus capitis. (Modified from Roberts RJ: Head lice. N Engl J Med 346:1646, 2002.)

Lice are found wherever people are found. Able to exist only briefly away from the human body, lice are spread by close personal contact and by sharing of clothing and bedding. The various species not only have a particular host but often prefer a particular part of the host’s body, so generalizing about transmission of the three varieties that parasitize humans is impossible. During biting and feeding, secretions from the louse cause a small red macule. Severe pruritus and marked inflammatory responses to bites are caused by the sensitization that occurs after repeated exposure to bites. Thus a victim may have lice for weeks before pruritus becomes marked. Not all people are equally attractive to lice, possibly because of differences in odor and chemical composition of sweat. Lice are medically important as vectors of systemic illnesses, as well as for dermatitis and discomfort.

CLINICAL ASPECTS The head louse localizes on the scalp and rarely on other hairy areas of the body. Children are most frequently affected, but adults, particularly women, may also be affected. Lice are particularly common in young girls, possibly because of their long hair. Infestation is uncommon in blacks, at least in the United States, probably because the shaft of African hair has an oval cross section that makes it difficult for the louse to grip while depositing eggs. However, pediculosis capitis is found in Africa, where the indigenous head louse is adapted to grip the oval hair shafts. Because nits initially attach to the hair shaft close to the skin and are carried higher as the hair grows, the presence of nits near the tips indicates a longstanding infestation. Itching is the principal symptom, and physical findings vary with duration and extent of the infestation, cleanliness, excoriations, and degree of secondary infection. Diagnosis is established by identifying nits and lice. It is not always easy to find lice, especially in early and mild cases, when they may be few in number. Lice are very active, but nits are always present and easy to identify. Nits are whitish ovals, about 0.5 mm long, and attach firmly to one side of the hair. Flakes of dandruff, which resemble nits superficially, are not attached to the hair shafts. Occipital and posterior cervical adenopathies are common and may be present even in less severe cases. A pruritic scalp

B FIGURE 50-54  A, Full-grown human head-louse, Pediculus humanus capitis. B, Adult louse embedded in scalp skin. (Modified from Roberts RJ: Head lice, N Engl J Med 346:1646, 2002.)

FIGURE 50-56  Pubic, or crab, louse, Phthirus pubis, grasping a hair.

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CHAPTER 50  Arthropod Envenomation and Parasitism

Lice (Order Anoplura)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

accompanied by adenopathy should prompt a thorough search for lice and nits. In severe cases, oozing and crusting may be present, sometimes with matting of the hair, and lice may be numerous. The body louse lives chiefly in the seams of clothing and is rarely seen on the skin. These lice leave clothing to feed on the skin or remain attached to the clothing while feeding, and thus are most abundant where clothing abuts the skin (e.g., at the belt line). The bite results in a small red macule with a characteristic central hemorrhagic punctum. Excoriations, crusts, eczematization, and other secondary lesions generally obscure the primary lesions by the time the victim seeks medical attention. Shoulders, trunk, and buttocks are favorite sites for bites, and parallel scratch marks on the shoulders are a common finding. The diagnosis is confirmed by identifying parasites or nits from the clothing. Bands of trousers, side seams, and underarm seams are sites of preference. Untreated cases may persist indefinitely, and massive infestations are sometimes seen in the homeless who have no ready access to frequent laundering or change of clothing or who cannot bathe regularly. Pediculosis pubis is usually acquired during sexual activity, and it may be a marker to search for other sexually transmitted diseases.194 It may result from unchanged bedding or nonsexual activity, either from lice that live briefly away from the human body or from egg-infested pubic hairs that are shed. The lice localize principally in the pubic hair, but are found occasionally in eyebrows, eyelashes,220,282 and axillary hairs. Adult pubic lice are not active and hug the skin at the bases of the hair shafts, with their heads buried in the follicular orifice. They are not easy to find, but one or more can usually be found if suspicion of the diagnosis is strong enough to prompt a thorough search. A loupe is helpful. Nits are more easily found. Primary bite lesions are almost never seen, but intense pruritus and pubic scratching are pathognomonic. The secondary infection, crusting, oozing, excoriations, and eczematization that often accompany head and body lice are rarely seen with pubic lice. Peculiar steel-gray macules (maculae caeruleae) may appear in association with some cases of pubic lice. These lesions do not appear until the infestation has been present for several weeks and are most common on the trunk and thighs.

TREATMENT AND PREVENTION Treatment of all types of lice strives to eradicate lice and nits and prevent reinfestation. Head lice may be treated with one application of 1% permethrin cream rinse (Nix) or 0.5% malathion lotion (Ovide).234,372 Most studies suggest that permethrin 1% is the most cost-effective treatment.153 Hair should be washed, rinsed, and dried, and the rinse is applied for 10 to 20 minutes before being washed off. Isopropyl myristate 50% in cyclomethicone solution (Full Marks Solution) is a new fluid treatment with a physical mode of action that uses a 10-minute contact time.356 A finetoothed comb may be used to remove nits after rinsing. Failure to remove all the lice is a frequent cause of treatment failure. Combing should be repeated in 1 to 2 days to confirm treatment success. A louse detection comb is a more effective method than visual screening for diagnosis.15 If lice are found after 7 days, retreatment is indicated. Household members and those in close contact with the patient should be screened for head lice and treated simultaneously if indicated. Extensive environmental cleanup is probably not warranted, although combs and brushes should be discarded or thoroughly washed with hot water.305 Hats and scarves should be machine-washed in a hot cycle and bed clothing dry-cleaned. Spraying or fogging a home with insecticide or pediculicides is not recommended.259 A child can return to school immediately after completion of the first proper application of an effective insecticide regardless of the presence of nits. This will avoid unnecessarily missing multiple days of school (and work days for the parents) as well as relieving public overreaction and hysteria.137,305,317 Regular weekly detection combing is recommended for up to 7 weeks after the first cure. Other pediculicides are available if the lice are resistant. Two products, RID and Triple X, contain 0.3% pyrethrins and 3.0% piperonyl butoxide. One application of either preparation usually eradicates both lice and nits. A few persons may require another 948

application 7 days after the initial treatment.27 Alcoholic formulations or vehicles of these products are flammable until dry. Lindane 1% (hexachlorocyclohexane, Kwell) may be used on persons who fail to respond or who are intolerant of permethrin. Kwell, which was formerly the medication most often used in the United States for treatment of louse infestations, is no longer recommended in children because of its safety profile, and it has been pulled off the shelves in many states.124 Lindane penetrates human skin and has potential for central nervous system toxicity manifesting as seizure activity. It is contraindicated in children and must be used with strict guidelines in older patients resistant to other treatment measures.372 Malathion (0.5% Ovide lotion) is an organophosphate and one of the only products that has retained its efficacy and safety profile over time. It is usually effective after one 20-minute application.234,372 However, this insecticide preparation is not recommended in children younger than age 2 years.305 Alternative treatments contain pyrethrums and piperonyl butoxide as active ingredients. Newer dry-on, suffocation-based pediculicide lotions are now being introduced that accomplish their mission without using neurotoxins, the need for nit removal, or extensive household cleaning. The results are comparable or superior with the efficacy of other pediculocides.276 Some sources warn that treatment failures may not result from improper application, noncompliance, or reinfestation but from increasing drug resistance,49,253 particularly in underdeveloped countries.102,110 Ivermectin, a macrocyclic lactone antibiotic highly effective against filarial worms, Strongyloides, and scabies (see later), has recently been demonstrated to be effective against lice both topically and orally.50,92 Body lice may be treated with the same medications, but parasites and nits are not generally found on the skin. Eradication of these from the clothing is the primary objective. Treatment includes bathing, laundering all clothing, and changing to fresh clothes free of lice and nits. Dry cleaning eradicates lice and nits, as does ordinary laundering on hot settings. Malathion preparations and gamma-benzene hexachloride formulations may be used for mass delousing. Pubic lice may be treated with the same medications used for head lice. Treatment consists of permethrin 1% cream rinse applied for 10 minutes and rinsed. Sexual partners should also be treated.125 Crotamiton lotion rubbed into the affected area daily for several weeks to destroy hatching ova may also be used. Eyelash infestations may be managed with physostigmine ophthalmic ointment using a cotton-tipped applicator. Machine washing and drying of sheets and clothing on hot settings will kill lice and nits.

Fleas (Order Siphonaptera) SPECIES, LIFE CYCLE, AND DISTRIBUTION Fleas are small ectoparasites of mammals and birds. The wingless body, which is covered by a hard shiny integument, is compressed laterally, enabling the fleas to scurry easily among hairs and feathers of the hosts. They are active insects with legs adapted for jumping, capable of prodigious leaps. Adult fleas subsist on blood. Some species must obtain blood from one particular host, others are less host specific, and all have mouthparts adapted for piercing and sucking. The eggs are laid on or near the host and drop to the ground as the host moves about or shakes. They hatch into small wormlike larvae that feed on droppings from adult fleas, flakes of dried blood from the host, and other organic matter. The life cycle varies among species and may vary considerably within the same species, because each developmental stage is influenced by prevailing temperature and humidity. The customary larval stage of 9 to 15 days may be prolonged for months by adverse conditions, and the pupal stage varies from a week to nearly a year. Individual adult fleas may live for years when circumstances are favorable and can live for months without feeding. Fleas exist universally, although the distribution of various species is restricted by climate and host. They are of medical importance because of the discomfort resulting from their bites, as a cause of papular urticaria, and as vectors of disease. They are more active in warm weather and cause more problems

Burrowing Flea Flea infestations tend to be similar clinically and associated with the distribution of animal hosts. However, one flea, Tunga penetrans, is responsible for a distinctive infestation known as tungiasis (Figure 50-57).377 The flea has a number of common names: burrowing flea, chigo, sand flea, and jigger.163 Infestation is common in Central and South America and in Africa, where the burrowing flea is widely distributed, but the incidence in the United States is rising as increasing numbers of tourists visit international exotic destinations.58 Vacationers who go barefoot on beaches in tropical Africa, South America, and subtropical Asia risk infestations.254 One resident of New York City developed lesions of tungiasis on her toes after visiting several countries in

East Africa, where she frequently wore sandals in rural areas.382 In Brazil, tungiasis is endemic in some resource-poor communities where domestic and sylvatic animals act as reservoirs for this zoonosis.281 The primary lesions of tungiasis are produced by the female flea. As soon as it is impregnated, it burrows into the skin until only the posterior end protrudes. Sucking blood, the insect becomes as large as a small pea and deposits eggs that fall to the ground. Lodged in the skin, the gestating female produces a firm itchy nodule, with the posterior end of the flea visible as a dark plug or spot in the center of the nodule. Lesions occur most often on the feet, buttocks, or perineum of persons who wear no shoes or frequently squat, because the burrowing flea is not a good jumper and abounds in the dusty soil surrounding human habitations. If the infestation is extensive, numerous papules may aggregate into plaques with a honeycomb appearance. After penetration under the nails of the feet, the ectoparasite enlarges and lesions become painful.35 Secondary infections become painful or even crippling, and severe infections may lead to death. If the burrowing flea is not removed, the pustule ruptures, leaving an ulcer. Wearing shoes prevents most cases of tungiasis.

CLINICAL ASPECTS The appearance of flea bites is not diagnostic, and the clinical features depend on the degree of sensitivity. A bite produces a small, central hemorrhagic punctum surrounded by erythema and urticaria. A small wheal at the bite site may be nonallergic because of primary urticariogenic substances in the flea saliva, but increasingly severe reactions are caused by sensitization to substances in the saliva. Bullae or ulcerations may result from flea bites in highly sensitive individuals. Flea bites are intensely pruritic, and scratching often results in crusting and impetiginization. Fleas have a habit of sampling several adjacent areas while feeding, and bites characteristically appear in irregular groups. Feet, ankles, and legs, as well as the hips and shoulder areas, where clothing fits snugly, are favorite targets. Although an

FIGURE 50-57  A to E, Tungiasis. B and C, Involvement of fingers. D and E, Toes and heel. (Courtesy Armed Forces Pest Management Board from World Health Organization Feldmeier H, Eisele M, Sabóia-Moura RC, et al: Severe tungiasis in under-privileged communities: case series from Brazil, Emerg Infect Dis 9:949, 2003.)

B

A

D

C

E 949

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in warmer climates with a longer breeding season, such as the southwestern United States. They are a particular nuisance in California. High standards of sanitation and personal hygiene in developed countries have discouraged the human flea, Pulex irritans, while at the same time, the popularity of household pets has been conducive to proliferation of dog and cat fleas, Ctenocephalides canis and Ctenocephalides felis. The incidence of other species on mammals and birds remains high. Because dog, cat, and many other fleas are only partially host specific, fleas associated with many mammals and birds cause disease in humans. Most current flea-bite problems are caused by animal fleas. Hungry fleas are more often attracted to people from an area frequented by an animal than from the animal itself. If the family dog is absent, hordes of hungry fleas may persist for months. Consequently, anyone with pet cats or dogs or near domesticated animals is more likely to be bitten, but outbreaks in the absence of pets are common. One epidemic of flea bites among children in a day nursery was traced to dog fleas in a deserted fox nesting area beneath the building.309 Another outbreak among poultry workers was caused by an infestation of hen fleas, Ceratophyllus gallinae.354 Fleas from flying squirrels also have been documented as the source of bites.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

individual lesion produced by a flea bite is not diagnostic, the typical clinical picture of grouped multiple bites is generally sufficient to establish a diagnosis, which is usually confirmed by locating and identifying fleas.

TREATMENT AND PREVENTION Ordinary flea bites require symptomatic treatment directed at relief of pruritus and prevention of secondary infection. Corticosteroid creams or calamine lotion with phenol, systemic antihistamines, and antibiotics are helpful when indicated, but the management of flea bites consists largely of prevention. The animals that host the fleas must be treated, as well as such places as chicken coops, rat nests, sleeping sites for dogs and cats, and often dwellings where pets live. Many effective insecticides are available. Typically, N,N-diethyl-meta-toluamide (DEET; also called diethyltoluamide), pyrethrins, piperonyl butoxide, and D-trans-allethrin are ingredients in sprays and foggers. An insect spray containing permethrin may be effective. Spraying or dusting must eradicate not only adult fleas but also the many larvae and pupae in grass, carpet, floorboards, furniture, and beds. Carbaryl and Malathion are the active ingredients in many sprays and dusts, and the services of professional exterminators may be necessary. Veterinary prescriptions are available for control of fleas on dogs and cats. Preparations containing 9.1% imidacloprid (Advantage) eliminate or reduce fleas on dogs when applied to the skin; 98% to 100% of fleas are killed within 12 hours of application, and reinfesting fleas are killed for 4 weeks after a single application. An oral preparation used for both dogs and cats contains lufenuron, an inhibitor of insect development. Lufenuron does not kill adult fleas, but rather controls flea populations by interrupting the life cycle at the egg stage. Cases of burrowing fleas should be treated promptly. One method is curettage of each nodule under local anesthesia, with concomitant use of systemic antibiotics to prevent secondary infection. Ether pledgets applied to the skin will kill fleas before curettage is begun. Where burrowing fleas are endemic, eradication is important. Floors must be swept free of dust, and insecticides may be sprayed or dusted.

Mites (Class Arachnida, Order Acarina) SPECIES, LIFE CYCLE, AND DISTRIBUTION Mites make up the largest group in the class Arachnida. Most are small arthropods, and many are barely visible. Mites have two body regions, a small cephalothorax and a larger, unsegmented abdomen. The cephalothorax and abdomen are broadly joined, giving most mites an oblong to globular appearance. Newly hatched larvae have three pairs of legs, and larvae acquire a fourth pair after the first molt. Mites are highly diverse. Some are parasitic, with both vertebrates and invertebrates serving as hosts; some are scavengers, some feed on plants, and many are free living and predacious. Although most species are oviparous, some are ovoviviparous, and a few are viviparous. They occur worldwide and frequently in great numbers. Mites have been associated with disease transmission, allergies, and dermatologic manifestations. Of the approximately 35,000 species, about 50 are known to cause human skin lesions, and most of the cutaneous lesions are caused by mites feeding or burrowing in the skin. Because children and adults of all races are susceptible to these ubiquitous arthropods, they are responsible for considerable morbidity. The mites of medical importance are some of the sarcoptic mites, some of the trombiculid mites, a number of other acariform mites that infest organic substances such as grains and produce, and the gamasid mites that are vectors of several rickettsial and viral diseases. Dermatologic manifestations of mite bites may be seasonal, as with the trombiculids; individual cases or outbreaks of varying magnitudes may be related to contact with mites that infest animals or various foods. Epidemics may occur, as is presently the case with scabies. 950

SCABIES Life Cycle.  The human scabies mite is Sarcoptes scabiei var. hominis, an obligate human parasite that completes its entire life cycle in and on the epidermis of humans (Figure 50-58). Unless treated, scabies can persist indefinitely. The adult female is responsible for the symptoms accompanying the infestation. After impregnation, she burrows into the epidermis and remains in the burrow for a life span of about 1 month. She slowly extends the burrow, feeding during travel, during which time several eggs are deposited daily. The ovoid female mite is approximately 0.3 to 0.4 mm long. Numerous transverse corrugations and dorsal spinous processes are adaptations to prevent backward movement in the burrow. The males are much smaller than the females, spend more time on the surface, and have a brief life, dying shortly after copulation. The mite is passed in the vast majority of cases by intimate contact, but adult human scabies mites can survive off the host for 24 to 36 hours at room conditions and still remain infestive.8 Thus, scabies can be acquired from infested bedding, furniture, and clothing. Outbreaks not related to sexual activity occur frequently among nursing home patients and personnel; epidemics in schools for small children are also common. Scabies became uncommon after World War II (during the war it was a common problem), but since 1964 the disease has increased to epidemic proportions worldwide.265 Large nosocomial outbreaks with considerable morbidity among patients and health care workers have been widely described.37,365 Clinical Aspects.  Severe nocturnal pruritus is the hallmark of scabies. Itching also may be provoked by any sudden warming of the body and generally does not involve the face. A warm bath or radiant heat may cause a paroxysm of itching. Because the pruritus is caused by sensitization, 4 to 6 weeks may elapse between infestation and the onset of severe pruritus. Reinfestation is common, because eradicating the disease from all contacts simultaneously is often difficult, and reinfestation after cure results in prompt recurrence of symptoms. Cutaneous manifestations are varied. The primary lesion is the epidermal burrow, a tiny linear or serpentine track, rarely longer than 5 to 10 mm (0.2 to 0.4 inch). The female mite may burrow anywhere on the body, but sites of predilection include the interdigital spaces, palms (Figure 50-59), flexor surfaces of the wrists, elbows, feet and ankles, belt line, anterior axillary folds, lower buttocks, and penis and scrotum. The distribution of burrows in infants may be atypical, with burrows frequently found in the scalp and on the soles (Figure 50-60). In the present epidemic, involving many people with excellent hygiene, cutaneous changes may be almost absent and burrows difficult to find. On the other hand, after the disease has been present for some time, eczematization, lichenification, impetiginization, myriad nonspecific papules and excoriations, and even urticaria may be present. The burrows are often the least conspicuous of various skin changes. The clinical picture varies with differences in personal hygiene, topical treatments used before diagnosis, and individual scratch threshold. Scabies can also result in secondary skin cellulitis, sepsis, and postinfective complications such as glomerulonephritis.225,313 Diagnosis is based on the combination of nocturnal pruritus and cutaneous findings and is confirmed by microscopic examination of burrow contents. The burrow and contents may be collected for examination by scraping with a scalpel blade or by pinching the skin to elevate it and shaving off a superficial layer. Burrows are often inflamed and no longer typical after the disease has been present for some time. The most productive sites to find burrows for examination are finger webs, sides of fingers, wrists, and elbows. Ectoparasites, ova, egg castings, feces, or pieces of mites are diagnostic. Norwegian scabies is a term describing a particularly severe form of scabies occasionally seen in senile and mentally impaired patients, those with debilitating illnesses, and immunosuppressed patients (Figure 50-61).346 Extensive crusting occurs, particularly of the hands and feet.61 Erythema and scaling may develop, and patients are literally “crawling with mites.” This form of scabies is highly contagious, resulting from the incredible number of mites on the patient and in the immediate vicinity.57,202

C

CHAPTER 50  Arthropod Envenomation and Parasitism

A

B

D

FIGURE 50-58  A to D, Scabies mite, Sarcoptes scabiei var. hominis. A, Scabies mite. B and C, Microscopic view of scabies. D, Scabies in subcutaneous skin layer near hair shaft. (From Centers for Disease Control and Prevention Public Health Image Library; courtesy Joe Miller, Reed and Crnrick Pharmaceuticals, 1975, and Wikimedia Commons.)

Treatment and Prevention.  A number of topical treatments are available. In most cases, a single overnight application of 5% permethrin cream (Elimite) is curative. Permethrin has the advantages of low mammalian toxicity and high cure rate.350 Even after adequate therapy, symptoms may persist more than a month until the mite and mite products are shed with the epidermis. The

chemical must be applied even beneath the fingernails, because ova and live mites are frequently lodged there as a result of frenzied scratching. If the itching has not abated in several weeks, the patient should be reexamined for treatment failure or reinfestation. Permethrin may be used for retreatment, or alternative scabicides may be considered. Lindane lotion is highly effective but has the potential for central nervous system toxicity, and percutaneous absorption may occur.25 It is contraindicated in infants and pregnant women and persons known to be allergic to hexachlorocyclohexane, and it is reserved for adults with resistant strains. Sulfur in petrolatum (5% to 10%) or another suitable vehicle applied for three consecutive nights is a suitable

FIGURE 50-59  Scabies—palm of hand. (From http://www.emedicine. com.)

FIGURE 50-60  Scabies—sole of foot. (From http://www.emedicine. com.)

Nodular scabies is another troublesome clinical variation. Persistent pruritic nodules develop, particularly on the male genitalia or in the groin, but usually on some covered body part. Nodules may be the only finding and may persist for months after adequate antiscabetic therapy.

951

PART 6  ANIMALS, INSECTS, AND ZOONOSES

closely associated with humans, have been known to harbor mites that can infest humans. Notoedres cati infestation is seen more often in Czechoslovakia and Japan than is dog sarcoptic scabies.60

TROMBICULID MITES

FIGURE 50-61  Case of Norwegian scabies. (From Wikimedia Commons.)

alternative. Crotamiton 10% cream or lotion applied for two consecutive nights is also used. In the treatment of Norwegian scabies, salicylic acid ointment may be needed to soften scales and permit penetration of the scabicide. Nodular scabies can be a perplexing therapeutic problem and may necessitate intralesional injections of corticosteroids in addition to adequate antiscabetic therapy. Application of crude coal tar to the nodules has been recommended. In France, a combination of 10% benzyl benzoate and 2% sulfiram has proved useful in scabies treatment.46 Household contacts and health care workers should be treated simultaneously.45 Clothing and linens should be laundered the morning after treatment to kill mites that may have strayed from the skin. When many members of a household are infested, live mites may be on the furniture; α-hexachlorobenzene sprays are available. Control of scabies outbreaks in nursing homes and similar epidemic situations can be almost insurmountable because of the number of patients and contacts that must be treated simultaneously. An uncured case of Norwegian scabies as the focus of an epidemic may be surrounded by millions of mites. Ivermectin is a cheap and effective alternative antiscabetic when taken orally and is useful in institutional epidemics.10,41,46,123,314 A single dose of 250 mg/kg cured 10 of 11 patients with crusted Norwegian scabies as well as all otherwise healthy persons with scabies.150,235 This agent is also approved for use in humans for strongyloidiasis and onchocerciasis. Albendazole has been used in immunocompromised patients with HIV and crusted scabies.101 Zoonotic Scabies.  Other burrowing mites similar to the human scabies mite infest animals, such as swine, cattle, horses, mules, sheep, dogs, and wild animals. They are relatively host specific but under conditions of close contact may cause self-limited dermatitis in humans. Because of humans’ close association with dogs, the most common animal scabies is canine, caused by Sarcoptes scabiei var. canis. Studies indicate that the dog scabies mites are able to survive for at least 96 hours on human skin, even burrowing and laying eggs, but whether a perpetual life cycle can be established is not yet determined.115 Infested dogs have reddish papules, scaling, crusting, and evidence of scratching. Humans develop itchy papules, often with some urtication, and scratching may give rise to varying degrees of secondary infection. The initial lesions are most often on areas of skin that come in contact with dogs: forearms, chest, anterior abdomen, and anterior thighs. Outbreaks are frequently traced to a kennel or litter of puppies. In one case, 15 patients developed an itchy dermatitis from five puppies in one litter.64 Human infestation with dog scabies mites subsides spontaneously when contact with dogs is discontinued or when the dogs are cured. The dogs must be treated with scabicides and the human victims with symptomatic therapy for pruritus. Cats, also 952

Mites of the family Trombiculidae are distributed worldwide. In the United States, the most important species is Eutrombicula alfreddugesi (red bug, chigger [Figure 50-62], harvest mite).112 Another species, Eutrombicula batatas, is also indigenous to parts of the United States. Adults are free living and predacious on small arthropods and their eggs, but the larvae are ectoparasites of vertebrates. Wild and domestic mammals, as well as reptiles, serve as hosts. The larval bite causes human dermatitis. Adult mites lay their eggs among vegetation, and newly hatched larvae crawl up on the vegetation, waiting to attach themselves to a passing host. They attach themselves to the skin with hooked mouthparts and feed on blood, falling off when full. However, humans are not good hosts, and larvae usually do not stay long. Severity of the response depends on the species of trombiculid, the irritating qualities of the mites’ saliva, and the host’s allergic response. The typical bite is a maddeningly pruritic, hemorrhagic punctum that usually becomes surrounded by intense erythema within 24 hours. Bites may number in the hundreds and can be associated with an allergic reaction. Hypersensitivity causes blisters and weeping of clear fluid with crusting. The surrounding area may be purplish in color, with severe swelling, particularly of the feet and ankles (Figure 50-63). The lesions regress in 1 to 2 weeks, but pruritus is persistent and often paroxysmal during this time, with secondary infection in excoriated skin. One pediatric case series reported a “summer penile syndrome,” describing a seasonal hypersensitivity reaction caused by chigger bites to the penis in 94 male patients over a 4-month period from June to September.337 Treatment is symptomatic and consists of topical antipruritic agents, corticosteroids, systemic antihistamines, and, occasionally, pulse therapy with systemic corticosteroids. Superpotent topical corticosteroid creams and ointments, such as 0.05% clobetasol, applied sparingly to individual bites several times daily, are effective but must be used properly. Prolonged application can result in dermal atrophy, and absorption can be significant if excessive body surface is treated. Phenol (1% in calamine) often is effective. As in all self-limited conditions with no satisfactory cure, home remedies abound, such as meat tenderizer rubbed into the moistened skin. Application of clear nail polish

FIGURE 50-62  Chigger mite, Eutrombicula alfreddugesi.

General Treatment of Insect Bites

FIGURE 50-63  Chigger bites.

to the individual lesions is a popular home remedy, even though no evidence suggests that this is effective. Preventive measures consist of avoidance, and insect repellents used on skin and clothing. Clothing pretreated with permethrin has resulted in a 74.2% increase in protection compared with unprotected controls.38 Other repellents suggested for treating clothing are ethyl hexanediol, DEET, and flowers of sulfur. Permanent residents in infested areas may develop tolerance to repeated bites.

MISCELLANEOUS MITES Parasitiformes.  The Parasitiformes group contains gamasid mites that are parasites of birds, mammals, snakes, insects, and, rarely, humans. In addition to being vectors of disease, gamasid mites are responsible for some cases of dermatitis. The chicken mite, Dermanyssus gallinae, is responsible for most of the dermatitis caused by this group. This pest of poultry is widespread and is associated with both domestic and wild birds. Poultry workers are common targets, but other persons may be infested from insidious sources, such as a pet canary or a bird nest near an intake for ventilation or air conditioning. The clinical picture is nonspecific, but the diagnosis may be made by identifying the mite. Treatment consists of symptomatic therapy and eradication of the mite source. The tropical rat mite Ornithonyssus bacoti has also been reported to cause dermatitis from such diverse sources as a rat nest in the attic or a colony of laboratory mice.63,126 Snake mites have been implicated as a cause of dermatitis. Four members of one family developed a vesicobullous eruption from Ophionyssus natricis harbored by a pet python.320 Acariniformes.  The Acariniformes are a huge group that includes mites that infest foods, feathers, and furs. Individual infestations and larger outbreaks are common, with increased exposure by occupation, resulting in such terms as grocer’s itch, miller’s itch, and copra itch. Dogs, cats, and rabbits are the primary hosts for mites of the genus Cheyletiella, and domestic pets are increasingly the source of mite dermatitis. Pet house cats are often involved.301 Mites of the genus Dermatophagoides are said to be the principal inhaled allergen of house dust. Dermatophagoides scheremetewskyi is an unusual mite that has been found in kapok and feather pillows, in a sparrow’s nest, in monkey food, and on rats and other animals. This mite has been reported as the cause of feather pillow dermatitis.13 The most common type of dermatitis in this group is grain itch caused by Pyemotes ventricosus. This tiny mite parasitizes various insects often found in and around grain and straw. It attacks humans when a large mite population has no ready

Oral antihistamines can be effective in reducing the symptoms of insect bites. Cetirizine was given prophylactically in a doubleblind, placebo-controlled, 2-week crossover trial to 18 individuals who had previously experienced dramatic cutaneous reactions to mosquito bites. Subjects given the active drug had a 40% decrease in both the size of the wheal response at 15 minutes and the size of bite papule at 24 hours. The mean pruritus score, measured at 15 minutes and 1, 12, and 24 hours after being bitten, was 67% less than that of the untreated controls. In highly sensitized individuals, prophylactic treatment with nonsedating antihistamines, such as loratadine, may safely reduce the cutaneous manifestations of insect bites.3,307 A 3.6% ammonium solution (After Bite) relieves the type I hypersensitivity symptoms associated with mosquito bites. In a double-blind, placebo-controlled laboratory trial, 64% of mosquitobitten subjects experienced complete relief of symptoms after a single application of the ammonium solution, and the remaining 36% had partial relief lasting 15 to 90 minutes. No subjects treated with placebo reported complete symptom relief.384

Protection and Prevention An integrated approach to personal protection is the most effective way to prevent arthropod bites, regardless of location and species (see Chapter 47). Protection from arthropod bites is best achieved by avoiding infested habitats, wearing protective clothing, and using insect repellents.127 Insect repellents containing DEET are the most effective products on the market, providing broad-spectrum repellency lasting several hours.127,304 Currently available non-DEET–containing repellents do not provide protection for as long as DEET-based repellents. DEET’s peak duration of action plateaus at a concentration of 50%, with no added benefit from products containing higher concentrations.127 Additionally, liberal use of higher-concentration products with ethanol bases can lead to increased skin absorption and perhaps neurotoxicity, particularly in young children.266,304 Topical insect repellents alone do not provide complete protection. Ethyl butylacetylaminopropionate (IR3535)–containing products can provide protection for up to 3 hours and can be added to sunscreen lotions without safety concerns or potential side effects.351,370 A piperidine derivative (Bayrepel) offers 2 to 8 hours of protection similar to DEET but is currently available only in Europe. Large doses of vitamin B1 have not been proved effective.127,128 Newer agents, such as picaridin, and natural products such as oil of lemon eucalyptus are becoming increasingly popular because of their low toxicity.182 BioUD is an arthropod repellent that contains the active ingredient 2-undecanone originally derived from wild tomato plants. In one recent study, no statistically significant difference in overall mean percentage repellency was found between BioUD and DEET.31 Mosquitoes can find and bite any untreated skin and may even bite through thin clothing. Deerflies, biting midges, and some blackflies prefer to bite around the head and will crawl into the hair to bite unprotected areas. Wearing protective clothing, including a hat, reduces the chances of being bitten. Treating clothes and hats with permethrin, in addition to spraying DEET on the skin, offers the greatest protection by also repelling any insect that crawls or lands on the treated clothing.127 DEET-impregnated anklets, wristbands, 953

CHAPTER 50  Arthropod Envenomation and Parasitism

access to normal hosts. Grain itch implies an occupational bias, but outbreaks not involving farmers or rural workers have been described. During a widespread epidemic of Pyemotes infestation of farm workers in the midwestern United States between 1950 and 1951, straw used at the Indiana State Fair was infested. During a 2-year period, 642 visitors were treated for grain itch at a dispensary maintained on the fairgrounds, and about 1100 animal attendants and fair workers were treated over the same period at a separate facility. The reservoir of infestation by Pyemotes may be quite obscure. Several reported cases were associated with the common furniture beetle Anobium punctatum in the floor joists of a house.120 Therapy is symptomatic. Large-scale eradication measures may require the services of professional exterminators.

shoulder, and pocket strips are also available.181 To prevent chiggers or ticks from crawling up the legs, pants should be tucked into boots or stockings. Persons traveling to a part of the world where insect-borne disease is a potential threat should be certain to learn about indigenous insects and the diseases they might transmit. Protective clothing, mesh insect tents or bedding, insect repellent, and permethrin spray should be carried.

Delusions of Parasitosis Patients with delusions of parasitosis are convinced, against all evidence to the contrary, that parasites infest their skin and often their homes and clothing. Ekbom syndrome is synonymous with delusional parasitosis or “invisible bug” infestations.35,165,275 No single cause is known for this condition, although some cases may be associated with proved parasitic infestation. The idea may also be suggested by infestations of relatives or acquaintances. Patients older than 50 years are most often female.345 Patients younger than age 50 years are equally male and female. Most cases of delusions of parasitosis commence with pruritus, which may be accompanied by crawling, creeping, stinging, and burning sensations. The initial reaction is to scratch, replaced soon by digging to remove the “parasites.” Self-mutilation and suicidal behavior may develop. Generally, the first contact with a physician is to bring in evidence of the “infestation.” Evidence typically consists of scales, lint, crusts, hairs, dust, and small pieces of skin, carefully collected in folded facial tissue or stored in a small box (defined as the “matchbox sign”).35 Medical attention is often sought not to relieve the symptoms but to eradicate the parasites. These patients tend to avoid psychiatrists and consult dermatologists, microbiologists, or general practitioners, but often lose faith in traditional medicine.133 Patients may take

the evidence to an entomologist for identification and may employ professional exterminators for repeated fumigation. Patients may be so convincing that household members or acquaintances come to share the delusion.66,116 Many patients with parasitophobia know that their fear is groundless but are still unable to overcome it. Other patients with delusions of parasitosis are convinced that they have an infestation and regard as incompetent the physician who makes the correct diagnosis of no infestation. A complete examination of the patient and the evidence is essential, and investigation of the home or workplace may be indicated. Other medical conditions that may produce cutaneous sensations include liver and renal disease, alcoholism and toxic states, diabetes mellitus, cardiovascular disease, lymphoma, anemia, sideropenia, vitamin B12 deficiency, pellagra, peripheral neuritis, dermatitis herpetiformis, drug reactions, and environmental irritants (e.g., arthropods, fiberglass).218,355,379 Neuroleptic medications, such as olanzapine,232 gabapentin,33 aripiprazole,22 and pimozide used to treat other monosymptomatic hypochondriacal psychoses, have been found useful in treating this condition.37,292,299,379 In one group, 14 patients were treated with pimozide and followed for an average of 34 months. Seven had complete remissions, three had relapses that responded to treatment with pimozide, and four were treatment failures.212 Psychiatric intervention is often unsatisfactory to both the patient and physician. Convinced that the physician is wrong, patients often seek repeated opinions and finally become despondent.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 51 

Tick-Borne Diseases STEPHEN J. TRAUB AND GREGORY A. CUMMINS

There are approximately 850 species of ticks, which rank second only to mosquitoes in importance as insect vectors of human disease.176 Tick-borne disease was first described by Hippocrates, who noted an epidemic of relapsing fever nearly 2500 years ago. In the early 18th century, European physicians described patients with signs and symptoms of Lyme disease. In 1857, David Livingstone, the British explorer of Africa, discovered that a human disease was caused by spirochetes from soft ticks. In the late 1880s, Dr. Arvid Afzelius in Europe described a ringlike lesion in association with the bite of the Ixodes ricinus tick. This lesion was almost assuredly Lyme disease, and a causative agent of Lyme disease in Europe, Borrelia afzelii, is named after him. The German physician Robert Koch confirmed the role of ticks in cases of tick-borne relapsing fever, previously thought to be a variant of malaria, in Africa in 1904. Ticks are the most common arthropod vectors of disease in the United States (Figure 51-1), and second worldwide, only behind mosquitoes. For those who have outdoor interests and enjoy outdoor activities, ticks are unavoidable. Ticks and the diseases they transmit may also afflict those who do not actively participate in outdoor activities, because pets may bring them into the home, where they may survive for weeks before transmitting disease. Several tick-borne diseases are readily transmissible by blood transfusion.223 New infectious diseases continue to emerge, and our awareness of them continues to grow. Ticks have recently been discovered to transmit several diseases that were formerly unknown, 954

that were not known in humans, or that were not formerly known to be transmitted by ticks. For example, ticks have recently been implicated in the transmission of West Nile virus.218 The overall global warming trend has expanded both the season in which ticks are found and the window of opportunity for exposure to them.81 The highest altitude at which tick-borne encephalitis is found in Europe has risen over the past 30 years,410 and ticks known to transmit diseases are now found at higher altitudes than they were found in the past.80,81 Ticks often harbor, and may transmit, multiple infectious organisms simultaneously.8,150,175,377,378 In one region, 24% of I. ricinus nymphs were infected with more than one infectiousorganism.284 Different genospecies of Borrelia have been documented in a single patient with Lyme disease,90 and it is likely that these multiple strains came from the same tick. In addition to the classic tick-associated illnesses described in this chapter, ticks may also harbor other bacteria. I. ricinus ticks may carry Pasteurella pneumotropica/haemolytica and other gramnegative organisms, including Pseudomonas aeruginosa.362 Ticks do not respect geographic borders. Many species of ticks feed on migratory animals, such as birds, that travel great distances.9,202 Ticks can survive unnoticed on a traveler, or in a traveler’s bag, from one continent to another. At least 29 different species of ticks have been introduced into the United States on imported reptiles.48 Outdoor pets, especially dogs, are welldocumented to carry infected ticks.26 One study indicated that dog owners are five times more likely to get spotted fever than are non–dog owners.265 International travel is now easier, and

areas not formerly accessible are easily visited. A group of American paleontologists working in Mongolia was recently tested for North Asian tick typhus, and four of the 13 researchers were infected.224 Many tick-borne illnesses are commonly researched in military biologic warfare laboratories and listed by the Centers for Disease Control and Prevention (CDC) as possible biologic weapons.36,65,192 Tularemia is listed as category A, and Q fever is listed as category

Ixodid Ticks Ixodid ticks, which transmit a plethora of diseases (Table 51-1), possess a hard, shield-like scutum. Their mouthparts are visible from the dorsal view (Figure 51-3). The scutum covers only the anterior portion of the dorsum of the females but the entire dorsal surface of the males. The presence of the scutum limits the size of the tick during feeding. Thus, the body of the female (to a much greater extent than of the male) may expand tremendously with a blood meal, because the tick ingests up to 50 times its weight in blood and body secretions. Ixodid females generally feed and mate only once as adults, whereas males may feed and

TABLE 51-1  Ixodid Ticks (Ixodidae) Tick Species

Transmitted Diseases

Geographic Distribution

Amblyomma americanum (lone-star tick)

Human monocytic ehrlichiosis (HME), southeastern tick-associated rash illness, tularemia Rocky Mountain spotted fever (RMSF)

Southeastern and south-central United States, Eastern Seaboard

Amblyomma cajennense (cayenne tick) Amblyomma hebraeum Dermacentor andersoni (Rocky Mountain wood tick Dermacentor marginatum Dermacentor Dermacentor Dermacentor Dermacentor

nuttalli occidentalis silvarum variabilis (American dog tick)

Haemaphysalis concinna Haemaphysalis leachi Haemaphysalis spinigera Hyalomma anatolicum Hyalomma asiaticum Hyalomma marginatum Ixodes holocyclus Ixodes pacificus (western black-legged tick) Ixodes persulcatus (taiga tick) Ixodes ricinus (castor bean tick) Ixodes scapularis (black-legged tick) Rhipicephalus sanguineus (brown dog tick)

Boutonneuse fever RMSF, Colorado tick fever (CTF), tularemia, tick paralysis Omsk hemorrhagic fever, Siberian tick typhus, tick-borne encephalitis (TBE) Siberian tick typhus, tularemia Tularemia, RMSF, CTF, tick paralysis TBE, Siberian tick typhus RMSF, tularemia, tick paralysis, human granulocytic ehrlichiosis (HGE) Siberian tick typhus, tick-borne encephalitis Boutonneuse fever Kyasanur forest virus Crimean-Congo hemorrhagic fever (CCHF) Siberian tick typhus, spotted fever group CCHF Tick paralysis, spotted fever group Lyme disease, HGE Lyme disease, Russian spring–summer encephalitis (RSSE) Lyme disease, TBE, babesiosis, tularemia, HGE Lyme disease, RMSF, HGE, babesiosis Spotted fever group, Q fever

Extreme south Texas, Mexico, Central America Southern half of Africa Western half of United States, Rocky Mountain states Europe, western half of Asia Northern Asia U.S. Pacific Coast, Mexico Eastern Europe, northern Asia Entire United States except Rocky Mountain states; Mexico Europe and temperate Asia Africa, Southeast Asia, Indonesia Southern half of India; Indonesia Northern half Africa, southern Europe, southern Asia South-central Asia Africa, southern Europe, southern Asia Australia United States and Canada west of Rocky Mountains Europe, northern half of Asia Northern Africa, Europe, Asia Eastern third of United States Worldwide

955

CHAPTER 51  Tick-Borne Diseases

FIGURE 51-1  Painting by Sue Oliver depicting the complex interaction among the tick vector, reservoir hosts, causative agent, and humans occurring in Lyme disease. (Courtesy Sue Oliver.)

B. Most other tick-borne diseases are listed as category C, meaning they are of concern but not easily grown, disseminated, or spread from person to person. Although an outbreak of any of these diseases may produce only a few fatalities, such an outbreak could seriously strain any advanced health care system. Most ticks are not species-selective with respect to their hosts, although some exhibit species preference. At least one, which feeds only on the Galapagos giant tortoise,178 is completely species specific. Some ticks are more anthropophilic (readily feeding on humans) than others. Different stages of a tick species may feed on different animals, and even different orders of animals. For example, Ixodes scapularis larvae and nymphs feed readily on mammals, reptiles, and birds, with varying degrees of host preference,184 whereas the adult ticks feed predominantly on large mammals. Once the tick initiates feeding, the hypostome (feeding organ) enters the skin. The hypostome contains hundreds of barbs, pointed in reverse direction from the entry into the skin to serve as an anchor (Figure 51-2). During feeding, the tick secretes a mixture of salivary proteins containing both anticoagulants and a proteinaceous cement. The combination of salivary proteins and mechanical irritation may cause a local reaction in the host, and the combination of reverse-pointing barbs and proteinaceous cement make embedded ticks difficult to remove. Ticks belong to the order Acari (which includes mites) and the class Arachnida (which includes spiders and scorpions). Taxonomists divide ticks into two major families: Ixodidae (hard ticks) and Argasidae (soft ticks).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Eggs Nymph

Eggs Spring Winter

Larva

Summer Fall Adults

FIGURE 51-2  Electron micrograph of the hypostome of an ixodid tick.

mate several times. Each female ixodid tick lays several thousand eggs in a single deposition, and then dies. These eggs hatch at approximately the same time, and if a potential host brushes by, thousands of larvae, or “seed ticks,” can attach nearly simultaneously. Some species live through all three life stages (larva, nymph, adult) on a single host (and are thus called one-host ticks), whereas most species feed, drop into leaf litter, molt, and seek another host for each life stage (and are called three-host ticks). A typical ixodid tick life cycle is depicted in Figure 51-4. It is typically a 2-year cycle, although in some areas it may be 1 year.106 The tick hatches as a six-legged larva and attaches to a small mammal, often a rodent. After feeding for 3 to 5 days, it drops off and molts to the eight-legged nymph. The nymph hibernates in the soil and becomes active again in the spring. It then attaches to and feeds on a larger animal for 4 to 9 days, after which it again drops off (into leaf litter) and molts a second time to the adult stage. The mature tick attaches to a third host, on which feeding and mating may occur. A large mammal, such as a deer, may support thousands of ticks.

FIGURE 51-4  Life cycle of Ixodes scapularis. The cycle of ixodid ticks typically spans 2 years and includes three blood meals in the spring. The adult female tick releases her eggs, which hatch as six-legged larvae, during the summer. The larvae take blood meals that last approximately 2 days. Larval ticks then enter a dormant phase with cooler fall weather. The ticks then molt in the spring, entering the second phase of their life cycle as eight-legged nymphal ticks. In the late spring or summer, nymphal ticks take blood meals that typically last for 2 to 3 days. The nymphal ticks then molt as eight-legged adults in the fall. The adults mate on white-tailed deer. After mating, the male dies, but the female takes one more blood meal before she lays her eggs and dies. (Modified from Habicht GS, Beck G, Benach JL: Lyme disease, Sci Am 257:78, 1987.)

Ticks do not find their hosts haphazardly. The tick’s front legs are equipped with chemoreceptors to detect respiratory gases (especially CO2) and proprioceptors to detect fine vibrations. Nymphs and adults actually climb up grass blades and “seek” a host (“seeking” or “questing”), holding up the front legs that also contain small barbs to help them attach. The ticks hook onto the

Hypostome

Hypostome

Chelicera within sheath Pedipalp

Pedipalp

Basis capitulum

Basis capitulum

Eye Gonopore

Scutum

Spiracle Anus

A

B FIGURE 51-3  Tick anatomy. A, Dorsal aspect. B, Ventral surface.

956

Argasid Ticks Argasid ticks do not exhibit sexual dimorphism or have a hard scutum. The mouthparts are not visible from above. The body typically has a wrinkled, leathery appearance (Figure 51-5). Argasid ticks move quickly in comparison to the ixodids. Argasid ticks usually feed completely in 10 to 30 minutes and do not cause pain. They generally feed at night, often moving unnoticed while their hosts sleep. After feeding, they drop off the host and lay dozens to a few hundred eggs and then repeat the cycle many times. The remainder of the life cycle is similar to that of the ixodids, except that nymphs may have multiple stages. Argasid ticks are generally found in animal burrows, dens, and caves, and in the floors and walls of huts and cabins. They thrive in hot, dry climates.

Ticks as Poisonous Arthropods TICK PARALYSIS In 1912, Todd371 recognized that an acute, ascending, flaccid motor paralysis followed the bite of certain ticks. Tick paralysis has been reported worldwide, although most human cases occur in North America and Australia.341,397 Forty-three species of ticks have been reported to cause tick paralysis.63 Human cases in North America are usually caused by Dermacentor andersoni, although Dermacentor variabilis, Amblyomma americanum (Figure 51-6), Amblyomma maculatum, and I. scapularis have also been implicated.158 In the United States, the Pacific

FIGURE 51-5  Soft ticks (family Argasidae) possess a leathery integument rather than the tough scutum possessed by hard ticks (family Ixodidae). North American argasid ticks of the genus Antricola possess a tuberculated, or “knobby,” roughened integument, as seen here from a close-up perspective. These ticks are parasites that use bats as hosts. (Courtesy CDC, 1975.)

CHAPTER 51  Tick-Borne Diseases

host’s fur, feather, scale, or skin and find a place to attach, often after climbing to an area with a relatively abundant blood supply.214 Ixodids are generally on their host for hours to a day or more before they begin to feed, and the feeding process may last from days to weeks. The duration of feeding depends more on the host than the tick; feeding on reptiles, for example, occurs more slowly than on other species. A blood meal and mating, which usually occurs on the host, are prerequisites to laying eggs. Females, once engorged, drop off the host, often in the night or early morning hours and typically into an animal’s nest or bedding area, and lay eggs nearby in leaf litter or nest material. This provides a meal for the larval ticks upon hatching. Ixodid ticks typically require dense vegetation and prefer areas of high animal traffic and humidity, such as leaf litter or moist soils. “Seeking” adults are often found on animal paths or game trails.144 They are found in temperatures from freezing to more than 38° C (100° F), although they move more slowly at cold temperatures. They can be frozen in a block of ice yet when thawed move freely and feed without difficulty.

FIGURE 51-6  Lone-star tick (Amblyomma americanum), implicated in cases of tick paralysis in North America. (Courtesy Sherman Minton, MD.)

Northwest and Rocky Mountain areas account for the vast majority of cases. In Australia, Ixodes holocyclus is primarily associated with the disease, although Ixodes cornuatus has been implicated.159,161 Tick paralysis usually occurs during the spring and summer months (April to June),95 when nymphs and mature wood ticks are feeding. Most cases occur in areas where ticks are endemic. Patients in urban areas may be affected if they have recently traveled,157 and the diagnosis should not be excluded on the basis of geography alone. Children are affected more often than adults, with most cases reported among girls less than 10 years of age. Among children, girls are affected twice as often as boys, probably because ticks on the female scalp are hidden in longer hair.1 Among adults, men account for most cases, presumably because of increased occupational and recreational exposures to tick habitats. A neurotoxic venom, ixobotoxin, is secreted from tick salivary glands during a blood meal and causes the paralysis. The venom inhibits membrane sodium flux, resulting in diminished acetylcholine release at the neuromuscular junction.157,267 Electrophy­ siologic measurements in humans consistently demonstrate slower motor conduction and reduction in muscle action potential amplitude.98,262,365 The neurotoxin may also increase the stimulatory current potential necessary to elicit a response at the motor end plate.203 The toxin appears to have central effects as well. Tick paralysis in humans develops 5 to 6 days after an adult female tick attaches, usually to the head or neck. Initially, the victim may be restless and irritable and may complain of paresthesias in the hands and feet. Over the next 24 to 48 hours, an ascending, symmetric, flaccid paralysis develops. Deep tendon reflexes are lost. Weakness is initially greater in the lower extremities, but within 1 to 2 days, severe, generalized weakness may develop, accompanied by bulbar and respiratory paralysis. Some victims develop cerebellar dysfunction with incoordination and ataxia.1,157 Exceptions to this general pattern are reported, including facial paralysis as an isolated finding278 and cranial nerve dysfunction out of proportion to muscular weakness.85,136 Case reports of Australian tick paralysis suggest that it may be more severe than its North American counterpart. Victims often appear more acutely ill. Paralysis may continue to progress for 48 hours after tick removal, and recovery may be prolonged.18,19,278 A recent report of six cases in children in Australia found little difference in the course between Australian and North American patients.159 Diagnosis is made solely on clinical grounds, as specific diagnostic laboratory tests to diagnose this condition are not available. White blood cell (WBC) count and cerebrospinal fluid (CSF) analyses are normal. If the tick is on the scalp, magnetic resonance imaging (MRI) performed as part of the diagnostic workup for other conditions may identify it incidentally as a small nodule that is hypodense to fat on T1 imaging, is isointense to fat on T2 imaging, and does not enhance with gadolinium.47 The diagnosis is confirmed on resolution of paralysis after removal of the 957

PART 6  ANIMALS, INSECTS, AND ZOONOSES

tick. Undiagnosed, tick paralysis may be fatal, as evidenced by a high (12%) mortality in older series prior to the widespread use of mechanical ventilation.321 Although a 60-year meta-analysis suggests that misdiagnosis has been more commonly reported in recent years,95 it is not clear if this represents an actual trend or simply publication bias. The most common misdiagnosis is Guillain-Barré syndrome. The clinical features of the two diseases are strikingly similar, although ataxia has been more common in tick paralysis.95 The results of electrophysiologic studies are often indistinguishable.379 Although the protein level of CSF in patients with Guillain-Barré syndrome is often elevated, this finding may be absent in up to 30% of patients,14 particularly in the early stages of the disease. For this reason, an abnormal CSF protein analysis strongly favors a diagnosis of Guillain-Barré, but a normal analysis does not exclude it. The differential diagnosis should also include botulism, myasthenia gravis, and potassium-associated paralyses, which can all be assessed via specific testing. Treatment includes removal of the offending tick followed by supportive care. Severely affected patients may require ventilatory support. Tick antivenom from hyperimmunized dogs has been developed for Australian tick paralysis and may be beneficial in victims with severe disease, although treated patients have a high incidence of acute allergy and serum sickness.159,278

Ticks as Vectors of Infectious Diseases Ticks transmit a wide variety of infectious agents, and may act either as amplifiers or as reservoirs for a given infectious agent.177 In the agent–tick amplifier system, an immature tick ingests the microorganism while feeding on an infected vertebrate, and the vertebrate is the reservoir for the disease. The pathogen replicates in the tick and is passed transtadially, from larval to nymphal to adult stage. The maturing tick transmits the agent to other vertebrate hosts when it feeds. A key epidemiologic feature of this system, transtadial survival of microorganisms, is common in ticks but rare in other hematophagous insects. This important difference is primarily due to the fact that tick anatomy is relatively unchanged as the tick molts.177 In the agent–tick reservoir system, the microorganism is passed transovarially from one generation of ticks to the next. The agent replicates within the tick and depends solely on the tick population for survival. The agent may also replicate within a vertebrate host, allowing for amplification and increasing the density and prevalence of the microorganism, but it need not do so. Table 51-2 lists the major tick-borne diseases in the United States. Lyme disease is now the most common tick-borne illness in the United States and throughout the world. Tularemia, ehrlichiosis, and Rocky Mountain spotted fever are observed throughout the United States and continue to produce significant morbidity and mortality. Tick-borne relapsing fever and Colorado tick fever occur in the western states and are particularly likely to affect campers, hikers, hunters, and others who frequent wilderness areas.

FIGURE 51-7  Lyme disease spirochete viewed under dark-field microscopy. (Courtesy CDC Public Health Information Library.)

TICK-BORNE BORRELIAL DISEASES The genus Borrelia belongs, along with Treponema and Leptospira, to the order Spirochaetales, which are helical bacteria. Borreliae are usually 10 to 20 µm long, with three to ten spirals.123 When live cultures are viewed under dark-field microscopy (Figure 51-7), the organisms are very motile. Borrelia species can be stained with aniline dyes, a feature that readily distinguishes them from Treponema and Leptospira genera.353 Borreliae can also be stained with Wright and Giemsa stains, although obtaining the organisms from blood is extremely difficult with most diseases (tick-borne relapsing fever being an exception). Culturing Borrelia species is technically challenging and must be done in properly formulated media incubated under specific conditions in specially equipped laboratories. In the relapsing fever borreliae, strains cannot be differentiated on the basis of morphology but are classified according to specificity of the tick– spirochete relationship, the range of animals susceptible to infection, and cross-immunity.20 The reservoir hosts, vectors, different species, and even different strains of Borrelia vary tremendously in different geographic areas.213,225,322,376,388 The medically important diseases caused by Borrelia species in the United States include Lyme disease (caused by Borrelia burgdorferi and Borrelia bissettii), tick-borne relapsing fever (caused by Borrelia recurrentis), and southern tick-associated rash illness (STARI, caused by Borrelia lonestari) (Figure 51-8). The Institut Pasteur currently lists approximately 12 species and nearly 200 different strains of Borreliae. Other important Borrelia species are being found regularly as more is learned about the spirochetes, hosts, and reservoirs.322,377,378 Lyme Disease In Europe, the rash known as erythema chronicum migrans (ECM) has been associated with the bite of I. ricinus for more than one hundred years.4

TABLE 51-2  Major Tick-Borne Diseases in the United States Disease

Organism

Major Vectors

Geographic Distribution

Lyme disease

Borrelia burgdorferi

Ixodes scapularis, I. pacificus

Rocky Mountain spotted fever Relapsing fever

Rickettsia rickettsii

Colorado tick fever Ehrlichiosis

Borrelia hermsii, Borrelia turicatae, Borrelia parkeri Orbivirus Ehrlichia chaffeensis

Dermacentor andersoni, D. variabilis Ornithodoros hermsi, Ornithodoros turicata, Ornithodoros parkeri Dermacentor andersoni Ixodes scapularis

Coastal mid-Atlantic states, northern West Coast, Wisconsin, Minnesota South-central states, coastal southern states

Babesiosis Tularemia

Babesia microti Francisella tularensis

Amblyomma americanum Ixodes scapularis A. americanum

958

Worldwide; most often rural and wilderness areas of western states Rocky Mountain states, California, Oregon Coastal mid-Atlantic states, northern West Coast, Wisconsin, Minnesota South-central states, coastal southern states Coastal southern New England and mid-Atlantic states South-central states, Montana, South Dakota

A

B FIGURE 51-8  Presumptive southern tick-associated rash illness. A, Rash on patient’s back. B, Close-up view of rash. (Courtesy Shannon B. Snyder, MD.)

In the mid-1970s, a team from Yale University School of Medicine investigated a cluster of cases of arthritis in children near Old Lyme, Connecticut. The arthritis was initially thought to be juvenile rheumatoid arthritis. On further examination, however, the clustering, rural setting, and some response to penicillins pointed to an infectious, most likely arthropod-borne etiology. The seasonality and frequent finding of a rash pointed to a tick vector.350 Epidemiologic evidence implicated the deer tick, I. scapularis, as the likely vector of what is now called Lyme disease. In 1982, Burgdorfer and associates46 isolated a treponeme-like spirochete, B. burgdorferi, from the midgut of I. scapularis ticks collected from a known endemic focus of Lyme disease.28 Subsequently, sera from nine patients clinically diagnosed with Lyme disease yielded high antibody titers to the spirochetes by indirect immunofluorescence.2 Isolation of B. burgdorferi from the blood, CSF, and skin lesions of affected patients finally confirmed the spirochetal etiology of Lyme disease.31,354 More than 12 species of Borrelia are now known to cause some variation of Lyme disease throughout the world. Most of these species cause disease in specific geographic regions and are transmitted almost exclusively by Ixodes ticks. In addition to numerous species of Borrelia, there are numerous strains of each species, and ongoing research is likely to lead to discovery of more. B. burgdorferi is the primary agent in the United States, Europe, and Asia. U.S. isolates of B. burgdorferi demonstrate regional genetic heterogeneity,248 and genetic comparison of European and North American strains indicate common ancestry.288 Borrelia garinii and B. afzelii are causative agents of Lyme disease in Europe, and still more agents are being identified.225 B. burgdorferi has been isolated in Morocco from I. ricinus ticks.318 The newly found B. bissettii (formerly Borrelia genomic group DN127) has been found in California, Florida, and other southeastern states and in Europe, and it is responsible for Lyme

Epidemiology.  Lyme disease surveillance began in 1982 at the CDC, and Lyme disease became a nationally reportable disease in 1991. In 2000, Lyme disease accounted for more than 90% of all reported cases of vector-borne illness in the United States.171 In the United States in 2001, 17,029 cases were reported in 43 states; in 2009, there were 38,468 cases from 50 states and the District of Columbia.68 Preliminary 2010 CDC data show 27,895 cases.69 The national incidence of Lyme disease is 8.2 cases per 100,000 population, although 12 states reported 95% of the cases. Columbia County, New York, reported the highest incidence of Lyme disease in both 2001 and 2002.67 Reasons for recent increases in the number of reported cases are multifactorial and most likely include public and physician awareness, increases of reservoir host populations, increased range of the vectors, efflux of people from urban cores to suburban areas (which results in more human–host–vector interfaces). Lyme disease is grossly underreported in many areas.55,75,254 Patients of any age may become infected, but the incidence has two peaks: among children aged 5 to 14 years and among adults aged 50 to 59 years. Fifty-nine percent had an onset of illness in June and July, and 78% of the cases occurred in the months of May through August. Fewer than 7% of the cases began in winter months. Lyme disease is a worldwide problem, diagnosed or found on all continents. Sporadic cases in Australia have yet to be proved as having originated in Australia and may have been imported in patients who spent time in areas endemic for Lyme disease.180,314 Polymerase chain reaction (PCR) analysis of approximately 12,000 field-captured ticks in Australia failed to find any evidence of Borrelia-like infection.315 The primary vectors for Lyme disease worldwide are ticks of the I. ricinus complex. In the eastern half of the United States, the primary vector is I. scapularis, known more commonly as the black-legged tick or deer tick. The primary vector in the western United States is Ixodes pacificus, the western blacklegged tick.274 In Europe, Asia, and Northern Africa, I. ricinus, the castor bean tick, is the main vector. In Japan, China, and eastern Russia, it is Ixodes persulcatus, the taiga tick. Transmission of the spirochetes to humans is almost exclusively by infected nymphs or adults. Larvae are usually not infected until they feed on an infected host, pick up the spirochetes from this host, and then become infective as a seeking nymph. Unlike in many other tick-borne diseases, there is minimal transmission of the causative spirochetes from an infected female to her eggs.271,285 Transmission of the disease in the United States outside of the areas in which I. ricinus complex ticks are found, although rare, does occur, thus implicating other vectors. Several other tick species (Amblyomma, Dermacentor, Haemaphysalis, Rhipicephalus, and other Ixodes species) have been found infected with the spirochetes, but they are not successful in transmitting the spirochetes to a host.234,263 Various nontick arthropods, including some biting flies, mosquitoes, and the cat flea, have been shown to harbor spirochetes, but they do not transmit spirochetes to a host or do so very rarely.230,234,300,368 In many of the nontick arthropod cases, disease transmission is presumed to take place by a “dirty syringe” type of mechanism, in which the vector feeds partially on a spirochete-laden host, only to momentarily later inject the spirochetes into the next host.230,235 Reservoir host species are numerous, and they vary worldwide depending on the location and climate. At least 125 species of mammals, birds, and reptiles are important hosts to Ixodes ticks throughout the world.199 In the northeastern United States, the preferred host for I. scapularis larvae and nymphs is the white-footed mouse, Peromyscus leucopus. In Europe and Asia, various rodents are the primary hosts for the larvae and nymphs. Larger mammals, most often deer, usually serve as hosts for the adults. In more temperate areas of the world, there is a much wider variety of hosts, including reptiles, birds, and mammals. In the southeastern United States, the cotton mouse (Peromyscus gossypinus), the cotton rat (Sigmodon hispidus), and other 959

CHAPTER 51  Tick-Borne Diseases

disease in those areas and most likely other areas yet to be discovered.287,322,380 Overall, Borrelia species are found nearly across the globe, and new species and geographic areas are being discovered regularly.

Clinical Manifestations.  Lyme disease has a myriad of constitutional, dermatologic, neurologic, cardiac, and musculoskeletal symptoms. The most common are vague myalgias, headache, fatigue, neck stiffness, and arthralgias. Rarely, gastrointestinal complaints or ocular complaints such as conjunctivitis, iritis, and keratitis may be reported. Collectively, these symptoms are difficult to distinguish from a benign viral syndrome, which is one of the reasons Lyme disease is easily misdiagnosed by both patients and physicians.16 Lyme disease is multisystemic and multiphasic. The disease is classically divided into three stages based on the chronologic relationship of symptoms to the original tick bite, with different clinical manifestations at each stage (Figure 51-9). There is no clear delineation distinguishing one stage from another, however, and signs and symptoms of different stages often overlap.

100 80 Patients (%)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

mammals, reptiles, and birds serve as primary hosts for larvae and nymphs.106,199,273 Bird species readily harbor spirochetes, whereas lizard species do not. The reptilian hosts, almost exclusively lizards, account for a large amount of the immature (larval and nymphal) tick population.273 Lizard sera and mule deer sera appear to deactivate spirochetes via a borreliacidal protein.213,376 The high numbers of ticks parasitizing lizards instead of mice and the lizards’ apparent inability to harbor the spirochetes may partially account for the differences in Lyme disease incidences between certain geographic areas.76 The migration of larger mammalian and avian hosts is one means by which ticks spread into new areas, often spreading various diseases with them.9,82,202 Host populations increase when appropriate predators are absent; these fluctuations can amplify tick populations tremendously. One deer can host several thousand ticks of various stages; deer population studies have shown that decreasing or eradicating deer populations leads to marked decreases in tick populations in subsequent years.143,292 The interaction between spirochete and host begins when the spirochete enters the salivary gland of the tick during the feeding process. Transmission to another vertebrate also occurs during the feeding process, which explains why disease transmission usually occurs only after a tick has been on a host for 48 to 72 hours. B. burgdorferi spirochetes show no transmission to mice in less than 24 hours, with maximal transmission occurring between 48 and 72 hours.94 Another study showed that tick attachment for greater than 72 hours was more likely to transmit disease.337

60

Stage I

Stage II

40 20

Stage III

0 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 Post-infection time (months) FIGURE 51-9  Time course and frequency of symptoms in Lyme disease. Approximately 50% of victims report recent tick bite. The initial stage I symptoms occur in approximately 70% to 80% of infected individuals. Weeks after the initial tick bite, the skin, nervous system, and joints are most often affected as the spirochete spreads hematogenously. Stage II symptoms typically begin 4 to 10 weeks after the initial infection and occur in approximately 50% of untreated patients. Stage III typically starts much later, often 1.5 to 2 years and rarely more than 5 years after initial infection. (Modified from Schmid GP: Epidemiology and clinical similarities of human spirochetal diseases, Rev Infect Dis 11[Suppl 6]:S1460, 1989.)

960

BOX 51-1  Lyme Disease: Stage I Incubation: 7-10 days (range, 3-32 days) Duration: 28 days (range, 1-14 months) Symptoms (Incidence) Erythema migrans (60%-89%) Mild lymphadenopathy (23%) Low-grade fever (19% to 39%) Mild fatigue and malaise (54%) Neck stiffness (35%) Mild arthralgia and myalgia (44%)

The disorder usually begins as a localized infection with constitutional findings and associated symptoms (stage I) (Box 51-1).139,268 Within days to weeks, spirochetes may disseminate through blood or lymph, and neurologic, cardiac, or joint abnormalities may develop (stage II). Finally, chronic, persistent infection of the joints, nervous system, skin, or eyes may occur months or years later (stage III). Although the exact roles of the infecting spirochete, spirochetal antigens, and host immune responses are unclear, tissue invasion and persistence of infection probably cause many of the later manifestations of Lyme disease. This concept is supported by isolation of B. burgdorferi from blood, skin lesions (erythema migrans), and CSF.28,354 The organism has also been identified in the eye,351 myocardium,239 and synovium.334 Patients at all stages of disease respond to appropriate antimicrobial therapy, and early treatment generally leads to an excellent long-term prognosis. Early Localized Disease (Stage I).  The ability of patients to remember a tick bite varies, frequently by species of tick, as some bites are more painful than others. Early localized disease typically begins as a localized erythema migrans rash or lesion, which occurs 7 to 10 days (range, 3 to 32 days) after a tick bite. Approximately 75% of patients with Lyme disease develop an erythema migrans lesion.148,211,264 In one prospective study in New England, erythema migrans was reported in almost 90% of patients with Lyme disease. A large number of these patients were children, however, who often have a greater febrile and dermatologic response.60,139,140,346 There are small regional variations in the development of erythema migrans, which may be due to infections with agents other than B. burgdorferi, such as B. lonestari or a similar agent.125,246,247,345 Erythema migrans may appear anywhere on the body but usually occurs at or near the site of the tick bite. In cases with a single erythema migrans lesion, the most common sites include the head and neck region (26%), extremities (25%), back (24%), abdomen (9%), axillae (8%), groin (5%), and chest (3%).139 In Europe, up to 18% of patients present with disseminated or multilocular erythema migrans.211 The erythema migrans rash is variable in size, ranging from 2 cm (0.8 inches) to more than 60 cm (24 inches) in diameter, and is usually in a circular pattern. To meet the CDC case definition of Lyme disease, the lesion must be at least 5 cm (2 inches). It usually begins as a red macule or papule, with an area of central clearing that becomes more apparent as the lesion expands in size (Figure 51-10). The central region may become indurated and, rarely, necrotic. The borders, which are usually bright red, may expand as much as 1 cm/day (0.4 inch day). These borders are usually flat, although rarely they may be raised or indurated. Occasionally, there are multiple, alternating concentric rings of erythema and clearing, a rash pattern referred to as “bull’s-eye.” The rash is usually warm to the touch. The lesions are sometimes difficult to differentiate from local immune reactions to the tick salivary proteins, and are sometimes confused with secondary bacterial cellulitic reactions. Local immune reactions usually occur within hours of the tick bite and are very pruritic. Secondary cellulitic reactions typically occur within a few days of the tick bite and lack central clearing and rapid expansion. Patients often describe the lesion as burning but may also report itching or pain. Children may develop temperatures to 40° C (104° F), but low-grade fevers are more common in adults.

Constitutional symptoms, such as malaise and myalgias, may also be present. Generalized lymphadenopathy is rare, but local lymphadenopathy may occur. Erythema migrans fades after an average of 3 to 4 weeks (range, 1 to 14 weeks) without treatment; with antibiotics, the lesion resolves after several days and seldom recurs.353 Although the erythema migrans lesions resolve without treatment, untreated patients are at risk for developing early (stage II) or late (stage III) disseminated disease. Early Disseminated Disease (Stage II).  Untreated Lyme disease may enter the second stage, early disseminated disease, within days to weeks after the initial infection. The spirochetes spread from the skin to other organs via blood or the lymphatics. Although organisms can be visualized in peripheral blood smears, they are very difficult to culture from blood. B. burgdorferi has a preference for certain tissues, but it can be found in nearly any organ.348 Dermatologic.  Disseminated erythema migrans is the most common manifestation of stage II disease. These secondary lesions are usually smaller, there are usually many of them, and they may lack the central clearing. They may appear anywhere on the body, with the exceptions of the palms and soles. Ten percent to 15% of patients have more than 20 such lesions; rarely, there are more than 100. Blistering and mucosal involvement do not occur—an important feature in differentiating these lesions from erythema multiforme. Other skin manifestations include a malar rash (10% to 15%) and (rarely) urticaria.353 Borrelial lymphocytoma, an unusual dermatoborreliosis, appears in Europe and western Asia in approximately 1% of patients. Patients typically present with a firm nodule that is red, purple, or blue and one to several centimeters in diameter. It is usually solitary, but multiple lesions may occur in approximately 25% of cases. It often occurs in areas of cooler body temperature, with approximately 80% on the nipple or areola, 10% on the earlobe, and 10% on other areas (including the scrotum).238 It is caused by Borrelia afzelii in approximately 90% of cases, although it has been seen with B. bissettii and B. garinii.238 Histologically, it consists of cutaneous lymphoid hyperplasia, usually in deep portions of the dermis. It may be confused with well-differentiated nodular lymphoma.264 There is associated pruritus, but otherwise it is benign and resolves with appropriate antibiotic therapy. Neurologic.  Neurologic manifestations occur in 10% to 40% of untreated or improperly treated patients.276 Meningitis, encephalitis, and meningoencephalitis are the major neurologic findings of early disseminated disease; lethargy, forgetfulness, disorientation, somnolence, dizziness, photophobia, and incoordination are the most common signs and symptoms. Mood disturbances may also be seen, especially in pediatric patients.27 Nuchal rigidity is sometimes present, along with a severe headache. Lumbar

FIGURE 51-11  An electrocardiograph of a patient with acute myopericarditis. (Courtesy Gregory A. Cummins.)

961

CHAPTER 51  Tick-Borne Diseases

FIGURE 51-10  Author’s leg with classic Lyme disease erythema migrans rash. (Courtesy Gregory A. Cummins.)

puncture reveals CSF with pleocytosis (usually less than 1000 cells/mm3), typically with lymphocyte predominance and high protein level. Paralysis of the facial nerve (cranial nerve VII) may occur and persist for months, and usually resolves spontaneously.72,279 Bilateral facial nerve paresis or paralysis may occur in 25% of cases with cranial nerve VII involvement, usually evolving asymmetrically. Bilateral facial palsy is an unusual physical finding and should suggest Lyme disease, although this finding may also be caused by sarcoidosis, herpes zoster, or the human immunodeficiency virus (HIV). Radiculoneuronitis may be present in various nerves, causing burning, stabbing, or shooting pain. Large nerve bundles such as the brachial plexus are more commonly involved. Mononeuritis multiplex may be present, with peripheral motor weakness and sensory pain. Other neurologic findings are rare but include pseudotumor cerebri, chorea, and dementia.138,185,302 Gastrointestinal.  Ten percent of patients may develop hepatitis, hepatomegaly, and generalized abdominal pain. Hepatic involvement does not progress to hepatic failure; symptoms usually resolve in less than 1 week but may persist for several weeks. Splenomegaly may also occur.268 Cardiac.  Untreated or improperly treated Lyme disease leads to cardiac manifestations in up to 10% of cases.349 Although cardiac involvement is usually self-limited and rarely lifethreatening, temporary intervention is required in some cases.162,197 The most common cardiac manifestation of Lyme disease is conduction delay, which may be of any degree and is found in 80% of cases with cardiac involvement.275 Electrophysiologic studies indicate that the block is at the level of the atrioventricular node. The block does not respond to atropine, suggesting a direct effect on the node.275,310 In cases of complete heart blocks, the presence of spirochetes can be confirmed in cardiac tissue by cardiac biopsy. Noninvasive imaging modalities such as cardiac MRI can be used to document improvement in response to antibiotics.89,197 Conduction delays usually, but not always, resolve with appropriate antibiotic therapy. Patients with first-degree atrioventricular block and a PR interval exceeding 300 msec, as well as all patients with second- and third-degree heart blocks should be admitted for observation and antibiotic treatment. Patients with third-degree heart block require temporary transvenous pacing and may require permanent pacemaker implantation. More diffuse cardiac involvement, such as myopericarditis, is found in about one-half of patients with cardiac involvement. The electrocardiograph (ECG) in such patients usually demonstrates diffuse, nonspecific changes (Figure 51-11). Radionuclide angiography may demonstrate left ventricular dysfunction, but this is seldom clinically significant. Cardiomegaly due to Lyme disease rarely occurs in U.S. patients, although dilated cardiomyopathy is often reported in Europe.336,344 Valvular involvement is uncommon. At least one death has been linked to cardiac involvement,239 but abnormalities usually resolve completely, often within 1 to 2

PART 6  ANIMALS, INSECTS, AND ZOONOSES

weeks.349 Severe cardiac complications have been described in pediatric patients but are relatively rare.139 Rheumatologic.  Monoarticular arthritis develops in 60% of patients with erythema migrans who are not treated, usually occurring between 4 weeks and 2 years after the onset of illness.358 Although common in North America, arthritis is rarely a finding in other areas of the world.71,348 In adult patients, arthritis may occur in a migratory pattern, involving many joints, usually one joint at a time. Joint involvement typically occurs for about a week (median, 8 days), but it may persist for months. Many patients have repeated episodes of arthritis, and each subsequent recurrence is less severe. Soreness often persists between episodes, never fully resolving, and persistent morning stiffness is common. The knee is most commonly affected, followed by the shoulder, elbow, temporomandibular joint, ankle, wrist, hip, metatarsals, and metacarpals.399 Joint swelling is not common except in the knee, and the joints are typically described as more sore than painful. Chronic effusions often occur. In pediatric patients, arthritis appears an average of 4.3 months after initial infection, with a broad range of a few days to 20 months.139,140 Approximately 50% of pediatric patients have multiple recurrences, although complete remission between episodes is typical and chronic arthritis is uncommon. Ninety percent of children in a large study had arthritis in at least one knee.140 Synovial fluid of involved joints has a median WBC count of 25,000/mm3, with polymorphonuclear leukocyte predominance. Synovial membrane biopsy shows cellular hypertrophy, vascular proliferation, and mononuclear cell infiltrate.352,356 PCR testing of synovial fluid is positive in 85% of cases of Lyme arthritis. The organism may also persist in synovial tissue. Four patients who completed antibiotic therapy for Lyme arthritis and who subsequently had negative PCR testing of synovial fluid had positive PCR testing of the synovial membrane.289 This persistence may account for the reactivation of Lyme arthritis that has been described after autologous chondrocyte transplantation for degenerative joint disease or cartilage injury.244 Late Disease (Stage III).  Late disease may occur a year or more after the initial presentation, and usually has rheumatologic, neurologic, and dermatologic manifestations. Recurrent hepatitis, eosinophilic lymphadenitis, acute respiratory distress syndrome (ARDS), and other rare manifestations may also be present. Rheumatologic.  Arthralgias and oligoarthritis occur in approximately 50% of untreated patients.355 In about 10% of patients, cartilage loss, subarticular sclerosis, osteophyte formation, cortical or marginal bone erosions, joint effusions, and other radiographic signs of degenerative arthritis may be seen.219 The rheumatologic workup, including erythrocyte sedimentation rate, C-reactive protein (CRP), antinuclear antibodies, and rheumatoid factor, is generally negative.355 Interestingly, late rheumatologic disease is rare in children.405 Neurologic.  Central nervous system (CNS) involvement may develop months to years after the initial infection. Patients most typically present with progressive encephalomyelitis, with ataxia, cognitive impairment, spastic paresis, and involvement of cranial nerves VII and VIII.2 Rarely, strokes, seizures, and dementia may occur.119 Lumbar puncture in patients with stage III CNS involvement reveals CSF with a lymphocytic pleocytosis and anti–B. burgdorferi antibodies. Magnetic resonance imaging (MRI) of the brain reveals white matter changes consistent with encephalop­ athy. In seropositive pediatric patients, the meningoencephalitic changes are often seen as behavioral changes and are noted more often in boys than girls.27,193 Peripheral nervous system involvement may manifest as peripheral paresthesias, painful radiculopathies, and motor nerve palsies. The underlying pathophysiologic mechanism appears to be mononeuritis multiplex.127 Such patients may present with radicular pain that is frequently asymmetric, originating in the spine and referring to the extremities. Nerve conduction and electromyographic studies show mild axonal polyneuropathy with decreased motor or sensory nerve conduction velocities, with denervation of spinal and limb muscles.127 Dermatologic.  Patients with late-stage dermatologic invol­ vement present with acrodermatitis chronica atrophicans, also 962

called diffuse idiopathic cutaneous atrophy. It is found almost strictly in central and southern Europe and is caused by B. afzelii. It may persist for many years.269 The dermatitis usually occurs on the distal extremities, often having started at a previous area of erythema migrans, commonly on the extensor surfaces of the extremities. It begins as inflammation, hyperpigmented with red or blue, and is followed by scarring and atrophy of the skin. The atrophy causes the skin to thin, and it later becomes hypopigmented. Hair loss and dysfunction of sweat and pilosebaceous glands also occur.264 Other findings, such as polyneuropathy, may accompany these skin changes. Borrelia has been cultured from 10-year-old lesions of acrodermatitis chronica atrophicans. Histologically, fibrosis occurs early, the glands become infiltrated, and the dermis reveals a patchy to bandlike mononuclear infiltrate composed of lymphocytes, histiocytes, and plasma cells in greater numbers than those found in typical erythema migrans lesions.264 “Chronic Lyme Disease.”  There is considerable debate over whether a chronic form of Lyme disease exists. Some patients develop chronic persistent Lyme disease symptoms despite repeated antibiotics. Whether this is a sequela of pathogen resistance or chronic auto-inflammation, auto-immunity or a form of fibromyalgia is highly debated.145 A collection of symptoms, lumped into a category sometimes referred to as postborreliosis syndrome or post–Lyme disease syndrome (PLDS), consists of signs and symptoms such as persistent fatigue, sleep disorders, depression, cognitive defects, mood swings, and other neuropsychiatric manifestations.228 This symptom complex fails to respond to traditional antibiotics. This collection of symptoms might be an entirely separate disease, or partially treated Lyme disease, or the disease complicated by the cystic form, which is difficult to treat. As early as the early 1900s, spirochetes were noticed to have developed into cysts, also called blebs or vesicles. Today, these cysts are called spherocytes, or the L-form of the spirochete.46 These spherocytes are induced under adverse conditions, such as the presence of antibodies targeted against the spirochetes, adverse pH, or adverse temperatures. Thus, the spherocytes may be responsible for the spirochetes’ surviving conditions that would kill or deactivate the typical spirochete form.266 When environmental conditions again become favorable for the spirochetes, the cysts or spherocytes convert back to the traditional spirochete form.40 Further research is likely to yield more information about the existence of and appropriate treatment of the cystic form of the disease, such as the addition of antiprotozoal medications to the treatment regimen.41,42 Patients afflicted with these persistent symptoms are very active in pursuing formal recognition and treatment of these disorders through political, legislative, and research means. However, at the present time, there is no evidence-based medicine to support prolonged antibiotic therapy for patients with any manifestation of Lyme disease.407 Lyme Disease in Pregnancy.  Fetal demise may result in mothers who develop Lyme disease in pregnancy.232,243,320,390 Transplacental transmission of Lyme disease is rare but appears to be associated with an increased risk of cardiac malformations.398 Lyme disease in pregnancy should be aggressively treated. A 1996 prospective study of 58 pregnant women with erythema migrans given oral or intravenous (IV) penicillin or ceftriaxone reported only seven adverse outcomes, none clearly associated with Lyme disease.237 The American College of Obstetrics and Gynecology recommends oral penicillin or amoxicillin for 3 weeks in pregnant women with cutaneous involvement or recent tick bites in endemic areas. For patients with severe acute disease, or disseminated or late disease, 3 weeks of parenteral penicillin is recommended. If the patient is allergic to penicillin, parenteral erythromycin is recommended.11,111 Tetracyclines should not be used in pregnancy. Diagnosis.  The CDC has established a surveillance case definition for Lyme disease. This case definition requires exposure to ticks in an endemic county and an erythema migrans lesion, diagnosed by a physician, that is larger than 5 cm (2 inches). In this definition, exposure requires outdoor activities within

would likely clarify the disease diagnosis.221 If another illness develops, as occurred in 20% of patients referred to the New England Medical Center clinic, it may be incorrectly attributed to Lyme disease. This is particularly problematic in patients with nonspecific symptoms of chronic fatigue or fibromyalgia, in whom the predictive value of a positive ELISA is low. Overdiagnosis of Lyme disease has significant health system and patient care implications. In another study of 209 individuals referred to a university-based Lyme disease clinic with a diagnosis of the disease, only 21% met the criteria for active Lyme disease, 60% had no evidence of current or previous infection, and 19% had evidence of previous but not active disease. The 79% of patients without active Lyme disease displayed significant anxiety and stress related to their diagnosis of Lyme disease, used considerable health care resources, and had frequent adverse antibiotic reactions.301 Treatment.  Although most manifestations of Lyme disease resolve spontaneously without treatment,317 treatment of Lyme disease with appropriate antibiotics hastens recovery in all stages of the disease. Both in vitro and in vivo studies have confirmed that B. burgdorferi is highly sensitive to tetracyclines, amino­ penicillins, ceftriaxone, and imipenem.170,188,189 The macrolides, oral second- and third-generation cephalosporins, and chloramphenicol all seem to have equal efficacies.5,188 Although fluoroquinolones have traditionally not been effective against Borrelia species, the fourth-generation fluoroquinolone antibiotics seem to have good efficacy in vitro.206 However, some B. burgdorferi strains are showing in vitro resistance to the newest fluoroquinolones.137 Table 51-3 lists general antimicrobial therapy options and recommendations for Lyme disease. In early localized Lyme disease (stage I), amoxicillin and doxycycline are the drugs of choice. Tetracyclines should not be used in pregnancy, in lactating women, or in children under age 9 years. The recommended treatment duration is 10 to 20 days. In one study, 10 days of treatment with doxycycline showed the same efficacy as 20 days, with fewer side effects. This may rarely be extended to 4 weeks if symptoms persist or recur, although no hard evidence exists for doing so.407 Medications that will penetrate the CSF are ideal and may lead to less disease recurrence.229 Sequestering of spirochetes in the brain may account for some apparent antibiotic failures, as not all antibiotics cross the blood–brain barrier. Within the first 24 hours of treatment with antibiotics, up to 15% of patients develop a Jarisch-Herxheimer reaction (JHR), which manifests as a rise in temperature, vasodilation, and hypotension.269 Normal saline infusion around the time of initial dosing of antibiotics may help reduce the degree of hypotension. In rare cases, JHR may be severe and fatal. Symptoms rarely persist beyond 24 hours. Disseminated disease (stages II and III) should be treated according to severity. In mild disseminated disease (such as secondary erythema migrans or cranial nerve VII palsy), 3 weeks of oral doxycycline is as effective as 2 weeks of parenteral ceftriaxone.84 In patients initially treated with oral antibiotics who are therapeutic failures or in whom disease recurs, parenteral antibiotics are indicated. Patients with severe disseminated disease (neuroborreliosis, high-degree heart block) require parenteral antibiotics for up to 4 weeks.83,227 Ease of once-daily administration of ceftriaxone makes it a better choice for both inpatient and outpatient administration than other typically used agents requiring administration three or four times daily.83,84 Neurologic symptoms begin to improve with therapy within 1 week, although full resolution may take 7 to 8 weeks.357 Prolonged oral antibiotics are often necessary to treat stage III arthritis, sometimes for as long as 4 to 8 weeks.357 Delayed clinical response in arthritis is not uncommon. Nonsteroidal antiinflammatory drugs (NSAIDs) may also reduce symptoms, and reduce disease recurrence by simultaneously treating the inflammation.145 No vaccines are presently available for the prevention of Lyme disease in humans. A vaccine based on recombinant outer surface protein A (OspA) was approved in 1998 but was removed from the market by the manufacturer in 2002. The vaccine had limited efficacy, required frequent boosters, was expensive, could not 963

CHAPTER 51  Tick-Borne Diseases

30 days of the onset of the lesion. An endemic county is one in which at least two confirmed cases of Lyme disease have been acquired, or known tick vectors are established. It is important to note that Lyme disease case definitions are designed for national reporting, not individual patient diagnosis. The clinical diagnosis of Lyme disease is based on history, clinical suspicion, and a working knowledge of the disease process and epidemiology; laboratory tests may be performed but generally serve only to confirm the presence of the disease. Routine laboratory examinations may reveal nonspecific findings, such as elevated liver enzymes (alanine transaminase [ALT], aspartate transaminase [AST], and/or gamma-glutamyltransferase [GGTP]) decreased leukocyte count, and elevated erythrocyte sedimentation rate. Immunoglobulins A and G (IgA and IgG) are usually normal, whereas IgM is usually elevated, especially in severe disseminated disease. Culture is the gold standard for diagnosis but is often difficult to obtain. Biopsy of an erythema migrans skin lesion is positive in 60% of punch biopsies from the leading edge of the lesion, and this figure may be as high as 80% in specialty centers.32 The production of anti–B. burgdorferi antibody develops slowly, and serologic assays in the first 3 to 6 weeks of illness are often negative unless severe disease is present.257,328 In some patients, treatment with antibiotics may blunt or entirely suppress the antibody response; in others, IgG and IgM antibodies may persist for years after resolution of clinical symptoms.121 Patients with complicated Lyme disease (with neurologic, cardiac, or joint involvement) or those in remission are more likely to have elevated specific antibody titers.257,328 Serologic testing has the highest predictive value in patients with a pretest probability of having Lyme disease between 20% and 80%.374 Patients from endemic areas with an 80% or higher pretest probability of having the disease benefit from empiric treatment, not testing. Patients with a pretest probability of less than 20% have a high likelihood of a false-positive testing. Indirect immunofluorescent assay (IFA), enzyme-linked immunosorbent assay (ELISA), and Western blot test are the most commonly used tools to detect antibodies to B. burgdorferi. For diagnostic purposes, ELISA appears to be the most accurate, with 89% sensitivity and 72% specificity. Low levels of agreement are common between various laboratories and individual assays.325 Western blot has proved to be a poor screening tool. New tests using recombinant proteins or synthetic peptides as ELISA antigens yield detection rates for serum antibodies of 20% to 50% for early disease, 70% to 90% for early disseminated disease, and nearly 100% in late disease.400 Although Western blot is a poor screening tool, it is useful to confirm a positive ELISA result. Only positive serologic assays confirmed by Western blot meet the criteria for laboratory diagnosis, according to the CDC national consensus panel. Many disease states, including other treponemal diseases, autoimmune diseases, and some viral diseases may give false-positive ELISA results.257 Antibodies directed toward oral flora may also cause false-positive results.10,257 A current research tool, reverse transcriptase DNA PCR, is both highly sensitive and specific for Lyme disease. With decreasing costs and increasing availability, PCR is rapidly finding its way into the diagnostic armamentarium.116,221 Patients with vague nonspecific symptoms such as chronic fatigue, musculoskeletal pains, and other neuropsychiatric signs and symptoms, in the absence of true Lyme disease signs and symptoms, should, in general, not undergo serologic testing for Lyme disease. Positive results in such patients are probably falsely positive and may create an inordinate amount of confusion and conflict. The importance of appreciating the limitations of serologic testing cannot be overstated. In one study, only 23% of patients referred to the Lyme Disease Clinic at New England Medical Center had active Lyme disease, and a majority of those without Lyme disease had been treated inappropriately with antibiotics.356 In this study, the most common reason for lack of response to antibiotics was misdiagnosis. The limitations of laboratory testing in Lyme disease include lack of sensitivity and specificity of serologic tests and considerable interlaboratory and intralaboratory variability in test results.325 Persistence of antibodies in patients with past or asymptomatic infection with B. burgdorferi also complicates serologic testing. PCR testing in these situations

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 51-3  Antimicrobial Recommendations for Lyme Disease Drug

Dose*

Duration (days)

Early Localized Disease Adults Tetracycline 250-500 mg PO QID 100 mg PO BID Doxycycline 500 mg PO TID Amoxicillin 500 mg PO TID Cefuroxime Children Amoxicillin 50 mg/kg/d PO divided TID Doxycycline (older than 8 yr) 100 mg PO BID 30-50 mg/kg/d PO divided QID Erythromycin Tetracycline (older than 8 yr) 250 mg PO QID 30-40 mg/kg/d PO divided BID Cefuroxime axetil Early Disseminated and Late Diseases† and Late Disseminated Neurologic Disease‡ Adults 2 g IV qd Ceftriaxone Cefotaxime 2 g IV q 8 hr Penicillin G 20 million IU/d IV divided q 4 hr Children Ceftriaxone 75-100 mg/kg/d IV qd 90-180 mg/kg/d IV q 8 hr Cefotaxime 300,000 U/kg/d IV q 4 hr Penicillin G Late Disseminated Arthritis Adults Amoxicillin 500 mg PO QID 100 mg PO BID Doxycycline Ceftriaxone 75-100 mg/kg/d IV qd Children Amoxicillin 50 mg/kg/d PO divided TID Ceftriaxone 80-100 mg/kg/d IM/IV divided BID–qd Disseminated Disease and Carditis Adults Doxycycline§ 100 mg PO BID Amoxicillin§ 500 mg PO q 8 hr Ceftriaxone¶ 2 g/d IV qd Children Ceftriaxone 75-100 mg/kg IV/IM qd 300,000 U/kg/d IV divided q 4 hr Penicillin G

14-28 14-28 14-28 14-28 14-28 14-28 14-28 14-28 14-28

14-28 14-28 14-28 14-28 (max, 2 g/d) 14-28 14-28 (max, 20 million U/d)

28 28 14 (max, 4 g/d) 28 14 (max 2 g/d)

21-28 21-28 14-28 14-21 (max, 2 g/d) 14-21 (max, 20 million U/d)

BID, Twice a day; IM, intramuscularly; IV, intravenously; PO, orally; QID, four times a day; qd, every day; TID, three times a day. *Total daily dose shown to be divided (if necessary) as indicated. † For multiple lesions of erythema migrans, use treatment for early localized disease for at least 21 days. For isolated facial palsy, use treatment for early localized disease for at least 21-28 days. ‡ Neurologic involvement limited to an isolated facial palsy should be treated as early disease. § For mild cardiac involvement (i.e., first-degree atrioventricular block with PR interval less than 0.30 second). ¶ For second- or third-degree heart block, although no evidence indicates that intravenous is better than oral regimens.

be used in children, and resulted in an apparent immunogenic reaction in some vaccinated individuals.163 Future vaccines, although still in their infancy, will most likely use polyvalent outer surface protein C (OspC). Treatment of asymptomatic tick bites in patients who are in areas endemic for Lyme disease is controversial, although this does not stop patients from requesting care. In one survey, physicians in Maryland reported seeing 11 times as many patients seeking help after “tick bites” as they did actual cases of Lyme disease.75 Three randomized, placebo-controlled studies have addressed antibiotic prophylaxis for tick bites.6,74,327 Of patients in the placebo groups, 1% to 3.4% developed Lyme disease or had evidence of seroconversion, even though 15% to 30% of ticks were infected; no patients in the treatment groups developed Lyme disease. A meta-analysis of the three studies concluded that there was no significant difference between the groups, and that routine prophylaxis of tick bites is not warranted except in pregnancy, even in endemic areas.389 Many physicians do not adhere to this recommendation, however. Maryland physicians ordered serologic testing in twothirds of patients with asymptomatic tick bites and treated more than one-half with prophylactic antibiotics.131 The concern often cited for such practices is that patients with tick bites who 964

become infected may not develop erythema migrans (when the disease is easily treated) but go on to develop the late and more serious manifestations of Lyme disease. Some of these decisions are likely driven by patient pressure, as well as defensive medicine. The risk of serious late sequelae in untreated patients with a tick bite, however, is extremely low, for three reasons. First, less than 5% of those bitten by the I. scapularis tick in endemic areas become infected. Second, most patients with an identified tick bite remove the tick before it has been attached for the 24 to 48 hours required to transmit an infectious inoculum of B. burgdorferi. Finally, 80% to 90% of the few patients who become infected develop erythema migrans, which makes diagnosis and treatment easy. Physicians must therefore weigh a number of factors related to the likelihood of disease acquisition in deciding whether to treat asymptomatic tick bites with antibiotics. These factors include species and stage of the offending tick, duration of attachment, geography, and patient factors such as pregnancy. If a decision is made to treat, reasonable initial antibiotic choices include a 10-day course of either amoxicillin or doxycycline. Overtreatment of presumed Lyme disease with antibiotics has significant health care ramifications. If the patient does not have Lyme disease, treatment failure is virtually ensured. Patients being

Southern Tick-Associated Rash Illness Since the mid-1980s, erythematous rashes similar to those seen in early Lyme disease have been found in persons from the southeastern and south-central states, a geographic area in which the presence of Lyme disease is in dispute.246 A correlation was noted between these rashes and the bite of the lone-star tick, A. americanum (see Figure 51-6). A causative agent, B. lonestari, has been discovered in ticks and in patients by detecting DNA from Borrelia in specimens and by culturing the organism.377,378 The disease has since been named southeastern tick-associated rash illness, or STARI, but it is also known as Master’s disease and southern Lyme disease.246 A new rickettsia, R. amblyommii, has been implicated in STARI (as well as in Rocky Mountain spotted fever in some southern states).13,272 A. americanum ticks are found throughout the southeastern and south-central United States, and along the eastern seaboard into Maine. All three stages of A. americanum feed aggressively on humans, and various stages are found in most of its distribution throughout the year. Patients with the disease present with a rash similar to erythema migrans, although it may lack the central clearing. Skin findings are followed by generalized fatigue, headache, myalgias, and other generalized symptoms.35 A. americanum ticks have proportionately large mouthparts (see Figure 51-6) and are very immunogenic; the rash is therefore sometimes difficult to distinguish from a local reaction. A local reaction is immunogenic and typically occurs within hours of the tick bite, whereas the STARI rash or a cellulitis occurs several days after the bite. Diagnosis at the present time is by gene amplification of B. lonestari using PCR. The disease is currently believed to be selflimited, although current recommendations are that it be treated with a course of an oral tetracycline. Research into STARI is in its infancy and will probably yield much more information over the next decade. Tick-Borne Relapsing Fever Tick-borne relapsing fever (TBRF) is an acute borrelial disease characterized by recurrent paroxysms of fever, separated by afebrile periods. It occurs in both endemic and epidemic forms. The endemic or sporadic form occurs worldwide and is caused by a group of closely related Borrelia species (Table 51-4). The epidemic form of relapsing fever, louse-borne relapsing fever (LBRF) is transmitted by the human body louse and has not been reported in the United States in recent years, although it is among the top ten causes of hospitalization in some African nations.77 The Ornithodoros ticks that transmit TBRF act as both vectors and reservoirs for Borrelia organisms; wild rodents also serve as reservoir hosts.372 Ticks ingest Borrelia organisms while feeding on an infected vertebrate, most often a rodent. Borreliae enter the tick hemocele and then spread to other tick tissues, including the salivary glands, coxal organs, and reproductive organs. The coxal organs in argasid ticks are specialized for excretion of excess fluids and solutes accumulated during feeding. In some Ornithodoros species, the coxal fluid is released near the mouthparts during feeding, allowing transmission of spirochetes to vertebrate hosts. Transmission may also occur through saliva or regurgitated gut contents.20 Borreliae remain infective within ticks for many months.338 Transovarial transmission allows all developmental stages to be potentially infective. The ticks generally feed at night and attach themselves to the host for a short time, usually less than 1 hour. The bite is seldom painful and frequently goes unrecognized. The ticks are extremely resilient and may survive for years between feedings. A high degree of specificity exists between the major strains of Borrelia that cause relapsing fever and their associated tick vectors. For example, the three Borrelia species found in the United States—Borrelia hermsii, Borrelia turicatae, and Borrelia

TABLE 51-4  Tick-Borne Relapsing Fever Arthropod Vector Ornithodoros hermsi Ornithodoros turicata Ornithodoros parkeri Ornithodoros moubata Ornithodoros tholozani Ornithodoros tartakovskyi Ornithodoros erraticus Ornithodoros graingeri Ornithodoros talaje Ornithodoros rudis Ornithodoros asperus Ornithodoros marocianus

Borrelia Species Borrelia hermsii Borrelia turicatae Borrelia parkeri Borrelia duttonii Borrelia persica Borrelia latyschevi Borrelia crocidurae Borrelia graingeri Borrelia mazzottii Borrelia venezuelensis Borrelia caucasica Borrelia hispanica

Geographic Distribution Western United States and Canada Southwestern United States and Mexico Western United States and Mexico Tropical Africa Central Asia, Middle East, Greece Iran, central Asia Russia, Middle East, East Africa, Turkey Kenya Mexico, Central America Central and South America Iraq, Russia Northern Africa, southern Europe

parkeri—show complete specificity for their respective tick vectors Ornithodoros hermsi, Ornithodoros turicata, and Ornithodoros parkeri. This specificity is used extensively in the classification of Borrelia species.86 Epidemiology.  Ornithodoros ticks generally inhabit rodent burrows and nests, and cracks and crevices in human and animal habitats, caves, and similar locations. Habits and patterns of infection vary between tick species. In parts of Africa, ticks live in the dust and cracks of earthen-floored huts, and sporadic cases are seen throughout the year. In the Middle East, Mexico, and southwestern United States, ticks live in the guano on cave floors, and human infection is often associated with visiting or camping in caves. The majority of cases of TBRF in the United States are attributed to B. hermsii. Its vector, O. hermsi, inhabits the coniferous forest biome, where it lives in remains of dead trees and burrows inhabited by mice, rats, and chipmunks. Ticks are carried by rodents into poorly maintained cabins and huts. Lodging in such shelters by hikers and hunters is a major factor in acquiring relapsing fever,126,179 and rodent-proofing such shelters dramatically reduces the risk of acquiring TBRF.277 Occasional cases are also caused by O. turicata (transmitting B. turicatae) in Texas (associated with travel into caves) and adjacent areas of the Southwest; O. parkeri (transmitting B. parkeri) rarely bites humans.177 TBRF is found throughout most of the world, and endemic areas include 14 western states, from Colorado to California up to the Pacific Northwest,109,126,179 and southern British Columbia in North America. TBRF is also found throughout the plateau regions of Central and South America, central Asia, Mediterranean countries, and most of Africa. TBRF is not a mandatory reportable disease, and is thus, like many tick-borne diseases, grossly underreported. In California, where reporting of relapsing fever is encouraged, two to 12 cases are reported per year, with only 25 cases per year nationwide.109,67 Large outbreaks have been reported from Spokane County in Washington,369 Colorado,372 and the north rim area of the Grand Canyon.61 Between 1985 and 1996, the 285 cases of TBRF reported in the United States occurred in California, Colorado, Idaho, Texas, Washington, Arizona, New Mexico, Nevada, Oregon, Utah, and Wyoming.372 Although the vast majority of cases occur in states where TBRF is endemic, a review of 450 cases of TBRF acquired in the United States from 1977 to 2000 noted that 7% of cases were diagnosed in states where it is not endemic.107 TBRF is more common in 965

CHAPTER 51  Tick-Borne Diseases

treated for Lyme disease have a significant amount of anxiety regarding the diagnosis.301 Adverse drug reactions may occur. Overuse of antibiotics has led to resistance to multiple antibiotics by many organisms, although resistance to tetracycline is not documented for Borrelia.12

PART 6  ANIMALS, INSECTS, AND ZOONOSES

men, presumably because of increased exposure to tick vectors, and occurs primarily during summer months. TBRF is rarely fatal in adults, but in infants younger than age 1 year, case fatality rates may be 20% or higher.220,338 Clinical Manifestations.  Ornithodoros ticks feed for a relatively short period (often less than 1 hour) and at night, so most patients have no recollection of a tick bite. After an incubation period of about a week, patients develop the characteristic clinical features of TBRF: abrupt onset of a fever lasting about 3 days (range, 12 hours to 17 days), followed by an afebrile period of variable duration, then relapse with return of fever and other clinical manifestations. The initial febrile period terminates with rapid defervescence or “crisis,” accompanied by drenching sweats and intense thirst. Febrile periods in TBRF are associated with spirochetemia. Resolution of fever occurs when the host develops an adequate antibody response to the spirochete. During afebrile periods, the spirochetes remain “hidden” in organ tissue and undergo antigenic conversion to a new serotype (see Antigenic Variation, later). Relapse occurs when the new serotype causes a new round of spirochetemia. After being bitten by an infected tick, victims may develop a pruritic eschar at the site of the tick bite, but the lesion is usually absent by the time the clinical symptoms appear. Victims typically develop fever, frequently accompanied by shaking chills, severe headache, myalgias, arthralgias, upper abdominal pain, photophobia, cough, nausea, and vomiting. The temperature is usually greater than 39° C (102.2° F), and patients may present with extreme muscular weakness and lethargy. Splenomegaly develops in approximately 40% and hepatomegaly in 18% of patients with TBRF. From 10% to 40% have neurologic involvement, approaching the incidence seen in Lyme disease. The most common neurologic complications are meningismus and facial nerve palsy.51 Facial palsy, when present, typically occurs after the second febrile episode and usually resolves within 2 to 9 weeks with or without treatment. Other reported neurologic complications include neuropsychiatric disturbances, encephalitis, peripheral neuropathy, myelitis, and pathologic reflexes. Iritis or iridocyclitis occurs in up to 15% of untreated cases, typically occurring later in the fever course. Formation of adhesions between the iris and anterior lens capsule may lead to visual defects. A rash, which may consist of a macular eruption, petechiae, or erythema multiforme, develops in 25% to 30% of patients.338 Mortality rates have been as high as 40% in some epidemics of louse-borne relapsing fever,115 but TBRF is generally selflimited. Only rarely are clinical features severe and prolonged. Neurologic complications generally resolve spontaneously, but severe depression may persist for months. Hemorrhagic complications, pneumonia, ARDS, hepatosplenomegaly, petechiae, or myocarditis may develop rarely.87,126,393 In a 6-month period in three western states, there were three separate cases of ARDS from TBRF, all requiring mechanical ventilation.67 Relapsing fever in pregnancy results in a high incidence of spontaneous abortion, premature birth, and perinatal morbidity.338 Fetal death is probably caused by direct placental invasion by spirochetes, resulting in thrombocytopenia and retroplacental hemorrhage.347 Prior studies have linked pregna­ ncy with a more serious maternal disease course.159,256,257 A more recent case–control study, however, found no significant difference in pregnant women’s mortality or complications.191 Infection in the neonatal period usually occurs by placental transmission and appears as overwhelming sepsis with very high mortality.408 Antigenic Variation.  The phenomenon of relapse in TBRF is caused by the ability of borreliae to undergo antigenic variation in an infected host. The organisms are capable of spontaneous conversion to many serotypes. Clinically, defervescence occurs when the dominant serotype is eradicated by interaction with host antibody. Spirochetemia probably persists at undetectable levels during the afebrile period and consists of mixed serotypes. Relapse occurs when a variant population reaches detectable levels. Antigenic variation is under complex genetic control and does not appear to require contact of the organism with host antibody.19,361 966

Diagnosis.  Clinical diagnosis of TBRF requires thorough knowledge of the epidemiology of the disease and a high index of suspicion. TBRF is uncommon and occurs only sporadically. A history of recent exposure to old cabins, caves, or any rodentfriendly environment should raise the specter of TBRF. Routine laboratory tests are of little value. The WBC count is usually normal but may be increased or decreased. A left shift is often present. Thrombocytopenia is common but nonspecific. The CSF is often abnormal, with lymphocytic pleocytosis (typically 10 to 2000 cells/mm3), usually with normal glucose and elevated protein. A false-positive serologic test for syphilis (Wassermann test) occurs in about 5% of cases.338 The diagnosis of relapsing fever is confirmed by demon­ strating spirochetes on peripheral blood smears, and carries a higher positive predictive value when obtained early in the course of the disease, during a febrile episode. A routine peripheral blood smear (Wright-Giemsa stain) from a febrile patient is initially positive in 70% of cases.338 The diagnostic yield can be increased by examining thick smears and by staining with acridine orange using fluorescence microscopy.326 Inoculating laboratory animals (rats, mice) with blood and examining blood smears from the animals will also increase the diagnostic yield. Visual yield of spirochetes in peripheral blood smears diminishes with each successive febrile sampling. B. hermsii can be cultured in BSK-II medium, with the yield increasing in acutely febrile patients. Serologic tests are difficult to perform and do not yet have practical usefulness.372 TBRF is probably under-recognized and underreported and has been misdiagnosed as Lyme disease.107 Treatment.  Tetracycline and erythromycin are both effective in treating relapsing fever. A single oral dose of 500 mg of either drug is effective in louse-borne relapsing fever.50 However, a 7- to 10-day course (500 mg orally four times a day) is generally recommended in the tick-borne disease.177,338 For children younger than age 9 years, erythromycin (30 to 50 mg/kg/day in four divided doses) is recommended, with the first dose given intravenously. The borreliae are also sensitive to penicillin and chloramphenicol, but treatment failures have been reported with all agents.50 A Jarisch-Herxheimer reaction ( JHR) has been documented after administration of ciprofloxacin in a pediatric patient.391 Animal studies have shown that early treatment with a β-lactam antibiotic within 24 hours of onset of spirochetemia decreases CNS involvement.51 JHR often occurs after the first dose of antibiotics. In one series, 54% of patients developed a JHR.107 It is often severe and may be fatal. The reaction begins with a rise in body temperature and exacerbation of existing signs and symptoms; vasodilation and a fall in blood pressure follow. This complex reaction is mediated in part by products of mononuclear leukocytes. The leukocytes are stimulated by increased contact with antibioticaltered spirochetes. Neither endotoxin nor complement appears to be necessary in the pathogenesis of JHR.49 JHR typically occurs within a few hours of initial antibiotic dosing. Waiting to begin treatment until the patient is afebrile does not prevent JHR.179 Pretreatment with acetaminophen and hydrocortisone results in only mild reduction of hypotension and does not prevent rigors.50 Patients who are receiving the initial dose of antibiotics for relapsing fever should receive an IV infusion of isotonic saline in anticipation of a possible JHR. This is generally sufficient to counteract hypotension. Lower initial dosages of tetracycline or erythromycin may reduce the frequency of JHR.179 In Israel, tick-borne relapsing fever is caused by Borrelia persica, transmitted by Ornithodoros tholozani ticks. In one study, doxycycline 200 mg PO day 1, then 100 mg PO days 2 through 5 was safe and efficacious in preventing disease following exposure to ticks in a high-risk environment.165

TICK-BORNE VIRAL DISEASES Tick-Borne Encephalitis Tick-borne encephalitis (TBE) is known by myriad names, including bi-undulating meningoencephalitis and biphasic milk fever. It is caused by a flavivirus and is found throughout Europe and

Colorado Tick Fever Colorado tick fever (CTF) is caused by a retrovirus of the genus Coltivirus. Also called mountain tick fever, mountain fever, and American mountain fever, CTF is the only tick-borne virus that occurs with significant frequency in the United States. CTF is found in the western third of the United States and Canada and is primarily transmitted by D. andersoni, although other vectors are implicated.216 Larval stages of D. andersoni ingest the virus while feeding on a viremic rodent host and pass it transtadially from larva to nymph to adult. Hibernating nymphs and adults carry the virus through the winter. Infected ticks emerge in the spring and feed on susceptible animals, renewing the cycle. Nymphal and adult ticks may also acquire the virus by feeding on viremic hosts. The virus does not appear to cause disease in its natural hosts; it cycles between the vector ticks and many reservoirs, primarily rodents.252 Typically, only adult ticks transmit the disease to humans, who are incidental and dead-end hosts. The attachment time required for transmission may be very brief. In human infection, viral

replication occurs in bone marrow, lymph nodes, spleen, and hematopoietic erythrocyte precursor cells, and virus is thus found in mature erythrocytes, protected from the body’s immune system.196 Disease transmission usually occurs from March through September, with the lower elevations yielding cases at the season’s extremes, and the higher elevations producing cases in the middle of the season. The incidence is 200 to 300 cases per year in the United States, usually confined to the western states, although remote cases are reported in other areas. CTF is primarily found in areas higher than 1219 m (4000 feet) above sea level. Blood transfusion has been documented as a means of its transmission, and the virus has been documented in blood samples up to 4 months after infection.53 Ninety percent of patients can recall a tick exposure. The incubation period is usually 3 to 6 days (range, 0 to 14 days),154,340 after which the disease typically manitest with acute onset of fever. The fever is classically taught as being biphasic (like dengue fever), with fevers to 40° C (104° F) for a few days to a week followed by a brief remission prior to another bout of similar duration. This “saddle-backed” temperature pattern, however, is present in only about one-half of patients.154,340 In some cases, further exacerbations of the fever cycle may occur. The fever may also be monophasic, presenting with persistent fever rather than defervescence and relapse. Other symptoms suggestive of a viral illness may occur in mild cases. Severe complications can occur, particularly in children younger than age 10 years. Meningoencephalitis has been described in several children.62,101,330,340 Two children developed a hemorrhagic diathesis and died.154 Other unusual complications associated with CTF include pericarditis,1,174 myocarditis,112 hepatitis,226 epididymo-orchitis,156 and pneumonitis.154 Information on CTF contracted during pregnancy is inconclusive, but of five cases reported, one terminated in a spontaneous abortion and in another, a live-born infant suffered multiple congenital anomalies.261 CTF virus is known to be teratogenic in mice.164 Laboratory abnormalities in CTF are not specific. Leukopenia involving both granulocytes and lymphocytes is common and may be helpful diagnostically, although one-third of patients have normal WBC counts.143 Thrombocytopenia may also develop; anemia associated with the virus is rare. Liver function tests may be elevated. Diagnosis is usually made on clinical grounds. The most reliable means of laboratory diagnosis is inoculating suckling mice or cell cultures with blood or CSF from a febrile patient. PCR is slowly finding use as a diagnostic tool as well, and is both highly sensitive and specific for this and many other tick-borne diseases.281,308 Serologic testing (neutralizing antibody, complement fixation, IFA) by immunoassay is available; however, antibody titers are slow to rise, making these tests better for following efficacy of treatment than for establishing the diagnosis. Treatment is entirely supportive. Recovery takes several weeks, especially in persons older than 30 years,154 and persistent malaise and weakness are common. Infection generally confers lifelong immunity. Pajaroello Tick Bites In the mountainous regions of coastal southern California, Mexico, and South America, the pajaroello (pajahuello) tick, Ornithodoros coriaceus, readily attacks cattle, deer, and humans. The bite may be painful and often results in a 10- to 30-mm (0.4- to 1.2-inch) erythematous papule that may become edematous also and progress to ulceration or necrosis.118 The Pajaroello has such a reputation that it has been depicted in ancient petroglyphs.117 The lesion gradually resolves over 3 to 4 weeks. Treatment consists of appropriate local wound care and administration of tetanus toxoid (if needed). Secondary infection is not uncommon. Although no data strongly link the bite of O. coriaceus to human miscarriage, it is strongly linked to epizootic bovine abortion, also called foothills abortion, a disease long known among cattle ranchers in these areas. Abortion rates in cattle run as high as 50%. 967

CHAPTER 51  Tick-Borne Diseases

northern Asia. It is actually a spectrum of diseases, varying in severity from louping ill in the British Isles to Russian spring– summer encephalitis (RSSE) in eastern Russia. Central European TBE often has a biphasic course, with an early viremic flu-like stage followed later by meningoencephalitis.260 Symptoms range from mild viral illness to high fevers, severe headache, nausea and vomiting, delirium, coma, paralysis, and death. After an incubation period of 7 to 14 days, patients usually develop viremia (2 to 4 days of flu-like symptoms), followed by an asymptomatic period of 8 days. Patients then develop the second stage of the disease, which consists of 2 to 4 weeks of mainly CNS involvement. Treatment is purely supportive. A vaccine is available in Europe and is recommended for those at high risk for exposure, such as farm workers, local residents, and travelers in peak incident seasons and areas. Transmission mainly occurs by I. ricinus and I. persulcatus ticks, as well as other Ixodes, Haemaphysalis, and Dermacentor species of ticks indigenous to northern Europe and Asia. Variants of TBE, also caused by flaviviruses, include Kyasanur Forest disease (KFD) in India, Omsk hemorrhagic fever (OHF) in Siberia, and Alkhurma virus in Saudi Arabia.70 Symptoms are similar to those of the rest of the TBE complex, except that CNS symptoms are less prominent and there is usually hemorrhage of mucosal surfaces and the respiratory tract. The vector for Kyasanur Forest disease is Haemaphysalis spinigera. OHF is transmitted by contact with infected animal carcasses, unpasteurized milk, and possibly ticks of the genus Dermacentor. Until recently, the only TBE agent known to be endemic to North America was the Powassan (POW) virus in Canada and the northeastern United States. The affliction resembles mosquitoborne encephalitis and has been found when investigation for the West Nile virus yields negative results in clinical situations typical for West Nile virus.66 It is also often mistaken clinically for aseptic meningitis. The fatality rate is approximately 50%, but fortunately the vector, Ixodes cookei, rarely bites humans.260 The incubation period is 7 to 14 days, after which the disease starts with sudden onset of fever to 40° C (104° F), chills, and occasionally seizures. Nausea, vomiting, and respiratory distress are also common. Care is purely supportive. Reservoirs are skunks, woodchucks, hares, raccoons, and other mammals. A newly identified TBE agent in the United States was first found in the New England states and subsequently identified in the northern Midwestern United States.108 It has been dubbed the deer tick virus, and it is transmitted by the deer tick, I. scapularis, in these areas.108,367 It is presumed to be similar to the POW virus, or some form of the European TBE, and the resulting clinical appearance is similar. Much is yet to be learned about this new entity. It remains to be seen if Dermacentor species in the United States may also be vectors, as they are in Europe. Treatment is entirely supportive. Overall, the case fatality rate for TBE is low (1% to 5%). Notable exceptions are pow (50%) and RSSE (25% to 30%).147

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 51-5  Human Rickettsial Diseases Disease Typhus Group Murine typhus Epidemic typhus Scrub typhus Spotted Fever Group Rocky Mountain spotted fever Eastern spotted fevers Rickettsial pox Other Q fever Trench fever Ehrlichial infections

Etiologic Agent

Arthropod Vector

Geographic Distribution

Rickettsia mooseri (typhi ) Rickettsia prowazekii Rickettsia tsutsugamushi

Flea Body louse Chigger

Worldwide Worldwide Asia, Australia

Rickettsia rickettsii Rickettsia conorii, Rickettsia sibirica, Rickettsia australis Rickettsia akari

Tick Tick Mite

Western Hemisphere Eastern Hemisphere United States, Russia

Coxiella burnetii Bartonella quintana Neorickettsia sennetsu, Neorickettsia risticii, Ehrlichia chaffeensis, Ehrlichia ewingii, Ehrlichia muris, Ehrlichia ruminatum

Tick Body louse Tick

Worldwide Africa, Mexico Worldwide

TICK-BORNE RICKETTSIAL DISEASES Species of the genus Rickettsia (family Rickettsiaceae) are small, fastidious intracellular parasites with gram-negative bacteria–like cell walls, a typical prokaryotic DNA arrangement, and considerable independent metabolic activity. Several major antigenic groups cause a variety of human diseases worldwide (Table 51-5). In the field of rickettsiology, there has been a plethora of new isolates of pathogens. Many of these manifest as diseases with much clinical overlap. The genetic differences between them are small, and they may not be distinguishable diagnostically.385 Three groups are potentially transmissible to humans by ticks: spotted fever group (SFG) diseases, Q fever, and ehrlichial infections. Exposure to crushed ticks, or fluid from ticks, may also transmit rickettsiae. Rickettsiae of the SFG share intracellular growth characteristics and a group-specific antigen. They are distributed worldwide and, with the exception of Rickettsia akari (rickettsial pox), are transmitted by bites of ixodid ticks (Table 51-6). Ticks serve as the natural hosts, reservoirs, and vectors for the rickettsiae.249 The organisms replicate freely within the tick host and are passed transovarially and transtadially. Amplification of the cycle occurs when uninfected ticks feed on an infected vertebrate host or concurrently with an infected tick. In most natural vertebrate hosts, the SFG rickettsiae induce a subclinical infection with transient rickettsemia. Human infection occurs through accidental intrusion into the natural cycle of infection or when ticks are transferred into human environments. Humans are incidental, dead-end hosts not involved in sustaining the life cycle of the organism. Rocky Mountain Spotted Fever The disease currently known as Rocky Mountain spotted fever (RMSF) was first recognized in the Snake River Valley area of Idaho in 1896 and was originally referred to as black measles because of the typical late appearance of the rash as dark papules. At the turn of the century, Dr. Howard Ricketts and others established the epidemiology behind the disease. They realized it was transmitted by tick vectors and named the causative organism Rickettsia rickettsii. (Ricketts died in 1910 from

typhus, another rickettsial disease.) RMSF is also known as tick typhus, Tobia fever (in Colombia), São Paulo fever and fiebre maculosa (in Brazil), and fiebre manchada (in Mexico). Epidemiology.  RMSF is found throughout the Western Hemisphere, with 1000 to 1500 cases reported in the United States per year in recent years, with 1527 cases of spotted fever reported by the CDC in 2010 from 33 states.69 Although the disease was first discovered in the Rocky Mountains, the name is a misnomer. Most cases are found in the eastern third of the United States, and between 1994 and 1998, less than 3% of the 2643 cases documented nationwide were reported from the Rocky Mountain states. The disease has now been reported in every state except Hawaii, Maine, Vermont, and Alaska, and it is found in southern Canada and Central and South America. Prior to the antibiotic era and in untreated cases, the mortality rate is 30%. With appropriate antibiotic therapy, the mortality rate is 3% to 5%. Ixodid ticks of the genus Dermacentor are the primary vectors of RMSF in the United States: D. andersoni, the wood tick, in the West, and D. variabilis, the American dog tick, in the East. Rhipicephalus sanguineus has recently been implicated in the transmission of RMSF in Arizona.92 Worldwide, ticks of the R. sanguineus complex have been implicated in transmission of various spotted fevers, each in a particular geographic distribution.141,142 In Mexico, the disease is also transmitted by R. sanguineus, the brown dog tick.22 In Central and South America, the main vector is Amblyomma cajennense, the cayenne tick. In North Carolina, the newest rickettsia, R. amblyommii, has been implicated in RMSF in southern states, and appears to be transmitted by A. americanum.13,332 Within a vector tick species, only 1% to 5% of ticks are infected with Rickettsia rickettsii, although coinfection of the tick with other rickettsial species that are nonpathogenic to humans is common.45 The duration of tick attachment required for disease transmission is as short as 6 hours. The bacterium is readily transmitted by the transovarial route, with 100% transmission in one study.231 Rickettsiae are well maintained in the tick population, as ticks may serve as both vectors and hosts. Large mammalian species serve as additional reservoirs. Dogs are an important host of

TABLE 51-6  Spotted Fever Group Diseases Disease

Etiologic Agent

Major Vector

Geographic Distribution

Primary Lesion

Usual Severity

Rocky Mountain spotted fever North Asian tick typhus Mediterranean spotted fever Queensland tick typhus

Rickettsia rickettsii

Dermacentor andersoni, Dermacentor variabilis Dermacentor, Haemaphysalis

Western Hemisphere

None

Moderate to severe

Europe to Russian Far East

Often present

Mild

Rhipicephalus sanguineus Haemaphysalis Ixodes holocyclus

Mediterranean littoral, South Africa, Kenya, India Australia

Often present

Moderate

Often present

Mild

968

Rickettsia sibirica Rickettsia conorii Rickettsia australis

Pathophysiology.  Rickettsia rickettsii are very small bacteria, 0.2 to 0.3 by 0.5 to 2.0 µm in size. Rickettsiae are usually introduced to the host via tick bite, although transmissions via blood transfusion and through aerosolization in a laboratory setting are reported. After inoculation, bacteria spread via the bloodstream and lymphatics and enter cells, specifically vascular endothelial and vascular smooth muscle cells. In RMSF the rickettsiae invade, proliferate within, and ultimately destroy capillary and precapillary endothelial cells. The organisms may also spread into larger arterioles and arteries and invade medial smooth muscle cells. Medial necrosis and destruction of the vascular wall may follow. At sites of endothelial cell damage, a perivascular inflammatory response ensues, and platelet and fibrin thrombi tend to form and occlude the vessel lumen. In severe cases, vascular thrombi lead to necrosis of peripheral parts, including fingers, toes, the external ear, and the scrotum. Antibodies develop 5 to 7 days after the onset of illness but do not appear to play a significant role in the pathogenesis of the vasculitis.403 Clinical Manifestations and Diagnosis.  The clinical appearance of RMSF ranges from very mild to fulminant, and it may be fatal within several days of onset. A history of tick exposure is present in 85% of confirmed cases.370 The incubation period is 2 to 14 days, with a median of 7 days; fulminant disease usually has a shorter incubation period. There is usually sudden onset of chills and fevers (in 94% of patients), with 66% reporting fever within the first 3 days, 86% reporting headache, and 85% reporting myalgias. RMSF produces a disseminated vasculitic rash in 85% to 90% of patients. The rash, which usually occurs after onset of constitutional symptoms, usually begins on the wrists, hands, ankles, and feet and spreads centripetally. It initially appears as blanching pink or red macules, 2 to 5 mm (0.1 to 0.2 inch) in diameter, that evolve into more pronounced, red, papular, nonblanching lesions. Finally, the rash becomes petechial and dark red to black; occasionally, areas of ecchymotic coalescence are noted (Figure 51-12). End-terminal vascular areas such as the fingertips, toes, nose, and genitalia may become necrotic. Involvement of the scrotum or vulva is a diagnostic clue.100 Ten percent of patients have a delayed rash, and 10% to 15% have no rash.166,167,169 Patients most likely to have no rash, such as the immunocompromised, are also those most likely to die from the disease.167 Neurologic manifestations range from minor headache to profound neurologic symptoms such as encephalopathy, seizures, ataxia, and delirium. Headache is common, occurring in approximately 90% of cases, and is of varying intensity. Lethargy and confusion are common and progress to stupor or coma in 10% of cases. Cerebral vasculitis may develop but is usually mild and transitory. CSF protein analysis may be normal or elevated, sometimes dramatically. Mild CSF pleocytosis of lymphocytes and polymorphonuclear cells (8 to 35 cells/mm3) may occur. Myocarditis is frequently found at autopsy in fatal RMSF; however, the clinical significance of the cardiac involvement is unclear. Pathologic study shows a patchy, interstitial, mononuclear infiltrate that appears to coincide with distribution of

CHAPTER 51  Tick-Borne Diseases

D. variabilis and can develop an acute rickettsial illness consisting of rash and fever. Additionally, dogs bring infected ticks home, and many cases of RMSF have been obtained by de-ticking dogs, as the ticks get crushed.26,156,265 Other tick species have been found to harbor rickettsiae, but they play an insignificant role in disease maintenance or transmission. RMSF is a seasonal disease: 95% of cases in the United States occur between April and September, with a peak in May through July. Exposure to habitats for the vector ticks, such as woods and grassy areas adjacent to woods, increases the chance of acquiring the disease. There appear to be “islands” of infection, which could be partially accounted for by transovarial transmission.245 The disease is slightly more common in males (60% of cases) and in individuals younger than age 20 years (50% of cases).78,366,370 Children aged 5 to 9 years in the mid-Atlantic and southern states have the highest individual incidence.78 The demographic groups most likely to contract the disease are also more likely to participate in outdoor activities in which ticks are encountered.

FIGURE 51-12  Typical vasculitic rash seen in Rocky Mountain spotted fever (RMSF). Note erythematous, vasculitic component and early black eschar formation. (Courtesy Gregory A. Cummins.)

rickettsiae in myocardial capillaries, venules, and arterioles.386 Abnormal left ventricular function can frequently be demonstrated echocardiographically in hospitalized patients.124,241 Overt clinical manifestations of left ventricular dysfunction are uncommon, however. Hypotension (present in 17% of cases) and pulmonary edema are generally attributable to noncardiogenic causes such as hypovolemia and hypoalbuminemia. Cardiac enlargement rarely may be seen on chest radiographs.222,242 ECG abnormalities include nonspecific ST-T changes, conduction abnormalities (primarily first-degree atrioventricular block), and arrhythmias (paroxysmal atrial tachycardia, nodal tachycardia, and atrial fibrillation).242 Most patients have complete resolution of cardiac abnormalities with clinical improvement, but persistent echocardiographic abnormalities have been noted.241 Infection of the pulmonary microcirculation by R. rickettsii results in interstitial pneumonitis and increased pulmonary vascular permeability. Although pulmonary involvement is not usually a prominent aspect of RMSF, a significant number of patients complain of cough, chest pain, or dyspnea.99 Patchy infiltrates are occasionally seen on chest radiographs, and noncardiogenic pulmonary edema may develop in severe cases, with potential progression to ARDS.99,222,316 Gastrointestinal symptoms are common in RMSF and are prominent complaints in some patients. On physical examination, 10% of patients have guaiac positive stool. At autopsy, rickettsial vascular lesions are frequently found throughout the gastrointestinal tract and pancreas, although actual necrosis appears to be a rare event.293 Occasionally, patients with RMSF present with an acute abdomen suggesting appendicitis or cholecystitis.384 In the kidneys, focal perivascular interstitial nephritis is concentrated near the corticomedullary junction. Clinically, however, significant renal involvement is usually caused by prerenal azotemia or acute tubular necrosis after a hypotensive episode.364 Monoarticular arthritis in the acute phase of RMSF has been reported.364 Major complications of RMSF result from direct vasculitic injury. In late stages of the disease, diffuse vasculitic lesions cause increased systemic capillary permeability, leading to hypovolemia and vascular collapse. Disseminated intravascular coagulation (DIC), acute renal failure, metabolic acidosis, and cardiac and respiratory dysfunction may ensue and are frequently preterminal events. Endothelial leukocyte adhesion molecules and cytokines are thought to play a important roles in pathogenesis of fulminant RMSF. Long-term sequelae include paraparesis, hearing loss, peripheral neuropathy, bladder and bowel incontinence, language disorders, and disability from limb amputation and cerebellar, vestibular, and motor dysfunction. Untreated, RMSF has a mortality rate approaching 30%.45 Mortality is higher in patients with elevated serum creatinine, elevated hepatic function tests, hyponatremia, and thrombocytopenia and associated immunosuppression.73 Acute renal failure has been linked to a 17-fold increase in mortality.73 Patients with 969

PART 6  ANIMALS, INSECTS, AND ZOONOSES

glucose-6-phosphate dehydrogenase (G6PD) deficiency are more likely to develop fulminant disease,383 and RMSF is nearly always fatal in these individuals. Persons of African, Middle Eastern, and Southeast Asian descents are most likely to have a G6PD deficiency. Diagnosis.  Early diagnosis and treatment substantially reduce morbidity and virtually eliminate mortality in RMSF. For this reason, suspicion of RMSF is sufficient to begin treatment. At the onset of illness, however, signs and symptoms are frequently nonspecific, leading to diagnostic confusion with viral or other infectious diseases.195 Serology is the best confirmatory test, but false-negative results early in the course of infection (before the body has mounted an appropriate antibody response) are common. A fourfold increase in titers, or a single titer over 64, is required for a serologic diagnosis; this is usually not achieved by the time testing is performed. Indirect IFA of R. rickettsii in skin biopsy specimens yields 70% to 90% sensitivity and 100% specificity and can detect rickettsiae early in the disease,404 but this is impractical for routine use. Routine laboratory analysis for hematology and chemistry may reveal common abnormalities that suggest RMSF. Thrombocytopenia is present in 35% to 50% of patients, and hyponatremia and anemia are also common.166,169,366 Treatment.  Antibiotics should be started empirically in patients living in or recreating in an endemic area who develop any of the constitutional symptoms (myalgias, headache, fever) of RMSF. The classic triad of rash, tick bite, and fever is present in only 18% of patients within the first 3 days of illness.169 Antibiotic treatment should not be withheld until the patient provides a self-diagnosis; patients started promptly on antibiotics are three times less likely to die than if started on antibiotics later.78 Tetracyclines and chloramphenicol are the antibiotics of choice in treating RMSF. Treatment is generally for 5 to 7 days, or until the patient has been afebrile for 48 hours or more. Parenteral antibiotics are not necessary in nontoxic patients, but they should be used in patients who are systemically ill or unable to tolerate oral medications. Although tetracyclines are generally not used in young children because of their propensity to permanently stain developing teeth, tetracyclines are superior to other antibiotics in the treatment of RMSF, and typical courses of treatment for RMSF have been shown to have no adverse effects in the pediatric population.52 Ciprofloxacin has been used in Europe to treat Mediterranean spotted fever.313 Other antimicrobials have been used in animal studies and are as effective or nearly as effective as tetracyclines, but there are no strong data to support their use in children.39 Even with timely and appropriate antibiotics, however, mortality is approximately 3% to 5%.167 The high mortality associated with improper treatment of RMSF warrants treatment of most young children with doxycycline, with a warning to the parents that permanent staining of teeth may occur. Supportive therapy, including aggressive fluid resuscitation in many cases, is a mainstay of treatment of RMSF. Corticoste­ roids may be of benefit in cases of severe vasculitis or encephalitis.250,403 Other Spotted Fever Group Diseases Mediterranean Spotted Fever.  Boutonneuse fever, also called Mediterranean spotted fever (MSF), Carducci fever, tick typhus, Indian tick typhus, and tick bite fever is caused by Rickettsia conorii and is endemic in the Mediterranean basin and in southern Asia and India. The major vector of MSF in Mediterranean countries is the dog tick, R. sanguineus. Several tick species have been implicated as vectors in other areas; these include Haemaphysalis leachi (Kenya, South Africa), Rhipicephalus simus, Dermacentor reticulatus, and Ixodes hexagonus.122 All stages of R. sanguineus occasionally attach to humans, and dogs may be important in transporting the ticks close to humans.373 Infection with Rickettsia conorii usually results in mild illness, although symptoms can be severe in 10% of patients, typically older adults or immunocompromised patients. Symptoms are fever, exanthems, and an eschar or necrotic plaque at the tick bite site. Fever of 39° to 40° C (102° to 104° F) is noted in 97.2% 970

FIGURE 51-13  Tick-bite eschar associated with African tick typhus. (From Armstrong D, Cohen J, editors: Infectious diseases, London, 1999, Mosby, with permission.)

to 100% of patients. Erythematous papules, primarily in the lower extremities, are noted in 96.1% to 100% of patients. A black eschar, appearing like a button at the site of the tick bite, is seen in 71.8% of patients (Figure 51-13). In addition, a vasculitic rash, similar to that seen in RMSF, may occur on the palms, soles, wrists, and ankles. In some cases, the only symptom is lymphadenopathy. The incubation period is typically from 4 to 15 days but may be as long as 28 days. Although the disease is usually mild in children and young adults, a malignant form resembling severe RMSF has been described.298,382 Older adults, alcoholics, and patients with G6PD deficiency appear particularly at risk.283 The incidence in Mediterranean rim countries and other countries varies from 51.6% of those reporting tick bites in Croatia, to 4.6% to 13.5% in a region of Spain, 13.3% of healthy patients in Turkey, and 16.7% in Zambia. Numerous cases have been imported, diagnosed, and confirmed in the United States and Canada from travelers to endemic regions. Abnormal laboratory values and other clinical symptoms share the clinical picture often seen with other tick-borne diseases. Treatment is with tetracycline, administered orally or parenterally. Chloramphenicol and the fluoroquinolones are reasonable second-line agents. Siberian Tick Typhus.  Siberian tick typhus, or North Asian tick typhus, caused by Rickettsia sibirica, is found throughout northern Russia and on islands of the Sea of Japan. It is primarily transmitted by various Dermacentor and Haemaphysalis species ticks. Symptoms are very similar to RMSF, although it is seldom fatal. Diagnosis and treatment are the same as those for the other spotted fever group diseases. African Tick Bite Fever.  African tick bite fever is caused by Rickettsia africae, a newly discovered agent of disease. It is similar to Boutonneuse fever but typically occurs without the rash. It is transmitted by Amblyomma hebraeum and is endemic to sub-Saharan Africa. Although rarely reported in indigenous peoples, it is well documented in travelers to the African continent.181,186 Queensland Tick Typhus.  Queensland tick typhus is caused by Rickettsia australis and is transmitted by I holocyclus, which is also the primary vector of tick paralysis in Australia. It is also very similar in appearance to the other spotted fever groups, and is diagnosed and treated in the same fashion.

Q FEVER Q fever is a worldwide zoonosis affecting both wild and domestic animals. It was first described in 1937 as an occupational disease of abattoir workers and dairy farmers in Australia.93 Aerosol spread of Coxiella burnetii, the causative organism, is the usual mode of transmission to humans. Sexual transmission has been implicated but not proved.212 Although ticks may become infected with C. burnetii after feeding on an infected vertebrate, tickborne transmission to humans appears to be very rare. Fewer than 10 cases of Q fever per year are reported in the United States. Serosurveys have shown widespread prevalence,

EHRLICHIOSIS In Texas in the 1940s, there was an epidemic of disease among World War II U.S. Army recruits. The illness was associated with bites from the lone-star tick, A. americanum. The location was Camp Bullis, and the disease became known as Bullis fever.402 In retrospect, it is very likely that Bullis fever was human ehrlichiosis.146,149 Ehrlichiosis was “discovered” in the mid-1980s when several individuals in rural areas of central and northern Arkansas became ill with a febrile disease that had many of the symptoms of Rocky Mountain spotted fever, with which they were initially diagnosed.130 Clusters of bacteria in intracytoplasmic inclusions were identified as an Ehrlichia species, similar if not identical to

Ehrlichia canis. E. canis had previously been known to infect only dogs. The new bacterium was later isolated and given the name Ehrlichia chaffeensis, after Fort Chaffee, Arkansas, the area from which the original cultures came. The late 1980s and early 1990s yielded several hundred cases, including some fatalities. By the year 2000, there were more than 1000 reported cases of ehrlichiosis. Most cases are sporadic; however, there are epidemics in some occupational and recreational groups, such as military personnel in field exercises and golfers with frequent errant shots.282,342,409 The taxonomy of the species that cause ehrlichiosis is very complicated and has undergone frequent change. This is a dynamic area of research, with new species and new vectors being found worldwide and nearly every day. The species that cause the various ehrlichioses belong to the family Anaplasmataceae and are obligatory intracellular gram-negative bacteria. They multiply in host cell vacuoles and form large mulberryshaped inclusion bodies called morulae. At present, about a dozen species are known in the family Anaplasmataceae. The bacteria causing human disease are divided into three genera: Neorickettsia (formerly Ehrlichia sennetsu and Ehrlichia risticii), Anaplasma (formerly Ehrlichia phagocytophila and Ehrlichia equi), and Ehrlichia. The Ehrlichia species consist of Ehrlichia ewingii, E. chaffeensis, E. canis, Ehrlichia muris, and Ehrlichia ruminatum.105 More than 21 different strains of E. chaffeensis have been isolated from U.S. patients in the southern states. Additional strains have been isolated from animal sources, although infectivity of these strains is not well established.103 There are two basic forms of ehrlichiosis in humans: human monocytic ehrlichiosis (HME) and human granulocytic ehrlichiosis (HGE). Human Monocytic Ehrlichiosis The first of the ehrlichiae identified as a cause of human disease was E. chaffeensis. Although reported in 46 states, E. chaffeensis is found predominantly in the south-central and southeastern United States. It causes HME, and is transmitted predominately by A. americanum, the lone-star tick. E. chaffeensis infects predominately mononuclear phagocytic cells, particularly monocytes, although other cell types may also be affected. Various organs are affected, particularly those with abundant mononuclear phagocytic cells. Cross-reactivity exists between the tests for E. chaffeensis, E. ewingii, and Anaplasma phagocytophila, so it is possible that not all cases attributed to E. chaffeensis are truly caused by this organism. This may change as tests become more specific. Less is known about the epidemiology of HME because the vector, A. americanum, has not been as extensively studied as I. scapularis ticks, the primary vectors for HGE and Lyme disease. The five states with the highest incidence of HME, compiled from data obtained from 1986 to 1997, were Arkansas, North Carolina, Missouri, Oklahoma, and New Jersey.253 In 2010, the CDC confirmed 586 cases of HME.69 HME occurs worldwide. The causative agent is always E. chaffeensis or very similar Ehrlichia species. There are multiple tick vectors worldwide, however, including primarily ticks of the I. ricinus complex in Eurasia, A. cajennense in South America, Amblyomma testudinarium, Haemaphysalis yeni, R. sanguineus in China, and others.56,303,392 Nontick transmission has been suggested by the occurrence of HME after contact with infected animal blood.17 E. chaffeensis can live in refrigerated blood for longer than 11 days, so transmission by blood transfusion is possible.251 In the United States, HME is transmitted primarily in the months of March through November, with 70% of the cases occurring between May and July.128,129,342 Cases are reported in the late fall and winter months from southern areas. HME has a male-to-female ratio of greater than 2 : 1, and it is reported more often in patients older than age 40 years.128 Younger patients may have less symptomatic disease and thus go unreported. History of a tick bite is present in approximately 68% to 80% of patients.115,128 The high rate of recollection of a tick bite is probably a result of the pain associated with the relatively long 971

CHAPTER 51  Tick-Borne Diseases

suggesting frequent asymptomatic infection or underdiagnosis and underreporting.160,329 The incubation period is typically 2 to 4 weeks, although the incubation period should not be used as an exclusion criterion. The most common clinical manifestation of Q fever is an influenza-like illness with fever, headache, myalgias, and pneumonitis. Abnormal liver function tests, jaundice, and hepatomegaly may be seen, and Q fever may cause acute acalculous cholecystitis.307 Glomerulonephritis has been reported with both acute Q fever and endocarditis-associated chronic infection.205 C. burnetii is not known to be teratogenic, but infection during pregnancy may cause placental insufficiency resulting in premature delivery or even intrauterine death297; the risk of miscarriage is also increased.295 Reported neurologic manifestations of Q fever include acute cerebellitis with tonsillar herniation,319 meningitis/encephalitis/meningoencephalitis,33 transverse myelitis,33,387 and peripheral neuropathies.33,335 Cardiac involvement in acute Q fever is rare but may include pericarditis,24,223 endocarditis, or myocarditis.133 In most patients, symptoms resolve spontaneously within 2 to 4 weeks of onset, with treatment hastening the resolution. Q fever may also be a chronic infection, with or without a history of an acute episode. Granulomatous hepatitis and culturenegative endocarditis are the major manifestations of the chronic forms of the disease. Endocarditis, fatal in 25% to 60% of patients, can affect native and prosthetic valves (underlying valvular disease is almost invariably present), and it has a predilection for the aortic valve.152 Infections of aneurysms and vascular prostheses have also been described.132 A post–Q fever syndrome involving fatigue, myalgia, arthralgia, night sweats, sleep disturbances, and mood alterations has been described and may occur in 20% to 42% of proven cases.15,280 Diagnosis of Q fever depends primarily on serologic testing. Two specific complement-fixing antibodies (phase 1 and phase 2) develop after infection with C. burnetii. In patients with acute Q fever, phase 2 antibody is usually detectable by the second week of illness; phase 1 is not detectable. The finding of phase 1 antibody indicates chronic infection. IgA subclasses (IgA1 seen in acute and chronic disease, IgA2 seen only in chronic disease) may also help differentiate between chronic and acute infection. Only patients with endocarditis were found to have IgA2 antibodies to phase 2 antigens.54 For the acute phase, tetracycline (500 mg orally four times a day) will hasten resolution. Treatment of chronic Q fever is not always successful. Patients probably need to be treated with tetracycline for at least 12 months, and up to 3 years if endocarditis is present.54 Some authorities recommend adding another drug, such as lincomycin or cotrimoxazole, but efficacy of this strategy is unproved.135,375 Patients with endocarditis typically receive treatment with tetracycline and a quinolone for at least 4 years, although new research supports shortened treatment with doxycycline and hydroxychloroquine.296 Some recent isolates of C. burnetii are showing resistance to doxycycline.306 A vaccine is used to prevent infection in high-risk abattoir workers. Preventive measures such as avoidance of potentially infectious animal tissues, especially raw milk and products of conception, should be taken. Pregnant patients should be aggressively treated with cotrimoxazole for the duration of the pregnancy, as insufficient treatment is associated with a higher rate of fetal loss.295

PART 6  ANIMALS, INSECTS, AND ZOONOSES

mouthparts of A. americanum and the immunogenic local reaction that often accompanies the bite. There are numerous reservoirs for the ehrlichiae. A. americanum is very nonselective in its feeding and is found on a variety of birds and mammals.34 In the United States, the whitetailed deer is the most important host. Domestic dogs also are vital in the epizootiology of the ehrlichioses. Dogs outnumber every other large mammal in the United States and are often highly infected, with a Virginia study showing 38% of dogs from southeastern Virginia positive for E. chaffeensis.88 Dogs also provide a large degree of interface between the wilderness areas and the domestic front, and often carry ticks into the home.26,265 A study of coyotes in Oklahoma documented infection rates of 71%.204 Wild turkeys also host A. americanum, which is so abundant on some turkeys that it is referred to as the “turkey tick” in some areas.91 Human Granulocytic Ehrlichiosis In the 1990s, E. phagocytophila (now Anaplasma phagocyto­ phila) and E. ewingii were also identified as human pathogens. These bacteria primarily infect neutrophils, causing HGE. These species cause disease in the north-central and northeastern United States, and they are transmitted by Ixodes species ticks, primarily I. scapularis, and D. variabilis. The numbers of reported cases quickly exceeded those from the original areas of E. chaffeensis. In 2010, the CDC reported 789 confirmed cases of HGE.69 The reservoir hosts are similar to those for HME. Clinical Features.  The clinical features of HME and HGE are very similar. Within 1 to 2 weeks of exposure to an infected tick, a prodrome of malaise, back pain, gastrointestinal symptoms, and fevers up to 39° C (102° F) develops. HME symptoms usually manifest within 3 to 4 days of onset and include fever (>95%), headache (60% to 75%), myalgias (40% to 60%), nausea (40% to 50%), arthralgias (30% to 35%), cough or dyspnea (20% to 25%), and malaise (30% to 80%).115,128 Respiratory complications are common; cough, pulmonary infiltrates, dyspnea, and respiratory failure have been reported. Rash is noted in both HME and HGE, although it is more common in the former (40%) than in the latter (8%).104 Meningoencephalitis is the most common neurologic complication. In one study of 15 patients with altered sensorium from ehrlichiosis who underwent CSF testing, eight had abnormalities, including elevated lymphocytes (up to 1000 cells/µL) and protein. In a review of 21 additional cases with CNS manifestations, 13 of 21 patients had abnormal CSF findings. Fourteen patients underwent brain computed tomography, revealing no abnormalities. Four of 21 patients with CNS symptoms died.299 Hematologic complications are also described. In HME, bone marrow and hepatic granulomas and multiorgan perivascular lymphohistiocytic infiltrates have been observed. In HGE, Ehrlichia-mediated defects in host defense and immune suppression have resulted in opportunistic fungal and viral infections.381 Up to 60% to 70% of patients require hospitalization.128,343 In severe cases, patients suffer renal failure, pancytopenia, DIC, ARDS, hepatic failure, profound hypotension, and death. There is an estimated 3% case fatality rate, down slightly from 5% in the mid-1990s.253 Of the fatal cases, 70% are male. Death usually results from multisystem organ failure, usually with profound pulmonary, hematologic, and gastroenterologic manifestations. Generally, immunocompromised patients, individuals older than age 60 years, and those not receiving appropriate antibiotics within 8 days of the onset of symptoms are at highest risk of mortality.128 Diagnosis.  In patients with symptoms suggestive of ehrlichiosis, the diagnosis is suggested by history of tick bite in an endemic area and confirmed by laboratory testing. Multiple abnormalities may be noted on routine blood testing. The complete blood count (CBC) shows mild to moderate thrombocytopenia in 70% to 90% of patients and mild to moderate leukopenia (principally lymphocytopenia) in 60% to 70% of patients. Hepatic transaminases are elevated in 80% to 90% of patients at some point in their illness, often early in the course. Hyponatremia is present in up to 50% of adult 972

patients and 70% of pediatric patients.115,182 Elevated creatinine, elevated fibrin degradation products, and prolonged coagulation times are indicative of more severe disease and carry a poor prognosis. Serologic tests confirm the diagnosis, but the results are not immediately available. The most widely used test is an IFA, which detects IgG and IgM. A rise in titer of fourfold or greater, or a single titer of 256 or greater is sufficient to confirm the diagnosis. The serologic tests use an antibody reactive to E. chaffeensis; the degree of cross-reactivity with other erhlichiae is unclear. The gold standard is the IFA, which is 95% sensitive and 100% specific when properly performed at appropriate times. Early testing may yield false-negative results, however, because of the relatively slow human antibody response to ehrlichiosis. Suspicion of disease in the appropriate setting should therefore prompt treatment, and a negative test early in the presentation should not preclude antibiotics. Western blot tests identify isolates of E. chaffeensis but do not play an important role in diagnosis. For E. ewingii, however, Western blot is useful for diagnosis, as there is no IFA test for this organism. ELISA tests are being developed but are not routinely used. PCR is beginning to complement IFA; it has the advantages that any tissue can be used and the disease can be detected early. Blood smear testing has very low sensitivity and specificity, is very operator dependent, and plays little role in diagnosis. Culture is feasible but is technically difficult, requires specially equipped laboratories and special media, and takes several weeks. Treatment.  E. chaffeensis is susceptible to tetracyclines but resistant to many antibiotics, including aminoglycosides, fluoroquinolones, penicillins, macrolides, and sulfa drugs. Doxycycline (100 mg orally or intravenously twice daily) is the drug of choice for the treatment of E. chaffeensis in adults and children older than 9 years of age. Treatment for 7 to 10 days (or for 3 days after the last febrile episode) is typically adequate. Failure to respond within 48 to 72 hours of initiation of antibiotics suggests a different diagnosis or coinfection. Other antibiotics may be considered when tetracyclines are contraindicated. Rifampin is very bactericidal in vitro, but it has not been used in large trials in vivo.38,43 Chloramphenicol, which has been used in children with varying degrees of success,23,233 has been shown to have weak inhibitory action against the ehrlichiae, but it is not bactericidal.201 Both rifampin and chloramphenicol are safe in children but are rated as category C for use during pregnancy. Despite this rating, a pregnant patient with HGE was treated successfully with rifampin.44

BABESIOSIS Babesia species, like malarial organisms, are pleomorphic intraerythrocytic protozoan parasites. More than 70 distinct species have been described from various vertebrate hosts.304 Some of the most important species include Babesia bigemina, Babesia bovis, and Babesia divergens (all in cattle); Babesia caballi and Babesia equi (horses); Babesia canis (dogs); and Babesia microti (rodents). Babesiae are transmitted to vertebrates primarily through the bites of ixodid ticks. Epidemiology.  Babesiosis has long been recognized as an important veterinary disease, receiving biblical reference as the “divine murrain” infecting cattle of the Pharaoh, Ramses II (Exodus 9 : 3). Various epidemics of cattle fever have been documented throughout history.37 Human disease was originally reported in 1957 in a splenectomized man in Yugoslavia.331 Five cases of human infection with bovine Babesia (B. bovis, B. divergens) were reported from Europe between 1957 and 1976; two cases of babesiosis of unknown species were reported from California in 1968 and 1981; a human case of B. gibsoni infection was reported in California in 1993; and a single Babesia caucasia infection was reported from Russia in 1978.187,304,309 These cases were widely separated geographically and all occurred in splenectomized individuals.

Pathogenesis.  Babesiae are transmitted from wild and domestic animal reservoirs to humans by Ixodes ticks. The life cycle of I. scapularis (the vector for transmission of B. microti to humans from rodents) spans 2 years, beginning in spring of the first year with hatching of the larval form. In late spring and summer months, the larvae feed on a variety of hosts and acquire babesial infection. Typically, larvae become infected from their preferred host, the white-footed mouse, P. leucopus. Ingested babesiae reach the gut of the feeding tick, where they reproduce asexually.

Tick Gut cell

10 –16 hr

Salivary gland 9 –10 mo

Asexual division

Erythrocyte cycle Erythrocyte Human FIGURE 51-14  Babesia life cycle. Within a tick, babesial parasites infect gut cells, undergo asexual division, and eventually migrate to the salivary glands. The organism is introduced into a human when the infected tick takes in a blood meal. Transmission usually involves the nymphal tick, but the duration of attachment required for transmission of Babesia species is not known. Babesia species can be transmitted to humans concomitantly with Borrelia burgdorferi. (Modified from Boustani MR, Gelfand JA: Babesiosis, Clin Infect Dis 22:612, 1996.)

The newly formed zygote eventually spreads throughout the body of the tick. After reaching the salivary glands, the babesial sporoblasts remain dormant until the next spring, when the tick larva molts to a nymph. The nymph then seeks a blood meal, infecting a new host (rodent or human). In endemic areas, as many as 60% of white-footed mice are infected by late summer. The nymph form of the tick transmits most human disease, although adult ticks may also do so. After inoculation by a tick bite, Babesia sporozoites enter erythrocytes, where they differentiate into merozoites. Great pleomorphism is displayed,263 but ring-shaped and ameboid trophozoites are the predominant forms. Multiplication occurs by asexual asynchronous budding. After the parasite multiplies, the infected erythrocyte ruptures, freeing the organisms to invade other red blood cells (RBCs). Severe hemolytic anemia may result (Figure 51-14). Infection with B. microti reduces malleability of erythrocytes, leading to microvascular stasis and decreased RBC life span. Electron microscopy has shown extensive RBC wall damage, including protrusions, perforations, and extrusions in the cell membrane. Asplenia or steroid therapy can worsen the disease and prolong parasitemia. An intact spleen preferentially destroys infected RBCs because of their decreased malleability, which plays an important role in resistance to Babesia organisms. Although the presence of a spleen is not protective against B. microti, the disease is often more severe in splenectomized patients. Age is also an important factor in susceptibility to babesiosis. Children and young adults usually have subclinical or mild, selflimited infections, whereas older adults and those with chronic medical problems30 are more likely to have severe, clinically apparent disease.29,312 Prolonged parasitemia is common in babesiosis.311 B. microti may persist for as long as 4 months in an otherwise healthy patient.394 Parasitemia may remain after clinical recovery or may develop in asymptomatic individuals. Clinical Manifestations.  Incubation is 1 to 4 weeks after a tick bite or 6 to 9 weeks after transmission by blood transfusion. Most victims of tick-transmitted disease do not recall a tick bite. Physical examination is usually normal, except for fever (steady or intermittent) and mild splenomegaly in some patients. Petechiae and ecchymosis rarely occur. Acute B. microti infection is characterized by gradual onset of malaise, anorexia, and fatigue, followed within several days to a week by fever, sweats, and myalgias. Other, less common symptoms include headache, nausea and vomiting, depression, abdominal pain, jaundice, and dark urine. In a review of 17 patients with babesiosis, 52.9% presented with temperature 973

CHAPTER 51  Tick-Borne Diseases

The incidence of B. microti is higher than that of other Babesia species because of its ability to produce disease in individuals with intact spleens. Since 1970, the incidence of human babesiosis has accelerated, primarily because of B. microti infections in the northeastern United States. In 1969, babesiosis was recognized in a patient with an intact spleen on Nantucket Island, Massachusetts.394 Since then, hundreds of cases have occurred in the United States.79,255 B. microti is endemic to the coastal regions of southern New England, where the principal vector is the northern deer tick I. scapularis. Most cases are contracted on Cape Cod and the offshore islands of Massachusetts (Nantucket, Martha’s Vineyard), New York (Shelter Island, Long Island), Rhode Island,79,305 and New Jersey.173 Cases have also been reported from Ontario,194 Wisconsin,283 and Minnesota, a known focus of I. scapularis.359 Although most cases of babesiosis in the United States involve B. microti, infection with other strains occurs. A strain of B. microti called WA-1, thought to be spread by I. pacificus, has been isolated from an immunocompetent patient with an intact spleen in Washington State.290 Another strain, termed MO1 and similar to (but distinct from) B. divergens, was isolated in Missouri.172 B. divergens infection is reported in the United States but is rare.25 Interestingly, B. divergens was found in 16% of cottontail rabbits in Nantucket, indicating an abundant reservoir in at least that area.151 The ecology of B. microti parallels that of B. burgdorferi, the agent of Lyme disease. The major vector in both diseases is I. scapularis. White-footed mice (Peromyscus leucopus) constitute the major reservoir for B. microti. Larval or nymphal ticks ingest the parasite during a blood meal from an infected rodent. Babesiae replicate within the tick and are passed transtadially. Amplification of the cycle occurs when the infected tick transmits the organism to a vertebrate host during the next blood meal. White-tailed deer (Odocoileus virginianus) are the principal hosts for adult ticks; larvae and nymphs feed on deer, mice, and other small mammals.339 Human babesiosis occurs when humans accidentally intrude on the natural cycle and are bitten by an infected tick. As is the case with other tick-borne diseases, the peak incidence is during the warm weather months from May to September, when ticks are actively feeding. An epidemiologic survey of 136 cases in New York State showed that the most important risk factors for severe babesiosis are advanced age, asplenia, and immunodeficiency. Babesial infection appears to be as prevalent in children as in adults, although the disease tends to be more severe in those older than age 40 years. In one study, 23% of patients with babesiosis had concurrent Lyme disease infection.255 Case reports have also shown multiple coinfections involving borreliosis, ehrlichiosis, and babesiosis,259 with more severe symptoms in coinfected individuals than in those infected with a single organism.210 Prolonged, subclinical infection creates the potential for transmission of B. microti through blood donation. Seroprevalence surveys in endemic regions show donor exposure rates from 1% to 3%,97,190 and transfusion-associated babesiosis is well-documented.96,215,240,333,401 Currently, control of transfusionrelated infection is limited to identifying donors at high risk of exposure (from endemic regions, history of tick bites, or seasonal exposure to tick-favorable landscapes). This strategy may become less effective as tick-endemic areas expand, however. Transfusion has also reportedly transmitted new species of Babesia, causing significant disease in immunocompetent individuals.174 Neonatal babesiosis may result from tick bites or transfusion (as in adults), but may also be acquired congenitally through vertical transmission.3,114,134

PART 6  ANIMALS, INSECTS, AND ZOONOSES

greater than 38.3° C (101° F), and four of the nine had morning fever spikes; eight had relative bradycardia.200 The CBC usually reveals mild to moderate hemolytic anemia, normal to slightly reduced WBC count, and (in some patients) mild to moderate thrombocytopenia. Serum lactate dehydrogenase (LDH) and bilirubin levels are mildly elevated in most patients, reflecting the hemolytic anemia.153,311 AST and ALT may be elevated, and urinalysis may be notable for proteinuria and hemoglobinuria. In one series, 13 of 17 patients (76.5%) had lymphopenia, and five (29.4%) had rouleau formation in the peripheral blood smear.200 A review of 139 hospitalized patients with babesiosis in New York from 1982 to 1993 attempted to identify common signs and symptoms and the prognostic factors associated with poor outcome.395 Of the 139 patients, 9 (6.5%) died, 35 (25.2%) were admitted to the intensive care unit, and 35 (25.2%) required more than 14 days of hospitalization. Among patients with severe disease, the mean age was 62.5 years, and 62% were male. The most common symptoms were fatigue, malaise, weakness (91%); fever (91%); shaking chills (77%); and diaphoresis (69%). Prognostic indicators for severe outcome included high alkaline phosphatase, male gender, and elevated WBC count. Only 12% of patients with severe disease had a history of splenectomy, and only 2% had received a prior blood transfusion. Although most patients with normal splenic function recover without specific therapy, prolonged fatigue and malaise are common.311 Splenectomized patients generally have more severe clinical disease, with higher levels of parasitemia and more severe hemolytic anemia.312 Older adult patients and immunocompromised patients, such as those with HIV infection, are also at higher risk for severe infection. Pulmonary edema has been reported.37 Typically, the level of parasitemia ranges from 1% to 10%. In Europe, babesiosis results from infection with B. divergens or B. bovis and has been reported only in splenectomized patients. The illness is characterized by high fever, chills, headache, and severe hemolytic anemia, often resulting in hemoglobinuria, jaundice, and renal insufficiency. Major findings on physical examination include fever, hepatomegaly, jaundice, and hypotension. More than one-half of the reported cases have been fatal.309 Diagnosis.  Babesiosis should be considered in any person with an unexplained febrile illness who has lived in or traveled to an endemic region in the midsummer months, especially with a history of a tick bite or tick exposure. The diagnosis of babesiosis can be confirmed by identifying the intraerythrocytic parasites on Giemsa-stained blood smears (Box 51-2). Persons with intact spleens usually have low levels of parasitemia (less than 5%), and examination of repeated smears may be necessary.153,311 The predominant forms of B. microti closely resemble the small rings of Plasmodium species. A later tetrad form (“Maltese cross”) may be seen and is positive morphologic evidence of babesiosis. Differentiating Babesia from Plasmodium may be difficult but is possible by noting the absence of pigment deposits in erythrocytes parasitized with the older stages of Plasmodium species. When organisms cannot be detected on blood smears, the diagnosis can be made by intraperitoneal inoculation of the patient’s blood into splenectomized hamsters. Serologic studies may also be helpful in confirming the diagnosis but are performed in only a few laboratories. A titer greater than 1 : 64 on IFA testing is considered consistent with seropositivity, and a titer greater than 1 : 256 is diagnostic of acute infection. No test for circulating Babesia antigen is available. PCR testing for Babesia BOX 51-2  Laboratory Diagnosis of Babesiosis Peripheral blood smear (Wright or Giemsa staining) showing intra-erythrocytic Babesia Polymerase chain reaction Indirect immunofluorescent assay Intra-peritoneal inoculation of splenectomized hamsters

974

can be as sensitive and specific as standard testing and may be reproducible enough for routine use in diagnosis of acute babesiosis.7,209 Treatment and Prevention.  First-line chemotherapy for patients with significant B. microti infection consists of 7 days of azithromycin (500 mg on day 1, 250 mg on days 2 to 7) and atovaquone (750 mg every 12 hours). This combination has equivalent efficacy to the previously used combination of clindamycin and quinine, with less adverse drug reactions,207 and has been used successfully in children.3,291 Resistance to azithromycinatovaquone therapy has been reported in severely immunocompromised individuals.406 Usually, therapy is reserved for patients with severe disease, those with asplenia or immunosuppression, or older adults.64 In seriously ill patients with high levels of parasitemia, exchange transfusion may also produce rapid clinical improvement.183,363 Patients with mild clinical disease typically recover without specific anti-Babesia chemotherapy, although few patients have been followed longitudinally. A recent prospective study showed that parasitemia lasted for a mean of 82 days in 24 asymptomatic subjects not treated with the standard regimen.208 Avoidance of ticks is the only currently effective method of preventing babesiosis. Splenectomized patients should be wary of visiting areas endemic for babesiosis.

TULAREMIA Please refer to Chapter 59 for information on Tularemia.

CRIMEAN-CONGO HEMORRHAGIC FEVER Crimean-Congo hemorrhagic fever (CCHF), also called central Asian hemorrhagic fever, is caused by a Nairovirus (circular, negative-sense, single stranded RNA [ssRNA]) in the Bunyaviridae family. Although these viruses are more of a problem in livestock than humans, human cases carry up to a 50% fatality rate. It is found in roughly 30 countries and is the most widespread tick transmitted viral disease. Two recent human cases involved livestock exposure and no tick bite.198 In Turkey in 2002, there were 2500 cases reported,236 and in 2007, there were at least 40 deaths, including two health care workers exposed to airborne virus. A new strain was found recently.110 The incubation period is generally one week if transmitted by tick bite and 7 to 10 days if contacted by airborne means or from bloody tissue exposure. Most cases occur between June and September. Primary symptoms are sudden onset of fever, headache, weakness, malaise, myalgias, anorexia, and mental status changes. Gastrointestinal symptoms are common, and patients present mainly with abdominal pain, hepatic enzyme elevation, and melena. A petechial rash usually occurs, sometimes leading to large areas of ecchymosis. Some cases proceed to hepatorenal syndrome, coma, and pulmonary failure within the first week. Cases with extensive multiorgan system involvement are often fatal. Several species of ixodid ticks are vectors; two species, Hyalomma marginatum and Hyalomma anatolicum, are anthropophilic and the most important vectors with respect to human disease. In areas endemic for CCHF, these ticks are found in very high numbers. Infection may also be transmitted via aerosols, either from crushing ticks or from the slaughter of infected animals. Nosocomial transmission is reported in hospitals in Africa. CCHF is diagnosed clinically and confirmed by laboratory tests. Treatment is mostly supportive, although ribavirin has been shown to provide some benefit.113,396 CCHF is listed by the CDC as a category C bioterrorism agent.

Tick-Borne Disease Prevention and Awareness Awareness of the ticks and the diseases necessary first step in prevention. Proper light-colored, as this makes ticks easier heavily infested areas reduces exposure,

they transmit is a clothing should be to spot. Avoiding as does reducing

FIGURE 51-15  Ideal tick removal method. Grasp the tick near the surface of the skin, withdraw from the skin in a steady, constant motion. Do not turn, jerk, or twist. (From Goddard J: Infectious diseases and arthropods, Totowa, NJ, 1999, Humana Press, with permission.)

contact with leaf litter.59,324 Reducing time in areas frequented by ticks reduces exposure further. A study of the upper surface of downed logs, as would be found and used by weary hikers, yielded a large number of I. scapularis nymphs.59,217 Boots provide better protection than do tennis shoes and socks.59 Tucking pant legs into the tops of the socks reduces the ticks’ ability to climb up the legs of potential hosts. A ring of masking tape or duct tape at the tops of the socks further reduces exposure. Insecticides containing diethyltoluamide (DEET) are generally safe, work well, and may be applied directly to the skin. A light spray of a permethrin-based acaricidal spray (such as Permanone) to clothing will persist through several washings and up to one month, and is highly toxic to ticks. Permethrin should not be applied to skin, as it has been associated with neurologic sequelae in mammals.286 A light spray around bedding may deter nighttime feedings. Some outdoor gear and clothing manufacturers now produce permethrin impregnated gear and clothing. In Europe, military-issue permethrin-impregnated clothing yielded a 95.5% mean protection from questing ixodid ticks.120 The use of the “four-poster” system in applying acaricides for wildlife or livestock has been shown to reduce tick populations significantly.58 This system, developed by researchers in Kerrville, Texas, involves creating a feeding station for deer or cattle that has four corner posts on which are rollers soaked in a 10% permethrin solution. When livestock or wild game feed at the station, the permethrin is applied to their heads, an area often heavily infested with ticks. Typically, there is a 92% to 98% reduction in the tick population within 3 years.323 However, ticks and other insects are showing resistance to even the most toxic of acaricidal treatments, primarily as a result of use of acaricides for livestock on a large scale.258,294 Frequent inspection of the body should be performed when in a tick-infested areas. Although some diseases require as much as 24 to 48 hours of tick attachment, others are transmitted within an hour. The argasid ticks feed in minutes, usually while the hosts are sleeping, so avoidance or protection through habitat selection or the use of physical or chemical barriers makes good sense.

Removal of attached ticks should never be done by bare or even gloved hands. A quality pair of fine-tipped forceps is necessary to safely remove embedded nymphal and adult ticks, by gently grasping the ticks as close to the skin as possible and gradually retracting outward in a straight line (Figure 51-15). Special tick-removal devices available from outdoor and camping supply companies provide some advantage over simple forceps but generally cost more.360 The area should then be cleaned with a local antiseptic. Other methods for tick removal, such as applying petroleum jelly to the tick, or using a lighted match or cigarette, isopropyl alcohol, or fingernail polish, do not ease removal of the tick. These and other “remedies” most likely increase expression of tick saliva and foregut contents, thus increasing the chance of disease transmission.21,270 Removal of larval ticks is easier, as their size and mouthparts are extremely tiny. A piece of tape, such as duct tape, applied to the skin and then removed, easily removes free-crawling or attached larval ticks. Alternatively, the thin edge of a plastic object such as a credit card or driver’s license scraped along the skin easily removes attached larvae. This method is appropriate only for larval ticks, not for nymphs or adults. Laundering clothing in hot water and drying on high heat after being in tick-infested areas generally works to kill ticks and keeps them from invading residences. However, despite exposure to hot water in the wash cycle, ticks may survive. High drying temperatures for 1 hour are generally required to kill ticks.57 Unfortunately, expensive Gore-Tex and similar outdoor clothing items do not tolerate high-heat drying. Free-crawling ticks can easily be transported from the field to a vehicle during a drive home from an endemic area, and then from the vehicle to the residence. For homeowners or landowners, proper landscaping, with an appropriate barrier or buffer zone of wood chips or gravel between forested areas and formal lawn areas, has been shown to reduce the potential tick–human interaction.102,168

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

975

CHAPTER 52 

Spider Bites LESLIE V. BOYER, GRETA J. BINFORD, AND JANICE A. DEGAN

Spiders and Their Venoms Spiders number nearly 42,000 described species and are found in all habitats except the open sea.38,64,225,227 They are carnivorous predators with important ecologic roles in most terrestrial ecosystems. Many are capable of wind-borne dispersal

(ballooning), which has led to colonization of even the most isolated land masses on Earth. As with ticks, mites, scorpions, and other arachnids, the spider’s body consists of an abdomen and an unsegmented cephalothorax (prosoma) with chelicerate jaws, pedipalps, and four pairs of legs (Figure 52-1). They are distinct from other arachnids 975

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 52-1  External anatomy of an araneomorph spider. A, Dorsal. B, Ventral (legs omitted).

Pedipalp

Chelicera

Eyes Carapace Coxa Trochanter Femur Patella Tibia

Cephalothorax

Tarsus Claws Spinnerets

A

Epigynum Lung slit Opisthosoma Genital furrow Tracheal spiracle

B

Poison gland

Eyes

Midgut diverticulum Apodeme

SEG ESO

Chelicera Fang Rostrum

P

S E

SUB

Aorta Intestine Abdominal nerve

Labium Pharynx muscle Mouth (depressor)

FIGURE 52-2  Longitudinal section of the prosoma. E, endosternite; ESO, esophagus; P, pharynx; S, sucking stomach; SEG, supraesophageal ganglion; SUB, subesophageal ganglion. (Modified from Foelix RF: Biology of Spiders, ed 2, Oxford, UK, 1996, Oxford University Press. With permission.)

in that they have no abdominal segmentation and the male pedipalpal tarsi are modified as secondary genitalia.273 In addition, spiders have venom that is produced in a gland in the anterior prosoma (Figure 52-2) and delivered through a cheliceral fang. On the abdomen, they have silk-producing glands and a set of spinnerets. The overwhelming majority of spider species is carnivorous, so eating involves the challenge of capturing live prey. Prey capture is a multistep process in which spiders must find prey, ensnare it, immobilize it, and digest it externally before the liquefied meal can be consumed. Venoms are a central tool in this process, and the primary function of venom in spiders is prey capture. They are also, but more rarely, used in defense. For their predatory function, venoms are complex mixtures of neurotoxic and proteolytic peptides, proteins, and biogenic amines.1,15,107,202,273 The venom of a single spider can have between 200 and 1000 distinct chemicals.89 In the past decade there has been a burst of research interest in spider venoms because they contain vast stores of unknown chemical compounds with potential application in research, pharmacology, or as insecticides. We direct the curious to Arachnoserver,336 a database of sequences, structural, and molecular target information of all published spider venom toxins. Transcriptomic and proteomic analyses are beginning to reveal patterns of complexity and variation in venom composition within and among species. We do not attempt to review the 976

Prosoma

Abdomen

Metatarsus

Pharynx muscle (levator)

Fangs Maxilla Labium Sternum Coxa

full literature of characteristics of spider venoms, but rather focus on what is known (and unknown) about venoms and their effects on humans. Most toxins in spider venoms have great target specificity, acting selectively on arthropods, vertebrates, or other groups, including some with mammalian-specific activity.1,126,221 Venom composition varies widely across spider species, and variation may exist within species between genders and among geographically isolated populations.136,200 Venom potency also varies within individuals, both seasonally and developmentally. Despite this tremendous venom diversity, only a few dozen spider lineages are considered harmful to humans because (1) most others have an insufficient quantity of venom, (2) the toxins do not affect mammals, or (3) the fangs cannot penetrate human skin. In a few species, although laboratory evidence suggests potential mammalian toxicity, human envenomations have not been reported, perhaps because of the rarity of encounters between spiders and humans in some habitats. Table 52-1 lists an assortment of spider families, including those with species that have been reported to bite humans. In addition to the direct action of venom toxins on humans, there are other ways in which spiders are suspected or known to be clinically relevant. Occasionally, spider digestate may infect wounds created by spider bites, which could in theory affect clinical appearance, although no direct evidence substantiates this suspicion. Similarly, mechanical punctures of human skin by spider fangs may introduce bacteria into wounds; however, this is another suspicion that has yet to be empirically substantiated. Outside of venom and bite mechanics, some theraphosids (tarantulas) produce urticating hairs that irritate skin or mucous membranes of animals or humans. Exposure to these may result from direct contact with a spider or from indirect exposure to materials, such as clothing, that may carry loose hairs.

General Assessment and Treatment of Spider Bites Awareness of the differential diagnosis is crucial for management of any patient presenting for evaluation of “spider bite,” because the offending creature is rarely observed and identified. In general, it is outside of normal biologic activity for spiders to bite humans, except in defense. A defensive bite risks the spider’s life and tends to occur only when its life is threatened by being crushed. Thus, true spider bites are much less common causes of skin lesions than are insect bites or cutaneous infections. Furthermore, no pathognomonic clinical signs prove the diagnosis without retrieval and identification of a spider that was seen actually biting.254 Diagnosis of arachnidism without direct evidence can lead to inappropriate treatment and inadequate consideration of more severe underlying medical issues.162,165,168,247,296

Scientific Name (Number of Genera and Species): Common Name Phylum Arthropoda, Class Arachnida, Order Aranea (3 suborders, 105 families, 3067 genera, approx. 34,000 species): Spiders Suborder Mesothelae (1 family, 2 genera, 40 species) Suborder Mygalomorphae (15 families, 260 genera, 2200 species): Mygales Theraphosidae (86 genera, 800 species): tarantulas and baboon spiders Aphonopelma (Rheochostica): tarantula

Geographic Range Worldwide Asia (part) Worldwide Worldwide New World

Rheochostica henzi (previously Dugesiella henzi ): tarantula Mygalarachne (previously Sericopelma) Pterinochilus: tarantula Pamphobaetus: tarantula Avicularia: tarantula Lasiodora: tarantula Grammostola cala: Chilean rose tarantula

Africa Brazil New World Brazil New World

Acanthoscurria: tarantula

New World

Euathlus (previously Brachypelma): tarantula

New World

Harpactirella lightfooti: baboon spider or bobbejaan-spinnekop Poecilothuria: tarantula Selenocosmia Phormictopus Lampropelma: tarantula Haplopelma minax: Thailand black tarantula Hexathelidae (11 genera, 74 species): funnel-web mygalomorphs Atrax Atrax robustus: Sydney funnel-web spider

Africa

New World

Australia East Indies, India, Australia South America, Caribbean Asia, India Asia, India Eastern Australia Eastern Australia

Hadronyche (Atrax) Hadronyche formidabilis: northern funnel-web spider Hadronyche versutus: Australian Blue Mountains funnel-web spider Hadronyche infensus

Eastern Australia Eastern Australia

Hadronyche cereberus

Southeastern Australia

Dipluridae (17 genera, 157 species): funnel-web mygalomorphs Trechona venosa

Worldwide

Idiopidae (18 genera, 267 species): front-eyed trapdoor spiders Aganippe subtristis Arabantis Mysgolas (previously Dyarcyops, Hermea) Ctenizidae (10 genera, 116 species): trapdoor spiders Bothriocyrtum Ummidia Actinopididae (3 genera, 41 species): trapdoor spiders Missulena bradleyi: mouse spider Suborder Araneomorphae (90 families, 2700 genera, 32,000 species): true spiders Filistatidae (12 genera, 87 species) Filistata Sicariidae (2 genera, 129 species): recluse, brown, or fiddle spiders Loxosceles: recluse, brown, or fiddle spiders DIC, Disseminated intravascular coagulation.

Clinical Remarks

Eastern Australia Eastern Australia

South America Pantropical, India Australia Australia Australia, New Zealand Worldwide, except South America North America North, Central America Australia, Central and South America Australia

Taxonomic References

Clinical References

64, 228 No species believed clinically relevant Opthalmic complications Minor local reaction; urticating hairs Minor local reaction Minor local reaction Minor local reaction Minor local reaction Minor local reaction Minor local reaction; urticating hairs Minor local reaction; urticating hairs Minor local reaction; urticating hairs Minor local reaction Minor local reaction Urticating hairs

Local pain; severe neurotoxicity Local pain; severe neurotoxicity Local pain; severe neurotoxicity Local pain; severe neurotoxicity Local pain; severe neurotoxicity Mammalian toxin; no human reports Minor local reaction Minor local reaction

229 237 237

268

237 237 237 237 237 237 237 237

37, 67, 68

237 237 237 237 237 237 237 237 237

42, 213, 215

37

237 237

95, 96, 133, 284, 285

237 237

11, 139

237

11

237

11, 118

237 237 237 237 237 237 237 237 237 237 237

Mammalian toxin; one case of systemic effects

237

Worldwide

172

Worldwide

229

New World, Mediterranean, Africa

110

148, 154

10, 20, 74, 335 Continued

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CHAPTER 52  Spider Bites

TABLE 52-1  Spiders of Clinical Interest

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 52-1 

Spiders of Clinical Interest—cont'd

Scientific Name (Number of Genera and Species): Common Name

Taxonomic References

Clinical References

110

116, 233

Geographic Range

Clinical Remarks

Loxosceles arizonica: Arizona brown spider

North America (central, southeast) North America (southwest)

Loxosceles rufescens Loxosceles intermedia Loxosceles gaucho Loxosceles spinulosa Loxosceles laeta: corner spider or spider behind the pictures

Worldwide Brazil Brazil South Africa South America, Australia, Finland

Local necrosis; systemic syndrome Local necrosis; systemic syndrome

Loxosceles parrami Sicarius: six-eyed crab spiders

South Africa Neotropics, South Africa

Dysderidae (20 genera, 371 species): giantfanged, six-eyed spiders Dysdera Desidae (28 genera, 200 species): long-jawed intertidal spiders Badumna insignis: black house spider

Worldwide

214 213, 215, 216 72

Worldwide Worldwide

72 249

Loxosceles reclusa: brown recluse spider

Australia, New Guinea

Zodariidae (350 species): hunting spiders Supunna picta Tetragnathidae (50 genera, 900 species): long-jawed orb-weaving spiders Nephila: golden-silk spiders Argyronetidae (1 genus, 1 species): water spiders Argyrontea aquatica Gnaphosidae (111 genera, 2156 species): ground and mouse spiders Herpyllus ecclesiasticus: parson spider

North America

Drassodes Lamponidae (1 genus, 50 species): white-tailed spiders Lampona cylindrata: white-tailed spiders

Worldwide Australia, Tasmania, New Zealand Australia, New Zealand

Miturgidae (23 genera): forest floor and cave spiders Miturga Heteropodidae (82 genera, 850 species): giant crab, huntsman, and large, wandering crab spiders Palystes natalius: lizard-eating spider Heteropoda Isopeda

Worldwide

Olios Delena cancerides: social huntsman spider Oxyopidae (9 genera, 400 species): lynx spiders Peucetia viridans: green lynx spider

Worldwide Australia Worldwide

Painful local lesion; systemic syndrome, antibiotic choice Local necrosis; DIC

Local pain, rarely necrosis Minor local reaction

110, 173 43 43 110, 172

123

182

Pantropical Europe

179 249

Europe Worldwide

249 228 Minor local reaction; brief systemic effects

Minor local reaction; rarely necrotic

Australia, New Zealand

South Africa Worldwide Australia, New Guinea, East Indies America, Australia Australia Worldwide

Minor local reaction

188, 328, 329 39

191

226 228 228

121, 150, 328

70

213

Minor local reaction Local pain, brief nausea Minor local reaction Minor local reaction

Salticidae (475 genera, 4500 species): jumping spiders Breda jovialis Phidippus

Australia New World

Holoplatys

Australia

Mopsus Thiodina Opisthoncus Thomisidae (160 genera, 1960 species): crab spiders Misumenoides Ctenidae (37 genera, 472 species): wandering spiders Phoneutria: armed spiders Phoneutria nigriventer: Brazilian armed spider

Australia America Australia Worldwide

Minor local reaction Local pain, minor ulceration Minor local reaction, itch, headache

251 78 40

44

82, 234

Minor local reaction

Americas Worldwide South America Brazil, Paraguay

134

10, 53, 203

98

North and Central America, West Indies Worldwide

978

110

252

76, 266 266

Local pain; systemic neurotoxin

84

261, 262

Spiders of Clinical Interest—cont'd

Scientific Name (Number of Genera and Species): Common Name Elassoctenus harpax Cupiennius

Geographic Range Australia South and Central America, West Indies Worldwide

Lycosidae (76 genera, 2196 species): wolf spiders Lycosa: wolf spiders Lycosa raptorial Lycosa tarentula: “tarantula” Lycosa godeffroyi Lycosa erythrognatha Miturgidae (28 genera, 590 species): sac, running spiders, and two-clawed hunting spiders Cheiracanthium: sac and running spiders Cheiracanthium mildei Cheiracanthium punctorium

Worldwide Holarctic Europe

Cheiracanthium japonicum

Japan, China

Cheiracanthium longimanus

Australia

Cheiracanthium lawrencei

Africa

Cheiracanthium mordax

Australia

Cheiracanthium inclusum Corinnidae (51 genera, 659 species): sac spiders Trachelas Supunna picta Tengellidae (5 genera, 18 species): running spiders Liocranoides Agelenidae (41 genera, 600 species): grass and funnel-web spiders Tegenaria agrestis: hobo or northwestern brown spider Agelenopsis aperta: grass spider or funnel-web spider Zoridae (12 genera) Diallomus Superfamily Orbicularia (13 families, 10,300 species) Theridiidae (62 genera, 2000 species) comb-footed spiders Latrodectus: widow spiders

America Worldwide

Latrodectus mactans: black widow spider Latrodectus mactans hasselti: redbacked spider Latrodectus hesperus: black widow spider Latrodectus tredecimguttatus Latrodectus pallidus Latrodectus indistinctus: black button spider Latrodectus geometricus: brown button spider Steatoda Steatoda paykulliana: false black widow spider Steatoda nobilis Steatoda foravae: false button spider Achaeranea tepidariorum Araneidae (155 genera, 2600 species): orb-weaving spiders Argiope: argiopes Argiope argentata Argiope trifasciata Araneus: cross, garden, and shamrock spiders Eriophora biapicata Neoscona: orb-weaving spiders Phonognatha graeffei

Clinical Remarks

Worldwide South America Palearctic Australia

78, 287 Local pain Local pain Subject of folklore Local pain

49, 147, 245

77

Minor local reaction; fever Minor local reaction; brief systemic illness Minor local reaction; brief systemic illness Local necrosis; systemic syndrome Minor local reaction, brief systemic illness Local pain, nausea Minor local reaction Minor local reaction

Appalachia, California Worldwide Europe, America (Pacific Northwest) Southwest United States, Mexico

Clinical References

193

Worldwide

Queensland New World

Taxonomic References

77 278

197, 198

339

222 30 213, 215 30

77 230, 338

30

230 71

224, 304

249 Local necrosis; systemic syndrome

250

2, 310, 312, 314

57

Australia Worldwide Worldwide North America Australia North America Mediterranean Libya to Russia Africa Worldwide Worldwide Europe, Mediterranean England Southern Africa Worldwide Worldwide Worldwide America Worldwide Worldwide Australia Worldwide Australia

338 Local pain; systemic neurotoxicity, cardiac effects

174, 180

87, 167, 258

180, 184 301

62 156, 327

184 184

Local pain; mild systemic effects Minor local reaction Trivial local reaction

Local pain; vesicle Minor local reaction Trivial local reaction

184 175 183

176

181 181 177, 178

61 196 206 206 323 208

305

29

DIC, Disseminated intravascular coagulation.

979

CHAPTER 52  Spider Bites

TABLE 52-1 

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Therefore, the medical history, physical examination, and laboratory evaluation of putative spider bites must usually take into consideration an alternative etiology. Treatment plans should include careful follow-up and patient counseling to manage any uncertainties in the final diagnosis. The differential diagnosis of a local lesion may include fungal, bacterial, and viral infections, especially herpes simplex and zoster; the vesiculobullous diseases; arthropod-borne infectious diseases (e.g., Lyme disease); other bites and stings; foreign body reactions; and systemic conditions that predispose to focal skin lesions (e.g., diabetes mellitus, leukemia, lupus erythematosus). First-aid interventions by the patient may mask an otherwise benign process by superimposition of trauma, burns, or chemical irritation. Systemic signs and symptoms may require differentiation from the effects of snake or scorpion neurotoxin, pesticide toxicity, sepsis, meningitis, hemolytic anemia, or acute abdomen, depending on the circumstances. The medical history should include details of the bite circumstances to demonstrate consistency with expected spider habitat and behavior. This includes location indoors or outside, time of day or night, and human activity at the time of injury. The victim should attempt to recall the appearance of the involved arthropod. If it was believed killed through garments or bedclothes, an attempt should be made to retrieve its remains. Crushed spider parts can be examined and identified by arachnologists or entomologists at many universities and museums. Until identified, spiders may be preserved in 70% to 80% ethanol. The evolution of subsequent wound and systemic symptoms should be noted, along with modifiers, including home treatment and underlying health of the patient. If the local geography lacks species consistent with the suspected pathophysiology, the recent travel histories of household contacts should be considered. Physical examination includes particular attention to the bite site, as well as general assessment for systemic effects. Local findings of importance include anatomic location (spiders are more likely to bite defensively at sites where clothing binds tightly; thin skin is more readily envenomed than callous skin) and number of separate lesions (multiple bites suggest parasitic insect bite rather than spider bite). Central punctae, vesicles, or erosions should be noted, as well as the pattern of peripheral changes, including erythema, pallor, hemorrhage, induration, tenderness or anesthesia, and local lymphatic involvement. Systemic findings, depending on the species involved, may include changes in vital signs, diaphoresis, generalized rash, facial edema, gastrointestinal distress, muscle fasciculations, spasm or tenderness, or altered mental status. The laboratory evaluation for envenomation is usually simple, seldom requiring more than a complete blood count and urinalysis. Assessment for other elements of the differential diagnosis, however, may be much more elaborate. Depending on circumstances, this may include viral, bacterial, or fungal culture; Lyme disease titer; radiography of the abdomen or of the injured part; stool test for occult blood; electrocardiogram; or skin biopsy. General supportive measures are the mainstays of therapy for most spider bites. These include basic local hygiene, tetanus prophylaxis, analgesics, hydration, and surgical follow-up if indicated for debridement and management of extensive necrotic lesions. Corticosteroids are of unproved benefit and are generally not indicated. Antibiotics, although not of value for simple venom injury, are prescribed when bacterial cellulitis cannot be eliminated from the differential diagnosis. Specific measures, including antivenom, for treatment of envenomation by particular spider species are discussed later in this chapter.

BOX 52-1  Clinically Important Spider Genera by

Geographic Distribution2,127,262,294

North America Loxosceles Latrodectus Tegenaria South America Loxosceles Latrodectus Phoneutria Africa Loxosceles Latrodectus Europe Loxosceles Latrodectus Australia Atrax Hadronyche (Atrax) Latrodectus Asia Latrodectus

the act of biting by directing professionals to proper identification keys. Table 52-1 includes species worldwide that are currently known or suspected to be medically noteworthy, even minimally, either through the effect of bites or urticating hairs. Geographic range and the most recent systematic work on each group are included. Box 52-1 lists the genera of serious medical significance for each continent. For effective communication, groups of spiders must be recognized by the same name worldwide. This chapter uses the current official nomenclature. Of the three spider suborders, two contain clinically significant species: Mygalomorphae and Araneomorphae. Mygalomorphs include the baboon spiders or tarantulas, trapdoor spiders, purseweb spiders, mygalomorph funnel-web spiders, and several other groups that lack common names. Most spiders are araneomorphs. These include jumping spiders, orb-weaving spiders, widow spiders, wolf spiders, and fiddleback spiders (see Table 52-1). The most conspicuous characteristics that distinguish these groups are the orientation of the chelicerae (jaws) and the number of book lungs. Spider fangs are located on the chelicerae, which open sideways in the Araneomorphae and move diagonally in the Mygalomorphae, requiring the latter to rear back for a downward, snakelike strike (Figures 52-3 and 52-4). Mygalomorphae have two pairs of book lungs, whereas most Araneomorphae have only one pair. Lung slits, which open into the book lungs, are easily visible in a ventral view of the anterior abdomen (see Figure 52-1). Characteristics that distinguish families, genera, and species include eye number and pattern, numbers of tarsal claws, and details of genitalia structure.

Guide to Spider Diversity and Identification This chapter provides more information on spider diversity than do most reviews in order to (1) inform the reader of the immense diversity of spiders that are medically insignificant and thus emphasize the rarity of spiders known to cause medical problems; (2) emphasize the need for accurate species identification, particularly in reporting of cases for publication or teaching; and (3) facilitate accurate identification of spiders that are caught in 980

A

B

FIGURE 52-3  Movement of the chelicerae in mygalomorphs (A) and araneomorphs (B). (Modified from Foelix RF: Biology of Spiders, ed 2, Oxford, UK, 1996, Oxford University Press. With permission.)

CHAPTER 52  Spider Bites

FIGURE 52-4  Fangs of mature male tarantula (Aphonopelma species). (Courtesy Michael Cardwell and Associates, 1992.)

FIGURE 52-6  Mature female Aphonopelma iodium. (Courtesy Michael Cardwell and Associates, 1997.)

Although many spider species are geographically localized (e.g., Atrax robustus in Australia, Phoneutria nigriventer in Brazil), some, such as the widow spiders (Latrodectus), are found worldwide (see Table 52-1). Others, such as members of the Loxosceles genus, are widely distributed in more than one continent, and still others, such as Tegenaria agrestis, appear to have naturalized in specific geographic regions distant from their point of ecological origin. Because of the resulting worldwide species diversity and overlap, the remainder of this chapter is structured according to spider taxonomy rather than isolated species or geographic location.

all continents, with the greatest abundance and diversity in tropical regions. They mature in 3 to 9 years and can live for 15 to 25 years. Individuals live in burrows, with trip-line threads extending from the entrance. These are sometimes located in abandoned rodent burrows or hollow trees. Theraphosids have dense tufts of specialized hairs on their tarsi (feet) that enable them to climb on smooth surfaces and may aid in prey capture. They have two tarsal claws, eight closely grouped eyes, and two pairs of spinnerets. As a group, they are found mainly in tropical and subtropical areas. Confusingly, the word tarantula was first applied to Lycosa tarentula, a species of European spider actually belonging to the wolf spider family, or Lycosidae, which are properly classified within the suborder Araneomorphae, described later in this chapter. In the United States, the term tarantula usually refers only to the large spiders of the family Theraphosidae, suborder Mygalomorphae. Grammostola mollicoma is the largest tarantula known, with a body length of 7 to 10 cm (3 to 4 inches) and leg spread of 21 to 27 cm (8.3 to 10.6 inches).42,111 Harpactirella lightfooti, the baboon spider or bobbejaan-spinnekop, is a mygalomorph spider found in South Africa. Body length is 3 cm (1.2 inches); the cephalothorax is brown with a yellowish border.

Suborder Mygalomorphae Mygalomorphs make up less than 10% of all spider species. They are found worldwide, with greatest abundance and diversity in tropical regions. Tarantulas (Theraphosidae) are the most famous mygalomorphs and include the largest spiders known, reaching up to 10 cm (4 inches) in body length. Most mygalomorphs are smaller, some less than 1 mm (0.004 inch) in adult body length. Most live multiple years (some up to 20), and females continue to molt after reaching adulthood. They have diverse habits but typically live in silk-lined burrows or silken tubes. For the purpose of prey capture, mygalomorph silk is only slightly sticky relative to araneomorph silk and is generally used to signal the presence of prey rather than to ensnare them. Once prey are detected, spiders run out of their retreat, seize prey in their jaws, and return to the retreat to feed. Individuals wander when dispersing, and males leave their retreats in search of females during mating season.

FAMILY THERAPHOSIDAE: TARANTULAS AND BABOON SPIDERS Theraphosidae is the largest mygalomorph family with respect to both numbers of species and sizes of the largest individuals (Figure 52-5). Approximately 800 described species are found on

FIGURE 52-5  Theraphosidae. (Courtesy Gita Bodner.)

Venom In the last few years our understanding of tarantula venoms has increased because of analyses of the venom transcriptomes and proteomes of multiple species.157 In the United States, Rheochostica henzi and members of the genus Aphonopelma (Figure 52-6) have venom containing hyaluronidase, nucleotides, and polyamines.48,58,172,259,260 Polyamines are thought to act as neurotransmitters and increase venom effectiveness, particularly with respect to paralysis of insect prey.273 Hyaluronidase is postulated to be a spreading factor, and the nucleotide adenosine triphosphate (ATP) potentiates the major effects of the venom on mice. Both venoms cause rapid, irreversible necrosis of skeletal muscle when injected intraperitoneally into mice.223 Dugesiella (Rheochostica) venom was found to have a necrotoxin with several similarities to sea snake venoms.172 In comparison, the venom of Scodra griseipes, an African tarantula, includes higher-molecularweight (greater than 25,000 daltons) proteins and enzymes plus lower-weight polypeptides (4000 to 9000 daltons); the second group is believed to contain polypeptide neurotoxins.56 S. griseipes venom toxins have an effect on mammalians, but this species is not known to be clinically relevant. Recent work suggests that venom chemotaxonomy may be a useful method of nondestructive species recognition, at least within the Brachypelma genus.88 Urticating Hairs Several genera of tarantulas, including Haplopelma, Lasiodora, Grammostola, Acanthoscurria, and Brachypelma, possess urticating hairs irritating to skin and mucous membranes. These genera are located throughout the western hemisphere, with 981

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many species indigenous to the United States. When one of these spiders is threatened, it rubs its hind legs across the dorsal surface of its abdomen and flicks thousands of hairs toward the aggressor. These barbed hairs can penetrate human skin, causing edematous, pruritic papules. Itching may persist for weeks. There are four morphologic types of urticating hairs. Tarantulas within the United States possess only type I hairs, which do not penetrate the skin as deeply as do type III hairs. Type II hairs are incorporated into the silk web retreat and are not thrown off by the spider. Type III hairs can penetrate up to 2 mm into human skin; this is the type of hair most likely to cause inflammation. They are typically found on Mexican, Caribbean, and Central and South American species. Type IV hairs, which belong to the South American spider Grammostola, are able to cause inflammation of the respiratory tract in small mammals. Rats and mice have been reported to die of asphyxia within two hours after exposure to the hairs.67,328 Clinical Presentation Despite the presence in venom of components toxic to rodent nerves and skeletal muscle, most tarantula bites result in only mild to moderate local symptoms in humans. A few can cause more severe pain and swelling, numbness, or lymphangitis. In a series of nine cases in Australia, by either Selenocosmia species or Phlogiellus species, no major effects occurred. Local pain was the most common effect, followed by puncture marks or bleeding. Severe pain occurred in four of seven patients, where severity of pain was documented. Mild systemic effects occurred in one case.149 Species of tarantula implicated as causes of human envenomation include those in genera Mygalarachne (formerly Sericopelma) of Panama, Pterinochilus of Africa, Aphonopelma of Mexico and the United States, Pamphobaeteus of South America, Euathlus of Costa Rica, Theraphosa of French Guyana, Grammostola of Colombia, Selenocosmia and Phlogiellus of Australia, Poecilotheria of India, Lampropelma of Thailand, Lasiodora of Brazil, and Avicularia of Central America and the southwestern United States. Envenomation usually involves immediate pain at the bite site, occasionally followed by some redness and swelling, and is usually without necrosis or serious sequelae.42,48,58,109,260 A paucity of reports in the peer-reviewed medical literature hinders proper characterization of occasional tarantula neurotoxicity, particularly in cases (e.g., Poecilotheria) that are reported anecdotally and in the pet trade, to provoke severe neuromuscular symptoms Although no fatalities have been reported, localized pain followed by emesis, weakness, and collapse have been noted after envenomation by Harpactirella lightfooti, the baboon spider of South Africa.42,129,213 Urticating hairs may cause intense inflammation, which may cause pruritus for weeks. Individuals who handle tarantulas may unwittingly transfer urticating hairs from hand to eye, causing keratoconjunctivitis or ophthalmia nodosa. Keratoconjunctivitis has been described after handling of a Thailand black tarantula, Haplopelma minax. Fine intracorneal hairs were noted at examination, and inflammation settled quickly with topical corticosteroid treatment; at a 36-month follow-up, the eye was normal.37 More severe ophthalmic complications occurred in two cases after handling Chilean rose tarantulas, Grammostola cala. In these victims, initial findings were similar, with intracorneal hairs and keratoconjunctivitis, but progressive panuveitis followed, with corneal granulomas, iritis, cataract, hyalitis, and chorioretinitis apparently related to migration of hairs through the media of the eye. The differences in outcome with exposure to the two species may result from differences in hair morphology, which may also explain differences in other reports of ophthalmic injury from tarantula or caterpillar hair exposure.37 Similar cases of ophthalmia nodosa have been described.24,171 Sheth and colleagues,268 in London, reported another case of ocular inflammation after handling a pet Chilean rose tarantula. A 9-year-old boy presented with new onset of painful red right eye, initially thought to be trauma-induced 2 weeks earlier. The left eye was unaffected and visual acuity was within normal limits. Slit-lamp examination showed right eye injection with multiple hairs at all levels of the cornea with associated opacities, and moderate anterior uveitis. In addition, hair-like vitreous lesions and peripheral full-thickness retinal infiltrates were seen. Topical therapy 982

FIGURE 52-7  Cornea showing multiple tarantula hairs with associated inflammatory infiltrate and scarring. (From Atkins JA, Wingo CW, Sodeman WA, et al: Necrotic arachnidism, Am J Trop Med Hyg 7:165, 1958.)

with corticosteroids and antibiotics was initiated and follow-up continued with long-term tapering topical steroids. Hair removal was not attempted because of the large number and depth of hairs. Eighteen-month follow-up revealed full resolution of inflammation, normal visual acuity, and no complications (Figures 52-7 and 52-8). Treatment Theraphosid bite management is symptomatic. Elevation and immobilization of the extremity and oral analgesics may help reduce pain. All bites should receive local wound care and appropriate tetanus prophylaxis. Urticating hairs can be removed from skin with repeated application and removal of sticky tape, followed by copious irrigation if necessary; exposed eyes should be irrigated primarily. Topical or systemic corticosteroids and oral antihistamines may also be useful for urticating hair reactions.

FAMILY HEXATHELIDAE: FUNNEL-WEB MYGALOMORPHS The family Hexathelidae includes 11 genera and approximately 74 species, which are currently known from the Old World and Chile.237 The funnel webs that typify members of this group are silk-lined tubular retreats that extend into a protected space, such as a burrow in the ground or a hole in a tree. Sheets of silk radiate from the retreat and signal the presence of prey. These webs superficially resemble webs of araneomorph spiders in the family Agelenidae. Distinguishing characteristics of the spiders include a shiny carapace; long, spiny sensory hairs on the legs;

FIGURE 52-8  Color photograph of retina showing punched-out fullthickness inflammatory lesions associated with embedded tarantula hairs. (From Atkins JA, Wingo CW, Sodeman WA, et al: Necrotic arachnidism, Am J Trop Med Hyg 7:165, 1958.)

and paired claws lacking claw tufts on the tips of the feet, with teeth lining the medial claw. Clinically significant hexathelid spiders are species of Atrax (Figure 52-9) and Hadronyche. Technically, taxonomists now consider Atrax and Hadronyche species as members of only one genus.237 To avoid confusion in the literature, species names still use either Atrax or Hadronyche, depending on their original names. We discuss these species as a cohesive taxonomic group. Among these, the species A. robustus is best known and most carefully studied. Atrax and Hadronyche species, all of which are believed to be dangerous, have been described in southern and southeastern Australia, Tasmania, Papua New Guinea, and the Solomon Islands. As a group, they prefer cool, moist coastal and mountainous regions.122,124,269 Genus Atrax/Hadronyche Biology.  Funnel-web spiders have a glossy ebony cephalothorax and velvety black abdomen. The abdominal undersurface may have brushes of red hair. The fangs reach 4 to 5 mm (0.16 to 0.19 inch) in length and are capable of penetrating a fingernail or a chicken’s skull, sometimes making removal of the spider difficult. Females are somewhat larger than males, with a body length of 4 cm (1.57 inches). Mature males are more delicate, with a tibial spur on the second pair of legs and pointed pedipalps.146,262 A. robustus, the Sydney funnel-web spider, is limited to a 160-km (100-mile) range around the center of Sydney, Australia. The spider creates a tubular or funnel-shaped, silk-lined shallow burrow under rocks, logs, fences, stumps, or thick vegetation or around foundations of houses. Colonies of up to 150 spiders have been found. Females rarely roam far from their webs; males live a vagrant life after reaching maturity. Wandering males may enter houses or other areas of human habitation, especially during the summer months after a heavy rain. Its aggressive behavior and potent venom make the male Sydney funnel-web arachnid one of the most dangerous spiders in the world. It is responsible for all known fatal Atrax envenomations.2,127,262,294 H. formidabilis, the northern funnel-web spider, is found in the central coastal region of New South Wales and the adjacent Blue Mountains. Its tree-dwelling habit was once thought to be unique, but it is now known that other species also live in trees. The webs may be camouflaged in rough-barked trees, such as melaleuca (paper bark), banksia, and eucalyptus.124 Venom.  Although many species have venom with significant in vitro toxicity, few have been implicated in human illness. The best described of these is A. robustus. Atrax venom causes widespread release of neurotransmitters.81,124,132,276,282 This may occur by a direct action of the venom on nerve membranes, producing spontaneous action potentials and consequently provoking a global outpouring of transmitters that accounts for the neuromotor and autonomic stimulation seen clinically. Early efforts to purify the active component of Atrax venom resulted in reports of neurotoxins of various molecular weights

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CHAPTER 52  Spider Bites

FIGURE 52-9  Funnel-web spider (Atrax species) wearing an engagement ring. (Courtesy Sherman Minton, MD.)

purified from venom preparations in separate experiments.281 These were termed atraxotoxin (10,000 to 25,000 daltons, from milked venom),124 robustoxin (4887 daltons, also from milked venom),270 and atraxin (9800 daltons, from ground venom glands).125 Venoms of A. robustus, H. cereberea, H. formidabilis, H. infensa, H. lanunstian, H. variela, H. versula, and an Atrax species preparation and Hadronyche species preparation have similar high- and low-molecular-weight protein electrophoretic patterns and Western blotting, suggesting that all of these species contain similar atraxotoxins. The relationships among these toxins are not clear, but atraxotoxin or atraxin may be a precursor to robustoxin. In addition to these components, Atrax venom contains various lower-molecular-weight compounds, including citric acid, lactic acid, phosphoric acid, glycerol, urea, glucose, γ-aminolevulinic acid, glycine, spermidine, spermine, tyramine, octopamine, and 5-methoxytryptamine.80 The best characterized of the toxins is robustoxin, whose 42–amino acid sequence was determined in 1985.270 It is the sole lethal toxin that can be isolated by cation-exchange chromatography, and its effects in monkeys duplicate the effects of crude venom preparations. A 5 mg/kg intravenous (IV) dose of robustoxin to monkeys causes dyspnea, blood pressure fluctuations culminating in severe hypotension, lacrimation, salivation, skeletal muscle fasciculation, and death within 3 to 4 hours of administration.209 Isolated human intercostal muscles were studied to determine the etiology of muscle fasciculations. Muscles treated with A. robustus venom developed marked contractions, which were abolished by d-tubocurarine.51 Muscles treated with venom for more than an hour stopped contracting and could be stimulated only by increasing the stimulus duration. A. robustus venom has been shown to lack anticholinesterase activity.280 Contractions are not a direct venom action on the muscle fiber, so acetylcholine appears to have been released from the presynaptic terminals.102 Muscle fasciculations are apparently caused by abnormal repetitive firing of motor neurons. It was hypothesized that the venom changes the membrane’s electric field, activating sodium channels without altering the transmembrane potential or damaging the neuronal membrane ultrastructurally.81,124,276 The initial hypertension in Atrax toxicity may have several causes. Morgans and Carroll204,205 demonstrated direct α-adrenergic stimulation with vasoconstriction of isolated arterial preparations exposed to A. robustus venom. In rabbit atria, an initial decrease followed by an increase in cardiac inotropy and chronotropy may result from vagal acetylcholine and myocardial norepinephrine releases, respectively.52 The combination of myocardial responses and peripheral vasoconstriction may explain the initial hypertensive response. Animal species vary in susceptibility to Atrax venom. Rabbits given 15 mg of crude venom intravenously and cane toads given 12 mg of female Atrax venom show no effects after envenomation. Primates, including humans, are among the most susceptible species. Newborn mice, also highly susceptible, have been used as an in vivo biologic assay for venom toxicity.124,285 Sutherland287 found that a lethal dose of venom from a male A. robustus could be neutralized in newborn mice by nonimmune sera from rabbits and other nonprimate vertebrates. Sheumack and co-workers271 later demonstrated that the active fraction of nonimmune rabbit sera contained immunoglobulins G and M (IgG, IgM). In addition, venom potency varies with time of year, recent feeding history, maturation, and gender of the individual spider.12 Between 1956 and 1963, Wiener330 demonstrated significant differences in the venoms of male and female Atrax spiders. Males had an average venom yield of 1.01 mg, less than the 1.84 mg average yield from females. On the other hand, guinea pig lethality was much greater after a bite by a male (75% to 90%) than by a female spider (20%). Weiner concluded that significant qualitative difference exists between the venoms of males and females. Monkeys, which have a pattern of envenomation similar to that in humans, provide a model in which Sutherland285,291 has described a biphasic clinical syndrome. Phase I begins minutes after venom injection, with local piloerection and muscle fasciculation. This extends proximally, becoming generalized over the

PART 6  ANIMALS, INSECTS, AND ZOONOSES

next 10 to 20 minutes. After another 5 minutes, severe hypertension, tachycardia, hyperthermia, and coma with increased intracranial pressure may occur, followed by diaphoresis, salivation, lacrimation, diarrhea, sporadic apnea, borborygmi, and grotesque muscle writhing. Death may result from asphyxia caused by laryngeal spasm, combined with copious respiratory secretions, apnea, or pulmonary edema. Laboratory evaluation reveals metabolic acidosis and elevated plasma creatine phosphokinase. Phase II begins 1 to 2 hours after envenomation as the phase I symptoms subside. The victim may return to consciousness and appear to recover. In severe cases, hypotension gradually worsens over 1 to 2 hours, with periods of apnea. Pulmonary edema and death may occur despite ventilatory support. Clinical Presentation.  Up to 90% of Atrax bites may not result in significant envenomation.328 Intense pain at the bite site may result from direct trauma as well as the venom’s effect, but the bite does not provoke cutaneous necrosis. Wiener330 studied the cutaneous effects of the venom on himself by injecting 0.5 mg intradermally. Local pain and a wheal surrounded by erythema lasted for 30 minutes, followed by localized sweating and piloerection. No systemic effects occurred. One case of cutaneous necrosis has been reported. Nayar and colleagues211 described a man visiting in New Zealand and reportedly bitten by a funnel-web spider when reaching into a bag of onions purchased at a shop. On return to England, he was treated at a hospital on two occasions with incisions and drainages for suspected infection of his thumb tip. Subsequently, his thumb became necrotic, with eventual osteocutaneous necrosis extending to the mid-terminal phalanx. Surgical treatment consisted of a Moberg flap reconstruction. No systemic involvement was seen, and he eventually returned to work. The earliest systemic signs and symptoms may include perioral tingling, nausea and vomiting, diaphoresis, salivation, lacrimation, and dyspnea. Pulmonary edema follows, along with a generalized central and peripheral neurologic syndrome that includes muscle fasciculations, tremor, spasms, weakness, and impaired consciousness. Death may occur secondary to pulmonary failure, hypotension, or cardiac arrest.282,328 Thirteen fatalities from A. robustus envenomation were recorded between 1927 and 1984. Children are particularly susceptible; those younger than 12 years of age may die within 4 hours of the bite.97,133,288 Before the development of specific antivenom in 1980, severe envenomations resulted in a minimum 8-hour critical period, followed by a 9- to 21-day hospital course.96,288,291 No fatalities caused by H. formidabilis have been recorded, although several severe envenomations have occurred.124 Venoms of A. robustus, A. versutus, A. infensus, and A. formidabilis appear to have comparable vertebrate toxicity in vitro.11 Treatment.  Immediate treatment after a bite is modeled after that for Australian snakebite and consists of four steps: (1) wrap the length of the bitten extremity with an elastic bandage, (2) splint to immobilize the extremity, (3) immobilize the victim, and (4) transport to the nearest hospital with the bandage in place.220,289 A human case report has illustrated utility of this method, with occurrence, disappearance, recurrence, and re-resolution of symptoms coinciding with compression wrap removal and replacement in a man bitten by a male A. robustus.118 An experimental model in Macaca fascicularis monkeys has supported efficacy of the pressure immobilization technique.284,285,292 Specific antivenom has been the mainstay of treatment for Atrax envenomation since 1981. The antivenom is a purified IgG product developed by Sutherland and associates286,293 at the Commonwealth Serum Laboratories by immunizing rabbits with a combination of male Atrax venom and Freund’s adjuvant. The antivenom was demonstrated to neutralize Atrax venom in vitro and to reverse symptoms in monkeys before its introduction for human use. It has been used with good effect in humans bitten by Atrax and Hadronyche species.75,291 If a tourniquet or bandage is in place when the victim presents for hospital care, an IV line should be initiated before removing the tourniquet or bandage in an intensive care setting, with careful observation for development or progression of symptoms. 984

If systemic signs or symptoms occur, victims are usually treated with antivenom administration. Two ampules of antivenom (100 mg of purified IgG per ampule) are administered intravenously every 15 minutes until symptoms improve. Dosing is the same for children as for adults, and total doses of two to eight ampules have been reported. During a 10-year period, antivenom was given to at least 40 persons, with no adverse effects or deaths reported.291 In addition to antivenom administration, management is symptomatic and supportive. Oxygen, mechanical ventilation, and IV fluid support may be indicated in severe cases. Atropine (0.6 mg) may be used to lessen salivation and bronchorrhea. β-Adrenergic blockers may be indicated for severe hypertension and tachycardia. Other than antivenom, no consistently effective agent has been found to enhance survival after Atrax envenomation. Diazepam, atropine, and furosemide have been found to increase survival in monkeys, but this may not be the case in humans.95,139 Sheumack and colleagues272 developed a toxoid from robustoxin by polymerization with glutaraldehyde. Immunization with the toxoid conferred protection against the lethal effects of 50 mg/kg Atrax venom in monkeys for at least 26 weeks after toxoid injection.

FAMILY DIPLURIDAE: FUNNEL-WEB MYGALOMORPHS Members of the family Dipluridae are found on all continents and are concentrated in tropical areas. Individuals build funnel webs similar to those of Hexathelidae. Diplurids are distinct from hexathelids in having posterior lateral spinnerets that are very long and widely separated. Most are 5 to 25 mm (0.2 to 1 inch) in length.

FAMILY ACTINOPODIDAE Genus Missulena: Mouse Spiders Biology.  Missulena are large spiders (10 to 35 mm [0.4 to 1.4 inches]) native to Australia, with one species found in Chile. Like all Actinopodidae, they are trapdoor spiders that burrow underground and seal the entrance with a lid that they open and close with their fangs. Silk lines spreading from the mouth of the burrow reveal the presence of prey that stumble across them. The spiders dash out, grab prey in their jaws, and retreat back into the burrow to feed. These spiders spend most of the time underground, with the exception of males searching for females in autumn. The larger females are most often encountered when their well-camouflaged burrows are accidentally dug up. Venom.  Missulena venoms have recently been confirmed to have a major bioactive component, δ-missulenatoxin-Mb1a,128 that is homologous to the δ-atraxotoxins of atraxine spiders (see earlier text). This toxin has strong insecticidal potency and acts by manipulation of tetrodotoxin-sensitive sodium channels. The discovery of this toxin and its homology with atraxotoxins indicate extreme conservation of this toxin family.128 This finding also provides a mechanistic explanation for observed similarities between the toxic effects of bites of Missulena bradleyi and those of Atracines in animals.236 Clinical Presentation.  In a series of 13 envenomations, pain was the most common complaint, severe in 10, with puncture marks, bleeding, redness, and edema being the next most common complaints. Three patients exhibited neurotoxic effects; all three exhibited paresthesias, one with accompanying diaphoresis. Nonspecific systemic effects occurred in five patients. There were no cases of severe envenomation in this series. There has been a total of 40 reported Missulena bites, with one case of severe envenomation. This occurred in a 19-month-old child in Queensland.148,154 Treatment.  Treatment is largely symptomatic and supportive. In the case of severe envenomation of the 19-month-old child,

Dipluridae, Genus Trechona Biology.  Trechona venosa is a large South American funnel-web tarantula with neurotoxic venom potentially dangerous to humans.42,109,129 As with all Trechona species, T. venosa is sedentary, living in holes or on plants in tropical forests along the Atlantic coast. The spider may be black or gray-brown with yellow stripes on the abdomen. Mature body length may be 3 to 4.5 cm (1.2 to 1.8 inches), with 6- to 7-cm (2.4- to 2.8-inch) legs and 3- to 4-mm (0.12- to 0.16-inch) fangs. T. venosa is not found in Chile, but in this region it has been confused, particularly in venom studies, with a spider in the family Nemesiidae, Acanthogonatus subcalpeianus, which it resembles.237 Venom.  The venom of T. venosa is extremely toxic to rats, with an apparent action similar to that of Phoneutria species.186 Little is known about venom composition. Clinical Presentation.  No cases of human envenomation have been reported, although it is presumed that symptomatic envenomation by T. venosa is possible. Treatment.  Treatment is symptomatic and supportive.

Suborder Araneomorphae Enormous diversity is found within the group Araneomorphae, which contains more than 85% of the approximately 42,000 currently described spider species.64,231,326 Araneomorphs, or true spiders, are found throughout the world in all terrestrial (and a few aquatic) habitats. They show tremendous variability in size, appearance, and habit; however, no araneomorphs are as large as the largest tarantulas. Characteristics that distinguish araneomorphs include features of the spinnerets that enable them to produce extremely sticky silk. All but a few groups have only one pair of book lungs. Most have eight eyes, but eye number varies from two to eight. Prey capture tactics usually determine where a spider will be found and are generally consistent within particular groups. Thus, these tactics often provide conspicuous clues that help identify spiders.

CHAPTER 52  Spider Bites

administration of funnel-web spider antivenom, raised against male A. robustus venom, produced dramatic improvement in her condition, with full recovery following a second dose.236 Although severe envenomation is rare, it is suggested that all suspected Mygalomorphae bites be observed for 4 hours to exclude such envenomation.148,154

FIGURE 52-10  Adult female desert violin spider (Loxosceles deserta). (Courtesy Michael Cardwell and Associates, 1994.)

human pathologic conditions. Several species have been associated with necrotic arachnidism in the United States: L. reclusa (the true brown recluse spider, Figure 52-11), L. rufescens, L. arizonica, and L. laeta. These spiders are native to all the southernmost states. In the Mississippi River Valley, their territory extends as far north as southern Wisconsin. Species native to one region or habitat may adapt successfully to new locations after transport by humans.216,322 Brown spiders regularly roam in search of new web sites, and males wander in search of females. They are most active at night from spring through fall, emerging from rock piles, woodpiles, and rats’ nests to hunt insects and other spiders. South African savanna species have been observed under stones and logs and in the tunnels of old termite nests; spelean species are found naturally in caves but have also appeared in homes and export warehouses.212,215,218 Brown spiders may infest homes, generally

FAMILY SICARIIDAE: RECLUSE SPIDERS Sicariidae includes two genera, Loxosceles and Sicarius, both of which are clinically important. The family falls within a larger group of families (Scytodoids) that all have only six eyes. In these two genera, the eyes are in dyad pairs. The chelicerae are fused at the base, and the labium is fused to the sternum. Males have more slender abdomens and more prominent pedipalps than do females. Previously, Loxosceles was placed in its own family, Loxoscelidae, but this was recently synonymized with Sicariidae.229 Genus Loxosceles: Brown or Fiddle Spiders Biology.  Loxosceles, commonly known as brown or fiddle spiders, build small, irregular, and sticky webs in small areas, such as under rocks or wood or in human-made habitats. The genus contains more than 100 species, with centers of diversity in North or South America and Africa.20,79,192,256,264 These spiders are 8 to 15 mm (0.3 to 1.6 inches) in adult body length, are light to dark brown, and have a dark, violin-shaped spot centered anterodorsally, such that the neck of the fiddle extends toward the posterior end of the cephalothorax. The shape and darkness of the fiddle, relative lengths of the first two pairs of legs, and genitalia characteristics are features that help distinguish species45,142,264 (Figure 52-10). From the South American Loxosceles laeta to the South African L. spinulosa, these small arachnids have been associated with

A

B FIGURE 52-11  Brown recluse spider. A, Loxosceles reclusa. B, Loxosceles vonwredei, a cave-dwelling species from Namibia. (A courtesy Indiana University Medical Center; B courtesy Greta J. Binford.)

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

preferring warm, undisturbed environments, such as vacant buildings and storage sheds. In Chile, the tendency to inhabit human dwellings has earned L. laeta the names araña de los rincones (corner spider) and araña de detrás de los cuadros (spider behind the pictures).265 Loxosceles distributions are patchy, but when they are present they can reach high densities. For example, 2055 individual L. reclusa were captured in a singlefamily home in Kansas in a 6-month period.318 Molts, or shed exoskeletons, are good indicators of the presence of resident Loxosceles. Webs are small, flocculent structures made in crevices with a bluish tint in bright light. Egg sacs are laid flat against surfaces, typically with a layer of fluffy silk on the exposed surface. Females may live 1 to 3 years, and longer in captivity.109,143 Naturally unaggressive toward humans, brown spiders are not prone to bite unless threatened or trapped against the skin. Bites typically follow retrieval of old bed sheets or jackets from storage. Thorough housecleaning with movement of boxes and stored items at least once per year highly reduces the likelihood of establishment of robust populations of Loxosceles in houses.110 A study by Vetter319 showed that of 1773 spiders thought to be L. reclusa by medical professionals, only 324 actually were Loxosceles. In addition, the true recluses were from regions historically known to be in their home range. Only one brown recluse spider was found outside the normal habitat region, and this case was explained by recent travel. Of the other 1449 submissions that were spiders, more than 38 families, 88 genera, and 158 species were identified. It was noted that more accurate identification occurred in areas with known historical populations. This study also suggests that the brown recluse has not migrated throughout the United States, but remains within its home regions. Venom.  Fractionated Loxosceles venom contains at least eight or nine major protein bands and three or four minor bands identifiable by 1-D protein gel electrophoresis36,242 and hundreds of proteins identifiable by 2-D gel electrophoresis.33a Recent proteomic and transcriptomic analyses have identified a minimum of 400 distinct toxic components in venoms of South American Loxosceles.93 Hyaluronidase was first identified as a component by Wright and associates.337 Hyaluronidase probably plays a facilitating role in lesion development, encouraging the spread of other venom components; however, it is not itself a cytotoxin. Hydrolytic enzyme activities include esterase,337 alkaline phosphatase,135 lipase,159 5′-ribonucleotide phosphorylase,108 and astacins302 but none of these alone appears to explain cytotoxicity. Sphingomyelinase D, a 32- to 35-kDa venom protein family, is the sufficient causative agent for formation of dermonecrotic lesions following Loxosceles bites.169,297,299 Homologs of sphingomyelinase D constitute up to 18% of the proteins in Loxosceles venom.93 The sphingomyelinase D enzyme activity is rare in nature and is currently only known elsewhere in tick saliva and as an exotoxin of pathogenic bacteria. Sphingomyelinase D is present in L. intermedia spiderlings starting with the third instar, with increasing activity throughout development until adulthood.114 Injection of expression products of cloned sphingomyelinase D–encoding genes isolated from L. intermedia, L. laeta, L. reclusa, and L. boneti produces characteristic lesions in rabbits.169,299,303 Sphingomyelinase D activity has been detected from a sampling of worldwide representatives of Loxosceles.35,36 Therefore, all species in this genus are suspected to be capable of bites resulting in dermonecrosis. Many of these species live in habitats that make them unlikely to encounter humans. Sphingomyelinase D is postulated to operate by a variety of mechanisms, including cell membrane–binding complement activation and polymorphonuclear leukocyte neutrophil (PMN) chemotaxis.105,241,274,307,308 Lesions are inhibited in rabbits by pretreatment with nitrogen mustard to deplete PMNs. Histologic studies suggest similarities between venom-induced lesions and those seen with the Arthus and Shwartzmann phenomena.274 Some vertebrate species, such as rats and fish, are essentially unaffected by Loxosceles venom; others, such as rabbits, mice, and dogs, are highly susceptible to its effects.263 Injected into humans, the venom is a hemolysin and cytotoxin, with enzymatic 986

activities that may cause dermonecrosis and hemolysis. Pathogenesis of the human lesion is not well understood but depends on the functions of complement and PMNs.17,264 Recent works suggest that venom toxins act as proteases against constituents of plasma and basement membranes. Because of their degenerative nature, these proteases may be a plausible mechanism for the hemorrhage, delayed wound healing, renal failure, and associated spreading of other toxins seen in Loxosceles envenomations.307 Venom from L. reclusa has a direct hemolytic effect on human erythrocytes; this process depends on the presence of serum components that include C-reactive protein and calcium.145,303 Platelet aggregation also is calcium dependent and is induced in vitro with sphingomyelinase D; this process may activate the prostaglandin cascade. Platelet aggregation appears to depend on serum amyloid protein, a serum glycoprotein of previously unknown significance.104,244,262 Lysis of erythrocytes has been shown to be induced by Loxosceles sphingomyelinases dependent on activation of complement by the alternative pathway, caused by induction of surface glycophorin cleavage. Cleavage of glycophorins, observed after incubation of erythrocytes and Loxosceles toxins, was a result of activation of an endogenous membrane–bound metalloproteinase.298,307 Because Loxosceles venom provokes an immune response in experimental animals, efforts to develop diagnostic tests are based on antigen or antibody detection in human blood. In 1973, Berger and associates28 reported an in vitro lymphocyte transformation assay for L. reclusa venom, which turned positive in the lymphocytes of exposed individuals within 4 to 6 weeks of initial exposure. This test may help to document prior exposure but not to diagnose envenomation at the time of the initial bite. Barrett and coworkers23 reported a passive hemagglutination inhibition test using rabbit antibody and human erythrocytes incubated in vitro with venom from L. reclusa. Cardoso and associates,50 observing that efforts to detect antigen in human serum may fail because of insufficient antigenemia, have demonstrated the presence of L. gaucho venom in biopsy homogenate using enzyme-linked immunosorbent assay (ELISA). Barbaro and colleagues21 demonstrated circulating IgG against L. gaucho venom detectable between 9 and 120 days after the bite in 4 of 20 patients. Some of the variability in clinical presentation among victims of Loxosceles envenomation may be caused by differences in the venom of males and females. Female L. intermedia spiders produce a greater amount of more potent venom than do males.69 Clinical Presentation.  Necrotic arachnidism, or loxoscelism in the case of bite by spiders of the genus Loxosceles, refers to the clinical syndrome that follows envenomation by a variety of spiders, for which L. reclusa, the brown recluse spider, is the prototype. The bites of these spiders often result in serious cutaneous injuries, with subsequent necrosis and tissue loss. Less often, severe systemic reactions may occur with hemolysis, coagulopathy, renal failure, and even death.144,321 Reports of severe reaction to spider bites possibly attributable to brown spiders date back to 1872, in a report of a 45-year-old Texan woman with a febrile illness accompanying a large necrotic lesion of her thigh.54 In 1896, death from renal failure accompanying another bite in Texas was reported.232 Spider bite was reported as a cause of blackwater fever (massive hemoglobinuria) in Tennessee in 1940.117 The first documented case of loxoscelism (from L. rufescens) was reported by Schmaus267 in Kansas in 1929. L. laeta was identified as the cause of similar lesions in South America in 1937, and L. reclusa was the cause of necrotic arachnidism in the midwestern Unite States by 1958.9,10 Since then, numerous cases of cutaneous and more severe reactions have been attributed to spiders of the genus Loxosceles. The clinical spectrum of loxoscelism ranges from mild and transient skin irritation to severe local necrosis accompanied by dramatic hematologic and renal injury. Isolated cutaneous lesions are the most common presentation, and most bites may resolve spontaneously without the need for medical intervention.27,28 Many clinicians distinguish between simple local presentation and more severe systemic, or viscerocutaneous, loxoscelism.

FIGURE 52-12  Brown recluse spider bite after 6 hours, with central hemorrhagic vesicle and gravitational spread of venom. (Courtesy Paul S. Auerbach, MD, and Riley Rees, MD.)

Local symptoms usually begin at the moment of the bite. A sharp stinging sensation is possible, although a victim may be unaware of having been bitten. Frequently, the bite site corresponds to a portal of entry or a region of constriction of clothing, such as cuff, collar, waistband, or groin area. The stinging usually subsides over 6 to 8 hours and is replaced by aching and pruritus as the lesion becomes ischemic from local vasospasm. The site then becomes edematous, with an erythematous halo surrounding an irregular violaceous center of “incipient necrosis” (actually hemorrhage and thrombosis).46,257,303 A white ring of vasospasm and ischemia may be discernible between the central lesion and the halo. Often, the erythematous margin spreads irregularly in a gravitationally influenced pattern that leaves the original center eccentrically placed near the top of the lesion (Figures 52-12 to 52-14). In more severe cases, serous or hemorrhagic bullae may arise at the center within 24 to 72 hours, and an eschar forms beneath. After 2 to 5 weeks, this eschar sloughs, leaving an ulcer of varying size and depth through skin and adipose tissue, but sparing muscle.138 Lesions involving adipose tissue may be extensive, perhaps from lipolytic action of the venom.159 The ulcer may persist for many months, leaving a deep scar.201,253,324 Local sequelae depend on the anatomic location. Persistent segmental cutaneous anesthesia has been attributed to nerve injury after a recluse bite on the side of the neck.127 Epiglottic and periepiglottic swelling severe enough to require endotracheal intubation has been reported in a recluse bite involving a child’s ear.137 The bite of the somewhat larger South American spider L. laeta is reported to cause intense pain and extensive edema, with proportionately less necrosis than that caused by L. reclusa. The edema is notoriously prominent with facial bites and resolves over 2 to 4 weeks.264

FIGURE 52-13  Brown recluse spider bite after 24 hours, with central ischemia and rapidly advancing cellulitis. (Courtesy Paul S. Auerbach, MD.)

Systemic involvement is less common but may occur in combination with cutaneous injury from any Loxosceles species; it occurs more frequently in children but may be seen in adults.233,300 Systemic reaction may develop in cases with minor-appearing local findings, making diagnosis difficult.303 When systemic involvement occurs, hemolytic anemia with hemoglobinuria is often the prominent feature, usually beginning within 24 hours of envenomation and resolving within 1 week.83 During this time, measured hemoglobin may drop markedly, accompanied by jaundice and hemoglobinuria. The anemia is usually Coombs’ test negative, but two cases of Coombs’ positive anemia have been reported.321 Fever, chills, maculopapular rash, weakness, leukocytosis, arthralgias, nausea, vomiting, thrombocytopenia, disseminated intravascular coagulation (DIC), hemoglobinuria, proteinuria, renal failure, and even death have been reported.32,111,210,321 McDade and co-workers190 reported on six adolescents treated for acute hemolytic anemia from presumed L. reclusa bites. The patients, all previously healthy, were treated for an acute systemic illness. Substantial anemia occurred in all six, with a median hemoglobin level of 7.1 g/dL. Direct antiglobulin test (DAT) was positive for surface complement component C3 in all, and surface immunoglobulin G (IgG) was detected in three patients. All patients developed reticulocytosis, hyperbilirubinemia, and local dermonecrosis. A case report by de Souza and associates74 illustrates critical complications of Loxosceles envenomation resulting in skin necrosis, rhabdomyolysis, hemolysis, coagulopathy, acute kidney injury, and electrolyte disorders. A 26-year-old man in Brazil was bitten on his trunk while getting dressed. Twenty hours later, he sought treatment at a hospital and was given anti-Loxosceles antivenom and supportive care. The spider was brought with the patient and was positively identified as Loxosceles. Over several hours, the man became critically ill with abdominal pain, headache, nausea and vomiting, oliguria, and respiratory distress. Forty eight hours after the bite, he was transferred to an intensive care unit in a specialty hospital. He had generalized exanthem, jaundice, and conjunctival hyperemia. The bite site was edematous, with vesicles and ecchymosis. Renal function deteriorated, and he was begun on hemodialysis on day 2, and progressed to develop hemolysis with Hgb of 4.7 g/dL on day 7. On day 30, hemoglobin levels stabilized in the absence of transfusions, and the lesion had evolved to eschar with areas of necrosis. Hemodialysis was discontinued on day 35 when creatinine levels began to normalize. He was discharged, and follow-up on day 61 indicated a normal creatinine level. The diagnosis of loxoscelism is based on spider observation and identification, typical history, and local and systemic signs. The differential diagnosis of the local injury includes bacterial and mycobacterial infection, herpes simplex, decubitus ulcer, burn, embolism, thrombosis, direct trauma, vasculitis, Lyme disease, and pyoderma gangrenosum.5,162,235,238,290 There is no universally accepted or available laboratory test to aid in diagnosis of Loxosceles envenomation. However, in one case, a venom-specific enzyme immunoassay was used to determine the cause of a suspicious skin lesion in a 57-year-old man. The assay was performed on both a lesional punch skin biopsy and a hair plucked from the lesion. In both samples, the presence of Loxosceles venom was detected, indicating that use of a hair from the lesion negated the need for a punch skin biopsy. 987

CHAPTER 52  Spider Bites

FIGURE 52-14  Brown recluse spider bite after 48 hours, with incipient central necrosis.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A series of five proved or suspected L. reclusa bites to women in the second and third trimesters of pregnancy has been reported. Despite significant local injuries, rash, and microhematuria, no fetal injury was noted.4 Treatment.  Treatment of loxoscelism depends on its severity. Cutaneous loxoscelism can usually be managed on an outpatient basis. Most mild cutaneous envenomations respond to application of local cold compresses,164 elevation of the affected extremity, and loose immobilization of the part. Tetanus prophylaxis should be provided where indicated. Necrotic lesions may need debridement after erythema has subsided to define the margins of the central eschar. This usually involves significant debridement 1 or 2 weeks after the bite, with close follow-up for several weeks. In severe cases, this can be followed with skin grafting or plastic surgery when the wound is stable. Severe necrotic or infected lesions may lead to hospitalization. Although many therapies have been used for Loxosceles envenomation, including dapsone, glucocorticoids, hyperbaric oxygen (HBO), electric shock, antivenom, metronidazole, diphenhydramine, phentolamine, and cyproheptadine, efficacy has not been established and clinical trials have not been done. Initial studies in small mammals have been inconclusive.85,296 Monteiro and colleagues203 found the anaerobic bacterium Clostridium perfringens in Loxosceles venom and fangs and suggested that it might be inoculated with the venom. In rabbits, the combination of venom and C. perfringens increased dermonecrotic damage. The authors suggested antibiotic therapy when treating loxoscelism in association with C. perfringens. Catalan and colleagues53 isolated and characterized several species of Clostridium, including multiply drug-resistant C. perfringens, from the fangs and venom glands of L. laeta. Some have advocated the use of dapsone for prevention of lesion progression in potentially necrotic wounds seen within 48 to 72 hours of a bite.101,106 Dapsone is a leukocyte inhibitor that in theory can minimize the local inflammatory component of cutaneous loxoscelism, thereby preventing or lessening subsequent skin necrosis. In 1983, King and Rees163 reported use of dapsone for envenomation in a human bitten by L. reclusa, based on a successful trial of dapsone pretreatment in guinea pigs injected with recluse venom. Since that time, no prospective, controlled human trial has proved dapsone efficacy, but a variety of case reports and series have supported its use in the treatment of potentially necrotic wounds treated in the first days after envenomation.3,25,137,187,325 Typical dosage recommendations are for 50 to 100 mg orally, twice daily. Risks of dapsone therapy include hypersensitivity,332 methemoglobinemia, and hemolysis in the presence of glucose-6-phosphate dehydrogenase (G6PD) deficiency. Because of these risks and the uncertain benefits, recent opinion has trended away from use of dapsone.316 Patients with systemic symptoms should be considered for admission when they have evidence of coagulopathy, hemolysis and hemoglobinuria, or rapid progression of other systemic signs. Care is mainly supportive, usually involving wound care, fluid management, presumptive treatment for bacterial superinfection, and, occasionally, blood transfusion. Rarely, hemodialysis has been required for oliguric renal failure.115 Discharge is appropriate when renal and hematologic status are stable. For patients with significant local or systemic signs or symptoms, laboratory evaluation should include peripheral blood cell count, basic coagulation screening, and urinalysis. Liver and renal function tests are indicated in severe poisonings. When use of dapsone is considered, a screening test for G6PD deficiency may be indicated. Frequency of follow-up testing depends on the course and severity of envenomation. Hospitalized patients may need close follow-up for several days of anemia and possibly altered renal function. Corticosteroids have been injected either at the wound site or systemically, but this remains of questionable benefit.26,240 Antihistamines may help control itching but do not change the lesion. Some clinicians advocate early surgical excision of the wound site,8,16,92,140 but others have demonstrated that outcomes are better with early medical management in human patients,73,242 as well as in experimental animals.240 HBO treatment has been tried empirically in uncontrolled human trials, with reports of good 988

outcome.295 Comparison of HBO with no treatment in rabbits showed enhanced recovery at 24 days at the histologic level, but with no apparent clinical difference between the two groups.279 Wong and co-workers335 studied negative-pressure wound therapy (vacuum-assisted closure [VAC]) in pigs. The size of the VAC-treated wounds on day 3 was significantly smaller when compared to control wounds. Loxosceles-specific antivenom has been tried in both North and South America. In the early 1980s, Rees and colleagues240 reported a protective effect of treatment with antivenom in rabbits before or up to 12 hours after envenomation. Small-vessel occlusion, leukocyte infiltration, and necrosis occurred but were diminished in antivenom recipients. Pretreatment in a separate study abolished symptoms of systemic loxoscelism.239 In one study, 17 patients were separated randomly into dapsone, antivenom, and combination therapy groups; all patients received erythromycin. Individual results suggested that the antivenom was efficacious when given early, but the overall trial was inconclusive, indicating the need for further study.243 Gomez and colleagues113 have studied intradermal use of anti-Loxosceles Fab-fragments in a rabbit model, suggesting therapeutic efficacy when the antivenom is injected up to 4 hours following envenomation. An F(ab′)2 antivenom for Loxosceles bites has been approved for use in Mexico, where anecdotal reports of improved outcomes suggest possible efficacy, but controlled trials have not been conducted (personal communication, A. Alagón). Currently, no Loxosceles antivenom is commercially available in the United States. In South America, an antivenom to L. laeta was developed in 1954 by Vellard using immune serum of the donkey. Furlanetto developed L. laeta antivenom using immune serum of horses.204 Reports of the efficacy of systemically administered L. laeta antivenom are mixed.264 Venom similarities throughout the genus suggest the potential for development of a globally effective antivenom treatment of Loxosceles bites.22 An ELISA assay, developed for detection of circulating venom antigen, has the potential to develop into a diagnostic tool for clinicians and epidemiologists.59 Genus Sicarius: Six-Eyed Crab Spiders Biology.  About 25 Sicarius species are known. Their range is limited to dry regions of South America and South Africa. Individuals live under stones or are sand dwellers. Some hide under sand and emerge to capture passing insects. Their bodies are flattened and their legs are laterigrade, meaning the tips point anteriorly as in a crab. Adult body size ranges from 12 to 22 mm (0.5 to 0.9 inch) (Figure 52-15). Venom.  The venom of the South African six-eyed sand spider Sicarius testaceus in a rabbit model demonstrated tissue necrosis and increased vascular permeability in the vicinity of the envenomation, as well as a dramatic decrease in platelet count. It is

FIGURE 52-15  Sicarius albospinosus male from Namibia. (Courtesy Melissa Callahan.)

Clinical Presentation.  Sicarius species are occasionally implicated in human bites in South Africa. They tend to bite only when provoked and are rarely implicated in human poisonings, despite fairly high toxicity of the venom in laboratory animals. Envenomation reportedly can cause edema, erythema, and necrosis and is occasionally associated with DIC.215-217

FAMILY GNAPHOSIDAE: GROUND SPIDERS AND MOUSE SPIDERS Gnaphosids are common and found worldwide, with the highest densities in temperate areas. They are small to medium sized (2 to 14 mm) and usually dark in color (black, gray, or reddish brown). They have long, slightly flattened abdomens, and two of their spinnerets are conspicuous and cylindric. Gnaphosids are nocturnal hunters, mostly on the ground, and during the day retreat under rocks and stones or other tight quarters. Herpyllus ecclesiasticus, the parson spider, is distributed widely throughout the United States under rocks and rubbish and in houses. One case report of a bite by H. ecclesiasticus described pruritus, arthralgia, malaise, and nausea beginning 1 hour after the bite. There was no necrosis.191,233

Treatment.  Treatment of Sicarius envenomation is symptomatic and supportive.

Treatment.  Treatment of bites is symptomatic and supportive.

FAMILY DESIDAE: LONG-JAWED INTERTIDAL SPIDERS

FAMILY LAMPONIDAE: WHITE-TAILED SPIDERS

About 200 species of Desidae are distributed worldwide. Their chelicerae often extend forward and have humps close to the prosomal attachment. Species range in body length from 4.5 to 12 mm (0.2 to 0.5 inch). Most spiders in this family build small, irregular webs under rocks or logs. Some desids are closely associated with marine habitats and live in the intertidal zone. These spiders feed on marine animals and at high tide retreat into empty snail shells and worm tubes and seal off the entrance with silk. Others are found only on the water surface. Genus Badumna: Black House Spider Biology.  Badumna insignis (Ixeuticus robustus), or the black house spider, is a common Australian spider associated with a few human bite reports. This species is a nocturnal forager that builds tangled webs with silk retreats in and around human habitations.328 Venom.  Venom gland extract from B. insignis is reported to cause increased vascular permeability, as well as dose-dependent decreases in arterial pressure in rats, apparently from the presence of a serotonin-like substance in the venom.155 Venom gland extract does not cause necrosis in cultured human or mouse skin.14 Venom of B. insignis has been found to contain fibrinogenolytic and gelatinolytic proteases. Sphingomyelinase activity has not been found in the venom of B. insignis, but has been identified in its abdominal contents.286 Clinical Presentation.  In one report, B. insignis caused local pain, itching, and swelling followed by regional lymph node tenderness and discoloration of the area around the bite. Over 2 weeks, the lesion resolved, with some tissue necrosis and sloughing centrally.188 In two series of B. insignis bites, local lesions were painful but transient and unaccompanied by necrosis.152,329 Systemic symptoms have rarely been reported, and include nausea, vomiting, abdominal pain, pruritus, and painful knees.328 Treatment.  Treatment of Badumna envenomation is symptomatic and supportive.

FAMILY ZODARIIDAE: HUNTING SPIDERS 153

Zodariids are a diverse group of hunting spiders. The estimated 350 species have worldwide distribution, but are primarily found in the tropics and subtropics. They are medium sized (3 to 15 mm), with the anterior spinnerets usually longer than the posterior structures. They hide under stones or burrow in pebbles or sand. Very few reports of documented human envenomation exist, although Supunna picta, a common leaf litter–dwelling spider of Australia, reportedly caused a transient erythematous rash and slight itch in a woman bitten at home. The lesion resolved uneventfully.39

Until recently, the genus Lampona was placed in the family Gnaphosidae. The group was changed to family status because members do not share many of the characteristics that define Gnaphosidae.228 Specialists believe that many undescribed genera in Australia belong to this group. Genus Lampona Biology.  Lampona cylindrata is a hunting spider with a distinctive cylindric shape and white spot at the tip of the abdomen. They are often found indoors in Australia and New Zealand.328 Individuals are wandering foragers that enter webs of other spiders and prey on them. Venom.  The venom of L. cylindrata appears to increase vascular permeability in rats, perhaps from the release of endogenous bradykinin and prostaglandins.166 Venom contains histamine and noradrenaline, both more highly concentrated in venom of male spiders.235 Venom of L. cylindrata contains fibrinogenolytic and gelatinolytic proteases. Sphingomyelinase activity has been identified in the abdominal contents, but not the venom, of L. cylindrata. This finding is similar to that for Badumna insignis.286 Clinical Presentation.  In a series of 130 Lampona bites, predominantly of L. cylindrata and L. murina, pain or discomfort occurred in all and was severe in 27%. Puncture marks were present in 17%, and redness or red mark in 83% of bites. Systemic effects occurred in 9% of bites. Necrosis was not reported. There were three distinct clinical patterns: pain only (21%), pain and red mark for less than 24 hours (36%), and persistent painful or red lesion (44%).150 Gray121 reported a case of more significant illness, with nausea, lethargy, and a small zone of necrosis after a known white-tailed spider bite. Although the vast majority of cases are relatively benign, significant skin necrosis occasionally may result from envenomation.328 Treatment.  Treatment of Lampona envenomation is symptomatic and supportive.

FAMILY: SPARASSIDAE CRAB SPIDERS AND HUNTING SPIDERS Biology Sparassids, or “giant crab spiders,” are distributed worldwide and are mostly tropical. They are large (10 to 40 mm [0.4 to 1.6 inches]) and resemble crabs, with the tips of all legs angling forward. They have flattened bodies and are capable of moving sideways. They have eight eyes in two straight rows. They are wandering hunters and typically nocturnal. In many places, they are welcome cohabitants with humans because they eat cockroaches. Palystes natalius, the lizard-eating spider, is one of the largest true spiders in South Africa. It has a brownish gray body with 989

CHAPTER 52  Spider Bites

not clear whether this pattern is the same in humans.306 South African Sicarius venoms have sphingomyelinase D activity, as discussed for Loxosceles venoms.35,36 The origin of this toxic enzyme in spider venoms is likely to have occurred in the most recent common ancestor of these two genera. South American Sicarius venoms have lost or reduced sphingomyelinase D activity.35 There are no records of clinically significant bites from South American Sicarius species.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

bright yellow and black striped legs. The female is larger than the male, with body length up to 4 cm (1.6 inches). Venom.  Venom from the Australian heteropodid Isopeda montana has direct β-adrenoreceptor action, and Delena cancerides, the social huntsman spider, appears to have both α- and β-adrenoreceptor activity, although neither of these has been involved in recognized human envenomation. Both have been shown to increase vascular permeability in rats.139 In a series of 173 spider bites, with 168 confirmed to be sparassid spiders, 95% percent of the bites were from four genera: Isopeda (32%), Isopedelia (21%), Neosparassus (27%), and Heteropoda (14%); other genera included Delena and Holconia. The majority (95%) of bites were on limbs, with 82% occurring distally. Pain or discomfort was present in all cases, and severe in 27%. The median duration of pain was reported as 5 minutes, significantly less than with other spiders. Puncture marks (40%) or localized initial bleeding (35%) occurred in 54% of bites. Redness or a red mark occurred in 57%, swelling in 16%, and itching in 44% of bites. Systemic effects occurred in 4% and consisted of nausea and/or headache. There were no cases of necrotic ulcers or allergic reactions.153 Clinical Presentation.  Only localized burning accompanied by slight swelling was noted after a female P. natalius bite to the left wrist.213,219 An Olios calligaster bite was followed by mild local symptoms, transient nausea, and faintness. Six bites by Isopeda species, predominantly I. pessleri, resulted in minimal local symptoms only.329 One case of acute conjunctival inflammation, secondary to material from a squashed I. villosa being accidentally rubbed in to the affected eye, has been reported. This type of injury is more commonly associated with small spiders, mainly Pholcidae (“daddy longlegs”).151 Treatment.  Treatment of heteropodid bites is symptomatic and supportive. In the case of the conjunctival inflammation, treatment consisted of a topical anesthetic followed by a normal saline flush for 1 hour. Redness and swelling began to resolve approximately 2 hours after injury. The patient experienced ongoing pain and mild photophobia and was discharged home with topical chloramphenicol ointment and an eye patch for 24 hours. Twentyeight hours after the injury, symptoms had resolved.151

FAMILY OXYOPIDAE: LYNX SPIDERS Lynx spiders are found worldwide, with the greatest abundance in the tropics. They are small to medium sized (4 to 18 mm [0.2 to 0.7 inch]) and have a distinctive eye pattern, with six eyes in a hexagon and two smaller eyes below. Their abdomens are pointed posteriorly. They have long leg spines (macrosetae) that help detect motion through vibrations in the air. They are diurnal hunters with good vision and actively search for prey. Most are found on vegetation, and some are arboreal. Genus Peucetia Biology.  Peucetia viridans, the green lynx spider of the United States and Mexico, is a diurnal hunting spider. P. viridans is translucent green, with red eyes and joints130 (Figure 52-16). This species is common in the desert Southwest of the United States and adult individuals are large (approximately 20 mm [0.8 inch]) and conspicuous. Venom.  Whole venom of P. viridans causes total and reversible block of non-N-methyl-D-aspartate receptor-mediated transmission in the chick central nervous system.155 Clinical Presentation.  A series of four cases in which the spider was identified as P. viridans showed immediate pain, burning sensation, pruritus, erythema, and induration resolving in a couple of days. Necrosis and systemic signs have not been reported.44 Treatment.  Treatment of Peucetia bites is symptomatic and supportive. 990

FIGURE 52-16  Green lynx spider (Peucetia viridans). (Courtesy Gita Bodner.)

FAMILY SALTICIDAE: JUMPING SPIDERS Salticidae is the largest family of spiders, with more than 5000 currently described species and many more yet to be described. They are distributed worldwide, with the highest densities in the tropics. Some have called them the “butterflies of the spider world” because most are brightly colored and some have iridescent scales. Some species mimic ants, beetles, pseudoscorpions, and bird droppings. Jumping spiders have excellent eyesight, with large, postero-median eyes. They visually search for prey, then stalk and ambush with catlike movements. Males are often more brightly colored than are females and perform elaborate courtship dances. They are always active during the day and are small, most less than 15 mm (0.6 inch). Bites from spiders of the genus Phidippus, such as the jumping spider Phidippus audax of the United States, can cause pain, erythema, pruritus, and sometimes minor ulceration. The swelling usually subsides within 2 days.252 In Australia, local pain has been reported with the bite of spiders from genera Mopsus, Breda, Opisthoncus, and Holoplatys. One patient bitten by a Holoplatys reported headache and vomiting.328

FAMILY CTENIDAE: WANDERING SPIDERS Ctenidae are abundant and conspicuous worldwide and mostly found in subtropical and tropical areas. They can be large spiders ranging from 4 to 40 mm [0.2 to 1.6 inches]. They nocturnally hunt on the ground or on vegetation. They resemble and are closely related to wolf spiders but are distinguished by their eye arrangement (three rows: two eyes, then four, then two, the last two being the largest). They sometimes travel as stowaways on bananas. Genus Phoneutria: Banana Spiders (Armed Spiders) Biology.  The Phoneutria spiders of South America are large, nocturnal creatures notorious for their aggressive behavior and painful bite. The best-known representative of the genus is P. nigriventer. It is known in Brazil as aranha armadeira, meaning “spider that assumes an armed display,” because of its characteristic defensive-aggressive display.262 P. nigriventer is the largest, most aggressive true spider found in South America, with an average body length of 35 mm (1.4 inches), leg length of 45 to 60 mm (1.8 to 2.4 inches), and fangs 4 to 5 mm (0.16 to 0.19 inch) in length for females. Males are slightly smaller.261 The body is gray to brown gray with white marks forming a longitudinal band on the dorsal abdomen. A distinguishing characteristic is the red-brown brush of hairs around the chelicerae. P. nigriventer is mainly found in southern Brazil, Argentina, and Uruguay. Other species have been found in Bolivia and Colombia. The spiders do not construct a web, because they are nocturnal hunters, often traveling several hundred meters in search of prey. They may enter houses during this time, hiding in clothes in the light of day. According to Bucherl,41 600 to 800 spider bites occur each year around the city of São Paulo alone.

Clinical Presentation.  P. nigriventer venom acts on both the peripheral and central nervous systems.129 Although the majority of cases are clinically insignificant,186 humans bitten by P. nigriventer may develop severe local pain that radiates up the extremity into the trunk, followed within 10 to 20 minutes by tachycardia, hypertension, hypothermia, profuse diaphoresis, salivation, vertigo, visual disturbances, nausea and vomiting, priapism, and occasionally death in 2 to 6 hours. Respiratory paralysis is generally the cause of death. Severe envenomation is more common among young children. Fatalities may occur in the debilitated or the young, but most people recover in 24 to 48 hours. Workers who handle bananas are frequently bitten because the spider hides in bunches of bananas. Bites have been reported in Switzerland and Argentina in produce workers inadvertently encountering these traveling spiders.129,261,262 Treatment.  In most cases, symptomatic care is all that is necessary. Local pain control may be achieved by infiltration of local anesthetic near the bite site; this reportedly suffices for 95% of cases treated at the Hospital Vital Brasil.186 For more severe cases, a polyvalent antivenom (Sero Anti­ aracidico Polivalente) and a monovalent antivenom (Belo Horizonte) active against Phoneutria species have been available in Brazil. Skin testing and antihistamine prophylaxis are recommended before their use. One to five ampules of antivenom are injected intramuscularly and/or intravenously, and clinical response is judged by the relief of pain or resolution of priapism. Opiates may potentiate the venom’s effects on respiration and are generally not recommended in cases of systemic envenomation.129,261,262 An ELISA has been developed, using anti–P. nigriventer antibodies, for rapid detection of venom antigens in suspected P. nigriventer envenomation. It has been tested in humans and shows promise as a diagnostic agent.60

FAMILY LYCOSIDAE: WOLF SPIDERS Lycosidae are among the most common spiders. They are diverse, with more than 3000 species distributed worldwide. They are found from beaches to grassy fields and pastures. The Greek name lycosa (wolf) comes from the former belief that they hunted in packs.66,334 They range in size from 3 to 25 mm (0.12 to 1 inch). Most species wander in active pursuit of prey, generally during the day. A few make deep burrows, and some even cover their burrows with doors. Most live on the ground, but some climb in vegetation. They have good vision, with

CHAPTER 52  Spider Bites

Venom.  Phoneutria venom is a complex mixture of histamine, serotonin, glutamic acid, aspartic acid, lysine, hyaluronidase, and other polypeptides. Histamine, serotonin, and incompletely characterized kallikrein-kinin activating fractions contribute to local tissue swelling from the increased vascular permeability that may occur with envenomation.6,194 In addition, the venom contains at least six neurotoxic polypeptides, with molecular weights between 3500 and 8500.68 The neurotoxic components include sodium channel poisons that appear to potentiate action potentials along axons, provoking erratic or rapid uncontrolled muscle twitches in invertebrates86 as well as in vertebrates.7,185 Microscopically, there is acute transient swelling of axons, particularly at the nodes of Ranvier, in a pattern similar to that caused by the venoms of scorpions Centruroides sculpturatus and Leiurus quinquestriatus. The axons recover within a few hours of exposure, but return of nodal width to normal takes several days.185 Effects of the venom have been studied in mice, rats, guinea pigs, rabbits, pigeons, and dogs. The venom has little or no effect on frogs and snakes, and it has four times greater toxicity in dogs than in mice. Rats and rabbits are very resistant to the venom’s effects, but rabbit vascular smooth muscle contractions appear to be stimulated by a venom protein that acts independently of voltage-dependent sodium and calcium channels.195 Dogs developed intense pain, manifested by yelping, followed by sneezing, lacrimation, mydriasis, hypersalivation, erection, ejaculation, and death after venom was injected subcutaneously.262 This is well within the dose that a single spider may inject.

FIGURE 52-17  Wolf spider (Lycosa species). (Courtesy Arizona Poison and Drug Information Center, 1996.)

conspicuously large, postero-median eyes. Their eyes are arranged in three rows (four eyes, then two, then two). To attract mates, males wave their legs and sometimes stridulate to make sound. The female carries the egg sac attached to her spinnerets. When the young hatch, they climb on their mother’s abdomen for transport. They have three claws on their tarsi. Genus Lycosa: Wolf Spiders Biology.  Lycosa is a large and widespread genus of wolf spiders (Figure 52-17). It includes various middle-sized to large spiders with mildly cytotoxic venom capable of provoking transient inflammation in humans. The most famous wolf spider species is Lycosa tarentula, to which “tarantula” was first applied. Its bite was once believed to cause “tarantism,” a syndrome of stupor, the desire to dance, and sometimes death, but this historic syndrome is now attributed to Latrodectus tridecimguttatus (neither a wolf spider nor a tarantula), and the wolf spider bite is now known to cause little more than stinging pain. The South American Lycosa raptoria has been reputed to be more dangerous than other wolf spiders, provoking necrosis at the site of envenomation. It now appears that this was also based on a misunderstanding. Necrotic arachnidism in South America is now attributed mainly to Loxosceles species. Venom.  Lycosid venom is thought to be primarily cytotoxic, without hemolytic or anticoagulant activity.334 Although scientific reports of necrosis are lacking after envenomation by the Australian wolf spider L. godeffroyi, media reports suggest that bites may lead to necrosis. Atkinson and Wright13 have demonstrated that the raw venom of L. godeffroyi causes a strong inflammatory response and cutaneous necrosis when injected into mice. They further hypothesized that this action may result from contamination of the venom with digestive juices, in that electrically collected raw venom caused necrosis, whereas venom gland extract did not.14 Clinical Presentation.  A series of 515 cases of confirmed Lycosa bites in Brazil showed that most occur between the hours of 6 AM and 6 PM, at a fairly consistent rate year-round. The most common bite sites were the feet (40%) and hands (39%). The most common signs and symptoms were all local, with pain in 83%, swelling in 19%, and erythema in 14%. No local necrosis was described.245 In a series of 45 Lycosidae bites in Australia, 73% were distal (hand or foot). Pain occurred in all bites and was reported as severe in all cases. Puncture marks or localized initial bleeding occurred in 33%, swelling in 20%, redness or a red mark in 67%, and itching in 13%. Three patients reported systemic effects, two with nausea, one with headache, and one with malaise. Necrosis or ulceration was absent in all cases.147 In the United States, five cases of Lycosidae bites have been documented. One resulted in skin necrosis at the bite site, probably from the combined results of envenomation and infection.49 991

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Treatment.  Although South American antivenom active against Lycosa venom was available in the past, it was used in only one case of 515 reviewed by Ribeiro and associates.245 Since 1985, the polyvalent Butantan Institute spider antivenom has not included the antilycosid fraction.186 Most Lycosa cases can be managed with tetanus immunization and ice or oral analgesics; occasionally, local anesthetic block has been used for pain management.245

FAMILY MITURGIDAE: SAC SPIDERS AND TWO-CLAWED HUNTING SPIDERS Clubionids are common and distributed worldwide, with the highest diversity of species in the neotropics. They are small to medium sized (2 to 15 mm [0.1 to 0.6 inch]) and are usually light brown to yellowish in color. They hunt nocturnally and make resting tubes in rolled leaves or under rocks or stones, where they retreat during the day. Genus Cheiracanthium: Running Spiders and Sac Spiders Biology.  The genus Cheiracanthium as a whole has no distinctive marks or patterns.117,334 Members may be pale yellow, brown, green, or olive. The dorsal abdomen may have a median longitudinal stripe. Body size ranges from 7 to 15 mm (0.3 to 0.6 inch), with a total diameter of 3 cm (1.2 inches), including long, slender legs. In the United States, Cheiracanthium inclusum (Figure 52-18) is the only indigenous species although several species have been introduced. C. diversum is widely found in the Pacific islands. It was transported into Hawaii from Australia approximately 50 years ago. C. mildei was introduced from Europe and is now found from New England to Alabama to Utah. It is a common biting spider in Boston; it is most abundant in autumn, when most bites occur.277 The South African sac spider C. lawrencei is a common nocturnal house spider that forages at night and may become trapped in bedding.215 During the day, these spiders hide in the concavities of leaves, curtains, or windowsills, encased in a silk sac. They are fast moving and aggressive when threatened.217 Venom.  Research on Cheiracanthium venom is limited. About 75% of guinea pigs bitten by C. mildei for the first time developed a wheal within 5 minutes, with 60% developing an eschar within 1 day.277 Fractionation of dissected venom gland extracts from C. japonicum resulted in five fractions with lethal activity in mice. These were considered neurotoxic based on symptoms of dyspnea, flaccid paralysis, and death after intraperitoneal injection.222 Clinical Presentation.  Spiders belonging to the genus Cheiracanthium have had a documented history of human envenomation since the 18th century. Species are known for their tenacious, painful bite. A pruritic, erythematous wheal appears within 30 minutes. Nausea, abdominal cramps, headache, and local necrosis have been reported.

FIGURE 52-18  Cheiracanthium inclusum. (Courtesy Sherman Minton, MD.)

992

In 1901, Kobert described local swelling, erythema, pain, and fever after the author’s third C. punctorium envenomation.29 Maretic197,198 described local redness, pain, and edema but no necrosis after C. punctorium envenomation. In another case, C. inclusum caused local pain that radiated from the forearm bite site up the arm, associated with nausea. No other signs developed.29 The Australian species C. mordax and C. longimanus caused local swelling, erythema, and pain associated with malaise, headache, dizziness, and nausea. Symptoms receded within 36 hours after treatment with antihistamines and local anesthetics.29 Ori222 found similar signs and symptoms after envenomation by C. japonicum. In South Africa, most C. lawrencei bites occur at night during sleep.213 Paired bite marks 6 mm (0.24 inch) apart are evident within the first few hours. Local edema and erythema may be slight. By the third day the marks may become necrotic, with more edema, erythema, and pain; headache and fever may accompany this stage. The small ulcer begins to heal 7 to 10 days after the bite.215 Treatment.  The lesion usually heals without problems, provided that secondary infections are avoided. Treatment is supportive, consisting of cool compresses, elevation, immobilization, analgesics, and tetanus prophylaxis.

FAMILY CORINNIDAE: SAC SPIDERS Corinnids are ground-dwelling spiders primarily found in tropical regions. They were previously placed in the family Clubionidae and have similar habits. Spiders of the Trachelas genus are often encountered in houses in late summer and fall. Trachelas volutus and several other Trachelas species reportedly cause mild local reactions without necrosis. Bites are painful initially and may swell. No systemic effects have been reported.224,304 Treatment is symptomatic and supportive.

FAMILY AGELENIDAE: HOBO, GRASS, AND FUNNEL-WEB SPIDERS The 600 species of Agelenidae are mainly found in temperate regions of the Northern Hemisphere. They are medium-sized spiders, ranging from 8 to 15 mm (0.3 to 0.6 inch) in body length. Individuals build sheet webs that lead to a long funnel, which the spider uses as a retreat. When prey contacts the web, the spider runs out, bites it, and carries it back into the funnel. The large and conspicuous webs of these spiders often are long lasting, with spiders adding silk to make the sheet larger as the individual grows. Males may be found searching for females. Genus Tegenaria: Hobo Spiders Biology.  Tegenaria agrestis is commonly called the hobo spider or Northwestern brown spider. It is a 10- to 15-mm (0.4- to 0.6inch), light-brown spider with a yellowish green tint and chevrons on the dorsal abdomen. Individuals typically build funnel webs in undisturbed habitats such as abandoned woodlots or along railroad tracks, with a hidden retreat beneath wood, rocks, or debris and small amounts of silk extending beyond the cover. Spiders mature to adulthood in midsummer and mate and lay eggs in July through September. Adult males live for 1 year, then senesce and die at the end of the mating season. Adult females live for 2 years, so adults are present throughout the year. T. agrestis spiders are common and widespread natives of Europe and western central Asia.131 This species was probably introduced to North America in a seaport near Seattle in the early 1900s and was first formally identified in the 1930s.90,91 It has since expanded its range to British Columbia, Alaska, Oregon, Idaho, Montana, and Utah.18,246,325 By the 1960s, individuals were often collected in and around human habitations in the Pacific Northwest. Venom.  The venom of T. agrestis has become of interest in the past 15 years because of reports suggesting that their bites result in necrotic lesions. T. agrestis venom chemistry is not well characterized, and no necrotoxic component has been identified.

Clinical Presentation.  T. agrestis has been implicated in several cases of necrotic arachnidism similar to that seen in Loxosceles envenomation. Systemic effects reported include headache, visual disturbances, hallucinations, weakness, and lethargy. Hemorrhagic complications have been reported in experimental animals. In general, direct observations are scarce of T. agrestis biting people, who then develop necrotic lesions.2 According to Vest,310,314 who studied 22 cases of “highly probable” T. agrestis envenomation, the local lesion followed a pattern reminiscent of loxoscelism. The initial lesion appeared as a small reddened induration, often surrounded by a large zone of erythema. Vesicles occurred within 36 hours, then burst; marked necrosis developed in 50% of cases. The most common symptoms included headache, weakness, and lethargy.312 If a spider has not been identified in association with a lesion, attribution of necrosis to T. agrestis bites is discouraged.317 Treatment.  No studies have investigated treatment for envenomation by Tegenaria species. As with mild cases of loxoscelism, patients should be treated supportively, with tetanus prophylaxis, careful wound debridement as needed, and observation.317 Genus Agelenopsis: Grass Spiders and Funnel-Web Spiders Biology.  Agelenopsis aperta is common in and restricted to the deserts of the southwestern United States, ranging from California to East Texas (Figure 52-19). They build large, conspicuous sheet webs, with retreats under rocks and logs or in tufts of grass. Adults are 13 mm (0.5 inch) in body length. Venom.  The venom of this species is among the best known of all spiders in terms of biochemical composition and neurophysiologic activity of the individual components. Its clinical relevance in humans, however, has only recently been recognized.

FIGURE 52-19  Agelenopsis aperta. (Courtesy Eileen Hebets.)

Nineteen toxins have been characterized in A. aperta venom, with three distinct classes that act synergistically to subdue insect prey rapidly and irreversibly.221 The µ-agatoxins modify sodium channel kinetics, increasing neurotransmitter release generally; the ω-agatoxins block presynaptic, voltage-sensitive calcium channels; and the α-agatoxins are a family of low-molecularweight acylpolyamines that block glutamate-sensitive receptor channels in insect muscle. The coexistence of toxins with different mechanisms of neurotoxicity appears to confer a synergistic action to the overall venom effect in insect prey. The ω-agatoxins range in target specificity from invertebrates to mammals.309 Clinical Presentation.  Two cases of envenomation by A. aperta have been reported in southern California. A 9-year-old boy developed a tender but nonnecrotic bite site, followed by a 2-day systemic syndrome that included headache, nausea, disorientation, pallor, and unsteady gait. A 54-year-old man developed a painful, indurated lesion that persisted for a week; he had no systemic symptoms.315 Treatment.  Treatment of Agelenopsis envenomation is symptomatic and supportive.

FAMILY THERIDIIDAE: COMB-FOOTED SPIDERS The family Theridiidae, sometimes called cobweb or combfooted spiders, is speciose, diverse, and distributed worldwide. The spiders are small to medium sized (1 to 14 mm [0.04 to 0.55 inch], usually less than 8 mm [0.3 inches]) and often have globose abdomens. They make irregular, tangly webs in which the spider hangs upside down. The silk is very sticky, easily entangling prey. Spiders throw silk over ensnared prey using a tiny comb at the end of the fourth leg. They then envenom prey and suck them dry through a small hole in the exoskeleton, because they have no cheliceral teeth for chewing. Genus Latrodectus: Widow Spiders Biology.  Latrodectus (Latin for “robber-biter”) species are among the largest theridiids. Females are 12 to 16 mm (0.47 to 0.63 inch) in body length. Males are much smaller, with longer legs relative to their body size. Individuals build typical theridiid cobwebs with very strong strands of silk. Arthropods are the most common prey, but widows also kill and consume vertebrates (e.g., small lizards and snakes). The folkloric belief that widow females kill and consume their mates is accurate, although this event does not as a rule occur. The 8- to 10-mm (0.31- to 0.39-inch) female black widow is shiny black with a characteristic red hourglass marking on the ventral abdomen. Species are distinguished based on hourglass shape and dorsal color patterns. Males are lighter in color, with white and gray markings and a faint hourglass. This feature becomes more prominent with maturity. The female spins an irregular web in sheltered corners of fields, gardens, and vineyards and under stones, logs, and vegetation. Uncommon in occupied dwellings, the spiders may be plentiful in barns, garages, trash heaps, and outbuildings. A few Latrodectus species (e.g., L. variolus) are arboreal. The web’s tattered “cobweb” appearance may belie an ongoing state of occupation, particularly during the daytime, when the spider is out of sight. The female seldom ventures far from the web, in which she suspends an ovoid or tear-shaped, whitish egg case. Latrodectus spiders are worldwide in distribution, most plentiful in temperate and subtropical regions, and most abundant during summer.31 L. mactans mactans, the black widow, is cosmopolitan and occurs in every state except Alaska (Figure 52-20). In North America, species include L. geometricus (the brown widow, Figure 52-21), L. bishopi (the red-legged widow), L. variolus, and L. hesperus (Figure 52-22). Species known to envenom humans are endemic to Australia (L. mactans hasselti, Figure 52-23) and to Europe and South America (L. tredecimguttatus). Related species are found in Asia and the Middle East (L. pallidus) and in Africa (L. indistinctus). The species L. tredecimguttatus is most important in the Mediterranean region, the Middle East, and parts of Russia, where it is 993

CHAPTER 52  Spider Bites

Johnson and colleagues158 identified potent insect-specific neurotoxic peptides and mammalian-specific peptides (5000 and 9000 daltons) that were lethal to mice at high dosage.317 Experimental envenomation of rabbits by live male spiders has resulted in extensive cutaneous injury and clear evidence of systemic poisoning. Local erythema appeared and faded within the first day; discolored patches were visible by day 4 and sloughed by day 6. Autopsy revealed petechial hemorrhages on the surfaces of the lungs, liver, and kidneys.310 Since the early 1980s, medically significant bites in the Pacific Northwest have been attributed to T. agrestis.2,311,313,314 In Europe, no medical problems have been associated with bites from these spiders.30,42,63 The venom chemistry of American spiders is no different from venoms of English spiders, so the cause of the alleged difference in medical significance is currently under investigation.34 Bites of males from the Pacific Northwest have more severe necrotic effects on mammalian tissues than do bites from females.310 Necrotic lesions have been attributed to this species all during the year, with a trend toward increased severity in the winter months.314

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 52-20  Adult female Latrodectus mactans mactans with fresh egg case. (Courtesy Michael Cardwell and Associates, 1999.)

sometimes referred to as L. lugubris. It may have red or orange spots or may be pure black and is known as kara kurt (Russian for “black wolf”). L. indistinctus, the black button spider of South Africa, has a narrow or broken red dorsal band or may be black. The red-backed spider (L. mactans hasselti) is medically important in Australia, New Zealand, and southern Asia. It has a dorsal red band similar to that of L. indistinctus, and the female also has a ventral red hourglass reminiscent of L. mactans mactans. L. geometricus is brown with black, red, and yellow markings and is common in southern Africa and warmer parts of the Americas. Widow spiders tend to bite defensively when accidentally crushed. In the Mediterranean basin, southern Russia, and South Africa, bites are associated with grain harvesting and threshing and with grape picking. In the United States, most bites occur in rural and suburban areas of southern and western states, with no special age, gender, or occupational predilection. In regions where outdoor privies are in common use, human envenomations are likely to involve the buttocks or genital area.33,112,197,333 Outbreaks of latrodectism may occur locally in epidemic fashion, lasting several years, and depend on changes in spider predator and parasite balance and on occupational variations in human– spider contact. Apparent outbreaks may also result from sudden increases in publicity and reporting.30,160

FIGURE 52-22  Mature female western black widow (Latrodectus hesperus). (Courtesy Michael Cardwell and Associates, 1993.)

molecular weight of 130,000, caused profound depletion of presynaptic vesicles with swelling of the presynaptic terminal at frog neuromuscular junctions; complete blockade of neuromuscular transmission followed within 1 hour. The toxin binds irreversibly with the lipid bilayer of the cell membrane, producing cationselective channels and interfering with endocytosis of vesicle membranes.55,94 The mechanism of action is not fully understood, but multivalent cations, including calcium, may enter the presynaptic nerve terminal through these channels, interfering with calcium-dependent intracellular processes.119,202 These effects appear to be specific to presynaptic nerves but independent of the transmitter involved. Acetylcholine, noradrenaline, dopamine, glutamate, and enkephalin systems are all susceptible to the toxin.248 Grishin126 has described the venom of L. tredecimguttatus, which has a family of seven protein toxins of high molecular weight. These all cause massive neurotransmitter release from presynaptic endings. They differ from each other in the specificity of the target animal. α-Latrotoxin acts selectively on vertebrate nerve endings; five latroinsectotoxins act on insects, and one toxin is specific for crustaceans. These large molecules have several functional domains responsible for ionophoric and secretogenic actions. Amino acid sequence analysis of precursor toxins reveals high levels of sequence identity between the different latrotoxins. It also reveals a series of ankyrin-like repeats that might be the structural basis of the interactions between the toxins and the membranes.126 L. indistinctus and L. geometricus also contain α-latrotoxin, the former with a greater venom yield per spider.207

Venom.  Unlike many other arthropod venoms, that of the widow spiders appears to lack locally active toxins capable of provoking inflammation. The venom contains several toxic components, including a potent mammalian neurotoxin, α-latrotoxin, that induces neurotransmitter release from nerve terminals. In 1964, Frontali and Grasso99 demonstrated three electrophoretically and toxicologically distinct fractions of Latrodectus venom. In 1976, Frontali and associates100 further purified and defined these fractions, encountering one major constituent (the B5 fraction, later renamed α-latrotoxin) with significant toxicity in mice and frogs (other fractions have effects more specific to insect physiology). α-Latrotoxin, a protein mix with an average

Clinical Presentation.  Latrodectism, the syndrome often resulting from Latrodectus envenomation, is best known for widespread, sustained muscle spasm rather than for local tissue injury. Although long-term outcomes are usually excellent, victims may have significant hypertension, autonomic and central nervous system dysfunction, and abdominal pain severe enough to be mistaken for an acute abdomen.

FIGURE 52-21  Mature female brown widow spider (Latrodectus geometricus). (Courtesy Michael Cardwell and Associates, 1999.)

FIGURE 52-23  Red-backed spider (Latrodectus mactans hasselti ). (Courtesy Sherman Minton, MD.)

994

Treatment.  Although the worst pain usually occurs during the first 8 to 12 hours after a bite, symptoms may remain severe for several days. All symptomatic children, pregnant women, and patients with a history of hypertension should be admitted to the hospital. Discharge is usually possible within 1 to 3 days, when

hypertension and muscle spasm have subsided. A patient with a satisfactory response to antivenom may be sent home after several hours’ observation. Care of the local site includes routine cleansing, intermittent application of ice, and tetanus prophylaxis. Severe pain and muscle spasm usually respond to IV narcotics or benzodiazepines. Careful observation of respiratory status is vital when either or both of these are used. Calcium gluconate infusion, advocated in the past, has proved only minimally useful and is no longer recommended. Hypertension may be treated with nifedipine or an infusion of sodium nitroprusside if the patient does not respond to pain control with narcotics or antivenom. Antivenom active against Latrodectus venom is available in the United States from Merck and Company; in Australia from Commonwealth Serum Laboratories; and in South Africa from the South African Institute of Medical Research. Standards for Latrodectus antivenom use vary around the world, as do guidelines for its administration.61,206,291 In the United States, Latrodectus antivenom, although it has never undergone clinical trials, has been used for many years and it is believed by many clinicians to be safe and effective for reversal of systemic effects and associated pain. When used properly, these products may prevent systemic sequelae resulting from envenomation, and even the need for hospitalization in some severe cases.62 Priapism, although refractory to treatment with opiates and benzodiazepines, has been reported to improve with antivenom.141 In general, antivenom should be used in cases involving respiratory arrest, seizures, uncontrolled hypertension, or pregnancy.256 In less severe settings, its value must be weighed against the risks of acute hypersensitivity and delayed serum sickness. In Australia, 0.5% to 1% of cases result in anaphylaxis, and some patients develop serum sickness.294 Death from anaphylaxis has been reported in the United States.61 The production of a Fab fragment specific for Latrodectus venom or α-latrotoxin could eliminate much of the concern surrounding the use of whole IgG in these patients.62 Fab fragments have less antigenicity, because of their lack of an Fc component present in whole IgG, prompting less of an immune response to the foreign protein by the recipient. An F(ab)2 product produced in Mexico is currently undergoing clinical evaluation in the United States. The usual therapeutic antivenom dose is one to three vials or ampules intravenously. Efficacy of antivenom is reported as satisfactory in 94% of patients in Australia,327 with anecdotal reports of efficacy even weeks to months after envenomation.19 Laboratory evaluation may include complete blood cell count, electrolytes, blood glucose, and urinalysis. Common findings include leukocytosis and albuminuria. In victims with severe muscle spasm, creatine phosphokinase levels may be elevated. Abdominal films and stool examination for occult blood, both of which should be normal after widow spider envenomation, may help with the differential diagnosis of abdominal pain. A pregnancy test should be done if indicated. No specific antigen or antibody detection technique is currently available for clinical diagnosis. Genus Steatoda: False Widow Spiders Biology.  Steatoda species are found worldwide. They are 3 to 8 mm (0.12 to 0.31 inch) in body length, smaller than Lactrodectus, and typically dark brown, often with white markings on the abdomen. They build tangly cobwebs and sit in crevices under stones, in tree bark, or in cracks of buildings near the web. S. paykulliana of Europe, S. foravae of southern Africa, and Steatoda grossa of the United States bear an external resemblance to members of the Latrodectus genus and therefore are referred to as false widow or button spiders. Venom.  The crude venom of S. foravae contains a major polypeptide of the same molecular weight as α-latrotoxin and can elicit a comparable neurotransmitter release syndrome in mice. The median lethal dose, however, is significantly higher, and the relative potency in mice is 10 to 20 times less than for venom of L. indistinctus.208 Clinical Presentation.  In humans, S. nobilis of southern England has caused brief local pain and slight swelling, followed 995

CHAPTER 52  Spider Bites

The initial bite may be sharply painful, but many bites are not recognized initially, so diagnosis is often presumptive and based on local and systemic signs. Local reaction is typically trivial, with only a tiny papule or punctum visible on examination. The surrounding skin may be slightly erythematous and indurated. In most cases, symptoms do not progress beyond this point. In one Australian series, 76% of victims presenting to a hospital for care had local symptoms only.156 The first reported case of Latrodectus envenomation in New Caledonia was L. macatans hasselti and involved local mild pain and inflammation, which only after several hours progressed to severe pain involving the entire extremity and requiring IV narcotic analgesia.189 In some cases, however, neuromuscular symptoms can become dramatic within 30 to 60 minutes as involuntary spasm and rigidity affect the large muscle groups of the abdomen, limbs, and lower back. Rhabdomyolysis has rarely been reported.87,103, A predominantly abdominal presentation may closely mimic an acute abdomen. Associated signs include fasciculations, weakness, ptosis, priapism, thready pulse, fever, salivation, diaphoresis, vomiting, and bronchorrhea. Compartment syndrome has rarely been described after a bite by Latrodectus species.65 Pulmonary edema has been described in Europe200 and South Africa.170,320 Respiratory muscle weakness combined with pain may lead to respiratory arrest. Hypertension with or without seizures may complicate management in elderly or previously hypertensive individuals. Isolated (normotensive) seizures do not appear to be a feature of latrodectism. Intractable crying may be the predominant feature in infants.47 Pregnancy may be complicated by uterine contractions and premature delivery.20,142,199,250,255 A characteristic pattern of facial swelling, known as Latrodectus facies, may occur hours after the bite and is sometimes mistaken for an allergy to drugs used in treatment. The usual course of an envenomation is to achieve complete recovery after a few days, although pain may last a week or more. The clinical picture of Latrodectus poisoning is similar around the world. In the 1980s in California, the most common site of envenomation referred to a toxicology service was the lower extremity (48%), followed by upper extremity (28%), trunk (18%), and head or neck (5%). The most common systemic symptom was abdominal or back pain (58%), followed by extremity pain (38%), hypertension (29%), and diaphoresis (22%).61 In Australia, a 1961 survey showed 37% of victims were bitten on the upper extremities, 27% on the lower extremities, 22% on the buttock or penis, 17% on the trunk, and 4% on the head or neck.331 A 1978 report showed a decline in the incidence of genital and buttock involvement (9.7%), perhaps related to a decrease in the use of outdoor lavatories.294 Australian envenomations showed a similar pattern of pain and diaphoresis, with more prominent local inflammation and lymphadenopathy and less hypertension than reported in the United States. In South Africa, envenomation by L. geometricus results primarily in local pain, whereas L. indistinctus provokes a syndrome of generalized pain, diaphoresis, and muscle rigidity similar to that seen in the United States.206 Victims bitten by L. tredecimguttatus may have spasms of facial muscles, swollen eyelids, lacrimation, and photophobia, more often resulting in recognized Latrodectus facies. A rash may appear 2 to 11 days after envenomation.196 Cardiac involvement is rarely reported. Three case reports of Latrodectus envenomation are reported in Turkey with cardiac manifestations. Erdur and associates87 reported a case of a young man bitten by L. tredecimguttatus who presented with anxiety, marked hypertension, nausea and vomiting, tremor, generalized pain, diaphoresis, rhabdomyolysis, and echocardiographic evidence of anteroseptal hypokinesia and depressed left ventricular function. Sari and co-workers258 reported myocarditis in a 65-year-old man within 3 hours of the bite with chest pain and electrocardiographic (ECG) changes. Kose and colleagues167 reported a young man with suspected Latrodectus bite who developed ileus, elevation of cardiac enzymes, and ECG changes. In all three cases, signs and symptoms resolved with time.

by local sweating and piloerection, facial flushing, and feverishness.323 One report of S. foravae bite in southern Africa showed minimal local inflammatory response without systemic toxicity.208 In one Australian report, a 2-year-old child bitten by a juvenile Steatoda (species unknown) developed lethargy, irritability, diaphoresis, and hypertension 22 hours after the bite. He improved gradually after administration of two ampules of red-backed spider (Latrodectus) antivenom.275 In another report, 30% of Steatoda bites (including S. capenis and S. grossa) studied in Australia presented to emergency departments and poison centers with systemic effects and persistent pain. Local and systemic symptoms were similar to those of Latrodectus envenomation, but overall they were less severe.152 Treatment.  In general, care is symptomatic and supportive. Similarities between the neurotoxins in Steatoda and Latrodectus venoms, however, suggest the use of Latrodectus antivenom in severely symptomatic cases. Several case studies from Australia using Latrodectus antivenom (red-backed spider antivenom, Commonwealth Serum Laboratories, Melbourne, Australia) for Steatoda bites have demonstrated improvement in and decreased duration of symptoms in victims. However, controlled studies have not been done.120,152 Genus Achaearanea: Grey House Spiders Biology.  Achaearanea are common spiders worldwide. They make classic theridiid cobwebs, often in corners and windows of houses. They are excellent predators of insects in homes. Individuals are mottled brown with globose abdomens and are easily distinguished from L. geometricus, the brown widow, by the lack of an hourglass in their ventral abdomen. Venom.  Little information is available about Achaearanea venom, although taxonomic proximity to other Theridiidae suggests the possibility of similar composition. Clinical Presentation.  One series of five cases in Australia indicates that redness or a red mark has been the only common local manifestation of Achaearanea bites. In case reports, bites to limbs produce pain that can become severe. Patients report increasing pain in the first hour that may persist for up to 24 hours. Local or regional diaphoresis is absent, with few reports of systemic effects. In two cases, headaches were reported, one with and one without nausea. This suggests that Achaearanea bites cause similar, but less severe, pain and systemic effects than do Latrodectus bites.152 Treatment.  Treatment of Achaeranea envenomation is symptomatic and supportive. Family Araneidae: Orb-Weaving Spiders Members of the family Araneidae are familiar to most people because they are common and build conspicuous, mainly circular, two-dimensional orb webs in open places. This is an abundant family, with 4000 species described and distributed worldwide. Species range in adult body size from 2 to 28 mm (0.07 to 1.10 inches) and often have extreme size dimorphism,

FIGURE 52-24  Orb weaver (Argiope species). (Courtesy Eileen Hebets.)

with males much smaller than females. They are extremely diverse in size, shape, web design, and prey capture tactics. They can be brightly colored, with typically ovoid abdomens and large chelicerae with several teeth. Although diverse and abundant, they are of minimal clinical concern. The venoms of many araneid spiders are known to have polyamine neurotoxins that postsynaptically block glutamate receptors in vertebrates.161 These are currently known from species of Nephila, Argiope, Araneus, and Neoscona. Genus Argiope: Argiopes Biology.  Argiope aurantia, known as the golden orb weaver or black and yellow garden spider, is common in California, Oregon, and the eastern United States (Figure 52-24). Other Argiope species are found throughout the United States, the Orient, and Australia.109 It is a large, brightly colored spider with a large, symmetric orb web and a leg spread of up to 7.5 cm (3 inches). Venom.  Although Argiope venom appears to be cytotoxic in vivo, research indicates the venom has neurotoxic effects in vitro. Venom gland extracts from A. trifasciata are postsynaptic blockers of neuromuscular transmission at locust glutamate receptors.305 Clinical Presentation.  Bites may cause local pain and erythema. Bites by A. argentata reportedly cause local pain, erythema, and vesicle formation, which resolve within 24 hours except for the bite marks.116,334 Treatment.  Treatment is symptomatic and supportive.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 53 

Scorpion Envenomation JEFFREY SUCHARD Scorpion stings occur commonly in tropical and subtropical regions around the world (Figure 53-1). Among causes of animalrelated human fatalities, scorpion stings rank second only to snakebites.196 The estimated annual number of scorpion stings worldwide is nearly 1.2 million, resulting in over 3000 deaths.54 More than 1800 scorpion species can be found, distributed on 996

all continents except Antarctica.165 The stings from most scorpion species cause local pain and inflammation, similar to bites or stings from other arthropods; mild systemic symptoms may also occur, but these stings are not serious. Basic first aid and symptomatic therapy, often only with nonprescription medications, are the only interventions necessary to treat most scorpion stings.

For online-only figures, please go to www.expertconsult.com

CHAPTER 53  Scorpion Envenomation

Incidence per 100,000 inhabitants Limits of distribution

<1

1 to 100

>100

FIGURE 53-1  Scorpion sting incidence around the world. (Modified from Chippaux JP, Goyffon M: Epidemiology of scorpionism: A global appraisal, Acta Tropica 107:71, 2008. With permission from Elsevier.)

Nevertheless, about 30 scorpion species are recognized as medically important and potentially fatal to humans. These dangerous scorpion species are distributed in both the Old World and New World, and all but one are from a single taxonomic family (Buthidae). Even among stings from dangerous scorpion species, many cases do not result in severe morbidity or mortality. Small children are particularly prone to developing more serious envenomation syndromes, probably because of the greater venom dose delivered per unit body weight. Stings are more common during the warmer months of the year, and in many countries they often occur in rural areas where access to health care may be more difficult. Seriously envenomed patients should certainly receive aggressive symptomatic and supportive care; however, the role of antivenom remains controversial, mostly because of the paucity of controlled clinical studies demonstrating its efficacy. Some differences exist between the full-blown envenomation syndromes that are typically seen. Most of the dangerous scorpions, including Tityus species in the Caribbean region and in South America, Androctonus and Buthus species in North Africa, Leiurus species in the Middle East (particularly L. quinquestriatus), and Hottentotta tamulus (formerly Mesobuthus tamulus) in India, cause an “autonomic storm” with prominent neurologic and cardiopulmonary effects, including hypertension, myocarditis, and pulmonary edema. A generally similar syndrome, but without the severe cardiopulmonary effects, occurs from stings of Centruroides species in the southwestern United States and Mexico and from Parabuthus species in southern Africa, which produce prominent neurologic effects associated with excess cholinergic tone. The non-Buthid scorpion Hemiscorpius lepturus, most commonly found in Iran, is the only dangerous species typically associated with local tissue necrosis and may also cause hemolysis and renal failure. Identification of new scorpion species and changes in taxonomy continue to occur. Names of scorpion genera, species, and even some families have changed since earlier editions of this book. Several species’ Linnean taxonomic names mentioned in the medical literature are now obsolete, and such changes will be generally noted in the text discussing those scorpions. The information provided in this chapter is believed to be current as of early 2010.

Scorpion Biology Scorpions are predatory arthropods of the class Arachnida. They have a lobster-like body shape with seven sets of paired appendages (Figure 53-2, online): the chelicerae, the pedipalps (claws), four sets of legs, and the pectines, a pair of comblike structures on the ventral surface. The segmented tail curves upward dorsally, ending in a terminal bulbous segment called the telson, which contains paired venom glands and the stinger (Figure 53-3). Scorpions feed primarily on ground-dwelling arthropods and small lizards. Scorpions grasp prey in their pedipalps and then rapidly thrust the tail overhead to sting. The chelicerae tear the food apart. The scorpion consumes only the juices and liquefied tissues of its prey, discarding the solid parts. Scorpions envenom by stinging, not biting, even though cases are occasionally misattributed to “bites” in the medical literature.20,165 Scorpions can sting multiple times; however, it appears that the first sting depletes or nearly depletes the telson of venom. A case series of three pairs of scorpion sting victims from India found that consecutive stings by Hottentotta tamulus caused severe cardiovascular manifestations in the first victim but not in the second.23 This author has anecdotally noted a similar difference in the severity of neurologic manifestations from consecutive Centruroides sculpturatus stings in Arizona. A characteristic physical property of scorpions is that they fluoresce when illuminated by ultraviolet light, as from a black light or a medical Wood’s lamp (Figure 53-4). This property is used in collecting scorpions for breeding or venom harvesting and in providing pest control. The fluorescent pigment in the scorpion cuticle is probably riboflavin.125

Venom Scorpion venoms are complex mixtures containing mucopolysaccharides, hyaluronidase, phospholipase, acetylcholinesterase, serotonin, histamine, protease inhibitors, histamine releasers, and protein neurotoxins.63,177 Neurotoxins are pharmacologically the most important venom constituents.177 The neurotoxins are single-chain, basic polypeptides of 60 to 70 amino acids, reticulated by four disulfide bridges. Each of the dangerous scorpion species’ venoms contains several neurotoxins, but they all share 997

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

C

B

FIGURE 53-3  A, Electron micrograph of scorpion telson. B and C, Close-up images demonstrating stingers with paired venom pores.

a similar structure and homologous sequences.91,177 In neuronal membranes, these toxins cause two effects with regard to fast sodium channels involved in action potential transmission: (1) incomplete inactivation of sodium channels during depolarization, resulting in a widening of the action potential, and (2) a slowly developing, inward sodium current after repolarization, leading to membrane hyperexcitability. The net result is repetitive firing of axons, enhancing release of neurotransmitters (acetylcholine, norepinephrine, dopamine, glutamate, aspartate, γ-aminobutyric acid) at synapses and at neuromuscular junctions.60,74,82,171,195 This is clinically demonstrated as excessive neuromuscular activity and autonomic dysfunction. Some scorpion neurotoxins also have effects on calcium-activated potassium channels,86,169 chloride channels,64 and L-type calcium channels.17 A few scorpion species have been demonstrated to produce a first droplet of “prevenom,” which has a different composition (less protein) and in vitro pharmacologic properties than does the subsequent normal venom.109 The clinical impact of prevenom, as compared with venom, is not known.

Regional Considerations: Epidemiology, Risk Factors, and Treatment Although scorpions are found throughout the world, the bulk of the published medical literature originates from only a few countries. The absence of data about a specific country here does not exclude the possibility of scorpion envenomation occurring there, particularly if that country is near a known scorpionendemic area; it simply means that such information is not available.

NORTH AFRICA

Morocco Scorpion stings are a major endemic hazard, accounting for 30% to 50% of all cases reported to the Moroccan Poison Control Center.2 The annual number of stings in Morocco has been estimated at 25,000 to 40,000.2,89 The majority of stings are caused by Androctonus mauretanicus, known as the “black scorpion” (Figure 53-5), and Buthus occitanus, the “yellow scorpion.”89 Stings are more commonly reported from Morocco’s southwestern provinces of El Kalaa, El-Jadida, Agadir, and Tan-Tan. Stings occur more commonly in rural areas, in the early evening when scorpions are active seeking prey.89 Most cases occur during the warmer summer months.2 Serotherapy has been advocated by some clinicians as the major therapeutic measure in Morocco since the 1970s.89 F(ab′)2 fragment antivenom is made by hyperimmunizing horses with crude A. mauretanicus venom; this product is cross-reactive with B. occitanus venom. In southwestern Morocco, 49% of patients are treated with antivenom, 35% with other drugs (calcium, steroids, antihistamines), and 16% with both. Patients given higher doses of antivenom (10 mL versus 2 to 5 mL or no antivenom) showed a decrease in serum venom levels and an increase in clinical improvement.89 However, in a 2009 series of 163 pediatric cases treated in Fez (north-central Morocco), none was treated with antivenom; the specific reason for symptomatic treatment was not explained, although the controversy regarding antivenom use was cited.2 Traditional first aid often includes scarification, which consists of local incision to induce bleeding that may result in venom release. Scarification was observed in nearly 40% of children evaluated at a university hospital in Fez, but this practice is considered medically contraindicated. Ninety percent of all fatal cases occur in children younger than 10 years old, with mortality rates ranging from 5.3% to 6.7%.2

Scorpion stings are a common problem throughout countries on Africa’s Mediterranean coast, where about 100,000 stings are reported annually.139

FIGURE 53-4  Scorpions fluoresce in ultraviolet light.

998

FIGURE 53-5  Androctonus mauretanicus, the “black scorpion” of North Africa. (Courtesy Jan Ove Rein.)

Algeria

SOUTHERN AFRICA

Tunisia Much of the published scorpion research from North Africa comes from Tunisia. Almost all stings are caused by five scorpion species: Androctonus australis, Androctonus bicolor, Buthus tunetanus (these first three are Buthid species), Scorpio maurus tenetanus, and Euscorpius sicanus.92 A. australis, locally known as the yellow scorpion (Figure 53-6), is the most common scorpion in Tunisia and accounts for most severe envenomations.80,92 A. aeneas is a dangerous black scorpion found only in the southern part of Tunisia, which constitutes only 1% to 2% of collected scorpion specimens. The non-Buthid scorpions are both relatively harmless and have thin tails and thick claws. The more dangerous Tunisian scorpions have long, thin claws and a thick tail (Figure 53-7).92,124 Stings occur most often outdoors (92%) on the victim’s extremities (95%) during the summer months.124 About 80% of all envenomations occur between June and September, with a peak in August.47,92 Scorpion envenomation occurs more in the less-populated middle and south of the country, so severely affected patients are usually admitted to rural hospitals with limited resources.47 Between 30,000 and 45,000 scorpion stings are reported annually in Tunisia, correlating to an incidence of 4.5 to 20 stings per thousand inhabitants, depending on the location. About 2.5% of

The majority of scorpion stings in South Africa, Zimbabwe, and neighboring countries do not cause systemic effects, although fatalities occasionally occur. The more dangerous scorpion species are members of the Buthidae family, most notably Parabuthus transvaalicus (centered around Zimbabwe and northernmost South Africa) and P. granulatus (found throughout the region).40,142 Parabuthus scorpions are some of the largest Buthid species in the world, ranging in size from 50 to 149 mm (2 to 6 inches).39,142 At least 20 Parabuthus species are distributed throughout South Africa, Namibia, Botswana, Zimbabwe, and Mozambique, also extending northward along the eastern coast into the Sahara and Arabia.142,149 It is recognized that Parabuthus scorpions have thin pincers and thick tails (Figure 53-8), whereas the relatively harmless species have thick pincers and thin tails (Figure 53-9).40,129,142 Parabuthus scorpions also have stridulatory granules on the dorsal aspects of the two proximal tail segments. When alarmed, these scorpions can scrape their stingers over these granules, making a warning sound.150 Also, several Parabuthus species are able to squirt their venom, an ability that has not been reported in other scorpions.149 Opistophthalmus glabrifrons, a member of the Scorpionidae family widespread in southern Africa, has infrequently caused systemic symptoms in addition to local swelling, but its sting is not considered potentially fatal.38 Stings from the Parabuthus species often cause only pain, although systemic effects occur less commonly. Severe envenomations are characterized by neuromuscular hyperactivity and excessive secretions (particularly hypersalivation and diaphoresis), but without the prominent cardiopulmonary effects from a hyperadrenergic state seen from the dangerous scorpions of

FIGURE 53-7  Androctonus amoreuxi, demonstrating the thin claws and thick tail characteristic of most dangerous scorpion species.   (Courtesy Jan Ove Rein.)

FIGURE 53-8  Parabuthus transvaalicus, a dangerous scorpion of southern Africa. (Courtesy Jan Ove Rein.)

Hundreds of deaths per year are caused by scorpion stings in Algeria.130 Most lethal scorpion stings in Algeria are caused by Androctonus australis. Antivenom therapy is advocated as the only indicated treatment for severe scorpion envenomation.173

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CHAPTER 53  Scorpion Envenomation

FIGURE 53-6  Androctonus australis, responsible for many severe scorpion envenomations in North Africa. (Courtesy Jan Ove Rein.)

stings (900 to 1100 per year) result in systemic manifestations requiring hospital admission.92 The mortality rate ranges from 0.25% to 0.4%, which is about 10% of victims with systemic envenomations, or 35 to 105 deaths per year.7,92,124-126 Two-thirds of reported stings affect adults and older adolescents, but nearly all fatalities occur in younger children; the mortality rate for children is about 1%.92,124 In a study of 951 patients admitted to the ICU between 1990 and 2002, the mortality rate was 7.5%.47 Scorpion antivenom is available in Tunisia and is commonly given to patients with systemic toxicity, but without good evidence of improved outcome.47 A randomized controlled trial of 825 patients given antivenom or placebo regardless of presenting clinical severity did not show any benefit of antivenom.5 Whether a subset of patients exists who would benefit from antivenom is not known. Horses are used as host animals to produce antivenom, although research has also been conducted with camels.139 Corticosteroids are often administered when treating scorpion stings in Tunisia, but this treatment appears to have no benefit; in fact, it is independently associated with the need for hospitalization.154 Dobutamine infusions are also used to treat severely affected patients with pulmonary edema.80

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 53-9  Hagodenes troglodytes, an impressive-looking yet relatively harmless scorpion of southern Africa, has large claws and a thin tail. (Courtesy R. David Gaban.)

northern Africa, South America, the Middle East, and India.39,40,142 This toxidrome appears identical to that seen in the American southwest from the stings of Centruroides sculpturatus. Stings typically occur in the early evening during the warmer months of October through April, with a peak incidence in January and February.39,40,142 Four children died in a series of 42 serious scorpion envenomations in South Africa.142 No fatalities were noted among 244 patients (17 with severe systemic symptoms) in Zimbabwe.40 In another study from Zimbabwe, however, five deaths occurred among 455 patients, with fatalities occurring in children less than 10 years old or adults over 55.39 Antivenom is produced in South Africa against Parabuthus venom, which is recommended for patients with severe systemic toxicity.39,40,129,142,150 Injection of local anesthetics for localized pain and intracutaneous sterile water injection for regional pain have also been advocated.40 Traditional herbal remedies are frequently used but have no apparent beneficial effect; indeed, rubbing the sting site, as commonly practiced with such herbal remedies, more than doubles the chance of developing a severe envenomation.39

ASIA Turkey Although scorpions are present throughout the country, only a limited number of medical publications about scorpion envenomation in Turkey are available, mostly from the southeastern portions of the country. Potentially dangerous species include Androctonus crassicauda (Figure 53-10), Leiurus quinquestriatus, Mesobuthus species, and a few others.10,46 As elsewhere,

FIGURE 53-10  Androctonus crassicauda, a “black scorpion” from the Middle East with a particularly painful sting. (Courtesy Jan Ove Rein.)

1000

stings occur more commonly during warm months, from May through September. Studies from the early 2000s had shown pediatric lethality rates as high as 12.5%, whereas a case series of 170 patients from 2007 involved no deaths.8 In a 2009 case series of 52 children hospitalized in southeastern Turkey, nearly one-half (46.2%) were stung by A. crassicauda, one (1.9%) was stung by L. quinquestriatus, and in the remaining cases the offending scorpion species was not known; one death was recorded. Admission from a rural area was a risk factor for severe envenomation, possibly because of increased time from envenomation to hospital presentation.46 Antivenom is widely used in Turkey for severe scorpion envenomation. A monovalent antivenom is produced by administering A. crassicauda venom to horses, then enzymatically digesting and purifying the serum. Hydrocortisone and antihistamines are commonly co-administered per the national poisoning treatment procedure.8 Israel Leiurus quinquestriatus, locally often called the “yellow scorpion,” is the most dangerous species found in Israel (Figures 53-11 and 53-12; Figure 53-12, online).44,77,107 Other native species include Hottentotta judaicus (formerly Buthotus judaicus, the “black scorpion”), Androctonus crassicauda, A. bicolor, Nebo hierochonticus, Scorpio maurus, and Orthochirus innesi.43,44,77 More than 90% of all scorpions encountered in neighboring Jordan are either yellow or black scorpions (L. quinquestriatus or B. judaicus), with the yellow being most common.77,107 Most scorpion stings occur during the warmer months of April through October.36 In the Negev desert region, Bedouin children are stung about six times more frequently than are Jewish children, probably because of more time spent outdoors and lack of protective footwear. Males are affected 2.3 times more often than females; this is most likely related to differences in gender roles, such as boys herding sheep or goats.107 The reported mortality rate in children was 18% among Palestinians living on the West Bank in 1965, 3.7% among children in the Jerusalem area in 1991,77 and 1.2% among children in the Negev area in 1985.107 Most scorpion stings have a mild clinical course; 13% of reported sting victims remain asymptomatic, 72% have mild illness, and 15% become moderately to seriously ill.36 In a case series of 18 Israeli pediatric patients stung by L. quinquestriatus between 1988 and 1996, 17 had mild to moderate toxicity, and only one patient was severely affected, suggesting that routine ICU admission was not necessary.35 Stings from L. quinquestriatus initially produce intense local pain, erythema, and edema, which can be followed by an outpouring of catecholamines and acetylcholine from nerve

FIGURE 53-11  Leiurus quinquestriatus, a dangerous “yellow scorpion” of North Africa and the Middle East. (Courtesy Jan Ove Rein.)

Saudi Arabia At least 14 species of scorpions are found in Saudi Arabia; the two species most commonly responsible for significant envenomation are Androctonus crassicauda, a black or dark brown scorpion, and Leiurus quinquestriatus, a yellow scorpion.* The “yellow scorpion” is usually reported to cause more stings than the “black scorpion,” except in one 5-year surveillance survey from the north-central Qassim province, where the distribution was roughly equal.119 Saudi Arabia averages 14,500 annual reported scorpion stings.121 These account for 3% to 4% of all pediatric hospital admissions in northwestern Saudi Arabia between May and August, with few admitted in other seasons.78,79 One author reported the incidence of “scorpion sting syndrome” as 1.3 cases per 1000 emergency department patients,148 whereas a 15-year retrospective analysis from another hospital in the same city (Riyadh), with over 100,000 visits annually, reported only 251 cases.9 Between 70% and 80% of cases occur between May and October, and 73% of stings occur at night between 6 PM and 6 AM.120,148 Many victims are barefoot children playing outdoors or persons tending flocks of goats or sheep. Males are affected at least twice as often as females.15,78,120,148 Mortality rates have decreased from 2% to 8%, as previously reported, to less than 0.05% in more recent studies.15,78,106 Antivenom is recommended and routinely administered for scorpion envenomation in Saudi Arabia; this may be related to decreasing mortality rates.15,78,79,113 L. quinquestriatus envenomations were reviewed earlier, in the section about Israel. A. crassicauda stings are similar to those of the yellow scorpion, causing hypertension and CNS manifestations, but differ in other ways.113 The pain from the A. crassicauda sting has been reported as particularly severe. Generalized erythema was noted in 20% to 25% of children less than 5 years of age; this is not usually seen with other scorpion stings. The cause of this erythema is not clear, especially because elevated catecholamine levels after scorpion envenomation appear to be protective against allergic reaction. Cholinergic effects are seen less often with A. crassicauda stings. Of special relevance to wilderness medicine, scorpion envenomation became an issue to U.S. soldiers deployed during the Gulf War.93 L. quinquestriatus and A. crassicauda were implicated in 57 scorpion stings over 4 months among 7000 troops of an armored cavalry division stationed in eastern Saudi Arabia. All patients with adequate data for further study recovered fully, usually with only supportive care in the field, probably reflecting that all were healthy adults. No antivenom was available. Typical signs and symptoms included local pain, tachycardia, hypertension, sweating, apprehension, headache, epigastric pain, nausea, restlessness, and local muscle cramping and paresthesias in lower extremity stings. Presumably, victims with only local pain failed to present to battalion aid stations, resulting in an apparently high incidence of systemic effects. Only two persons had serious presentations or subsequent complications. One had a clinical picture consistent with anaphylaxis and required intubation for respiratory support. The other developed a cutaneous ulcer that healed in 3 weeks with oral antibiotic therapy.93 *References 15, 79, 106, 113, 120, 128, 148.

Iran More than 44 scorpion species are found in Iran, including at least seven whose stings are considered medically important.159 Scorpion stings are most prevalent in Khuzestan, a hot and humid province in the southwest adjacent to the Persian Gulf; about 60% of all reported stings in Iran occur in this province. In 1990, the distribution of stings by species to persons seeking medical attention in Khuzestan was 41% Androctonus crassicauda, 45% Mesobuthus eupeus, and 13% Hemiscorpius lepturus, the only non-Buthid scorpion generally recognized as dangerous to humans.160 A more recent collection of 418 scorpions brought with patients evaluated at various medical centers in Khuzestan after being stung found 120 (28.7%) A. crassicauda specimens, 104 (24.9%) H. lepturus, 91 (21.7%) M. eupeus, 86 (20.6%) Compsobuthus matthiesseni, and minor contributions by three other species.66 Nonspecialists can rarely identify species by sight, but most can easily identify the scorpion’s primary coloration. The most dangerous “black scorpions” of Iran are A. crassicauda and Hottentotta schach, whereas the dangerous “yellow scorpions” are M. eupeus, Hottentotta saulcyi, Odontobuthus doriae, and Hemiscorpius lepturus.175 Stings occur more commonly during the warmer months of the year (90% occurring between April and October), and most occur during the night or early morning hours, reflecting times of peak scorpion activity.159,175 In Iran, 90% to 95% of all fatal stings are caused by H. lepturus (sometimes previously called H. lepturus), making it the most dangerous scorpion in Iran.121,159,175 This member of the Hemiscorpiidae family causes a spectrum of disease distinctly different from that caused by the dangerous scorpions of the Buthidae family. Severe envenomation by H. lepturus is characterized by hemolysis, renal failure, and local tissue necrosis. Stings by H. lepturus are stated to not induce an acute painful response (unlike stings from other species), resulting in many patients delaying medical attention until the local tissue destruction is advanced.121,161 This last point sounds similar to many alleged brown recluse spider bites in the United States and alleged whitetailed spider bites in Australia, where dermonecrotic lesions of unknown etiology (often from bacterial infection of the skin and soft tissue) are erroneously ascribed to arthropods by laypersons and health care personnel alike. However, this author is not aware of any published evidence refuting the observation that H. lepturus stings are not initially painful. Envenomation by A. crassicauda in Iran produces pain, neuromuscular agitation, and signs of parasympathetic hyperstimulation (e.g., lacrimation, salivation, increased bronchial secretions) similar to other Buthid scorpions.160 However, this report does not comment on signs and symptoms specifically related to the adrenergic/hypertensive crisis seen with many other dangerous species. India Nearly all of the medical literature regarding Indian scorpions relates to Hottentotta tamulus, sometimes called the “red scorpion,” the single most dangerous native species (Figure 53-13).143 Until recent taxonomic changes, this scorpion had been called Mesobuthus tamulus (and before that Buthus tamulus and Buthotus tamulus); therefore the bulk of previously published observations and research now refers to obsolete genus names. H. tamulus is a particular problem in southern coastal India. Stings occur predominantly in April, May, and June at night among young farmers wearing minimal clothing.24,30 In many cases, stings occur at the tip of an extremity, with the only symptom being pain, which can be controlled with local anesthetic injections.30,62 Systemic toxicity occurs from release of catecholamines, with major morbidity and mortality resulting from cardiopulmonary toxicity.* Fatality rates between 30% and 40% were reported in the 1960s and 1970s, but these have fallen to 2% to 3% with treatment using vasodilators and calcium channel blockers.25,27,33 An 11.8% mortality rate, however, was found *References 21, 24, 27, 30, 41, 62.

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CHAPTER 53  Scorpion Envenomation

endings. In severe cases, clinical signs of sympathetic overload predominate, with severe hypertension, tachyarrhythmias, and pulmonary edema.3,97,98,162 Parasympathomimetic action of the venom may also cause bradyarrhythmias or atrioventricular block, usually preceding the sympathetic overload. Cardiomyopathy and myocardial damage with electrocardiographic (ECG) and serum marker (creatine kinase [CK], CK-MB, troponin) changes have been reported.77,97,176,183 Other common findings from severe stings include agitation, convulsions, encephalopathy, hypersalivation, diaphoresis, priapism, and pancreatitis.178,179 Treatment recommendations differ, but all emphasize aggressive symptomatic and supportive care for severely envenomed patients. However, some clinicians propose the routine use of antivenom,77 whereas others argue that serotherapy does not significantly alter outcome based on experimental pharmacokinetic data.97,98,101 Antivenom had no demonstrable effect in one clinical series of Israeli patients.180

PART 6  ANIMALS, INSECTS, AND ZOONOSES

by small Buthid scorpions from the Lychas genus; however, all five stings from Tasmania were from Cercophonius squama, the only known species on that island.110 Urodachus scorpions are larger but less commonly encountered.111 No neurotoxins were found in U. novaehollandiae, the only Australian species that has had its venom studied.185 No antivenom exists for native Australian scorpions. Supportive treatment, often with only oral analgesics, appears to be adequate. Similar to the treatment of some other envenomations, the application of hot water (e.g., immersing a stung finger) has been advocated, but this has not been studied systematically.111,185

SOUTH AMERICA

FIGURE 53-13  Hottentotta tamulus, the dangerous “red scorpion” of India. Until recent taxonomic changes, it was most widely known as Mesobuthus tamulus. (Courtesy Jan Ove Rein.)

among 152 children admitted to hospitals in Calcutta from 1985 to 1989, but treatment details were not reported.41 H. tamulus antivenom had not been available for clinical use until quite recently. Starting in 2002, scorpion antivenom has been distributed to primary health centers (PHCs) in India free of charge; however, its use is not standard, especially because envenomation cases are commonly admitted, which does not occur at PHCs.33 Bawaskar and Bawaskar, from Maharashtra, a state in western coastal India, are the world’s foremost proponents of using antihypertensive agents (primarily oral prazosin, an α-adrenergic blocker) to treat the catecholaminergic effects of severe scorpion envernomation.22-33 They cite the limited medical resources available for the majority of victims, many of whom live in rural settings and are poor, in addition to the potential risks of transporting unstable patients. Other vasodilators that have been advocated include nifedipine, IV sodium nitroprusside, and captopril.127 Administration of H. tamulus antivenom did not appear to improve clinical outcome compared with treatment with oral prazosin in a nonrandomized observational study of 53 patients.33 A potential confounder is the fact that patients treated with antivenom were all referred from PHCs to the study hospital, whereas those treated with prazosin presented directly to the hospital. Some researchers have instituted protocols relying on oral prazosin for early-presenting patients, but using dobutamine and nitroprusside for those with pulmonary edema.42,147 In 2010, the Bawaskars published a randomized, open-label study comparing patients treated with oral prazosin alone with those treated with prazosin plus H. tamulus antivenom. Enrolled in each group were 35 patients with grade II envenomation (systemic signs and symptoms present, but without pulmonary edema or shock). The recovery time in the antivenom group was reduced (8 hours versus 17.7 hours), and there was no significant difference in clinical deterioration rate. They noted that the total cost of treatment with antivenom “approaches a month’s salary for a laborer in the region” (Rs350, $7.77), whereas prazosin costs less than one-tenth this amount.34

AUSTRALIA Australia is home to more than 40 named scorpion species and is believed to harbor as many as 200 species in total. However, scorpion stings are uncommon there and do not cause major envenoming.110,111 In a 27-month study in the early 2000s, only 192 scorpion stings were reported to Australian poison centers. The majority of stings occurred during the warmer months of the year, and they tended to occur at night and indoors. These stings generally caused severe pain (defined as greater than that from a bee sting) lasting a few hours, although 11% of the victims had systemic complaints of nausea, headache, and malaise. The majority of victims were managed without seeking additional medical attention. In 95 cases, the offending scorpion was collected and identified by an arachnologist. Most stings (72) were 1002

Colombia A case series of 129 patients admitted after scorpion stings in Colombia has been reported.156 The most commonly implicated species were Tityus pachyurus, T. fuehrmanni, and Centruroides gracilis. Most envenomations were mild (76%), and only children less than 6 years old were in the severe group (four patients). A commercially available Mexican antivenom against the venom of four Centruroides species was used in 19 cases with systemic findings, which decreased the duration of some clinical signs and had no reported adverse effects. Thirty-two cases occurred on an Air Force base, where servicemen put on clothes or boots in which scorpions had sought shelter overnight.156 Venezuela Envenomation by scorpions of medical importance in Venezuela is endemic to the densely populated northernmost sections of the country, with the northeastern states of Monagas and Sucre being particularly affected.71,72 Tityus discrepans is the most common species causing stings, although 184 scorpion species were described by 2006, with 52 from the Tityus genus.71,72,75 Intravenous antivenom is commonly given for severe envenomations, and there appears to be a trend toward a better outcome with earlier administration.136,137 Trinidad Tityus trinitatis accounts for almost 90% of the scorpion population on Trinidad. Fatalities are rare but occur more often in children. Stings are more frequent in summer months.19 Systemic effects of serious T. trinitatis envenomations include tachypnea, restlessness, vomiting, hypersalivation, cerebral edema, pulmonary edema, hypovolemic shock, seizures, and myocarditis.63 The most striking clinical observation is the high incidence (up to 80%) of acute pancreatitis; scorpion stings are the most common cause of acute pancreatitis in Trinidad.19,88 Brazil About 10,000 cases of scorpion envenomation are reported annually in Brazil, with 80% occurring in southeastern regions.141,151 One-half of the reported stings occur in the state of Minas Gerais, although scorpions are also problematic in São Paulo and Bahia.50,141 Most stings occur between December and February.85 Tityus serrulatus, popularly known as the “yellow scorpion,” is the most prevalent species in Brazil and accounts for most fatal stings, as a result of its widespread distribution in populous urban centers and high venom potency.11,59,141 T. serrulatus is considered by some to be “the most dangerous scorpion in South America.”158 T. bahiensis is the second-most common species, although severe envenomations are much more likely from T. serrulatus.49,151 Equine-derived antivenom for either T. serrulatus or both T. serrulatus and T. bahiensis is able to neutralize venom from all Brazilian scorpions studied.151 Children are much more likely than adults to have severe envenomations.84 In Minas Gerais, children less than 14 years of age accounted for 27% of scorpion envenomation admissions but for all cases of significant morbidity and mortality; 16% were treated in an intensive care unit (ICU) setting. Mortality with current treatment now ranges from 0.7% to 1.1% in children and is 0.28% overall.84,104,141,166 A “tripartite approach” has been advocated, which employs symptomatic measures, support of vital functions, and immunotherapy.167 Antivenom from a few manufacturers is available in Brazil and routinely used in severe envenomations.50,84,166

Argentina Scorpions of medical importance in Argentina belong to the Tityus genus. Tityus trivittatus is generally recognized as the only species capable of causing severe envenomations or death, although T. confluens has also been implicated in a few cases.69,70 Over a 7-year period, 511 scorpion envenomations were reported to public health authorities. Most cases occurred indoors and during the warmer months, November through April. Scorpions are hyperendemic in the provinces of Córdoba and Santiago del Estero, where 85.6% of the envenomations occurred. Local pain and inflammation were most common, whereas systemic envenomation occurred in 7% of children 10 years and younger and in 2% of older victims. Antivenom therapy was provided in 84% of cases with available treatment records; only three fatalities occurred, and none of these victims had received antivenom. Until 1996, the Argentinians used a cross-reactive Brazilian antivenom against T. serrulatus. Since 1997, Argentina has produced a F(ab′)2 fragment equine antivenom.69

NORTH AMERICA Mexico An estimated 250,000 scorpion stings occur annually in Mexico.157 The number of resultant deaths per year has been variously reported from “about 100,” to “700 to 800,” to “over 1000”; regardless of the actual number, this certainly represents a serious public health concern.55,157,164 Of at least 221 native species and subspecies, only eight members of the Centruroides genus (Figure 53-14) are recognized as significantly dangerous.56,65,73,155 The Centruroides scorpions are relatively small and described as yellow, tan, or brown. Clavigero recognized as early as 1780 that “the venom of the small and yellow scorpions is more active than that of the big grey ones.”138 Mexican states on the Pacific Coast, particularly Colima, Durango, Guerrero, Morelos, and Nayarit, report the highest number of scorpion stings.55,65,138,164 In 1999, Morelos had the highest incidence, with a total of 30,663 stings and nine deaths. Nearly 2% of the population in Morelos is stung annually, and in some hyperendemic villages this figure is over 10%.164 In urban areas of Colima, 3 stings per 1000 people occur annually; this figure rises to 18 to 30 stings per 1000 in more rural areas.55 The peak incidence of scorpion stings occurs during the warmer months, but has been variably reported as from “March to July, coinciding with scorpion reproduction,” or between “June and October,” correlating with rainfall statistics.56,155 The following signs and symptoms have been reported with Mexican scorpion stings, although not all effects are necessarily seen in the same victim, and no apparent sequence of effects has been observed: hyperexcitability, restlessness, hyperthermia, tachypnea, dyspnea, tachycardia or bradycardia, diaphoresis, nausea, vomiting, gastric distention, diarrhea, lacrimation, nystagmus, mydriasis, photophobia, excessive salivation, nasal secretion, dysphagia with foreign body sensation, dysphonia, cough, bronchorrhea, pulmonary edema, arterial hypertension or hypotension, heart failure, shock, convulsions, ataxia, fasciculations,

United States More than 40 species of scorpions are found in the United States.51 However, only one American species, the Arizona bark scorpion (Figure 53-15), causes a significant number of systemic reactions and is known to be potentially fatal.37,51,60,172,186 For many years, controversy has existed regarding proper taxonomy and the medical importance of this scorpion.194 This species has at times been called Centruroides sculpturatus, C. exilicauda, or C. gertschi. Current taxonomy holds that the Arizona bark scorpion is properly called C. sculpturatus, which is medically important and found in the southwestern United States (particularly Arizona), of which C. gertschi is a striped subspecies. C. exilicauda is a different species found in Baja California, Mexico; its sting is considered medically insignificant, and no fatalities have been documented.170,194 Nevertheless, a significant proportion of the medical literature regarding scorpions refers to the medically important American species as C. exilicauda. Approximately 30 Centruroides species are found distributed throughout the New World, several of which are medically important and are mostly found in Mexico.172 Centruroides sculpturatus is called the “bark scorpion” because of its preference for residing in or near trees. These scorpions also often hide under wood (old stumps, lumber piles, firewood, loose bark, or fallen trees), in ground debris, or in crevices during the daytime. This is troublesome to humans, because the scorpions may hide in shoes, blankets, or clothing left on the floor during daylight hours, as well as under common ground covers and tents. C. sculpturatus is found statewide in Arizona and also in some areas of Texas, New Mexico, northern Mexico, small areas of California, and near Lake Mead, Nevada.60 The bark scorpion is relatively small, measuring up to 5 cm in length. Specimens are variously described as being a uniformly yellow, brown, or tan; stripes are uncommon. The pincers (pedipalps) and tail are thin, giving the scorpion a streamlined appearance

FIGURE 53-15  Centruroides sculpturatus, the Arizona bark scorpion; the only species in the United States known to cause severe neurotoxic envenomations. (Courtesy Jan Ove Rein.)

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CHAPTER 53  Scorpion Envenomation

FIGURE 53-14  Centruroides limpidus limpidus, one of several closely related, dangerous Mexican scorpions. (Courtesy R. David Gaban.)

and coma.65 Unpublished verbal reports by physicians who have treated scorpion-envenomed patients in Mexico suggest that the clinical presentation is virtually identical to that caused by C. sculpturatus in the United States. The higher mortality from Mexican scorpion stings compared with American stings may be the result of differences in venom potency between species, differences in human and scorpion population densities, differences in the ease of access to medical care (e.g., monitoring equipment, ICUs, and antivenom), and perhaps also from cultural differences in housing and protective clothing that promote human–scorpion interactions in Mexico. Antivenom is recommended and commonly used for severe scorpion envenomation in Mexico.56,65,73,131,155 A F(ab′)2 fragment antivenom is produced domestically and is commercially available. It is prepared from the venoms of four native Centruroides scorpions and is also under investigation for use against C. sculpturatus in the United States.49

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 53-16  Distinctive features of Centruroides sculpturatus include the nearly uniform yellow/tan color, thin pedipalps and tail, and subaculear tooth (indicated by arrow) on the telson.

(Figure 53-16), in contrast to several of the larger but less dangerous scorpions with thick claws and tails. The presence of a subaculear tooth, a tubercle at the base of the stinger, is distinctive to C. sculpturatus and is helpful in differentiating this neurotoxic scorpion from other species.60,186 The bark scorpion presents a significant public health problem in Arizona. About 10% of all calls received by the poison control center in Phoenix are related to scorpion stings, the vast majority of which are known or highly suspected to have been caused by C. sculpturatus. The bark scorpion was at one time the number-one killer among Arizona’s venomous animals. From 1931 to 1940, more than 40 deaths were attributed to envenomation by this scorpion, mostly in young children and infants. The fatality rate fell dramatically between 1940 and 1970, probably because of improved pest control measures and advances in medical technology and supportive care. In 1972, these scorpion stings were still considered generally fatal to infants without treatment, extremely dangerous to older children, and occasionally fatal to adults with hypertension.184 However, no deaths have been reported in the medical literature from scorpion envenomation in Arizona since 1968.37 In 2001, a scorpion-related fatality was reported in Arizona, although death was ascribed to anaphylaxis rather than to direct venom toxicity, in a patient previously stung and presumably sensitized to the venom.48 A more recent, unpublished pediatric death may have been caused by a lack of adequate airway control and/or allergic reaction to antivenom. Because death can apparently be prevented with currently available supportive care, earlier fatalities were probably caused by loss of upper airway and respiratory muscle control with the potential for aspiration, exacerbated by metabolic acidosis, hyperthermia, and rhabdomyolysis from excessive muscular activity.60 Centruroides vittatus, the common striped scorpion, accounts for the next most reported envenomations in the United States. C. vittatus has a black intraocular triangle and black stripes on the thorax (Figures 53-17 and 53-18). A review of 558 C. vittatus stings reported to Texas poison centers in 1997 found that 96% produced local symptoms of pain, bleeding, burning sensations, erythema, edema, hives, local paresthesias, and pruritus; systemic reactions occurred in 20% of victims.187 The most common systemic features were paresthesias of the face, tongue, and perioral region, followed by dysgeusia, chills, sweating, dysphagia, fasciculations, nausea, and vomiting. C. vittatus is found primarily in the Southwest and Texas but also extends into southern Indiana and Illinois.191 Hadrurus species are the longest and most heavy-bodied scorpions native to North America and are known as “giant hairy scorpions” because of their size and conspicuous bristles (Figure 53-19). They are native to Arizona, California, and parts of Utah, Nevada, Idaho, and Mexico. Vaejovis species have a wide distribution from southern Canada, south through Wyoming, Colorado, and Texas, and west to California. Hypersalivation after Vaejovis envenomation has been reported. Uroctonus species are found in mountain habitats from southern California to Oregon.172 Isometrus maculatus is the only scorpion found in Hawaii and 1004

FIGURE 53-17  Centruroides vittatus, the American common striped scorpion: male specimen. (Courtesy Jan Ove Rein.)

FIGURE 53-18  Gravid female Centruroides vittatus. (Courtesy Jan Ove Rein.)

is also found in southern Florida and California.51,135 Envenomations cause mild systemic effects (myalgia and nausea); no fatalities have been reported.135 Diplocentrus species have been found in Florida, Texas, and California.51 The Midwest and New England are not natural scorpion habitats, although three envenomations in Michigan were caused by scorpions unintentionally transported with personal belongings or with produce—two by Centruroides hentzi from Florida and one by C. sculpturatus from Arizona.191 The poison control center in Phoenix has also been consulted regarding stings from bark scorpion stowaways in mail to Minnesota and in personal belongings to Germany.

FIGURE 53-19  Hadrurus arizonensis, a “giant hairy scorpion” of the American Southwest. (Courtesy R. David Gaban.)

BOX 53-1  Grading of Centruroides sculpturatus

Envenomation

Grade I: Local pain and/or paresthesias at site of envenomation Grade II: Pain and/or paresthesias remote from the site of the sting, in addition to local findings Grade III: Cranial nerve dysfunction or somatic skeletal neuromuscular dysfunction A. Cranial nerve dysfunction: blurred vision, wandering eye movements, hypersalivation, difficulty swallowing, tongue fasciculations, upper airway problems, slurred speech B. Somatic skeletal neuromuscular dysfunction: jerking of the extremity/(ies), restlessness, severe involuntary shaking and jerking that may be mistaken for a seizure Grade IV: Cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction Modified from Curry S, Vance MV, Ryan PJ, et al: Envenomation by the scorpion Centruroides sculpturatus, J Toxicol Clin Toxicol 21:417, 1983-1984.

and multisystem organ failure have also been reported in a few severely ill children.38 After envenomation, symptoms may begin immediately and progress to maximum severity within 5 hours. Infants can reach grade IV in 15 to 30 minutes.60 The symptoms abate at a rate that depends on the age of the victim and the grade of envenomation. Symptomatic improvement occurs within 9 to 30 hours without antivenom therapy.45,57,60,186 Pain and paresthesias are exceptions and have been known to persist for days to 2 weeks. Although adults appear to be envenomed more often, children are more likely to develop severe illness requiring intensive supportive care.60 A review of 673 patients found that 67.8% of stings occurred in adults older than 20, with 14.9% in children younger than 11. Many more unreported envenomations probably occur in adults, placing the relative incidence for children even lower. Of the patients, 621 (92.3%) had symptoms of either grade I or II envenomations or were asymptomatic and thus required no specific therapy. Younger patients had a higher percentage of the more severe envenomations; 25.9% of children younger than 6 years of age had grade III or IV envenomations, or 34% if asymptomatic patients (most likely never stung) are excluded. Only 6.1% of adults had grade III or IV envenomations.60 Medically reliable descriptions of the victim’s perspective of neurotoxic scorpion envenomation are rare, primarily because of the young age of those most severely affected. Box 53-2 is a personal description of C. sculpturatus envenomation by a critical care physician. A notable natural experiment occurred in the United States with regard to antivenom use for scorpion envenomation. For many years, the only domestic scorpion antivenom was produced at Arizona State University (ASU) in Phoenix. A goat-derived whole IgG antivenom was first produced in 1966.87 This antivenom was produced by hyperimmunizing a small herd of goats against C. sculpturatus venom and then intermittently harvesting and freezing or lyophilizing their serum. Probably because of the limited geographic need, this antivenom was never approved by the U.S. Food and Drug Administration and was not available commercially; however, it was distributed free of charge on a humanitarian basis within the state by special action of the Arizona State Board of Pharmacy.45 Nevertheless, it was not universally agreed that this antivenom should be the primary therapy for severe scorpion envenomation, and debate persisted between opposing schools of thought among local toxicologists. In general terms, the toxicologists based in Phoenix preferred to use antivenom, whereas the toxicologists in Tucson promoted advanced supportive care measures, often in an ICU setting with administration of intravenous sedatives to mitigate the involuntary neuromuscular agitation.90,133 Production of scorpion antivenom at ASU ceased around the year 2000, the last batch of antivenom expired in 2004, and hospital pharmacies used up their last supplies in 2005.49,168 By default, the only available therapy was supportive care, which resulted in increased pediatric ICU admissions in Arizona.168 Although no manufacturer in the United States is currently producing any scorpion antivenom, research has been conducted with a polyvalent anti-scorpionic F(ab′)2 fragment produced in Mexico using a horse host and venom from other Centruroides species. This product is commercially available in Mexico. Anascorp, Centruroides (Scorpion) Immune F(ab′)2 (Equine) Injection was subsequently approved as an orphan drug by the U.S. Food and Drug Administration on August 3, 2011, based on safety and efficacy data collected from 1534 patients in a study coordinated by investigators from the University of Arizona.192,193 This antivenom is to be marketed to health care facilities in areas where C. sculpturatus is found, which includes Arizona, and portions of Clark County, Nevada and New Mexico.193

Pathophysiology and Clinical Effects CARDIOVASCULAR EFFECTS Detailed descriptions of myocardial damage and other cardiovascular manifestations from the scorpions of Israel, India, Trinidad, Tunisia, and Brazil have been reported since the 1960s.97,103 The 1005

CHAPTER 53  Scorpion Envenomation

Centruroides sculpturatus Envenomation.  Stings from C. sculpturatus often produce significant neuromuscular effects without severe cardiopulmonary toxicity. Curry and co-workers reviewed clinical findings after C. sculpturatus envenomation and proposed four clinical grades of envenomation intended to direct treatment (Box 53-1).60 Grade I envenomation is characterized by local pain and paresthesias at the sting site. Usually, no local inflammation occurs, and the puncture wound is too small to be observed. If no scorpion is seen, the diagnosis may require historic or epidemiologic clues or other physical signs. The “tap test” has been empirically recommended to confirm a bark scorpion sting, although its reliability has not been rigorously tested. With the patient looking away or otherwise distracted, gently tapping the sting site will greatly exacerbate the pain, a sign that does not occur with other envenomations.60,186 Victims with grade II envenomations have local symptoms plus pain and paresthesias remote from the sting site. The more distant symptoms often radiate proximally up the affected extremity but may occur in even more remote sites (e.g., contralateral limbs) or as generalized paresthesias. Victims may complain of a “thick tongue” and “trouble swallowing” in the absence of objective motor abnormalities. Children and adults frequently rub their nose, eyes, and ears, and infants may present with unexplained crying.60 Cranial nerve or somatic skeletal neuromuscular dysfunction is found in grade III envenomations. Cranial nerve dysfunction can be demonstrated as blurred vision, abnormal eye movements, slurred speech, tongue fasciculations, and hypersalivation. The combination of bulbar neuromuscular dysfunction and increased oral secretions may cause problems with airway maintenance. Abnormal eye movements most often are involuntary, conjugate, slow, and roving. Chaotic multidirectional conjugate saccades resembling opsoclonus and unsustained primary positional nystagmus may also be seen.58 Many patients with abnormal eye movements prefer keeping their eyes closed. Somatic skeletal neuromuscular dysfunction can cause restlessness, fasciculations, alternating opisthotonos and emprosthotonos, and shaking and jerking of the extremities that can be mistaken for a seizure. The abnormal skeletal muscle activity appears more undulating and writhing, however, than the tonic–clonic movements of generalized seizures. Also, unlike victims with seizures, these victims often remain awake and alert the entire time. Grade IV envenomation is characterized by both cranial nerve dysfunction and somatic skeletal neuromuscular dysfunction. On close examination, victims with skeletal muscle hyperactivity (at least grade III) usually also have cranial nerve dysfunction, meeting criteria for grade IV. In the most severe cases, stridor and wheezing occur, suggesting foreign body aspiration or reactive airways disease. Hyperthermia up to 40° C (104° F) can occur, probably resulting from excess motor activity. Respiratory failure, pulmonary edema, metabolic acidosis, sterile cerebrospinal fluid pleocytosis, rhabdomyolysis, coagulopathy, pancreatitis,

PART 6  ANIMALS, INSECTS, AND ZOONOSES

BOX 53-2  Personal Account of Centruroides

sculpturatus Envenomation by a Critical Care Medicine Specialist

Arriving home in the early evening, I decided to go for a run. My running shoes were in the kitchen area, where I had left them the day before. As usual, I would wear my shoes without socks. As I put my left foot into the shoe, I felt an intense burning pain on the dorsum of my first toe. I pulled my foot out of the shoe and along with it came a 1.5- to 2-inch, clear-brown scorpion. Having no idea what to do for a scorpion envenomation, I called the poison control center. I was informed that the systemic toxicity was usually mild for someone my age, and that if the pain was too severe, I should come in and be evaluated. As the minutes went by, I began to salivate and feel perioral paresthesias. As I walked, the paresthesias became more generalized, with a very noticeable paravertebral tingling with each step. After a few more minutes, I decided to call the poison control center to ask for advice. After dialing the number, I was unable to speak clearly because of severe dysarthria and excess salivation. The toe pain seemed to abate as other neurologic symptoms developed. Since I was unable to talk on the phone, and no neighbors were home to drive me to the hospital, I decided to drive myself. The normal 10-minute drive took 45 minutes. I had coordination difficulties with the gas pedal, clutch, and gear shifting. It was also nighttime, and I could not process the multiple visual inputs of car lights, street lights, and road lines in a way that would allow me to drive more than 5 to 10 miles per hour. I not only had to stop frequently and close my eyes for a few seconds but also had difficulty keeping the car in my driving lane. After arriving at the emergency department, I was ataxic, dysarthric, and drooling and had difficulty giving the admitting nurse a proper history. I’m certain that I was thought to be either mentally retarded or intoxicated. Examination by the emergency department physician revealed many abnormal cerebellar findings, continued salivation, inability to swallow liquids, continued symptomatic paresthesias, but no objective motor or sensory deficits. There were no physical signs of envenomation [at the sting site], but tapping the toe produced worsening pain. As my story became clearer to the ED physician, antivenom was ordered and administered. Within 20 minutes of finishing the infusion, all neurologic signs and symptoms were gone, except for toe pain. Courtesy Dr. Thomas Bajo, Phoenix, Arizona.

cardiovascular effects of scorpion envenomation are complex and varied. Stimulation of the sympathetic and parasympathetic branches of the autonomic nervous system results in different clinical presentations that may change with time. Distinct syndromes may dominate the clinical picture in severe scorpion stings. Hypertension or hypotension can occur with or without pulmonary edema, and rhythm disturbances may consist of sinus bradycardia or tachycardia, premature depolarizations, supraventricular tachycardia, atrioventricular block, and ventricular tachycardia.83,99 Some clinicians have postulated that the cardiovascular effects follow a predictable pattern of progression from an initial hyperdynamic and hypertensive phase to a hypokinetic, hypotensive phase with left ventricular dysfunction, with or without pulmonary edema, depending on the patient’s volume status.1,122,153 Transient parasympathetic effects may occur initially, resulting in bradycardia and hypotension, and are followed by sustained adrenergic hyperactivity.25 Sinus tachycardia and hypertension are related to venominduced catecholamine and angiotensin release.25,63,100,122,128 Significant hypertension may be seen in up to 77% of patients with systemic envenomation, although a 17.5% to 30% incidence of hypertension is more common.97 A loud protosystolic gallop, systolic parasternal lift, and transient apical murmur of papillary muscle dysfunction are associated with systemic hypertension.25,97 1006

Myocarditis, with ECG changes and biochemical evidence of cardiac injury, is often reported. This myocardial damage is most likely caused by massive catecholamine discharge and sympathetic overstimulation, although direct venom cardiotoxicity has not yet been ruled out.* Many ECG changes consistent with myocardial ischemia and myocarditis, including Q waves, ST-segment elevation or depression, peaked or inverted T waves, U waves, prolonged QTc intervals, and atrioventricular and bundle branch blocks, have been found in persons stung by scorpions.24,97,176 Most ECG abnormalities are transient, lasting only as long as the most severe clinical effects. Prolonged QTc intervals last for 48 to 72 hours, however, and T-wave inversions have persisted for 4 to 6 weeks.19 Echocardiography has demonstrated left ventricular systolic dysfunction, which usually resolves by the next day.128 Concurrent right ventricular dysfunction supports primary global scorpionic myocarditis rather than secondary myocardial ischemia from systemic hypertension.153 Elevated serum levels of CK and CK-MB have been found in about one-half of persons with systemic envenomation. Only about one-half of those with elevated CK-MB levels also have ECG changes consistent with myocardial injury.181 Concurrent CK, CK-MB, and troponin-I elevations have also been reported in a victim with transient bradycardia and second-degree (Mobitz type I) atrioventricular block.176 Troponin-I was found to be a more specific marker for clinical signs of myocarditis (such as heart failure, cyanosis, shock, abnormal heart sounds, and ECG changes) than were total CK, CK-MB, or LDH among scorpionenvenomed children.140 Even in patients with severe Tityus serrulatus envenomation, troponin-I may be normal at admission, typically peaking within 24 to 36 hours of the sting.61 Histologic examinations of cardiac tissue in fatal human cases have shown a mixed picture of toxic myocarditis and myocytolysis, with interstitial edema and hemorrhage, inflammatory cell infiltrates, necrotic foci, and fatty droplet deposition.61,97

RESPIRATORY EFFECTS Respiratory failure after scorpion envenomation has been attributed to direct CNS depression, hypertensive encephalopathy, upper airway obstruction, bronchospasm, impaired surfactant synthesis, and pulmonary edema.14,143,178,180 Pulmonary edema is the most severe respiratory feature in severe scorpion envenomation, occurring in 7% to 35% of victims and accounting for approximately 25% of scorpion-related deaths.3,4,162 The etiology and pathogenesis of pulmonary edema from scorpion stings are not clear, and both cardiogenic and noncardiogenic factors have been implicated. Left ventricular systolic dysfunction may cause pulmonary edema through venom-induced myocarditis and acutely increased afterload.4,5,95,162 Increased pulmonary capillary wedge pressures,4 abnormal radionuclide scans,162 and left ventricular dysfunction demonstrated by Doppler ECG studies3 support a cardiac origin of pulmonary edema. Noncardiogenic causes for pulmonary edema are less well documented and include shock, primary venom-induced lung injury, oxygen toxicity,95 the presence of various inflammatory mediators (interleukins, kinins, platelet activating factor),5 and decreased lung liquid clearance.58 Histologic and biochemical evidence of increased alveolocapillary membrane permeability has been demonstrated in animal studies and in a fatal human case of Tityus serrulatus envenomation.12 Rabbit studies with T. discrepans venom found abundant intravascular microthrombi in lungs with pulmonary edema, and heparin prevented the development of pulmonary edema.75 Such findings are atypical of noncardiogenic pulmonary edema, or adult respiratory distress syndrome (ARDS), and the researchers therefore suggest that scorpion venom respiratory distress syndrome (SVRDS) be recognized as a distinct clinical entity.

NEUROLOGIC EFFECTS Stings from dangerous Buthid scorpion species around the world can produce prominent neurologic effects. Scorpion venom causes repetitive and uncontrolled neuronal discharges through *References 25, 63, 84, 97, 153, 183.

PANCREATITIS Scorpionic pancreatitis was reported by Waterman in 1938 from Tityus trinitatis stings and was found in 80% of patients studied by Bartholomew in 1970.19 Most patients had epigastric pain radiating to the back starting within 5 hours of the sting and resolving within 24 hours. Some patients with hyperamylasemia (38%) did not complain of abdominal pain, suggesting that the true incidence of pancreatitis may be significantly higher. Scorpion stings are the most common cause of acute pancreatitis in Trinidad.19 Acute pancreatitis is the most common form of the disease, but edematous, hemorrhagic, and chronic relapsing pancreatitis may also occur.88 Transient pancreatitis has also been reported from Centruroides sculpturatus in the United States and in 93% of children envenomed by Leiurus quinquestriatus in Israel.36,184 Hyperamylasemia was found in 46% of patients envenomated by T. discrepans in Venezuela.76 The systemic severity of the envenomation or amount of abdominal pain does not appear to correlate with the degree of elevation in the serum amylase level.19,184 Scorpion venom is known to be a potent secretagogue, stimulating exocrine secretion of the stomach, salivary glands, and pancreas.53,60,190 Enhanced release of proteolytic enzymes, accompanied by spasm of the sphincter of Oddi, is hypothesized to cause acute scorpionic pancreatitis.53,88

OTHER GASTROINTESTINAL EFFECTS Nausea, vomiting, gastric distention, abdominal cramping, and occasional diarrhea are reported in victims with severe systemic symptoms.65,107,128,142 Gastric distention associated with agitation and depressed level of consciousness place scorpion sting victims at increased risk for pulmonary aspiration of gastric contents. T. serrulatus venom increases the volume, acid output, *References 30, 50, 77, 98, 126, 180.

and pepsin output of gastric juice in rats, probably mediated by release of acetylcholine and histamine. Serum gastrin levels are also elevated.190 Pig studies with Leiurus quinquestriatus venom found that despite an increase in oxygen transport and consumption, oxygen utilization in the GI tract was impaired.178 Such impairment in oxygen utilization may occur in other tissues as well, contributing to metabolic acidosis in severe envenomations.

ENDOCRINE AND OTHER HUMORAL EFFECTS Scorpion envenomation has long been known to cause an autonomic storm with increased release of endogenous catecholamines, contributing to hypertension, tachycardia, and potentially fatal cardiopulmonary dysfunction. Envenomed patients with abnormal ECG tracings excrete elevated levels of free epinephrine, norepinephrine, and vanillylmandelic acid.102 Elevated circulating catecholamine levels have also been reported.12 Release of catecholamines may be caused by direct stimulation of postganglionic sympathetic neurons and the adrenal glands. Hypertension may also be caused by activation of the renin-angiotensin endocrine axis. Elevated levels of renin and aldosterone were found in victims stung by Leiurus quinquestriatus.96 Stings often induce hyperglycemia, possibly related to suppression of insulin secretion, in contrast to the enhanced secretion by the exocrine pancreas.59,76,143 Murthy and Hase propose that this results in a syndrome of fuel-energy deficits related to inability to use existing metabolic substrates, exacerbating the cardiopulmonary insult.143 Insulin therapy has been found to reverse ECG changes, reduce angiotensin levels and circulating free fatty acids in experimental animals, and reverse hemodynamic changes and pulmonary edema in children stung by scorpions.143,144 Hottentotta tamulus venom also lowers thyroxine and triiodothyronine levels in experimental myocarditis.145 Kinins and other inflammatory mediators may play a role in the cardiovascular toxicity. T. serrulatus and Centruroides sculpturatus venoms potentiate the action of bradykinin by inhibiting angiotensin-converting enzyme (ACE).132 Animal experiments show reversal, using aprotinin (a kallikrein-kinin inhibitor)81,119 and icatibant (a bradykinin antagonist),81 of venom-induced cardiovascular effects and augmentation with captopril, an ACE inhibitor, of adverse effects.18 Serum interleukin-6 (IL-6) levels were greatly elevated in 8 of 10 Israeli children, gradually decreasing toward normal over 24 hours.181 High levels of circulating IL-1, IL-3, IL-6, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF) have also been found in a severely envenomed Brazilian patient.5 The IL-8 level appeared to correlate with envenomation severity caused by Buthus occitanus in Egypt.140

GENITOURINARY EFFECTS Priapism is frequently reported among male patients with systemic envenomation. Priapism results from enhanced parasympathetic tone and is often associated with vomiting and profuse sweating.20,22 The reported incidence of priapism ranges from 4% to 10%,7,15,160 to as high as 78% to 96%.107,182 In India, priapism, vomiting, and diaphoresis are considered premonitory diagnostic signs of severe Hottentotta tamulus envenomation. Priapism is reduced or absent within 6 hours of the sting even in severe cases, and the degree of priapism does not appear to correlate with the severity of envenomation.24 In Tunisia, however, the incidence of priapism positively correlated with degree of severity.126 Urinary retention is found in 33% of victims with systemic envenomation in southern Africa.38,39,142 This finding, however, is not consistent with increased cholinergic tone, which should produce increased urination, as seen in other series.15 A dorsal nerve block with 1% lidocaine was successful in treating severe local pain from a T. serrulatus sting to the penis.152

HEMATOLOGIC EFFECTS Scorpion stings are not generally noted to produce coagulop­ athies or other significant hematologic effects, although DIC has been reported.15,132 The occasional “defibrination syndrome” is 1007

CHAPTER 53  Scorpion Envenomation

incomplete sodium-channel inactivation.60 Neurologic signs are fairly common, even from scorpions categorized as cardiotoxic. Actually, all scorpions that produce systemic effects are primarily neurotoxic; however, the neurotoxic effects from some species can induce massive release of endogenous catecholamines, resulting in cardiopulmonary effects that are more prominent clinically. Neurologic signs reported with cardiotoxic scorpions include local or diffuse paresthesias, tremors, shivering, agitation, hyperirritability, apprehension, restlessness, myoclonus, oculogyric crisis (opsoclonus), convulsions, confusion, delirium, hypo­ reflexia, and coma.* In fatal human cases, a preterminal encephalopathic phase is typical.119 Intracranial pathology, such as hemorrhagic strokes thought to be related to vascular rupture from acute hypertension,85,163 vasculitis,20 or disseminated intravascular coagulation,16 has been noted in several case reports of scorpion envenomation. Ischemic strokes have also been reported, probably related to cardiogenic shock.94 Although pain and paresthesias lasting hours to a few days from the neurotoxic effects of scorpion stings are common, strokes and other persistent neurologic sequelae are rare. Many persons with systemic scorpion envenomation exhibit anxiety and agitation, consistent with CNS excitation. Animal experiments have shown that intracerebroventricularly administered Hottentotta tamulus venom produces effects similar to those caused by yohimbine, a known anxiogenic agent.40 Although in fatal cases of Leiurus quinquestriatus envenomation, CNS manifestations always precede terminal hypotension and cardiac arrest, the venom crosses the blood–brain barrier poorly, if at all,114,119,166 so any encephalopathy would be secondary to peripheral effects. Others suggest that CNS manifestations of scorpion stings are caused by hypertensive encephalopathy or excessive levels of circulating catecholamines, rather than a direct venom effect.179,180 Hypoxia and pain may also contribute to agitation. Video clips demonstrating the neuromuscular hyperactivity in young children with severe Centruroides sculpturatus envenomation are available online (http://www.youtube.com/ watch?v=DE60ig0CIZc&feature=channel, or http://www.youtube. com/watch?v=MbuGEQs6aSw).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

seen more often in children, probably because of a higher relative dose, and can be experimentally reproduced in dogs. Platelet aggregation can be induced by catecholamines alone and may therefore be an indirect effect of scorpion venom. Increased osmotic fragility of red blood cells has been demonstrated in some experimental models.132 The only scorpion routinely implicated in dangerous hematologic effects is Hemiscorpius lepturus, which can cause severe hemolysis and consequent renal failure.121,159,161,175 Case reports from Saudi Arabia associate severe Nebo hierochonticus stings with DIC and intracranial hemorrhage.15,16 Neither of these species is from the Buthidae family, which more characteristically causes cardiopulmonary and neurologic toxicities.

IMMUNOLOGIC EFFECTS Scorpion toxins are antigenic and therefore capable of eliciting an immune response. Positive skin prick, intradermal skin tests, and radioallergosorbent assays have been found with the venom from Centruroides vittatus and Androctonus australis hector in previously stung patients.66,130 Envenomation by C. sculpturatus has produced an anaphylactic reaction, with urticaria, wheezing, and facial angioedema but without systemic neurotoxic findings, in an otherwise healthy adult patient previously stung by a scorpion.197 Fatality from scorpion envenomation in the United States is extremely rare; however, a reported death in 2001 appears to have been caused by anaphylaxis to scorpion venom, rather than direct venom effect.48 Treatment with animal-derived antivenom puts the patient at risk for both immediate and delayed immunologic reactions. Because the treatment for hypersensitivity reactions includes epinephrine, and because many persons envenomed by cardiotoxic scorpions have elevated circulating catecholamines, such persons should be less likely to have anaphylactic reactions to antivenom. Brazilian patients stung by T. serrulatus were separated into groups with or without adrenergic manifestations, and both groups received antivenom.13 The group with adrenergic toxicity developed significantly fewer signs and symptoms of early anaphylaxis (8% compared with 42.9%).

Differential Diagnosis Bites or stings from other arthropods should be considered in the differential diagnosis of scorpion envenomation. Pain at the site of Centruroides sculpturatus sting may be similar to latrodectism (widow spider bite; see Chapter 52). Patients with severe scorpion envenomation are often unable to lie still, whereas patients with latrodectism can maintain a position for short periods before moving again to seek a comfortable position. Widow spider envenomation may produce hypertension, tachycardia, sweating, and other signs of adrenergic excess, but it does not produce the abnormal eye movements, fasciculations, or paresthesias, or induce a positive tap test, as those found with scorpion stings. Widow spider bites frequently produce a characteristic halo lesion at the site, whereas no lesion is usually visible after neurotoxic scorpion stings. Many other arthropods can produce a small puncture wound accompanied by local tissue inflammation; this may be difficult to differentiate clinically from scorpion sting in the absence of cardiovascular or neurologic toxicity or without tentative visual identification of the arthropod involved. The tachycardia, respiratory distress, excessive secretions, and occasional wheezing that occur from C. sculpturatus stings may be mistaken for asthma, airway obstruction with a foreign body, or poisoning with a cholinergic agent, such as an organophosphate insecticide. In the absence of the history of a scorpion sting, other disorders to be considered include CNS infection, tetanus, dystonic reaction, seizure, hysteria, and intoxication with an anticholinergic agent, sympathomimetic agent, phencyclidine, nicotine, or strychnine. Autonomic storm from a cardiotoxic scorpion sting may be confused with pheochromocytoma or a monoamine oxidase inhibitor–tyramine reaction. A victim of severe scorpion envenomation presenting late in the course may appear to have cardiac failure or sepsis. 1008

Toxicity from illicit amphetamines is sometimes mistaken for envenomation by C. sculpturatus. Young children from endemic areas presenting with unusual neurologic symptoms (agitation, choreiform or repetitive motion of the trunk and extremities, abnormal eye movements) may be assumed to have been envenomed even without history of a sting or scorpion.146 Occasionally, caregivers are aware of this potential for misdiagnosis and claim their child was stung when they believe the child ingested methamphetamine. A series of 18 inadvertent methamphetamine poisonings among children in Arizona included three victims initially misdiagnosed with a scorpion sting and inappropriately treated with antivenom; one patient had an anaphylactic reaction.123

Treatment The great majority of the medical literature regarding treatment of scorpion envenomation relates to evaluation and care rendered in a hospital setting, often within intensive care units. This information, therefore, is often not directly applicable to the prehospital setting or to the provision of medical care in austere environments. For many scorpion species, stings cause only local pain and inflammation that will respond well to local care measures. On the other hand, there is little medical treatment that can be provided on-scene for the autonomic storm that can occur with envenomation by the world’s dangerous scorpion species. Ismail and colleagues summarized the current understanding of treating scorpion stings when noting, It is strange that despite the long experience with scorpion envenomation, most of the treatment protocols advocated are based on isolated clinical observations, are sometimes controversial, and not instituted on rigid or strictly controlled animal or clinical studies. … Even in serotherapy there are no quantitative studies regarding antivenom dosage, routes of administration, time-effectiveness relationship and titre of the antivenom used.119 Although much controversy surrounds the proper treatment of scorpion envenomation, some consensus exists. Most victims, even those stung by potentially dangerous scorpions, demonstrate only local signs and symptoms and require only symptomatic outpatient treatment. It is prudent to observe such persons for several hours after the sting to ensure that progression to severe envenomation does not occur. Experience with Centruroides sculpturatus envenomation in Arizona shows that progression of envenomation grade occurs rapidly, with a mean time of 14 minutes and a median time of less than 1 minute.134 For localized pain, several clinicians have recommended local anesthesia with lidocaine, bupivacaine, or dehydroemetine by infiltration or nerve block, such as a digital block for fingers or toes.30,38,39,112,152 In southern Africa, Bergman has reported successful treatment of poorly localized pain radiating up an extremity with an intracutaneous sterile water injection (ISWI), usually also with a local anesthetic infiltrated at the sting site.38,39 ISWI is performed by injecting small amounts (about 0.1 mL) of sterile water intradermally into points of maximal pain, producing up to 10 wheals. Pain relief is said to occur within 1 to 5 minutes, but pain may return in 4 to 12 hours and can be persistent. ISWI therapy cannot be generally recommended because it has not been tested in prospective or controlled trials or with scorpion stings elsewhere in the world. Scorpion stings are traumatic puncture wounds, and victims should be given appropriate wound care and tetanus prophylaxis if indicated. The local trauma from neurotoxic scorpion stings, however, tends to be minimal. For instance, it is common to see no local soft-tissue findings in patients with severe toxicity from C. sculpturatus stings. Victims with significant systemic scorpion envenomations should receive supportive and symptomatic care in a monitored hospital setting.78,84,98,102 Many require admission to an ICU, although treatment should begin in the emergency department or outlying facility if available. Airway control must be addressed and continuous cardiovascular and respiratory monitoring instituted. Fluid resuscitation may be indicated secondary to fluid losses from vomiting, sweating, and increased insensible losses from hyperthermia. Both hyperthermia and hypothermia have been reported

PHARMACOLOGIC THERAPY Many drugs have been recommended for the treatment of scorpion envenomations, but few have been rigorously tested. Recommendations regarding the use of atropine vary. Many victims exhibit signs of excess cholinergic tone, such as bradycardia, vomiting, sweating, and hypersalivation. If venom induces prominent adrenergic effects, the rescuer should not administer atropine.26,84,98 Parasympathetic venom effects are usually transient and not life threatening, although atropine may be indicated for severe bradycardia. Also, in subsequent phases with more prominent adrenergic toxicity, atropine could worsen tachycardia and hypertension. Atropine may be safe, however, for cholinergic effects from scorpion species that do not cause prominent cardiotoxicity. Published cases from southern Africa and Arizona suggest that atropine can reverse hypersalivation that interferes with airway control, which may obviate the need for intubation and decrease the risk for aspiration, although caution is still advised.38,142,188 Scorpion envenomation in these areas is characterized by neuromuscular and dysautonomic effects but does not typically involve serious cardiopulmonary effects. Protocols for the use of atropine and its optimal dosage have not been prospectively determined. Treatment with corticosteroids has been regularly recommended and is still common in many countries; however, a prospective, randomized, placebo-controlled human study of antiinflammatory corticosteroids showed no benefit.7 In Tunisia, 600 consecutive patients received either 50 mg/kg of hydrocortisone hemisuccinate or a placebo. No differences between the two groups were found in clinical severity (baseline and four hours after treatment), mortality, need for artificial ventilation, or duration of hospitalization. Glucocorticoids and antihistamines are not recommended unless administered as treatment for allergic manifestations (e.g., anaphylaxis to antivenom).40,142 Vasodilator therapy has received much attention. Because excessive adrenergic tone appears to cause the most significant morbidity, vasodilators should block or reverse severe cardio­ pulmonary effects from scorpion envenomation. Prazosin is a selective α1-adrenergic blocker, which may lower blood pressure and help reverse other cardiopulmonary effects. Prazosin is also thought to reverse the inhibition of insulin secretion.28,29 In India, an initial dose of 0.5 mg by mouth for adults and 0.25 mg for children is given to relieve hypertension and pulmonary edema. Repeat doses are given in 4 hours, then every 6 hours as needed for up to 24 hours. Sodium nitroprusside is used in cases of lifethreatening pulmonary edema.30 Nifedipine, 5 to 10 mg “sublingually” by puncturing and swallowing the gelatin capsule, has also been used in India, along with the initial dose of prazosin. When this protocol was compared with “conventional treatment” (with digoxin, furosemide, hydrocortisone, antihistamines, and atropine), the cohort treated with prazosin had significantly reduced morbidity and shortened recovery time.29 In Israel, hypertension from scorpion sting unresponsive to analgesics and sedatives has been treated with IV hydralazine or sublingual nifedipine, which are believed to reverse hypertensive encephalopathy.179 A potential benefit of vasodilators over antivenom is the rapidity of onset of therapeutic effect.101 Captopril has also been used to treat hypertension, but theoretically this could worsen pulmonary edema.18,30,114,122 Insulin infusion has been used in India.143,144 Because scorpion venoms inhibit insulin secretion, this treatment may help reverse the consequent metabolic derangements. A series of six patients treated with an insulin infusion (0.3 units of regular insulin per gram of glucose, at a rate of 0.1 g glucose per kilogram bodyweight per hour) showed improvement in pulmonary edema and hemodynamics, although furosemide and hydrocortisone appeared to offer little benefit.143 Insulin therapy for scorpion envenomation is not standard in India and has not been reported from other locations. Dobutamine infusions of 7 to 20 mcg/kg/min improved cardiac function in a series of seriously envenomed Tunisian

patients.80 Digoxin, β-adrenergic blockers, dantrolene, aminophylline, quinine, and aspirin have also been suggested as potential therapeutic adjuvants in scorpion envenomation, but these are not widely recommended.30,105

ANTIVENOM Treatment recommendations seriously diverge regarding antivenom. Most medical researchers believe that antivenom plays a crucial role in the treatment of seriously envenomed patients.* Proponents believe that (1) antivenom is the only specific therapy available against the primary physiologic insult and (2) it greatly improves outcome. Any previous disappointing experience with antivenom, they argue, probably results from inadequate dosing.113,114 Researchers from Israel and India do not recommend antivenom.22,98,182 Opponents believe that (1) morbidity and mortality are not caused by the venom but by autopharmacologic agent release, which should not be reversed by antivenom therapy, (2) pharmacokinetic data do not support a role for antivenom, (3) antivenom has not improved outcomes in Israeli studies, and (4) antivenom is often unavailable and would be prohibitively expensive in India, so other options must be chosen. Treatment without antivenom consists of managing serious cardiopulmonary and neurologic effects with pharmacologic agents and supportive care. Even when antivenom is administered by its proponents, adjunctive therapies to treat cardiac failure, pulmonary edema, and other physiologic treatments are also used. A major issue in the debate regarding the usefulness of antivenom relates to the pharmacokinetics of scorpion venom. Detectable circulating venom supports the use of antivenom to neutralize the toxins. Tityus serrulatus venom injected subcutaneously in rodents rapidly distributed to various tissues, with peak serum levels in 30 to 60 minutes.166,174 After 2 hours, the venom decreased rapidly and was no longer detectable after 8 hours. Therefore IV serotherapy should be initiated as soon as possible, because it would become less effective when administered many hours after envenomation.166 Ismail and co-workers reported that scorpion venoms in animal experiments were rapidly absorbed and distributed to tissues, but had more prolonged elimination phases.114,117 Scorpion venom has a half-life of 4.2 to 24 hours.114 The clinicians concluded that although antivenom would theoretically be most efficacious if given immediately after envenomation, it is still indicated after a delay of several hours or more.128,174 It is interesting to note, however, that Gueron and colleagues reviewed these data and concluded instead that serotherapy would be ineffective and recommended against it.97,98 They suggested that the most severe cardiopulmonary effects would be present early and would not be reversed by antivenom given later. The clinical effects of scorpion envenomation are related to tissue concentrations of Androctonus amoreuxi venom in experimental animals, although the slower distribution of antivenom to tissues suggests that it may be less effective when given after a significant delay.116 A series of 56 victims stung by T. serrulatus in Brazil correlated clinical severity to plasma venom concentrations.67 This correlation between venom levels and clinical severity of envenomation has been seen in other studies.76,89 IV antivenom lowers circulating levels of venom and presumably the clinical severity of envenomation; however, the effectiveness of antivenom on venom bound to other tissues has not been well defined. The role of serotherapy depends on the time to administration, becoming less effective with increasing delay.124,136 Because scorpion venom acts indirectly through the release of auto­ pharmacologic substances, treatment with specific blockers may be more effective than antivenom in persons with delayed presentation.116 In 1999, a large (825-patient), randomized, placebo-controlled Tunisian clinical trial of scorpion antivenom in humans found no significant benefit to giving antivenom in terms of progression to systemic illness.5 However, the majority of patients in this study had mild envenomations, possibly obscuring an effect that *References 4, 45, 60, 68, 83, 112, 142.

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CHAPTER 53  Scorpion Envenomation

from scorpion stings, and both appear to worsen toxicity.118 Hyperthermia usually resolves with standard acetaminophen doses, and hypothermia resolves with warm blankets.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

could be seen only in more serious cases. One canine study showed that whereas simultaneous administration of antivenom and venom prevents clinical manifestations of envenomation, delayed administration of antivenom does not alter the clinical course.6 A small series of pediatric cases from India published in 2003, after antivenom became available, is consistent with these findings. Four children with severe envenomations by Hottentotta tamulus who received scorpion antivenom within 1.5 hours of the sting were not observed to have any clinical improvement.31 Another canine study found that the administration of antivenom 20 minutes after venom improves cardiac output, as does the administration of IV fluid; combination therapy worked better than either single treatment alone.189 A treatment protocol using high doses of IV polyvalent antivenom (i.e., doses greater than the in vitro neutralizing dose) is used in Egypt and has reduced mortality from 4.6% to 8% down to less than 0.05%.115 The entire body of literature on scorpion antivenom appears to be a muddle, with many contradictory findings. This confusion may stem from differences between benchwork and clinical studies, differences in study design, venom and antivenom dosing, patient susceptibility, and many other factors. Based on this author’s own clinical experience with stings from Centruroides scorpions in the United States, the use of IV antivenom is favorable for severe scorpion envenomation in cases where it is available. Scorpion antivenom is generally administered intravenously (IV). Indeed, some antivenom preparations have been approved only by their respective drug regulatory agencies for IV use. Some antivenoms (against scorpions and against other envenomations) have been administered by the intramuscular (IM) route. When

compared with IM, administration of IV scorpion antivenom results in faster onset of action and shorter recovery times.65 Given the small size of the patients most likely to suffer the highest-grade scorpion envenomations and the resultant neuromuscular hyperactivity, in some instances IV access may not be possible to obtain or maintain. Successful administration of scorpion antivenom in the United States by the IM and/or intraosseous (IO) routes has been reported in a few cases.108

TREATMENT IN AUSTERE ENVIRONMENTS If travel within a scorpion–hyperendemic area is planned and evacuation to modern facilities will not be possible, consideration should be given to carrying oral prazosin in the medical kit. This treatment has been advocated in India for complications of severe scorpion envenomation (e.g., pulmonary edema) without rapid access to advanced medical care.30,31,33 Recommended prazosin dosing is 250 mcg for children and 500 mcg for adults by mouth, then repeated four hours later if needed, and then every 6 hours as long as needed (usually 24 hours).30 More extensively prepared travelers might possibly carry antivenom against the area’s dangerous scorpions, if it is available. However, out-ofhospital administration of biologic products, with its attendant risk for severe allergic reaction, should be performed only by trained medical personnel with access to appropriate resuscitation drugs and equipment. It is hard to imagine an expedition of such importance, preparation, and funding that would justify carrying scorpion antivenom, yet did not have access to urgent evacuation measures, such as by helicopter.

BOX 53-3  Previously Recommended Procedures for Administration of Goat-Derived Whole IgG Centruroides

Scorpion Antivenom in the United States

1. Assess for contraindications—Any of the following relative contraindications (in decreasing order of importance) should suggest withholding antivenom in favor of symptomatic and supportive care only: a. Prior administration of antivenom derived from the same host animal species b. Current β-adrenergic blocker use c. History of asthma or atopy d. Current ACE inhibitor use e. History of allergy to the animal species from which the antivenom is derived, allergy to that animal’s milk, or prior extensive exposure to the animal, especially its blood 2. Monitoring a. Continuous ECG monitoring b. Continuous pulse oximetry monitoring c. IV access obtained, preferably with two IV lines 3. Equipment and medications for treating anaphylaxis and respiratory arrest are made available. Medications are not given prophylactically, but are given only if an allergic reaction occurs: a. Epinephrine drip—Add 1 mg epinephrine to 250 mL of 5% dextrose in water (D5W) or normal saline (NS) on a primed IV line with a pump b. IV methylprednisolone c. IV diphenhydramine 4. Antivenom Preparation a. If lyophilized, antivenom is reconstituted with as much sterile NS or D5W as can fill the vial, with gentle rocking to avoid foaming b. Antivenom is then withdrawn from the vial and dissolved in 50 mL of crystalloid and placed on an IV pump 5. Skin Testing a. Up to 0.02 mL of a 1 : 10 dilution of reconstituted antivenom is injected intradermally with a 27- or 30-gauge needle, the site marked with a pen b. Patient is observed for at least 10 minutes for development of a wheal, rash, wheezing, or hemodynamic signs of

1010

anaphylaxis, any of which constitute a positive skin test, which contraindicates further antivenom therapy c. Any allergic reactions treated appropriately with the medications made available above 6. Antivenom Administration a. The antivenom is initially administered at a very slow rate (5 mL/hr), which is doubled every 2 to 3 minutes as long as the patient tolerates the infusion (i.e., develops no signs of anaphylaxis), up to 150 mL/hr b. Infusion of one vial by this method takes approximately 30 minutes, and most patients require only one vial of antivenom c. The patient is observed for at least 1 hour after the initial antivenom infusion is complete before proceeding with additional vials, because most symptoms resolve in this period. If the symptoms have resolved or regressed to a grade I or grade II envenomation and no complications (e.g., aspiration) are suspected, the patient is discharged 7. Discharge Instructions a. Because many patients treated with antivenom develop a delayed hypersensitivity reaction, the patient and caregivers are informed about signs and symptoms of serum sickness before discharge. An urticarial rash developing within a few days to weeks is the most common sign, although malaise, myalgias, and arthralgias also may occur; more serious problems are rare b. The patient may be discharged with prescriptions for antihistamines (hydroxyzine or diphenhydramine) and a tapering dose of corticosteroids to be started if serum sickness develops. Filling these prescriptions and initiating therapy immediately as prophylaxis against serum sickness are not recommended c. Patients treated with whole IgG antivenom should be   warned that they are now likely to be allergic to serum products from the animal species used. Use of   antivenom for subsequent envenomations is relatively contraindicated but can be undertaken with extreme   caution if necessary

ANTIVENOM ADMINISTRATION RECOMMENDATIONS Standard practices for administration of scorpion antivenom vary considerably around the world. Because antivenoms are biologic products, their use carries the risk for inducing both immediate and delayed allergic reactions (i.e., anaphylaxis and serum sickness, respectively). In general, therefore, antivenom is indicated for patients who are more seriously ill with systemic signs and symptoms, rather than for patients with local pain and paresthesias or other minor effects. Most scorpion anti­ venoms available worldwide are whole IgG products, which carry a higher risk for allergic reactions than do Fab fragment antivenoms. Although, in the United States, the older goat-derived whole IgG antivenom is no longer available and the Fab fragment antivenom was only recently approved, considerable experience exists with the administration of these products. The typical procedure previously used for administering whole IgG scorpion antivenom is shown in Box 53-3. This procedure can be considered whenever giving animal-derived whole IgG antisera for scorpion envenomation. Since early 2010, a Fab fragment antivenom produced in Mexico has been frequently used in the United States (Arizona) for serious Centruroides scorpion envenomation, initially only through an experimental protocol but now approved for wider use. Patients given Fab fragment antivenom are closely monitored with continuous ECG and pulse oximetry in a setting where rapid treatment of acute allergic reaction is possible, usually in an emergency department or ICU. The product package insert recommends readiness with intravenous therapy with epinephrine, corticosteroids, and diphenhydramine should an allergic reaction occur, but preadministrative skin testing is not performed. Consultation with toxicologists experienced in treating C. sculpturatus envenomations can be obtained by calling the Banner Good Samaritan Poison and Drug Information Center in Phoenix at 602-495-4884 or the Arizona Poison and Drug Information Center in Tucson at 520-626-7899.

Prevention Because on-scene treatment options for scorpion stings are quite limited, preventive measures are a larger concern for wilderness medicine. The following guidelines are recommended when staying or traveling in scorpion-endemic areas: • Shake out your clothes and shoes before putting them on • Check your sleeping bag/blanket before going to sleep, especially if it is located on the ground • Consider clearing debris from the campsite, to decrease places where scorpions can hide • Be on higher alert for scorpions during the warmer months of the year, when stings are more common Many scorpion stings result from human practices that place persons at risk. Residences with small cracks and crevices offer many hiding places, increasing the risk for human–scorpion interactions. In several countries, playing or working outdoors with inadequate protective clothing, especially in the early evening during warm months, is associated with most scorpion stings. In scorpion-infested areas, clothing, shoes, packages, and camping gear should be shaken out and checked for scorpions. Footwear is recommended. Unnecessary ground cover and debris should be removed from around homes to reduce potential nesting places. Certain insecticides, including organophosphates, pyrethrins, and several chlorinated hydrocarbons, are known to kill scorpions. Home spraying is often ineffective because the insecticide does not come in contact with the scorpion. Spraying insecticides around the home can work indirectly by killing other insects in the area and reducing the scorpions’ food supply. A village-wide scorpion eradication program with pyrethroid insecticides in the state of Morelos, Mexico, reduced the incidence of scorpion stings by 17%.164

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 54 

  Bites by Venomous Reptiles in Canada, the United States, and Mexico ROBERT L. NORRIS, JR., SEAN P. BUSH, AND JENNIFER COHEN SMITH

The medical impact of venomous reptiles in the “New World” is relatively low when compared with that in the Eastern Hemisphere. Recent estimates suggest approximately 300,000 snakebites per year in North America and Latin America, with approximately 4000 deaths, compared with more than 2 million bites per year in the Eastern Hemisphere, with approximately 80,000 deaths.83 Although these estimates are inexact, given major barriers to data gathering in developing regions of the world, they paint a picture of snakebite at a “macro” level in the New World as an annoyance, but as a major health issue on the other side of the planet. However, the bites of rattlesnakes or Gila monsters that occur in North America are very significant to the individual victims and to those called on to render care in the field and hospital. This chapter reviews venomous reptiles of major medical importance in Canada, the United States, and Mexico, detailing clinical effects and proper approach to management of their bites. A general discussion of antivenom therapy is included. Venomous snakes are discussed first, followed by venomous lizards.

Venomous Snakes SCOPE OF THE PROBLEM The oft-quoted number of venomous snakebites in the United States is 7000 to 8000 per year. This estimate stems from work originally done in the late 1960s by Dr. Henry Parrish164 and expanded on by Dr. Findley Russell.176 Parrish estimated deaths due to snakebite in the United States to be about 15 per year.164 No rigorous, systematic review has ever been done in the United States to determine a precise incidence of venomous snakebite, but compared with much of the developing world, the problem is relatively uncommon. A review of bites by native U.S. venomous snakes reported to the American Association of Poison Control Centers (AAPCC) from 2001 through 2005 revealed 23,676 cases (average 4735 per year) with 14 total deaths (just under 3 per year).190 Given that some unknown percentage of snakebites go unreported to poison control centers, these

For online-only figures, please go to www.expertconsult.com

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

numbers are an underestimate but give an idea of the scope of the problem in the United States. The incidence of snakebite in Canada is much lower than in the United States because of fewer snake species and numbers in colder climates. In Mexico, snakebite has greater medical importance because Mexico has more venomous snake species than any other nation in the New World.34 An estimated 3000 snakebites, with as many as 150 deaths, occur in Mexico each year.74,192 Table 54-1 lists the species of dangerous venomous reptiles found in Canada, the United States, and Mexico.35 All of the medically important North American venomous snakes are in the families Viperidae (subfamily Crotalinae, the pit vipers) and Elapidae (subfamily Elapinae [the coral snakes] and subfamily Hydrophiinae [the sea snakes]). Being poikilothermic, snakes rely on environmental heat energy to support locomotion, feeding, digestion, and reproduction. Thus the number of species decreases as the distance from the equator increases. Pit vipers are widely dispersed throughout most of the New World south of southern Canada (i.e., south of 55° north latitude).148 North American pit vipers include the rattlesnakes (genera Crotalus and Sistrurus); copperheads, cottonmouth water moccasins, and cantils (genus Agkistrodon); and numerous species unique to Latin America (genera Atropoides [jumping pit vipers], Bothriechis [palm-pit vipers], Bothrops [lancehead pit vipers], Cerrophidion [montane pit vipers], Ophryacus [Mexican pit vipers], and Porthidium [hognose pit vipers]). There are three pit viper species (all rattlesnakes) found in Canada, 18 in the United States, and approximately 50 in Mexico.35 Rattlesnakes are the most widespread pit vipers, found throughout much of North America (Figures 54-1 to 54-10). At least one species is found in each of the 48 contiguous states except Maine. Copperheads (Agkistrodon contortrix) are found in the central and southeastern United States and westward into the Big Bend region of Texas (Figure 54-11). Cottonmouth water moccasins (Agkistrodon piscivorus) are found in the southeast

from Virginia to Florida and extend westward into central Texas (Figure 54-12). In Mexico, copperhead and cottonmouth snakes are replaced by the cantils, Agkistrodon bilineatus (Figure 54-13) and Agkistrodon taylori. In terms of elapids, coral snakes (akin to cobras [Naja sp.]), mambas (Dendroaspis sp.), and kraits (Bungarus sp.) of the Eastern Hemisphere are the only land-dwelling members of this family in North America, with two genera (Micrurus and Micruroides) on the continent (Figures 54-14 to 54-16). There are no coral snakes indigenous to Canada and only three species in the United States, but 16 species are found in Mexico. In the United States, these colorful reptiles are found in Arizona (Sonoran coral snake, Micruroides euryxanthus), the southeastern United States (eastern coral snake, Micrurus fulvius), and Texas (Texas coral snake, Micrurus tener [formerly M. fulvius tenere]). Mexican coral snakes include Micruroides euryxanthus and 15 Micrurus species.35 One species of sea snake (Pelamis platurus) reaches the southwestern coast of North America, occasionally visiting the coast of southern California. Sea snakes are discussed in Chapters 55 and 81. The largest and most cosmopolitan snake family, Colubridae, consists largely of species that are completely harmless. However, there are occasional reports, particularly in tropical regions of the world, of human envenomations and even deaths caused by a handful of colubrid species (see Chapter 55). These species possess secretory glands (Duvernoy’s glands) and enlarged maxillary teeth (sometimes grooved) in the rear of their mouths (opisthoglyphous). Secretions from these glands are variable, depending on the species, with a number including proteolytic enzymes and phospholipases.98 The venoms may help to immobilize, kill, and digest prey and, when injected into humans, may cause envenomation—generally limited to pain, soft tissue swelling, bruising, and blister formation. Such local consequences have been reported in the United States after bites by the western hognose snake (Heterodon nasicus)214 and the wandering garter

TABLE 54-1  Venomous Reptiles of Canada, the United States, and Mexico Genus Pit Vipers Agkistrodon

Atropoides

Bothriechis

Bothrops Cerrophidion

Crotalus

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Species

bilineatus contortrix piscivorus taylori mexicanus nummifer occiduus olmec aurifer bicolor rowleyi schlegelii asper barbouri godmani petlalcalensis tzotzilorum adamanteus aquilus atrox basiliscus catalinensis cerastes enyo horridus intermedius lannomi

Common Name Cantils, copperheads, water moccasins Common cantil Copperhead Cottonmouth water moccasin Taylor’s cantil Jumping pit vipers Central American jumping pit viper Mexican jumping pit viper Guatemalan jumping pit viper Tuxtlan jumping pit viper Palm pit vipers Yellow-blotched palm pit viper Guatemalan palm pit viper Mexican palm pit viper Schlegel’s viper Lanceheads Terciopelo Montane pit vipers Barbour’s montane pit viper Godman’s montane pit viper Petlalcala montane pit viper Tzotzil montane pit viper Rattlesnakes Eastern diamondback rattlesnake Querétaro dusky rattlesnake Western diamondback rattlesnake Mexican west coast rattlesnake Santa Catalina rattlesnake Sidewinder Baja California rattlesnake Timber/canebrake rattlesnake Mexican small-headed rattlesnake Autlán rattlesnake

Canada

U.S.

Mexico

— — — —

— + + —

+ + — +

— — — —

— — — —

+ + + +

— — — —

— — — —

+ + + +

—

—

+

— — — —

— — — —

+ + + +

— — — — — — — + — —

+ — + — — + — + — —

— + + + + + + + + +

Genus

Ophryacus Porthidium

Sistrurus

Elapids Micruroides Micrurus

Pelamis Lizards Heloderma

Species

Common Name

lepidus mitchelli molossus oreganus oreganus abyssus oreganus caliginus oreganus cerberus oreganus concolor oreganus helleri oreganus lutosus oreganus oreganus polystictus pricei pusillus ravus ruber scutulatus simus stejnegeri tigris tortugensis totonacus transversus triseriatus viridis

Rock rattlesnake Speckled rattlesnake Black-tailed rattlesnake Western rattlesnake Grand Canyon rattlesnake (formerly C. viridis abyssus) South Coronado Island rattlesnake (formerly C. viridis caliginus) Arizona black rattlesnake (formerly C. viridis cerberus) Midget faded rattlesnake (formerly C. viridis concolor) Southern Pacific rattlesnake (formerly C. viridis helleri) Great Basin rattlesnake (formerly C. viridis lutosus) Northern Pacific rattlesnake (formerly C. viridis oreganus) Mexican lance-headed rattlesnake Twin-spotted rattlesnake Tancitaran dusky rattlesnake Mexican pygmy rattlesnake Red diamond rattlesnake Mohave rattlesnake Middle American rattlesnake Long-tailed rattlesnake Tiger rattlesnake Tortuga Island diamond rattlesnake Totonacan rattlesnake Cross-banded mountain rattlesnake Mexican dusky rattlesnake Prairie rattlesnake (formerly C. viridis abyssus [Grand Canyon rattlesnake], C. viridis caliginis [Coronado Island rattlesnake], C. viridis cerberus [Arizona black rattlesnake], C. viridis concolor [midget faded rattlesnake], C. viridis lutosus [Great Basin rattlesnake], C. viridis nuntius [Hopi rattlesnake], C. viridis viridis [prairie rattlesnake]) Ridge-nosed rattlesnake Mexican horned pit vipers Black-tailed horned pit viper Mexican horned pit viper Hognose pit vipers Dunn’s hognose pit viper Colima hognose pit viper Rainforest hognose pit viper Yucatán hognose pit viper Rattlesnakes Massasauga Pygmy rattlesnake

willardi melanurus undulates dunni hespere nasutum yucatanicum catenatus miliarius euryxanthus bernadi bogerti browni diastema distans elegans ephippifer fulvius (formerly M. fulvius fulvius) laticollaris latifasciatus limbatus nebularius nigrocinctus pachecogili proximans tener (formerly M. fulvius tenere) platurus

suspectum horridum

Canada

U.S.

Mexico

— — —

+ + +

+ + +

— — — — — — + — — — — — — — — — — — — — +

+ — + + + + + — + — — + + — — + — — — — +

— + — — + — — + + + + + + + + + + + + + +

—

+

+

— —

— —

+ +

— — — —

— — — —

+ + + +

+ —

+ +

+ —

Coral snakes Sonoran (Arizona) coral snake Coral snakes Blotched coral snake Bogert’s coral snake Brown’s coral snake Variable coral snake West Mexican coral snake Elegant coral snake Oaxacan coral snake Eastern coral snake, Harlequin coral snake

—

+

+

— — — — — — — —

— — — — — — — +

+ + + + + + + —

Balsan coral snake Long-ringed coral snake Tuxtlan coral snake Ixtlán coral snake Central American coral snake Azpotitlán coral snake Nayarit coral snake Texas coral snake

— — — — — — — —

— — — — — — — +

+ + + + + + + +

Sea snakes Yellow bellied sea snake (see Chapters 55, 80, and 81 for discussion of sea snake bites)

—

+

+

— —

+ —

+ +

Venomous lizards Gila monster Beaded lizard

Modified from Campbell JA, Lamar WW: The venomous reptiles of the Western Hemisphere, Ithaca, NY, 2004, Comstock. +, Present.

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

TABLE 54-1  Venomous Reptiles of Canada, the United States, and Mexico—cont’d

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 54-1  Eastern diamondback rattlesnake (Crotalus adamanteus) is the largest pit viper of the United States and can attain lengths  of 2 m (6.5 feet). (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-2  Western diamondback rattlesnake (Crotalus atrox) causes many serious bites in the U.S. Southwest. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-3  Mohave rattlesnake (Crotalus scutulatus) has two geographic populations in terms of venom composition, one with predominantly neurotoxic effects and one with more local sequelae. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-4  Timber rattlesnake (Crotalus horridus) is a large, dangerous snake of the eastern United States. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-5  Canebrake rattlesnake (Crotalus horridus), a form of the timber rattlesnake found in Florida, Georgia, and South Carolina, possesses a more neurotoxic and myotoxic venom than does its more northern variant. (Courtesy Michael Cardwell and Medtoxin Venom Labs.)

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FIGURE 54-6  Prairie rattlesnake (Crotalus viridis viridis) is a widely distributed species of the western United States. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-9  Tropical rattlesnake (Crotalus simus, formerly C. durissus durissus) is a large, dangerous species found in southern Mexico. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-11  Southern copperhead (Agkistrodon contortrix contortrix) has markings that make it almost invisible when lying in leaf litter. (Courtesy Michael Cardwell and Medtoxin Venom Labs.)

FIGURE 54-8  Southern Pacific rattlesnake (Crotalus oreganus helleri, formerly C. viridis helleri) replaces C. oreganus oreganus in southern California and northwestern Mexico. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-10  Western pygmy rattlesnake (Sistrurus miliarius streckeri) is one of the smaller rattlesnake species of North America. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

FIGURE 54-12  Cottonmouth water moccasin (Agkistrodon piscivorus) exhibiting its threat display. This snake is found most often around standing water sources in the southeastern United States. (Courtesy Sherman Minton, MD.)

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

FIGURE 54-7  Northern Pacific rattlesnake (Crotalus oreganus oreganus, formerly C. viridis oreganus) is a moderate-sized but very toxic snake of the Pacific Northwest. (Courtesy Joel Levis, MD.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 54-13  Cantil (Agkistrodon bilineatus) is a close relative of the copperheads (A. contortrix) and cottonmouths (A. piscivorus) of the United States. This pit viper is found in Mexico and Central America. (Courtesy Michael Cardwell and William W. Lamar.)

FIGURE 54-16  Sonoran coral snake (Micruroides euryxanthus) is also known as the Arizona coral snake. No documented fatality has followed a bite by this species. (Courtesy Michael Cardwell and Jude McNally.)

Throughout North America, pit vipers are responsible for approximately 98% of venomous snakebites.190 Coral snakes tend to be secretive in nature and possess a less efficient venom delivery mechanism compared with pit vipers (see Anatomy, later). Coral snake bites are infrequent, even in regions where the snakes are relatively common. The 2008 report of the AAPCC Toxic Exposure Surveillance System recorded 99 coral snake bites in the United States that year.15

ANATOMY

FIGURE 54-14  Eastern coral snake (Micrurus fulvius) has a highly potent venom but is secretive, and bites are uncommon. (Courtesy Michael Cardwell, Extreme Wildlife Photography and Medtoxin Venom Labs.)

snake (Thamnophis elegans vagrans).75 Effective envenomation generally requires that these snakes maintain a bite for several minutes in order to get sufficient venom into the tissues via their posterior teeth. These bites in the United States do well with conservative treatment alone, but it is important that they be differentiated from bites by pit vipers that may require antivenom therapy. A careful description of the involved snake should be obtained.

Pit Vipers Pit vipers of North America come in a wide range of sizes. Smaller rattlesnakes include the sidewinders (Crotalus cerastes), ridgenosed rattlesnakes (Crotalus willardi), and pygmy rattlesnakes (Sistrurus miliarius), whose adult lengths are routinely less than 65 cm (25.6 inches).114 At the other extreme, the eastern diamondback rattlesnake (Crotalus adamanteus) can exceed 2 m (6.5 feet).114 The term pit viper comes from the presence of paired, thermal receptor organs (pits) present on the forward portion of the snakes’ heads (Figure 54-17). Also known as foveal organs, these structures assist with prey location, aiming strikes (Figure 54-18),

Pit vipers

Triangular head

Keeled scales Elliptical pupil Nostril

Pit

FIGURE 54-15  Texas coral snake (Micrurus tener, formerly M. fulvius tenere), which although dangerous, tends to cause less severe envenomation than does Micrurus fulvius. (Courtesy Michael Cardwell and the Gladys Porter Zoo.)

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FIGURE 54-17  Pit viper’s head. Note the elliptical pupil and the heatsensing pit for which these reptiles are named. Viewed from above, the head has a distinctly triangular shape. Many nonvenomous snakes also possess triangular heads, and this is not a reliable means of differentiation. (Courtesy Marlin Sawyer, 1994.)

Elliptical pupil

FIGURE 54-18  Paired heat-sensing pits of the pit vipers used to help the snake locate its prey, direct its strike, and probably determine the volume of venom to be expended. (Courtesy Marlin Sawyer, 1994.)

and metering venom dose through a neurologic feedback loop with the elaborate crotaline venom delivery apparatus221 (Figure 54-19). Encased in the muscularis compressor glandulae, bilateral venom glands are located at the sides of the head behind the eyes. These glands, which produce and store venom, are connected through ducts to more anterior accessory glands, whose secretions serve to potentiate the venom.178 From here, the venom moves forward through other ducts into the venom sheaths located adjacent to the proximal portion of the hollow, needle-like fangs with which the snake pierces its victim in a stabbing motion. These fangs, found on the anterior surfaces of the maxillary bones, are large (up to 20 mm [0.79 inches] in big rattlesnakes114) and highly mobile. At rest, the snake folds the fangs against the roof of its mouth. For a strike, the fangs are brought into an upright position, perpendicular to the maxillae. The snake has voluntary control over its fangs and can open its mouth without raising the fangs or can raise each fang individually at will. The fangs are relatively brittle and fracture or become dull with time and use. Replacement fangs, at varying stages of development behind the functional set, move forward on the

Maxilla Fangs Duct Accessory gland Duct Main venom gland

FIGURE 54-19  Venom delivery apparatus of a pit viper. Venom is produced in large venom glands just posterior to the eyes and is passed through a duct system into the hollow, anterior fangs when the snake bites. (Courtesy Marlin Sawyer, 1994.)

FIGURE 54-20  Rattlesnake skull. Replacement fangs are behind the primary, functional fangs. The smaller teeth of the palatine, pterygoid, and mandibular bones are used for gripping food. (Courtesy Michael Cardwell/Extreme Wildlife Photography.)

maxillary bone when needed (Figure 54-20). Pit vipers can strike at speeds of up to 2.4 m (8 feet) per second and reach distances of approximately one-half their body length.221 Table 54-2 lists venom yields for various North American pit vipers. The fastest pit viper can crawl at a maximum speed of approximately 4.8 km (3 miles) per hour, which approximates an average adult walking pace.221 Crotaline snakes do not chase people. Accounts suggesting otherwise can be explained by snakes’ poor eyesight; when threatened, they may unwittingly retreat in the direction of people.

TABLE 54-2  Venom Yields of Some Medically

Important Snakes of North America

Species Crotalus adamanteus Crotalus atrox Crotalus cerastes Crotalus durissus Crotalus horridus Crotalus molossus Crotalus oreganus helleri (formerly C. viridis helleri) Crotalus oreganos (formerly C. viridis oreganus) Crotalus scutulatus Crotalus viridis Sistrurus catenatus Sistrurus miliarius Agkistrodon contortrix Agkistrodon piscivorus Micruroides euryxanthus Micrurus fulvius Micrurus nigrocinctus

Maximum Venom   Yield (mg Dry Weight) 848 1145 63 514 (average) 229 540 390

Reference * * * * * * *

289

*

141 162 33 18 (average) 45 150 6 38 20

* * † * ‡ ‡ § § §

*From Klauber LM: Rattlesnakes: Their habits, life histories, and influence on mankind, ed 2, Berkeley, Calif, 1997, University of California Press. †From Glenn JL, Straight RC: The rattlesnakes and their venom yield and lethal toxicity. In Tu AT, editor: Rattlesnake venoms: Their actions and treatment. New York, 1982, Marcel Dekker, pp 3-119. ‡From Parrish HM: Poisonous snakebites in the United States, New York, 1980, Vantage Press. §From Roze JA: Coral snakes of the Americas: Biology, identification, and venoms, Melbourne, Fla, 1996, Krieger.

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

Nostril

Pit

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 54-21  Although most members of the largely harmless Colubridae snake family have round pupils, some, like this lyre snake (Trimorphodon biscutatus), a mildly venomous, rear-fanged colubrid of the southwestern United States, have elliptical pupils similar to those of pit vipers. (Courtesy Robert L. Norris, Jr., MD.)

The characteristic forked tongue of the snake is an olfactory tool and possesses none of the offensive “stinging” function ascribed to it in folklore. The snake extends its tongue to detect chemical odors in its environment. The tongue is then retracted and its tips placed into the paired Jacobson’s organs, lined with olfactory epithelium, in the roof of its mouth. This sensory system is highly sensitive, allowing the snake to identify potential mates, locate prey, and track down an intended food item that has been bitten by the snake and released to die. Pit vipers have elliptical, or “catlike,” pupils (see Figure 54-17), whereas most North American harmless snakes have round pupils. A few, essentially harmless, rear-fanged colubrids in the United States, such as the night snake (Hypsiglena torquata) and lyre snake (Trimorphodon biscutatus) (Figure 54-21), also possess elliptical pupils but lack facial pits. Although these opisthoglyphous species possess Duvernoy’s glands (see earlier discussion), they are innocuous creatures. They are reluctant to bite humans, and their salivary toxins are likely to cause few signs or symptoms, other than slight swelling, bruising, and pain, in the event of a bite. The two small species of boas in North America, the rosy boa (Lichanura trivirgata) and the rubber boa (Charina bottae), also possess elliptical pupils, but their body form (more cigar-shaped and lacking the broad, triangular head of a pit viper) and skin patterns are very different from those of any crotaline. The caudal rattle of the rattlesnake is composed of loosely interlocked plates of keratin that emit a buzzing sound when the snake rapidly vibrates its tail. This characteristic sound serves as a warning to a perceived threat. A new segment is added to the rattle each time the snake sheds its skin, which can occur from one to several times each year, depending on its age, health, and feeding success. Newborn rattlesnakes have a single button present at birth (Figure 54-22). Not until after their first shed do they possess a true rattle that can create a sound. Rattles are commonly broken off during the snake’s life, so the number cannot be used reliably to determine age. Although rattlesnakes are generally quick to sound a warning when threatened, it is a misconception that they will always do so before striking. Another helpful anatomic feature of pit vipers in the United States is the scale pattern on the underside of the tail—the subcaudal scales. The junction of a dead snake’s body and its tail can be easily ascertained by viewing its ventral side. At this location is a large scale (sometimes divided) known as the anal plate. Just distal to this in U.S. pit vipers is a sequence of single scales that entirely cross the ventral surface. In nonvenomous snakes and in coral snakes (as well as some Latin American pit vipers), the subcaudal scales are paired (i.e., each covers approximately half the width of the tail) (Figures 54-23 and 54-24). This feature 1018

FIGURE 54-22  Newborn western diamondback rattlesnake (Crotalus atrox). Note the single “button” of its “rattle.” (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

becomes clinically useful when a U.S. snakebite victim brings in the body of a decapitated snake for identification and when the skin pattern is unfamiliar to the physician. Coral Snakes Coral snakes are identified primarily by color pattern. U.S. coral snakes are banded in a red-yellow-black-yellow-red pattern (Figure 54-25), and the bands completely encircle the snake’s body. The contiguity of the red and yellow bands distinguishes U.S. coral snakes from a number of harmless mimics (e.g., several kingsnakes and milksnakes, genus Lampropeltis), which generally have red and yellow bands separated by black bands. This can best be remembered by recalling the phrase “red on yellow, kill a fellow; red on black, venom lack” or by considering that the red and yellow lights on a traffic signal are the warning lights. Contiguous red and yellow bands can be used to reliably identify coral snakes only in North America, north of Mexico City. Farther south, bicolor (red and black) coral snake species may be found, and there are many harmless mimics that closely resemble these venomous serpents.150 One harmless U.S. colubrid, the shovelnosed snake (Chionactis species), has contiguous red and yellow bands, but the bands do not completely encircle its body and the snake is completely inoffensive. In exceptionally rare cases, coral snakes can be all black (melanistic) or albino.143 The coral snake venom apparatus is much less complex than that of pit vipers. The paired venom glands connect through

Single row of subcaudal scales Anal plate

Anal plate (may be divided) Anal plate

Double row of subcaudal scales

Rattles

Rattlesnakes

No rattles Copperheads and cottonmouths

Colubrids and coral snakes

FIGURE 54-23  Subcaudal scale patterns of U.S. snakes. In the United States, pit vipers have a single row of scales on the ventral side of the tail, just distal to the anal plate. Most harmless colubrid snakes have double rows of subcaudal scales, as do coral snakes and some species of Latin American pit vipers. (Courtesy Marlin Sawyer, 1994.)

Single subcaudal scale

Anal plate

Fixed fang

Double subcaudal scales

FIGURE 54-26  Coral snake’s skull. Note the slightly enlarged anterior maxillary fang that is fixed in its upright position. (Courtesy Marlin Sawyer, 1994.)

VENOMS Pit Vipers

FIGURE 54-24  Comparison of the subcaudal scale pattern of a rattlesnake on the left with a harmless rat snake on the right. (Courtesy Robert L. Norris, Jr., MD.)

ducts to slightly enlarged, hollow fangs that are fixed in an upright position in the forward portion of the maxillae (Figure 54-26). For the coral snake to inflict a potentially serious bite, it must chew on the victim to inject a sufficient volume of venom through its relatively small fangs. These animals are not capable of striking out with the stabbing motion of a pit viper. In the vast majority of coral snake bite cases, the victim was handling the creature when bitten; in some cases, this occurred when the victim misidentified the snake as a harmless kingsnake.167

FIGURE 54-25  Comparison of the Texas coral snake (Micrurus tener) with the harmless Mexican milk snake (Lampropeltis triangulum annulata). Coral snake (bottom) has contiguous red and yellow bands, whereas red and yellow bands of the milk snake are separated by black. (Courtesy Charles Alfaro.)

Snake venoms are extraordinarily variable and complex chemical cocktails of approximately 100 distinct molecular moieties. Some of the better characterized and more interesting of these include the phospholipase A2 neurotoxins, metalloproteinases, and thrombin-like enzymes.53,109 Phospholipase A2 neurotoxins are among the most toxic of pit viper venom components and can increase lethality of the venom 10- to almost 100-fold.69 The first of these, crotoxin, was isolated in 1938 from the South American rattlesnake (Crotalus durissus terrificus).1 Phospholipase A2 neurotoxins noncompetitively bind to presynaptic calcium channels, inhibiting acetylcholine release and thereby blocking neurotransmission at the neuromuscular junction, inactivating the muscle. This can cause paralysis of the muscles of respiration, for example, and lead to respiratory difficulty. Additionally, phospholipase A2 damages muscle cell membranes, allowing calcium influx and release of creatine and creatine kinase (CK), which can progress to diffuse myonecrosis and rhabdomyolysis.110 Metalloproteinases, the enzymes that cause much of the locally destructive effects of pit viper envenomation, activate tumor necrosis factor alpha and stimulate endogenous human metalloproteinases, intensifying inflammation. Certain metalloproteinases, the hemorrhagins, cause leakage of red blood cells out of the vasculature, leading to ecchymosis (characteristic of more severe pit viper bites) and fluid shifts.82,217 High venom toxicity is generally associated with phospholipase A2 neurotoxins, which are typically (but not always) inversely related in proportionate concentrations to the tissue-damaging metalloproteinases.137 Thrombin-like enzymes cause consumptive coagulopathy but do not directly activate coagulation factors or form a complex with antithrombin III (and so are not affected by heparin). Disintegrins bind to proteins on blood platelets, blocking their combination with fibrinogen necessary to form clots.31 Bradykinins cause hypotension, vomiting, and pain. Hyaluronidase decreases the viscosity of connective tissues, allowing venom to spread. Lysolecithin, a by-product of the enzymatic action of phospholipase A2, damages mast cell membranes and results in histamine release.42 Pit viper venom has both offensive (i.e., food gathering) and defensive functions. In predatory strikes, venom immobilizes prey, facilitates its retrieval by altering its scent, and accelerates digestion.41,88,95 Defensive strikes are meant to deter predators and tormentors. The amount of venom injected differs from bite to bite. Factors such as prey size and species, duration of fang contact, and time elapsed since last meal influence the amount of venom released.88,95 Rattlesnakes have been shown to inject significantly more venom into large mice than into small mice.88 The mass of venom expended differs between predatory and defensive bites. In comparison studies, venom expenditure by North American pit vipers appears to be greater in defensive bites than in predatory bites.95 In one comparison, the northern Pacific rattlesnake (Crotalus oreganus [formerly C. viridis oreganus]) expended almost four times more venom when biting a hand model (defensive) than when biting a mouse (predatory).88,95 The most important factor influencing potential venom delivery is the size of the snake.95 A direct relationship in both predatory and 1019

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

Anal plate

PART 6  ANIMALS, INSECTS, AND ZOONOSES

defensive bites has been demonstrated between snake length and mass of venom expended.85,95 A popular belief is that juvenile rattlesnakes are more dangerous than are adult snakes because their venom is more toxic and they are unable to control the volume released. The venom of some juvenile rattlesnakes may be slightly more toxic, but larger rattlesnakes are capable of delivering much greater amounts of venom in a bite. Juvenile prairie rattlesnakes (Crotalus viridis [formerly C. viridis viridis]) have been shown in one small study to possess venom that is 2 to 3 times more toxic than that of adults.62 Large adult snakes, however, deliver an average of 17 times (range, approximately 10 times to greater than 100 times) more venom than do juveniles.85 The ability to control venom expenditure has been demonstrated in juvenile rattlesnakes. In a series of first exposures to different-sized prey, “naive” juvenile rattlesnakes injected similar quantities of venom into all size classes. However, in the second series of exposures, “experienced” snakes injected significantly more venom into larger prey.86 The clinical relevance of this is uncertain. In many species, venom composition appears to change as the snake ages. Phospholipase A2 activity decreases with age, probably accounting for some decrease in toxicity. Proteolytic activity increases with age, possibly to aid digestion of larger prey eaten by older, larger snakes.85 Coagulopathic effects can be different between juvenile and adult western diamondback rattlesnakes (Crotalus atrox), partly because of the greater amounts of thrombin-like enzymes in younger snakes.172 Clinical studies showing that envenomations by large rattlesnakes are generally more severe than are envenomations by smaller ones corroborate and complement these findings in the laboratory and the field.87,105 Juvenile pit vipers can, however, deliver a very serious, even life-threatening, envenomation. Venom characteristics vary with geographic origin of the snake.71 For example, certain populations of the Mohave rattlesnake (less correctly spelled “Mojave”) (Crotalus scutulatus) cause human neurotoxicity with severe envenomation while causing minimal local tissue destruction and no hemorrhagic effects.46,106 Neurotoxic findings may include respiratory difficulty, generalized weakness, and cranial nerve palsies.46 The venoms of these snakes possess a presynaptic neurotoxin, originally designated “Mojave toxin”6 (and this spelling persists), and are classified as venom A populations. Venom B populations lack Mojave toxin and are less toxic. Bites by venom B snakes result in consequences more typical of most rattlesnake envenomations: soft tissue swelling, necrosis, and coagulopathy. Venom A populations are found in California, western Arizona, Nevada, Utah, New Mexico, and Texas. Venom B populations are found in eastern parts of Arizona. A zone of intergradation between venom A and venom B populations occurs along a line between Phoenix and Tucson.89,219 Envenomations manifesting both venom A and venom B effects (i.e., neurotoxicity plus coagulopathy and swelling) have been observed in inland southern California. Toxins with structures and physiologic effects similar to those of Mojave toxin have been isolated from venoms of other species of rattlesnakes, including southern Pacific rattlesnakes (Crotalus oreganus helleri [formerly C. viridis helleri ]), prairie rattlesnakes (C. viridis [formerly C. viridis viridis ]), midget faded rattlesnakes (C. concolor [formerly C. viridis concolor ]), tropical rattlesnakes (C. durissus), timber rattlesnakes (Crotalus horridus), and tiger rattlesnakes (Crotalus tigris).64,70,72,94,215 Geographic differences occur in the venoms of other snakes as well. Timber rattlesnakes (sometimes referred to as canebrake rattlesnakes) (C. horridus) from Florida, Georgia, and South Carolina possess more “canebrake toxin,” a neurotoxic and myotoxic component, than do specimens from Alabama, Mississippi, Tennessee, and North Carolina.72 Differences in concentration of this toxin correlate with varying clinical effects seen after bites by this species from different geographic regions.39 Neurotoxicity has been clinically associated with severe myotoxicity in many cases.28,39,50,106 Severe rhabdomyolysis and myoglobinuric renal failure have been reported after Mohave rattlesnake envenomation and are thought to be related to Mojave toxin.106 The association between neurotoxicity and myotoxicity has been confirmed in laboratory animals.7 C. horridus specimens possessing significant amounts of the neurotoxin, canebrake 1020

toxin, produce a rise in serum CK levels as a biochemical signature of significant envenomation. The rise in CK level appears to parallel severity of envenomation by these snakes.39 Autopsy findings have demonstrated that myonecrosis in this setting is systemic and not limited to the bite site.39,112 Concomitant rises in MB fractions of CK can occur in the absence of any clinical evidence of cardiac damage. In one such case, troponin-T level was normal despite abnormal total CK and CK-MB levels.39 Lesser CK elevations (usually less than 500 units/L) may be seen with other rattlesnake bites, such as that of the eastern diamondback (C. adamanteus). In these cases, the elevations appear to more closely parallel local effects.39 Mojave toxin is thought to inhibit acetylcholine release at the presynaptic terminal of the neuromuscular junction.46 Myokymia, or muscle fasciculations, may be considered by some to be a manifestation of neurotoxicity. This phenomenon, however, occurs through a different mechanism than does Mojave toxin– induced neurotoxicity. Myokymia is believed to be caused by interaction of certain venom components with calcium or calciumbinding sites on the nerve membrane.46 Myokymia has been reported to occur after envenomation by certain species of rattlesnakes, most notably the southern Pacific rattlesnake, C. oreganus helleri (formerly C. viridis helleri).14,211 The variability of southern Pacific rattlesnake venom, for example, has clinical implications. It has been suggested that envenomation by specimens possessing Mojave toxin responds well to treatment with the current U.S. pit viper antivenom, CroFab Crotalidae Polyvalent Immune Fab (Ovine) likely because the antivenom was developed using C. scutulatus venom A, which contains Mojave toxin. In contrast, certain clinical manifestations, such as myokymia, are much less responsive to CroFab, possibly because of non-neutralized or partially neutralized components in southern Pacific rattlesnake venom. These envenomations often require more antivenom than do those by Mojave toxin–possessing specimens. Novel venom components, such as hellerase or yet-to-be characterized small, basic, neurotoxic peptides, may explain this phenomenon.183 Many modern medicines are derived from reptile venoms. These are being investigated and used for treatment of heart disease, stroke, cancer, diabetes, hypertension, pain, and other conditions. Some of the most promising of these venom-derived pharmaceuticals come from the disintegrins.31 Coral Snakes Coral snake venoms are less complex than are pit viper venoms and have received less research attention. Micrurus and Micruroides venoms have minimal proteolytic activity but contain the spreading enzyme hyaluronidase and some phospholipase A2.182 The primary lethal component is a low-molecular-weight, postsynaptic neurotoxin that blocks acetylcholine binding sites at the neuromuscular junction.40,204 In addition, the venom contains at least one myotoxic component that may clinically produce a rise in serum CK level.81 What coral snake venom lacks in complexity, it makes up in potency. Among U.S. snakes, Micrurus and Micruroides venom potency, as determined by median lethal dose (LD50) values in mice, is surpassed only by that of the Mohave rattlesnake (C. scutulatus).178 It is indeed fortunate that these reptiles are shy and inoffensive and possess a less effective venom delivery device than do pit vipers.

CLINICAL PRESENTATION Pit Vipers The clinical presentation of pit viper envenomation is quite variable and depends on the circumstances of the bite. Important factors include the species, size, and health of the snake, age and health of the victim, circumstances that led to the bite, number of bites and their anatomic locations, and quality of the care rendered to the victim, both in the field and hospital. Although statistics vary, most bites occur to the lower extremities.164 The next most common anatomic site is an upper extremity, often bitten while the victim is intentionally interacting with the snake (e.g., tormenting the animal, trying to catch it, or

A

TABLE 54-3  Signs and Symptoms Following

Rattlesnake Bites

Sign or Symptom Fang marks Swelling and edema Pain Ecchymosis Vesiculations Change in pulse rate Weakness Sweating and/or chill Numbness or tingling of tongue and mouth or scalp or feet Faintness or dizziness Nausea, vomiting, or both Blood pressure changes Change in body temperature Swelling regional lymph nodes Fasciculations Increased blood clotting time Spherical red blood cells Tingling or numbness of affected part Necrosis Respiratory rate changes Decreased hemoglobin Abnormal electrocardiogram Cyanosis Hematemesis, hematuria, or melena Glycosuria Proteinuria Unconsciousness Thirst Increased salivation Swollen eyelids Retinal hemorrhage Blurring of vision Convulsions Muscle contractions Increased blood platelets Decreased blood platelets

Frequency* 100/100 74/100 65/100 51/100 40/100 60/100 72/100 64/100 63/100 57/100 48/100 46/100 31/100 40/100 41/100 39/100 18/100 42/100 27/100 40/100 37/100 26/100 16/100 15/100 20/100 16/100 12/100 34/100 20/100 2/100 2/100 12/100 1/100 6/100 4/25 42/100

From Russell FE: Snake venom poisoning, New York, 1983, Scholium International, p 281, with permission. *Number of times symptom or sign is reported as observed per total number of patients.

Systemic findings after pit viper bites are extremely variable; any organ system can be affected. Nausea with or without vomiting is common and may occur early in serious bites. The victim may complain of an overall sense of weakness. An odd sense of taste, such as a rubbery, minty, or metallic taste, may be present.178 The victim may complain of numbness of the mouth or tongue.

B

FIGURE 54-27  Rattlesnake envenomation can lead to varying degrees of ecchymosis over time. A, Mottled rock rattlesnake (Crotalus lepidus lepidus) bite in a young man at 24 hours. Note the exudation of red cells into the soft tissues remote from the bite site. The man was bitten on his left thumb. B, Northern Pacific rattlesnake (Crotalus oreganus oreganus) bite to the left pretibial region resulted in extensive ecchymosis of the right lower extremity and extended into his flank (seen here one week after the bite). (Courtesy Robert L. Norris, Jr., MD.)

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

handling a captive specimen). Less often, bites occur to the head, neck, or trunk. Most bites occur around dawn or dusk and during warmer months, when snakes and people are more active outdoors.164 A young, intoxicated male bitten on the hand while intentionally interacting with a snake is a common clinical profile in the United States. About 75% to 80% of pit viper bites result in envenomation. Approximately one in every four to five bites is “dry,” meaning no venom has been injected.165,178 The precise mechanisms behind “dry bites” are unclear. The snake may elect to save its venom for its next meal rather than waste it on a large human. Alternatively, the feedback mechanism may “short-circuit” between the heat-sensing pit organs and the venom delivery apparatus, so that when faced with a huge, heat-radiating mass (a human), the system fails and no venom is expelled. Other possible causes of dry bites include glancing blows that fail to penetrate the skin and an exhausted venom supply. Approximately 35% of bites result in mild envenomations, 25% moderate, and 10% to 15% severe.165 The clinical findings found in crotaline envenomation can be divided into local and systemic signs and symptoms (Table 54-3). After most pit viper bites, severe burning pain at the site begins within minutes. Soft tissue swelling then progresses outward to a variable distance from the bite site. Over hours, a bitten extremity can swell all the way to the trunk. Bites to the face or neck may result in rapid, severe swelling that can compromise the airway.173 Blood may persistently ooze from fang marks, marking the presence of anticoagulant substances in the venom. Ecchymosis is common, both locally and at more remote sites, as the vasculature becomes leaky and red blood cells (RBCs) escape into soft tissues (Figure 54-27). Over a period of hours to days, the patient may develop hemorrhagic or serum-filled vesicles and bullae at the bite site and more proximally, especially if there is a delay in obtaining care (Figure 54-28). Fang marks are usually evident as small puncture wounds, but the precise bite pattern can be misleading.153 Most nonvenomous snakebites result in multiple rows of tiny puncture wounds (from the maxillary, palatine, pterygoid, and mandibular teeth) that usually cease bleeding quickly. Pit vipers also possess palatine, pterygoid, and mandibular teeth, which can result in more than the classic paired puncture marks from the maxillary fangs. Also, a snake may make contact with only a single fang. For this reason, associated signs and symptoms should carry more significance than the bite pattern in determining whether a bite was inflicted by a pit viper or another snake. Some rattlesnake bites result in little or no local pain or swelling despite serious envenomation. For example, serious bites by specimens of Mohave rattlesnakes (C. scutulatus) coming from regions where their venom contains substantial quantities of Mojave toxin (venom-A, see earlier discussion) may result in little if any local findings such as pain, swelling, or ecchymosis. Such a presentation could result in early underestimation of the severity of envenomation by the treating physician.221

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 54-28  Hemorrhagic bleb at the site of a western diamondback rattlesnake (Crotalus atrox) bite at 24 hours. (Courtesy Robert L. Norris, Jr., MD.)

Vital signs may be abnormal, with respiratory and heart rates increased. The victim may experience respiratory distress as a result of neurotoxic components of the venom, especially after bites by venom A–producing Mohave rattlesnakes (C. scutulatus).178 Another important cause of respiratory distress is pulmonary edema from pulmonary artery congestion and translocation of intravascular fluid into alveoli. This can be compounded by myocardial depressant factors in some venoms.178 The victim’s blood pressure may be elevated; however, hypotension, which may progress to frank shock, is more common in severe cases. In the first several hours, hypotension is usually caused by blood pooling in the pulmonary and splanchnic beds. Later, as swelling progresses and fluid exudes into soft tissues, intravascular volume can become significantly depleted. A rare cause of early shock is nonallergic (and possibly allergic) anaphylaxis to the venom itself (see Allergy to Reptile Venom, later).18,29,56,158 Musculoskeletal and neurologic abnormalities may be present. As mentioned previously, some rattlesnake venoms possess one or more components that can cause local or systemic myokymia as a sign of significant envenomation. These repetitive, fine muscle contractions may persist for many hours and are variably responsive to antivenom administration.138,206 Myokymia involving the shoulders, chest wall or torso has been associated with respiratory insufficiency and the need for endotracheal intubation.206 Other findings of neurologic dysfunction can include paresthesias, numbness, and frank motor weakness, especially after bites by some Mohave rattlesnakes (C. scutulatus) and eastern diamondback rattlesnakes (C. adamanteus). Although uncommon, hemorrhage can occur at multiple anatomic locations because of the complex procoagulant, anticoagulant, and metalloproteinase components of some venoms.178 Bleeding can occur in the gingival membranes, renal system (microscopic or frank hematuria), gastrointestinal tract (occultly heme-positive stool, frank blood per rectum, or hematemesis), pulmonary tree (hemoptysis) or central nervous system. Laboratory evaluation of a victim of pit viper bite may reveal significant abnormalities. The white blood cell count may be elevated, reflecting neutrophilic leukocytosis. Hematocrit may be elevated from hemoconcentration or may be depressed secondary to bleeding or hemolysis. Platelet count can drop precipitously as a result of consumptive coagulopathy, sequestration at the bite site, or direct venom effects.216 Serum chemistries may be abnormal. Blood glucose level may be elevated. Muscle damage can result in elevated serum potassium and CK levels. Renal dysfunction may result from hypotension, myoglobin and hemoglobin deposition, and direct venom effects.43 Hepatic dysfunction with elevations of serum transaminases may be seen.142 Coagulation studies may reveal significant abnormalities. Prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT) can be elevated. Fibrinogen levels may be depressed, along with elevation of fibrin degradation products and D-dimer levels.9 In resourceconstrained environments, a 20-minute whole blood clotting test 1022

can be used to diagnose coagulopathy. A few milliliters of blood are drawn and placed in a clean, new, dry, glass test tube and allowed to sit, undisturbed, for 20 minutes. After this time, the tube is tipped once to 45 degrees. If the blood is still liquid, coagulopathy is present.207 Major abnormalities may be seen in serum coagulation studies in the absence of any clinically significant bleeding (i.e., no evidence of bleeding or nothing more serious than gingival oozing or microscopic hematuria).19 This is particularly relevant for determining when to use blood products in treating these victims (see Hospital Care, later). Recurrent coagulopathic parameters (e.g., thrombocytopenia and/or hypofibrinogenemia) may persist or recur for as long as 2 weeks after envenomation, particularly after rattlesnake bites (see Indications for Antivenom, later).8,46,48 Urinalysis should be performed to identify hematuria. Proteinuria and glycosuria may be seen.181 Each time the victim voids, the urine should be evaluated with bedside testing strips for the presence of blood. If envenomation is severe or if the victim has significant underlying medical problems (e.g., cardiovascular or respiratory disease), an electrocardiogram (ECG), arterial blood gases (ABGs), and chest radiograph should be obtained. The ECG may reveal evidence of myocardial ischemia. ABGs give important information regarding adequacy of tissue perfusion and respiratory status, but caution should be used in performing arterial puncture in the setting of potential coagulopathy. Pulmonary vascular congestion or frank pulmonary edema may be confirmed radiographically. Coral Snakes Given their less efficient venom delivery system, coral snakes effectively envenom their victims only about 40% of the time.178 Following envenomation, the effects are predominantly neurotoxic. In the United States, bites by the eastern coral snake (Micrurus fulvius) tend to be more severe than those by Texas coral snakes (Micrurus tener), and both are significantly more severe than those of the Sonoran coral snake (Micruroides euryxanthus).152,175,185 The victim may have variable, early, and transient pain of the bitten extremity.177 Local swelling is uncommon. Fang marks may be difficult to see and should be carefully sought.155 Systemic signs and symptoms may be delayed as long as 13 hours after significant bites and can then progress rapidly.113 The earliest findings may be nausea and vomiting, followed by headache, abdominal pain, diaphoresis, and pallor.57 Victims may complain of paresthesias or numbness. They may have altered mental status, such as drowsiness or euphoria.143 The victim may develop cranial nerve dysfunction (e.g., ptosis, difficulty speaking, difficulty swallowing), followed by peripheral motor nerve dysfunction.143 In severe cases, respiratory insufficiency and aspiration are significant risks.113 Cardiovascular insufficiency may also be seen.181 Unlike with many crotaline envenomations, coagulop­ athy is not a feature of coral snake envenomation. Laboratory studies are of little value in evaluation of a victim of coral snake bite. Occasionally, a rise in serum CK and myoglobinuria occur, reflecting myotoxicity.113 ABGs may be useful in evaluating the victim’s respiratory status if endotracheal intubation is considered or performed. A chest radiograph is indicated in the setting of apparent cardiac dysfunction or after endotracheal intubation.

MANAGEMENT Prehospital Care Pit Vipers.  The factors that most reduce venomous snakebiterelated injury and mortality in the United States are rapid transport, antivenom therapy, and intensive care.21 All victims should be transported to the hospital as expeditiously and safely as possible, preferably through activating the emergency 911 system (where available). Increasing the area of coverage for cellular phone services provides snakebite victims with easier access to ambulance or helicopter rescue (Figure 54-29, online). Attempts to kill the snake are not recommended because of the risk for additional bites to the victim or rescuer and because precious time can be wasted. All emergency personnel should

rate of progression. These measures suffice as adequate prehospital care for the vast majority of pit viper bites in the United States. To be avoided are measures such as incision, suction, tourniquets, electric shock, ice, alcohol, and folk therapies. Incising the bite site is contraindicated. This creates additional injury and has never been shown to be effective. Because viperid fangs are curved, incisions may miss the track along which venom is actually injected. Incisions made by laypersons can cause serious injury to underlying blood vessels, nerves, or tendons. Because of venom-induced coagulopathy, bleeding from such incisions can be severe.89 Furthermore, the lack of sterile conditions in the field increases the risk for infection. Although use of the Sawyer Extractor Pump to apply mechanical suction was recommended for a number of years, at least three studies using different methodologies independently found that the Extractor does not work for venomous snakebite and can make things worse.2,26,27,22 Mouth suction is contraindicated for the additional concern of potentially contaminating the wound with oral flora. Venom sequestration techniques, such as application of a lymphatic or superficial venous constriction band or pressure immobilization, may inhibit the systemic spread of venom.20,199 It is not clear, however, whether such measures improve outcome after pit viper envenomation. Some argue that restricting the spread of potentially necrotizing venom to local tissues may intensify injury.92 Because local sequelae are the predominant complications after pit viper envenomation (see Morbidity and Mortality, later), and because permanent systemic injury and death are rare, especially in North America, any attempt to strictly limit venom to the bite site is ill advised.56 Tourniquets have worsened injury when used for snakebite and are contraindicated.89 Pressure immobilization (P-I) has been used effectively in Australia for field management of elapid snakebites (see Chapter 55).200 This technique involves immediately wrapping the entire bitten extremity with an elastic wrap or crepe bandage as tightly as would be done for a sprain, and then splinting and immobilizing the extremity (Figure 54-30). P-I resulted in significantly longer survival, but higher intracompartmental pressures after artificial, intramuscular western diamondback rattlesnake (C. atrox) envenomation in a pig model.24 In a separate small pig

Fang marks

4 1

5

2

3 FIGURE 54-30  The Australian pressure-immobilization technique. This technique has proved effective in the management of elapid and sea snake envenomations. Its efficacy in viperid bites has yet to be fully evaluated clinically.

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

be able to distinguish native venomous from nonvenomous snakes. However, if rescuers are uncertain about whether a particular snake is venomous, photographs may be taken of the snake from a safe distance (at least 2 m [6.5 feet] away) using a digital camera. These images may help facilitate clinical decisions. Although helpful in identifying the species of snake,23,25 transporting it (alive or dead) is discouraged because of inherent dangers. On scene, snakes should be moved or contained only if absolutely necessary (i.e., for safety). A snake hook or long shovel may be helpful to move a snake into a large, empty trash canister where it can be recovered by a professional, such as an animal control agent. Serious morbidity and even death have been reported after envenomation by decapitated rattlesnake heads.39,112,198 A recently killed snake or severed snake head can maintain a bite reflex for at least 90 minutes after its death. Emergency personnel and hospital care providers should exercise extreme caution in handling any specimen accompanying the victim, even if it appears dead. Recommendations for first aid and prehospital treatment of pit viper envenomation have historically been based on speculation and anecdotal experience, although better evidence is accumulating in the literature. In one large retrospective series, first aid treatment had no relationship to ultimate envenomation severity.220 Some first aid measures recommended in the past have caused more injury than have the bites, and delays in care have been shown to increase morbidity and mortality.56,90 It is inappropriate to use any technique that could potentially injure the patient or delay travel to the nearest facility where antivenom is available. General support of the airway, breathing, and circulation should be provided, depending on the capabilities at hand. Oxygen, cardiac monitoring, and intravenous (IV) fluids should be used in the field when available. Although it may be necessary for the victim to hike out from the scene of the incident, exertion should be minimized as much as possible. Alternative methods (e.g., stretcher, helicopter, boat) of extracting the victim from a wilderness setting can be used when available and when conditions such as weather and terrain allow. Jewelry and tightfitting clothing are removed from the involved extremity in anticipation of swelling. The border of advancing edema is marked with a pen every 15 minutes so that emergency personnel can estimate the severity of envenomation by following the

PART 6  ANIMALS, INSECTS, AND ZOONOSES

study using C. atrox venom, P-I again prolonged survival without evidence of worsening local tissue sequelae.147 Additional conclusive research is necessary to definitively assess the risk–benefit ratio of using P-I in bites by snakes with necrotizing venoms. Furthermore, studies have shown that lay people as well as physicians have difficulty properly applying the bandage, generally underestimating the necessary tightness for effective application.36,156 Further complicating the clinical use of P-I is the fact that the victim must be carried out of the field following application of pressure immobilization, because walking stimulates muscular pumping of venom into the systemic circulation and negates any benefit, even in upper extremity bites.102 For these reasons, P-I is not routinely recommended at this time for use in pit viper bites. Certain scenarios may, however, warrant consideration of its use. Although it is difficult to predict snakebite severity at the time of the bite, certain factors may suggest an increased likelihood of a more severe envenomation: large snake size, particularly dangerous snake species, small patient size, prolonged fang contact, previous venomous snakebites (treated or not) or exposures to snakes, and delays to medical care and antivenom administration.105 Individuals who consider using P-I must thoroughly familiarize themselves with the technique and must assess risks, benefits, and alternatives on a case-by-case basis. If P-I is applied after a snakebite, however, the wrap should not be removed until a source of definitive care is reached. Loosening the wrap may result in release of a venom bolus into the systemic circulation. Antivenom must be immediately available to treat such an event, and medications and equipment available to treat an immediate hypersensitivity reaction (see Allergy to Reptile Venom, later). Electrotherapy was proposed in the late 1980s for first aid treatment of snakebites and subsequently was popularized by the lay press.79,97 Early proponents recommended application of high-voltage, low-amperage, direct current (DC) shocks to the bite site using a source such as an outboard motor or lawn mower engine.78 A “stun gun,” typically designed for self-defense, was even modified by one company and marketed for snakebite treatment.89 This marketing was halted by the U.S. Food and Drug Administration (FDA) in 1990 because of total lack of testing or evidence of efficacy. In subsequent controlled animal studies, electric shock showed no efficacy in reducing morbidity or mortality after rattlesnake venom injection in mice, rats, or rabbits.103,107,196 In humans, application of electric shock for snakebite has been associated with acute myocardial infarction and increased local tissue damage secondary to electrical burns.54,55,179 Because of its lack of efficacy and inherent risks, electric shock should not be used in the treatment of snakebites. Local application of ice to the bite wound as a first aid measure has not been adequately studied in terms of its benefits or risks. This should not be confused with “cryotherapy,” or packing the injured limb in ice for extended periods. This form of treatment was popularized in the 1950s and 1960s. Use of cryotherapy resulted in a significant increase in tissue loss and amputation rates after pit viper bites, and it has now been completely abandoned.177 Whether brief (e.g., less than 1 hour) local application of ice is beneficial (by reducing venom activity or decreasing pain and inflammation) or harmful (by worsening local ischemia and resulting necrosis) is unknown. In any case, ice should not be applied directly to the skin for any prolonged period. Although indigenous peoples in many parts of the world have long used plants, either topically (Figure 54-31) or systemically, for treatment of snakebite, little formal research has been done in this area. No current data support the use of any plants in the management of snakebite.101 Other first aid measures that lack therapeutic value or have potential for being more harmful than the snakebite itself include scarification of the bite wound, ingestion of alcohol, use of stimulants, and various folk remedies such as application of ammonia, silver nitrate, oil, potassium permanganate, or saliva. Similarly ineffective is application of poultices made from various parts of the offending reptile (or other creatures), such as the snake’s crushed head, bile or fat, or use of snake stones.178 Insufficient evidence exists regarding efficacy of splinting or specific positioning (e.g., above or below the level of the heart) 1024

FIGURE 54-31  Neem leaves (Azadirachta indica) applied by a victim in an effort to treat saw-scaled viper (Echis sochureki) bite in Rajasthan, India. (Courtesy Robert L. Norris, Jr., MD.)

of the limb. Theoretically, elevation may hasten systemic spread of venom, whereas lowering the extremity may worsen swelling. In the absence of any reliable data, it is recommended at this time that the extremity be maintained in a neutral position of comfort until it can be ascertained whether the predominant effects of the bite will be systemic or local. For the victim of a pit viper bite who is many hours or days from medical care, the best course of action depends on the situation. If present, a companion may hike out for help, if conditions allow for prompt return of a rescue team. At times, if sufficient rescuers are available, the victim can be carried out. The victim who must hike out should use a makeshift crutch (for a lower extremity bite) or sling (for an upper extremity bite), rest frequently, and maximize oral intake of clear liquids as tolerated. Antivenom use in the field can be recommended only when a qualified medical provider is on scene and when all equipment (including definitive airway management equipment) and drugs are available to manage acute reaction to the antiserum. Studies and clinical experience show that newer, purified Fab-fragment antivenoms may be safer than are whole immunoglobulins (see Antivenom Production, later). Adverse reactions that occur with new-generation antivenoms are less frequent and less severe than those reported with previous preparations. Antivenom has been shown to retain activity for at least 60 days under conditions of increased heat and motion (as might be encountered in a field setting).59 With the safety profile and stability of new antivenoms, field use may be worth reconsidering, although monetary costs may be prohibitive. Coral Snakes.  When a bite by a coral snake is suspected, the animal’s skin color pattern should be noted. Because of the potential delay in onset of signs and symptoms after coral snake envenomation, distinguishing between a coral snake and a harmless mimic is important. It may be helpful if the snake can be quickly and safely photographed, as mentioned previously. Recent research suggests that the Australian P-I technique may be useful in the field management of coral snake bites. This technique has been shown to be effective in one small-animal study using Micrurus fulvius venom.67 Being elapids, coral snakes are related to the venomous snakes in Australia, for which this technique has been shown in animal models to be effective in limiting venom absorption (see Chapter 55). This intervention remains problematic, however, because rescuers frequently have difficulty applying this technique with the precision required for it to be effective156 and because the victim must be fully immobilized and carried out of the field. Hospital Care Pit Vipers Initial Management.  Initial focus of emergency medical care for a pit viper bite (Figure 54-32) is on the victim’s airway, breathing, and circulation. Victims should receive supplemental oxygen

Assess Patient

See Post-Discharge Planning (box 14)

Yes

No progression of any venom effect during the specified observation period No unfavorable laboratory trends in protime, fibrinogen, or platelets

Determine if Patient Meets Discharge Criteria

Perform serial examinations Maintenance antivenom therapy may be indicated Read Box 13 (Maintenance Antivenom Therapy) Observe patient 18-24 hours after initial control for progression of any venom effect Follow-up labs 6-12 hours after initial control and prior to discharge If patient develops new or worsening signs of envenomation, administer additional antivenom per box 4

Monitor Patient

Yes

Swelling and tenderness not progressing Protime, fibrinogen, and platelets normal or clearly improving Clinically stable (not hypotensive, etc.) Neurotoxicity resolved or clearly improving

Determine if Initial Control of Envenomation has been Achieved

Establish IV access and give IV fluids Pediatric antivenom dose = adult dose Mix 4-6 vials of crotaline Fab antivenom (CroFab ®) in 250 ml NS and infuse IV over 1 hour For patients in shock or with serious active bleeding Increase initial dose of antivenom to 8-12 vials Call physician expert (see box 12) Initiate first dose of antivenom in ED or ICU For suspected adverse reaction: hold infusion, treat accordingly, and call physician-expert Re-examine patient for treatment response within 1 hour of completion of antivenom infusion

Administer Antivenom

Present

Swelling that is more than minimal and that is progressing, or Elevated protime; decreased fibrinogen or platelets, or Any systemic signs

Check for Indications for Antivenom

Present

Swelling, tenderness, redness, ecchymosis, or blebs at the bite site, or Elevated protime; decreased fibrinogen or platelets, or Systemic signs, such as hypotension, bleeding beyond the puncture site, refractory vomiting, diarrhea, angioedema, neurotoxicity

Check for Signs of Envenomation

Mark leading edge of swelling and tenderness every 15-30 minutes Immobilize and elevate extremity Treat pain (IV opioids preferred) Obtain initial lab studies (protime, Hgb, platelets, fibrinogen) Update tetanus Contact poison control center (1-800-222-1222)

No

None

None

11

10

9 Apparent Dry Bite / No Bite

If initial control is not achieved after 2 doses of antivenom, call physician expert (see box 12)

Repeat antivenom until initial control is achieved.

Do not administer antivenom Observe patient 12-24 hours Repeat labs at 4-6 hours and prior to discharge If patient develops progression of any signs of envenomation, return to box 3

Apparent Minor Envenomation

Do not administer antivenom Observe patient ≥ 8 hours Repeat labs prior to discharge If patient develops signs of envenomation, return to box 2

When to Call a Physician-Expert

14

13

Follow-up visits: Antivenom not given: PRN only Antivenom given: Copperhead victims: PRN only Other snakes: Follow up with labs (protime, fibrinogen, platelets, hemoglobin) twice (2- 3 days and 5-7 days), then PRN

Bleeding precautions (no contact sports, elective surgery or dental work, etc.) for 2 weeks in patients with Rattlesnake envenomation Abnormal protime, fibrinogen, or platelet count at any time

Instruct patient where to seek care if symptoms of serum sickness (fever, rash, muscle/joint pains) develop

Instruct patient to return for Worsening swelling that is not relieved by elevation Abnormal bleeding (gums, easy bruising, melena, etc.)

Post-Discharge Planning

Follow local protocol or contact a poison center or physician-expert for advice.

Maintenance therapy may not be indicated in certain situations, such as Minor envenomations Facilities where close observation by a physicianexpert is available.

Maintenance therapy is additional antivenom given after initial control to prevent recurrence of limb swelling Maintenance therapy is 2 vials of antivenom Q6H x 3 (given 6, 12, and 18 hours after initial control)

Maintenance Antivenom Therapy

If no local expert is available, a physician-expert can be reached through a certified poison center (1-800-222-1222) or the antivenom manufacturer’s line (1-877-377-3784).

Complicated wound issues

Uncommon clinical situations Bites to the head and neck Rhabdomyolysis Suspected compartment syndrome Venom-induced hives and angioedema

If transfusion is considered

Allergic reactions to antivenom

Recurrence or delayed-onset of venom effects Worsening swelling or abnormal labs (protime, fibrinogen, platelets, or hemoglobin) on follow-up visits

Hard to control envenomation Envenomation that requires more than 2 doses of antivenom for initial control

Life-threatening envenomation Shock Serious active bleeding Facial or airway swelling

Direct consultation with a physician-expert is recommended in certain high-risk clinical situations:

12

16

15

This worksheet represents general advice from a panel of US snakebite experts convened in May, 2010. No algorithm can anticipate all clinical situations. Other valid approaches exist, and deviations from this worksheet based on individual patient needs, local resources, local treatment guidelines, and patient preferences are expected. This document is not intended to represent a standard of care. For more information, please see the accompanying manuscript, available at www.biomedcentral.com.

All treatment recommendations in this algorithm refer to crotalidae polyvalent immune Fab (ovine) (CroFab®).

Notes:

Cutting and/or suctioning of the wound Ice NSAIDs Prophylactic antibiotics Prophylactic fasciotomy Routine use of blood products Shock therapy (electricity) Steroids (except for allergic phenomena) Tourniquets

Treatments to Avoid in Pit Viper Snakebite

FIGURE 54-32  Unified treatment algorithm for the management of pit viper snakebite in the United States. (From Lavonas EJ, Ruha AM, Banner B, et al: Unified treatment algorithm for the management of crotaline snakebite in the United States: Results of an evidence-informed consensus workshop, BMC Emergency Medicine 11:2, 2011. With permission. http://www.biomedcentral.com/ 1471-227X/11/2.)

8

7

6

5

4

3

2

1

Includes: Rattlesnakes, Copperheads, and Cottonmouths (Water Moccasins)

Emergency Department and Hospital Management of Pit Viper Snakebite

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

1025

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

B

FIGURE 54-33  A, This patient was bitten by a 3-foot-long southern Pacific rattlesnake (Crotalus oreganus helleri ) 72 hours earlier. The snake hung on for 15 seconds and the patient suffered an extraordinarily severe systemic envenomation. Prolonged fang contact is a factor associated with increased snakebite severity. These bullae were left in place and the hand ultimately healed without any surgical intervention. B, The patient’s hand at 3-week follow-up. At 1-year follow-up, this patient had nothing more than a slightly stiff index finger. (Courtesy Sean P. Bush, MD.)

until it is clear that they are stable. Patients with bites to the face or neck may require early endotracheal intubation to prevent loss of the airway caused by severe swelling. Pulse oximetry and cardiac monitoring should be instituted and two large-bore IV lines established. In the setting of potential coagulopathy, venipuncture attempts should be minimized and noncompressible entry sites (e.g., subclavian vein) should be avoided. As lines are placed, blood is drawn for initial laboratory analysis (complete blood count, coagulation studies, electrolytes, renal and hepatic function studies, and blood typing and screening). Initial management of hypotension or shock should include vigorous fluid resuscitation with crystalloid (normal saline or Ringer’s lactate) infusion and prompt antivenom administration. If organ perfusion remains inadequate after aggressive crystalloid infusion (e.g., 2 L in an adult, 20 to 40 mL/kg in a child) and antivenom, a trial infusion of 5% human albumin can be started (e.g., 250 to 500 mL for older children and adults and 15 to 20 mL per kilogram body weight for infants and young children, given intravenously and repeated in 30 minutes as needed). Evidence supports the usefulness of adding albumin early in this setting because of the rapid onset of increased vascular permeability after significant pit viper envenomation.187 Vasopressors (e.g., dopamine) should be used to treat venom-induced shock only after adequate volume infusion and initiation of antivenom therapy. Prolonged, inadequately treated hypotension has been strongly implicated in fatal cases of envenomation.56,92 The mainstay of medical management of significant snake envenomation is prompt administration of appropriate antivenom in order to bind deleterious venom components that are being absorbed and circulated from the bite site. Time is of the essence, because venom components can be bound and deactivated only before they attach to target tissues. Once attachment occurs, they cannot be displaced and will inflict damage. The medical team responsible for a snakebite victim should begin the process of locating and obtaining appropriate antivenom as soon as possible. Hospitals in regions where snakebites are likely to occur should maintain a stock of antivenom at least sufficient to begin therapy and have plans in place to procure more as needed. Guidelines for managing pit viper bites in North America with CroFab Crotalidae Polyvalent Immune Fab (Ovine) including guidelines for administration and dosing, are summarized in Figure 54-32. Initial control of envenomation may require larger doses of antivenom in the setting of thrombocytopenia, bleeding, neurologic abnormalities, or an otherwise severe bite.224 Further details regarding antivenom use, including adverse reactions and their management, are found later in General Concepts of Antivenom Therapy. Snake envenomation is a complex and dynamic syndrome best managed under the guidance of a physician experienced with the use of antivenom. Regional poison control centers throughout the United States, under the auspices of the AAPCC, are manned by trained personnel who maintain a list of physician toxinology experts available for consultation to assist 1026

with managing cases of native or exotic snakebite. The central emergency phone number is 1-800-222-1222. Centers that handle snakebite cases regularly include the University of Arizona Poison and Drug Information Center, Rocky Mountain Poison and Drug Center, and California Poison Control System, San Diego Division. The Antivenom Index, published jointly by the AAPCC and the American Zoo and Aquarium Association, lists antivenom sources within the United States. This list is readily available to poison control center personnel. Analgesia and Wound Care.  Pain can be substantial after pit viper envenomation. Analgesia is best obtained using titrated doses of narcotics. In the presence of hypotension, it may be prudent to start with a short-acting, easily titratable agent, such as fentanyl, until blood pressure stabilizes. Aspirin and nonsteroidal antiinflammatory drugs should be avoided, because they may exacerbate coagulopathy. Wound care for pit viper envenomation follows standard principles. Tetanus immunization is recommended if the patient’s immunization is not up to date. Any wounds should be cleaned. The extremity is then kept above heart level to reduce swelling. Wound infections from venomous snakebites are uncommon in North America, and prophylactic antibiotics are unnecessary in most cases.45,213 A variety of bacteria, including Clostridium species, Bacteroides fragilis, Pseudomonas species, Proteus species and Staphylococcus aureus, have been isolated from the oral cavities of pit vipers.73 Aeromonas hydrophila has been reported to cause necrotizing fasciitis following cottonmouth water moccasin (Agkistrodon piscivorus) bite.3 If infection occurs, initial antibiotic choice should be broad to cover gram-positive and gram-negative bacteria, aerobes, and anaerobes, and should be further guided by wound cultures and sensitivities. Intact blisters should be protected as much as possible from rupture (Figure 54-33). Debridement of clearly necrotic tissue or ruptured blebs and bullae should await full reversal of any ongoing coagulopathy. The patient should begin a physical therapy regimen as soon as possible to expedite return of function. Swelling of the bitten extremity can be quite severe following pit viper envenomation, and is often accompanied by discoloration, tenderness, and pain on range-of-motion of the digits. This may raise clinical concern for a compartment syndrome. The majority of swelling, in most cases, however, occurs in the subcutaneous tissues, and compartment syndrome is an uncommon complication.65,154 Muscle necrosis after pit viper envenomation is primarily caused by direct myotoxic venom effects rather than increased intracompartmental pressures.66 Differentiating subcutaneous swelling from intramuscular swelling is achieved by objectively measuring intracompartmental pressures using a digital readout device. If compartmental pressure exceeds 30 to 40 mm Hg, antivenom should be started or continued while the extremity is elevated. The hemodynamically stable patient should receive IV mannitol (1 to 2 g/kg) over 30 minutes. These

51

measures may reduce pressures to safe levels. If pressures fail to decrease within 60 minutes and ischemia within the compartment is suspected, fasciotomy is required (Figure 54-34). While animal evidence suggests that myonecrosis associated with venomous snakebite may actually be worsened by fasciotomy,201 surgical decompression is necessary to prevent pressure necrosis of intracompartmental nerves.93 A knowledgeable surgical consultant (hand, orthopedic, plastic, or general) should be involved if compartment syndrome is a possibility. Prophylactic fasciotomy is not recommended. In some cases of finger bites, if the vascular supply to the digit is compromised despite antivenom and elevation of the extremity, digital dermotomy may be needed. Occasionally, after a bite to a digit, severe necrosis results, requiring eventual amputation of the appendage. Such an extreme procedure should be delayed until a confident level of demarcation of damage can be ascertained. A digit may also require amputation if the bite results in severe contracture deformity and chronic, severe pain. Disposition.  Disposition decisions for patients bitten by pit vipers are generally straightforward. Admission to the hospital should be strongly considered for all persons with apparent envenomation. In one series, more than one-half of persons with minimal or no signs of envenomation at presentation subsequently developed significant envenomation with moderate to severe swelling, elevated PT, or thrombocytopenia.104 Approximately 25% of these persons deteriorated more than 8 hours after envenomation. Even with apparent resolution of swelling, victims may later develop severe toxicity.80 Because onset and progression of signs and symptoms after a pit viper bite vary greatly, all potential victims should be closely watched in the emergency department for a minimum of 8 hours if not admitted to the hospital. Discharge may be considered after 8 hours for victims with no symptoms or signs other than puncture wounds. All laboratory studies and vital signs must be normal. On discharge, such patients should be instructed to return for onset of swelling, increased pain, bleeding, blood in the urine, severe headache, difficulty breathing, rash, joint pain, swollen lymph nodes, fever, or signs of wound infection. The victim should be scheduled for a follow-up reexamination in 24 to 48 hours and should be accompanied and assisted by another responsible adult. Because of the delayed onset of findings with some Mohave rattlesnake (Crotalus scutulatus) bites, all persons with suspected bites by this snake should be admitted to the hospital for 24 hours of observation. Admission is also highly recommended for children with potentially venomous snakebites. Admission to an intensive care unit (ICU) is prudent for victims with severe envenomation or with progressive clinical findings despite initial antivenom administration. Persons bitten in the head, neck, or trunk should be monitored in an ICU because of the greater risks associated with these bites. Any patient who develops a serious acute reaction to antivenom (see Adverse Reactions to Antivenoms, later) should also be admitted to the ICU. Victims who require a higher level of care than is available at the treating institution should be transferred to an

FIGURE 54-35  Victims of rattlesnake bite often develop delayed recurrence of coagulopathy up to 2 weeks following envenomation. This patient was bitten by a large northern Pacific rattlesnake (Crotalus oreganus oreganus) to the left foot. Her initial platelet count was 73,000/µL, and she received four vials of CroFab 2 hours after the bite. Platelet count improved to 238,000/µL one hour later. Labs were otherwise normal, including hemoglobin and fibrinogen. Sixteen vials of antivenom were given during the hospital course, and the patient was discharged after 2 days with normal platelets, hemoglobin and fibrinogen as well as regression of local effects. The patient returned 2.5 days after the last dose of antivenom and last lab draw with profound thrombocytopenia (platelets = 1000/µL), anemia (hemoglobin = 4 g/ dL) and extensive ecchymosis (photo). At no time did she develop hypofibrinogenemia. (Courtesy Sean P. Bush, MD.)

appropriate facility, but antivenom therapy should be initiated prior to transfer. After antivenom infusion and clinical stabilization, victims of mild or moderate envenomation can be admitted to a regular hospital floor, but they should be carefully watched, particularly if repeat doses of antivenom are planned. At hospital discharge, patients who received antivenom should be reminded about the possibility of developing serum sickness (see Adverse Reactions to Antivenoms, later) and the need for prompt medical attention if they develop fever, rash, arthralgias, myalgias, urticaria, or other findings consistent with serum sickness within the first few weeks after treatment. Patients who developed coagulopathy should be warned of potential delayed recurrence and should have follow-up arranged for repeat testing (see Antivenom Administration, later) (Figure 54-35). They should be told to return if they experience any bleeding and to avoid high-risk activities (such as contact sports or mountain climbing) and elective surgical procedures for 2 to 3 weeks following their bite. Patients with substantial local tissue effects should have follow-up arranged for on-going wound management and physical therapy. Discharge instructions to patients should also include information on ways to prevent venomous snakebite. More than one-half of bites occur during intentional interactions with snakes.151 These usually involve attempts to handle, harass, capture, or kill the animal. Commonly, the bite is inflicted by a specimen in captivity. Avoiding intentional interaction with venomous snakes can prevent many injuries. Wearing shoes and long pants can prevent some strikes.96 In areas where snakes are common, children should be closely supervised and educated to avoid snakes. Animal control services should be called to remove snakes found close to human habitation. If a snake is encountered in the wilderness, people should carefully move a safe distance away as they enjoy the experience. Coral Snakes.  Hospital management of coral snake bite victims (Figure 54-36) can be challenging. The first priority in the stable victim is to determine that a coral snake was actually the culprit. Photographs of coral snakes and nonvenomous mimics indigenous to the area can be useful. If a coral snake is identified and 1027

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

FIGURE 54-34  Rarely indicated fasciotomy in a victim of a severe bite from a rattlesnake (Crotalus oreganus helleri). Compartment pressures were greater than 60 mm Hg despite aggressive antivenom therapy. (Courtesy Robert L. Norris Jr., MD.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

appears to have inflicted an effective bite, management should proceed in anticipation of a significant envenomation, even if systemic abnormalities are currently absent. The patient should receive cardiac and pulse oximetry monitoring, and an IV line should be established. A history and careful physical examination should be performed; local findings are minimal, and fang marks can be difficult to see.155 The victim typically has little or no swelling and variable local pain. The victim should be carefully assessed for any neurologic abnormalities. Aggressive airway management is essential with any sign of

respiratory dysfunction or difficulty swallowing secretions. Early endotracheal intubation in such cases may prevent pulmonary aspiration and its complications. Bedside spirometry testing can be helpful in monitoring the respiratory status of these patients. Laboratory studies have little benefit, except for ABGs if respiratory insufficiency is suspected or endotracheal intubation is required. The preferred therapy for an effective coral snake bite includes administration of appropriate coral snake antivenom. The only currently approved antivenom for coral snakes in the United

1 Assess Patient • Evaluate airway, breathing, and circulation and support as needed • Establish IV access • If there is any difficulty with breathing or swallowing, secure the airway by endotracheal intubation and begin mechanical ventilation • Attempt to identify the offending snake (see text) • Mark leading edge of swelling every 15 minutes (will likely be minimal) I bili and d elevate l t th t it • Immobilize the extremity • If pressure-immobilization has been applied in the field, attempt to locate antivenom before removing (see text) • Treat pain as needed (with cautious titration of opioids) • Initial lab studies unlikely to be beneficial (unless victim has significant underlying medical disorders) • Update tetanus • Contact poison center (1-800-222-1222)

2 •

•

Check for Indications for Antivenom Any evidence of envenomation • Local pain out of proportion to puncture wounds • Evidence of neurotoxicity (e.g., ptosis, difficulty swallowing, weakness, numbness, shortness of breath, altered mental status) A prolonged bite by a confirmed coral snake (i.e., the snake was able to chew on the victim), even if the victim is otherwise asymptomatic

Present 3

Appropriate Coral Snake Antivenom Available?

Absent

No

Yes

Administer Antivenom

4 • • • • •

Infuse IV fluids (20 ml/Kg) Pediatric antivenom dose = adult dose Ad i i t antivenom ti di tto package k iinsertt – b i iin ED or ICU Administer according begin • Starting dose for Wyeth’s North American Coral Snake Antivenom = 3 to 5 vials (mixed in 250-500 ml NS and infused over 1 hour) For suspected acute adverse reaction: hold infusion, treat accordingly, and call physician-expert Assess response 1 hour after infusion. If signs of envenomation have progressed, repeat starting dose (once)

6

5

Supportive Care

• • •

Close monitoring of airway and breathing (and secure/support as needed) IV normal saline boluses for hypotension Add a vasopressor (e.g., dopamine) infusion for refractory hypotension

Admit All Patients with Possible Coral Snake Bites to an ICU for a Minimum of 24 Hours of Observation

FIGURE 54-36  Emergency department and hospital management of possible coral snake bite in North America. Includes patients bitten by a brightly colored, unidentified snake in areas where coral snakes are indigenous.

1028

• • •

When to Call a Physician-Expert Victim has any evidence of envenomation Advice/assistance needed re: obtaining an appropriate antivenom Allergic reactions to antivenom

If no local expert is available, a physician-expert can be reached through a certified poison center (1-800-222-1222)

8

Post-Discharge Planning (after a minimum of 24h of observation)

• •

Instruct patient to return for any evidence of recurrence or new neurotoxicity or evidence of wound infection I t t patients ti t who h received i d antivenom ti h t seek k care if Instruct where to symptoms of serum sickness (fever, rash, muscle/joint pains) develop

9

Treatments to Avoid in Coral Snake Bite

• • • • • • •

Cutting and/or suctioning of the wound I Ice Prophylactic antibiotics Prophylactic fasciotomy (swelling is rarely significant in these bites) Shock therapy (electricity) Steroids (except for allergic phenomena) Tourniquets

FIGURE 54-36, cont'd.

States (Wyeth Antivenin) has been discontinued by the manu­ facturer. At the time of this writing, there remains a single lot of Antivenin (Micrurus fulvius) [equine, also known as North American Coral Snake Antivenin] with an extended expiration date of October 31, 2011. Plans are reportedly in place for Pfizer Inc. to resume manufacturing coral snake antivenom in a new plant currently under construction.108 The first documented coral snake–related human death in the United States since the Wyeth Antivenin was initially released occurred in 2006.157 Although this victim did not seek medical care, the case emphasizes the lethal potential in bites by these snakes and the need for an efficacious antiserum. Physicians treating victims of coral snake bite in the United States should consult a poison control center for advice regarding availability of antivenom. In the absence of antivenom, treatment is supportive and includes early intubation at any sign of respiratory distress or difficulty swallowing oral secretions. Close observation for such complications must occur for at least 24 hours following the bite of a coral snake. If intubation is required, respiratory support may be required for as long as a week.113 Bites by the Sonoran coral snake (Micruroides euryxanthus) have always been managed supportively. There has never been an antivenom for this small, inoffensive species, and no deaths have been reported after its bite.57 The role for anticholinesterase agents in the management of bites by coral snakes remains to be determined. These agents have been used in some parts of the world to reverse postsynaptic neurotoxicity in patients envenomated by elapids (see Chapter 55).207 Anticholinesterase drugs are not, however, a substitute for antivenom administration, and their use does not obviate the need for close monitoring of respiratory and cardiovascular status or airway control with ventilator support if the patient’s status worsens. In the unusual case of hypotension following coral snake bite, the victim should be initially resuscitated with intravascular crystalloids. Once intravascular volume is expanded, vasopressors may be added as needed (e.g., dopamine starting dosage, 2.5 to 5 mcg/kg/min by IV infusion).

All victims who have possibly been bitten by a coral snake, even if asymptomatic, should be admitted to an ICU for 24 hours for close cardiac and respiratory monitoring.

GENERAL CONCEPTS OF ANTIVENOM THERAPY A Brief History of Antivenom Therapy Antivenoms are immunobiologics designed to neutralize venoms. Scholars of ancient Greek history believe that King Mithridates VI of Pontus (132 BC to 63 BC) was the first documented user of immunotherapeutic principles. He ingested sublethal doses of numerous venoms in attempts to render himself immune to the toxins.58 However, it was not until 1895 that French scientist Albert Calmette developed the first therapeutic antivenom, against the monocellate cobra, Naja kaouthia.30 In the early 1900s, Brazilian physician Vital Brazil worked to develop and distribute antivenoms for various venomous snakes in South and Central America.84 In order to ensure a sufficient venom supply to conduct his research, Dr. Vital worked with the Brazilian government to provide free rail passage for all snakes shipped to his institute. Participants sending snakes received free snake-capture equipment and transport crates, as well as one vial of antivenom per snake.84 His work greatly decreased Brazil’s snakebite mortality,13,84 and he subsequently founded the nowfamous Instituto Butantan in São Paulo, Brazil, which still produces antivenoms. These products were historically termed antivenins, derived from venin, the French word for “venom.” In 1981, however, the World Health Organization (WHO) declared that the preferred term in the English language is antivenom.222 Although modern purification processes have improved tremendously over the years, the basic principles of antivenom production remain the same. Antivenom continues to be the mainstay of treatment for bites and stings of many venomous creatures. Antivenoms exist for various species of snakes (see also Chapter 55), spiders 1029

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

(discussed in Chapter 52), scorpions (discussed in Chapter 53), and for some marine creatures (discussed in Chapters 80 and 81). Antivenom Production Antivenoms are currently produced by injecting animals, such as sheep or horses, with sublethal doses of venom. This is done repeatedly and with gradual escalation in dose until the animals develop antibodies directed against the venom proteins. Serum is then removed and purified to extract the useful IgG antibodies while filtering out potentially harmful foreign proteins. Antivenoms are generally lyophilized and require reconstitution before administration. Some antivenoms are available as liquids and require a cold chain for storage. After it is given to a snakebite victim, antivenom imparts immediate passive immunity against venom antigens circulating in the body. Most antivenoms are administered intravenously, although a few may be given intramuscularly (e.g., widow spider [Latrodectus] antivenom and box jellyfish [Chironex fleckeri] antivenom [see Chapters 52 and 80]). Antivenom may be produced by immunizing an animal against a single species of venomous creature, in which case it is referred to as “monovalent.” It may also be made by immunizing an animal against several different species, making it “polyvalent.” Mixing several monovalent products together produces a “mixed monovalent” product that covers all species included in the mix. Monovalent antivenoms provide antibodies against the venom of one particular species and therefore necessitate precise identification of the offending snake. Polyvalent and mixed monovalent antivenoms contain antibodies against a number of different species; exact identification is not as important, so long as the offending species is covered by the product chosen. Use of a broad-spectrum antivenom results in administration of extraneous, potentially allergenic foreign proteins that are of no benefit to the victim. Antivenoms often provide some cross-protection among species with closely related venoms. For example, CroFab, an antivenom derived from four North American pit viper species, has an FDA-approved indication for all North American pit vipers; however, cross-protection has not been studied for all species and efficacy may vary from snake to snake.25,47,48 In contrast, specimens of the same species of snake from different regions may have substantial venom differences that limit the efficacy of antivenoms produced with specimens outside the region where the bite occurred. Good examples of this include Russell’s vipers (Daboia russelii) in Asia, and carpet and sawscaled vipers (Echis sp.) of middle Asia and Africa.223 An IgG antibody molecule contains two functional domains (Figure 54-37). The desired effects of antivenom administration, binding and neutralization of venom, are achieved by the two Fab fragments. The IgG molecule also contains an Fc or effector region, which activates the immune system and may lead to immediate hypersensitivity reactions. The fear of allergic reaction is a reason why many physicians unfamiliar with the treatment

Antigen-binding region

+H N 3

NH3+

Fab

Disulfide bridge

Effector region

Fc OOC

COO

IgG molecule FIGURE 54-37  Schematic diagram of an IgG molecule. The antigenbinding region (Fab portion) is present at the amino-terminal end. The effector region (Fc portion) interacts with the immune system cells and resides at the carboxyl end of IgG. Note the disulfide bridge.

of envenomation may be hesitant to use antivenom, even in situations where it is clearly indicated. Newer methods of antivenom production attempt to retain the useful Fab fragments of the IgG molecule while eliminating the allergenic Fc fragment. Two different methods of cleaving the IgG molecule are used. Cleavage with pepsin or trypsin yields a single F(ab′)2 fragment and an Fc fragment (Figure 54-38), whereas cleavage with papain yields two Fab fragments and an Fc fragment (Figure 54-39). The various fragments have different advantages and disadvantages when compared with one another and with the parent IgG molecule. An ideal antivenom would have pharmacokinetics and dynamics similar to those of venom. A whole IgG molecule has a long half-life, and the venom-antivenom complex is slowly removed by the reticuloendothelial system (RES). Because venom may be slowly absorbed into the circulation over time from a “depot” of venom at the bite site, the persistence of whole IgG may help to prevent the phenomena of recurrent venom effects requiring repeat antivenom dosing. However, this persistence also leads to increased rates and severity of delayed hypersensitivity reactions. The longer the antigen-antibody (i.e., venom

F(ab′)2

Pepsin

Fc portion

Fc portion

IgG molecule FIGURE 54-38  Proteolytic cleavage of IgG results in predictable substituent fractions. Pepsin digestion produces Fc and F(ab′)2 fractions for each IgG molecule. F(ab′)2 consists of two Fab portions connected by a disulfide bridge. The molecular weight of F(ab′)2 is 100,000 daltons.

1030

Papain

Fab

Papain

Fc portion IgG molecule

Fc portion

FIGURE 54-39  Proteolytic cleavage of IgG results in predictable substituent fractions. Papain digestion yields the Fc and two Fab segments for each IgG molecule. The molecular weight of Fab is 50,000 daltons.

component-antivenom) complex circulates, the more likely it is that host antibodies will be formed against this foreign complex. These host antibody-antivenom immune complexes may then precipitate in susceptible tissues (such as skin, synovium, and glomeruli) to cause serum sickness (see Adverse Reactions to Antivenoms, later). Additionally, the fact that the whole IgG molecule retains the immunogenic Fc fragment (as well as other non–venom-neutralizing proteins) leads to an increased risk for immediate hypersensitivity reactions. These principles are supported by clinical data. Antivenin (Crotalidae) Polyvalent (ACP) (equine), a whole IgG product that is no longer available, was reported in the literature to have at least a 20% rate of immediate hypersensitivity reactions, and at least 50% of patients who received it developed delayed serum sickness.55 Acute reactions were often persistent and difficult to treat. Initial post-marketing studies of the ovine Fab product currently used in the United States, CroFab, reported a 17% rate of immediate hypersensitivity reactions and 12% rate of delayed serum sickness.174 The reactions reported were generally short lived and mild. Additionally, it is suspected that the actual rate is significantly lower because this study contained a batch of im­ properly purified antiserum contaminated with Fc fragments. A follow-up study with properly purified antivenom reported a 5.4% rate of immediate hypersensitivity reactions.37 Reaction rates also appear to be relatively low with quality F(ab′)2 products. A study evaluating acute reaction rates with Thai green pit viper (Trimeresurus albolabris) and cobra (Naja kaouthia) equine F(ab′)2 antivenoms revealed rates of 2.3% and 12.5%, respectively.202 Another potential benefit of Fab fragment antivenoms is that their smaller molecular sizes may allow better penetration into tissue compartments and larger volumes of distribution compared to whole IgG antivenoms.189 Further work is needed to elucidate the clinical importance of this potential size advantage. One clear drawback to Fab antivenoms is the fact that they are cleared more quickly by the kidneys, resulting in shorter half-lives than whole IgG antivenoms cleared by the RES.189 The half-life for whole IgG antivenoms is in the range of 61 to 194 hours, whereas that of an Fab product such as CroFab is probably less than 12 hours.12 This is likely responsible, to some degree, for the recurrence of venom effects that commonly follows initial control with Fab antivenoms, necessitating repeat or maintenance antivenom dosing. With CroFab, recommended maintenance dosing after initial control of the envenomation process is two vials every 6 hours for three additional doses (see Figure 54-32).48 Even with such redosing, however, rattlesnake bite victims have a significant rate of recurrent thrombocytopenia and/or coagulopathy, which may be relatively unresponsive to

further doses of CroFab and difficult to manage.11,189 Patients may develop severe thrombocytopenia (platelets counts below 10,000/ cu mm) and/or complete defibrination (undetectable fibrinogen and elevations in PT) roughly 2 to 12 days after initial treatment. Clinical bleeding is rare, although recent case reports have emerged of patients with delayed life-threatening or fatal bleeding following initial stabilization with CroFab.61,111,159 Research is ongoing in an effort to find a way to effectively prevent or mitigate delayed recurrent coagulopathy. Alternative dosing regimens, such as by continuous infusion, are being explored. In addition, another antivenom, Crotalinae (Pit Viper) Equine Immune F(ab′)2 (Anavip), is in ongoing Phase III clinical trials at the time of this writing.203 Safety and efficacy data will be forthcoming from this study. Anavip, developed with the venoms of two Latin American pit vipers, Crotalus durissus (South American or tropical rattlesnake) and Bothrops asper (ferde-lance or terciopelo), has been shown in mouse models to offer cross-protection against the North American pit vipers with which it was tested.184,186 It is hypothesized that the longer halflife of this F(ab′)2 product will reduce the late hematologic recurrences in patients treated with CroFab. One drawback with current antivenom production techniques using sheep or horses is the expense of maintaining the animals and the laborious nature of extracting and purifying animal sera. Research is being done using chicken hens immunized against snake venoms as a source of antivenoms. Anti-snake–venom antibodies (IgY) can then be extracted from the yolks of the hens’ eggs. The costs associated with obtaining and maintaining chickens is far lower than that of large mammals, and the antibody extraction process is less labor intensive. Each egg produces between 80 and 120 mg of antibodies, and the antibodies remain present in the eggs for 100 days following immunization.60,140 Preliminary studies (animal models and neutralization studies) using avian antivenoms produced against the Russell’s viper (Daboia russelii), saw-scaled viper (Echis carinatus), Indian cobra (Naja naja) and the banded krait (Bungarus caeruleus) have demonstrated efficacy.145,146 In addition to traditional methods of antivenom production, researchers are studying polymer nanoparticle technology to create synthetic plastic antibodies. Nanoparticles are polymerized in the presence of a target molecule (i.e., venom components) in a process known as “imprinting.” The resultant polymers bind to target proteins with affinity similar to antibodies produced in animals. The particles are inert and have low affinity for molecules other than the ones with which they are imprinted. The cost of production would likely be relatively low compared with animal-derived antivenoms. Thus far, researchers have created 1031

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

Fab

PART 6  ANIMALS, INSECTS, AND ZOONOSES

nanoparticles that successfully bind to mellitin, a key component of honeybee venom.100 Indications for Antivenom With regard to pit viper bites, antivenom is indicated for patients presenting with progressive local findings or any evidence of systemic envenomation. This includes evidence of worsening local injury or presence of thrombocytopenia, coagulopathy, or other systemic effects (hypotension, muscle weakness, etc.). Antivenom can generally prevent progression of venom effects, but cannot reverse all effects (e.g., tissue damage) that have already been set in motion. For this reason, antivenom is usually more effective the earlier it is administered. However, if ongoing venom effects, such as persistent thrombocytopenia or coagulopathy, are noted, antivenom may still provide benefit when administered late in the course of envenomation.5 Of note, antivenom, not blood products, is the first-line treatment in patients with venom-induced coagulopathy or thrombocytopenia. Although blood products may be indicated in patients with severe active bleeding,19 antivenom should always be administered first in order to avoid fueling an ongoing consumptive coagulopathy. Different recommendations exist for when antivenom is indicated for late recurrence of thrombocytopenia and/or coagulop­ athy. Existing recommendations are based on bleeding risks in patients with other bleeding disorders (such as leukemia, congenital hypofibrinogenemia, and overtreatment with oral anticoagulants). These numbers may not necessarily be applicable to snakebite patients. It is generally accepted that severe thrombocytopenia (platelet counts below 25,000/cu mm) or combined thrombocytopenia and significant coagulopathy should be treated with repeat antivenom dosing. There is controversy, however, as to whether isolated delayed coagulopathy or hypofibrinogenemia without thrombocytopenia requires treatment, as well as how many vials should be administered.11,33 A reasonable approach is to follow patients who developed coagulopathy during their acute envenomation with repeat blood work at 2 to 3 days following antivenom therapy and again at 5 to 7 days. Thereafter, follow-up should be as needed (ongoing until hematologic disturbances have resolved and wounds are healing). On follow-up, if hematologic derangements have recurred, antivenom should be repeated for any of the conditions in Box 54-1.11 Large doses (up to ten vials of CroFab) may be required to reverse delayed hematologic effects, which appear to become less responsive to antivenom over time.191 If significant active bleeding is present, it may necessitate transfusion with platelets, packed red blood cells, fresh frozen plasma, and/or cryoprecipitate in addition to antivenom. Patients who must be on aspirin or anticoagulants may also require more aggressive treatment. Antivenom Administration When possible, it is prudent to get informed consent from the patient before administering antivenom because of the risks of adverse reactions (see Adverse Reactions to Antivenoms, later). BOX 54-1  Indications for Administration of Additional

Antivenom in Patients With Recurrent Coagulopathy or Thrombocytopenia After Initial Control*

• Evidence of clinically significant bleeding • Platelet count below 25,000/cu mm • INR greater than 3 • aPTT greater than 50 sec • Fibrinogen less than 50 mg/dL • Presence of multicomponent coagulopathy • Worsening trend in a patient with prior severe coagulopathy • High-risk behavior for trauma • Certain comorbid conditions (e.g., systemic vasculitis, seizure disorders, prior stroke) aPTT, Activated partial thromboplastin time; INR, international normalized ratio. *See Indications for Antivenom, earlier in text.

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Snake antivenoms should be administered intravenously.142 Other routes of administration are inadequate to allow effective circulation of the antiserum in order to quickly bind venom components. Many antivenoms, including CroFab, are supplied in lyophilized form and require reconstitution before administration. Although the manufacturer of CroFab recommends reconstituting each vial to be given with 10 mL of sterile water for dilution, it appears that using 25 mL per vial and hand-mixing via continuous rolling and inverting of vials significantly reduces the amount of time it takes to get the product into solution and ready for administration.170 All reconstituted vials that are to be administered should then be injected into a 250-mL bag of normal saline for intravenous infusion. The infusion should be started slowly, with the attending physician at the bedside in order to intervene at the first evidence of an acute adverse reaction (see Adverse Reactions to Antivenoms, later). All drugs and equipment needed to treat acute anaphylaxis should be immediately available. The infusion is run slowly over the first 10 minutes, and in the absence of an acute reaction, the rate is increased to get the total starting dose administered over 1 hour. Adverse Reactions to Antivenoms The most common adverse reactions associated with antivenom administration are immediate and delayed hypersensitivity reactions. Immediate hypersensitivity reactions include type I allergic anaphylaxis and clinically indistinguishable, nonallergic anaphylaxis (anaphylactoid reaction). Allergic anaphylaxis results from IgE-mediated mast cell and basophil degranulation and requires prior sensitization. Clinical manifestations may include urticaria, angioedema, laryngeal edema, bronchospasm, and hypotension. Anaphylactoid reactions produce the same clinical findings via direct mast cell and basophil degranulation or complement activation by heterologous antivenom proteins, without involvement of IgE, and thus do not require prior sensitization. Such reactions may be related to the dose, concentration, and infusion rate of the antivenom and are more common than true allergic anaphylaxis following antivenom administration. Whenever antivenom administration is first started, the treating physician should be at the bedside to recognize the first signs of anaphylaxis and to intervene as needed. Immediate hypersensitivity reactions are managed by temporarily stopping the antivenom infusion and immediately treating with epinephrine. The safest and most effective route of administration of epinephrine is 0.01 mg/kg given intramuscularly into the thigh. Epinephrine should only be administered intravenously if hypotension is profound, and then a slow intravenous infusion should be initiated and titrated to clinical effect (see Chapter 62). Crystalloid fluid infusions should also be used if hypotension is present. Antihistamines (both H1 and H2 blockers) and steroids should be administered intravenously as second-line therapy for anaphylaxis. Once the reaction has been reversed, the antivenom infusion should be restarted. If the reaction was particularly severe and more life threatening than the envenomation, it may be necessary to proceed with management of the envenomation without further antivenom. In all such cases, an expert in envenomation medicine should be consulted for assistance. Delayed, type III hypersensitivity reactions, or serum sickness, may occur a few days to a few weeks after antivenom administration.63 Such reactions occur as a result of vascular deposition of immune complexes (host antibody-antivenom) in tissues such as the skin, kidneys, and synovium. Clinical findings may include fever, rash, arthralgias, neuropathies and renal dysfunction. The presence of non-neutralizing proteins in whole IgG antivenoms and their prolonged elimination half-lives make serum sickness more likely and often more severe than that with Fab fragment products.55 Delayed hypersensitivity reactions are generally not life threatening, though they may be quite debilitating. Serum sickness should be treated with oral steroids (e.g., prednisone, 1 mg/kg/day) until the symptoms have resolved and then tapered over approximately 1 week. Symptomatic relief can be furthered with oral antihistamines and acetaminophen. Clinical illness usually resolves in 1 to 2 weeks with appropriate therapy. It is not possible to accurately predict patients who will have an acute reaction to antivenom. Skin testing is of no benefit in this regard and should not be used.202,218 Patients who have

SPECIAL SNAKEBITE SCENARIOS Allergy to Reptile Venom Snake (and lizard) venoms are highly immunogenic substances. Occasionally, a bitten victim presents with an acute, allergic anaphylactic reaction.18,76,168 The risk for such reactions increases in victims previously bitten by venomous reptiles or those who work with venoms (e.g., in a venom-extraction or research facility). In addition, snake venoms can trigger an autopharmacologic response in victims, with resulting release of vasoactive compounds (e.g., histamine and bradykinin) that cause nonallergic anaphylactic (anaphylactoid) reactions.32,188 The presentation in either scenario can be typical for anaphylaxis, with bronchospasm, laryngeal edema, hypotension, and urticaria, but differentiating between an acute immunologic reaction to venom and severe direct venom toxicity can be difficult. If the precise etiology for hypotension or respiratory distress is unclear, treatment can be rendered for anaphylaxis (beginning with intramuscular aqueous epinephrine 1 : 1000, 0.01 mg/kg) while antivenom preparation (in the case of snakebite) and supportive care proceed. Bites in Children When children are bitten by venomous snakes, they receive venom loads similar to those received by adults, resulting in higher relative venom doses per unit body weight. It remains unclear, however, whether children suffer more severe envenomations.49,160,190,212 Dosing of antivenom in pediatric victims is the same as for adults. Antivenom is not dosed on any weightbased formulation. With adequate antivenom administration, children do not appear any more susceptible to systemic venom effects than are adults.56 The total volume of diluent used in administering antivenom in children can become a factor, particularly in very small children (less than 10 kg body weight) or those with underlying cardiovascular, pulmonary, or renal disease.160 In such cases, the total volume of diluent can be reduced as needed. For CroFab, the recommended dilution of the total initial dose in 250 mL of saline is a reasonable volume tolerated by most children weighing more than 10 kg. CroFab appears to be safe and effective in children.169 Although CroFab is preserved using thimerosal, an organic mercurycontaining preservative, its benefit far outweighs any mercury toxicity risks when used in young children, because the maximum total mercury contained in a vial is 104.5 mcg, resulting in a total exposure of no more than 1.9 mg of mercury in a child receiving a large (18-vial) total dose of this product.48,77,160 Bites in Pregnant Women Snakebites are rare in pregnant women.117 The fetus is best served by an approach that optimally treats the mother. Potential effects of snake venom on the fetus have not been well studied, although fetal malformation has been described.139 Preterm labor, abruptio placentae, and fetal and neonatal deaths have also been reported after pit viper envenomation.117,162,225 Anticoagulant and proteolytic actions in many crotaline venoms are probably responsible for disrupting integrity of placental attachment to the uterus. To inhibit these systemic venom effects, antivenom administration is important, even though all U.S. antivenoms carry an FDA Category C designation for safety in pregnancy. The benefit of antivenom outweighs the risks in this population, although informed

consent should be obtained before administration, if possible. Standard doses of antivenom should be used, although the severity rating should be liberally upgraded in pregnant patients. If an acute allergic reaction develops during antivenom administration, antivenom should be temporarily stopped. Epinephrine should be avoided, if possible, because of its adverse effects on uterine blood flow. Instead, ephedrine should be given at a dose of 5 to 25 mg by slow IV push.163 This dose can be repeated every 5 to 10 minutes as needed (maximum 150 mg in 24 hours). If the reaction is refractory to ephedrine, however, epinephrine should be used. Other drugs (e.g., antihistamines, steroids) should be given as for the nonpregnant patient. Antivenom administration can usually be restarted in a more dilute concentration and at a slower rate. Additional consultation with an envenomation specialist is advisable. Other management principles for snakebitten pregnant women include early obstetric consultation, fetal monitoring, and early ultrasonography for fetal and placental assessment. Exotic Snakebites With the growing popularity of keeping venomous snakes in private collections in the United States, bites by captive venomous reptiles have increased. A physician anywhere in North America may see a victim who has been bitten by a king cobra (Ophiophagus hannah), a black mamba (Dendroaspis polylepis), or another exotic species. Management principles in these cases are similar to those outlined earlier (see also Chapter 55). In 2008, 144 exotic snakebites were reported to the AAPCC.15 Such cases present unique clinical challenges given the lack of readily available antivenoms for these species. The online Antivenom Index, maintained by the AAPCC and American Association of Zoological Parks and Aquariums, is a helpful resource to locate U.S. stores of antivenoms (at zoos) for exotic venomous creatures. Additionally, the Miami-Dade Fire Rescue Venom Response Program stocks rare and exotic antivenoms and may be willing to ship or transport antivenom to other locations when needed.149 Injuries Caused by Giant Snakes Snakes of the family Boidae (subfamily Boinae, the boas; subfamily Pythoninae, the pythons) have become quite popular as exotic pets in the United States. Although not venomous, larger boids can cause serious bites and even deaths in humans. Bites by large snakes can be quite painful, with substantial local bleeding from multiple puncture wounds inflicted from numerous fine, sharp teeth in the upper and lower jaws. If the victim reflexively jerks the bitten body part away from the snake, substantial skin tears can occur. Teeth may be dislodged and remain embedded in the victim’s soft tissues. Bleeding generally stops quickly with direct pressure. Management includes cleaning the wounds, updating tetanus status as needed, and attempting to rule out retained teeth. Soft tissue radiographs or ultrasound can be used for this purpose. If teeth are not seen, the victim should still be warned of the possibility of retained teeth and instructed to return on evidence of secondary infection. Antibiotics are not indicated unless an infection occurs. The boids kill prey by constriction. Approximately once a year, a human is killed in North America by a large captive boid. Implicated species have included the Indian and Burmese pythons (Python molurus ssp), African rock python (P. sebae), reticulated python (P. reticulatus), amethystine python (Morelia amethistina) and anaconda (Eunectes murinus). In human fatalities, the constriction may occur in several situations. Victims, including adults, may be killed by a snake that is draped over their shoulders as they clean its cage, or as they sleep in a house with a snake that has escaped from its enclosure or been allowed to roam freely. In all such cases, the snake wraps the victim’s neck and body in its coils and the victim dies as a result of asphyxiation.141,161 Precautions against such tragic events include maintaining the animal in a secure, escape-proof, and locked enclosure; never cleaning or feeding a large boid while alone; never keeping large boids in the home of a small child; and never allowing children to handle large boids unsupervised. Any boid in excess of 2 m (6.5 feet) in length should be handled with caution. There are no documented cases of humans actually being consumed by giant snakes in the United States, and if this 1033

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

previously received antivenom may be at some increased risk for allergic reaction, but this is not a contraindication to antivenom use.44 Other patients at increased risk include those with known allergy to horse or sheep serum (depending on which animal was used to prepare the antivenom), and victims with known allergy to papaya or papain. Patients on beta-adrenergic blocking agents are also of concern, because this may predispose to refractory anaphylactic reactions. In all of these cases, a careful risk– benefit analysis should be done based on severity of envenomation before deciding whether or not to proceed with antivenom therapy. If the risk for reaction is deemed high, extra care should be taken and pretreatment with antihistamines may be considered, though this strategy is unproven.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

occurs in regions of the world where these animals are found in the wild, it is an exceptionally rare occurrence.

MORBIDITY AND MORTALITY Pit Vipers Reliable numbers for morbidity and mortality from snakebite in North America are not available, but it is generally accepted that deaths in the United States and Canada are uncommon. Recent assessments suggest that annual snake-related fatalities average fewer than 6 per year (range: 0 to 12) in the United States, ranking snakes far behind dogs and stinging insects in terms of animal-related fatalities.116,118 Another source of information on snakebite-associated morbidity and mortality is the AAPCC. Over a 26-year period (1983 to 2008), 33 deaths from endemic venomous snakes were reported to the AAPCC (Table 54-4).* When the reptile implicated was identified, almost all were rattlesnakes. These numbers are underestimates and can be used only as a rough gauge of incidence and mortality. Not all venomous snakebites, even fatal ones, are reported to the AAPCC. Snakebite is not classified as a reportable disease, and there exist no reliable government statistics. Although causes of death vary following venomous snakebite, delay in reaching emergency medical care is a major contributing factor.91 When death results, it may rarely occur within a few minutes, or more commonly, it can take several hours to days. A quick death can be caused by anaphylactic or anaphylactoid reactions to venom or antivenom (see Allergy to Reptile Venom and Adverse Reactions to Antivenoms, earlier), by venom-induced respiratory insufficiency, or by airway obstruction following bites to the head or neck. Prolonged hypotension, shock, and tissue hypoxia can lead to hypoxic encephalopathy, cerebral edema, and herniation. Venominduced coagulopathies can lead to life-threatening bleeding complications, such as intracranial or gastrointestinal bleeding. Multiinfarct encephalopathy has been observed to occur in patients with true disseminated intravascular coagulation, which is very rare. Renal failure may take several days to manifest and can cause death if untreated. Comorbidities, such as coronary artery disease, can affect the chances of surviving snakebite. Iatrogenic complications, such as adverse drug reactions or nosocomial infections, can also lead to death. Before the introduction of Wyeth’s pit viper antivenom in 1954, mortality rates were estimated to be as high as 5% to 25%.165 After that time, mortality rates in patients treated without antivenom declined to approximately 2.6%, largely because of improvements in other aspects of care (e.g., development of ICUs and of fluid resuscitation principles). Antivenom, however, further reduced the mortality rate to 0.28%, a statistically and clinically significant tenfold reduction.165 The challenge and focus of future research are likely to shift from mortality issues to measures that reduce morbidity, disability, pain, and inconvenience (e.g., issues associated with prolonged monitoring after treatment).52 Other than death, permanent systemic morbidity after pit viper envenomation is rare.56 Local sequelae, such as the partial or complete loss of a limb or digit, loss of function at a joint (Figure 54-40), or permanent sensory loss, are more common.56 The reported incidence of permanent local morbidity is less than 10%, although this does not include complications that may follow surgical interventions.74 Most patients recover fully after rattlesnake envenomation in the United States, but the incidence of local complications is probably underestimated. Unless careful follow-up is done, including objective range-of-motion and sensory testing, permanent disabilities that impact lifestyle and occupation can be missed.193 Although not clearly substantiated, it has been suggested that children are more susceptible than are adults to systemic morbidity and mortality from snakebites (see Bites in Children, earlier).49,160,212 However, of the 142,516 snakebite exposures and 39 deaths (including endemic and exotic snakes) described by

*References 15-17, 115, 119-136, 205, 208-210.

1034

the AAPCC since its first report in 1983, only two deaths were in pediatric patients.* Better pediatric supportive care and improved understanding of how antivenom should be administered have blurred any distinction between the pediatric and adult prognosis.56 Older adult patients appear to have a higher case-fatality rate, probably related to co-morbid conditions.56 Morbidity and mortality from snakebites can also result from efforts to treat the victim. Significant wound complications can follow ill-advised incisions in and around the bite site and application of mouth suction.68,221 Serious burns and systemic complications, such as myocardial infarction, can follow application of electric shocks to the wound.179 Tourniquets or ice may increase the risk for tissue damage. Antivenoms can precipitate early anaphylactic or anaphylactoid reactions that can add to morbidity and even result in death (see Adverse Reactions to Antivenoms, earlier). Coral Snakes Deaths due to coral snake bites are quite rare, but the potential should not be underestimated. In fact, the mortality rate for an untreated bite has been estimated to be approximately 10%.166 Although animal research suggests that death can occur as a result of cardiovascular collapse,171 the cause of death is much more likely to be related to paralysis and respiratory failure. Prolonged muscle weakness is common after severe envenomation, and victims with respiratory compromise may require mechanical ventilation for many days. There are no reports of permanent sequelae in patients who survive coral snake envenomation.

Venomous Lizards The only two known species of venomous lizards in the New World are found in North and Central America, and they belong to the genus Heloderma. The Gila monster (Heloderma suspectum) is found in the southwestern United States (Arizona, western New Mexico, southeastern California, the southern tip of Nevada, extreme southwestern Utah) and northwestern Mexico (Figure 54-41).197 The range of the Mexican beaded lizard (Heloderma horridum) is south of that of the Gila monster, extending to Guatemala (Figure 54-42).182

SCOPE OF THE PROBLEM Establishing credible estimates of the incidence of venomous lizard bites is even more difficult than for snakes. The vast majority of victims are bitten while intentionally interacting with the lizard, and truly accidental bites are rare. Because these creatures are legally protected, many bites are probably never reported.

ANATOMY The two New World venomous lizards are impressive creatures about which much misinformation has been spread for centuries. They have been thought to possess supernatural features such as poisonous breath, a stinging tail, and the ability to spit their venom.178 The Gila monster (Heloderma suspectum) reaches a maximum length of approximately 50 cm (19.7 inches), whereas the beaded lizard (Heloderma horridum) is larger, reaching almost 1 m (39.4 inches). They are both heavily built and possess massive muscles of mastication with powerful biting capacity. The venom delivery apparatus consists of a pair of anterior, multilobed glands that open through a series of ducts into the labial mucosa of the lower jaw. Their teeth are lancet shaped, grooved, and loosely attached to the jaws (Figure 54-43). When the lizard becomes agitated, it salivates heavily, producing a flow of venom into the labial mucosa. It bites with a powerful, chewing motion, instilling venom into the wounds by capillary action along the grooves of the teeth. Teeth may be left in the wounds, especially if the animal must be forcefully removed from the victim. The tenacious creature may still be attached when help arrives. Effective envenomation occurs in about 70% of bites.10

*References 15-17, 115, 119-136, 205, 208-210.

Year

Total Bites Reported*

Deaths

1983 1984 1985 1986 1987 1988 1989

717 1347 1676 2416 2701 3076 3851

1 1 0 0 1 0 1

1990 1991

4461 5255

0 1

1992

1055

2

1993 1994

5653 6317

0 2

1995

7100

2

1996 1997

7494 7045

0 2

1998 1999

7194 6832

0 2

Specifics of Deaths 1 rattlesnake 1 rattlesnake — — 1 rattlesnake — 1 prairie rattlesnake: A 27-year-old man was bitten on two fingertips by a 2-foot-long prairie rattlesnake (Crotalus viridis, formerly C. v. viridis). He arrived in the ED 15 minutes later. Swelling rapidly progressed to the upper arm over the next 2.5 hours. He was pretreated with diphenhydramine, epinephrine, and methylprednisolone, and 5 vials of antivenom in 250 mL of D5W were started. Twenty minutes later, 60% of the antivenom had been given, and he developed anaphylaxis. He was given IV epinephrine, and a cricothyroidotomy was performed; he could not be intubated because of laryngospasm. He suffered cardiac arrest. Autopsy revealed bronchospasm but no swelling of the upper airway. — 1 unidentified rattlesnake: A 52-year-old man was bitten on his thumb by an unidentified rattlesnake in central Oregon at high altitude. In the ED 20 minutes later, he complained of circumoral numbness, tingling, and flushing. BP was 140/94 mm Hg, HR was 92, RR was 16. On his thumb were “two entrance wounds and minimal swelling.” He had been given 6 mL of a solution of 5 vials of antivenom in 500 mL D5W when he became diaphoretic and dyspneic with increased pulmonary secretions. He became near-syncopal. The antivenom was discontinued, and he was intubated and given epinephrine and steroids. He became hypotensive and developed asystole within 15 minutes. Laboratory values showed acidosis, hemoconcentration, and mild coagulopathy. Autopsy revealed extensive coronary artery disease. 1 northern Pacific rattlesnake: A 20-year-old man was handling a northern Pacific rattlesnake (Crotalus oreganus oreganus, formerly C. viridis oreganus) when it bit him on the lips. He collapsed, began vomiting, and was driven 3 miles to the hospital. He was intubated 40 minutes later, but he suffered cardiac arrest during the procedure. He was resuscitated for 30 minutes with epinephrine, atropine, and 5 vials of antivenom before recovering a sinus rhythm and BP of 100/60 mm Hg. He developed profound coagulopathy and was given 30 vials of antivenom. He was later determined to be brain dead. Autopsy showed brain edema and herniation. Blood alcohol level was 207 mg/dL. 1 black Indian cobra: A 25-year-old male “snake expert” was bitten on the toe by his captive, pregnant black Indian cobra. He died within minutes. Autopsy revealed bloody pulmonary exudate, cerebral edema, and a fine petechial rash. — 1 presumptive Mohave “green” rattlesnake: A 40-year-old man was bitten while working in bushes. He collapsed 20 minutes later. In the ED 4.5 hours later, he was comatose and in atrial fibrillation with labile blood pressure. He was intubated for poor respiratory effort. Fasciculations and metabolic acidosis were noted. Two small puncture wounds, which had been initially overlooked, were noted 1 cm apart on the forearm and lower leg. The presumptive diagnosis of Mohave “green” rattlesnake (Crotalus scutulatus scutulatus) was made, and antivenom was administered. He was cardioverted to normal sinus rhythm and dopamine was started, but he remained hypotensive. He developed disseminated intravascular coagulopathy and died on day 8. 1 rattlesnake: A 34-year-old male “snake handler” was bitten on the hand when he picked up a rattlesnake on the road. He collapsed 10 minutes later and his family began cardiopulmonary resuscitation. When medics arrived 30 minutes later, he was in full cardiopulmonary arrest. He was intubated and given IV fluids, dopamine, antivenom, and hydrocortisone. He died within 3 hours. Autopsy revealed hemorrhage in the myocardium, alveoli, pancreas, and kidneys. The airway was patent, but there was laryngeal edema, pulmonary edema, and evidence of aspiration. His right coronary artery was 75% stenosed. Blood alcohol level was 118 mg/dL. 1 canebrake rattlesnake: A 35-year-old man was bitten near the radial artery while playing with a Crotalus horridus atricaudatus (now classified as C. horridus). He was asystolic when medics arrived 30 minutes later. At autopsy, no necrosis was noted. Blood alcohol level was 250 mg/dL. 1 unknown reptile — 1 rattlesnake: A 4-year-old boy bitten on the thigh was treated with 5 vials of antivenom and transferred. He was intubated en route and subsequently developed massive extremity swelling. He suffered cardiac arrest, was resuscitated and given additional antivenom, and then arrested again in the PICU 7 hours after envenomation. 1 venomous exotic snake — 1 rattlesnake: A 43-year-old man who was drinking with his friends was bitten on the hand by a rattlesnake presumed to be dead. After further ethanol consumption, he presented 1 hour later with complaints of hand pain and mild abdominal cramping. His HR was 134, RR was 28, and BP was 81/46 mm Hg. Tongue swelling, fang marks, and minimal edema of the hand were noted. Hypotension necessitated vasopressor therapy, and increased tongue edema was treated with diphenhydramine and steroids. Unsuccessful attempts at intubation were complicated by hypoxia, and cricothyroidotomy was performed. Further treatment included sodium bicarbonate for metabolic acidosis, 1 unit of polyvalent antivenom, and fresh frozen plasma. The course was complicated by acute renal failure secondary to hemolysis requiring hemodialysis, rhabdomyolysis, and prolonged ventilatory support. On day 13 in the hospital, cardiac arrest secondary to pulmonary embolism occurred, after which the patient was declared brain dead. 1 unknown snake Continued

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

TABLE 54-4  Snakebite-Related Deaths Reported to the AAPCC, 1983-2008

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 54-1  Snakebite-Related Deaths Reported to the AAPCC, 1983-2008—cont’d Year

Total Bites Reported*

Deaths

2000

7316

2

2001

7463

2

2002

7829

2

2003

7952

2

2004

8313

3

2005

7714

6

1036

Specifics of Deaths 1 eastern diamondback rattlesnake: A 2-year-old boy was bitten just proximal to the knee by an eastern diamondback rattlesnake (Crotalus adamanteus). Findings included one fang mark and minimal local signs. On arrival at the hospital, BP was 98/48 mm Hg and HR was 130. Listlessness, progressive swelling at the site of the bite, hypotension, and bleeding from his cutdown site, nose, mouth, and gastrointestinal tract ensued. Treatment included 90 vials of polyvalent Crotalidae antivenom, vasopressors, and blood products. Within 24 hours, he had fixed, dilated pupils and no response to pain. A CT brain scan revealed bilateral cerebral infarctions and he was declared brain dead. 1 timber rattlesnake: A 45-year-old man was bitten under the right nipple by a timber rattlesnake (Crotalus horridus horridus [now classified as C. horridus]) during a snake-handling congregational meeting. Church members reportedly prayed over him for the next 2 days until he died. At autopsy, systemic petechiae, marked ecchymosis of his anterior chest wall, and hemorrhagic mediastinitis were noted. 1 rattlesnake: A 30-year-old man was comatose after a bite from his pet rattlesnake. In the ED, he was found to have coagulopathy and a subarachnoid hemorrhage. On admission, his INR was 5.5, and his platelet count was 7000/µL. He received 10 to 20 vials of crotalid antivenom and was admitted to the ICU. His condition continued to worsen and life support was withdrawn on the day after admission. 1 unknown crotaline 1 timber rattlesnake: A 43-year-old man was reportedly bitten by a timber rattlesnake (Crotalus horridus horridus [now classified as C. horridus]) while he was trying to capture it. He was unstable in the ED 1 hour after the bite, requiring endotracheal intubation and epinephrine for a BP of 60/47 mm Hg. He was treated with 10 vials of crotaline polyvalent antivenom, diphenhydramine, corticosteroids, morphine, and diazepam. He was transferred to another hospital. An additional 16 vials of antivenom were administered. Dopamine and epinephrine were administered for hypotension. Four hours after the admission, there was laboratory evidence of coagulopathy. Six vials of Fab antivenom were given. Over the next few hours, he appeared to stabilize and vasopressors were discontinued. Several hours later epistaxis and bleeding from his mouth began. An additional 7 vials of antivenom, fresh-frozen plasma, platelets, and cryoprecipitate were given. Renal failure developed and required hemodialysis. By the third day he had developed multisystem organ failure. He died on day 10 in the hospital. 1 rattlesnake 1 rattlesnake: A 33-year-old man was hospitalized for a bite to his hand by a Crotalus viridis lutosus [now classified as C. oreganus lutosus]. He was treated with CroFab and discharged within 24 hours after developing minimal symptoms. He was given a prescription for acetaminophen/oxycodone on discharge. That night he was noted to be snoring in bed and was difficult to arouse, and in the morning he was found dead in bed. Autopsy revealed pulmonary edema, thick secretions occluding the trachea and bronchi, and cerebral edema. Postmortem heart blood had an oxycodone concentration of 200 ng/mL. The medical examiner attributed the death to respiratory arrest from an opiate intoxication. 1 venomous exotic snake 1 canebrake rattlesnake: A 55-year-old man was bitten on his hand by a captive canebrake rattlesnake (Crotalus horridus horridus [now classified as C. horridus]) while feeding the snake. He became dizzy within seconds of the bite. He drove himself to a nearby ED, where he immediately became hypotensive and unresponsive. He was intubated, intravenous access was obtained, and pressors were started. He had a single puncture wound. The treating facility had no antivenom, so he was transferred to a regional referral hospital. He remained hypotensive most of the 2 hours from the time of the bite to arrival at the referral hospital. He was given 14 vials of CroFab and further resuscitation. However, he ultimately developed circulatory collapse, coagulopathy, and renal failure. He died 7 hours after the bite. 1 unknown crotaline (presumed copperhead): A 50-year-old man was bitten on the finger by a snake presumed to be a copperhead (although not positively identified). He was treated with CroFab, digit dermotomy, and fasciotomy of his arm. He became thrombocytopenic down to a platelet count of 51,000/µL and was transfused. Past medical history was significant for alcoholism, hepatitis C, cirrhosis and chronic thrombocytopenia. The patient was also given lorazepam for alcohol withdrawal; however, he became increasingly agitated and was given diazepam, haloperidol, and fentanyl. He subsequently had a respiratory arrest, which responded to naloxone. He was intubated and put on mechanical ventilation, but was later extubated. He was then taken back to the operating room for debridement of his wounds. During the procedure, he had another respiratory arrest and was reintubated. He appeared to have aspirated during this episode. Later he developed adult respiratory distress syndrome. He also had myoglobinuria. Eventually life support was withdrawn, and the patient died. 1 venomous exotic snake 1 eastern diamondback rattlesnake: A 55-year-old man was bitten on the hand by an eastern diamondback rattlesnake (Crotalus adamanteus). He had immediate dyspnea and aphonia. Upon arrival at the ED, he was hypotensive and diaphoretic. Cardiac monitoring showed ectopy. Swelling extended into his forearm. He was given 4 vials of CroFab and amiodarone and showed clinical improvement. Laboratory results: PT 17 sec; platelet count 109,000/µL. Approximately 27 hours after presentation, 16 vials of antivenom had been given. Labs: PT 20 sec; fibrinogen 195 mg/dL. On the sixth hospitalized day, he had coagulopathy recurrence. Labs: platelet count 93,000/µL; fibrinogen <35 mg/dL; PT and PTT both >150 sec. It is not clear whether blood products or additional antivenom were given. Later that day he developed focal neurologic deficits and became unresponsive. Head CT showed intracranial hemorrhage. He died the following day. 1 rattlesnake (Crotalus horridus horridus): A 25-year-old man was bitten on the hand by a rattlesnake (Crotalus horridus horridus [now classified as C. horridus]). He was being driven to a rural hospital when the car had a flat tire. The patient became unconscious and was taken on to the hospital by a passing motorist. He was dead on arrival to the ED. Autopsy revealed a bite mark on the back of the hand, with hemorrhagic necrosis of the underlying soft tissue. A blood ethanol level was 290 mg/dL.

Year

2006 2007 2008

Totals:

Total Bites Reported*

Deaths

7311 7330 7098

4 0 3

142,516

39

Specifics of Deaths 1 rattlesnake: A 32-year-old man with a history of snakebites in the past was bitten by a rattlesnake. Upon arrival to the ED 10 minutes later, he had a respiratory arrest due to anaphylaxis. His pupils were fixed and dilated. The patient was resuscitated and antivenom was given. Oxygen saturation improved to 98%, and blood pressure stabilized. He was transferred to a higher level of care hospital. Labs: PT and PTT were slightly prolonged; platelet count 120,000/µL. Additional antivenom was given. His neurologic status throughout hospitalization was consistent with anoxic brain injury, confirmed by head CT and EEG. The patient died on day 4. 1 presumed crotaline: A 44-year-old man saw a 4-foot long snake (presumed crotaline) and chased it into a wooded ravine to catch it. His body was found 2 days later. Autopsy showed 4 puncture marks on his hand with swelling, discoloration, and cellular lysis of the surrounding muscle and tissue. Marked edema of the larynx, epiglottis, and surrounding upper airway was noted as well. A blood ethanol level was 120 mg/dL. 2 unknown crotalines 3 rattlesnakes 1 unknown crotaline 1 rattlesnake: A 37-year-old man was bitten on his thumb by a rattlesnake at home. He called his wife, who arrived 30 minutes later and found him cyanotic and unresponsive after vomiting. EMS personnel defibrillated and intubated the victim and started CPR. His past medical history included asthma and two prior rattlesnake bites with reported “allergy” to rattlesnake venom. Physical exam revealed him to be unresponsive with fixed and dilated pupils and a small (<1 cm) laceration on his thumb. He had respiratory and metabolic acidosis, and cardiac rhythms during his resuscitation included asystole, VF, and VT. His T was 35.6° C (96.1° F). In the ED, he received IV fluids, sodium bicarbonate, epinephrine, atropine, methylprednisolone, diphenhydramine, 6 vials of antivenom, norepinephrine, lidocaine, clindamycin, levoquinalone, midazolam, vecuronium, naloxone, and vitamin K. Labs approximately 4 hours after the bite demonstrated PT 19.6 seconds; fibrinogen 155 mg/dL; platelets 232,000/µL; and Hgb 19.1. The patient was flown to a tertiary hospital. Six more vials of antivenom were given. No ecchymosis or oozing was noted. On day 2, he was still on a ventilator and shaking; swelling was present in his hand, and the thumb was black. He was on an insulin infusion and antibiotics, and diphenhydramine and 4 units of fresh frozen plasma were given. On day 2 his platelets were 142,000/µL; INR 1.5; fibrinogen 223 mg/dL; and fibrin degradation products >40 mcg/mL. On day 3 he had a GCS of 5T. He remained on insulin and received nebulized albuterol, morphine, hydrocortisone, antibiotics, and vitamin K. He developed poor urine output and was started on NG feedings. The tip of his thumb became necrotic. His platelets were 84,000/µL, fibrinogen 330 mg/dL; and Hgb 11.5. On day 4, he had no cough or gag reflex, and his GCS was 3T. On day 5, the patient’s family requested comfort measures only; he expired on day 6. 2 unknown crotalines Of the cases where circumstances were described: • All victims were male. • Ages (in years) were 2, 4, 20, 25 (two), 27, 30, 32, 33, 35, 37, 40, 43 (two), 44, 45, 50, 52 and 55 (two). • 26 rattlesnakes, 7 unidentified crotalines, 4 exotics, 2 unknown. • Time to death varied from minutes to 10 days. • At least 6 bites were associated with alcohol ingestion. • Crotalus horridus was the most commonly implicated snake (5 cases) when species was reported. • 1 appeared to be related to coagulopathy recurrence. • 1 appeared to be related to self-overmedication with opiates.

From references 15-17, 115, 119-136, 205, 208-210. AAPCC, American Association of Poison Control Centers; bpm, beats/min; BP, blood pressure (mm Hg); CPR, cardiopulmonary resuscitation; CT, computed tomography; D5W, 5% dextrose in water solution; DIC, disseminated intravascular coagulation; ED, emergency department; EEG, electroencephalogram; EMS, emergency medical services; FabAV, Fab fragment antivenom; FFP, fresh frozen plasma; GCS, Glasgow Coma Scale; HR, heart rate (beats per minute); Hgb, hemoglobin (g/dL); ICU, intensive care unit; INR, international normalized ratio; IV, intravenous; NG, nasogastric; NSR, normal sinus rhythm; PICU, pediatric ICU; PT, prothrombin time; PTT, partial thromboplastin time; RR, respiratory rate (breaths per minute); RCA, right coronary artery; T, temperature; VF, ventricular fibrillation; VT, ventricular tachycardia. *Includes all bites by reptiles (including exotics, nonvenomous, and unknowns).

A

B

C

FIGURE 54-40  A, Soft tissue swelling, hemorrhagic blebs, and early necrosis after red diamond rattlesnake (Crotalus ruber) bite to the long finger (day 2). Victim received ten vials of antivenom (Crotalidae) polyvalent 6 hours after the bite and ten more vials for severe thrombocytopenia on day 2. B, Seven weeks later. Note the degree of necrosis. C, Five years later. Extensor function was never regained. (A and B courtesy Sean P. Bush, MD; C courtesy Kent Denmark, MD.)

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CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

TABLE 54-1  Snakebite-Related Deaths Reported to the AAPCC, 1983-2008—cont’d

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 54-41  Gila monster (Heloderma suspectum) is one of only two known venomous lizards and the only species found in the United States. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

VENOMS Gila monster and beaded lizard venoms are similar in composition and are as potent as some rattlesnake venoms.195 They possess enzymatic components, including hyaluronidase (spreading factor), protease, phospholipase A2, kallikrein-like substances, and nonenzymatic substances such as serotonin. Venom kallikreins stimulate the release of vasoactive kinins, such as bradykinin, which may be responsible for occasional hypotension seen after helodermatid bites.197 These venoms contain no neurotoxic components and no components that directly interfere with coagulation.144 Of note, Gila monster venom inspired production of a drug that helps diabetics get better control of their blood glucose levels.194

CLINICAL PRESENTATION Following the bite of a helodermatid, bleeding usually occurs from punctured and torn tissues, but it is generally not excessive.144 Throbbing or burning pain may radiate proximally along the bitten extremity and may be severe. Local edema may be progressive (Figures 54-44 and 54-45; Figure 54-44, online). Victims may complain of generalized weakness, nausea and vomiting, difficulty breathing, profuse sweating, dizziness, and paresthesias.4,99,178,197 On examination, the victim may be tachycardic, hypotensive (related to kinin release), and diaphoretic.4,99 There may be significant local tissue trauma. The site may be cyanotic or ecchymotic with local vasospasm.178 Regional lymphadenopathy may be present.10 Apparent anaphylactic reactions to helodermatid venom have been reported.38,168

FIGURE 54-42  Mexican beaded lizard (Heloderma horridum) is located south of the Gila monster’s range in Mexico. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

1038

FIGURE 54-43  Teeth of the helodermatid lizards are grooved to aid instillation of venom during a bite. These teeth are loosely adherent and may become dislodged in the bite wound. (Courtesy Michael Cardwell, Extreme Wildlife Photography.)

MANAGEMENT Prehospital Care Data are minimal regarding prehospital care of venomous lizard bites. In some cases, the first priority is to detach the lizard from the victim. The lizard can be placed under running hot water, or the jaws can be pried apart using a stick or metal instrument.197 Care must be taken not to injure the victim further and to avoid a second bite, perhaps to the rescuer. Once freed from the lizard, the victim should be placed at rest and the bite site rinsed and cleaned as much as possible. Any bleeding should be stopped with direct pressure. There is no evidence to support the use of suction devices, ligatures, or pressure immobilization, and incisions and electrotherapy should be strictly avoided. Local application of ice may be harmful because it may increase the risk for vasospasm and tissue damage.180 A bandage to stop bleeding and a splint to limit movement may be beneficial. The victim should be expeditiously transported to a medical facility. Hospital Care Assuming the lizard has been detached before arrival at the hospital, the victim’s airway, breathing, and circulation are assessed. Vital signs should be obtained while the patient is being placed on oxygen and cardiac and pulse oximetry monitoring. At least one large-bore IV line should be established with normal saline. If the victim is hypotensive or tachycardic, a second line should be placed, and physiologic saline should be given (1 to 2 L for an adult, 20 to 40 mL/kg for a child). Hypotension rarely persists after volume resuscitation. If necessary, vasopressors can be added after the victim’s intravascular volume has been repleted.197

FIGURE 54-45  Bite of a captive beaded lizard (Heloderma horridum). (Courtesy Michael Cardwell.)

MORBIDITY AND MORTALITY No fatalities from helodermatid bites have been documented in at least 60 years,144 but a bite could prove fatal if a large lizard were to hang on to a victim and deposit a large volume of venom. Bites to children are especially concerning because of a potentially larger venom load per body mass compared with adults. Likewise, given their complicating comorbidities,

chronically ill or older adult victims are at higher risk for a serious outcome. Pain and tenderness may be prolonged for days or weeks after these bites,180 although necrosis is rare.144,178

Considerations Before Going Into the Wilderness Before leaving on a trip into habitat in which venomous reptiles may be encountered, it is important to plan the steps to be taken should a bite occur. The traveler should become familiar with local dangerous fauna, using field guides or Internet resources. A plan should be developed for field management of a bite. How will a victim be evacuated from the location? What will be the destination hospital? Does the hospital have antivenom and personnel knowledgeable in the management of snakebite? Appropriate supplies should be gathered, such as dressings and splints (e.g., SAM SPLINTs are lightweight and easily carried). The question often arises of whether to carry antivenom on a trip to a remote location. If this is considered, an appropriate, preferably broad-spectrum, polyspecific product is ideal. Such products are best purchased in the destination country, because advance importation of exotic antivenoms into the United States is time consuming and difficult. If a foreign product is to be carried, its package insert should be translated, if necessary, before the trip begins. If traveling to Central or South America, it is likely that CroFab would provide broad enough coverage for most pit vipers that might be encountered (although further research is needed in this area, and it is certainly more expensive than antivenoms produced by Latin American countries). CroFab has been studied and found to be relatively stable despite prolonged exposure to high temperatures and rough handling.55 It should stand up to the punishment of vigorous hiking in tropical regions. If antivenom is to be taken into the field, all equipment necessary for its administration (IV supplies, a bag of normal saline, airway equipment, and drugs needed to adequately treat an acute reaction) must also be carried, and an expedition member must have the skills needed to give the drug and treat adverse reactions. Although it may be possible to administer CroFab intramuscularly,189 the intravenous route is preferred. Further research is needed to determine whether the smaller molecular size of Fab fragments allows adequate distribution by the intramuscular route to be of any benefit in field management of snake envenomation. The most important consideration when entering the field is, of course, prevention. Long pants and boots should be worn in snake country, and team members should be especially vigilant about visually clearing any location where they will place hands and feet when hiking, climbing, or gathering firewood. If going outside in the dark for any reason, each expedition member should wear proper footwear and carry a flashlight, because many venomous snakes are more active after dark. If a snake or venomous lizard is encountered, it is best appreciated and photographed from a safe distance.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

1039

CHAPTER 54  Bites by Venomous Reptiles in Canada, the United States, and Mexico

Laboratory testing should include a complete blood count, serum electrolytes, renal function studies, and coagulation studies. Total white blood cell count may be elevated, and in severe cases, platelets may be decreased.178 Despite the fact that lizard venoms do not appear to possess anticoagulant fractions, rare hemostatic abnormalities have been reported after severe bites and are probably related to endothelial cell damage.10,197 Urinalysis is useful to assess for microscopic hematuria or renal casts. Helodermatid bites can cause transient ECG abnormalities, such as T-wave anomalies and conduction delays.10,99 A single case of apparent myocardial infarction after a Gila monster bite has been reported in a patient with a history of cocaine abuse.10 It is reasonable to obtain an ECG and markers of cardiac ischemia if the victim shows any sign or symptom of envenomation. Once the victim’s overall status is stabilized, attention focuses on wound care. A soft tissue radiograph or ultrasound of the bite site may identify retained lizard teeth (see Figure 54-44, B, online) but does not replace careful exploration of the wounds.99 After an assessment of functional status, the wound can be anesthetized using a local or regional block. The bite site should then be carefully explored for damage to underlying vital structures and for retained teeth. Thorough cleansing and irrigation should follow exploration. The wounds are dressed and splinted with generous padding. The extremity is then elevated to reduce swelling and discomfort. Narcotics may be necessary for pain management during the victim’s initial evaluation and for any pain not controlled by local or regional anesthesia. The victim’s tetanus immunization status should be updated as needed. Infections are uncommon and prophylactic antibiotics are not required.197 If secondary infection occurs, cultures should be obtained and the victim started on broad-spectrum antibiotic coverage for both gram-positive cocci and gram-negative rods. Culture and sensitivity results should guide further treatment. Daily wound care should include cleansing with soap and water, followed by saline irrigation, application of a topical antiseptic, and redressing. Physical therapy is helpful in returning the patient more rapidly to full function. Victims who are relatively asymptomatic, with normal vital signs and diagnostic studies, may have received a dry bite and can be discharged home after 8 hours of medical observation. These patients must have proper resources for care at home and the ability to return if they worsen. Proper wound care instructions should be given and patients should be scheduled for reevaluation in approximately 24 to 48 hours. An oral narcotic analgesic may be prescribed. Evidence of envenomation (i.e., signs or symptoms besides simple wounds; laboratory or ECG abnormalities) necessitates admission. Systemic findings (e.g., chest pain, ECG changes, hypotension, and rare coagulopathy) require monitoring for at least 24 hours.197 There is no antivenom for venomous lizard bites.

CHAPTER 55 

Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide  DAVID A. WARRELL

Dangerous Reptiles Within the class Reptilia, some alligators and crocodiles (order Crocodylia), notably Crocodilus niloticus and C. porosus, are able to kill and eat humans (see Chapter 58); even large sea turtles (order Testudines) can be dangerous. The leatherback turtle (Dermochelys coriacea), which can reach 3 m (9.8 feet) in length and 900 kg (1984 lb) in weight, is reported to have capsized small boats. Giant pythons and Komodo dragons occasionally prey on humans (see later text). Many species of the clade Toxi­ cofera, constituting 60% of the Squamata (snakes and lizards),66 including snakes of Canada, the United States, and Mexico, and helodermatid lizards of the southern United States and Mexico are capable of venomous bites (see Chapter 54). This chapter covers dangerous snakes and lizards, venomous and nonvenom­ ous, found in the rest of the world and therefore considered “exotic” in North America.

Venomous Snakes TAXONOMIC REVOLUTION Snake taxonomy is based on morphologic features, such as numbers and arrangement of scales (lepidosis), dentition, osteol­ ogy, myology, sensory organs, form of the hemipenes (paired male genital organs), and, increasingly, sequence analysis of DNA encoding of important mitochondrial and other enzymes.167,237,238 The accelerating pace of taxonomic revision of medically impor­ tant taxa has left clinicians and nonherpetologists confused and frustrated. To change familiar names and split genera and species of medically important taxa can be misleading, even though it may be well justified on evolutionary and taxonomic grounds. Correct identification and designation of species responsible for bites is important for optimal clinical management and choice of appropriate antivenom. Therefore the latest taxonomic designa­ tions are employed in this chapter, with obsolete but familiar names in parentheses. Use of correct taxonomy is essential when designing regional antivenoms and selecting appropriate venoms for their manufacture. It is also crucial for laboratory toxinologists who work on venoms that are sometimes of uncertain prove­ nance. Several toxins have been misnamed because of ignorance of the correct nomenclature for the source species. For instance, “ceruleotoxin” was named after Bungarus caeruleus, although its true origin was Bungarus fasciatus. “Grambin” and “graminely­ sin” were named after Trimeresurus gramineus, but were obtained from Viridovipera (Trimeresurus) stejnegeri. In an attempt to improve the flow of information between taxonomists, toxinologists, and clinicians, an important series of reviews was published in Toxicon,295,296 succeeded by an invaluable web­ site (http://www.bangor.ac.uk/~bss166/update.htm). Some pub­ lished work on toxins can never be reproduced because the venoms used, their origins shrouded in incorrect snake nomen­ clature, can never be identified.297 Fortunately, nomenclature and identification have been clari­ fied for several groups of medically important snakes: African spitting cobras,294,299 Afro-Asian saw-scaled vipers,161 Asian cobras,293,294,298,301 Russell’s vipers,301 arboreal pit vipers,132,178 and Bothrops atrox.300 Many of the most important causes of snakebite 1040

in each country have been identified and their geographic dis­ tributions mapped (http://www.who.int/bloodproducts/snake_ antivenoms/en/). New species of both clinical and toxinologic interest continue to be discovered, for example New Guinea small-eyed snake (Micropechis ikaheka),270 Indo-Chinese spitting cobra (Naja siamensis),301 hump-nosed pit viper (Hypnale hypnale) in India,101,129 the greater black krait (Bungarus niger) in Bangladesh,57 Wall’s kraits and the Sind krait in Nepal and Bangladesh,113 and the southern African swamp adder (Proatheris superciliaris).259 Based on their nuclear and mitochondrial genes, advanced snakes (Caenophidia), including all venomous snakes, are now classified into three superfamilies:237,238 • Colubroidea—including families Natricidae (e.g., Asiatic keelbacks genus Rhabdophis), Colubridae (e.g., African boomslang Dispholidus typus and twig snakes genus Thelotornis) and Dipsadidae (e.g., South American racers genus Philodryas) • Elapoidea—including families Lamprophiidae (subfamily Atractaspidinae, burrowing asps genus Atractaspis) and Elapidae (terrestrial elapids, sea snakes and sea kraits) • Viperoidea—including Viperidae, subfamilies Viperinae (Old World vipers) and Crotalinae (pit vipers)

Identification of Venomous Snakes DISTINGUISHING SNAKES FROM LEGLESS LIZARDS, AMPHIBIANS, AND SNAKE-LIKE FISH Most lizards have eyelids, external ear orifices (Figure 55-1, Pogona barbata), thick and fleshy tongues that are forked and snake-like in Varanidae, Teiidae, Lacertidae, and Anguidae, and very long friable tails; they lack the enlarged ventral scales of snakes. Legless lizards include slow worms and glass lizards (family Anguidae), worm-like geckos (family Pygopodidae) (Figure 55-2, Lialis jicari), and skinks (family Scincidae), some of which have vestigial limbs (Figure 55-3, Chalcides armitagei) and may be confused with snakes unless these features are detected. The fossorial amphisbaenid lizards have worm-like annular grooves along the length of their bodies (Figure 55-4, Amphisbaena fuliginosa; Figure 55-5, A. mertensii). Caecilians (legless amphibians) (Figure 55-6, Dermophis mexicanus) have no obvious eyes or scales. Eels and pipe-shaped fish are easily distinguished by their gills and fins from snakes.

DISTINGUISHING VENOMOUS FROM NONVENOMOUS SNAKES There is no quick, simple, and absolutely reliable method for distinguishing venomous from nonvenomous snakes. The fangs may be very small in elapids, or they may be folded back inside a sheath in vipers (Figure 55-7, Bothrops atrox). In a dead snake, a needle may be swept along the upper jaw from the angle of the jaw to the snout to engage upon and reveal the fangs. Some key morphologic features are subtle. Most elapid snakes lack the loreal scale (between the preocular and nasal scales) possessed by most colubroid snakes (Figure 55-8, Dendroaspis angusticeps and Philodryas viridissimus). Pit vipers (Crotalinae) possess a

For online-only figures, please go to www.expertconsult.com

FIGURE 55-2  Papuan snake-lizard (Lialis jicari: family Pygopodidae) (Madang, Papua New Guinea), a legless lizard, showing external ear opening, distinguishing it from snakes. (Copyright D.A. Warrell.)

FIGURE 55-5  Mertens’ worm lizard (Amphisbaena mertensii: family Amphisbaenidae) (Brazil). (Copyright D.A. Warrell.)

FIGURE 55-6  Mexican caecilian (Dermophis mexicanus: family Caeciliidae). (Copyright D.A. Warrell.)

FIGURE 55-3  Armitage’s cylindrical skink (Chalcides armitagei: family Scincidae) (The Gambia) showing vestigial limbs. (Copyright D.A. Warrell.)

heat (infrared)-sensitive pit organ, situated between the eyes and nostrils, whose functions include heat regulation and detection of warm-blooded prey and predators (Figure 55-9, A, Popeia popeiorum). Pythons and boas have labial heat-sensitive organs (Figure 55-9, B, Morelia viridis). Snakes of the subfamily Viperi­ nae, the Old World vipers and adders, lack this pit organ. Fortunately, the most dangerous species tend to be well known in the areas where they are medically important. The

characteristic hood of cobras and some other elapids is visible only when the snake is rearing up in a defensive attitude (Figure 55-10, Naja mossambica). Vipers and pit vipers are often identifi­ able by their striking and sometimes colorful dorsal pattern (Figure 55-11, Bitis arietans; Figure 55-12, Deinagkistrodon acutus). Russell’s vipers (Daboia russelii) (Figure 55-13, A), Daboia siamensis (Figure 55-13, B), and puff adders (B. arietans) (see Figure 55-11) hiss loudly by expelling air through their large nostrils. The saw-scaled or carpet vipers (genus Echis) and some other desert vipers produce a characteristic rasping sound by rubbing their coils together (Figure 55-14, A, Echis pyramidum, and Figure 55-14, B, Cerastes cerastes), and king cobras (Figure 55-15, Ophiophagus hannah) are said to “growl.” The tail tip series of interlocking and resonating modified scales of 1041

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

FIGURE 55-1  Eastern bearded dragon (Pogona barbata: family Agamidae) (Australia) showing eyelids and external ear orifice typical of lizards. (Copyright D.A. Warrell.)

FIGURE 55-4  Speckled worm lizard (amphisbaenid) (Amphisbaena fuliginosa: family Amphisbaenidae) (Peru) showing distinctive annular rings, distinguishing it from snakes. (Copyright D.A. Warrell.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

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B FIGURE 55-8  A, Eastern green mamba (Dendroaspis angusticeps: family Elapidae) (KwaZulu-Natal, South Africa) showing the absence of a loreal scale between the preocular and nasal scales typical of elapid snakes. B, Brazilian green racer (Philodryas viridissimus: family Dipsadidae, Colubridae) (Manaus, Brazil) showing loreal scale (arrow) lacking in most elapid snakes. (Copyright D.A. Warrell.) FIGURE 55-7  Long front fangs of vipers fold flat, concealed by a sheath. Common lancehead (Bothrops atrox: family Viperidae) (Icoaraci, Brazil). (Copyright D.A. Warrell.)

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FIGURE 55-10  Mozambican spitting cobra (Naja mossambica: family Elapidae) (Harare, Zimbabwe) showing the hood spread in a threatening/defensive attitude and sensing forked tongue. (Copyright D.A. Warrell.)

B FIGURE 55-9  Heat-sensitive pit organs in snakes. A, Between nasal and preocular scales (arrow) in Pope’s pit viper (Popeia popeiorum: family Viperidae; subfamily Crotalinae) (Thailand). B, On the upper lip (arrows) in New Guinea green python (Morelia viridis: family Pythonidae) (Papua New Guinea). (Copyright D.A. Warrell.)

FIGURE 55-11  Puff adder (Bitis arietans) (South Africa) showing the distinctive repeated U (chevron) dorsal pattern. (Copyright D.A. Warrell.)

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FIGURE 55-12  Hundred-pacer (Deinagkistrodon acutus) (China) showing the striking dorsal pattern. (Copyright D.A. Warrell.)

B FIGURE 55-14  Desert snakes. A, Saudi Arabian saw-scaled or carpet viper (Echis pyramidum) showing its defensive coiling movement, during which the rough lateral scales rub together to produce a characteristic rasping sound. B, Algerian Saharan horned viper (Cerastes cerastes), this specimen without horns. (Copyright D.A. Warrell.)

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FIGURE 55-15  King cobra (Ophiophagus hannah) (Thailand). (Copyright D.A. Warrell.)

B FIGURE 55-13  Russell’s vipers. A, Western species (Daboia russelii ) from Anuradhapura, Sri Lanka. B, Eastern species (Daboia siamensis) from Eastern Java, Indonesia. (Copyright D.A. Warrell.)

rattlesnakes produce their familiar castanet-like warning sound (Figure 55-16, Crotalus durissus cumanensis). However, in a world increasingly densely inhabited by humans, this sound may no longer be protective to these snakes but rather attract lethal attention. There is some evidence that natural selection now favors rattlesnakes that are more reticent about sounding their rattles. Less spectacularly, several genera of South American pit vipers (Agkistrodon, Bothrops, Lachesis), especially their juve­ niles, vibrate the tips of their tails when aroused, producing a whirring sound in the undergrowth. Mimics, Misidentification, and Mismanagement Some nonvenomous or less-venomous colubroid snakes closely resemble highly venomous species in their appearance and behavior. This is probably an example of Batesian mimicry. There are examples from all continents: in Europe, Hemorrhois nummifer (coin-marked snake) mimics Macrovipera lebetina

FIGURE 55-16  South American rattlesnake (Crotalus durissus cumanensis) showing rattle (Colombia). (Copyright D.A. Warrell.)

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FIGURE 55-17  Mimicry—Europe. A, Coin-marked snake (Hemorrhois [Coluber] nummifer : family Colubridae) (Symi). B, Levantine viper (Macrovipera lebetina: family Viperidae) (Cyprus). (A courtesy Matt Wilson; B copyright D.A. Warrell.)

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FIGURE 55-18  Mimicry—Africa. A, Tiger snake (Telescopus variegatus: family Colubridae) (Nigeria). B, Egg-eating snake (Dasypeltis scabra: family Colubridae) (Kenya). C, West African carpet viper (Echis ocellatus: family Viperidae) (Nigeria). (Copyright D.A. Warrell.)

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FIGURE 55-19  Mimicry—Asia. A, Spotted cat snake (Boiga multomaculata: family Colubridae) (Thailand). B, Eastern Russell’s viper (Daboia siamensis: family Viperidae) (Supanburi, Thailand). (Copyright D.A. Warrell.)

(Levantine viper) (Figure 55-17); in Africa, Telescopus variegatus (tiger snake) (Figure 55-18, A) and Dasypeltis scabra (egg-eating snake) (Figure 55-18, B) mimic Echis spp. (saw-scaled viper) (Figure 55-18, C); in Southeast Asia, Boiga multomaculata (Figure 55-19, A) mimics D. siamensis (Eastern Russell’s viper) (Figure 55-19, B), various species of Dryocalamus (e.g. D. davisonii [Figure 55-20, A]) and Lycodon (e.g., L. aulicus Figure 55-21, A) mimic kraits (Bungarus candidus [Figure 55-20, B] and B. caeruleus [Figure 55-21, B]); and in the Americas, Dipsas (Figure 55-22, A, D. indica), Xenodon (Figure 55-22, B, Xenodon neuwiedii; Figure 55-22, C, X. severus), Waglerophis merremi (Figure 55-22, D), and many others mimic Bothrops species (Figure 55-22, E, B. brazili). The best known examples are mimics of coral snakes (Micrurus) (Figure 55-23, A to E: M. corallinus, M. decoratus, M. frontalis, M. mipartitus, M. spixii obscurus), which include Oxyrhopus, Rhinobothryum, and Simophis spp. (Figure 55-24). The familiar jingle “red on yellow kills a fellow, red on black venom lack (or, “OK Jack”)” safely distinguishes North American coral snakes (Micruroides euryxanthus, Micrurus fulvius, M. tener 1044

[Figure 55-25]) from harmless scarlet snakes (Cemophora coccinea), king snakes, and milk snakes (Lampropeltis spp.), but in Central and South America this does not apply, because many species of Micrurus have “red on black” (see Figure 55-23). Similarities between the superficial appearances of venomous and nonvenomous species, or even between different venomous species, may lead to choice of the wrong antivenom or inap­ propriate use of antivenom. For example, in a study of 860 snakebites in Sri Lanka,9 snakes were misidentified by the hos­ pital staff on 51 occasions, resulting in unnecessary use of anti­ venom. Hump-nosed pit vipers (Hypnale hypnale, Figure 55-26) were misidentified as Russell’s vipers (Daboia russelii, see Figure 55-13, A) on 36 occasions; cat snakes (Boiga ceylonensis [Figure 55-27], and B. trigonata trigonata) were misidentified as humpnosed pit vipers twice, as Russell’s vipers three times, and as a saw-scaled viper (Echis carinatus, Figure 55-28) once; pythons were misidentified as Russell’s vipers twice; wolf snakes banded phase (L. aulicus [see Figure 55-21, A]), and L. striatus sinhalayus) were misidentified as common kraits (B. caeruleus) five

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FIGURE 55-20  A, Blanford’s bridal snake (Dryocalamus davisonii: family Colubridae) (Thailand). B, Malayan krait (Bungarus candidus) (Thailand). C, Banded krait (Bungarus fasciatus) (Thailand). (Copyright D.A. Warrell.)

skin of their prey or human victim or inoculated by chewing. One or two reserve fangs may be situated immediately behind the active fang on each side. Colubroidea: Natricidae, Colubridae, Dipsadidae Venom from supralabial (Duvernoy’s) glands is inoculated by enlarged posteriorly situated (opisthoglyphous) maxillary teeth that can be formidably long (hence the term “rear-fanged snake”) (Figure 55-29, Tomodon dorsatus). These teeth may have anterior grooves or be solid. To envenom a human, the snake must seize, hold onto, and chew the finger of its victim, who is often a herpetologist. Duvernoy’s glands are surrounded by muscles (adductores superficialis, medialis and profundus and retractor quadrati that may help to express the secretions).

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B FIGURE 55-21  Mimicry—kraits. A, Wolf snake (Lycodon aulicus: family Colubridae) (Sri Lanka). B, Ceylon krait (Bungarus ceylonicus: family Elapidae) (Sri Lanka). (Copyright D.A. Warrell.)

times and rat snakes (Ptyas mucosus) as cobras twice. Antivenom was given inappropriately on 13 occasions because a nonvenom­ ous species or a hump-nosed viper had been mistaken for one of the four species covered by Indian polyspecific antivenom. In a study of 1631 snakebites in Thailand,239 Oligodon dorsolateralis was mistaken for Calloselasma rhosostoma twice and for D. siamensis once, common kukri snakes (O. cyclurus) for C. rhodostoma on six occasions, B. multomaculata (see Figure 55-19, A) for D. siamensis on seven occasions, Lycodon laoensis for B. candidus once, Rhabdophis subminiatus for C. rhodostoma once, and Dryocalamus davisonii (see Figure 55-20, A) for B. candidus (see Figure 55-20, B) or B. fasciatus (see Figure 55-20, C) on four occasions. Bungarus candidus was confused with B. fasciatus on five occasions with the result that inappropriate mono­ specific B. fasciatus antivenom was given.

FANGS AND VENOM APPARATUS* Venomous snakes have one or more pairs of enlarged teeth (fangs) in their upper jaws. The fangs usually contain grooves or venom channels through which venom is injected through the *References 112, 283.

Elapoidea: Lamprophiidae, Subfamily Atractaspidinae The genus Atractaspis (African and Middle Eastern burrowing asps, stiletto snakes, burrowing or mole vipers or adders, false vipers, or side-stabbing snakes) have long front fangs upon which they impale their victims by a side-swiping motion of the fang protruding from the corner of the partially closed mouth (Figure 55-30, Atractaspis aterrima). In some species, the venom glands are very long—perhaps one-sixth the snake’s total length. The Natal black snake (Macrelaps microlepidotus) possesses two very large grooved opisthoglyphous fangs at the posterior ends of its maxillae. Elapoidea: Elapidae Cobras—Naja; kraits—Bungarus; mambas—Dendroaspis; shieldnosed and African coral snakes—Aspidelaps; Asian coral snakes— Calliophis; African garter snakes—Elapsoidea; terrestrial venomous Australasian snakes—for example, Acanthophis, Pseudechis, Pseudonaja, Oxyuranus, Notechis; and sea snakes—for example, Laticauda, Enhydrina, Hydrophis, and Lapemis, have relatively short, proteroglyphous (fixed) front fangs mounted on a rela­ tively fixed maxilla so that they cannot be folded flat against the jaw (Figure 55-31, Oxyuranus scutellatus canni). However, mambas can rotate their fangs in the sagittal plane because the maxilla has a posterior articulation with the prefrontal bone (Figure 55-32, Dendroaspis angusticeps). This allows the snake to close its mouth despite having unusually long elapid type of fangs and to increase its gape when striking at large prey. Venom glands are situated behind the eyes and are compressed by adductor externus superficialis (equivalent to levator anguli oris) muscles. Some coral snakes possess inferolabial glands in the lower jaw that also secrete venom conducted by shallow grooves in the mandibular teeth. Spitting Elapids.41  The fangs of African and Asian spitting cobras and the South African ringhals or rinkhals (Hemachatus haemachatus) have venom channels that turn forward at their point of exit near the tips of the fangs. Compressor muscles produce a stream of venom under high pressure so that a spray of venom can be ejected forward for a meter or more into the eyes of an aggressor (Figure 55-33, Naja nigricollis).23,41,298,299 This is a defensive strategy that temporarily blinds the aggressor, 1045

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

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FIGURE 55-22  Mimicry—South American pit vipers. A, Amazonian snail eater (Dipsas indica: family Dipsadidae) (Amparo Granja, Sao Jose, Brazil). B, Neuwied’s false fer de lance (Xenodon neuwiedii: family Dipsadidae) (Cajamar, Brazil). C, Amazon false fer de lance (Xenodon severus: family Dipsadidae) (Porto Velho, Brazil). D, Wagler’s snake (Waglerophis merremi: family Dipsadidae) (Brazil). E, Brazil’s lancehead (Bothrops brazili: family Viperidae) (Moreno Santiago, Ecuador). (Copyright D.A. Warrell.)

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FIGURE 55-23  South American coral snakes (family Elapidae). A, Painted coral snake (Micrurus corallinus) (Brazil). B, Decorated coral snake (M. decoratus) (Brazil). C, Cerrado coral snake (M. frontalis) (Brazil). D, Red-tailed coral snake (M. mipartitus) (Colombia) showing tail curling display. E, Amazonian coral snake (M. spixii obscurus) (Ecuador). (Copyright D.A. Warrell.)

usually a large, threatening mammal, thus allowing the snake to escape. To eject venom 2 m, pressures of 1.5 kg/cm2 (21.3 psi) would be required. Viperoidea Viperidae (vipers, adders, and pit vipers) have highly evolved, long, curved front solenoglyphous (hinged, venom-conducting) 1046

fangs, mounted on a rotatable maxilla so that they can be erected when the snake strikes and folded flat against the jaw in a pro­ tective membrane when not in use. They contain a closed venom channel and resemble hypodermic needles (Figure 55-34, A, Bothrops jararacussu, and Figure 55-34, B, Bitis rhinoceros). The venom glands are squeezed by compressor glandulae, adductor externus profundus, and pterygoideus muscles.

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FIGURE 55-24  Coral snakes mimics (family Dipsadidae). A, Duméril’s false coral snake (Oxyrhopus clathratus) (Juquitiba, Brazil). B, Brazilian false coral snake (Oxyrhopus trigeminus) (northeast Brazil). C, Rhinobothryum bovallii (Rio Bogota, Esmeraldas, Ecuador). D, Simophis rhinostoma (Brazil). (Copyright D.A. Warrell.)

FIGURE 55-25  Texas coral snake (Micrurus tener) (Kingsville, Texas) showing “red on yellow” pattern. (Copyright D.A. Warrell.)

FIGURE 55-27  Ceylon cat snakes (Boiga ceylonensis). (Copyright D.A. Warrell.)

FIGURE 55-26  Sri Lankan hump-nosed pit viper (Hypnale hypnale: family Viperidae; subfamily Crotalinae; scale in cm). (Copyright D.A. Warrell.)

FIGURE 55-28  Sri Lankan saw-scaled viper (Echis carinatus). (Copyright D.A. Warrell.)

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FIGURE 55-30  Long front fang of a slender burrowing asp (Atractaspis aterrima: subfamily Atractaspidinae) (Zaria, Nigeria). (Copyright D.A. Warrell.) FIGURE 55-29  Long maxillary fangs of Pampas snake (Tomodon dorsatus: family Dipsadidae) (Ibiuna, Brazil). (Copyright D.A. Warrell.)

FIGURE 55-32  Eastern green mamba (Dendroaspis angusticeps) (coastal Kenya) showing articulation of the maxilla (bearing the fangs) on the prefrontal bone (arrow), allowing rotation of the long elapid type of fangs. (Copyright D.A. Warrell.) FIGURE 55-31  Short front fangs of a Papuan taipan (Oxyuranus scutellatus: family Elapidae) (Port Moresby, Papua New Guinea). (Copyright D.A. Warrell.)

FIGURE 55-33  Black-necked spitting cobra (Naja nigricollis) (Zaria, Nigeria) in the act of “spitting” venom from its fang tips toward the snake charmer’s hand. (Copyright D.A. Warrell.)

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FIGURE 55-34  Erectile front fangs of Viperidae. A, Large front fangs of jararacuçu (Bothrops jararacussu: subfamily Crotalinae, Brazil). B, Enormous solenoglyphous front fangs of a West African Gaboon viper/adder (Bitis rhinoceros: subfamily Viperinae, Cameroun) erected as when the snake strikes its prey. Gaboon vipers have longer fangs than do other snakes, up to 8 cm (3.1 inches) in length. (Copyright D.A. Warrell.)

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Snakes have evolved the most complex of all venoms, the venom of each species containing more than 100 different components. The evolutionary origins of these molecules are of great current interest.63,69 More than 90% of the dry weight is protein, compris­ ing a variety of enzymes, nonenzymatic polypeptide toxins, and nontoxic proteins. Nonprotein ingredients include carbohydrates and metals (often part of glycoprotein metalloprotein enzymes), lipids, free amino acids, nucleosides, and biogenic amines such as serotonin and acetylcholine.

ENZYMES Eighty percent to 95% of viperid and 25% to 70% of elapid venoms consist of enzymes (molecular weights 13 to 15 kDa), including digestive hydrolases (proteinases, exopeptidase, endo­ peptidases, phosphodiesterases, metalloproteinases, and phos­ pholipases), hyaluronidase,106,165,166 and activators or inactivators of physiologic processes. Most venoms contain L-amino acid oxidase (containing riboflavin 5′-phosphate prosthetic group that confers the yellow color of many venoms), which may have a digestive function,208 phosphomonoesterase, diesterase, 5′nucleotidase, deoxyribonuclease, nicotinamide adenine dinucle­ otide nucleosidase,49 phospholipase A2 (PLA2), and peptidases. Elapid venoms in addition contain acetylcholine esterase,3 phospholipase B, and glycerophosphatase, whereas viperid venoms have endopeptidase, arginine ester hydrolase, kininoge­ nase (which releases bradykinin from bradykininogen), and procoagulants—thrombin-like serine proteinases126 and factor V, factor X, and prothrombin-activating enzymes, which cause dis­ seminated intravascular coagulation leading to consumption coagulopathy. PLA2s are the most widespread and extensively studied of all venom enzymes.50,128 Under experimental condi­ tions, they damage mitochondria, red blood cells, leukocytes, platelets, peripheral nerve endings, skeletal muscle, vascular endothelium, and other membranes, and produce presynaptic neurotoxic activity, opiate-like sedative effects, and autopharma­ cologic release of histamine. Hyaluronidase promotes the spread of venom through tissues. Proteolytic enzymes (endopeptidases or hydrolases) are responsible for local changes in vascular per­ meability, leading to edema, blistering, bruising, and necrosis. Metalloproteinases cause local and systemic hemorrhage and local myonecrosis, blistering, and edema through their actions on vascular endothelium, platelets,102 muscle, and other tissues.59,79

NECROTOXINS Many snake venoms contain myotoxic and cytolytic factors that contribute to tissue destruction around the site of the bite. These include zinc-dependent metalloproteinases and myotoxic PLA2s, other digestive hydrolases, and hyaluronidase. Myotoxins are proteins that can damage the muscle cell plasma membrane directly. Most are PLA2s, either enzymatically active (aspartate-49) or enzymatically inactive (lysine-49).78 Cobra cardiotoxins are low-molecular-weight polypeptides with cytotoxic action.

NEUROTOXINS Postsynaptic Three-Finger-Fold Neurotoxins† These polypeptide curarimimetic or α-neurotoxins are lowmolecular-weight, nonenzymatic proteins found in elapid and some colubroid venoms.64,127,156 They are termed “short” (60 to 62 amino acids) or “long” (66 to 74 amino acids, such as α-bungarotoxin and cobrotoxin). They bind to the nicotinic ace­ tylcholine (ACh) binding sites of motor endplates of skeletal muscles, at the interfaces between the α/ε and the α/δ subunits of the ACh receptor, thereby preventing the interaction between ACh and the receptor, to cause a rapidly developing neuromus­ cular paralysis and eventually death from bulbar and respiratory muscle weakness. They have a distinctive “three-finger-fold” *References 85, 128, 141, 264. † Reference 141.

structure, complementary in shape to their receptor, and have also been found in some colubrid venoms. Presynaptic Phospholipases A2 Neurotoxins These β-neurotoxins, such as β-bungarotoxin, crotoxin, and taipoxin, contain about 120 to 140 amino acid residues and a phospholipase A subunit. They damage nerve endings at neuro­ muscular junctions, targeting voltage-gated potassium channels, causing sequential suppression, enhancement, and finally com­ plete failure of ACh release. The resulting paralysis is clinically indistinguishable from that caused by postsynaptic toxins, except that the latter may be ameliorated by anticholinesterases, such as edrophonium or neostigmine. Many neurotoxic PLA2s and other phospholipases have myotoxic activity.

MAMBA TOXINS Mamba (Dendroaspis) venoms contain a number of distinctive neurotoxins.85,141 Dendrotoxins (7 kDa, 57-60 amino-acid pro­ teins), such as α-dendrotoxin from eastern green mamba (Dendroaspis angusticeps) (see Figure 55-8) venom, which binds to some classes of voltage-gated potassium channels at nerve endings to cause polarizing block by ACh release, and calciclu­ dine, which blocks calcium channels, are “pear”-fold structures. Two “three-finger-fold” neurotoxins are unique to mamba venoms. Fasciculins (61-amino-acid residues) inhibit some ace­ tylcholinesterases, causing persistent muscle fasciculations,86 whereas calciseptine binds to calcium channels.

KRAIT BUNGAROTOXINS In the venoms of kraits (Bungarus spp.), a number of neurotox­ ins have been identified that have proved useful to neurophysi­ ologists and neuropharmacologists. They include β-bungarotoxins (β-BTXs) that act presynaptically, α-bungarotoxins (α-BTXs), and γ-bungarotoxins (γ-BTXs) that antagonize binding of ACh postsynaptically at peripheral neuromuscular junctions, and κ-bungarotoxins (κ-BTXs) that block neuronal nicotinic recep­ tors. β-BTXs are heterodimeric neurotoxins consisting of a PLA2 chain and a Kunitz type of protease inhibitor chain. Like most neurotoxic PLA2s, they have been shown to cause a significant loss of labeling by antisynaptophysin (reflecting a loss of synaptic vesicles) at the mammalian neuromuscular junction and degen­ eration of intramuscular branches of the terminal motor axon and are implicated in the resistance of the neuromuscular weakness of krait bite victims to antivenom and anticholinesterases.

CARDIOVASCULAR TOXINS Shock in snakebite victims is variously attributable to permeabil­ ity factors causing hypovolemia from extravasation of plasma and toxins acting directly or indirectly on cardiac muscle, vascular smooth muscle, and other tissues. ACE Inhibitors and Bradykinin-Potentiating Peptides Oligopeptides (molecular weight 600-1,600 Da) from venom of the Brazilian jararaca (Bothrops jararaca) activate bradykinin and, through a bradykinin-potentiating peptide (BPP) activity, prolong bradykinin’s hypotensive effect by inactivating the pep­ tidyl dipeptidase that destroys bradykinin and converts angioten­ sin I to angiotensin II. This provided the structural model for captopril, first of the synthetic angiotensin-converting enzyme (ACE) inhibitors. BPPs and ACE-inhibiting peptides have been found in several other crotaline and viperine venoms.51 Sarafotoxins18,53,201 Venoms of the Israeli burrowing asp (Atractaspis engaddensis: Atractaspidinae) and some other members of this genus contain endothelin-like sarafotoxins. They are 21-amino-acid polypep­ tides that cause coronary artery vasoconstriction and prolonged atrioventricular conduction and are positively inotropic. Natriuretic Peptides Natriuretic peptides been found in many viperid and Dendroaspis, Bungarus, and Micrurus venoms. A B-type natriuretic peptide 1049

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

Venom Composition*

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 55-1  Venom Yield on Milking and Mouse Lethality of Selected Venoms in Declining Order of Lethal

Potency in Mice

Venom Yield: (Dry Weight) (mg) Species

Range

Average

Papuan taipan (Oxyuranus scutellatus )

90-420

Beaked sea snake (Enhydrina schistosa) Australian (Eastern) taipan (Oxyuranus scutellatus)

7-20 40

120

Western/inland taipan or small-scaled snake (Oxyuranus microlepidotus) Eastern brown snake (Pseudonaja textilis) Russell’s viper (Daboia russelii ) Common krait (Bungarus caeruleus) Mainland tiger snake (Notechis scutatus) Indian cobra (Naja naja) Tropical rattlesnake (Crotalus durissus terrificus) Mohave rattlesnake (Crotalus scutulatus) Florida coral snake (Micrurus fulvius) Black mamba (Dendroaspis polylepis) Common lancehead (Bothrops atrox) Hundred pacer (Deinagkistrodon acutus) Green mamba (Dendroaspis angusticeps) European adder (Vipera berus) Southern Pacific rattlesnake (Crotalus oreganus helleri ) West African carpet viper (Echis ocellatus) Terciopelo (Bothrops asper) Eastern diamondback rattlesnake (Crotalus adamanteus) Cerrado coral snake (Micrurus frontalis) Jararacuçu (Bothrops jararacussu) King cobra (Ophiophagus hannah) Central American rattlesnake (Crotalus simus) Indian saw-scaled viper (Echis carinatus) Bushmaster (Lachesis muta)

44

110

130-250 8-20

Maximum 420 400

8

67

35 169

189 610 220 141 38 300

60-95 6-18 1.4-24.8 370-720

20-35

485 410 421 159

390 25 1530 848 53 830 1000 360 1760

Mouse Median Lethal Dose (LD50): mg/kg (Reference) 0.0023+/−0.006 (IP*) 0.0047+/−0.006 (IV*) 0.05 (subcutaneous)206 0.01 (0.164) (IV) 0.015 (IV) 0.099 (subcutaneous) 0.025 (subcutaneous) 0.053 (IV) 0.08 (IV) 0.09 (IV) 0.118 (IV) 0.13-0.42 (IV) 0.17 (IV) 0.18 (IV) 0.21 (IV) 0.26-2.9 (IV) 0.35 (IV) 0.38 (IV) 0.45 (IV) 0.55 (IV) 0.84 (IV) 0.99 (95% CI, 0.83-1.20) (IV†) 1.10 (IV) 1.2 (IV) 1.5 (subcutaneous) 1.75 (IV) 1.80 (IV) 1.84 (IV) 2.30 (IV) 5.6 (IV)

From Bolaños R: Toxicity of Costa Rican snake venoms for the white mouse, Am J Trop Med Hyg 21:360, 1972; Broad AJ, Sutherland SK, Coulter AR: The lethality in mice of dangerous Australian and other snake venom, Toxicon 17:661, 1979; Mebs D: Pharmacology of reptilian venoms. In Gans C, editor: Biology of the reptilia, vol 8, London, 1978, Academic Press, pp 437-560; and references 109, 170, and 198. CI, Confidence interval; IP, intraperitoneal; IV, intravenous. *Data from Vargas M, Segura A, Herrera M, et al: Preclinical evaluation of caprylic acid-fractionated IgG antivenom for the treatment of Taipan (Oxyuranus scutellatus) envenoming in Papua New Guinea, PLoS Negl Trop Dis, 5:e1144, 2011. † Data from Theakston RDG: Personal communication, August 2010.

from eastern green mamba venom (Dendroaspis angusticeps) is under therapeutic trial for congestive cardiac failure.

VARIATIONS IN THE QUANTITY AND COMPOSITION OF VENOM INJECTED BY A SNAKEBITE

BIOGENIC AMINES

In human victims of snakebite, the amount and composition of venom injected by the snake are the most important, but inde­ terminate, factors influencing evolution of envenoming and prog­ nosis. Apart from inferring the quantity and quality of injected venom from the range and severity of clinical manifestations of envenoming, the only currently available objective method of assessment is to measure venom antigenemia when the patient is admitted to the hospital. This has been found to correlate with clinical severity in the case of several different species of snake, including European vipers,13 Burmese Russell’s viper,233 Martini­ can lancehead (Bothrops lanceolatus),220 jararaca (B. jararaca),61 and common lancehead (B. atrox).197 Box 55-1 summarizes the factors that determine severity of envenoming. Clinical assessment suggests that the amount of venom injected at a bite is very variable. A proportion of human victims of snakebite, more than one-half in some series, show negligible or no signs of envenoming, even though the snake was identified as being venomous and there were obvious punc­ ture marks indicating that the fangs had penetrated the skin.148,159 These so-called “dry bites” have led to the belief that snakes can somehow control the amount of venom injected, according to the size of their natural prey,88 and that they can inflict an inten­ tionally “defensive bite,” choosing not to expend venom when they strike at an enemy. However, when humans are bitten, the usual circumstances of the bite, inadvertently picking up or step­ ping on a snake in foliage, may mitigate against mechanical

Biogenic amines, such as histamine and 5-hydroxytryptamine, found particularly in viper venoms, may contribute to local pain and permeability changes at the site of a snakebite.

VENOM POTENCY AND LETHALITY The activities of different venoms can be compared in the labora­ tory using in vitro and animal in vivo assays. The only practicable index of lethality is the median lethal dose (LD50) measured in mice of specified strain and size (Table 55-1). However, this value cannot be extrapolated easily to give a reliable idea of the lethal dose or even the relative lethality of different venoms in humans. Quite apart from the marked species variations in vulnerability to venoms, the mode of death in different animals may not be the same. For example, in mice, venom of the black-necked spitting cobra (N. nigricollis) causes death with convulsions fol­ lowing paralysis (intravenous LD50 0.40 to 1.37 mg/kg), but humans envenomed by this species do not show neurotoxic­ ity.222,269 A series of standard World Health Organization (WHO) assays for assessing different aspects of venom activity has been developed.212 It is hoped that an assay in insensate chick embryos189 and increasing use of tissue culture assays may reduce the need for studies in living animals. 1050

Severity of Envenoming

Incidence of Bites • Frequency of contact between snakes and humans depends on: • Population densities (snake, human) • Diurnal and seasonal variations in activity • Types of behavior (e.g., human agricultural) • Snakes’ “irritability”—readiness to strike when alarmed or provoked—varies with species Severity of Envenoming • Dose of venom injected—depends on mechanical efficiency of bite and species and size of snake • Composition and hence potency of venom—depends on species and, within a species, the geographic location, season, and age of the snake • Health, age, size, and specific immunity of human victim • Nature and timing of first aid and medical treatment

efficiency of the snake’s venom apparatus in injecting venom, because humans are unexpected and abnormal targets. The idea that a snake might exhaust its supply of venom by a recent strike and therefore be less venomous after killing and swallowing its prey or after striking another person has been refuted. Snakes do not exhaust the contents of their venom glands during the first strike. The proportion of unexpended venom after the first strike was found to be 0% to 85% for the Australian death adder (Acanthophis), 5% to 81% for Australian tiger snakes (Notechis), 40% for the Indian cobra (Naja naja), and 30% for the saw-scaled viper (E. carinatus).112 Palestine vipers (Daboia palaestinae) con­ tinue to deliver substantial quantities of venom after nine or more consecutive strikes.112 In several reports of consecutive strikes by a single snake on several human victims, the first victim was not always the most severely envenomed. In the case of Russell’s viper bites in Burma (Myanmar), snakes that had recently fed (those in which a rodent was found in their stomachs) inflicted bites that were no less venomous than those with empty stom­ achs.233 Although the largest snakes do not always inflict the most highly venomous bites, there is a tendency, in most species that have been studied, for the severity of local and systemic enven­ oming to increase with the size of the individual snake respon­ sible.233 Venom yield has been shown to increase with ambient temperature, but no definite seasonal variation has been documented.

EFFECT OF THE SITE AND DEPTH OF THE BITE In experimental animals, the route of venom administration (topical, intradermal, subcutaneous, intramuscular, intraperito­ neal, intravenous, intracerebral) affects the speed, pattern, and lethality of envenoming. This is virtually impossible to study clinically, but in anecdotal cases of human envenoming, in which systemic effects develop rapidly after a bite with minimal local signs, it has been assumed that venom entered the bloodstream directly as a result of a fortuitous intravenous puncture (Figure 55-35, online) (Bothrops atrox bite).

Epidemiology of Snakebite SNAKE SPECIES RESPONSIBLE FOR MOST BITES Table 55-2 lists the species responsible for most snakebite deaths and severe morbidity outside North America. Fortunately, some species notorious for the potency of their venom (e.g., sea snakes and the reclusive Australian inland taipan, Oxyuranus microlepidotus) or their great size (e.g., the south Asian king cobra, O. hannah [see Figure 55-15], which can grow longer than 5.8 m [19 feet]; Gaboon vipers, Bitis gabonica and B. rhinoceros [see Figure 55-34, B], which may exceed 2 m [6.6 feet] in total length and weigh more than 8 kg (17.6 lb); and bushmasters (genus Lachesis) that grow to more than 4 m [13 feet]) (Figure 55-36, Lachesis stenophrys) rarely bite humans. African night adders and burrowing asps (genera Causus [Figure 55-37] and Atractaspis [Figure 55-38]),276 Asian green pit vipers (e.g., genera Cryptelytrops [Figure 55-39], Trimeresurus, Viridovipera [Figure 55-40])96,239 and Sri Lankan and southwest Indian hump-nosed pit vipers (H. hypnale)12,48,101 are responsible for many bites, but severe enven­ oming is rare or uncommon.

Distribution of Venomous Snakes Venomous snakes are distributed from sea level up to high alti­ tudes. The Himalayan pit viper, Gloydius himalayanus, normally confined below 1500 m (4921 feet), has been recorded at the base of the Dharamsala glacier in northern India as high as 4877 m (16,000 feet),187 and the rattlesnake (Crotalus triseriatus

INTRASPECIES VARIATION IN VENOM COMPOSITION* In many snake species, venom composition has been found to change as the snake grows older, presumably to accommodate a changing range of prey species. Most of the species that have been studied are from the Americas (see Chapter 54), but in the rest of the world, Indian cobra (Naja naja) venom has been shown to have decreasing lethality with increasing age, whereas venoms of the saw-scaled viper (E. carinatus) and black-necked spitting cobra (N. nigricollis) show decreasing lethality despite increasing protein concentration.252 Seasonal variation in the venom composition of a particular species has been suspected but not proved. There is now abundant literature describing variations in venom lethality, composition, and activities between individuals of a particular species at the same geographic focus or from different places within the snake’s geographic range.45,162,252 In the case of the Malayan pit viper (Calloselasma rhodostoma),45 Echis spp.,17,33 and Sistrurus spp.,73 available prey species seemed to have had a major evolutionary influence on venom composi­ tion in different parts of its geographic range. *Reference 252.

A

B FIGURE 55-36  Bushmasters (genus Lachesis). A, South American bushmaster (L. muta) (Brazil). B, Central American bushmaster (L. stenophrys) (Costa Rica). (Copyright D.A. Warrell.)

1051

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

BOX 55-1  Determinants of Snakebite Incidence and

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 55-2  Species of Snake Probably Responsible for Most Deaths and Morbidity Outside North America

and Mexico

Geographic Area

Scientific Name

Common Name

Europe

Vipera and Macrovipera spp. Vipera ammodytes Naja nigricollis, N. mossambica, etc. Naja haje, N. annulifera, N. anchietae Naja senegalensis Dendroaspis spp. Echis ocellatus, E. jogeri, E. leucogaster, E. pyramidum, etc. Bitis arietans Naja oxiana Echis spp. Macrovipera lebetina Daboia palaestinae Naja naja, N. kaouthia, N. siamensis Bungarus spp. Daboia russelii, D. siamensis Calloselasma rhodostoma Echis carinatus Hypnale hypnale Cryptelytrops, Trimeresurus, and related genera Naja atra Bungarus multicinctus Protobothrops flavoviridis Protobothrops mucrosquamatus Gloydius blomhoffii and G. brevicaudus Acanthophis spp. Pseudonaja spp. Pseudechis spp. Notechis spp. Oxyuranus scutellatus Micropechis ikaheka Micrurus spp. Bothrops atrox Bothrops asper Bothrops jararaca Bothrops bilineatus (Bothriopsis bilineata) Agkistrodon, Bothriechis, Porthidium, and related genera Lachesis spp. Micrurus lemniscatus, M. circinalis Bothrops asper Bothrops caribbaeus Bothrops lanceolatus Crotalus durissus Lachesis muta

Vipers, adders Long-nosed viper African spitting cobras Egyptian and snouted cobras

Africa

Asia, Middle East

Asia, Indian Subcontinent, and Southeast Asia

Asia, Far East

Australasia, New Guinea

Central, South America

Caribbean

FIGURE 55-37  Velvety-green night adder (Causus resimus: subfamily Viperinae) (Watamu, Kenya). (Copyright D.A. Warrell.)

1052

Mambas Saw-scaled or carpet vipers Puff adder Oxus cobra Saw-scaled or carpet vipers Levantine viper Palestine viper Asian cobras Kraits Russell’s vipers Malayan pit viper Saw-scaled or carpet vipers Hump-nosed pit viper Arboreal and other pit vipers Chinese cobra Chinese krait Japanese habu Chinese habu Mamushis Death adders Brown snakes Black snakes Tiger snakes Taipan New Guinean small-eyed snake Coral snakes Common lancehead Terciopelo Jararaca Papagaio Cantils and other pit vipers Bushmasters, surucucu Coral snakes (Trinidad) Mapepire (Trinidad) Serpent (St Lucia) Fer de lance (Martinique) Colebre (Aruba), Islas Los Testigos Mapepire zanana (Trinidad)

FIGURE 55-38  Burrowing asp (Atractaspis fallax: subfamily Atractaspidinae) (Watamu, Kenya). (Copyright D.A. Warrell.)

FIGURE 55-40  Chinese bamboo viper (Viridovipera stejnegeri: subfamily Crotalinae) (China). (Copyright D.A. Warrell.)

A

B FIGURE 55-46  Fresh water sea snake. A, Lake Taal (Lake Bombon), Luzon, Philippines home of Garman’s sea snake (Hydrophis semperi) (B). (A copyright D.A. Warrell; B courtesy George Watt.)

FIGURE 55-41  High-altitude rattlesnake. Mexican dusky rattlesnake (Crotalus triseriatus) found on Mt Popocatepetl and Ajusco and Volcán Pico de Orizaba in Mexico at altitudes up to 4600 m (15,092 feet). (Copyright D.A. Warrell.)

triseriatus) (Figure 55-41) has been found on Mt Popocatepetl and Ajusco and Volcán Pico de Orizaba in Mexico at altitudes up to 4600 m (15,092 feet).110 The European adder, Vipera berus, is very widely distributed, from England, Scotland, and Wales in the west, across Europe and Asia to North Korea and Sakhalin Island in the east, and north into Scandinavia and the Arctic Circle (Figure 55-42, online). No other venomous species is found in the Arctic, and none occurs in the Antarctic, Crete, Ireland,

Iceland, Madagascar, New Caledonia, New Zealand, and Hawaii. Most of the islands of the western Mediterranean Sea and Atlantic and Pacific Oceans are free of venomous snakes (Figure 55-43, online). Sea snakes occur in the Persian Gulf and Indian and Pacific Oceans between latitudes 30 degrees north and 30 degrees south, as far south as New Zealand and Tasmania, and as far north as Siberia (yellow-bellied or pelagic sea snake Pelamis platurus) (Figure 55-44, online).137,172,248 The beaked sea snake (Enhydrina schistosa) and Hydrophis species frequent estuaries and have been found 130 to 160 km (80 to 100 miles) up rivers. In Papua New Guinea, E. schistosa was taken in the Ramu River, 30 km (18.6 miles) from the sea, where it had caused fatal envenoming (Figure 55-45). In freshwater lakes, Hydrophis semperi occurs in Lake Taal (also called Lake Bombon) (Figure 55-46) in the Philip­ pines and E. schistosa in Tonle Sap in Cambodia. There are no sea snakes in the Atlantic Ocean or the Red Sea.248

Snakebite Mortality and Morbidity In the tropical countries where snakebite is most common, there are few reliable data. There have been only three serious attempts to assess global snakebite mortality.38,105,207 However, community-based studies have revealed gross underreporting of deaths in these studies. One reason is that records of patients 1053

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

FIGURE 55-39  White-lipped green pit viper (Cryptelytrops albolabris: subfamily: Crotalinae) (Thailand). (Copyright D.A. Warrell.)

FIGURE 55-45  Beaked sea snake (Enhydrina schistosa: subfamily Hydrophiinae) found in estuaries and up rivers (Bunapas Mission, Ramu River, Papua New Guinea). (Copyright D.A. Warrell.)

PART 6  ANIMALS, INSECTS, AND ZOONOSES

treated by traditional methods are missing from official hospitalbased statistics, and deaths reported at the hamlet or district level may not be sent on to ministry headquarters. Population surveys* have given a far more accurate picture of snakebite incidence, morbidity, and mortality. The prevalence of chronic morbidity following snakebite is unknown, but it is possible that, for every person killed by snakebite, one or two may survive with a longterm physical handicap.

AMERICAS (CENTRAL, SOUTH, AND THE CARIBBEAN) Estimates of the total number of deaths caused by snakebites each year in Central and South America (including Mexico) were as follows: in 1954, between 3000 and 4000207; in 1998, 5000 out of 300,000 bites38; and in 2008, 3300 to 4500 deaths out of 81,427 to 137,123 bites.105 The incidence is high among indigenous Amerindian tribes. In Acre, western Brazil, snakebite accounted for 3.3% of all deaths and 24% of deaths in the 15- to 44-year-old age-group among 100 families of Kaxinawa of the Rio Tejo, Upper Juruá rubber extraction area.24 A survey of forest-dwelling Amazonian Indians and rubber tappers of the Juruá Valley found that 30% of the population had been bitten during their lifetime. Mortality was estimated at about 400 deaths per 100,000 popula­ tion per lifetime.160 Brazil At the beginning of the 20th century, Vital Brazil estimated that, among 19,200 probable bites in Brazil, there were 4800 deaths. In 1949, 2000 deaths were estimated.207 During the period 1990 to 1993, there was an average of 27,200 cases per year with 120 deaths per year, the overall case fatality being 0.4%. In 2005, 28,711 snakebites were reported (15/100,000 population) with 114 deaths (Secretaria de Vigilância em Saúde). Costa Rica In 1943, 24 deaths were attributed to attacks by venomous animals.207 Annual mortality (per 100,000 population) has declined, from about 5 in 1952 to 0.15 in 1996. Currently there are an estimated 600 bites, with 2 to 5 deaths each year.

ASIA Estimates of snakebite deaths in Asia range between 15,000 and 100,000/year,40,105 reflecting the difficulty in assessing an occupational/environmental disease that exacts so much of its mortality outside hospitals. The highest recorded incidence was 162 deaths per 100,000 population per year, determined in the Eastern Terai area of Nepal.193 In this study, only 20% of deaths occurred in hospitals. Increased risk for fatality was associated with being bitten inside the house while resting between mid­ night and 6:00 AM, which suggests bites by the common krait (B. caeruleus) (see later discussion). Other risk factors were an initial visit to a traditional healer and delayed transport to the hospital. In Bardhaman (Burdwan) District, West Bengal, a field survey in randomly selected villages suggested that among the total popu­ lation of nearly 5 million people, nearly 8000 were bitten and 800 killed by snakes each year.87 Bangladesh Nineteen thousand people in nearly 4000 randomly selected households throughout the country provided information about snakebites. National totals of approximately 600,000 bites and approximately 6000 deaths per year were calculated by extra­ polating to the total population of rural Bangladesh.168 Burma In the 1930s, the annual snakebite mortality reported in Burma exceeded 2000 (15.4 per 100,000 population per year). Russell’s viper (Daboia siamensis) bite was once the 5th and is now the 12th leading cause of death in the country. In 1991, there were 14,000 bites with 1000 deaths and in 1997, 8000 bites with 500 *References 60, 87, 145, 164, 185, 198, 225, 265.

1054

deaths. From 2005 until 2008, 8994 to 11,172 bites were reported annually, with 748 to 794 deaths. The average case fatality is 7.9%. Underreporting is estimated to be about 12%. In some townships in the Irrawaddy division, case fatality still ranges from 10% to 40% and may be increasing. Ninety percent of bites are caused by Russell’s vipers (D. siamensis). India From 1869, when Joseph Fayrer first solicited data from “British India,” around 20,000 human deaths each year were attributed to snakebite. Based on a nationally representative study of 128,000 deaths in 6671 randomly selected areas of India from 2001 to 2003, a total of about 46,000 snakebite deaths was esti­ mated for 2005.145 Japan In the Amami and Okinawa Islands of Japan, there were 5488 bites by the habu (Protobothrops [Trimeresurus] flavoviridis), resulting in 50 deaths during the 9 years from 1962 to 1970.184 The highest incidence of bites on one of the islands was 4.6 per 1000 population per year. Sri Lanka Snakebite numbers increased from 12,175 per year in 1991 to peak at 37,244 in 2002 and 36,861 in 2005. Fatalities peaked at 194 in 2000, and there were 134 in 2005. There are currently 30,000 to 35,000 bites and 100 to 150 deaths each year. In hospitals, case fatality decreased from 3.5% in 1985 to 0.2% in 2006. Thailand Improved surveillance explained the reporting of increasing numbers of snakebite cases from an average of 2316 per year in the 1950s to 9071 (14.5/100,000) in 2002 and 8299 (13.25/100,000) in 2006. Mortality has declined from an average of 178 deaths per year in the 1950s to fewer than 10 per year recently. Over the last 5 years, both incidence and case fatality have declined to 8000 to 10,000 bites per year (12 to 18 per 100,000 population per year), with an admirably low case fatality of 0.5%.

AFRICA There are probably more than 100,000 envenomings and 5000 deaths in Africa each year. However, Chippaux38,39 has estimated fivefold higher figures of 1 million bites, 500,000 envenomings, and 20,000 deaths. Burkina Faso Snakebites (Echis leucogaster) are said to be common, even in the suburbs of Ouagadougou (7.5 envenomings per 100,000 population per year). In rural areas, the incidence is 35 to 120 per 100,000 population per year, with a case fatality of 3%. Health services claim 7000 to 10,000 envenomings and 200 fatalities. Few patients are admitted to hospitals, and there is virtually no antivenom available. Nigeria Seventy-four snakebites per 100,000 population per year are reported.149 The saw-scaled or carpet viper (Echis ocellatus) is responsible for 90% of bites and 60% of deaths.149 In the Benue Valley of northeastern Nigeria, the incidence of snakebite was found to be about 500 per 100,000 population per year with a mortality of 12.2%.265 A community survey of snakebites by the black-necked spitting cobra (N. nigricollis) in Malumfashi, north­ ern Nigeria, found that in a population of 43,500 there were 15 to 20 bites per 100,000 population per year. Only 8.5% of the victims had visited a hospital. The case fatality rate was 5%, and 19% of survivors had persistent physical disability from the locally necrotic effects of the venom.164 Senegal In Bandafassi, in the southeast, in a population of 10,509, snake­ bite mortality was 14 per 100,000 population per year. Saw-scaled vipers (E. jogeri), puff adders (B. arietans), and spitting cobras (Naja katiensis) were implicated.225

In Kenya, a preliminary survey based on Ministry of Health, hospital, clinic, and dispensary records in Kakamega and western Kenya, Lake Baringo, Laikipia, Kilifi, Malindi, and northern Kenya suggested an overall average frequency of snakebite of 14 (range 2 to 68) per 100,000 population per year with a minimum death rate of 0.45 per 100,000 population per year. Puff adders, black mambas, and spitting cobras were responsible for the fatalities.43 However, a community-based study on the coast in the Kilifi district discovered 15 adult snakebite fatalities per 100,000 popu­ lation per year.198 South Africa Three hospital-based studies in KwaZulu-Natal reported inci­ dences of bites of 31 to 89 per 100,000 population per year, and a study from Transvaal reported an incidence of 34 per 100,000 population per year. There were few deaths. The species respon­ sible included B. arietans, Naja nivea, N. mossambica, Dendroaspis polylepis, Causus rhombeatus, and Atractaspis bibronii.

OCEANIA In Australia, 1000 to 2000 bites occur per year with an average of 2 to 3 deaths. In Papua New Guinea, the incidence of bites was 215 and of deaths was 7.9 per 100,000 population per year in Central Province, whereas in Kairuku subprovince, there were 526 bites per 100,000 population per year.122 The number of deaths may have increased recently because of inadequate anti­ venom supplies. It seems likely that 200 to 300 people die each year of snakebite in Papua New Guinea.

were 21 deaths in 25 years with an annual incidence of almost 200 bites.

SNAKEBITE AS AN OCCUPATIONAL DISEASE In tropical countries, farmers, plantation workers, herders, and hunters are most frequently bitten. Rice farmers in Burma, Sri Lanka, and central Thailand tread on Russell’s vipers or inadver­ tently pick them up in a handful of paddy during the harvest148 (Figure 55-47, A). Cobras (Naja philippinensis) are an occupational hazard to rice farmers in the Philippines.280 The Chinese predilec­ tion for snakes and their organs, both as food and medicines, has resulted in many bites in snake restaurants and snake farms in China and Southeast Asia. In the savanna of West Africa, farmers are bitten by Echis species as they dig the fields at the start of the rainy season (Figure 55-47, B).265 Rubber tappers in Southeast Asia tread on Malayan pit vipers (Calloselasma rhodostoma) in the dark and are bitten as they make their early morning rounds of the rubber trees (Figure 55-47, C ).272 This species is also responsible for numerous fatal bites among coffee and rubber plantation workers in Vietnam, especially in Song Be province. Sea-snake bites were an occupational hazard of fishermen in Southeast Asia where hand nets were used.174 Mechanization of fishing methods in this region has resulted in a dramatic decrease in sea-snake bites, but they still occur along the coast of south Vietnam (Figure 55-47, D).248 The beaked sea snake (E. schistosa) (see Figure 55-45) has caused most bites and deaths. Other common and medically important species are Hydrophis cyanocinctus, Hydrophis spiralis, and Lapemis curtus.

BITES BY SNAKES KEPT IN CAPTIVITY

EUROPE In Britain, there are more than 200 adder (V. berus) bites each year, but there have been only 14 deaths during the last hundred years, the last in 1975.204,232,257 There were 44 deaths caused by this species in Sweden between 1911 and 1978; in Finland, there

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Especially in more industrialized countries, venomous snakes are increasingly popular exotic pets. Many are kept illegally. Most bites are inflicted on the hands when the snakes are picked up by an owner who is under the influence of alcohol or recreational drugs.4,257,261

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FIGURE 55-47  Snakebite as an occupational hazard. A, Rice harvest, Sri Lanka. B, Early tilling, Kaltungo, Nigeria. C, Rubber tapping, Trang, Southern Thailand. D, Fishermen, Long Hai, Vietnam. (Copyright D.A. Warrell.)

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RISK TO WILDERNESS TRAVELERS The risk for snakebite is a major anxiety among members of expeditions and wilderness travelers. Provided that sensible pre­ cautions are taken (see later text), the risk is small. However, for field biologists working in snake-infested areas, especially those who are interested specifically in finding and capturing snakes, the risk is far higher. The death of Joe Slowinski in 2001 illus­ trated the mortal danger of handling snakes in places far from medical help. He was an expert herpetologist from the California Academy of Sciences who died at Rat Baw in remote northern Burma, 32 hours after being bitten by a 30-cm juvenile krait (Bungarus near multicinctus) that he pulled out of a bag with his bare hand, believing it to be the harmless krait-mimic Dinodon septentrionalis.124 Snakebite is a rare accident for ordinary back­ packers, but people have been bitten even while walking down the main trail into the Grand Canyon.

CIRCUMSTANCES IN WHICH SNAKEBITES OCCUR Most people are bitten after inadvertent contact with snakes while doing agricultural work in fields or plantations or while walking to and from work along unlit paths after dusk. Unpro­ voked attacks are unusual, but snakes will bite if they are cornered or feel threatened. Asian kraits, notably B. caeruleus (see Figure 55-72) in Pakistan, India,177 Nepal, Bangladesh, and Sri Lanka10; B. candidus and B. multicinctus in Southeast Asia94,218,230,273; and African spitting cobras, N. nigricollis, in western Africa269 and N. mossambica in South Africa222 enter human dwellings at night in pursuit of their prey (rodents, lizards, toads) and may strike at a person who moves in his or her sleep. Epidemics of snakebite can be caused by flooding, the building of new roads through jungles, and implementation of irrigation schemes. In Western countries, a larger proportion of people, especially young men, are bitten on their hands, either in the wild (including such bizarre events as rattlesnake roundups in the United States) or by captive specimens, while showing off under the influence of alcohol or other recreational drugs.

Principal Clinical Features of Envenoming and Their Pathophysiology (Table 55-3)* Fear, direct and indirect effects of venom, results of prehospital treatment, and later complications all contribute to the symptom­ atology and clinical picture in a snake-bitten patient by the time he or she presents for medical treatment.

LOCAL SIGNS AT THE SITE OF THE BITE Local swelling at the site of the bite is the most usual feature of envenoming, but a constricting band applied as first aid may cause misleading swelling (“factitious swelling”) that is not neces­ sarily indicative of envenoming. Other fashionable first-aid methods, such as suction pumps, incisions, tattooing, application of herbs and chemicals, electric shocks, ice, or fire may create their own dramatic signs and obscure the evidence of envenom­ ing (see below). Puncture wounds can be useful evidence, but they are not diagnostic of snakebite and do not help to distinguish venomous snakebites from those of nonvenomous snakes. Bites that are responsible for fatal envenoming may leave no discernable mark. The differential diagnosis includes bites and stings by other animals, including Hymenoptera, spiders, scorpions, centipedes, rodents, and, in estuaries and the sea, various aquatic stingers (Figure 55-48). Fang and other teeth punctures may be the sites of persistent bleeding, suggesting coagulopathy (Figure 55-49). Local signs of envenoming include progressive swelling, tender painful enlargement of lymph nodes draining the bite site, bruising, red lymphangitic lines, inflammation and erythema resembling cellulitis, blistering, and signs of necrosis, such as an anesthetic hyperpigmented or hypopigmented area smelling of putrefaction (Figure 55-50). Complications include ischemia sec­ ondary to raised intracompartmental pressure or thrombosis, and wound infection or local abscess. *References 140, 249, 250, 290, 291.

TABLE 55-3  Clinical Manifestations of Snakebite Envenoming With Suggested Pathophysiologic Mechanisms Sign or Symptom Local Envenoming Swelling, bruising, and blistering Severe local/regional pain (coral snake envenoming) Enlarged, painful, and tender lymph nodes draining the bitten area Tissue necrosis/gangrene Peripheral nerve lesion Systemic Envenoming Hypotension and shock Bleeding, coagulopathy, thrombosis Intravascular hemolysis Acute kidney injury: acute tubular necrosis Neurotoxicity Autonomic hyperactivity Abdominal pain (krait bite envenoming) Generalized rhabdomyolysis

Proposed Mechanism Increased vascular permeability (digestive enzymes, metalloproteinases, PLA2 myotoxins) Cystine knot peptides activating noxious transient receptor potentiating V1 receptor Absorption and passage of large-molecular-weight venom toxins via the lymphatic system Venom myotoxins, cytotoxins, metalloproteinases, etc; secondary ischemia (iatrogenic from tourniquet, thrombosis, intracompartmental syndrome) Iatrogenic from pressure of tourniquet (e.g., lateral popliteal nerve), compartment syndrome, hematoma Hypovolemia from extravasation of blood/plasma into the swollen limb Vasodilation by venom toxins and autacoids (ACE inhibitors and bradykinin-potentiating peptides) Myocardial damage, cardiac arrhythmias, (rarely) venom hypersensitivity anaphylaxis Vascular endothelial activation and damage by metalloproteinase hemorrhagins, consumption coagulopathy by venom procoagulant enzymes, fibrinolysis/fibrinogenolysis by venom toxins and endogenous plasmin, anticoagulant effects of venom PLA2s, platelet activation and inhibition by venom C-type lectins, fibrin deposition in small to large arteries PLA2-mediated, complement (cobra venom C3b) activation or microangiopathic (endothelial activated) Hypotension, disseminated intravascular coagulation, direct nephrotoxicity, pigment nephropathy (hemoglobinuria, myoglobinuria), associated with microangiopathic hemolysis, secondary to hyperkalemia Presynaptic and/or postsynaptic neuromuscular block Release of adrenergic/cholinergic mediators Hyperalgesic AVIT sequence cysteine-rich protein (e.g., mamba intestinal toxin—prokineticin) Myotoxic phospholipases A2

ACE, Angiotensin-converting enzyme; PLA2, phospholipase A2.

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FIGURE 55-48  A, European adder (Vipera berus) bite in Oxford, England. B, Fatal Sri Lankan Russell’s viper bite (Daboia russelii ). C, Bite by nonvenomous water snake (rice paddy snake) (Enhydris plumbea) in Thailand. D, Bite by rat. E, Bite by Brazilian wandering spider (Phoneutria nigriventer). (A, B, C, and E copyright D.A. Warrell; D courtesy Dr. Yamin, São Paulo.)

or enzymatically inactive (lysine-49).78 Cobra cardiotoxins are low-molecular-weight polypeptides with cytotoxic action.

SIGNS OF SYSTEMIC ENVENOMING Hypotension and Shock Usually blood pressure falls and shock develops within hours of the bite as a result of hypovolemia (Figure 55-51, A). However, patients may suffer shock within minutes of the bite, manifested by faintness, loss of vision, collapse, and unconsciousness, which is usually transient. Victims may injure themselves falling during syncopal attacks. There may be associated features of anaphy­ laxis, for example following envenoming by vipers (Vipera berus, V. aspis): urticaria, angioedema, bronchospasm, nausea, vomit­ ing, and abdominal colic. People who have become hypersensi­ tive to snake venoms, usually habitual snake handlers, may develop anaphylactic shock soon after exposure.

FIGURE 55-49  Persistent bleeding from fang marks 40 minutes after a bite by Malayan pit viper (Calloselasma rhodostoma) in Thailand. (Copyright D.A. Warrell.)

Pathophysiology Increased vascular permeability leads to swelling and bruising. The factors responsible include endopeptidases, metalloprotein­ ase hemorrhagins, membrane-damaging polypeptide toxins, phospholipases and endogenous autacoids released by the venom, such as histamine, 5-hydroxytryptamine, and kinins. Venoms of some Viperidae, such as D. russelii, D. siamensis, and V. berus, can also produce a generalized increase in vascular permeability resulting in pulmonary edema, serous effusions, conjunctival and facial edema, albuminuria, and hemoconcentra­ tion. Local tissue necrosis results from the direct action of myo­ toxins and cytotoxins, and ischemia caused by thrombosis; compression of blood vessels by first-aid methods such as tight tourniquets; or by swollen muscle within a tight fascial compart­ ment. Myotoxins damage the muscle cell plasma membrane directly. Most are PA2s, either enzymatically active (aspartate-49)

Pathophysiology.  Leakage of plasma or blood into the bitten limb and elsewhere, or massive gastrointestinal hemorrhage, may cause hypovolemia after viper bites. Vasodilation, especially of splanchnic vessels, and a direct effect on the myocardium may contribute to hypotension after viper bites. Profound hypotension is part of the autopharmacologic syndrome that occurs within minutes of bites by European Vipera, Daboia palaestinae, D. siamensis, D. russelii, burrowing asps (Actractaspis engaddensis), and Australian elapids. Presumably this is caused by oligopep­ tides (ACE inhibitors and BPPs) and vasodilating autacoids (see earlier discussion), but massive clot formation in the heart and great vessels has been suggested as an explanation for early col­ lapse in victims of Australian elapid envenoming.206 Hypotensive collapse associated with bradycardia in a susceptible person might be explained by vasovagal syncope. This might occur even in the absence of envenoming. In some cases, direct myocardial effects of venom may be suggested by electrocardiographic (ECG) changes and autopsy findings of epicardial or endocardial hemorrhages and histopathologic evidence of cardiac myonecro­ sis (Figure 55-51, B and C; see Figure 55-66, D). Bleeding and Clotting Disturbances* Hemostatic disturbances are an important feature of envenoming by vipers, pit vipers, Australasian elapids, and dangerously ven­ omous colubrids. These manifest clinically as persistent bleeding from the fang punctures (see Figure 55-49) and other sites of *References 97, 102, 126, 286.

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FIGURE 55-50  Local signs of envenoming. A, Tender, painful enlargement of local lymph nodes in a man bitten on the left foot by a Papuan taipan (Oxyuranus scutellatus) in Papua New Guinea. B, Tense swelling, bruising, blistering and necrosis at the site of bite (dorsum of the foot) (Calloselasma rhodostoma) in Thailand. C, Swelling and blistering extending up the bitten arm (C. rhodostoma) in Thailand. D, Bleeding and hemorrhagic blisters (C. rhosdostoma) in Thailand. E, Tense swelling of bitten limb and scrotum (Bothrops atrox) in Pastaza, Ecuador. F, Tense swelling and bruising (Echis ocellatus) in Nigeria. G, Necrosis (Naja nigricollis) in Nigeria. H, Sloughing of necrotic skin (N. nigricollis) in Nigeria. (Copyright D.A. Warrell.)

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FIGURE 55-51  A, Shock (Daboia russelii ) (Burma). B, ECG changes caused by European adder (Vipera berus) envenoming in England. C, Premortem tachyarrhythmia, epicardial hemorrhages at autopsy (Daboia siamensis) (Burma). (Copyright D.A. Warrell.)

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FIGURE 55-52  Spontaneous systemic bleeding after snakebites. A, Gums (Bothrops atrox, Ecuador). B, Floor of mouth (Echis ocellatus, Nigeria). C, Hemoptysis (Calloselasma rhodostoma, Thailand). D, Brain (Daboia siamensis, Burma). E, Rectal (D. russelii, Sri Lanka). F, Generalized (E. ocellatus, Nigeria). (A to C, E, and F copyright D.A.Warrell; D courtesy Hla Mon.)

acute or recent trauma (e.g., partially healed wounds) and spon­ taneous systemic bleeding from gums, nose, gastrointestinal and genitourinary tracts and into skin, conjunctivae, the brain, and other tissues (Figure 55-52). Pathophysiology.  Snake venoms affect hemostasis in several ways: Procoagulant enzymes activate intravascular coagulation, producing consumption coagulopathy and incoagulable blood. For example, procoagulants in the venom of Colub­ ridae, Echis and Bothrops species,191 and Notechis scutatus activate prothrombin, whereas those in venoms of Daboia russelii and D. siamensis activate factors V and X (see earlier discussion). Thrombin-like enzymes in venoms of many crotaline snakes have a direct action on fibrinogen. Some venoms cause defibrinogenation by activating the endogenous fibrinolytic (plasmin) system. Anticoagulant activity is attributable to venom phospholi­ pases. Platelet activation or inhibition and thrombocytopenia are common accompaniments of systemic envenoming. Acti­ vators of platelet agglutination are C-type lectins of viperoid and elapid venoms.52 Mucrocetin (Protobothrops [Trimeresurus] mucrosquamatus), ophioluxin (Ophiophagus hannah), and stejnulxin (Viridovipera stejnegeri) target platelet gly­ coprotein receptor GPIb; alboaggregin A and alboluxin (Cryptelytrops [Trimeresurus] albolabris) and convulxin (Crotalus durissus terrificus) act through both receptors GPIb and GPVI; aggretin (Calloselasma rhodostoma) activates platelet receptor CLEC2 and agkaggregin (Deinagkistrodon acutus), and rhodoaggretin (C. rhodostoma) and crotacetin (Crotalus durissus terrificus) are platelet agonists acting through an undetermined receptor. Proatherocytin (Proatheris superciliaris) is a platelet receptor PAR-1 agonist.259

Platelet inhibitors also include C-type lectin. Dabocetin (Daboia siamensis) binds with GPIb and rhodocetin (C. rhodostoma) and inhibits platelets via interaction with α2β1 integrin receptor. Mocarhagin (Naja mossambica) and jararhagin (Bothrops jararaca) are metalloproteinases that cleave GPIbα and GPIa-IIa, respectively, thus inhibiting platelet responses depending on those receptors. Arg-GlyAsp (RGD) tripeptide sequence–containing venom pep­ tides, such as trigramin, echistatin, contortrostatin, and flavoviridin, are powerful inhibitors of the fibrinogen recep­ tor GPIIb-IIIa. Few studies of platelet function have been attempted in envenomed humans. In patients bitten by Malayan pit vipers and green pit vipers (Cryptelytrops albolabris), there was initially inhibition of platelet agglutina­ tion, followed by activation and appearance of circulating clumps of platelets.96,97 Hemorrhagins: In the absence of trauma, defibrination/ defibrinogenation induced by venom coagulants, such as ancrod (Arvin, Arwin) from C. rhodostoma venom, is a rela­ tively benign state.173 Potentially lethal spontaneous sys­ temic bleeding is attributable to distinct venom components, known as hemorrhagins, which damage vascular endothe­ lium. These metalloproteinases are zinc metalloendopepti­ dases (reprolysins), some of which have disintegrin-like, cysteine-rich, and lectin domains.102 The combination of incoagulable blood, thrombocytopenia, and vessel wall damage result in massive bleeding, a common cause of death from viper bite. Complement activation:151,241,269 Elapid and some colubroid venoms activate complement via the alternative pathway (“cobra venom factor” is the snake’s C3b), whereas some viperid venoms activate the classic pathway.241 This has been documented in human victims of snakebite.151,269 Com­ plement activation could in turn affect platelets, the blood coagulation system, and other humoral mediators. 1059

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FIGURE 55-53  Neurotoxicity after snakebite. A, Ptosis (Bungarus caeruleus, Sri Lanka). B and C, Ptosis and external ophthalmoplegia (Oxyuranus scutellatus, Papua New Guinea). Patient is trying to look at the finger. D, Restricted jaw opening (O. scutellatus, Papua New Guinea). E, Ptsosis and jaw hanging open due to paralysis of masseter muscles (Crotalus durissus terrificus, Brazil). F, Late generalized flaccid paralysis (B. caeruleus, Sri Lanka). G, Persistent mydriasis unresponsive to light 25 days after a bite by Bungarus multicinctus on the right index finger in Hanoi, Vietnam. White line indicates pupillary diameter before (above) and 20 minutes after (below) instillation or 1% eilocarpine drops. (Copyright D.A. Warrell.)

Neurotoxicity Paralytic symptoms may emerge within 15 to 30 minutes of the bite, or they may be delayed for 9 or more hours. Preparalytic symptoms include nausea, vomiting, abnormal taste sensations, paresthesias, hyperacusis, blurred vision, feeling of heaviness of the eyelids, and drowsiness. Ptosis, external ophthalmoplegia, mydriasis, and paralysis of muscles innervated by the facial and other cranial nerves ensue, eventually involving muscles of deglutition and respiration, the trunk, and limbs (Figure 55-53). Autonomic nervous system symptoms include sweating, hyper­ salivation, gastrointestinal symptoms, and changes in blood pres­ sure and pulse rate. These symptoms are characteristic of envenoming by most elapids, such as kraits, coral snakes, mambas, cobras and the king cobra, but not of African spitting cobras, whose venoms are not paralytic in humans. Venoms of terrestrial Australasian snakes,28-30,42,206 sea snakes, and a few species of Viperidae, notably the Chinese and Japanese mamu­ shis (Gloydius [Agkistrodon] blomhoffii and G. brevicaudus), Sri Lankan and South Indian D. russelii, the southern African berg adder (Bitis atropos), and some other small Bitis species of south­ ern Africa (B. peringueyi, B. xeropaga), are also neurotoxic in humans. Pathophysiology.  Neurotoxic polypeptides and PA2s of snake venoms cause paralysis by blocking transmission at the neuro­ muscular junction.42,227 Patients with paralysis of the bulbar muscles may die of upper airway obstruction or aspiration, but the most common mode of death after neurotoxic envenoming is respiratory paralysis. By prolonging the activity of ACh at neuromuscular junctions, anticholinesterase drugs may improve paralytic symptoms in patients bitten by snakes with neurotoxins that are predominantly postsynaptic in their action (e.g., Asian cobras and Australasian death adders [genus Acanthophis]). Some patients bitten by elapids or vipers are unphysiologically drowsy in the absence of respiratory or circulatory failure. This is unlikely to be an effect of neurotoxic polypeptides, which do not cross the blood–brain barrier. It may be caused by endogenous opiates released by a venom component. Intracerebral injection of β-RTX 1060

(a receptor-active protein), a potent antagonist of opiate recep­ tors from D. russelii venom, produced sedation in rats.86 Myotoxicity Patients with generalized rhabdomyolysis develop myalgia, muscle tenderness on palpation or passive stretching, and trismus, and they pass dark brown or black urine (Figure 55-54). Pathogenesis.  PLA2 myotoxins and metalloproteinases are prin­ cipally responsible.78,79 They are present in venoms of most species of sea snakes,172 many terrestrial Australasian elapids such as tiger snakes (Notechis scutatus and N. ater), king brown or mulga snake (Pseudechis australis), taipan (O. scutellatus), rough-scaled snake (Tropidechis carinatus), Australian small-eyed snake (Rhinoplocephalus/Cryptophis nigrescens),206,285 some species of krait (Bungarus)57,94,230 coral snakes (Micrurus)109,135 and Viperidae, such as the Sri Lankan Russell’s viper (D. russelii),159 tropical rattlesnakes (Crotalus durissus),15,16,256 and North American rattlesnakes.108 Release into the bloodstream of myoglobin, muscle enzymes, uric acid, potassium, and other muscle constituents is an effect in humans of presynaptic neuro­ toxins. Patients may die of bulbar and respiratory muscle weak­ ness, acute hyperkalemia, or renal failure.

ACUTE KIDNEY INJURY Acute kidney injury is a common event and cause of death fol­ lowing bites by Russell’s vipers148,196,219,224 and sea snakes172,196,248 and is not uncommon following bites by South American rattle­ snakes (Crotalus durissus terrificus)15 and some Bothrops spp. It can complicate severe envenoming, even by species that usually cause only mild envenoming, such as Cryptelytrops albolabris, the hump-nosed pit viper (H. hypnale),12,48 V. berus,171,257 and Cerastes cerastes.186 Clinical presentation may be dramatic and is often associated with a period of profound hypotension (Figure 55-55, A). The patient claims to have passed no urine since he or she was bitten. More commonly, there is declining urine output and, much more

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FIGURE 55-54  Myotoxicity after snakebite showing myopathic facies, pain on passive stretching of muscles, brown staining of plasma (myoglobinemia) and myoglobinuria. A, Crotalus durissus terrificus, São Paulo, Brazil. B to D, Sea snake, Western Malaysia. (A copyright D.A. Warrell; B to D courtesy the late H. Alistair Reid.)

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C FIGURE 55-55  Acute kidney injury following snakebite. A, Shocked kidneys (demarcation between cortex and medulla) after Daboia siamensis bite in Burma. B, Fibrin (stained red) deposition in glomerular and peritubular vessels after D. siamensis bite in Burma. C, Fibrin deposition after Bothrops jararaca bite. (A courtesy Hla Mon; B courtesy Nicholas Francis; C courtesy Carlos Amaral.)

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BOX 55-2  Renal Histopathologic Changes in Human

Snakebite Victims

Glomerular Changes • Toxic mesangiolysis, platelet aggregation, mesangial proliferation • Proliferative glomerulonephritis; endocapillary, exocapillary, mesangiocapillary • Fibrin deposition • Ischemia

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Tubular Changes • Direct nephrotoxicity “lower nephron nephrosis” • Secondary ischemic changes (fibrin deposition) • Acute tubular necrosis (prerenal) • Cortical infarction, calcification

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FIGURE 55-56  Microangiopathic hemolysis following Cerastes cerastes bite. A, Blood film showing schistocytes (helmet cells). B, Showing hemoglobinemia (right) compared with control (left). (Copyright D.A. Warrell.)

rarely, polyuria. Some patients present late with symptoms of uremia. There may be evidence of pigment nephropathy associ­ ated with myotoxicity (see earlier discussion) or intravascular hemolysis, as in victims of envenoming by the colubroid genera Dispholidus, Thelotornis, and Rhabdophis who develop hemo­ globinemia, hemoglobinuria, and mild jaundice. Acute kidney injury associated with features suggestive of hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP) has been recognized in patients envenomed by Australian elapids, especially brown snakes (genus Pseudonaja)98 and several vipers, including Cerastes cerastes.186 Severe and often refractory renal failure is associated with thrombocytopenia, and intravascular hemolysis with the presence of circulating schisto­ cytes (helmet cells, fragmented erythrocytes) (Figure 55-56), indicating microangiopathic hemolysis with or without consump­ tion coagulopathy. Preexisting chronic renal disease and the effects of antivenom (serum sickness) may confuse clinical and histopathologic interpretations. Pathophysiology A wide range of renal histologic changes has been described after snakebite (Box 55-2). Acute tubular necrosis is the most common, but proliferative glomerulonephritis, toxic mesangioly­ sis with platelet agglutination, fibrin deposition, ischemic changes, distal tubular damage (“lower nephron nephrosis”), suggesting direct venom nephrotoxicity, and bilateral renal cortical necrosis with subsequent calcification are also reported.196 Acute tubular necrosis may result from prolonged hypotension and hypovole­ mia (see Figure 55-55, A), disseminated intravascular coagulation, direct toxic effect of the venom on the renal tubule, hemoglo­ binuria, myoglobinuria, and hyperkalemia. Russell’s viper venom

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produces hypotension, disseminated intravascular coagulation, direct nephrotoxicity,169 and, in Sri Lanka and India, intravascular hemolysis and rhabdomyolysis.159 In Burmese patients enven­ omed by Russell’s vipers (D. siamensis), high urinary concentra­ tions of β2-microglobulin, retinal binding protein, and N-acetyl glucosaminidase suggested failure of proximal tubular reabsorp­ tion and tubular damage.224 High plasma concentrations of active renin suggested that renal ischemia with activation of the reninangiotensin system was involved in development of renal failure. A marked but transient capillary and glomerular leak of albumin was an early sign of oliguric renal failure.219 Snake venom– induced disseminated intravascular coagulation may result in deposition of fibrin on vascular endothelium (see Figure 55-55, B and C ) that has been activated by, for example, metallopro­ teinases, producing microangiopathic hemolysis. Although the clinical picture (see earlier discussion) is reminiscent of hemolytic uremic syndrome, there is no reason to postulate autoantibodies (as in some forms of TTP) and no justification for plasmapheresis (see below).

CLINICAL PATTERN OF ENVENOMING BY DIFFERENT TAXA OF VENOMOUS SNAKES COLUBROIDEA (BACK-FANGED SNAKES)* Species Capable of Causing Fatal Envenoming In Africa, the boomslang (Dispholidus typus) (Figure 55-57) and the bird, twig, vine, or tree snake (Thelotornis kirtlandii and Thelotornis capensis [Figure 55-58]) have caused fatalities, including *References 249, 250, 284.

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FIGURE 55-57  Boomslang (Dispholidus typus), an arboreal colubrid snake capable of fatally envenoming humans. A, South African specimen (Johannesburg, South Africa). B, Showing large back fangs. (A copyright D.A. Warrell; B courtesy Dave Ball.)

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FIGURE 55-58  Bird, twig, vine, or tree snake (Thelotornis capensis), an arboreal colubrid snake capable of fatally envenoming humans. A, South African specimen. B, Showing back fangs (Johannesburg, South Africa). (Copyright D.A. Warrell.)

among their victims two famous herpetologists, Karl P. Schmidt (bitten by D. typus) and Robert Mertens (bitten by T. kirtlandii). In Asia, the Japanese yamakagashi (Rhabdophis tigrinus) and the Southeast Asian red-necked keelback (R. subminiatus) (Figures 55-59 and 55-60) have caused severe or fatal envenoming. Species Capable of Causing Systemic Envenoming In Europe, the Montpellier snake (Malpolon monspessulanus) (Figure 55-61) has been reported to cause neurotoxic symptoms. In Oceania, the brown tree snake (Boiga irregularis) (Figure 55-62), exported from Australia and New Guinea to Guam, has been known to attack and possibly envenom infants.62 In South America, a green racer (Philodryas olfersii) (Figure 55-63, A and B) and possibly other members of this genus can cause systemic hemostatic disturbance with ecchymoses distant from the bite (Figure 55-63, C and D). If these colubrid snakes are able to engage their rear fangs and chew for 15 seconds or longer, severe envenoming may result. Envenoming by D. typus, Thelotornis spp., R. tigrinus, and R. subminiatus gives rise to similar symptoms with onset that may be delayed for many hours or even days after the bite.249,250 There are nausea, vomiting, colicky abdominal pain, and head­ ache. Bleeding develops from old and recent wounds, such as

FIGURE 55-59  Yamakagashi (Rhabdophis tigrinus tigrinus). Japanese specimens. (Courtesy S. Mishima and the late Yoshio Sawai: The Snake 6:cover, 1974.)

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FIGURE 55-60  A, Red-necked keelback (Rhabdophid subminiatus) (Chanthaburi, Thailand), a dangerously venomous colubrid snake of Southeast Asia. B, Showing back fangs. (Copyright D.A. Warrell.)

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consciousness, and transient hypertension; and in three, there were ECG changes (ST-T changes and prolonged PR interval) (Figure 55-66, D).114 Mild abnormalities of blood coagulation and liver function have also been described. Atractaspis venoms have high lethal toxicity. The venom of A. engaddensis contains four 21-amino-acid peptides, sarafotoxins, that have 60% sequence homology with endogenous endothelins. They can cause coro­ nary vasoconstriction and atrioventricular block.18,53,201 The venom also contains hemorrhagic and necrotic factors, but no true neu­ rotoxins. Bites by the Natal black snake (M. microlepidotus) are said in two cases to have resulted in collapse and loss of con­ sciousness for up to 30 minutes.

ELAPIDAE Elapidae comprise cobras, kraits, mambas, African shield-nosed snakes, garter snakes (Elapsoidea), coral snakes (Aspidelaps), Asian coral snakes (Calliophis [including Maticora], Sinomicrurus, Hemibungarus), American coral snakes (Micruroides, Micrurus), sea kraits (genus Laticauda), and true sea snakes (subfamily Hydrophiinae). They are best known for systemic neurotoxic effects, but cytotoxic elapids, such as African spitting cobras and Asian spitting and nonspitting cobras, produce severe local envenoming (see later discussion).

FIGURE 55-61  Montpellier snake (Malpolon monspessulanus), 180-cm (70.9-inch) long male in Cartagena, Spain. (Courtesy Matt Wilson.)

venipunctures, and there is spontaneous gingival bleeding, epi­ staxis, hematemesis, melena, subarachnoid or intracerebral hem­ orrhage (Figure 55-64, A), hematuria, and extensive ecchymoses (Figure 55-64, B). Intravascular and microangiopathic hemolyses have been described. Most fatalities followed renal failure from acute tubular necrosis, many days after the bite. Local effects of the venom are usually trivial (Figure 55-65, online), but several patients showed local swelling; one person bitten by D. typus had massive swelling with blood-filled bullae. Investigations reveal incoagulable blood, defibrination, elevated fibrin/ fibrinogen degradation products (FDPs), severe thrombocytope­ nia, and anemia. These clinical features are explained by dis­ seminated intravascular coagulation triggered by a venom prothrombin activator. There is also complement activation.151

ATRACTASPIDINAE, GENUS ATRACTASPIS (BURROWING ASPS OR STILETTO SNAKES) (See Figures 55-30 and 55-38) Fatal envenoming has been reported from the Sudan (Kassala and Kordofan) (“Atractaspis microlepidota”*), from Nigeria (A. irregularis), and from the Arabian peninsula (“A. microlepidota andersoni”).1 However, in many parts of Africa and the Middle East, bites by the approximately 17 species of burrowing asp are common and rarely cause more than local symptoms.247,249,276 There is local pain, swelling, blistering, necrosis (especially of bitten fingers) (Figure 55-66, A to C), tender enlargement of local lymph nodes, local numbness, and paresthesias. The most common systemic symptom is fever. Most of the fatal cases died soon after the bite suffering vomiting, profuse salivation, and coma.276 In Israel, severe envenoming by A. engaddensis may produce violent autonomic symptoms (nausea, vomiting, abdom­ inal pain, diarrhea, sweating, and profuse salivation) within minutes of the bite. One patient developed severe dyspnea with acute respiratory failure; one had weakness, impaired *The taxonomic status of Arabian and Sudanese “Atractaspis micro­ lepidota” is currently uncertain.

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Neurotoxic Elapids Kraits,10,94,216,230 mambas, most of the Australasian elapids (see later text), some of the cobras (e.g., Philippine cobra, Naja philippinensis279,280; Cape cobra, N. nivea) and sea snakes176,248 cause minimal local effects. Rapidly evolving neurotoxicity is the domi­ nant clinical feature of envenoming by many elapid species, including African mambas, some African and Asian cobras, king cobras and kraits, Australasian elapids, American coral snakes and sea snakes. The earliest symptom of systemic envenoming is repeated vomiting, but sometimes the use of emetic herbal medicines confuses interpretation of this symptom. Other early preparalytic symptoms include contraction of the frontalis muscle (before there is demonstrable ptosis), blurred vision and loss of visual accommodation attributable to mydriasis, paresthesias (especially around the mouth), hyperacusis, loss of smell and taste, headache, dizziness, vertigo, and signs of autonomic nervous stimulation such as hypersalivation, congested conjunc­ tivae, and piloerection (“goose bumps”). Paralysis is first detect­ able as ptosis and external ophthalmoplegia, because ocular muscles are most sensitive to neuromuscular blockade (see Figure 55-53, A to C). These signs may appear as early as 15 minutes after the bite (cobras and mambas) but may be delayed for 10 hours or more following krait and cobra snakebites. Later, facial muscles, palate, jaws, tongue, vocal cords, neck muscles, and muscles of deglutition may become paralyzed. Pupils are usually dilated. Many patients are unable to open their mouths, but this can be overcome by force. In a minority, the jaw hangs open (see Figure 55-53, E). Respiratory arrest may be precipitated by obstruction of the upper airway by the paralyzed tongue or inhaled vomitus. Intercostal muscles are affected before limbs, diaphragm, and superficial muscles, and the pattern of breathing becomes abdominal or paradoxical (protrusion of the abdomen during inspiration). Even in patients with generalized flaccid paralysis (see Figure 55-53, F), slight movements of the digits may be possible, allowing the patients to signal. Loss of

FIGURE 55-62  Brown tree snake (Boiga irregularis) (Papua New Guinea). (Copyright D.A. Warrell.)

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FIGURE 55-63  Brazilian green racer (Philodryas olfersii). A, Specimen from Brazil. B, Details of back fangs. C, D, Bruising distant from the bite. (A and B copyright D.A.Warrell; C and D courtesy João Luiz Costa Cardoso.)

consciousness and generalized convulsions are due to respiratory paralysis, shock, or massive cerebral hemorrhage or thrombosis. Drowsiness may develop before significant paralysis. Drooping eyelids from tiredness may be misconstrued as ptosis, unless the extent of lid retraction with upward gaze is formally assessed. Patients with systemic envenoming suffer from headache, malaise, and generalized myalgia. Intractable hypotension may occur in patients envenomed by Asian and Australasian elapids, despite adequate respiratory support. Neurotoxic effects are completely reversible, either acutely in response to antivenom (e.g., in Asian cobra and Australasian death adder bites) or to anticholin­ esterases,* or they may slowly wear off spontaneously.28,29,119,216 In the absence of specific antivenom, patients supported by mechanical ventilators usually recover sufficient respiratory muscle function to breathe adequately in 1 to 4 days; ocular muscles recover in 2 to 4 days, and there is usually full recovery of motor function in 3 to 7 days.29-32,119 However, especially in the absence of antivenom treatment, paralysis may persist. Patients have recovered after 30 days of manual ventilation (in a case of envenoming by the Chinese krait, B. multicinctus) and after 10 weeks of mechanical ventilation (Australian rough-scaled snake, Tropidechis carinatus). Neurotoxic deaths are claimed to have occurred as soon as 15 minutes after the bite in the case of N. naja and from 1.25 to 60 (mean 12.6) hours in the case of N. kaouthia.125,240

*References 118, 227, 228, 273, 278, 282.

Envenoming by Mambas (Genus Dendroaspis)* These are justifiably the most dreaded snakes in Africa. All four species (D. polylepis, D. angusticeps, D. jamesoni, and D. viridis) (Figure 55-67, A to E; see Figures 55-8 and 55-32) are capable of causing rapidly progressive and fatal respiratory paralysis. Mamba venom toxins (see earlier discussion) are responsible for a distinctive clinical syndrome of envenoming: paresthesias, signs of autonomic nervous system stimulation, muscular fascicula­ tions, and paralysis (Figure 55-68). The speed of evolution of envenoming is well illustrated by a patient seen in Harare, Zim­ babwe. After a bite by a 3-m (9.8-foot) long black mamba (D. polylepis), the victim noticed tingling of the tongue and lips within 1 minute, followed by generalized tingling, abdominal pain, and light-headedness. Within 20 minutes, he was sweating profusely, had dilated pupils, and was too weak to stand up. He became nauseated and vomited 30 minutes after the bite, by which time he was unable to pass urine and had detectable ptosis. He became breathless and found it difficult to clear his throat of thick secretions. Forty minutes after the bite, he felt cold all over and noticed gooseflesh, his conjunctivae were con­ gested, and he was unable to open his mouth or protrude his tongue. There was then rapid deterioration in his breathing and level of consciousness. Generalized fasciculations were noticed. He was treated with antivenom after 75 minutes and, 4.5 hours after the bite, was intubated and mechanically ventilated for 40 hours, after which he made a complete recovery.249 *References 249, 256.

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Several patients bitten by captive eastern green mambas (D. angusticeps) in Western countries developed atypical envenom­ ing: extensive local swelling, blistering, and mild antihemostatic disturbances in the absence of classic neurotoxicity. Envenoming by African Neurotoxic Cobras (Naja anchietae, N. annulifera, N. haje, N. melanoleuca, N. nivea, and N. senegalensis) (Figure 55-69) Bites may cause some local swelling, but no necrosis develops unless the bite is on a finger pulp. Classic neurotoxic symptoms develop as early as 30 minutes after the bite and can evolve to the point of fatal respiratory paralysis 2 to 16 hours after the bite (Figure 55-70).249,256,266,291 Envenoming by the King Cobra (Ophiophagus hannah) (See Figure 55-15)* The world’s largest venomous snake can cause extensive local swelling, but neurotoxicity is the most prominent feature, reput­ edly capable of leading to death “soon” or in a “few minutes” after the bite. One patient, bitten by a 2-m (6.6-foot) long speci­ men in Burma, began to feel dizzy 15 minutes after the bite, had difficulties with speech and breathing after 30 minutes, showed bilateral ptosis after 40 minutes, and at 90 minutes suffered a respiratory arrest requiring 38 hours of mechanical ventilation (Figure 55-71, A to D). He made a full recovery (Figure 55-71, E).223 Severe envenoming by the king cobra (O. hannah) results in swelling of the whole limb and formation of bullae at the site of the bite, but local necrosis is minimal or absent (Figure 55-71, F).223,250

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B FIGURE 55-64  Yamakagashi (Rhabdophis tigrinus) bite in Japan. A, Cerebral hemorrhage. B, Extensive ecchymoses on bitten leg. (Courtesy the late Yoshio Sawai.)

Envenoming by Asian Kraits (Genus Bungarus) (See Figures 55-20, B and C and Figure 55-21, B)† The common Indian krait (B. caeruleus) (Figure 55-72) is consid­ ered to be the most dangerous species of venomous snake in the Indian subcontinent, together with N. naja.216 It is responsible for 22% to 44% of snakebite deaths in Anuradhapura, Sri Lanka, and *References 223, 236, 250. † References 10, 46, 94, 216, 230.

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FIGURE 55-66  Envenoming by burrowing asps. A, Local blistering at site of bite by slender burrowing asp (Atractaspis aterrima) in Nigeria. B, Atractaspis engaddensis bite in Israel. C, Atractaspis fallax bite, Diani Beach, Kenya. D, Electrocardiographic changes after A. engaddensis bite in Israel. (A copyright D.A.Warrell; B and D courtesy Elazar Kochva;114 C courtesy Thomas Sollacher.)

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FIGURE 55-67  Mambas (genus Dendroaspis). A, Black mamba (D. polylepis) (Zimbabwe). B, Showing long fangs and black lining of mouth, which gives this species its name (specimen from Watamu, Kenya). C, Eastern green mamba (D. angusticeps). D, Showing fangs (Watamu, Kenya). E, Western green mamba (D. jamesoni kaemosi) (Kakamega, Kenya). (Copyright D.A. Warrell.)

for 33% of all venomous snakebites in West Bengal. The epide­ miologic pattern is distinctive.10 Most patients are bitten while asleep on the floors of their huts, the bites occurring particularly at the time of night when sleepers are particularly restless during rapid eye movement sleep. At that time, they are more likely to inadvertantly touch or trap a snake that is prowling around their home in search of its natural prey. Because people are bitten while lying down, the target may be any part of the body, includ­ ing the head, neck, and shoulders. In one series of 88 cases of proved B. caeruleus envenoming in Sri Lanka, all patients were bitten while sleeping on the ground, at night, indoors. Only 23% of bites were on the lower limbs (compared with 82% by other species). Only 9% of patients had any sign of local envenoming,

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but 64% developed respiratory paralysis and the case fatality rate was 6%, twice as high as with other species.10 Krait bites usually produce invisible or scarcely perceptible puncture marks; no local symptoms apart from mild tenderness, itchiness, numbness, or some other paresthesia; and negligible or no local swelling. As a result, snakebite may not be suspected, and patients com­ monly present to the hospital after waking in the morning with descending paralysis (“early morning paralysis”).177 A virtually identical syndrome has been described following Malayan krait (B. candidus) (see Figure 55-20, B) bites in Southeast Asia, Ceylon krait (B. ceylonicus) (see Figure 55-21, B) bites in Sri Lanka, and bites by the banded krait (B. fasciatus) (see Figure 55-20, C) and the Chinese krait (B. multicinctus) (Figure 55-73).

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FIGURE 55-68  Envenoming by black mamba (Dendroaspis polylepis) bite in KwaZulu-Natal, South Africa. A, B, Eight hours after bite on leg—no local signs, drooling saliva, ptosis, but still breathing well. C, Improved after antivenom treatment. (Courtesy Iain Thirsk.)

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FIGURE 55-69  African neurotoxic cobras (genus Naja). A, Snouted cobra (N. annulifera, South Africa). B, Egyptian cobra (“asp”) (N. haje, Nigeria). C, Arabian cobra (N. haje arabica, Saudi Arabia). D, Forest cobra (N. melanoleuca). E, Cape cobra (N. nivea, South Africa). F, Senegalese cobra (N. senegalensis). (A to D copyright D.A.Warrell; E courtesy John D. Visser; F courtesy Jean-François Trape.)

Patients envenomed by B. candidus and B. multicinctus in Vietnam often suffer from persistent mydriasis (see Figure 55-53, G).94,230 Rare differential diagnoses of this type of neurologic pre­ sentation would include acute idiopathic inflammatory polyneu­ ropathy (Guillain-Barré syndrome, especially its variants, Miller Fisher syndrome and polyneuritis cranialis), Bickerstaff brainstem encephalitis, myasthenia gravis, and botulism. Rarely, local lymph nodes may be painfully enlarged. Noncolicky, increasing (cre­ scendo) pain (resembling classic gallstone or renal “colic”), epi­ gastric or central in location, is a prominent and characteristic early symptom of B. caeruleus envenoming, which may be the manifesting feature before development of neurotoxicity.10 This symptom seems to be less prominent in B. candidus and B. multicinctus envenoming. AVIT sequence cysteine-rich proteins,

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like mamba intestinal toxin (prokineticin), which cause painful gut spasm and hyperalgesia, may be responsible. Paralysis may develop within 2 hours or be delayed for 7 to 12 hours. Severe generalized muscle pains were noticed by a few patients in whom moderately elevated plasma myoglobin concentrations suggested the possibility of generalized rhabdomyolysis. Rhabdo­ myolysis and acute kidney injury have been described in victims of greater black krait (B. niger) bite in Bangladesh57 and, com­ bined with profound hyponatremia, in patients envenomed by B. multicinctus and B. candidus in Vietnam.92,94,230 Bungarus sindanus and B. walli have caused cases of severe neurotoxic enven­ oming in Nepal and Bangladesh.113 Reported case fatality rates in the absence of antivenom treatment and assisted ventilation were as high as 77% in India and 100% in Sri Lanka.

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FIGURE 55-70  Envenoming by Cape cobra (Naja nivea). A, Negligible local envenoming after 5 days. B, Respiratory paralysis on ventilator after 8 hours. C, Mydriasis. (Courtesy John D. Visser.)

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FIGURE 55-71  Envenoming by king cobra (Ophiophagus hannah). A, Patient paralyzed and ventilated 30 minutes after the bite. B, Local swelling and multiple fang marks. C, Bilateral ptosis. D, Conjunctival congestion. E, After recovery, back at work with the snake responsible for the bite. F, Minimal local necrosis at the site of a bite on the thumb in another reptile handler in Bangkok. (Copyright D.A. Warrell.)223

Envenoming by Australian and New Guinean Elapids (Figure 55-74; See Figure 55-31)* Venoms of these snakes cause a distinctive triad of symptoms: neurotoxicity similar to that seen with other elapid bites, general­ ized rhabdomyolysis, and hemostatic disturbances (Figure 55-75). Local signs are usually mild, but extensive local swelling and bruising with necrosis have been reported, especially after bites by the king brown or mulga snake (Pseudechis australis). Painful and tender local lymph nodes are a common feature in patients developing systemic envenoming. Early symptoms include vomiting, headache, and syncopal attacks similar to those experienced after some viper bites. ECG changes were common in patients envenomed by taipans *References 28-30, 42, 117-122, 206, 285.

FIGURE 55-72  Common krait (Bungarus caeruleus) (Hyderabad, India). (Copyright D.A. Warrell.)

(Oxyuranus scutellatus canni) (see Figure 55-31) in Papua New Guinea, and some had elevated cardiac troponin-T levels, sug­ gesting myocardial damage.119,120 In dogs, common brown snake (Pseudonaja textilis) venom caused myocardial depression attributed to disseminated intravascular coagulation, and tiger snake (Notechis scutatus) venom caused formation of thrombi within the heart, leading to pulmonary and coronary artery thromboembolism.206 All Australian elapid venoms are potentially neurotoxic to humans.227 Some patients lose their senses of smell and taste, in a few cases permanently, which is reminiscent of bites by the African berg adder, Bitis atropos (see later text). Many of the venoms contain myolytic PLA2s,202,206,270 and generalized rhabdo­ myolysis has been confirmed after bites by Notechis, Pseudechis, Oxyuranus, Austrelaps, Tropidechis, Rhinoplocephalus/Cryptophis nigrescens, Micropechis ikaheka, and Acanthophis.118,192,214,270,285 Persistent bleeding from wounds and spontaneous systemic bleeding from gums and the gastrointestinal tract are found in association with incoagulable blood following bites by many Australasian species. Venoms of 15 out of 19 species exhibited

FIGURE 55-73  Chinese many-banded krait (Bungarus multicinctus) (China). (Copyright D.A. Warrell.)

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FIGURE 55-74  Australasian elapid snakes. A, Death adder (Acanthophis laevis) (Papua New Guinea). B, New Guinea small-eyed snake (Micropechis ikaheka). C, Tiger snake (Notechis scutatus) spreading hood. D, Inland taipan (Oxyuranus microlepidota). E, Eastern taipan (Oxyuranus scutellatus). F, King brown or mulga snake (Pseudechis australis). G, Eastern brown snake (Pseudonaja textilis). H, Rough-scaled snake (Tropidechis carinatus). (Copyright D.A. Warrell.)

procoagulant activity in vitro.206 Some venoms (e.g., Pseudechis, Acanthophis, Micropechis ikaheka, and Pseudonaja) are antico­ agulant and might cause incoagulable blood without evidence of activation of coagulation and fibrinolysis.103,118,203,270 Hemostatic abnormalities are particularly frequent and serious in patients bitten by tiger snakes (Notechis spp.), taipans (Oxyuranus spp.), and brown snakes (Pseudonaja spp.); uncommon with bites by black snakes (Pseudechis spp.); and rare with bites by death adders (Acanthophis spp.).118 Envenoming by American Coral Snakes (See Figures 55-23 and 55-25)* Local signs are usually reported as minimal, consisting of mild swelling and some erythema, or are entirely absent (Figure 55-76, A and E). However, local symptoms may be severe and persis­ tent, including pain that may be excruciating (Micrurus lemniscatus)135 and sometimes generalized to bones, joints, and tooth sockets, paresthesias such as numbness radiating up the bitten limb, and, in some cases, extensive swelling. The earliest symptom of systemic envenoming may be nausea, retching, and repeated vomiting, sometimes with abdominal pain. Other early prepara­ lytic symptoms include euphoria (M. fulvius), blurred vision, perioral paresthesias, hyperacusis, loss of the senses of smell and taste, headache, dizziness, vertigo, and signs of autonomic nervous system stimulation, such as hypersalivation producing unusually sticky secretions, congestion of the conjunctivae, and piloerection. Descending paralysis is usually first detectable as ptosis and external ophthalmoplegia, appearing as early as 15 minutes but sometimes as late as many hours after the bite, progressing to total flaccid paralysis (Figure 55-76, B, C, D, and *References 109, 135, 256.

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F). Symptoms of systemic envenoming include headache, malaise, and generalized myalgia with, in rare cases, evidence of gen­ eralized rhabdomyolysis (M. fulvius, M. lemniscatus helleri, M. laticollaris), hemolysis, mild coagulopathy and bleeding into gastrointestinal and urinary tracts.109,135 Envenoming by Sea Snakes (Hydrophiinae) and Sea Kraits (Laticaudinae) (Figures 55-77 and 55-78; see also Figures 55-45 to 55-47)* The bite is usually painless and may not be noticed by the wader or swimmer. Fangs and other teeth may be left in the wound. There is minimal or no local swelling (Figure 55-78, A), and involvement of local lymph nodes is unusual. Generalized rhab­ domyolysis is the dominant effect of envenoming by many species. Early symptoms include headache, a thick feeling of the tongue, thirst, sweating, and vomiting. Generalized aching, stiff­ ness, and tenderness of the muscles become noticeable between 30 minutes and 210 minutes after the bite. Trismus is common (Figure 55-78, B). Passive stretching of the muscles is painful (see Figure 55-54, C). Later there is progressive flaccid paralysis start­ ing with ptosis, as in other neurotoxic envenomings (see Figure 55-78). The patient remains conscious until the respiratory muscles are sufficiently affected to cause respiratory failure. Myo­ globinemia and myoglobinuria develop 3 to 8 hours after the bite (see Figure 55-54, B to D, sea-snake bite). These are sus­ pected when the serum/plasma appears brownish and the urine dark reddish brown. Bedside “stix” tests will appear positive for hemoglobin/blood in urine containing myoglobin. Myoglobin and potassium released from damaged skeletal muscles may cause acute kidney injury, whereas hyperkalemia developing within 6 to 12 hours of the bite may precipitate cardiac arrest. *References 172, 174, 206, 248, 285.

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FIGURE 55-75  Envenoming by Papua New Guinean elapids. A, Negligible local envenoming after Papuan taipan (Oxyuranus scutellatus) bite. B, Ptosis after death adder (Acanthophis laevis) bite. C, Paralytic and hemorrhagic signs after Papuan taipan bite. D, Bleeding gums after Papuan taipan bite. (Copyright D.A. Warrell.)

Cytotoxic Elapids Patients bitten by African spitting cobras (e.g., N. nigricollis) and Asian cobras (e.g., N. naja, N. kaouthia) commonly develop tender local swelling, which may be extensive, and regional lymphadenopathy.222,240,269 A characteristic lesion may appear within 24 to 48 hours. Blistering often surrounds a demarcated pale or blackened anesthetic area of skin. The lesion smells putrid and eventually breaks down, with loss of skin and sub­ cutaneous tissue that may be extensive. Skip lesions, separated by areas of apparently normal skin, may extend proximally up the limb. Prolonged morbidity may result, and some patients may lose a digit or the affected limb if there is secondary infection. Envenoming by the black desert cobra (Walterinnesia aegyptia) may result in marked local swelling as well as neurotoxicity.247,249,253 Envenoming by African Spitting Cobras (Genus Naja) (Figure 55-79; See Figures 55-10 and 55-33) Bites by N. ashei, N. katiensis, N. mossambica, N. pallida, N. nigricincta, N. nigricollis, and N. nubiae cause severe local envenoming without neurotoxicity.222,242,249,269 Most bites occur at night inside homes while the victims are asleep. There is immedi­ ate pain, followed by vomiting within 6 hours and extensive local swelling, blistering (60%), and tissue necrosis (70%) (see Figure 55-50, G and H, N. nigricollis bite). Tissue necrosis usually involves the skin and subcutaneous connective tissues only. There may be the appearance of skip lesions, in which areas of necrosis are separated by strips of apparently normal skin. There is leukocytosis and evidence of complement activation, princi­ pally by the alternative pathway (Figure 55-80).242,269

Envenoming by Asian Cobras (Genus Naja) (Figure 55-81) In victims of spitting and nonspitting Asian cobras, severe local effects, as described for African spitting cobras, can develop, but with classic elapid neurotoxicity (Figure 55-82). Species include Chinese cobra (N. atra), monocellate cobra (N. kaouthia), Indian spectacled cobra (N. naja),216 and Southeast Asian spitting cobras (N. siamensis301 and N. sumatrana). The Philippine cobra, which is responsible for about one-half of all snakebites in Luzon Island, rarely causes local swelling or necrosis.279,280 Snake Venom Ophthalmia* Venom ophthalmia results when venom of the spitting elapids (African and Asian spitting cobras, genus Naja; southern African rinkhal, Hemachatus haemachatus) enters the eye. There is intense local pain, blepharospasm, palpebral edema, and leukor­ rhea (Figure 55-83, A to C, N. nigricollis spit). Slit-lamp or fluo­ rescein examination reveals corneal erosions in more than one-half the patients spat at by N. nigricollis.164,242,274 Secondary infection of the corneal lesions may result in permanent opacities (Figure 55-83, F ), causing blindness or panophthalmitis with destruction of the eye (Figure 55-83, E). Rarely, venom is absorbed into the anterior chamber, causing hypopyon and anterior uveitis (Figure 55-83, D).157 Seventh (facial) cranial nerve paralysis is a rare complication that results from tracking of venom from the conjunctival sac through lymphatics posteriorly to the superfi­ cially situated seventh cranial nerve. *Reference 41.

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FIGURE 55-76  Envenoming by American coral snakes. A, Showing lack of local envenoming (Micrurus corallinus). B, Neurotoxic signs (M. corallinus. C, Neurotoxic signs appearing first 15 hours after the bite (Micrurus lemniscatus helleri ).135 D, Ptosis and facial paralysis during the first day after the bite (Micrurus mipartitus) (Colombia). E, Bite site on palm of hand showing lack of local envenoming. F, Neurotoxicity after bite by M. mipartitus in Colombia. (A and B courtesy Instituto Butantan, São Paulo; C courtesy Steve Manoch;135 D to F courtesy Rafael Otero-Patiño.)

VIPERIDAE (OLD WORLD VIPERS AND ADDERS, ASIAN AND LATIN AMERICAN PIT VIPERS)* Local envenoming is usually more severe than that caused by other snakebites. Swelling may develop immediately but is some­ times delayed for several hours. It may spread rapidly, sometimes *References 256, 262.

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involving the whole limb and adjacent trunk (see Figure 55-50 B, C, E, and F). There is associated pain, tenderness, and enlarge­ ment of regional lymph nodes. Bruising is common, especially along the path of superficial lymphatics and over regional lymph nodes. Persistent bleeding from the fang marks suggests coagu­ lopathy (see Figure 55-49, C. rhodostoma bite). Swollen limbs can accommodate many liters of extravasated blood, leading to hypovolemic shock. Blistering may appear at the bite site within a few hours after the bite (see Figure 55-50, C and D). These contain clear or bloodstained fluid. Necrosis of

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FIGURE 55-77  Sea snakes. A, Blue-spotted sea snake (Hydrophis cyanocinctus) (Tachalab, Thailand). B, Hydrophis fasciatus atriceps (Thailand). C and D, Hardwick’s sea snake (Lapemis curtus) showing tiny fangs. E, Sea krait (Laticauda colubrina) (Madang, Papua New Guinea). (Copyright D.A. Warrell.)

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FIGURE 55-78  Sea-snake bite. A, Fang marks; note lack of local envenoming. B, Ptosis, external ophthalmoplegia, facial paralysis, and trismus in a Malaysian fisherman bitten 24 hours previously by a beaked sea snake (Enhydrina schistosa). (Courtesy the late H. Alistair Reid.)

skin, subcutaneous tissue, and muscle develops in up to 10% of hospitalized cases, especially following bites by Asian pit vipers (e.g., Calloselasma rhodostoma, Deinagkistrodon acutus, and Protobothrops flavoviridis), African vipers (genus Bitis), sawscaled vipers (genus Echis), and the Palestine viper (Daboia palaestinae). Bites on the digits and in areas draining into tight fascial compartments, such as the anterior tibial compartment,

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are particularly likely to result in necrosis. High intracompart­ mental pressure may cause ischemia that contributes, together with direct effects of the venom, to muscle necrosis.70 Severe pain associated with tense swelling, segmental anesthesia, and pain on stretching the intracompartmental muscles (e.g., dorsi­ flexion of the foot in the case of the anterior tibial compartment) should raise the possibility of raised intracompartmental pressure.

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FIGURE 55-79  African spitting cobras (genus Naja). A, N. ashei (Watamu, Kenya). B, N. nigricollis (Abuja, Nigeria). C, N. nubiae (Egypt). D, N. pallida (Kenya). (Copyright D.A. Warrell.)

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C FIGURE 55-80  Envenoming by African black-necked spitting cobra (Naja nigricollis). A, Swelling, blistering, and necrosis after a bite on the elbow. B, Loss of skin and subcutaneous tissue after a bite on the dorsum of the foot. C, Extensive necrosis of skin and subcutaneous tissues in a Mende woman in Sierra Leone bitten 2 weeks earlier. Note the “skip lesions”—areas of necrosis separated by intact skin. (Copyright D.A. Warrell.)

Sudden severe pain, absence of arterial pulses, and a demarcated cold segment of limb suggest thrombosis of a major artery. Deep vein thrombosis has been described but is surprisingly rare. The absence of detectable local swelling 2 hours after a viper bite usually means that no venom has been injected, but fatal systemic envenoming by the Burmese Russell’s viper (D. siamensis) and tropical rattlesnake (Crotalus durissus sub spp.) may occur in the absence of local signs. Systemic Envenoming Hemostatic Abnormalities.  Hemostatic abnormalities are char­ acteristic of envenoming by Viperidae but are usually absent in patients bitten by the smaller European vipers (e.g., V. berus, V. aspis, V. ammodytes).171,257 Persistent bleeding (>10 minutes) from the fang puncture wounds and from new injuries such as veni­ puncture sites and old partially healed wounds is the first clinical evidence of consumption coagulopathy. Spontaneous systemic hemorrhage is most often detected in the gingival sulci (see Figure 55-52, A). Bloodstained saliva and sputum usually reflect bleeding gums or epistaxis. True hemoptysis is rare. Hematuria may be detected a few hours after the bite. Other types of spon­ taneous bleeding are ecchymoses; intracranial and subconjuncti­ val hemorrhages; bleeding into the floor of the mouth, tympanic membrane, and gastrointestinal and genitourinary tracts; pete­ chiae; and larger discoid and follicular hemorrhages. Bleeding into the iliacus muscle may result in weakness of hip flexion. Hemorrhagic infarction of the anterior pituitary (resembling post­ partum Sheehan’s syndrome) may complicate envenoming by Russell’s vipers in Burma and India,234 and single cases have been 1074

reported from Brazil (alleged to have been caused by Bothrops jararacussu) and Sri Lanka.6 Menorrhagia and antepartum and postpartum hemorrhage have been described after envenoming by vipers.20 Severe headache and meningism suggest subarach­ noid hemorrhage. Evidence of a developing central nervous system lesion (e.g., hemiplegia), irritability, loss of consciousness, and convulsions suggest intracranial hemorrhage (see Figure 55-52, D) or cerebral thrombosis. Abdominal distention, tender­ ness, and peritonitis with signs of hemorrhagic shock but no external blood loss (hematemesis or melena) suggest retroperi­ toneal or intraperitoneal hemorrhage. Incoagulable blood result­ ing from defibrination or disseminated intravascular coagulation is a common and important finding in patients systemically envenomed by members of the following genera: Atheris, Daboia, Vipera, Echis, Gloydius, Calloselasma, Deinagkistrodon, and Trimeresurus (sensu lato). Intravascular hemolysis, causing hemoglobinemia (pink plasma) and black or grayish urine (hemoglobinuria or methe­ moglobinuria), has been convincingly described in patients bitten by Sri Lankan Russell’s viper (Daboia russelii),159 the Saharan horned viper (Cerastes cerastes)186 (see Figure 55-56), and Aus­ tralian western brown snakes (Pseudonaja spp.).98 Features of microangiopathic hemolysis that have suggested hemolytic uremic syndrome may progress to severe anemia and renal failure.186 Circulatory Shock (Hypotensive) Syndromes A decrease in blood pressure is a common and serious event in patients bitten by vipers, especially in the case of some of the Old World Viperinae (e.g., D. russelii, D. siamensis, D. palaestinae, V. berus, Bitis arietans, B. gabonica, and B. rhinoceros) (see Figure 55-51).138,148,275 Sinus tachycardia suggests hypovolemia resulting from external hemorrhage, blood loss into the tissues, or local or generalized increase in capillary permeability. Patients envenomed by Burmese Russell’s viper (D. siamensis) may develop conjunctival edema, serous effusions, pulmonary edema, hemoconcentration, and decrease in serum albumin concentra­ tion, all evidence of increased vascular permeability (see later discussion).148,219 Pulse rate may be slow or irregular if the venom affects the heart directly or reflexly (e.g., V. berus, B. arietans, Calloselasma rhodostoma). Vasovagal syncope may be precipi­ tated by fear and pain. Early, repeated, and usually transient syncopal attacks with features of anaphylaxis develop in patients bitten by some Viperidae (e.g., D. palaestinae, V. berus, V. aspis, D. siamensis, and D. russelii). Vomiting, sweating, colic, diarrhea (with incontinence), shock, bronchospasm, urticaria, and angio­ edema of the face, lips, gums, tongue, and throat may appear as early as 5 minutes or as late as many hours after the bite. Hypo­ tension is an important feature of anaphylactic reactions to anti­ venom (see later text). Renal failure can complicate severe envenoming by any species of snake, but it is common and the most frequent cause of death in victims of Russell’s viper. People bitten by Russell’s viper may become oliguric within a few hours of the bite. Loin pain and tenderness may be experienced within the first 24 hours and, in 3 or 4 days, the victim may become irritable, comatose, or convulsing, with hypertension and evi­ dence of metabolic acidosis. Neurotoxicity Neurotoxicity attributable to venom PA2s is a feature of enven­ oming by a few species of Old World Viperidae (e.g., Gloydius blomhoffii, G. brevicaudus, Bitis atropos, other small South African Bitis species, and Sri Lankan and south Indian Russell’s viper), some populations of Vipera aspis and V. berus,133,134 and New World tropical rattlesnakes (Crotalus durissus sub spp.). The clinical features are the same as with elapid envenoming (Figure 55-84; see Figures 55-53, E, and 55-54, A). Progression to respiratory or generalized paralysis is unusual but has been described. Associated generalized myalgia suggests the possibil­ ity of rhabdomyolysis. Pupillary dilation, causing visual distur­ bance from loss of accommodation, is a feature of severe envenoming by small Bitis species (e.g., B. peringueyi) and may be a permanent neurologic sequela that can be corrected tran­ siently by instillation of pilocarpine, as in some cases of krait bite envenoming.

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FIGURE 55-81  Asian cobras. A, Chinese cobra (Naja atra) (Hong Kong). B, Monocellate cobra (N. kaouthia) (Thailand). C, Indian spectacled cobra (N. naja) (Sri Lanka). Black and white (D) and brown (E) phases of Indo-Chinese spitting cobra (N. siamensis) (Thailand). F, Equatorial spitting cobra (N. sumatrana) (Singapore). (Copyright D.A. Warrell.)

ENVENOMING BY VIPERINAE Europe Envenoming by European Vipers (Figure 55-85).*  The common viper, or adder (V. berus) (Figure 55-85, C), the only venomous snake found in Britain, occurs in England, Wales, Scotland, and northern Europe (Figure 55-85, D and E), extending into the Arctic Circle and through Asia as far east as Sakhalin Island and south to northern Korea (see Figure 55-42, online). Four other vipers are widely distributed in mainland Europe: the nose-horned or sand viper (V. ammodytes) (Figure 55-85, A and B) in the Balkans, Italy, Austria, and Romania; the asp viper (V. aspis) in France (south of Paris), Spain, Germany, Switzerland, and Italy; Lataste’s viper (V. latastei) in Spain and Portugal; and Orsini’s viper (V. ursinii) in southeastern France, central Italy, and Eastern Europe. The Ottoman viper (Montivipera xanthina) (Figure 55-85, G) occurs around Istanbul and in some eastern Aegean islands, northern Greece, and Asia Minor. The Milos viper (Macrovipera schweizeri) (Figure 55-85, F) inhabits some of the Cyclades Islands, southeast of Greece, whereas the Levantine viper (Macrovipera lebetina) occurs on Cyprus. Clinical Features of the European Adder (Vipera berus) Bite.  Pain usually develops quickly at the site of the bite, and local *References 104, 140, 171, 251, 254, 257.

swelling is evident within a few minutes but is sometimes delayed for 30 minutes or longer. Local blisters containing blood are uncommon (Figure 55-86, A). Swelling and bruising with lymphan­ gitis may advance to involve the whole limb within 24 hours, extend to the trunk, and, in children, become generalized (Figure 55-86, B to D). A few cases of compartment syndromes and necro­ sis have been described. Pain, tenderness, and enlargement of local lymph nodes are sometimes noticeable within hours. Dra­ matic early systemic symptoms may appear within 5 minutes of the bite or be delayed for many hours. These include retching; vomiting; abdominal colic; diarrhea; incontinence of urine and feces; sweating; vasoconstriction; tachycardia; shock; angioedema of the face, lips, gums, tongue, throat, and epiglottis; urticaria; and bronchospasm. These symptoms may persist for as long as 48 hours. Hypotension is the most important sign. It usually develops within 2 hours. It may be transient, resolving spontaneously within 2 hours, persistent and recurrent, or progressive and fatal. ECG changes (see Figure 55-51, B) include flattening or inversion of T waves, ST-segment elevation, second-degree heart block, bradyar­ rhythmias or tachyarrhythmias, atrial fibrillation, and myocardial infarction. Defibrination (incoagulable blood) or milder degrees of coagulopathy and spontaneous bleeding into the gastrointesti­ nal tract, lungs, (see Figure 55-86, E) or urinary tract are uncom­ mon. Other clinical features include fever, drowsiness, and, rarely, coma and seizures secondary to hypotension or cerebral edema, respiratory distress/pulmonary edema (in children), acute kidney injury, cardiac arrest, intrauterine death, acute gastric dilation, 1075

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FIGURE 55-82  Envenoming by monocellate Asian cobra (Naja kaouthia). A, Local swelling and early darkening. B, Blistering and demarcated necrotic area. C, After debridement of necrotic tissue. D, Severe hypoxic brain damage in a boy bitten on his left ankle in Vietnam. There was a delay in resuscitating him after development of respiratory paralysis. (Copyright D.A. Warrell.)

paralytic ileus and acute pancreatitis. Laboratory findings include neutrophil leukocytosis (more than 20 × 109/L in severe cases), thrombocytopenia, initial hemoconcentration and later anemia, resulting from leakage of plasma and blood cells out of blood vessels into the bitten limb, and, rarely, hemolysis, elevation of serum creatine kinase, and metabolic acidosis. Deaths usually

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occur from 6 to 60 (average 34) hours after the bite. Most adder bites cause only trivial symptoms; patients must be assessed indi­ vidually. Children may be severely envenomed; in a French series, there were three deaths in a group of seven children between 2.5 and 10 years of age. The dangers of adder bite should not be underestimated.

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FIGURE 55-83  Venom ophthalmia after venom “spitting” by black-necked spitting cobra (Naja nigricollis) in Nigeria. A to C, Acute effects— blepharospasm, inflammation, leukorrhea, epiphora. D, Hypopyon. E, Panophthalmitis following neglected corneal abrasion. F, Corneal opacity causing blindness. (Copyright D.A. Warrell.)

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FIGURE 55-84  Neurotoxic envenoming by Viperidae. Ptosis (A) and mydriasis (B) after berg adder (Bitis atropos) bite in Drakensberg, South Africa. C, B. atropos specimen from South Africa. (A and B courtesy Craig Smith; C copyright D.A. Warrell.)

Envenoming by other European and Mediterranean vipera produces similar features, most severe in the case of M. lebetina (Cyprus), V. ammodytes, and V. aspis bites, and least severe in V. ursinii and V. latastei bites. It is surprising that bites by M. schweizeri (Cyclades Islands, Greece) do not appear to result in severe envenoming. Some populations of V. aspis zinnikeri and V. aspis in southeastern France and of V. berus in Hungary can cause mild neurotoxic envenoming.133,134

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Africa Envenoming by Saw-Scaled or Carpet Vipers (Genus Echis) (Figure 55-87; See Figures 55-14, A and 55-18, C).*  This genus of vipers is of great medical importance. It is widely distributed in *References 249, 265, 267.

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FIGURE 55-85  European Viperidae. A, Vipera ammodytes. B, V. ammodytes (Montenegro). C, Vipera berus (England). D, Melanistic V. berus (Russia). E, V. berus bosniensis (Hungary). F, Macrovipera schweizeri (Milos). G, Montivipera xanthina (Turkey). ( A to D, F, and G copyright D.A. Warrell; E courtesy Tamás Malina.)

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FIGURE 55-86  Envenoming by Vipera berus. A, Hemorrhagic blister at site of bite. B, Swelling of bitten limb. C, Bruising of the bitten limb. D, Generalized swelling and bruising in a 4-year-old child in Sweden. E, Chest radiograph showing extensive intrapulmonary bleeding. (A copyright D.A. Warrell; B courtesy Mark Brueton; C and E courtesy H. Bowker; D courtesy Hans Persson.)

the northern third of Africa from Senegal in the west to the Tana River in Kenya in the south and through the Middle East. Through­ out this range, it is usually the most important cause of human snakebite morbidity and mortality. Bites are most common in West Africa, where E. ocellatus (see Figure 55-18, C) is the most important species.55,242,267,268 In Nigeria, only 4% of patients admit­ ted to the hospital lacked signs of envenoming, the lowest rate of “dry bites” reported in any large case series. The remainder had both local and systemic envenoming. Twelve percent devel­ oped local blistering, and 9% developed necrosis (Figure 55-88, A and B). Coagulopathy (attributable to venom prothrombin activators and factor X activators) was universal; 55% of victims showed spontaneous systemic bleeding (see Figures 55-52, A, B, E, and F and 55-88, C to G), usually from the gingival sulci (Figure 55-88, C), but thrombocytopenia (platelet count less than 103 × 109/L or 103,000/mm3) was detected in only 7%. Soluble fibrin complexes and fibrin/fibrinogen breakdown products were detected, but heparin does not inhibit Echis thrombin in vitro or in patients.55,97,267 The case fatality rate of 3.6% was attributable to hemorrhagic shock (three cases) (Figure 55-88, E to G; see Figure 55-52, F) and intracerebral hemorrhage (two cases) (Figure 55-88, D). Envenoming by eastern and North African E. pyramidum is generally less severe, but fatalities are reported in Turkana and Wajir in northern Kenya and in Somalia. One patient bitten by a Tunisian E. leucogaster developed transient ptosis.74,262 Echis species cause most fatal snakebites in the Middle East.247,249,253 Envenoming by African Puff Adders (Bitis arietans) (Figure 55-89; See Figure 55-11).*  This species (or species complex) is thought to be responsible for many of the bites throughout the African savanna region. Local swelling is often very extensive, commonly extending to involve the entire bitten limb and spread­ ing to the trunk (Figure 55-90, A).275 This extravasation of plasma causes hypovolemic shock, a common manifesting feature. Local blistering and necrosis may be extensive, requiring amputation of the bitten digit or even part or all of the bitten limb (Figure 55-90, B). Major arteries may become thombosed or entrapped by swollen tissue22 in the bitten limb, increasing local tissue damage. Compartment syndromes may develop, especially involving the anterior tibial compartment after bites on the feet *References 249, 284.

1078

and ankles. These may lead to ischemic muscle necrosis, as in Volkmann’s ischemic contracture of the forearm. Direct myocar­ dial effects and arrhythmias, commonly sinus bradycardia, may contribute to hypotension. In West Africa, envenoming by B. arietans causes spontaneous bleeding, bruising and petechial hemorrhages on serosal surfaces, attributable to thrombocytope­ nia but not coagulopathy. However, in East and South Africa, coagulopathy, and rarely even cerebral thrombosis, have been reported. This regional variation in the pattern of envenoming suggests that there may be different species of puff adder. Envenoming by Giant Rain Forest Vipers or Adders (Bitis gabonica, Bitis rhinoceros and Bitis nasicornis) (Figure 55-91; See Figure 55-34, B).*  These giant rain forest species are the commonest cause of snakebite in some areas of Africa, for example in southern Nigeria and the eastern Democratic Repub­ lic of Congo. In light of their wide distribution, prodigious size, enormous fangs, and massive yield of highly potent venom, it is surprising that so few cases of envenoming have been reported. Local effects of envenoming may be less severe than those pro­ duced by puff adder bites, but swelling, bruising, blistering, and necrosis are common (Figure 55-92). Systemic symptoms may be early and dramatic, including dizziness, chest tightness, nausea, and vomiting. In one case, there was early paralysis of visual accommodation and deafness, suggesting neurotoxicity. Cardio­ vascular abnormalities, including hypotension and hypovolemic and cardiogenic shock, arrhythmias, and ECG changes, are reported. Spontaneous systemic bleeding is a common feature, whereas hemostatic abnormalities include thrombo­cytopenia, inhibition of platelet aggregation, and evidence of thrombin-like and fibrinolytic activities.138 Envenoming by the Berg Adder (B. atropos) (See Figure 55-84).  This mountain species has been responsible for enven­ oming rock climbers and mountain travelers in Zimbabwe and South Africa. It is the most neurotoxic of African vipers and can cause other unusual symptoms. After initial severe pain and rapidly spreading local swelling (with rare development of necro­ sis), there are paresthesias of the tongue and lips, blurring of vision, loss of the senses of taste and smell, nausea, vomiting, *References 249, 262.

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FIGURE 55-87  Saw-scaled or carpet vipers. A, Echis carinatus carinatus (Tamil Nadu, India). B, Echis carinatus multisquamatus (Russia). C, Echis carinatus sochureki. D, Echis coloratus (Saudi Arabia). E, Echis jogeri (Senegal). F, Echis pyramidum leakeyi (Baringo, Kenya). (A to D, F and G copyright D.A. Warrell; E courtesy Wolfgang Wüster.)

and dizziness. In one series of cases, ptosis, external/internal ophthalmoplegia, dilated pupils, loss of visual accommodation, and anosmia were reported in 93% of cases (see Figure 55-84). There was respiratory paralysis in 72%, hyponatremia (attributed to a natriuretic hormone–like toxin) and dysphagia in 64%, and convulsions in 29%.146Only one fatal case has been reported. Envenoming by Bush Vipers (Genera Atheris, Proatheris, and Others) (Figure 55-93).*  These mainly arboreal species seem more likely to bite Western snake enthusiasts than indig­ enous Africans. Envenoming by them has been underestimated. Bites by Atheris ceratophora, A. desaixi, and A. nitschei caused only local effects: transient pain, swelling, bruising, and residual arthrodesis. However, a prominent feature of severe envenoming by A. squamigera and A. chlorechis was hypotension, perhaps attributable to a new class of peptides containing small poly-His and poly-Gly segments identified in venoms of A. squamigera, A. chlorechis, and A. nitschei. A man bitten by a large green bush viper (A. squamigera) developed massive swelling of the bitten limb and incoagulable blood. He died 6 days later in hemorrhagic shock following hematemesis. In other cases of bites by this species, there were immediate severe pain, swelling, local bruis­ ing, dizziness, shivering, nausea, and local lymphadenopathy. A man bitten by a Western bush viper (A. chlorechis) developed a severe bleeding diathesis, hypotension, acute kidney injury, and

*References 259, 262.

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hemolysis but survived. Three men were bitten by captive speci­ mens of lowland or swamp adders (P. superciliaris). All experi­ enced severe and persistent pain, initially in the bitten limb but later spreading to the trunk and back; local swelling (local necro­ sis in one); intravascular hemolysis (schistocytes in one) with hyperbilirubinemia; thrombocytopenia; fibrinolysis (elevated Ddimer); elevated aspartate aminotransferase and other serum enzymes; oliguric acute kidney injury requiring dialysis in two cases; and slow recovery over several weeks. One presented with severe persistent nausea, vomiting, and diarrhea. Two had con­ sumptive coagulopathy, two hematuria or hemoglobinuria, and two became hypertensive and developed pulmonary congestion with arterial desaturation. In one case, imaging suggested bilat­ eral intrarenal vascular occlusion that progressed to renal cortical necrosis, and later myocardial ischemia, leaving him with intrac­ table renal failure.259 Envenoming by Desert Vipers (Genus Cerastes) (Figure 55-94).*  C. cerastes, C. gasperettii, C. vipera, and Pseudocerastes persicus inhabit the vast arid deserts of North Africa and the Middle East, where they are the most common cause of snake­ bite. A few fatal cases were reported in the 19th-century French colonial military literature, but there have been no recent reports. Envenoming usually results in local pain and swelling, compli­ cated by necrosis in some cases. Nausea, vomiting, spontaneous

*Reference 186.

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FIGURE 55-88  Envenoming by West African carpet viper (Echis ocellatus) in northern Nigeria. A and B, Local necrosis. C, Bleeding from gums and into floor of mouth. D, Subarachnoid hemorrhage causing meningism. E to G, Autopsy finding of bleeding into the lungs, kidneys, and bladder. (Copyright D.A. Warrell.)

Asia Envenoming by Saw-Scaled or Carpet Vipers (Genus Echis) (See Figure 55-88, A to C ).*  E. carinatus occurs in western Asia, as far north as the Aral Sea, and throughout the Indian subcon­ tinent, including Sri Lanka, as far as the border of West Bengal. It is prodigiously common in some areas of India and Pakistan (e.g., in Sind and Jammu), where it is the major cause of snake­ bite morbidity and mortality.20,111,265 In northern India ( Jammu) and in western India (Rajasthan), envenoming by E. carinatus sochureki caused symptoms similar to those observed in Nigeria (see Figures 55-50, F, 55-52, B and F, and 55-88, D to G).20,111

Envenoming by Western and Eastern Russell’s Vipers (Daboia russelii and D. siamensis) (See Figure 55-13).*  These medically important species occur from Pakistan in the west through India and Sri Lanka, north into Nepal21 and Bhutan (D. russelii), and as far east as West Bengal; and in Southeast Asia, southern China, Taiwan, and in parts of Indonesia19 (D. siamensis) (Figure 55-95, online). Throughout this range, there are intriguing geographic variations in the clinical mani­ festations of envenoming that reflect differences in venom composition.56,162,231,243,244 Sri Lanka.  D. russelii (see Figure 55-13, A) is a major cause of venomous snakebites. Of patients bitten by this species, 28% showed no clinical evidence of envenoming.8,11,159 Apart from typical features of viperine envenoming (local envenoming, coag­ ulopathy, bleeding, and sometimes shock [see Figures 55-50, B to F, and 55-51]), there were distinctive features of neuromyo­ toxicity attributable to venom PLA2: ptosis (77%), external

*References 250, 262.

*References 244, 262.

bleeding, and coagulopathy have been observed in some cases. Recently, disseminated intravascular coagulation, microangio­ pathic hemolysis, and acute tubular necrosis were described in two proven cases of envenoming by C. cerastes (see Figure 55-56).186

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FIGURE 55-89  African puff adder (Bitis arietans). A, Specimen from Saudi Arabia. B, Dorsal view of head showing large nostrils. C, Showing fangs. (Copyright D.A. Warrell.)

ophthalmoplegia (82%) (Figure 55-96, A), inability to open the mouth (23%) or to swallow and protrude the tongue, generalized muscle tenderness (32%), and myoglobinuria (27%) (Figure 55-96, B). Most patients showed evidence of intravascular hemo­ lysis. Acute renal failure was a common feature of severe enven­ oming. Single or multiple medium-to-large cerebral arterial thromboses have been described,71 as well as the more familiar hemorrhagic strokes. Similar findings have been reported from envenoming by D. siamensis in Tawain.95 A single case of hypo­ pituitarism has been detected.6 India.  In most parts of the country, D. russelii is an important cause of snakebite, but in Jammu in the northeast, only 4 of 310 identified viperine bites were caused by this species.20 In Kerala, South India, neurotoxic signs, such as ptosis and ophthalmople­ gia, associated with hemostatic disorders, are familiar signs of envenoming by this species, and bilateral parotid enlargement is also described.54 Features of panhypopituitarism, manifesting between 1 month and 1 year after the bite, were observed in 7 of 1000 cases of snakebite, and there was 1 case of diabetes insipidus. Especially in the south, Russell’s viper bite is the most common cause of acute kidney injury in both adults and children. Burma.  Russell’s viper (D. siamensis) is the most important cause of snakebite morbidity and mortality. However, about onethird of all patients hospitalized after proved Russell’s viper bites

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B FIGURE 55-90  Envenoming by puff adder (Bitis arietans). A, Swelling and blistering of bitten limb. B, Necrosis in neglected case (KwaZulu Natal, South Africa). (A copyright D.A. Warrell; B courtesy Paul Rollinson.)

develop no clinical evidence of envenoming at any stage. In Tharrawaddy, north of Rangoon, two distinct populations of Rus­ sell’s vipers were found to be responsible for bites during the November to January rice harvest. Smaller snakes (125 to 375 mm [4.9 to 14.8 inches] in total length) had probably been born that year, whereas the larger snakes (500 to 1125 mm [19.7 to 44.3 inches] in total length) had been born in previous years.233 Bites by larger snakes were associated with more intense local swelling (Figure 55-96, C) and a higher risk for systemic envenoming.233 Severe systemic envenoming can result, despite there being little or no local evidence of envenoming. Spontaneous bleeding (gums, epistaxis, hemoptysis, hematemesis, hematuria) develops within a few hours and may result in fatal cerebral hemorrhage (see Figure 55-52, D). A sign, apparently unique to Russell’s viper bite in Burma, is orbital and conjunctival edema with conjunctival hemorrhages (Figure 55-96, D and E), which develops in severe cases and is evidence of generalized increase in capillary perme­ ability. Other manifestations of this permeability syndrome are facial edema, pleural effusions, ascites, pulmonary edema (Figure 55-96, F), and transient proteinuria with hypoalbuminemia.219 Other clinical features include hypotension and shock (see Figure 55-51, A and C), epigastric and chest pain, and development of acute renal failure within 3 to 4 days of the bite (see Figure 55-55, A and B). This is associated with bilateral loin tenderness and hypertension. In some cases, spontaneous diuresis began within 7 to 10 days, followed by complete recovery without residual renal abnormalities. Some patients developed a late hemorrhagic syndrome with recurrent shock and at autopsy were found to have hemorrhagic infarction of the anterior pituitary (Figure 55-96, G), and in some cases adrenal glands, intracranial hemor­ rhage, and swollen hemorrhagic kidneys.6,234 Renal angle tender­ ness predicted the development of oliguria (sensitivity 0.7, specificity 0.9).219,224 Russell’s viper venom contains a number of different components that affect hemostasis, including procoagu­ lants (activating factors X, IX, and V, and protein C), fibrinolytic agents, platelet aggregating and inhibiting factors, an anticoagu­ lant, and a hemorrhagin.97 In human patients, the most striking laboratory features are depletion of fibrinogen, factors V, X, and XIIIa, antithrombin III, plasminogen, antiplasmin, protein C, and platelets. There are high levels of fibrin/fibrinogen-related antigen, mostly cross-linked in the form of D-dimer.210,211 At autopsy, there is widespread evidence of bleeding but also fibrin deposition, occluding small blood vessels in the pituitary, lungs (Figure 55-96, H), and kidneys.209 Some patients who survived the acute pituitary adrenal crisis described presented later with more insidious symptoms of panhypopituitarism, including loss of libido, impotence, loss of secondary sexual hair, hypotension, amenorrhea, and features of hypothyroidism (Figure 55-96, I).234 Thailand.  Russell’s viper bites are common in the central rice-growing area of Thailand, but although the snake is appar­ ently the same species (D. siamensis) as in adjacent Burma, clinical features are generally less severe, although there have been deaths attributed to shock, cerebral hemorrhage, and acute kidney injury.125 1081

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FIGURE 55-91  Giant rain forest vipers or adders. A, Eastern Gaboon/Gabon viper (Bitis gabonica) (South Africa). B and C, Western rhinoceros viper (Bitis rhinoceros) (Ghana). D to F, Rhinoceros-horned viper or river jack showing nasal horns (B. nasicornis) (Cameroon). (Copyright D.A. Warrell.)

pain, shock, acute renal failure, bleeding gums, and ecchymoses. Neurotoxic features are confined to ptosis and external ophthal­ moplegia, which can develop between 1 and 48 hours after the bite. In the oriental region of China, north of latitude 25 degrees north, the Chinese mamushi (G. brevicaudus) is the most common cause of snakebite. There is local swelling, together with neuro­ toxic symptoms, such as blurring of vision, ptosis, and diplopia within 24 hours of the bite. Breathlessness, dysphagia, and dif­ ficulty opening the mouth are associated with symptoms suggest­ ing generalized rhabdomyolysis. Some patients require assisted ventilation.

ENVENOMING BY PIT VIPERS (CROTALINAE)* Envenoming by Japanese and Chinese Mamushis (Gloydius [Agkistrodon] blomhoffii, G. brevicaudus, and others) (Figure 55-97) In Japan, bites by the Japanese mamushi (G. blomhoffii) are mainly inflicted on the hands. There is local swelling with blister­ ing, nausea, vomiting, fever, headache, abdominal and lumbar *References 249, 256.

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FIGURE 55-92  A and B, Envenoming by Gaboon viper (Bitis gabonica) showing pulmonary edema, swelling, and bruising after a bite on the wrist. (From McNally T, Conway GS, Jackson L, et al: Accidental envenoming by a Gaboon viper (Bitis gabonica): The haemostatic disturbances observed and investigation of in vitro haemostatic properties of whole venom, Trans Roy Soc Trop Med Hyg 87:66, 1993; copyright D.A. Warrell).

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D

FIGURE 55-93  African bush vipers. A, Usambara bush viper (Atheris ceratophora) (Tanzania). B, Mt Kenya bush viper (A. desaixi) (Kenya). C, Rough-scaled bush viper (A. hispida) (Kakamega, Kenya). D, A. squamigera. E, Swamp adder (Proatheris superciliaris) (Malawi). (Copyright D.A. Warrell.)

Envenoming by the Malayan Pit Viper (Calloselasma rhodostoma) (Figure 55-98)*

55-52, B and D). Most patients have profound thrombocytopenia, probably resulting from sequestration. Fatal cases in Thailand were attributed to cerebral hemorrhage, shock, tetanus, septice­ mia, and anaphylaxis.125

This species is an important cause of snakebite in northwestern Malaysia, Thailand, Laos, Cambodia, Vietnam, and Java (see Figure 55-98, A). It inhabits coffee and rubber plantations and rice fields in areas of cleared jungle. Bites are a major occupa­ tional hazard of plantation workers (see Figure 55-47, C). About one-half the patients develop minimal or no envenoming, but in the remainder, local swelling starts within minutes and reaches its maximum after 24 to 72 hours (see Figure 55-50, B to D). Local necrosis develops in 11% of victims and is always preceded by blistering (Figure 55-99, A to C). Secondary infection by bac­ teria peculiar to the venom and oral cavity of the snakes is common, and fatal tetanus may ensue (Figure 55-99, E).215 The blood becomes incoagulable as early as 30 minutes after the bite and, in untreated patients, may persist for 1 to 26 days.173 There is associated bleeding from sites of trauma (see Figure 55-49), gums, ecchymoses, and elsewhere (see Figures 55-50, D and

Envenoming by Asian Arboreal Pit Vipers (Genera Trimeresurus, Cryptelytrops [Trimeresurus], Viridovipera, Protobothrops [Trimeresurus], and others) (See Figures 55-39 and 55-40)* In Thailand, the white-lipped green pit viper (C. albolabris) is the most widely distributed venomous snake and the second most common cause of snakebite (27% of cases).239 Pain and swelling develop early after the bite, spreading to involve more than one-half the bitten limb in 46% of cases. Local bruising and tender enlargement of local lymph nodes are common, whereas local blistering and necrosis are rare (Figure 55-100, A to C ). Coagulopathy, thrombocytopenia, and leukocytosis may develop. In Burma, C. erythrurus bites resulted in no evidence of envenoming in 65% of cases. In the rest, there

*References 173, 175, 272.

*References 96, 250, 271.

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FIGURE 55-94  A and B, Sahara horned viper (Cerastes cerastes) (Algeria) showing supraocular horns. (Copyright D.A. Warrell.)

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

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G

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I

FIGURE 55-96  Envenoming by Russell’s vipers in Sri Lanka (Daboia russelii)—A, Neurotoxicity. B, Myotoxicity. In Burma (Daboia siamensis). C, Local swelling, blistering, and necrosis. D and E, Chemosis and subconjunctival hemorrhage. F, Pulmonary edema. G, Hemorrhagic infarction of anterior pituitary. H, Fibrin deposition in pulmonary blood vessels. I, Chronic pan-hypopituitarism showing loss of secondary sexual hair and testicular atrophy. (A to G and I copyright D.A. Warrell; H courtesy Nicholas Francis.)

FIGURE 55-97  Chinese (short-tailed) mamushi (Gloydius brevicaudus) (Beijing). (Copyright D.A. Warrell.)

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was local swelling without necrosis, incoagulable blood, and thrombocytopenia. In Bangladesh, most victims of bites by this species show no coagulopathy and recover without antivenom treatment. Although the Indian bamboo viper (T. gramineus) is the most abundant pit viper in the southern half of India, there is little reliable information about the effects of envenom­ ing. In south India, the Malabar pit viper (T. malabaricus) is said to commonly cause local necrosis.96 In Thailand, the dark green pit viper (Cryptelytrops [Trimeresurus] macrops) is a common cause of mild envenoming in some areas, notably in gardens in central Bangkok, whereas the Kanchanaburi pit viper (Cryptelytrops [Trimeresurus] kanburiensis) is capable of causing severe envenoming (Figure 55-100, D).271 The Chinese habu (P. mucrosquamatus) causes about one-third of venom­ ous snakebites in Taiwan and results in an 8% case fatality rate, whereas the Chinese green pit viper (V. stejnegeri), although responsible for 53% of bites in Taiwan, carries a case fatality rate of only 1%. Bites by P. mucrosquamatus are more likely to cause local necrosis and rhabdomyolysis.36

Probable distribution range Localities from which specimens have been collected

Burma (Myanmar)

Laos

Thailand Vietnam

?

Cambodia

Brunei Sabah

West Malaysia

B

Sarawak Kalimantan Sumatra

A

Karimunjawa Archipelago Kangean Islands Java

D

C

FIGURE 55-98  Malayan pit viper (Calloselasma rhodostoma). A, Distribution. B to D, specimens from Thailand showing dorsal pattern and fangs (A courtesy Jenny Daltry; B to D copyright D.A. Warrell.)

Envenoming by Latin American Pit Vipers (Genera Bothrops, Bothriopsis, Crotalus, Lachesis)* Agkistrodon, Bothrops (Bothriopsis), and Others (Figure 55-101; See Figures 55-7, 55-22, E, and 55-34, A).  Local envenom­ ing may appear within 15 minutes but rarely may be delayed for *Reference 256.

A

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E

several hours. Swelling spreads rapidly, sometimes to involve the entire bitten limb and adjacent areas of the trunk (Figure 55-50, E). There are associated pain, tenderness, and enlargement of regional lymph nodes. Bruising may extend up the bitten limb, especially in lines along the path of superficial lymphatics and over regional lymph nodes. There may be persistent bleeding from the fang marks if the blood is incoagulable. Blistering may appear at the site of the bite within the first 12 hours, and necro­ sis of skin, subcutaneous tissue, and muscle develops in up to

C

FIGURE 55-99  Envenoming by Malayan pit viper (Calloselasma rhodostoma). A, Severe blistering and bruising. B, Diffuse ecchymoses, shock, and gangrene of the bitten arm 4 days after the bite, when the patient was finally brought to the hospital. C, Gangrene. D, Bleeding gums. E, Tetanus complicating snakebite wound infection. (Copyright D.A. Warrell.)

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China

PART 6  ANIMALS, INSECTS, AND ZOONOSES

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FIGURE 55-100  Envenoming by arboreal green pit vipers (genus Cryptelytrops [Trimeresurus]): bites by white-lipped green pit viper (C. albolabris). A and B, Swelling of bitten arm and the snake responsible (Thailand). C, Local necrosis (Vietnam). D, Local swelling after a bite by a Kanchanaburi pit viper (C. kanburiensis) (Thailand). (Copyright D.A. Warrell.)

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FIGURE 55-101  Latin American pit vipers. A, Cantil (Agkistrodon bilineatus) (Mexico). B, Central American jumping viper (Atropoides mexicanus) (Guatemala). C, Small-eyed toad-headed pit viper (Bothrocophias microphthalmus) (Garagoa, Boyaca, Colombia). D, Terciopelo (Bothrops asper) (Caucasia, Colombia). E, Common lancehead (Bothrops atrox) (Para, Brazil). F, Papagaio (Bothrops bilineatus smaragdinus/Bothriopsis bilineata smaragdina) (Napo, Ecuador).G, Jararaca (Bothrops jararaca). H, Jararacuçu (Bothrops jararacussu) (Brazil). I, Serpent of St. Lucia (B. caribbaeus). (Copyright D.A. Warrell.)

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epistaxis, hematemesis, hematuria, intracranial (Figure 55-102, J) and subconjunctival hemorrhages and bleeding into the gastro­ intestinal and genitourinary tracts. Women may develop menor­ rhagia and pregnant women antepartum or postpartum may develop hemorrhages with hemorrhagic abortion of the fetus. Severe headache and meningism suggest subarachnoid hemor­ rhage, whereas hemiplegia and other lateralizing neurologic signs, irritability, loss of consciousness, and convulsions suggest intracranial hemorrhage or cerebral thrombosis. Abdominal

C

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J

FIGURE 55-102  Envenoming by South American lanceheads (genus Bothrops). A, Swelling and bruising after bite on hand by papagaio (B. bilineatus smaragdinus) (Largo Agrio, Ecuador). B, Local blistering after bite by jararaca (B. jararaca) (São Paulo, Brazil). C, Severe blistering after bite by common lancehead (B. atrox) (Pucallpa, Peru). D, Blistering and necrosis after bite by B. atrox (Pucallpa, Peru). E, Liquefaction-necrosis of anterior tibial compartment after bite by B. marajoensis (Marajo, Brazil). F, Gangrene after bite by terciopelo (B. asper) (Pedro Vicente Maldonado, Ecuador). G, Abscess developing 5 days after bite by B. atrox (Pastaza, Ecuador). H, Bleeding gums after bite by B. jararaca (São Paulo, Brazil). I, Spitting out blood in sputum after B. atrox bite (Pastaza, Ecuador). J, Cerebral hemorrhage after bite by B. atrox (Pastaza, Ecuador). (A to E and G to J copyright D.A. Warrell; F courtesy David Gaus.)

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10% of hospitalized cases (Figure 55-102, A to F). Bites on the digits (fingers and toes) and in areas draining into the tight fascial compartments, such as the anterior tibial compartment, are par­ ticularly likely to cause necrosis. Absence of detectable local swelling 2 hours after a viper bite usually means that no venom has been injected. Secondary bacterial infections may manifest as subcutaneous abscesses or more diffuse cellulitis (Figure 55-102, G). Spontaneous systemic hemorrhage occurs from the gingival sulci (see Figures 55-52, A and 55-102, H and I) as

PART 6  ANIMALS, INSECTS, AND ZOONOSES

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FIGURE 55-103  Latin American rattlesnakes (genus Crotalus). Tropical rattlesnakes (Brazil). A, C. durissus cascavella. B, C. durissus collilineatus. C, C. durissus ruruima. D, Central American rattlesnake (C. simus) (Guerrero, Mexico). (Copyright D.A. Warrell.)

distention, tenderness, and peritonism with signs of hemorrhagic shock but no external blood loss suggest retroperitoneal or intra­ peritoneal hemorrhage. Hypotension and circulatory shock causing loss of vision and then consciousness may occur a short time after the bite. Acute kidney injury can complicate cases of severe envenoming (see Figure 55-55, C). Thromboses of smallto medium-sized cerebral, pulmonary, coronary, or mesenteric arteries are features of envenoming by the fer de lance of Marti­ nique (B. lanceolatus) and the serpent of St Lucia (B. caribbaeus) (see Figure 55-101, I).80,131,220 Cerebral thrombosis has also been described in patients envenomed by Daboia russelii in Sri Lanka, D. siamensis in Taiwan, Bitis arietans in South Africa, and some species of North American rattlesnakes (e.g., Crotalus oreganus helleri). The terciopelo (B. asper) and common lancehead (B. atrox) are responsible for many cases of severe envenoming in Central and South America, resulting in death or permanent disability.155 The larger, B. asper (exceptionally up to 2.5 m (8.2 feet) in total length), seems even more inclined than B. atrox to strike if cor­ nered, molested, or inadvertently trodden upon or touched. Its habit of raising its head high off the ground can result in bites above knee level. The jararaca (B. jararaca) is an important cause of envenoming in southeastern Brazil and in adjacent northeastern Paraguay and northern Argentina. Clinical effects are generally less severe than with B. asper and B. atrox enven­ oming, but coagulopathy, bleeding, and local necrosis are common.31,181,256 The jararacuçu (B. jararacussu) is a bulky snake with a high yield of unusually potent venom. It has a formidable reputation for causing severe bleeding, fibrin deposition, local necrosis, shock, and acute kidney injury that often prove fatal.143 Crotalus (Figure 55-103; See Figure 55-16).  The two species of Latin American (tropical) rattlesnake, Crotalus simus in Central America and C. durissus in South America, pose a serious medical problem in many parts of their ranges. Severe systemic envenom­ ing by the tropical rattlesnake (C. durissus terrificus) may occur in the absence of local signs. Neurotoxic envenoming develops only in victims of populations of some subspecies of C. durissus, such as C. d. terrificus, C. d. collilineatus, and C.d. cascavella. 1088

Typical elapid-type descending paralysis (Figure 55-104, A; see Figure 55-53, E) may result in life-threatening respiratory paraly­ sis. Venom myotoxins cause myoglobinemia and myoglobinuria (see Figure 55-54, A), which may result in acute kidney injury.15,16 Other life-threatening clinical effects include coagulopathy and spontaneous systemic hemorrhage,180,256 hypotension, and shock. Local envenoming, however, is usually trivial, restricted to pain, mild swelling, and erythema (Figure 55-104, B and C). In contrast, envenoming by C. simus in Central America produces clinical effects more reminiscent of rattlesnake bites in North America: severe local envenoming with massive swelling, blistering, and necrosis. Systemic envenoming involves some hemostatic disor­ ders such as hypofibrinogenemia, but spontaneous systemic bleeding is unusual, acute kidney injury has rarely been reported, and neurotoxicity is controversial. Lachesis (See Figure 55-36).  Bushmasters may reach a length of nearly 4 m (13.1 feet) and are the longest venomous snakes in the western hemisphere. Envenoming by all four species may cause local swelling, blistering, bruising, and necrosis with coag­ ulopathy, spontaneous systemic bleeding, shock, and acute kidney injury reminiscent of other pit vipers. However, a distinc­ tive syndrome has been described in a proportion of cases. Within 10 to 15 minutes of the bite, there are nausea, abdominal colic, repeated bilious vomiting, watery diarrhea with profuse sweating, hypersalivation and other features of autonomic hyper­ activity, bradycardia, visual disturbances, profound shock, and syncope. Local effects of envenoming may leave permanent impairment.100

RISK FOR ENVENOMING Even when the fangs of a venomous snake have pierced the skin, envenoming is not inevitable. About 20% of patients bitten by Calloselasma rhodostoma and Daboia russelii show absolutely no evidence of envenoming, and as many as 80% of those bitten by sea snakes and Australasian eastern brown snakes (Pseudonaja textilis) and 50% by C. rhodostoma or Russell’s vipers, have trivial or no envenoming. These are the so-called dry bites.

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FIGURE 55-104  Envenoming by tropical rattlesnakes (Crotalus durissus) in Brazil. A, Neurotoxicity (C. durissus marajoensis) (Marajo, Brazil). B and C, Evolution of local swelling and demarcated erythema after bite by C. durissus terrificus (São Paulo, Brazil). (A courtesy Pedro Pardal; B and C copyright D.A. Warrell.)

RISK FOR DEATH Untreated snakebite mortality is hard to assess, because hospital admissions include a disproportionate number of severe cases, and data for untreated snakebites are available only from the preantivenom era or from occasions when antivenom supply is limited, an antivenom of low potency is used,265 or when anti­ venom is withheld by doctors who doubt its efficacy. The mortal­ ity rate of E. ocellatus bites has been reduced from about 20% to 3% with antivenom.265,267 In Brazil, untreated and treated case fatalities for Bothrops and Crotalus durissus terrificus envenom­ ing were estimated as 8% and 0.7% and 72% and 12%, respec­ tively.176 In Australia, case fatality before development of antivenom was 50% for Acanthophis, 45% for Notechis, and 19% for Pseudonaja.221 Prognosis appears to be the worst in infants and in older adults, but there is no convincing evidence that older children have a worse prognosis than do young adults, despite the larger dose of venom they may receive relative to their body weight.

INTERVAL BETWEEN BITE AND DEATH Death after snakebite may occur as rapidly as within a few minutes (reputedly after a bite by the king cobra, O. hannah) or as long as 41 days after a bite by the saw-scaled or carpet viper (E. carinatus). However, the speed of killing has been exaggerated. Most elapid deaths occur within hours of the bite, most sea-snake bite deaths between 12 and 24 hours, and viper bite deaths within days.

RATE OF EVOLUTION AND RECOVERY OF ENVENOMING Local swelling is usually evident within 2 to 4 hours of bites by vipers and cytotoxic cobras. Swelling is maximal and most exten­ sive on the second or third day after the bite. Resolution of swelling and restoration of normal function in the bitten limb may be delayed for months, especially in older people (e.g., after bites by the European adder V. berus). The earliest systemic symptoms, such as vomiting and syncope, may develop within minutes of the bite, but even in the case of rapidly absorbed elapid venoms, patients rarely die less than an hour after the bite. Defibrination may be complete within 1 to 2 hours of the

bite (e.g., saw-scaled or carpet viper E. ocellatus).242,267 Neuro­ toxic signs may progress to generalized flaccid paralysis and respiratory arrest within a few hours. If the venom is not neutral­ ized by antivenom, these effects may be prolonged. Defibrination can persist for weeks (Echis spp. and C. rhodostoma).173,242,267 Patients with neurotoxic envenoming have recovered after being artificially ventilated for up to 10 weeks. Tissue necrosis usually declares itself within a week of the bite. Sloughing of necrotic tissue and secondary infections including osteomyelitis may occur during subsequent weeks or months. Deaths occurring from neurotoxic envenoming are caused by airway obstruction or respiratory paralysis, whereas later deaths may result from technical complications of mechanical ventilation or intractable hypotension. Late deaths, more than 5 days after the bite, are usually the result of acute kidney injury. Delayed shock with recurrent spontaneous hemorrhage has been described in victims of Burmese Russell’s viper; pituitary and other intracranial hemor­ rhages have been found at autopsy.

CHRONIC SEQUELAE OF SNAKEBITE Tissue loss, amputations, contractures, arthrodeses, hypertrophic and keloid scars, tendon damage, and complications of surgery are the most common causes of persistent morbidity in survivors of snakebites (Figure 55-105, A). Chronic ulcers, pyogenic arthri­ tis, and osteomyelitis are described. Malignant transformation (Marjolin’s ulcer) has been seen in patients with chronic ulcer­ ation after bites by N. nigricollis269 and C. rhodostoma (Figure 55-105, B).90,272 Chronic renal failure (bilateral cortical necrosis) and panhypopituitarism (from Sheehan’s-like syndrome) are reported complications of Russell’s viper bites.6,234,244 An unknown number of patients who develop acute bilateral renal cortical necrosis after viper bite envenoming, even by small species such as Hypnale hypnale, may be left with chronic renal failure.12 Cerebral hemorrhage complicating viperid, colubrid, and Austral­ asian elapid bites may result in chronic neurologic deficits, and it is possible that survivors of severe presynaptic neurotoxicity (e.g., from krait and Australasian elapid envenoming) may be susceptible to a late poliomyelitis-like syndrome. Apart from these purely objective abnormalities, snakebite victims may com­ plain of chronic or recurrent symptoms in the bitten limb and attribute a wide variety of physical and mental problems to that unforgettable, dramatic, and traumatic event of their snakebite. 1089

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

muscle-derived enzymes, myoglobin, and potassium concentra­ tions. Plasma is stained brownish by myoglobin and pink by hemoglobin. Heparinized blood should be allowed to sediment spontaneously (without centrifugation) to reveal these pigments. Evidence of Intravascular Hemolysis Patients with intravascular hemolysis have black urine (as in malarial “blackwater fever”). It is brownish, pinkish, or reddish in patients with hematuria or myoglobinuria.

A

B FIGURE 55-105  Permanent sequelae of snakebite. A, Hypertrophic scar with contractures and arthrodeses at site of spitting cobra bite (Naja nigricollis, Nigeria). B, Marjolin’s ulcer—malignant transformation to squamous cell carcinoma at site of chronic osteomyelitis following bite by Calloselasma rhodostoma in Thailand. (Copyright D.A. Warrell.)

Laboratory Investigations HEMATOLOGY Systemic envenoming is usually associated with a neutrophil leukocytosis: counts above 20 × 109/L indicate severe envenom­ ing. Initially, hematocrit may be high from hemoconcentration when there is generalized increase in capillary permeability (e.g., Burmese D. siamensis). Later, hematocrit falls because of bleeding into the bitten limb and elsewhere, and from intravas­ cular hemolysis or microangiopathic hemolysis in patients with disseminated intravascular coagulation. Thrombocytopenia is common (e.g., D. russelii, C. rhodostoma, B. arietans).

EVIDENCE OF RENAL DYSFUNCTION AND ACID-BASE IMBALANCE Blood urea or serum creatinine and potassium concentrations should be measured in patients who become oliguric, especially in cases with a high risk for renal failure (e.g., D. russelii, ter­ restrial Australasian snakes, sea snakes, and Colubridae). All snake-bitten patients should be encouraged to empty their bladder on admission. Urine should be examined for blood/ hemoglobin and protein (by dipstick test) and for microscopic hematuria and red cell casts. Severely sick, hypotensive, and shocked patients will develop lactic acidosis (suggested by an increased anion gap). Those with renal failure will also develop metabolic acidosis (decreased plasma pH and bicarbonate con­ centration, reduced arterial PCO2), and patients with respiratory paralysis will develop respiratory acidosis (low pH, high arterial PCO2, decreased PO2), or respiratory alkalosis if they are mechani­ cally overventilated.

ELECTROCARDIOGRAPHIC ABNORMALITIES (See Figures 55-51, B and C and 55-66, D)* ECG abnormalities include sinus bradycardia, ST-T wave changes, varying degrees of atrioventricular block, and evidence of hyper­ kalemia. Shock may induce myocardial ischemia or infarction in patients with diseased coronary arteries.

CHEST RADIOGRAPHY (See Figures 55-86, E and 55-96, F ) Chest radiography is useful for detecting pulmonary edema (e.g., European Vipera and D. russelii/D. siamensis), pulmonary hemorrhages and infarcts, pleural effusions, and secondary bronchopneumonia. *References 119, 120, 171, 242, 254, 257, 267.

Twenty-Minute Whole Blood Clotting Test* Incoagulable blood is a cardinal sign of systemic envenoming by most of the Viperidae, many of the Australasian elapids, and the medically important Colubridae. For clinical purposes, a simple, bedside, all-or-nothing test of blood coagulability is adequate. A few milliliters of blood taken by venipuncture are placed in a new, clean, dry, glass vessel; left undisturbed at room tempera­ ture for 20 minutes; then tipped once to see if there is clotting (Figure 55-106).

OTHER TESTS OF HEMOSTASIS More sensitive laboratory tests that are rapid and relatively simple to perform are whole blood or plasma prothrombin times and detection of elevated concentrations of FDP by agglutination of sensitized latex particles or of D-dimer. Serum concentrations of creatine kinase, aspartate transferase, and blood urea are com­ monly elevated in patients with severe envenoming, because of local muscle damage at the site of the bite. Evidence of Muscle Damage Generalized rhabdomyolysis caused by sea snake, Australasian elapid, tropical rattlesnake, and Sri Lankan Russell’s viper bites causes a steep rise in serum creatine kinase and other *References 179, 267.

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FIGURE 55-106  Twenty-minute whole blood clotting test. Blood taken by venipuncture from a patient bitten by Papuan taipan (Oxyuranus scutellatus), placed in a new, clean, dry glass tube and left for 20 minutes undisturbed has failed to clot, indicating consumption coagulopathy or presence of venom anticoagulants. (Copyright D.A. Warrell.)

Detection of venom antigens in body fluids of snakebite victims using enzyme immunoassays has proved a valuable research tool for confirming the species responsible for envenoming (immu­ nodiagnosis), as a prognostic index of the severity of envenom­ ing, and to assess efficacy of antivenom treatment*. Venom gland mRNA has been detected in stored venom samples using reverse transcription–polymerase chain reaction (RT-PCR).35 Of the various techniques used, enzyme immunoassay has proved the most rapid, sensitive, and specific. However, commercial venom detection kits for clinical diagnosis are available only in Australia (Venom Detection Kit).206 They are highly sensitive, but specific­ ity may be inadequate to distinguish between envenoming by different species in the same genus or in closely related genera.206,229 Envenomed patients develop persisting levels of antibodies to venom antigens, including individual toxins190 detectable by enzyme immunoassay, but they have proved insuf­ ficiently specific to allow reliable retrospective diagnosis.90,240

Management of Snakebite† FIRST-AID TREATMENT‡ Principles of First Aid • Reassure the victim, who is often terrified. • Do not tamper with the bite wound in any way, but immo­ bilize the bitten limb using a splint or sling. If the patient is thought to have been bitten by a dangerously neurotoxic elapid snake (including sea snakes), consider pressureimmobilization (see later text). • Take the patient as quickly as possible to the nearest medical care facility. The entire patient should be immobi­ lized, especially the bitten limb, because any muscle con­ tractions will promote spread of venom. Ideally the patient should be transported by motor vehicle, bicycle (as a pas­ senger), boat, or on a stretcher. • Avoid harmful and time-wasting treatments (see later text). • Because species diagnosis is critically important, the snake should be taken along to the hospital if it has already been killed. However, if the snake is still at large, do not risk further bites and waste time by searching for it. Even snakes that appear to be dead should not be touched with bare hands, but carried in a bag or dangling across a stick. Some species (e.g., Hemachatus haemachatus) sham death, and even a severed head can inject venom!

PRESSURE IMMOBILIZATION AND PRESSURE-PAD The splinting and pressure bandaging method (illustrated in Chapter 54) developed and advocated by Struan Sutherland in Australia proved effective in limiting the absorption of Australian elapid toxins in restrained monkeys.205 Although never subjected to formal clinical trials, the method has proved successful and safe, as judged by some anecdotal reports of delayed systemic enven­ oming and rapid deterioration after release of the bandage, in some cases supported by measurements of venom antigenemia. However, there have been practical difficulties in implementing this discovery, and, even in Australia, only 18% to 53% of the bandages in place when patients arrived in the hospital had been correctly and effectively applied. The method is still regarded by some experienced physicians as of unproved benefit.37 Bandaging aims to exert a pressure of about 55 mm Hg (1.06 psi), that of a venous tourniquet. In practice, it is difficult to judge how tightly the bandage should be applied and difficult for the patient to put it on unaided,258 explaining why so many are incorrectly applied.37 A recent study found that the technique was difficult to teach and that elasticized bandages were superior to traditional crepe ban­ dages.264 External compression increases intracompartmental pres­ sure and may accentuate the effects of some necrotic snake *References 76, 90, 91, 152, 195, 213, 214, 235. † References 29, 123, 140, 206, 226, 255, 263, 264, 285. ‡ References 37, 245, 246, 258, 264.

venoms, but animal studies found little evidence that this was deleterious and reinforced the lifesaving effects of lymphatic/ venous compression.25,139 However, if a patient is bitten by a dan­ gerously neurotoxic elapid (such as a mamba, king cobra, or taipan) or by a sea snake, there is a risk that respiratory paralysis might develop en route to the hospital. In these cases, it is recom­ mended that an elastic bandage and splint be applied firmly, but not so tightly as to obliterate the peripheral arterial pulse. Lym­ phoscintigraphy studies in simulated envenoming showed that excessive pressure (>70 mm Hg [1.35 psi]) and movement of the other limbs increased lymphatic flow.93 The patient should lie down and remain as immobile as possible during the journey to hospital. A recent study of lymaphatic flow in human volunteers and in rats showed that nitric oxide (NO) donating drugs, such as glyceryl trinitrate, applied topically to the bitten limb, slowed lymphatic flow substantially, presumably by inhibiting the intrinsic lymphatic pump, despite movement of the limb. In rats challenged with Eastern brown snake venom, death was delayed. It is sug­ gested that topical application of NO donating drugs might prove to be a useful adjunct to pressure-immobilisation and pressure-pad (see below) first-aid methods.182 Monash Pressure-Pad Method An alternative, simpler method of local compression was devel­ oped by Anker and colleagues5 and tested in Burmese Russell’s viper bite cases by Tun-Pe and colleagues in Burma.232 Applica­ tion of a foam rubber pad directly over the bite wound, at a pressure of about 70 mm Hg, delayed systemic envenoming, as assessed by measurements of venom antigenemia, and the method appeared safe and effective in a preliminary field trial.232

REJECTED OR CONTROVERSIAL FIRST-AID METHODS* Traditional treatments are widely preferred by inhabitants of rural parts of the developing world.150 However, even in the West, tourniquets, constriction bands, wound cauterization, incision or excision, amputation of the bitten digit, suction by mouth, vacuum pumps26 or “venom-ex” apparatus, instillation of chemi­ cal compounds such as potassium permanganate, application of ice packs (cryotherapy), “snake stones,” electric shocks, and many other outlandish first-aid treatments have been advocated. These are absolutely contraindicated in that they are harmful and have no proved benefit.83,246 Incisions can provoke uncontrolled bleeding when the blood is incoagulable; may damage nerves, blood vessels, or tendons; and introduce infection.20 Suction, chemicals, and cryotherapy can cause tissue necrosis. Snake stones do not remove venom from the wound and usually require an incision to make them adhere. This can result in persistent bleeding and infection.

DANGERS OF TIGHT TOURNIQUETS Tight (arterial) tourniquets have been responsible for terrible morbidity and even mortality in snakebite victims and should never be used. Dangers of tourniquets include ischemia and gangrene if they are applied for more than about 2 hours, damage to peripheral nerves (especially the lateral popliteal [common peroneal] nerve when a tourniquet presses against the neck of the fibula), increased fibrinolytic activity, congestion, swelling, increased bleeding, increased local effects of venom, and shock, rapid development of life-threatening systemic envenoming, or even pulmonary embolism after their release (see later text).245,246

TREATMENT OF EARLY SYMPTOMS BEFORE THE PATIENT REACHES THE HOSPITAL Distressing and dangerous manifestations of envenoming may appear before the patient reaches the hospital: • Local pain: This may be intense. Oral acetaminophen is preferable to aspirin or nonsteroidal antiinflammatory *References 246, 257.

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

IMMUNODIAGNOSIS

PART 6  ANIMALS, INSECTS, AND ZOONOSES

agents, which carry the risk for gastric bleeding in patients with incoagulable blood. Severe pain should be treated with opiates. • Vomiting: This is a common early symptom of systemic envenoming. Patients should be laid in the recovery posi­ tion (on their left side) with the head down to avoid aspira­ tion. Persistent vomiting can be treated with intravenous promethazine (12.5 to 25 mg in adults, 0.1 to 0.25 mg/kg in children older than 2 years of age). • Syncopal attacks and anaphylactic shock: Patients who collapse within minutes of the bite may show features of either a vasovagal attack with profound bradycardia or of anaphylaxis with angioedema, urticaria, asthma, abdominal colic, and diarrhea. Anaphylaxis should be treated with aqueous epinephrine 0.1% (1 : 1000) (0.3 to 0.5 mL in adults, 0.01 mL/kg in children) by intramuscular injection, followed by a histamine H1-blocker such as chlorphenira­ mine maleate (10 mg in adults, 0.2 mg/kg in children) given by intravenous or intramuscular injection. In patients with incoagulable blood, injections can cause hematomas. Pressure dressings should be applied to all injection sites to prevent oozing. • Respiratory distress: This may result from upper airway obstruction if the jaw, tongue, and bulbar muscles are para­ lyzed or from paralysis of the respiratory muscles. Patients should be placed in the recovery position, the airway cleared if possible using a suction pump, an oral airway inserted, and the jaw elevated. If the patient is cyanotic or respiratory movements are weak, oxygen should be given by any available means. If clearing the airway does not produce immediate relief, artificial ventilation must be initi­ ated. In the absence of any equipment, mouth-to-mouth or mouth-to-nose ventilation can be lifesaving. Manual ventila­ tion by bag-valve-mask device is rarely effective for a prolonged period of time. Ideally, a cuffed endotracheal tube should be introduced using a laryngoscope, or a cuffed tracheostomy tube inserted. The patient can then be ventilated by bag. If no femoral or carotid pulse can be felt, external cardiac massage should be instituted. Examination of Pregnant Women Potential complications of envenoming in pregnancy include antepartum and postpartum hemorrhage indicated by vaginal bleeding, premature labor, abortion/stillbirth, and fetal dis­ tress.81,82 If possible, uterine contractions and fetal heart rate should be monitored continuously. Fetal distress may be signaled by fetal bradycardia, tachycardia, or late deceleration after each uterine contraction. If there is vaginal bleeding or the likelihood of imminent surgery, correction of antihemostatic abnormalities after antivenom treatment should be accelerated using blood products. Lactating women should be encouraged to continue breastfeeding.

MEDICAL TREATMENT IN THE HOSPITAL Snakebite is a medical emergency. The history, symptoms, and signs must be assessed rapidly to direct urgent appropriate treat­ ment. Patients may arrive at the hospital soon, or in some cases many days, after being bitten. They may therefore show early or late signs of envenoming or its complications. It is essential that all patients with a history of snakebite be assessed rapidly; they may be moribund but still salvageable by appropriate resuscita­ tion. Cardiopulmonary resuscitation may be needed, including clearance of the airway, oxygen administration by face mask or nasal catheter, and establishment of intravenous access to allow treatment with drugs and intravenous fluids. Airway, respiratory movements (breathing), and arterial pulse (circulation) must be checked immediately. Vital signs must be recorded: blood pres­ sure, pulse rate, and respiratory rate.

NEEDS FOR RAPID ASSESSMENT AND RESUSCITATION Patients with severe envenoming may present with the following problems requiring urgent intervention: 1092

• Profound hypotension and shock, resulting from: • Direct cardiovascular effects of the venom (e.g., V. berus, D. russelii, D. siamensis, B. arietans, O. scutellatus). • Hypovolemia secondary to blood loss, persistent vomit­ ing, or other causes of dehydration. • Autopharmacologic effects of the venom (activation/ inhibition of physiologic vasomotor systems, such as the angiotensin-renin-bradykinin systems, by venom toxins). • Rarely, anaphylaxis provoked by antivenom given outside the hospital and, even more rarely, provoked by venom in habitual snake handlers who have been sen­ sitized by previous exposure. • Sudden deterioration after release of a tourniquet or com­ pression bandage, resulting in shock, bleeding, or respira­ tory paralysis.281,290 These bands, bandages, or ligatures are often removed too hastily by hospital staff before antive­ nom treatment has been initiated and appropriate staff and equipment are on hand in the event that resuscitation is needed. • Airway obstruction, resulting from aspirated vomitus, a foreign body, or the tongue blocking the upper airway, especially in patients with evolving bulbar paralysis who have not been transported to hospital in the left lateral (recovery) position. Vomiting can be the result of systemic envenoming or ingestion of emetic herbal remedies. • Terminal respiratory failure from progressive neurotoxic envenoming that has led to paralysis of respiratory muscles. • (Hours after the bite) Cardiac arrest resulting from hyper­ kalemia in patients with massive generalized skeletal muscle breakdown (rhabdomyolysis) after sea-snake bites. • (Days after the bite) Acute renal failure. • (Days after the bite) Septicemia complicating aspiration pneumonia (see earlier text) or infection of incisions made at the site of the bite.

CLINICAL ASSESSMENT Four important preliminary questions are as follows: 1. In which part of your body have you been bitten? 2. When and under what circumstances were you bitten? 3. Where is the snake that bit you? Did you bring it and, if not, what did it look like? 4. How are you feeling now? If the snake has been killed but not brought, someone should be dispatched to collect it. Alternatively, a high-quality digital photograph(s) may be obtained. Only if the snake can be identi­ fied confidently as nonvenomous can the bitten patient be dis­ charged after a booster dose of tetanus toxoid. Patients should be asked whether they have taken any drugs or alcohol, whether they have vomited, fainted, or have noticed any bleeding or other ill effects of the bite, and whether they have passed urine since being bitten. Physical signs should be assessed before any com­ pression bandage or tourniquet is removed. Fang marks are sometimes invisible and rarely help the diagnosis, although the discovery of only two or three discrete puncture marks suggests a bite by a venomous snake. Local swelling, tenderness, and lymph node involvement are early signs of envenoming. The gingival sulci are usually the earliest site of detectable spontane­ ous bleeding (see Figures 55-52, A, 55-75, C and D, 55-88, C, 55-99, D, and 55-102, H). Bleeding from venipuncture sites, recent wounds, and skin lesions suggests incoagulable blood. If the patient is in shock (collapsed, sweating, cool, cyanotic extremities, low blood pressure, tachycardia), the foot of the bed should be raised, and an intravenous infusion of a plasma expander, such as fresh frozen plasma, dextran, Haemaccel (3.5% colloidal solution), Gelofusine (succinated gelatin), or fresh blood started immediately. The central venous pressure should be observed. The earliest symptoms of neurotoxicity after elapid bites are often blurred vision, feeling of heaviness in the eyelids, and drowsiness. The earliest sign is contraction of the frontalis muscle (raised eyebrows and puckered forehead) even before true ptosis can be demonstrated. Signs of respiratory muscle paralysis (dyspnea, “paradoxical” abdominal respiration, and cya­ nosis) are ominous. Patients with generalized rhabdomyolysis may have trismus and muscles that are stiff, tender, and resistant

Early Clues That a Patient May Be Severely Envenomed • The snake is identified as a dangerously venomous species and was perhaps a large specimen. • Rapid early spread of local swelling from the site of the bite. • Enlarged, painful, and tender lymph nodes draining the site of the bite indicate early spread of large-molecular-weight venom components into the lymphatic system. • Early symptoms of systemic envenoming include collapse (hypotension, shock); nausea, vomiting, and diarrhea; severe headache; “heaviness” of the eyelids; pathologic drowsiness or early ptosis/ophthalmoplegia. • Early spontaneous systemic bleeding occurs, for example, from the gums or nose, or in vomitus, feces, or urine. • Urine is dark brown or black.

ANTIVENOM (ANTIVENOM, ANTIVENENE, ANTISNAKEBITE SERUM)* Antivenom is the concentrated whole gamma immunoglobulin (IgG) or enzyme-refined gamma IgG fragments (F[ab′]2 or Fab) of horses or sheep, which have been immunized with venom.77,154,218,289,292 It is the only specific treatment available and has proved effective against many of the lethal and damaging effects of venoms. In the management of snakebite, the most important clinical decision is whether or not to give antivenom, because only a minority of snake-bitten patients need it, it may produce severe reactions, and it is expensive and often in short supply. Clinical testing of the effectiveness and safety of antivenoms in human patients has been generally neglected in favor of inad­ equate testing in animals, usually mice. Recently, attempts have been made to encourage routine preclinical and phase I (equiva­ lent) and phase II/III clinical trials.†

neutrophil leukocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, hemoconcen­ tration, uremia, raised serum creatinine, oliguria, hypox­ emia, acidosis, and vomiting in the absence of a history of ingesting emetic agents • Severe local envenoming: local swelling that is spreading rapidly or that extends more than halfway up the bitten limb; extensive blistering or bruising, especially in patients bitten by species known to cause local necrosis (e.g., Viperidae, Asian cobras, African spitting cobras). Bites by these species inflicted on the digits carry a high risk for necrosis and warrant antivenom treatment. In Europe, to improve the rate of recovery after bites by V. berus, anti­ venom has been recommended in adults with swelling extending beyond the wrist or ankle within 2 hours of a bite.171,251,254,257 Special Indications for Antivenom in Specific Areas Europe (Adder—Vipera berus—and Other European Vipera).*  Zagreb antivenom, or Protherics ViperaTAb (Table 55-4), is indicated to prevent morbidity and reduce the length of convalescence in patients with moderately severe envenoming, as well as to save the lives of severely envenomed patients. Indications are as follows: • Fall in blood pressure with or without signs of shock • Other signs of systemic envenoming (see earlier text), including spontaneous bleeding, coagulopathy, pulmonary edema or hemorrhage (shown by chest radiograph), ECG abnormalities, peripheral leukocytosis, profound anemia, or elevated serum creatine kinase • Severe local envenoming—swelling of more than one-half the bitten limb developing within 48 hours of the bite— even in the absence of systemic envenoming • In adults, early swelling extending within 4 hours of the bite beyond the wrist after bites on the hand or beyond the ankle after bites on the foot Patients bitten by European Vipera who show any evidence of envenoming should be admitted to a hospital for observation for at least 24 hours. Antivenom should be given whenever there is evidence of systemic envenoming (see earlier text) even if its appearance is delayed for several days after the bite. Contraindications to Antivenom Treatment There are no absolute contraindications to antivenom in cases of life-threatening envenoming. However, patients with atopic asthma and those who have reacted to equine antiserum on previous occasions have an increased risk for developing severe antivenom reactions. In such cases, antivenom should not be given unless there is evidence of systemic envenoming. If anti­ venom is given, pretreatment with adrenaline (epinephrine), an antihistamine, and a corticosteroid is recommended. Rapid desensitization is not recommended.

CHOICE OF ANTIVENOM IN A PARTICULAR CASE: MONOVALENT AND POLYVALENT ANTIVENOMS

Indications for Antivenom • Systemic envenoming • Hemostatic abnormalities: spontaneous systemic bleed­ ing, incoagulable blood or prolonged clotting time, severe thrombocytopenia • Cardiovascular abnormalities: hypotension, shock, abnormal ECG, cardiac arrhythmia • Neurotoxicity • Generalized rhabdomyolysis • In patients with definite signs of local envenoming, the following indicate significant systemic envenoming:

The range of venoms neutralized by an antivenom is usually stated on the package insert and is to be found in compendia of antivenoms.† If the biting species is known or strongly sus­ pected, the appropriate monovalent (monospecific) antivenom should be used. Monovalent antivenom is raised against the venom of a single species and is effective for treating envenom­ ing by that species of snake alone, or, in some cases, for enven­ oming by a few closely related species. They are generally less expensive than polyvalent antivenoms,226,229 but this is no longer true for CSL taipan and polyvalent antivenoms. In cases of known taipan envenoming, CSL polyvalent antivenom is preferred. In parts of the world where several species produce identical signs, patients who fail to bring the dead snake (or, in Australia, who cannot be diagnosed by venom detection kits) must be treated with polyvalent (polyspecific) antivenom. Polyvalent antivenom

*References 289, 292. † References 1, 2, 40, 197, 218, 292.

*References 104, 251, 254, 257. † References 140, 217, 285, 290-292.

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

to passive stretch. Urine output may dwindle very early in the course of Russell’s viper bite. Dark urine suggests myoglobinuria or hemoglobinuria. If there is initially no evidence of envenoming, the patient should be admitted for observation, ideally for 24 hours.84 Every hour, symptoms, level of consciousness, degree of ptosis, pulse rate and rhythm, blood pressure, respiratory rate, extent of local swelling, and other new signs should be recorded. If there is any evidence of neurotoxicity, ventilatory capacity should be recorded every hour. Useful investigations include the 20-minute whole blood clotting test (or other tests of coagulation), peripheral leukocyte count, hematocrit, urine microscopy and dipstick testing, and electrocardiography. If a tourniquet or tight compression bandage is in place, it may create distal edema through venous congestion even in the absence of envenoming and, if applied tightly enough to prevent arterial perfusion, might cause a cold, pulseless, and cyanotic extremity. Blockage of venous drainage from a limb into a pow­ erfully procoagulant venom that has been injected by the snake may promote deep vein thrombosis and subsequent pulmonary embolism when the tourniquet is released. Such occlusive devices must not be released until intravenous access has been estab­ lished and antivenom, plasma expanders, and adequate medical staff are available to cope with the dramatic deterioration that may follow.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

is raised against the venoms of a selection of the most important species of snakes in a particular geographic region. Polyvalent antivenoms do not necessarily contain lower concentrations of species-specific antibody per unit volume (or total protein content) than do monovalent antivenoms, because immunizing animals with the venoms of two or more related species may produce an augmented antibody response to conserved epit­ opes.170 Polyvalent antivenoms do not necessarily carry a higher risk for reactions than do monovalent antivenoms. The chosen antivenom must have demonstrated ability to protect against the venom of the species thought to have been responsible. Non­ specific antivenom is generally of no benefit to the patient and

may cause reactions (see later text). Some antivenom manufactur­ ers claim a wide range of “para-specific” neutralization for their products, but mere immunologic cross-reactivity in the laboratory is inadequate grounds for relying on an antivenom to be effective clinically.158 Table 55-4 lists some important antivenoms for this region. In some cases, clinical trials have established an average initial dose. Conservation of Antivenom and Expiration Dates Liquid antivenoms stored at temperatures below 8° C (46.4° F) usually retain most of their activity for 5 years or more.289 Freezedried (lyophilized) antivenoms are even more stable. Under

TABLE 55-4  Guide to Initial Dosage of Some Antivenoms for Treating Bites by Medically Important Snakes

Outside the Americas

Species Latin Name

English Name

Manufacturer, Antivenom

Acanthophis species Bitis arietans Africa

Death adder Puff adder

Bitis arietans Middle East

Puff adder

Bothrops asper Bothrops atrox Bothrops bilineatus Bothrops jararaca Bothrops lanceolatus B. caribbaeus Bungarus caeruleus Bungarus candidus

Terciopelo Common lancehead Papagaio Jararaca Lesser Antillean fer de lance Common krait Malayan krait

CSL* Death Adder or Polyvalent Antivenom Sanofi-Pasteur (“Fav Afrique” or “FaviRept” polyvalent; SAVP† polyvalent NAVPC‡ Polyvalent Snake Antivenom Vacsera Polyvalent or Anti-Viper Venom Antiserum ICP§ polyvalent, LBS|| Antivipmyn Tri Butantan, FED¶ Antibotropico polyvalent Butantan polyvalent Butantan polyvalent Sanofi-Pasteur BothroFav

Bungarus fasciatus

Banded krait

Bungarus multicinctus

Chinese krait

Calloselasma (Agkistrodon) rhodostoma Cerastes species

Malayan pit viper

Crotalus durissus

Tropical rattlesnakes

Crotalus simus Cryptelytrops albolabris, C macrops Daboia (Vipera) palaestinae

Central American Green pit vipers

Daboia (Vipera) russelii, D siamensis

Russell’s vipers

Dendroaspis species Dispholidus typus Echis species Africa

East/South African mambas African boomslang Saw-scaled or carpet Vipers

Echis species Middle East

–––––––––

Echis carinatus India Gloydius (Agkistrodon) blomhoffii Hydrophiinae Lachesis sp

––––––––– Chinese Mamushi

Micropechis ikaheka

New Guinean small-eyed snake

1094

Desert (horned) vipers

Palestine viper

Sea snakes Bushmasters

Indian manufacturers** polyvalent TRC†† Malayan Krait Antivenin monovalent or neuro-polyvalent TRC†† Banded Krait Antivenin Monovalent or neuro-polyvalent Shanghai Vaccine & Serum Institute Antivenom of Bungarus multicinctus Blyth Taiwan NIPM Taipei Naja-Bungarus antivenin TRC†† Malayan Pit Viper Antivenin monovalent or haemato-polyvalent NAVPC‡ Polyvalent Vacsera AntiViper or Polyvalent Butantan or FED¶ Anticrotalico or Antibotropico-crotalico ICP§ LBS|| polyvalent TRC†† Green Pit Viper Antivenin or haematopolyvalent Rogoff Medical Research Institute, Tel Aviv, Palestine viper monovalent Myanmar Pharmaceutical Factory, monovalent Indian manufacturers** polyvalent TRC†† Russell’s Viper Antivenin monovalent or haemato-polyvalent SAVP† Dendroaspis or Polyvalent Antivenoms SAVP† Boomslang Antivenom SAVP†, Echis, monovalent Sanofi-Pasteur (“Fav Afrique”) MicroPharm EchiTAb-G ICP§ EchiTAb-plus-ICP NAVPC‡ Polyvalent Snake Antivenom Vacsera Polyvalent and Anti-Viper Venom Antiserum Indian manufacturers|| polyvalent Shanghai Vaccine & Serum Institute Mamushi antivenom CSL* Sea Snake Antivenom ICP§ polyspecific, FED¶Antibotropico laquetico, Butantan Antiophidico CSL* Polyvalent Antivenom

Approximate Average Initial Dose (reference) 1-3 vials (285) 80 mL (275) 80 mL (247,253) 80 mL 5-20 vials (154) 2-12 vials (197) 2-4 vials (197) 2-12 vials†† 2-6 vials (220) 100 mL 50 mL 50 mL 5 vials 5 vials 100 mL (272) 30-50 mL 30-50 mL 5-20 vials 5-15 vials 100 mL (96) 50-80 mL 80 mL (148) 100 mL (8,11) 50 mL 50-100 mL 1-2 vials 20 mL (267) 100 mL 1 vial (1,2) 3 vials (1,2) 50 mL 50 mL 50 mL 5 vials 1-10 vials 10-20 vials ?2 vials

Outside the Americas—cont'd

Species Latin Name

English Name

Manufacturer, Antivenom

Approximate Average Initial Dose (reference)

Micrurus corallinus, M. frontalis M. nigrocinctus,   M. mipartitus,   M. multifasciatus Naja kaouthia

Brazilian coral snakes

Butantan “Antielapidico”

1-5 vials

Central American coral snakes

ICP monovalent

1-5 vials

Monocellate Thai cobra

TRC†† Cobra Antivenin monovalent or neuro-polyvalent Indian manufacturers** polyvalent SAVP2 and Sanofi-Pasteur Polyvalent

100 mL

Vacsera Polyvalent Venom Antiserum NAVPC‡ Bivalent Naja/Walterinnesia or Polyvalent Snake Antivenom SAVP† and Sanofi-Pasteur Polyvalent

100 mL 100 mL

Vacsera Polyvalent Venom Antiserum TRC†† neuro-polyvalent antivenom

100 mL 100 mL

CSL* Tiger Snake or Polyvalent Antivenom TRC†† King Cobra Antivenin or neuro-polyvalent CSL* Polvalent (or Taipan) Antivenom CSL* Brown Snake or Polyvalent Antivenom CSL* Black Snake Antivenom Japanese Snake Institute, Nitta-gun   Yamakagashi antivenom

1-3+ vials (285)

Naja naja, N oxiana Naja haje, N anchietae,   N annulifera, N melanoleuca, cobras   N nivea, N senegalensis Naja haje (Middle East) Naja haje arabica

Indian cobras African neurotoxic

Naja nigricollis, N mossambica etc Naja (nigricollis) nubiae Naja siamensis, N. sumatrana Notechis scutatus

African spitting cobras

Ophiophagus hannah

King cobra

Oxyuranus scutellatus Pseudonaja species Pseudechis species Rhabdophis tigrinus,   R subminiatus

Australian/Papuan taipans Australian brown snakes Australian black snakes Japanese yamakagashi,   SE Asian red-necked keelback Green pit vipers

Trimeresurus albolabris,   T macrops Vipera berus and other European Vipera

Walterinnesia aegyptia

§

Egyptian cobra Arabian cobra

Egyptian spitting cobra Indo-Chinese and other SE Asian spitting cobras Tiger snake

European adder

Black desert cobra

100 mL 100 mL

100 mL (269)

100-200 mL 1-6+ vials (285) 1-6+ vials (285) 1-3 vials (285) 1-2 vials

see Cryptelytrops above Immunoloski Zavod-Zagreb Vipera polyvalent Protherics Fab monovalent “ViperaTAb” NAVPC‡ Bivalent Naja/Walterinnesia or Polyvalent Snake Antivenom

10-20 mL (257) 100-200 mg 50 mL

*Commonwealth Serum Laboratories, Parkville, Australia † South African Vaccine Producers, formerly SAIMR, Johannesburg ‡ National Antivenom and Vaccine Production Center, National Guard Health Affairs, Riyadh, KSA § Instituto Clodomiro Picado, San Jose, Costa Rica || Laboratorios Bioclon, Silanes, Mexico ¶ Fundação Ezequiel Dias, Belo Horizonte, Brazil **Indian Manufacturers: Bharat Serums and Vaccines, Mumbai, Biological E (Evans), Vins Bioproducts, Hyderabad †† Thai Red Cross Society, Bangkok

expedition conditions, liquid antivenoms can be expected to retain their activity even if exposed to environmental tempera­ tures above 30° C (86° F).289 Antivenoms retain much of their activity well beyond stated expiration dates. Although the use of such out-of-date material could never be recommended, situa­ tions may arise in the developing world when there is no alterna­ tive.153 Opaque solutions should not be administered, because precipitation of protein indicates denaturing with loss of activity and increased risk for adverse reactions.

SUPPLY OF ANTIVENOMS Antivenom manufacturers and suppliers change often, so avail­ ability of antivenom is uncertain. For this reason, a timely Internet search (see Useful Websites) followed by confirmation of clinical efficacy and safety, as well as immediate availability, are essential, well in advance of the time when antivenom is needed. In urgent cases, some national poison centers (e.g., London, UK) and zoo

networks hold stocks of antivenoms covering most exotic and local species. Europe, Asia, and Australia are reasonably well supplied with antivenoms, but there is currently a crisis in anti­ venom supply to the sub-Saharan countries of Africa and to New Guinea.77,115,116,287 This problem may be relieved by the production of new “pan-African” polyvalent antivenoms, raised against appropriate African venoms, by manufacturers outside of Africa.27,77,115,116,188 Purchasers of antivenom should be aware that some clinically ineffective, nonspecific but highly reactogenic antivenoms raised against Indian venoms (e.g., Naja, Echis) are sold in African and Asian countries and in Papua New Guinea, where they are pur­ ported to be effective against venoms of the local snakes.260

ANTIVENOM REACTIONS Antivenom treatment may be complicated by early anaphylactictype, pyrogenic, or late (serum sickness–type) reactions. 1095

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

TABLE 55-4  Guide to Initial Dosage of Some Antivenoms for Treating Bites by Medically Important Snakes

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Early Anaphylactic–Type of Reactions These reactions usually develop within 10 to 180 minutes of starting antivenom. There are itching, urticaria, fever, tachycardia, palpitations, cough, nausea, and vomiting. Up to 40% of patients with early reactions show features of severe systemic anaphy­ laxis: bronchospasm, hypotension, or angioedema—but deaths are rare. The reported incidence, which varies between antiven­ oms and according to dose, ranges from 3% to 84%. Safety can be improved by attention to the manufacturing processes.218,292 These reactions are not usually type I IgE-mediated hypersensitiv­ ity reactions to equine serum proteins and are therefore not predicted by hypersensitivity tests.44,130 For this reason, it is inap­ propriate and misleading to apply the adjectives immediate, allergic, or hypersensitivity to early antivenom reactions in general. Antivenoms activate complement in vitro,204 whereas the clinically similar reactions to homologous serum are associated with complement activation and immune complex formation in vivo. The complement system is probably activated by aggregates of IgG or its fragments, but there is little evidence that pepsin digestion, which removes complement-activating Fc fragments, reduces the incidence of reactions.154 Unless patients are watched carefully for 3 hours after treatment, mild reactions may be missed and deaths misattributed to the envenoming itself. Early reactions should be treated as for anaphylaxis of any cause.97,199 They respond readily to aqueous epinephrine/adrenaline given by intramuscular injection of between 0.5 and 1.0 mL of 0.1% (1 : 1000, 1 mg/mL) in adults (children, 0.01 mL/kg) at the first sign of trouble. Antihistamines, such as chlorphenamine maleate (adult dose 10 mg, children 0.2 mg/kg), should be given by intravenous injection to combat the effects of histamine released during the reaction. Pyrogenic Reactions Pyrogenic reactions result from contamination of the antivenom by endotoxin-like compounds. High body temperature develops 1 to 2 hours after treatment and is associated with rigors, followed by vasodilation and decreased blood pressure. Febrile convul­ sions may be precipitated in children. Patients should be physi­ cally cooled and given antipyretic drugs such as acetaminophen by mouth, via nasogastric tube, or by suppository. Aspirin and nonsteroidal antiinflammatory agents are not safe in patients with hemostatic problems. Late (Serum Sickness–Type) Reactions Late reactions develop 5 to 24 (mean 7) days after treatment. Their incidence and speed of development increase with the dose of antivenom. Symptoms include fever, itching, urticaria, arthralgias (which may involve the temporomandibular joint), lymphadenopathy, periarticular swellings, mononeuritis multi­ plex, albuminuria, and (rarely) encephalopathy. This immune complex disorder responds to an antihistamine such as chlorphe­ niramine (adults, 2 mg 4 times a day; children, 0.25 mg/kg per day in divided doses), or, in more severe cases, to corticosteroids (prednisolone 5 mg 4 times a day for 5 days in adults; 0.7 mg/ kg per day in divided doses for 5 days for children).

PREDICTION OF ANTIVENOM REACTIONS Hypersensitivity testing by intradermal or subcutaneous injection or intraconjunctival instillation of diluted antivenom has been widely practiced in the past. However, these tests delay the start of antivenom treatment, are not without risk, and have no predic­ tive value for early (anaphylactic) or late (serum sickness type) antivenom reactions, which are not usually manifestations of IgE-mediated type I hypersensitivity.44,130

PREVENTION OF EARLY ANTIVENOM REACTIONS Prophylactic antihistamines (anti-H1 and anti-H2), corticosteroids, and epinephrine have been very widely used, singly or in combination, on empirical grounds, but not without risk. A few randomized controlled trials have now been completed, and several more are in progress. Intramuscular promethazine proved 1096

ineffective,58 but in two published studies, subcutaneous epi­ nephrine (adrenaline) (0.1%, adult dose 0.25 mg) reduced the incidence of early antivenom reactions.163,288 A study purporting to demonstrate the efficacy of combined hydrocortisone and antihistamine infusion was underpowered.72 A review of 10 years of experience with various premedication regimens in Papua New Guinea288 illustrated the heterogeneity and lack of standard­ ization of snakebite victim care in developing countries while suggesting efficacy of some prophylactic regimens, as did the study of Caron and colleagues32 in Ecuador. Recently, data were published comparing the premedication of 1007 Sri Lankan snakebite victims with promethazine, hydrocortisone, and adren­ aline in a dose of 0.25 mL of 1:1000 subcataneously, each alone and in various combinations. Compared with placebo, adrenaline significantly reduced severe reactions to antivenom by 43% (95%, CI 25 to 67) at 1 hour and by 38% (95%, CI 26 to 49) up to and including 48 hours after antivenom administration. Hydrocorti­ sone and promethazine were ineffective and addition of hydro­ cortisone negated the benefit of adrenaline.47

ADMINISTRATION OF ANTIVENOM Antivenom should be given as soon as it is indicated, but it remains potentially effective as long as signs of systemic enven­ oming persist (e.g., up to 2 days after a sea-snake bite and many days or even weeks for prolonged defibrination following bites by Viperidae).172,173,267,268 In contrast, local effects of venoms are probably not reversible by antivenom delayed for more than 1 to 2 hours after the bite.222,242,269,275 Route of Administration The intravenous route is most effective. Although intramuscular injection is associated with a lower rate of early anaphylactoid reactions, absorption is very slow, especially when the gluteal site is used (but see later text). An infusion over 30 to 60 minutes of antivenom diluted in isotonic fluid may be easier to control than an intravenous “push” injection of reconstituted but undi­ luted antivenom given over 10 to 20 minutes. There is no differ­ ence in the incidence of severity of antivenom reactions in patients treated by these two methods,130 but greater dilution and slower infusion should be tested.29 Further trials are in progress.7 Snakebite in Remote (Wilderness) Locations If someone is bitten by a snake in a remote location and signs of envenoming develop, but there is no one in the group capable of giving an intravenous injection, antivenom may be given by deep intramuscular injection at multiple sites into the anterolat­ eral aspect of the thighs (not into the gluteal region, from which absorption is exceptionally slow), followed by massage to promote absorption. An algorithm has been developed to guide the use of antivenom in these circumstances (Figure 55-107). However, the volumes of antivenom normally required would make this route not practical, as would the risk for hematoma formation in patients with incoagulable blood. Dose of Antivenom Ideally, the initial dose of a particular antivenom should be based on results of clinical studies when available, depending upon species of snake responsible and severity of envenoming. However, most manufacturers’ recommendations are based on mouse assays, which may not correlate with clinical findings.278 Clinical trials of antivenom have been carried out since 1973,268 but are inappropriately neglected, even though they are the only reliable means of obtaining efficacy and safety data. Initial doses of some important antivenoms are given in Table 55-4. The apparent serum half-lives of antivenoms in envenomed patients range from 26 to 95 hours, depending on which IgG fragment they contain.89,213 Children must be given the same doses of antivenom as adults. Recurrent Envenoming Recurrence of clinical and laboratory features of systemic enven­ oming, including recurrent venom antigenemia, several days after an initially good response to antivenom, was clearly documented

No or ?

Signs of envenoming appear (in less than 30 minutes)

Yes Reassure, clean wound (tetanus toxoid)

No Observe and reassess every 30 minutes: signs of envenoming appear

No

Yes

Hospital less than two hours away

Available: someone capable of giving intravenous injection  antivenom.1 Epinephrine (adrenaline) 2 and other drugs for treating anaphylactic antivenom reaction 3

No Available: someone capable of giving intramuscular injection  antivenom.1 Epinephrine (adrenaline) 2 and other drugs for treating anaphylactic antivenom reaction 3 No Conservative management. Then evacuate on stretcher.

Yes

CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

Snake definitely nonvenomous

Yes

No

Yes

Immobilize bitten limb (pressure).4 Then evacuate on stretcher to hospital.

Yes

Give antivenom1 by slow intravenous injection with full precautions. Observe carefully for signs of antivenom reaction. Then evacuate on stretcher.

Give antivenom1 by intramuscular injection with full precautions. Observe carefully for signs of antivenom reaction. Then evacuate on stretcher. Notes: “Antivenom” means appropriate specific antivenom for the species of snake involved. “Epinephrine (adrenaline)” means 0.1% (1:1000) adrenaline for intramuscular injection (adult dose 0.3-0.5 mL). “Other drugs for treating anaphylactic antivenom reaction” means antihistamine and hydrocortisone for intravenous injection. 4 “Immobilize bitten limb (pressure)” means immobilization of the bitten limb with a splint or sling. “Pressure” means use of the pressure immobilization method employing several long elasticized bandages on the pressure-pad method (see previous text). This should only be used when a bite by a neurotoxic elapid snake cannot be excluded. 1 2 3

FIGURE 55-107  Algorithm indicating appropriate management for snakebite in a patient while in a remote wilderness location. (From Warrell D, Anderson S, Dallimore J, et al: Oxford handbook of expedition and wilderness medicine, New York, 2008, Oxford University Press, pp 517-520.)

in patients envenomed by Malayan pit vipers (C. rhodostoma) in Thailand in the 1980s, although this work was overlooked when the phenomenon was rediscovered after the introduction of CroFAb in the United States.90,246,272 Recurrent envenoming is probably the result of continuing absorption of venom from the injection site after antivenom has been largely cleared from the circulation or perhaps by redistribution of venom from tissue in response to antivenom.13,90 Paradoxically, venom absorption may increase after a hypotensive, shocked patient has been resusci­ tated. It is more likely to occur when a rapidly eliminated small IgG fragment antivenom, such as Fab, is used.8,142 This suggests that an initial dose of antivenom, however large, may not prevent late or recurrent envenoming. Repeated Dosing The response to antivenom will determine whether further doses should be given. Neurotoxic signs may improve within 30 minutes of antivenom treatment, but this usually takes several hours. Hypotension, sinus bradycardia, and spontaneous sys­ temic bleeding may respond within 10 to 20 minutes. Blood coagulability is usually restored between 1 and 6 hours, pro­ vided sufficient antivenom has been given. A second dose of antivenom should be given if severe cardiorespiratory symptoms persist for more than about 30 minutes and when incoagulable

blood persists for more than 6 hours after the start of the first dose. The “6-Hour Rule” Studies of envenoming by several species of snakes whose venoms cause coagulopathy have demonstrated that once an adequate neutralizing dose of antivenom has been given, blood coagulabil­ ity (assessed by the 20-minute whole blood clotting test) will be restored within a median of 6 hours.264 This reflects the ability of the liver, highly activated by circulating fibrin/fibrinogen break­ down products, to restore coagulable levels of clotting factors in patients with consumption coagulopathy. This important observa­ tion is the basis for a simple method of titrating antivenom dosage in individual patients whose blood is initially incoagulable. The 20-minute whole blood clotting test is performed at 6-hour inter­ vals, and the initial dose of antivenom is repeated every 6 hours until blood coagulability is restored. After that, the 20-minute whole blood clotting test is checked at 12-hour intervals for at least 48 hours to detect recurrent envenoming. Very large doses of antivenom may be required to treat patients bitten by species capable of injecting enormous amounts of venom or extremely potent venom. A patient bitten by the king cobra (O. hannah) was given 1150 mL of specific anti­ venom and prolonged artificial ventilation and survived.223 1097

PART 6  ANIMALS, INSECTS, AND ZOONOSES

SUPPORTIVE TREATMENT (ASSUMING THAT AN ADEQUATE INITIAL DOSE OF ANTIVENOM HAS BEEN GIVEN) Neurotoxic Envenoming Artificial Ventilation.  This was first suggested for neurotoxic envenoming more than 130 years ago, but patients continue to die due to lack of vital respiratory support. Bulbar and Respiratory Muscle Paralysis.  Inability to swallow is indicated by accumulation of secretions in the pharynx. Stridor indicates paralysis of the vocal cords; it can be accentuated by extending the neck. Early paralysis of intercostal respiratory muscles is suggested by “abdominal breathing” (or “paradoxical respiration”) in which exaggerated compensatory contraction of the diaphragm causes the paralyzed abdomen (rather than the chest) to expand on inspiration. Objective measurement of ven­ tilatory capacity is very useful to monitor respiratory paralysis. This can be achieved with a peak flow meter, spirometer, or respirometer (if the patient is using a face mask or is intubated) or by asking the patient to blow into the tube of a sphygmoma­ nometer to record the maximum expiratory pressure. If patients are adequately oxygenated, even those with profound general­ ized flaccid paralysis from neurotoxic envenoming are fully con­ scious. However, because their eyes are closed (ptosis) and they do not move or speak, they are commonly assumed to be uncon­ scious, and their level of consciousness cannot be properly assessed by the conventional Glasgow Coma Scale. Tactless remarks made by medical staff can be heard by the apparently comatose patient! Opening his or her eyes so that he or she can see the surroundings is very reassuring for a ptotic and com­ pletely paralyzed patient. They may still be able to flex a finger or toe, allowing simple “yes or no” communication. It is very important not to assume that patients with snakebite neurotoxic­ ity have irreversible brain damage, although they may be are­ flexic, unresponsive to painful stimuli, and have fixed, dilated pupils. Neurotoxic effects are fully reversible with time. A patient bitten by B. multicinctus in Canton recovered completely after being ventilated manually for 30 days, and a patient probably envenomed by T. carinatus recovered after 10 weeks of mechan­ ical ventilation in Queensland, Australia. Endotracheal intubation or tracheostomy using a cuffed tube is needed. The patient can be ventilated manually with an anesthesia bag or, preferably, with a mechanical ventilator. For technical details of airway management and assisted ventilation, see http://www.searo. who.int/EN/Section10/Section17.htm. Anticholinesterase Drugs Anticholinesterase drugs have limited usefulness in neurotoxic envenoming but may produce rapid improvement in neuromus­ cular transmission in patients suffering the effects of postsynaptic neurotoxins, for example, from envenoming by some species of Asian and African cobras, mambas, death adders (Acanthophis species), and kraits.118,273,278,282 It is worth trying the “Tensilon test” in all cases of severe neurotoxic envenoming, as for a patient with suspected myasthenia gravis. Baseline observations or mea­ surements are made against which to assess the effectiveness of the anticholinesterase. Atropine sulphate (0.6 mg for adults; 50 mcg/kg for children) or glycopyrronium is given by intrave­ nous injection followed by neostigmine bromide or methylsul­ phate (Prostigmin) (or distigmine, pyridostigmine, ambenomium, and others in appropriate doses) by intramuscular injection 0.02 mg/kg for adults, 0.04 mg/kg for children. Short-acting edrophonium chloride (Tensilon) is ideal for this test but is rarely available in the region. It is given by slow intravenous injection in an adult dose of 10 mg or 0.25 mg/kg for children. The patient is observed over the next 30 to 60 minutes (neostigmine) or 10 to 20 minutes (edrophonium) for signs of improved neuromus­ cular transmission. Ptosis may disappear and ventilatory capacity (peak flow, forced expiratory volume in 1 second [FEV1], or maximum expiratory pressure) may improve. Patients who respond convincingly can be maintained on neostigmine meth­ ylsulphate, 0.5 to 2.5 mg every 1 to 3 hours up to 10 mg/24 1098

hours maximum for adults or 0.01 to 0.04 mg/kg every 2 to 4 hours for children by intramuscular, intravenous, or subcutane­ ous injection together with atropine to block muscarinic side effects. Patients able to swallow tablets may be maintained on atropine 0.6 mg twice each day, neostigmine 15 mg 4 times each day, or pyridostigmine 60 mg 4 times each day. Patients must be observed closely for symptoms of cholinergic crisis. The “ice test” is a possible alternative to the Tensilon test.75 In patients with myasthenia gravis who have bilateral ptosis, application of an ice-filled plastic glove to one eye for 2 minutes resulted in improvement in ptosis on that side, possibly due to inhibition of anticholinesterase. This quick and simple test might obviate the need for the Tensilon test. However, it has not yet been evalu­ ated in patients with neurotoxic snake envenoming.

HYPOTENSION AND SHOCK Hypovolemia is a common cause of hypotension and shock and should be treated by infusing a plasma expander. Central venous pressure is the safest way to control volume replacement. Hypo­ tensive patients envenomed by the Burmese Russell’s viper responded to dopamine, 2.5 mcg/kg per minute by intravenous infusion; however, methylprednisolone, 30 mg/kg, and naloxone were not effective.148 Anaphylaxis, whether it is a primary response to envenoming, the result of hypersensitization, or a reaction to antivenom, should be treated promptly with epinephrine/adrenaline.199,200

ACUTE KIDNEY INJURY* If urine output drops below 400 mL/24 hours, urethral and central venous catheters should be inserted. If urine flow fails to increase after cautious rehydration, diuretics should be tried (e.g., furosemide by slow intravenous injection, 100 mg followed by 200 mg if urine output fails to increase). If these measures fail to restore urine flow, the patient should be placed on strict fluid balance. Peritoneal dialysis or hemodialysis will be required in most patients with established renal failure. For technical details of assessment and treatment of acute kidney injury, see http:// www.searo.who.int/EN/Section10/Section17.htm.

LOCAL INFECTION A booster dose of tetanus toxoid should be given. Following bites by Latin American pit vipers99 and some other species such as Malayan pit vipers (C. rhodostoma),215 local bacterial infections with formation of wound abscesses occur in about 10% of cases. A wide range of bacteria has been implicated, some peculiar to snakes’ oral cavities and venom.194 Even a case of Buruli ulcer (Mycobacterium ulcerans) has been attributed to snakebite. Pro­ phylactic antibiotics are not justified unless the wound has been incised or there is evidence of necrosis.99 Penicillin, erythromycin, or chloramphenicol is appropriate, as would be an antibiotic effective against the bacterial flora of the buccal cavity and venoms of local snakes.215 An aminoglycoside such as gentamicin should be added for 48 hours. Bullae are best left intact.

NURSING SNAKE-BITTEN LIMBS Excessive elevation of snake-bitten limbs should be avoided, in that this has been shown to increase the risk for compartment syndromes.136

SURGICAL MANAGEMENT OF SNAKE-BITTEN LIMBS† Debridement of Necrotic Tissue Necrotic tissue should be debrided as soon as possible and the denuded area covered with split-thickness skin grafts. Muscle should not be excised just because it looks dark or even black, *References 196, 290. † Reference 277.

COMPARTMENT SYNDROMES* In a snake-bitten limb, swelling of muscles within tight fascial compartments, such as the anterior tibial compartment, may raise tissue pressure to such an extent that perfusion is impaired and ischemic damage (as in Volkmann’s contracture of the forearm) is added to the effects of the venom. Risk factors include pressure bandaging and excessive elevation of the limb that reduce arterial perfusion pressure in the compartment but cannot reduce local venous pressure below tissue pressure. Reduction of the arteriovenous pressure gradient was associated with decreased muscle PO2 and nerve conduction velocity.136 The classic signs of compartment syndrome include excessive pain, weakness of the compartment muscles and pain when they are passively stretched, hypoesthesia of areas of skin sup­ plied by nerves running through the compartment, and obvious tenseness of the compartment.136 These features have been char­ acterized as “the seven P’s:” pain at rest, pain on possible movement, paralysis, pallor, paresthesia, poikilothermia, and pulselessness. Unfortunately, local effects of envenoming often result in a painful, immobile, pale, cyanotic, cold, tensely swollen, and apparently pulseless limb with poor capillary refill in the absence of any demonstrable compartment syndrome. These appearances may mislead inexperienced surgeons into diagnosing compartment syndrome without objective evidence and encourage them to proceed to fasciotomy. The discovery of dark or even black-looking muscle tissue may reassure the surgeon that the operation was necessary, but envenomed yet viable muscle often looks black because of hemorrhage. Dangers of fasciotomy include neglect of early adequate antivenom treat­ ment, severe persistent bleeding if the venom-induced hemo­ static abnormalities have not been corrected by adequate doses of antivenom, delayed recovery of function, prolonged hospital admission, persistent morbidity from damage to sensory nerves, and contractures from keloid formation or hypertrophic scarring in some ethnic groups. Palpation of peripheral pulses or their detection by Doppler ultrasound does not exclude compartmen­ tal ischemia. However, direct measurement of intracompartmen­ tal pressure is reasonably simple, using a perfusion pump and saline manometer system or a commercial transducer such as the Stryker apparatus. An intracompartmental pressure of more than 45  mm Hg in an adult or 30  mm Hg in a child indicates a high risk for ischemic necrosis. In these circumstances, fasci­ otomy may be justified to relieve the pressure in the compart­ ment, but this treatment did not prove effective in saving envenomed muscle in animal experiments.70 Necrosis occurs most frequently after digital bites. Fasciotomy must never be undertaken until blood coagulability has been restored by ade­ quate doses of specific antivenom, followed by transfusion of fresh whole blood, clotting factors, or platelets as required.

2. Analgesia by vasoconstrictors with weak mydriatic activity (e.g., 0.5% adrenaline/epinephrine) or a single topical administration of local anesthetic (e.g., 0.4% oxybupro­ caine hydrochloride (Novesin), 4% lidocaine hydrochlo­ ride, or tetracaine hydrochloride (Dicaine). 3. Exclusion of corneal abrasions by fluorescein staining and/or slit lamp examination and application of a pro­phylactic topical antibiotic such as tetracycline, chloram­ phenicol, soframycin, ciprofloxacin, gatifloxacin, penicillinstreptomycin or polymixin B sulphate. 4. Prevention of posterior synechiae, ciliary spasm and dis­ comfort with a topical cycloplegic such as 2% atropine, scopolamine, or homatropine. 5. Antihistamines in case of allergic keratoconjunctivitis. Topical or intravenous antivenom and topical corticosteroids are contraindicated. Topical heparin proved promising experi­ mentally but has been untested clinically.

Prevention of Snakebite The risk for snakebite can be reduced by simple precautions. Snakes should never be disturbed, attacked, or handled unneces­ sarily, even if they are thought to be harmless species or appear to be dead. Some venomous species, such as the ringhals (Hemachatus haemachatus), a South African spitting elapid, sham death (Figure 55-108). Venomous species should never be kept as pets or as performing animals. Protective clothing—boots (not open sandals), socks, long pants (trousers)—should be worn when walking in undergrowth or deep sand, and a flashlight should always be carried at night. Particular care should be taken while collecting firewood; moving logs, boulders, boxes, or debris likely to conceal a snake; climbing rocks and trees covered with dense foliage; or swimming in overgrown lakes and rivers. Where there are sea snakes, wading in the sea, especially in sand or near coral reefs, is a dangerous pastime and should be avoided if possible. Shuffling is safer than a high-stepping gait. Divers should keep clear of sea snakes. Fishermen who catch sea snakes in nets or on lines should return them to their element without touching them; their heads and tails may be difficult to differentiate. In the camp, sleep off the ground in a hammock, on a camp bed or in a tent with a sewn-in ground sheet, especially in krait country. A study in Nepal proved that a well tucked-in mosquito net afforded good protection against snakebites.34 Remove unnecessary junk and litter that might attract rodents, because rodents attract snakes. Various toxic chemicals, such as naphtha­ lene, sulfur, insecticides (e.g., DDT, dieldrin, and pyrethrins), and fumigants (e.g., methyl bromide, formaldehyde, or tetrachloro­ ethane), are lethal to snakes, but no true repellent has been identified that is acceptably safe for peridomestic use where there are children, domestic animals, and valuable wildlife. Prophylactic immunization against snakebite using venom toxoids has been attempted, for example, against habu

INAPPROPRIATE TREATMENTS Corticosteroids, heparin, antifibrinolytic agents such as aprotinin (Trasylol) and ε-aminocaproic acid, antihistamines, trypsin, and a variety of traditional herbal remedies have been used and advocated for snakebite. Most are potentially harmful and none has been proved to be effective.

TREATMENT OF SNAKE VENOM OPHTHALMIA† Management of venom ophthalmia consists of the following: 1. Urgent decontamination by copious irrigation: The “spat” venom should be washed from the eye or mucous mem­ brane as soon as possible using large volumes of water or any other available bland fluid. Even urine is better than nothing! *References 136, 290. † References 41, 255, 274.

FIGURE 55-108  South African ringhals, a spitting elapid (Hemachatus haemachatus: family Elapidae), shamming death. (Copyright D.A. Warrell.)

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

because intense hemorrhage may produce this appearance in viable muscle.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

(Protobothrops flavoviridis) among farmers in the Amami and Ryuku Islands of southern Japan, where it proved ineffective.183 The analogy with immunization against infectious diseases is misleading, because the immunized person would not have time to develop an enhanced secondary (anamnestic) response to the venom after being bitten. Protection would depend solely on levels of neutralizing antibody circulating at the time of the bite.

Venomous Lizards The overtly venomous helodermatid lizards (Gila monster and Mexican beaded lizard) are discussed in Chapter 54. Recently, evidence has been published that the saliva of other groups of lizards contains toxins: Iguania (e.g., iguanas and agamids) (see Figure 55-1, Pogona) and Anguimorpha (e.g., varanid or monitor lizards) (Figure 55-109, A, Varanus salvator).65 These lizards have mandibular glands, but only those of Varanidae/Lanthanotidae and Helodermatidae are segregated into specialized serous protein-secreting glands with thick capsules. Glands of members of four Anguimorph families (Anguidae, Lanthanotidae, Shinisau­ ridae [Figure 55-109, B], and Varanidae) were shown to secrete a variety of toxins, including cysteine-rich secretory proteins (CRiSP), kallikrein, helokinestatin, hyaluronidase, lectin, natri­ uretic peptides, PLA2s, and new cardiopetides.67 The clinical significance of these findings is doubtful, because lizard bites rarely cause more than mild trauma, transient pain, and swelling. However, it has been claimed that envenoming might contribute to the massively traumatic predatory attacks launched by Komodo dragons against large mammals and occasionally humans (see later text).

Dangerous Large Reptiles GIANT PYTHONS (FAMILY BOIDAE) Bites by most species of python can be locally traumatic and sometimes complicated by infection (Figure 55-110, B). Several species have been responsible for rare fatal attacks reported from South America (anaconda, Eunectes murinus) (Figure 55-111, A); Africa (rock python, Python sebae) (Figure 55-111, B to D); south and Southeast Asia, especially Indonesia (reticulated python, Python reticulatus [Figure 55-111, E], and the Indian python, Python molurus); and Australia, where a 5.2-m (17-foot) long scrub python, Morelia amethistina, killed its keeper.144 The victims were asphyxiated and crushed by constriction and in some cases swallowed after the clavicles had been broken147,263 (Figure 55-110, A). In 1974, a man attacked by P. sebae near Harrar, Ethiopia, died 48 hours later as a result of perinephric

A

A

B FIGURE 55-109  Lizards whose saliva contains toxins.67 A, Asian water monitor (Varanus salvator: family Varanidae) (Muda Ganga, Balapitiya, Sri Lanka). B, Chinese crocodile lizard (Shinisaurus crododilurus: family Shinisauridae) (Yao Shan E Xi, China). (Copyright D.A. Warrell.)

hematomas resulting from crush injuries. Recently, a 34-year-old man in the United States was strangled to death by his 2.7-m (9-foot) long, 11.3-kg [25-lb] boa constrictor, reemphasizing the danger posed by even modest-sized pythons.

KOMODO DRAGON (VARANUS KOMODOENSIS) This giant lizard, which can reach 3.1 m (10.2 feet) in length and 166 kg (366 lb) in weight, is restricted to Komodo, Rinca, Flores, and Gili Motang Islands in Indonesia. Until recently it was believed that it killed its prey (deer, cattle, pig, and occasionally humans) by brute force or through debilitation through contami­ nation of bite wounds with pathogenic bacteria, such as Pasteurella multocida.14 Recently, Fry and associates68 found that these

B

FIGURE 55-110  Attacks by pythons. A, Man killed and swallowed by a large reticulated python (Python reticulatus). B, Tooth marks made by a brown water python (Liasis fuscus) that seized a 7-year-old child while she was asleep near the Adelaide River in Australia. (A courtesy Exel Sawuwu; B courtesy Bart Currie.)

1100

B

D

C

E

FIGURE 55-111  Giant pythons. A, Anaconda (Eunectes murinus) (Brazil). B to D, African rock python (Python sebae) showing head (note supralabial heat-sensitive pit organs) and multiple teeth. E, Reticulated python (Python reticulatus). (Copyright D.A. Warrell.)

monitors possessed compound mandibular venom glands whose six compartments ducted to openings between the serrated pleur­ odont teeth. The venom contains toxins capable of causing hypotension (CRiSP, kallikrein, and natriuretic toxins), bleeding (PLA2 toxins), and hyperalgesia (cramping AVIT toxins), which, they argue, contribute to the predation strategy. In support of envenoming, they note that prey animals are reported to be unusually quiet after being bitten and that they rapidly go into shock. There are anecdotal reports of persistent bleeding in human victims after bites by V. komodoensis.

Internet Resources SNAKEBITE MANAGEMENT AND ANTIVENOMS Africa http://www.afro.who.int/en/clusters-a-programmes/ hss/essential-medicines/highlights/2358-whoafro-issuesguidelines-for-the-prevention-and-clinical-management-ofsnakebite-in-africa.html South and Southeast Asia: http://www.searo.who.int/EN/ Section10/Section17.htm (see under Technical Guidelines) Global (“Antivenoms website” [Venomous Snakes Distribution and Species Risk Categories] and “WHO Guidelines” [for the Production, Control and Regulation of Snake Antivenom

Immunoglobulins]): http://www.who.int/bloodproducts/ snake_antivenoms/en/ Global (especially Australasia): http://www.toxinology.com/ Global VAPA Guide: http://vapa.junidas.de/cgi-bin/WebOb jects/vapaGuide.woa/wa/getContent?type=page&id=1

ANTIVENOMS ONLY Munich AntiVenomINdex (MAVIN): http://toxinfo.org/anti venoms/ CSL Australian antivenoms: http://www.toxinology.com/gene ric_static_files/cslb_index.html Global crisis solutions center: http://globalcrisis.info/late stantivenom.htm For poison centers’ prescribers only: https://www.pharmacy. arizona.edu/avi/verify.pl#top

VENOMOUS SNAKE TAXONOMY UPDATES http://pages.bangor.ac.uk/~bss166/update.htm

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 55  Envenoming and Injuries by Venomous and Nonvenomous Reptiles Worldwide

A

CHAPTER 56 

Bites and Injuries Inflicted by Wild and Domestic Animals JOHN E. BRADFORD AND LUANNE FREER

Wild and domestic animal bites are distinct from other injuries suffered by humans. Tearing, cutting, and crushing injuries may be combined with blunt trauma caused by falls. Animal bites may cause local infection, and offending bacteria reside in numerous environmental sources. However, few traumatic lacerations are as regularly contaminated with as broad a variety of pathogens as are animal bites. Domestic animal bites are common, and their incidence is rising.43,201,297 Wild animal attacks are often more spectacular; however, in the developed world, injuries from domestic animals have a much greater health and economic impact. Humans are not a preferred natural prey of any animal, and, although some attacks are predatory, most attacks are caused by fear of humans (real or perceived), territoriality, protective instinct, or accident. Unfortunately, wild animal attacks may be sensationalized by the lay press, and animals given anthropomorphic characteristics that do not accurately reflect their instinctive responses; this may lead to public misunderstanding of animal behavior. Press reports may ignore the fact that wild animal attacks are rare and that wild animals are far less likely to cause injury than are their domestic counterparts. As human settlements and populations continue to grow and encroach on the natural world, the incidence of human–animal encounters will increase. Adventure-seeking humans may also seek out animal encounters that historically would have been avoided. A wolf sighting 100 years ago would have been cause for alarm, yet today people travel to Yellowstone National Park to see wolves in the wild and hope to get close enough to take pictures. The increased pressure of human proximity to animals increases the likelihood of an encounter resulting in a negative outcome (Figure 56-1).40 Other special features of human–animal encounters include attacking animals that may terrorize the victim and transmission of systemic diseases, many of which might cause substantial morbidity and mortality (for a discussion of zoonoses, see Chapter 59). In addition, treatment decisions are often made without a strong scientific basis, and management of wild animal attack victims is often based on a much more robust experience with domestic animal attacks (i.e., dog and cat bites). It is important to note that animal-caused injuries are usually preventable. When experience allows humans to understand the typical behavior of a species, people can take proper precautions

FIGURE 56-1  Yellowstone visitors approach bull elk. (Courtesy Luanne Freer, MD.)

1102

near potentially dangerous animals. For instance, when an animal attacks to defend itself or its territory, it is likely to cease this behavior when the person leaves and the perceived threat is diminished. However, during a predatory attack, the intent of the animal is to kill and not allow its prey to escape. Understanding how to react in these situations decreases the potential for a disastrous outcome. This chapter interprets the present state of knowledge and makes logical and specific recommendations for all of these conditions.

General Epidemiology According to the 2008 National Pet Owner Survey, 39% of all households in the United States own a total of 74.8 million dogs, and 34% own 88.3 million cats.10 During 1 year in Pennsylvania, county health officials reported 16,000 animal bites, 75% of which were dog related; the highest incidence of dog bite was among children less than 5 years old. Three-quarters of persons injured received wound treatment, and one-half received antimicrobials. Postexposure rabies prophylaxis administration was prescribed for attacks by species as follows: 44% for cats, 30% for dogs, 7% for raccoons, 4% for bats, 2.5% for squirrels, 2.1% for groundhogs, 2% for foxes, and 8% for all other species.230 Each year, dogs bite 1.8% of all Americans, resulting in 4.7 million wounds. More than 750,000 of these victims seek medical attention.75 Bites to children are common, especially among boys between the ages of 5 to 9 years.75 Over the course of 1 year in Pittsburgh, Pennsylvania, 790 dog bites were reported, but an estimated 1388 went unreported; the annual incidence was 58.9 bites per 10,000 individuals.81 Of 279 reported injuries caused by animals to travelers, 51% were caused by dogs, 21% by monkeys, 8% by cats, and 1% by bats.144 In India, where stray dogs cause 96% of rabies cases, the annual dog bite rate is 25.7 per 1000 individuals, and the most common victims are males.3,86 The annual incidence of cat bites in the United States is approximately 400,000.303 A cat bites one in every 170 people each year, and 80% of these bites become infected.156 Biting cats are typically stray females, and most human victims are female. Of the approximately 30 million Americans who ride horses, 50,000 a year are treated for horse-related injuries in an emergency department, principally because the rider is unrestrained and can fall off while traveling at speeds of up to 64.4 km/hr (40 mph). Horses can kick with a force of up to 907 kg (1 ton), and frequently bite. A 2-year review of animal bites in Oslo, Norway, revealed that horses caused 2% of 1051 recorded bites; 53% of these horse bite victims were children.104 The American Ferret Association estimates that 6 to 8 million domesticated ferrets reside in the United States. The Centers for Disease Control and Prevention (CDC) reports that the number of bites inflicted by ferrets—65 reported bites in 10 years—is substantially lower than that caused by dogs and cats (i.e., between 1 and 3 million)23 (Table 56-1). In Arizona, 11 ferret bites were reported over 11 months; with the ferret population estimated at 4000, the reported bite-to-ferret population ratio is approximately 0.3%.316 The risk of attack by a ferret is greatest among infants and small children. In Sweden, 3 in 1000 citizens are injured by animals each year.46 Domestic animals accounted for more than 90% of injuries, moose accounted for 6% (almost all were involved in auto accidents), and all other animals accounted for 4%. However, bites were not examined separately, and many injuries occurred during

For online-only figures, please go to www.expertconsult.com

Study Species Dog Cat Rodent Monkey Skunk Lagomorph Large mammal Reptile Bat Raccoon Human Other animal

A

B

C

89 4.6 2.2 0.1*

91.6 4.5 3 0.2 0.02 0.5 0.01‡

78 16 <1 2.2 0.02

65 15 0.1

1.2

3§

1 0.5

0.3 1

6 3||

0.7 0.5

0.2 0.03† 0.1

0.004 0.08

D

E 75 20 2.5 0.2

F 85-90 5-10 2-3

2-3 <1

G 80-85 10

5-10¶

A: Marr J, Beck A, Lugo J: An epidemiologic study of the human bite, Public Health Rep 94:514, 1979. B: Scarcella J: Management of bites, Ohio State Med J 65:25, 1969. C: Sinclair CL, Zhou C: Descriptive epidemiology of animal bites in Indiana, 1990-1992: A rationale for intervention, Public Health Rep 110:64, 1995. D: Kizer K: Epidemiologic and clinical aspects of animal bite injuries. JACEP 8:134, 1979. E: Spence G: A review of animal bites in Delaware: 1989 to 1990, Del Med J 62:1425, 1990. F: UpToDate: Initial management of animal bites. http://www.uptodate.com/online/content/topic.do?topicKey=.peds_env/5288&source=preview&anchor=H2#H2. G: Answers.com: Animal bite infections. http://www.answers.com/topic/animal-bite-infections. *Includes 21 monkeys, 4 raccoons, 3 ferrets, 1 weasel, 1 coatimundi, 1 skunk, and 1 goat. † Includes 3 lions, 1 ocelot, 1 leopard, 1 polar bear, and 1 anteater. ‡ Includes 1 goat, 1 ocelot, 1 jaguar, and 1 groundhog (which inflicted a bite on Groundhog Day). § Includes 1 coyote. || Includes 1 kinkajou. ¶ Includes rodents, rabbits, horses, raccoons, bats, skunks, and monkeys.

vehicular accidents with animals. Some officials estimate there are two additional bites for every one reported, but a survey of children between the ages of 4 and 18 years old estimated an incidence of more than 36 times the reported bite rate. These figures are most likely based on domestic bites, although this was not specifically stated.32,33 During a 7-year period in Texas, 2% of all large-animal–related trauma was caused by wild animal attacks.243 From 2001 to 2005, there were 472,760 reports by poison control centers of animal bites and stings, which is an average of 94,552 reports per year.202 A 2006 GeoSentinel review of injuries to travelers from 1998 to 2005 showed a total of 320 reported animal-related injuries (i.e., 1.8% of all reported injuries).144 The review revealed that, among travelers, women were more likely than men to be injured by animals. Men were more likely to be injured by dogs, women by monkeys, and children suffered animal injuries at a higher rate than any other travel-related injury. By geographic region, travelers were most likely to experience animal-related injuries in Southeast Asia, followed by Asia, Australia and New Zealand, Africa, Latin America, North America, and Europe.144

Typical Victim No published reports characterize the typical wild animal attack victim. Two U.S. state health departments report that, if all animal bites (including domestic) are considered, animal bites occur most often among male children between the ages of 5 and 9 years.302,306 However, more than 90% of animal attacks in these states are caused by domestic animals, so this group may not accurately reflect the typical victim of a wild animal attack. In developing countries, many persons are exposed daily to biting animal species that are considered “exotic” in the developed world. Persons in certain occupations in developed countries (e.g., veterinary and animal control workers, laboratory workers) are at greatest risk for wild animal bites. One study reported that 65% of veterinarians had suffered an animal-related injury during the preceding 12 months.200 The U.S. Bureau of Labor Statistics reported that, during a 5-year period, 186 occupational injury fatalities were caused by animal attacks and that the majority involved cattle.58 In one study of 102 animal control officers, the overall bite rate was 2 per 57 individuals per working day, which is 175 to 500 times the estimated rate for the general population (this study did not differentiate between wild and domestic

animal bites).32 The incidence of biting varies with species exposure. In 2003, 93% of Wisconsin and Minnesota veterinarians were victims of dog or cat bites. Cattle and horses inflict the most injuries to veterinarians, with kicking, biting, and crushing being the top three mechanisms of injury.116 In every statistical series of bites, small numbers of exotic animals—including ocelots, jaguars, lions, leopards, polar bears, wolves, anteaters, and weasels—are represented. Bites from these animals occur as a result of exposure to wild and zoo animals and because of the increasing popularity of keeping wild animals as pets. This practice, which commonly involves exotic animals being kept illegally and without adequate training and understanding of animal care and behavior, all too often ends in tragedy. Several thousand people per year are killed by mammalian bites, with most of the deaths inflicted by maneating lions and tigers in Africa and Asia (Table 56-2). By way of comparison, the World Health Organization estimates that 5 million people per year are bitten and 125,000 killed by snakes and that additional millions are killed by insect-borne diseases.349 An estimated 200 persons are killed by animals in the United States each year; 131 of these die in traffic accidents involving deer.170 Bees kill approximately 43 persons, dogs 14, and rattlesnakes 10. Wild animals (e.g., bears, cougars) kill fewer people than do goats, rats, jellyfish, and captive elephants. More than 3 million people visit the wilderness in Yellowstone National Park every year, but the incidence of serious injuries by bears in the park is less than that of being struck by lightning.162

Circumstances Surrounding and Prevention of Animal Bites: Animal Behavior Analysis of unintentional injuries shows that these are not random events but rather, are predictable events and have identifiable personal and environmental risk factors similar to those of diseases.350 For example, family pets cause most bites, and the animals are usually provoked in some way. Boys experience 150% to 250% the rate of injuries as compared with girls at every age350 (Table 56-3). Injuries are frequently sustained while playing with the animal.81 Most bites occur in the summer months during the late afternoon. Children sustain a higher percentage of head and neck bites than do adults and are more likely to require 1103

CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

TABLE 56-1  Incidences (%) of Bites by Species in the United States as Reported in Seven Studies

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 56-2  Human Deaths from Animal Attacks Species

Estimated Deaths Annually

Humans Wolves Hyenas Domestic dogs Other canines Tigers Leopards Lions Cougars African buffalo Elephants Black rhinoceri Hippopotami American bison Moose Deer Domestic herbivores Snakes Crocodiles Alligators Ostrich Kangaroos

200,000 20-50 10-50 10-20 1-5 800 30-100 300-500 <1 20-100 600 1 200-300 3 3 50 20-25 100,000 2000 1-2 1-2 1-2

Estimated Attacks Annually 1-5 Hundreds 4.7 million 200-250 800 400 — <1 — — — — 56 368 injuries 1.5 million accidents 50,000-100,000 injuries — — — — 100-200 accidents

Predominant Area

Comments

Worldwide Worldwide (mostly Eurasia) Africa United States Australia India Africa and India Africa and India United States Africa Worldwide Africa Africa United States British Columbia, Canada United States United States and Australia Worldwide Africa United States

Murders only

medical attention.130 Of all dog bites, 9% to 36% occur to the head and neck region, whereas this area is affected in 6% to 20% of persons who sustain cat bites.130 Understanding such patterns of animal bite injuries allows for improved prevention and treatment. Prevention of animal bites requires thorough knowledge of the patterns of behavior and personalities of various species of animals. A person who wishes to avoid the bite of a particular species will often be able to gain expertise about that species’ behavior only from those who work with it regularly. Detailed information about animal behavior and the attack patterns of animals is also available on the Internet (Box 56-1).

Domestic animals of any kind rarely attack unless provoked, although unrestrained dogs are sometimes exceptions. Physical attack is usually a last resort, but an animal will fight if it perceives that it is trapped. Reducing the risk of injury is often based on common sense and knowledge of animal behavior. For example, horses kick backward and with both rear feet, whereas cattle kick forward with only one foot. How a person reacts

Increasingly threatened by habitat loss Unpredictable Auto accidents only Auto accidents only

Auto accidents only

BOX 56-1  Animal Behavior and Attack Prevention

Websites

Dog and cat bite prevention Dog bite prevention

Dog bite prevention and   legal information Moose attack prevention Cougar attack prevention

Basic Principles for Avoiding Animal Bites

Frequently maneaters Frequently maneaters Frequently maneaters 20 deaths during the last century

Wolf behavior and human encounters Hunter education General animal attack   information Wild animal attack   compilation

http://www.cityoffortwayne.org/ animal-bite-prevention.html http://www.petplace.com/dogs/ preventing-dog-bites-things-  to-do-before-you-get-a-dog/  page1.aspx http://www.dogbitelaw.com http://www.survivaltopics.com/ survival/survive-a-moose-attack/ http://www.arkanimals.com/dlg/ cougar_attack.htm http://fwp.mt.gov/wildthings/wolf/ human.html http://www.hunter-ed.com/ index.html http://www.articlesbase.com/ health-and-safety-articles/ how-to-avoid-animal-attack-  injury-444613.html http://www.attack.igorilla.com

TABLE 56-3  Selected Demographics for Animal-Related Fatalities in the United States From 1991 to 2001*

(Based on the International Classification of Diseases Reporting System Codes)

Type of Animal Dog Rat Unspecified animal Specified animal† Other animal‡ Alligator Marine animal Other mammal

Number of Deaths 208 3 32 846 32

Percentage

Average Number of Deaths

Range

Death Rate per Million per Year

17 0.25 2.70 71.5 2.70

18.9 0.27 4 76.9 4

11-26 0-1 1-8 51-113 2-8

0.07 0.0001 0.011 0.285 0.011

Male

Female

0 to 19 Years Old

≥20 Years Old

134 3 21 416 15 4 4 157

74 0 11 148 17 1 0 40

123 1 10 125 5 0 1 34

85 2 22 439 27 5 3 163

From Langly R: Animal-related fatalities in the United States: An update, Wilderness Environ Med 16:67, 2005. *This does not include fatalities related to vehicle–animal collisions or fatalities from falling off ridden animals, because these categories are classified differently under the International Classification of Diseases reporting system. † This category is described as follows: “Other specified animal includes many large animals, such as bears, sharks, cows, and horses. The actual number of fatalities caused by each species is not known for many animals.” ‡ This category does not include arthropods. It does include cats, moray eels, sharks, and rodents (except rats).

1104

Common Pets*

Dogs • Do not leave a young child alone with a dog. • Never approach or try to pet an unfamiliar dog, especially if it is tied up or confined. • Always ask the dog’s owners if you can pet the dog. • Do not lean over a dog or pet it directly on the head. • Do not kiss a dog. • Avoid quick or sudden movements that may startle a dog. • Never pet or step over a sleeping dog. • Never try to take a bone or toy away from a dog (other than your own dog). • Know the appearance of an angry dog: barking, growling, snarling with teeth showing, ears laid flat, legs stiff, tail up, and hair on the back standing up. • Never step between two fighting dogs; if you need to separate them, use a bucket of water or a hose. • Do not approach a female dog that is nursing her pups. • Teach injury prevention advice to children from an early age. Cats • Be aware that some cats do not like prolonged petting. • Know warning signs of an impending bite: twitching of the tail, restlessness, and “intention” bites (i.e., the cat moves to bite but does not bite). Ferrets • Do not sell or adopt a ferret that is known to bite. • Do not push your fingers through the wires of a ferret cage. • Reach for a ferret from the side with the palm upward rather than from above. • Do not handle food and then handle young ferrets without washing your hands first. • Do not poke a ferret or pull on its tail or ears. • Never leave a ferret alone with a child or infant. • If a ferret bites and locks on very tightly, pour cold and fast-running water over its face.

and capture are considered high risk, and careful study of the species’ behavior, the individual animal, and the physical environment and available resources should precede actual attempts at restraint (see Chapter 61). Because people seem drawn to raising wild animals as pets,211 a large and lucrative market exists, particularly in the United States. No matter how they are raised, these animals remain wild and will never be as predictable, trustworthy, and nonaggressive as animals that have been domesticated for centuries. Often owners of these animals demonstrate a lack of common sense; consider the case of a pet Bengal tiger that attacked and killed its trainer, then did the same to its owner 6 weeks later.21,112 Most wild species have a strong sense of territoriality. Individuals, pairs, and larger groups establish a territory that ranges from square feet to miles and aggressively prevent any intrusion into that territory, particularly by members of their own species. During mating season and later during protection of the nest and young, this drive may stimulate even small animals to threaten or attack humans. A major principle of animal behavior is that physical attack is often the animal’s last resort. Animals generally give ample warning regarding their intentions. Elaborate rituals and rules that encourage a nonviolent solution so that the victor may successfully defend its territory and itself with little or no injury govern spectacular contests between animals that occur in the wild. Humans can often avoid attack and injury by successfully interpreting visual, auditory, and olfactory warning signs. If a human slowly and carefully backs away without making sudden or threatening gestures, usually no harm will be done. However, the ideal reaction depends on the species. For example, mountain lions have been turned from a full charge by a human who acted aggressively or fought back.35 Given a choice of victims, such a predator prefers the fleeing and panicked victim who demonstrates expected behavior patterns. If capture of an animal is essential, detailed preparation should be undertaken. For small animals, using nets or heavy cloth and wearing extremely heavy gloves and other protective clothing are advisable. Desperate animals can bite with tremendous force; large carnivores can easily amputate a gloved digit. A wolf can tear apart a stainless steel bowl with its teeth, and a hyena can bite through a 2-inch–thick wooden plank.92 Four men

*The prevention of bites and injuries from other animals is addressed in the appropriate sections of this chapter.

BOX 56-3  Suggested Actions If You Are Under Threat

or Attacked By a Dog

during a confrontation with an animal is also important. Nonpredator species (e.g., cattle, deer) are very susceptible to human intimidation, whereas a direct stare at a canine may be seen as a challenge. Expert recommendations can reduce the chance of being attacked and bitten by a domestic animal (Box 56-2). Specific actions can be taken when an individual is threatened or under attack by a dog (Box 56-3). Dogs are guided by memory and instinct; fear and self-preservation are very strong instincts, so any perceived threat could lead to an attack. Territoriality is still ingrained in domestic dogs, even if humans provide for them. Protection of food can cause aggression, even in a docile dog. Any threat to a dog’s mate, offspring, or owner may result in an attack. Personality changes may lead to aggression; causes include illness (e.g., distemper) and physiologic factors (e.g., a female in heat). Like their domestic counterparts, wild animals rarely attack humans without provocation. Exceptions are large apex carnivores, which may be relatively unafraid of humans, and creatures infected with rabies. However, carnivores do not commonly hunt humans as preferred prey. The animal’s perception of provocation may not be readily apparent to the inexperienced individual. Patterns of behavior and attack differ by species. People often capture or restrain wild animals, thereby creating stress that may cause even the most benign animal to attack its captor. Allegedly tame animals are very likely to struggle. Even shy animals that are being captured for treatment of an injury may attack in self-defense and can inflict a life-threatening injury (e.g., goring). Therefore, all situations that involve animal restraint

Stand totally still, and let the dog come to you. Remain calm, assume a nonthreatening stance, and never run. Do not pat the dog. Keep your eye on the dog, but do not stare at it. Avoid smiling at the dog. To reprimand the dog, say “no” in a harsh voice; do not attempt to hit the dog. Do not make any threatening or provocative movement. Do not fight back, especially against a “fighting” dog. Do not let the dog get behind you; keep turning to face it. If you are knocked down, feign death, and curl up into a ball until the dog loses interest. If the dog punches you with its nose, ignore it. If a dog puts one of your legs in its mouth without tearing the flesh, waiting for a reaction, stay still if you can. If you are attacked by more than one dog, try and stand with your back to a wall or car. Back away slowly and leave the area when the dog loses interest in you. After an attack, contact the dog’s owner and the appropriate authorities, and attend to any wounds. If the interaction occurs when you are cycling, dismount, and keep the bike between you and the dog. Modified from Wilson S: Bite busters: How to deal with dog attacks, New York, 1997, Simon & Schuster; and wikiHow: How to handle a dog attack. http:// www.wikihow.com/Handle-a-Dog-Attack.

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CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

BOX 56-2  Advice for Avoiding the Bites and Attacks of

PART 6  ANIMALS, INSECTS, AND ZOONOSES

BOX 56-4  Animal Capture and Immobilization

Considerations

Types of Equipment* Nets Vehicles Helicopters Drugs Feed Bomas (holding pens)

Considerations Type of animal Number, gender, and age Animal health Time of year Area of capture Physical condition of animal Postcapture transport†

Successful Captures Planned No unnecessary personnel‡ Are not performed during late winter Animals are not chased§

Capture Methods Immobilizing drugs¶ Tranquilizing drugs¶ Cage traps with or without bait Darting from a vehicle or helicopter

Modified from Wildlife Campus: Game capture: Part A. http://www.docstoc. com/docs/19872015/Game-Capture-Part-A. *The welfare of the animal is always paramount † Large carnivores should remain tranquilized for transport for ease of handling and animal safety. ‡ Bystanders increase the potential for injury to both humans and animals. Observers are usually inexperienced and may hinder operations. § Chasing animals for long distances or periods of time is not advised. Animals do not act this way in natural settings, and such stress could prove fatal. ¶ In South Africa, the most common drugs used are a compound called M-99 and fentanyl.

are needed to subdue an adult chimpanzee; an orangutan can maintain a one-fingered grip that an adult human cannot break. Larger animals generally require a team approach by animal control specialists with equipment such as nets, barriers, cages, and immobilizing drugs. Ideal immobilization techniques for various species are detailed in veterinary and wildlife management publications137,142 (Box 56-4).

Evaluation and Treatment of Injuries: Prehospital Care Attacks by domestic and farm animals are fairly predictable and preventable; this is unlike many attacks in the wilderness. In Africa and Southeast Asia, life-threatening attacks by large animals such as water buffalo, lions, tigers, and elephants are common. Attacks by larger animals can result in major blunt or penetrating trauma, with possible major arterial blood loss, airway damage, broken ribs, pneumothoraces, and intraperitoneal bleeding. The victim’s condition and availability of rapid evacuation determine the extent of treatment in the field. Medical personnel or supplies are often not available, so the victim must be moved to a hospital or clinic as soon as possible. Many of the complications and serious infections that occur as a result of animal bites are caused by inadequate first aid and delays in medical care. Local wound treatment should be initiated at the scene of the bite (Box 56-5); more than any other therapy, this can determine the course of healing. Simple first-aid measures must be initiated immediately unless definitive or better treatment is available within a short time. Pressure on the wound or pressure points controls most bleeding; avoid tourniquets unless blood loss cannot otherwise be controlled. If the victim is more than 1 hour from a treatment facility, cleanse the wounds at the scene as soon as resuscitation efforts are complete. Early cleansing reduces the chance of bacterial infection and is extremely effective for killing rabies and other viruses. Potable water, preferably boiled or treated with germicidal agents, is adequate for wound irrigation. Ordinary hand soap adds some bactericidal, virucidal, and cleansing properties. If 1% to 5% povidone–iodine in normal saline solution is available, it should be used as an irrigant. Alternatively, thoroughly irrigate the wound with at least a pint of soapy water and then gently debride 1106

it of dirt and foreign objects by swabbing with a soft, clean cloth or sterile gauze. Irrigation with a syringe is preferable (see Chapter 22). After cleansing, cover the wound with sterile dressings or a clean, dry cloth. Wounds of the hands or feet require immobilization. If the wounds are at high risk for infection, treatment is hours away, and an antibiotic such as amoxicillin–clavulanate (first line), a fluoroquinolone plus clindamycin, trimethoprimsulfamethoxazole plus clindamycin, amoxicillin plus cephalexin (less effective), azithromycin, or doxycycline is available,1,102,308 then it is reasonable to start immediate treatment with an oral dose (Box 56-6). To most effectively prevent subsequent wound infection, antibiotics should be started within 1 hour of wounding. However, with a severe wound, it is worthwhile to provide the antibiotic, even if delivered substantially later. If antibiotics are unavailable, the wound is infection prone, and medical care is delayed, a simple remedy such as filling the wound with honey may be an effective antibacterial strategy.264 Because of its high osmolarity and weak hydrogen peroxide concentration when diluted, honey can be effective as an antibacterial when used in adequate quantities, although there are no randomized controlled trials to support this recommendation. The wound should be flooded with honey that has been slightly thinned with water and kept flooded like this until definitive treatment is available. The amount of honey needed will depend on the amount of exudate from the wound (because of dilution), and the frequency of dressing changes will depend on how rapidly the exudate dilutes the honey. Whenever possible, even in prehospital settings, wounds should be cleansed and irrigated thoroughly. Irrigation should be delivered with pressure equal to about 8 to 12 psi and debrided as effectively as possible. For some wounds that are not at high risk, attempting field closure is reasonable, and a loose closure with a dressing may help to decrease bleeding, prevent infection and make self-evacuation possible. However, in general, field closure of contaminated bite and claw wounds is not recommended. Further discussion of bandaging and

BOX 56-5  Summary of Mandatory Animal Bite Wound

Treatment for All Wounds

1. Evaluate for potential blunt trauma and injury to deeper and vital structures caused by penetrating teeth, claws, or horns. 2. Ensure appropriate tetanus immunization. 3. Irrigate wound with a copious volume (minimum, 100 to 300 mL) of normal saline or 1% to 5% povidone–iodine in saline solution. 4. Debride obviously crushed and devitalized tissue. 5. If the animal is suspected to be rabid (e.g., atypical behavior, high-risk species), do the following: a. Infiltrate wound edges with 1% procaine hydrochloride. b. Swab wound surface vigorously with cotton swabs and 1% benzalkonium chloride (Zephiran) solution or other soap. c. Rinse wound with normal saline. d. Assess need for rabies immune globulin and vaccine. 6. Assess risk factors to make decisions about further (selective) treatment (see Box 56-3). 7. Do not culture fresh wounds. 8. Do not give prophylactic antibiotics for routine low-risk bite wounds. Selective Treatment (Wounds Selected By Risk Factors) 1. Suture, staple, or use adhesive strips to close all skin wounds in the usual fashion, unless wounds are high risk (e.g., hand wounds, high-risk species, immunosuppressed patient). 2. Culture infected wounds only if they show signs of established infection or if there is evidence of systemic sepsis. 3. Consider surgical consultation and delayed primary closure for high-risk wounds. Strongly consider administration of prophylactic antibiotics to victims with high-risk wounds.

Antibiotic Agent of Choice A)  Amoxicillin–clavulanate Alternate Combination Therapy: B or B)  Metronidazole Or: C)  Clindamycin Plus One of the Following: D)  Doxycycline E)  Trimethoprim–sulfamethoxazole F)  Penicillin V potassium G)  Cefuroxime H)  Moxifloxacin

Recommended Adult Dose

Recommended Child Dose*

875/125 mg twice daily 45 mg/kg per dose (amoxicillin component) twice daily C (With Anaerobic Activity) Plus E, F, G, H, or I 500 mg three times daily 10 mg/kg per dose three times daily 450 mg three times daily

10 mg/kg per dose three times daily

100 mg twice daily 160/800 mg (1 DS tab) twice daily 500 mg four times daily 500 mg twice daily 400 mg once daily

Not for use in children <8 yr old 4 to 5 mg/kg (trimethoprim component) per dose* twice daily 12.5 mg/kg per dose four times daily 10 mg/kg per dose twice daily Use with caution in children

Adapted from Endom EE: Initial management of animal and human bites. In Danzi DS, editor: UpToDate. Waltham, Mass, 2011, UpToDate. *Child dose should not exceed recommended adult dose.

wound-repair techniques may be found in Chapters 21, 22, and 23. In addition to treating the bite victim, try to capture the offending animal for examination, if this can be done without risk of human injury in the process. Unusual behavior, such as unprovoked attack by a wild animal in broad daylight or a complete absence of fear of humans, should raise the suspicion for rabies (see Chapter 60). Live animal capture is optimal, but freshly killed animals are usually satisfactory for examination for fluorescent rabies antibody. Avoid damaging the animal’s head and brain (e.g., by gunshot or bludgeoning), because brain tissue is needed for analysis. Availability of the animal can eliminate the need for costly and uncomfortable rabies prophylaxis. If more than 1 hour will elapse before the animal can be transported to a hospital or public health department prepared to process the body for the determination of rabies, then refrigerate the body. For shipping, wrap the animal’s head and transport it in an insulated container with ice or ice packs. Do not use preservatives. Be sure to include the type of animal, details of the exposure, date of the animal’s death, victim information, and a description of the animal’s behavior in the report accompanying the specimen.304 An examination of the animal is not useful for most other diseases and will not help predict local wound infections. Therefore, use good judgment when deciding how much time and energy to expend on capture.

Evaluation and Treatment of Injuries: Hospital Care Resuscitation with fluids and possibly blood products may be needed if there is extensive volume loss. When considering diagnostic imaging, the type of animal and its particular attack characteristics should be considered. Blunt trauma often accompanies penetrating injuries such as goring and trampling. Animal attack wounds classified as high risk for infection (Box 56-7) include deep puncture wounds, moderate or severe wounds with associated crush injury, wounds with areas of underlying venous or lymphatic compromise, wounds on the hands or in close proximity to a bone or joint, and bite wounds in compromised hosts (e.g., immunocompromised, absent spleen or splenic dysfunction, diabetes mellitus). Surgical consultation and hospital admission should be considered early in such cases.

WOUND MANAGEMENT Animal bites are not clean lacerations, and wounding may be compounded by crush injuries with devitalized tissue. All bites should be treated as contaminated wounds. Evaluate all victims of animal bites for blunt trauma and internal injuries, which may be less obvious than the bite wound (see Box 56-5). Internal organ, deep artery and nerve damage, and penetration of joints are all possible. Particularly in children, animal bites can

BOX 56-7  Risk Factors for Infection from Animal Bites High Risk Location Hand, wrist, or foot Scalp or face in patients with high risk of cranial perforation; computed tomography or skull radiograph examination is mandatory Over a joint (possibility of perforation) Through-and-through bite of cheek Type of Wound Punctures that are difficult or impossible to irrigate adequately Tissue crushing that cannot be debrided (typical of herbivores) Carnivore bite over vital structure (e.g., artery, nerve, joint) Patient Older than 50 years Asplenic Chronic alcoholic Altered immune status (e.g., chemotherapy, acquired immunodeficiency syndrome, immune defect) Diabetic Peripheral vascular insufficiency Chronic corticosteroid therapy Prosthetic or diseased cardiac valve (consider systemic prophylaxis) Prosthetic or seriously diseased joint (consider systemic prophylaxis) Species Large cat (canine teeth produce deep punctures that can penetrate joints and the cranium) Primates Pigs (anecdotal evidence only) Alligators and crocodiles Low Risk Location Face, scalp, ears, and mouth (all facial wounds should be sutured) Self-bite of buccal mucosa that does not go through to skin Type of Wound Large clean lacerations that can be thoroughly cleansed (the larger the laceration, the lower the infection rate) Partial-thickness lacerations and abrasions Species Rodents Quokkas Bats (although there is a high risk for rabies)

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CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

BOX 56-6  Recommended Empiric Oral Antibiotics for Bite Wound Prophylaxis and Treatment

PART 6  ANIMALS, INSECTS, AND ZOONOSES

penetrate vital structures, such as joints or the cranium.53,68 Radiographs may be employed whenever these injuries are suspected. A complete head-to-toe evaluation for trauma is advised in all but the most trivial and isolated bite injuries. Laboratory tests are of little use when evaluating animal bite injuries. Unless hematocrit is being assessed for evidence of blood loss, the complete blood cell count is not useful, because it is a nonspecific and unreliable gauge of infection. Definitive trauma evaluation and treatment are discussed in detail in Chapter 21. Routine wound cultures obtained at the time of initial wounding do not reliably predict whether infection will develop or, if it does develop, the causative pathogens.135 Therefore, culturing an uninfected bite wound does not yield any useful data.49,60,135 If a bite wound appears infected, cultures and gram staining should be obtained before antibiotics are administered. It is useful to alert the laboratory technician that the culture is from a bite wound, because organisms such as Pasteurella multocida are often misidentified. Many bite injuries are simple contusions that do not break skin. The infection potential of these injuries is low; superficial wound cleansing and symptomatic treatment of pain and swelling suffice. Treatment should include prompt and liberal application of ice or other cold packs during the first 24 hours. However, this is not beneficial for snakebite (see Chapters 54 and 55), and is obviously impractical in many locations. When skin is broken, the risks of local wound infection or transmission of systemic disease are incurred. Infection can be caused by organisms carried in the animal’s saliva or nasal secretions, by human skin microbes carried into the wound, or by environmental organisms that enter the wound during or after the attack.225 Debridement removes bacteria, clots, and soil far more effectively than does irrigation.135 In addition, debridement is intended to create cleaner surgical wound edges that are easier to repair, heal faster, and produce a smaller scar. Topical antiseptic ointments (e.g., neomycin, bacitracin, polymyxin) are highly effective for promoting healing of minor skin wounds.146,206 Although topical ointments are appropriate for abrasions produced by animal bites, they may be less effective for punctures and sutured lacerations. A sutured wound is covered by a simple, sterile, dry dressing to protect it from rubbing against clothing or repetitive minor trauma. Delayed primary closure requires that the wound be kept moist; this is usually done with a wet saline dressing twice daily until closure, which is generally planned for 72 hours after wounding.135

WOUND CLOSURE AND INFECTION RISK FACTORS Three major considerations govern the decision of whether to suture a wound: cosmetics, function, and risk factors. Cosmetic appearance virtually mandates suturing all facial wounds, which are usually low risk. Similar reasons may dictate closure of wounds on other visible portions of the body. Function is of critical importance for wounds of the hand, a high-risk area in which infection can have disastrous consequences. Thus, in general, all but the least complex hand wounds should initially be left open. Risk factors are many and complex, and provide a useful logical framework for making the decision of whether to suture, administer antibiotics, or undertake other treatments. For more information about surgical procedures, see Chapters 21 and 22. The amount of time elapsed after wounding is a critical risk factor; the longer the interval, the more likely the chance for infection. After the first few hours, adequate wound cleansing is unlikely to be carried out. In developed countries, many victims are seen within hours of wounding, and the results are usually very good. In remote and undeveloped areas and countries, wounds commonly do not receive medical attention for half a day or more, thereby putting them into a high-risk category that may eliminate the possibility of primary repair. Certain species— including primates, wild cats, pigs, and large wild carnivores— seem to inflict infection-prone wounds. Wounds that involve crush injuries, puncture wounds, hands or feet, or affect a 1108

compromised host are at high risk for infection, and primary closure should only be attempted after careful consideration and with surgical consultation and concurrence in most cases. If primary closure is not chosen or deemed too risky, surgical consultation for a discussion of other options, including delayed primary closure or vacuum-assisted closure, is prudent.55,135 Many minimally contaminated bites can be safely sutured after proper wound preparation. Data suggest that carefully selected mammalian bite wounds can be sutured with approximately a 6% rate of infection.84 Two separate studies examining the risk of infection after primary closure reported rates of 7.8% (6 of 92 cases)214 and 5.5% (8 of 145 cases).84 The authors of the latter study concluded that the rate of infection after primary closure was acceptable, particularly if a good cosmetic outcome was needed.84 Optimal conditions for primary repair include prompt medical treatment, which is seldom available in remote and undeveloped areas. In these circumstances, leaving bite wounds open (or with a drain, although this is also controversial) is the more prudent course.

BITES OF THE HAND Because hand bites are common and infection can be disastrous,334 the hand is considered at high risk for complications (see Box 56-7). The hand contains many poorly vascularized structures and tendon sheaths that poorly resist infection. The fascial spaces and tendon sheaths of the hand communicate with each other, and movement seals off the wound from external drainage and spreads bacteria and soil internally. Because of the unique anatomy of the hand, thorough irrigation of wounds is often impossible. Data regarding hand wound infection have been collected mostly from experience with domestic dog and cat bites. From a retrospective study in Oslo, Norway, it was determined that nearly all hand bite wounds healed uneventfully when the wounds were left open, either without antibiotics or with penicillin after wound treatment.104 In another European center, the total infection rate was 18.8% in hand bite wounds; this rose to 25% when the hand wound was closed primarily. The average time from the injury to the first medical treatment was 11 hours in infected wounds and 2 hours in noninfected ones.7 Because of the high morbidity and permanent residual impairment that occurs with hand infections, treating them aggressively is best (see Box 56-5). Hand bite wounds should be irrigated, debrided if possible, and, in higher-risk wounds, initially left open.135,334 Small, uncomplicated lacerations can be repaired within 12 to 24 hours. The hand should be immobilized with a bulky mitten dressing in an elevated position, and the victim usually should be started promptly on antibiotics. Specialty consultation and follow up are mandatory for persons with established infection, and hospitalization should be considered. Persons who are not hospitalized should be rechecked daily until signs of infection clear. In the patient without initial evidence of infection, 5 days of splinting and oral antibiotics should suffice if no complications develop.62 Radiographic examination to search for fractures and imbedded foreign bodies should be considered for all significantly injured extremities.

PUNCTURE WOUNDS Punctures may occur as a result of biting, clawing, or goring. The infection rate is related to difficulty irrigating properly and degree of contamination, which is highest in bites. Puncture wounds can be contaminated with pieces of the victims’ clothing or shoes as well. Usually, attempts to irrigate narrow punctures simply result in rapid development of tissue edema from infused irrigant solution, which does not cleanse the wound. However, if the wound is large or can be held open wide enough to permit fluid to escape, irrigation is worth the effort. Large goring-type puncture wounds up to 20.3 cm to 25.4 cm (8 to 10 inches) deep from bison have a low incidence of infection when closed primarily after irrigation and debridement.96 For most smaller puncture wounds, irrigate or debride them as well as possible, suture only if cosmetic or functional considerations require it, and treat

FACIAL AND SCALP WOUNDS Facial and scalp wounds tend to heal rapidly, with little risk of infection; in general, they may be sutured primarily, and do not require prophylactic antibiotics. Typical dog bites of the face and neck (including punctures) have an infection rate of only 3%, even when sutured.7,104,107,342 Generally the cosmetic closure of facial wounds is afforded by the lower incidence of infection. Standard of care in most cases is primary closure of an animal bite wound of the face.342 A major risk associated with facial and scalp wound victims of large carnivores is that the teeth can easily perforate the cranium, producing depressed skull fracture, brain laceration, intracranial abscess, or meningitis.78,260 In young children with such wounds, or in adult victims of large carnivore bites, computed tomography (or in the absence of computed tomography, skull radiography) should be routinely employed to look for evidence of perforation that would mandate immediate neurosurgical consultation and admission to the hospital.

FOLLOW-UP CARE Assuming that the possibility of major or occult trauma has been ruled out, follow-up care for animal bites depends on the risk factors present (see Box 56-7) and the patient’s response to treatment. With only a superficial abrasion, infection is unlikely, and no return visit is needed. With an ordinary low-risk bite wound, one follow-up visit in 2 days to assess any infection will suffice. If the patient is very reliable and no sutures have been placed, a return visit may not be necessary. Infected wounds dictate much closer follow up, with the frequency depending on the wound’s response to treatment and the patient’s risk factors. In a high-risk wound or compromised patient, the initial follow-up visit should be made within 24 hours if the patient is not hospitalized.

INFECTION: ZOONOSES AND RABIES Immense numbers of bacteria inhabit animals’ mouths and can be inoculated into a bite wound. Claw and scratch wounds may be contaminated with soil, urine, and feces. The exact pathogens vary depending on the biting species (Box 56-8). If inoculated in sufficiently large numbers, these microorganisms can cause localized cellulitis and abscess formation, the most common forms of infection. Wild animals also act as vectors for diseases, such as rabies, cat scratch fever, monkeypox virus, simian herpes virus, tularemia, hantavirus, tetanus, Q fever, and toxoplasmosis (see Chapters 59 and 60).

RABIES Rabies is discussed in detail in Chapter 60, so comments here are limited to brief remarks about epidemiology, assessment of risk in the bite victim, and local wound treatment. Rabies is a rhabdovirus that occurs in wild and domestic animals and is transmitted through the saliva of an infected animal. It is generally believed that no true reservoir host exists for rabies (i.e., no species harbors a latent and nonfatal infection). The epidemiology of rabies varies widely in different parts of the world. In the United States, Western Europe, and Canada, wild animals are by far the main vectors of rabies, accounting for more than 88% of all reported cases from the past two decades.196 In India, 95% of rabies postexposure prophylaxis treatment is the result of bites from stray dogs.86 In recent years, rabies in humans has become an extremely rare disease in the United States, with only two cases occurring in 1997196 and one case in 2001.123 Since 1980, rabies-infected bats caused 58% of

BOX 56-8  Common Bacteria in Animal Bites

Dog Bites Staphylococcus species Streptococcus species Eikenella species Pasteurella species Proteus species Klebsiella species Haemophilus species Enterobacter species DF2 or Capnocytophaga canimorsus Bacteroides species Moraxella species Corynebacterium species Neisseria species Fusobacterium species Herbivore Bites Actinobacillus lignieresii Actinobacillus suis Pasteurella multocida Pasteurella caballi Staphylococcus hyicus subspecies hyicus

Cat Bites Pasteurella species Actinomyces species Propionibacterium species Bacteroides species Fusobacterium species Clostridium species Wolinella species Peptostreptococcus species Staphylococcus species Streptococcus species

Swine Bites Pasteurella aerogenes Pasteurella multocida Bacteroides species Proteus species Actinobacillus suis Streptococcus species Flavobacterium species Mycoplasma species

Large Reptiles (e.g., crocodiles, alligators) Aeromonas hydrophila Pseudomonas pseudomallei Pseudomonas aeruginosa Proteus species Enterococcus species Clostridium species

Rodent Bites (i.e., rat-bite fever) Streptobacillus moniliformis Spirillum minus

Data from Garth AP: Animal bites in emergency medicine. http://emedicine.medscape.com/article/768875-overview.

the human cases of rabies diagnosed in the United States.196 Of the more than 7437 cases of animal rabies reported in the United States in 2001, raccoons accounted for nearly 40% of the total. Foxes, bats, and skunks accounted for all but less than 1% of the remainder. Hawaii is the only state without any reported rabies.123 Foxes are the primary offenders in Europe; some countries have eliminated rabies in wild populations by using innovative vaccination programs.89 Because of local variations in animal vectors and endemics, consultation with the state or local health department is prudent before a decision is made to initiate rabies postexposure prophylaxis (PEP).196 Although the number of human cases has declined, about 18,000 people per year in the United States receive rabies PEP.134 In the rest of the world, virtually all rabies occurs in dogs. Worldwide, dogs account for 91% of all human rabies cases; cats 2%, other domestic animals 3%, bats 2%, foxes 1%, and all other wild animals only 1%.89,347 However, in the United States and Puerto Rico in 2004, 92% of all rabies cases were attributed to wildlife, with the majority being raccoons, skunks, and bats.196 It is important to note that 75% of animal injuries to travelers occurred in rabies-endemic countries, including Thailand, India, Indonesia, China, Nepal, and Vietnam.144 Each year in India, 25,000 humans die from rabies, and one-half million receive rabies vaccine.310 In Thailand, 50% of human rabies cases occur among children who are less than 15 years old.315 In Africa, Latin America, and most of Asia, dogs are the principal vector, although jackals are also a factor. In South America and Mexico, rabid vampire bats cause occasional human infection. During recent years, disruption of the natural ecology of vampire bats as a result of introducing humans and domestic animals to the rain forest has produced epidemics of rabies. In Israel, wolves and jackals are the chief vectors, and the mongoose prevails in Puerto Rico. 1109

CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

as having a high risk of infection.135 Use delayed primary closure liberally.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

In Eastern and Central Europe, the raccoon dog (Nyctereutes procyonoides) is an increasingly common vector.89 Risk of rabies exposure rests on several factors, including the type of animal, its behavior, and endemicity of the country or region in which it is located. The incidence of rabies in local species is important; in the United States, urban dogs and cats, domestic ferrets, rodents, and lagomorphs (i.e., rabbits and hares) are at low risk. Description of the animal’s behavior is sometimes helpful, and is easily evaluated in wild animals because most tend to shun humans. The appearance of a skunk, fox, or bat in an urban setting that has no fear of human beings during broad daylight should raise suspicion for rabies. The incidence of rabies is so high for dogs in some developing countries that rabies PEP should always be given serious consideration. In addition to situations involving animal bites, contact of mucous membranes with rabid saliva or an animal scratch should prompt consideration for rabies PEP. In the United States and other areas in which bat rabies is endemic, if a person is found in a room with a bat and is unable to reliably report the absence of contact that could have resulted in exposure (e.g., an unattended child, a sleeping or mentally incompetent adult), then rabies PEP should be administered. Thorough and rapid early treatment of wounds from suspected rabid animals may decrease viral load. Immediately cleanse all bite wounds and scratches with soap and water and a virucidal agent (e.g., povidone–iodine solution).302 Evaluate all persons exposed to a possibly rabid animal for rabies PEP. The CDC guidelines issued in 2009 recommend that, for previously unvaccinated persons, the entire dose of rabies immune globulin [20 IU/kg body weight] should be infiltrated at the wound site, if possible. In the United States, two types of rabies vaccine are currently available: human diploid cell vaccine and purified chick embryo cell vaccine. The chosen vaccine is given in 1-mL doses on days 0, 3, 7, and 14 after exposure. Rabies immune globulin should not be administered to previously vaccinated persons. Persons previously vaccinated should instead receive two 1-mL doses of vaccine (either purified chick embryo cell vaccine or human diploid cell vaccine) given on days 0 and 3.74 Further information about rabies pre-exposure prophylaxis and PEP is provided in Chapter 60.

OTHER NEUROTROPIC INFECTIONS Although Creutzfeldt-Jakob disease (CJD) is not caused by bites or wounds, oral transmission of this spongiform encephalitis has been reported to result from the regionally common practice of eating the brains of wild goats, pigs, or squirrels (even when cooked). CJD is characterized by progressive dementia, ataxia, and myoclonus, and is untreatable. It is caused by a virus also identified in the brains of domestic sheep and mule deer.187 Chronic wasting disease (CWD) is another transmissible spongiform encephalitis that is found in elk and deer in the Four Corners area of the United States (i.e., where Colorado, New Mexico, Arizona, and Utah meet). Food-borne transmission of CJD has raised concerns that the species barrier (i.e., the difficulty an infectious disease encounters during transmission from one species to another as a result of structural protein differences between the agent and host) may not protect against CWD. In vitro conversion of CWD to a human infective form has been demonstrated, but further studies are needed. Between 2001 and 2003, six people—all of whom died—were identified as having a CJD variant. All were known to have consumed venison from CWD-endemic areas, although strong data linking CJD with exposure to CWD were lacking. The risk of transmission to humans, even in CWD endemic areas, remains extremely low.36 Mad cow disease is discussed in Chapter 59.

INDICATIONS FOR WOUND CULTURE Culture of fresh animal bite wound surfaces, whether judged quantitatively or qualitatively, is useless as a predictor of infection. Some of the pathogens of greatest concern (e.g., genus Eikenella) can take 10 days to grow out in culture, by which time most therapeutic decisions have been made. Other organisms (e.g., genus Pasteurella) are fastidious, hard to identify, and 1110

frequently missed by laboratory technicians, who rarely encounter them.150 If a wound is infected or if animal bite sepsis is suspected, obtain wound cultures to guide subsequent antibiotic therapy. In certain cases, cultures should be sent to reference laboratories, such as those in state health departments or at the CDC in Atlanta, Ga, because reference laboratories have successfully isolated more pathogens on identical samples sent simultaneously to both reference and local laboratories.314

PROPHYLACTIC ANTIBIOTICS Currently, the weight of evidence does not support use of prophylactic antibiotics for wounds that are not high risk. Many animal bites, human and otherwise, are treated with prophylactic antibiotics, particularly bites to the hands or feet or if the victim is immune suppressed. Human-to-human bites, although outside the scope of this chapter, have similar risks for infection compared with other animal bites. A recent double-blind study of 125 people with superficial human bites showed no statistically significant difference in infection rates between antibiotic and placebo groups.52 A Cochrane Database Systems review of eight randomized controlled trials found no evidence that the use of prophylactic antibiotics is effective for cat or dog bites, except in the case of bites to the hand.225 The use of prophylactic antibiotics is advisable for wounds of the hand; the speed of development, frequency, severity, and complications of hand wound infections can be impressive.135,334 Persons with other risk factors may benefit from prophylactic antibiotics (see Box 56-6). These risk factors include prolonged time from injury to treatment; complex wounds with massive crushing; heavily contaminated wounds; wounds communicating with tendons; fractured bones or joint spaces; or medical conditions such as asplenia, diabetes mellitus, vascular insufficiency, and immune deficiency. For bite wounds, treatment can begin only after wounding and bacterial inoculation; thus, antibiotics are never truly prophylactic. For major surgery, prophylactic antibiotics are of proved value only in carefully selected high-risk procedures and only if begun before surgery.329 Several controlled studies of dog bite wounds found no significant benefit for using prophylactic antibiotics to treat low-risk facial and scalp wounds.111,206 Other studies recommend the use of prophylactic antibiotics only for high-risk wounds or patients.104,107,155,334,342 To be most effective, prophylactic antibiotics must be administered early. The offending bacteria are already present in the wound when the victim is first seen. Therefore, bite victims who require early antibiotic treatment should be identified promptly, preferably during triage on entry to the treatment facility. The victim should receive immediate antibiotics by protocol; the intravenous route is by far the quickest. The current recommendation for duration of antibiotic prophylaxis is 3 to 5 days (see Box 56-6). Therapy should be tailored to the largest variety of most likely pathogens for a particular type of bite. For most terrestrial mammals, the choice of antibiotic is based on experience with human, dog, and cat bites. However, with an alligator or crocodile bite, or other wounds incurred in freshwater, antibiotic choice should be directed against Aeromonas hydrophila174,226 (see Chapter 58).

TETANUS PROPHYLAXIS In the United States, cases of human tetanus from animal bites exceed cases of rabies infection by a ratio of 2 : 1 each year.30 The spores of Clostridium tetani are ubiquitous in soil, on teeth, and in the saliva of animals; therefore, the risk of tetanus may be present from any animal injury that penetrates the skin. Rates of tetanus vaccination are highest in the developed world and fall dramatically in the developing world, with Somalia and Samoa having the lowest rates.346,348 For adults in the United States in 2007, the CDC reported that, out of a sample of 3525 people, 2.1% had received a tetanus booster (tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis) in the past 2 years, and the vaccination rate for tetanus during the prior 10 years was 57% (n = 1727).26,77 Because tetanus is preventable and many

Clean and Minor Wound

All Other Wounds

Previous Doses of Adsorbed Tetanus Toxoid*

Tetanus Toxoid†

Tetanus Human Immune Globulin‡

Tetanus Toxoid§

Tetanus Human Immune Globulin

<3 or unknown ≥3

Yes Only if last dose given ≥10 yr prior

No No

Yes Only if last dose given ≥5 yr prior

Yes No

From Hibberd PL: Tetanus-diphtheria toxoid vaccination in adults. In: Weller PF, editor: UpToDate, Waltham, Mass, 2011, UpToDate. *Tetanus/diphtheria is preferred to tetanus toxoid for those who received tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis previously; when tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis is not available; and for persons >64 yr old. † Toxoid: Adult: 0.5 mL of diphtheria–tetanus given intramuscularly. Child <5 yr old: 0.5 mL of diphtheria–tetanus given intramuscularly. Child >5 yr old: 0.5 mL of diphtheria–tetanus given intramuscularly. Child <7 yr old: diphtheria/tetanus/acellular pertussis. ‡ Tetanus immune globulin: 250 to 500 units given intramuscularly in limb contralateral to toxoid. § ≥7 and <11 yr old: tetanus/diphtheria. 11 to 64 yr old: tetanus toxoid, reduced diphtheria toxoid, and cellular pertussis is preferred to tetanus/diphtheria for those who have never received tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis.

persons still do not receive tetanus immunoprophylaxis in accordance with guidelines, proper emergency prophylaxis against tetanus remains an important but often underaccomplished intervention (Table 56-4). For a clean wound that contains little devitalized tissue and that can be easily irrigated and debrided, a previous full course of tetanus immunization plus a booster within the last 10 years is sufficient. For a deep puncture or wound with much devitalized tissue that is difficult to irrigate and debride (which is thus predisposed to anaerobic growth), a full series of previous immunizations plus a booster within the last 5 years is sufficient. If there is any uncertainty regarding the status of the victim’s prior immunizations, 0.5 mL of diphtheria–tetanus or tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis booster vaccine should be administered. A high-risk wound should also prompt consideration of administration of an intramuscular injection of 250 to 500 units of tetanus human immune globulin.

GENERAL COMPLICATIONS Wound infection is generally diagnosed on the basis of increasing redness, swelling, and tenderness of the wound margins that eventually progresses to production of pus, cellulitis, lymphangitis, and local lymphadenopathy. Lymphadenitis and lymphangitis, which are much less common, occur as local defenses are overwhelmed. Symptoms of systemic infection are rare and suggest bacteremia or sepsis. Wound infection from animal bites should be treated like infection of any other traumatic wound. Elevate the wound, immobilize the affected part, remove sutures or staples if present, and provide antibiotic therapy (see Box 56-6). The 1999 Emergency Medicine Animal Bite Infection Study Group findings recommended that empiric treatment include a combined β-lactam/β-lactamase inhibitor antibiotic, a second-generation cephalosporin with anaerobic activity, or combination therapy with either penicillin and a first-generation cephalosporin or clindamycin and a fluoroquinolone.135,314 Additional studies recommend azithromycin, trovafloxacin, or telithromycin, which demonstrate good in vitro activity against unusual aerobic and anaerobic animal pathogens.150-152,314 In 2002, a study showed that garenoxacin, a des-fluoro(6) quinolone, was very active against 240 aerobic and 180 anaerobic isolates from bite victims. It inhibited 403 of 420 (96%) isolates, including those of Moraxella spp., CDC group EF-4, Eikenella corrodens, all Pasteurella spp., and Bergeyella zoohelcum. Fusobacterium russii and 6 of 11 Fusobacterium nucleatum isolates of animal bite origin were resistant.153 Extremely rare pathogens can cause infection (see Box 56-8). Culture of debrided tissue is the only reliable identification technique, and sensitivity testing may take weeks. In 2002, a 7-yearold girl developed a wound infection as a result of a tiger bite; DNA sequence analysis revealed that one of the causative organisms was a previously undescribed subspecies of Pasteurella multocida, which the authors designated “Pasteurella multocida subspecies tigris.”63 This organism is usually sensitive to

ciprofloxacin, cefoxitin, and perhaps rifampin.266 A diabetic patient developed tenosynovitis caused by Mycobacterium kansasii after an accidental bite by his pet dog,305 and Bergeyella zoohelcum has been reported as a fastidious species that is difficult to culture from patients with infected cat bites.294

SEPTIC COMPLICATIONS Bacteremia and sepsis, although theoretic risks with any animal bite pathogen, have so far been reported with only a limited number of species.9,133,197,260 Clinical manifestations include cellulitis, endocarditis, meningitis, pneumonitis, WaterhouseFriderichsen syndrome, renal failure, shock, and death. Purpuric lesions are seen in one-third of cases and may progress to symmetric peripheral gangrene and amputation. House cats are an increasing source of human plague in the Southwest United States. Since the onset of the human immunodeficiency virus epidemic, Rochalimaea infection (bacillary angiomatosis) has also become more prominent, and is closely associated with exposure to cats. Although sepsis after an animal bite incident is reported more often among immunosuppressed patients (e.g., there was a case of fatal Pasteurella dagmatis peritonitis and septicemia in a patient with cirrhosis188), there are reports of fatal cases of purpura fulminans with gangrene, sepsis, and meningitis caused by Capnocytophaga canimorsus among previously healthy patients after dog bites. 109,204

ALLERGIC REACTIONS Up to 11% of laboratory workers have allergic reactions to laboratory animal dander, hair, or urine.343 One case of proved hypersensitivity to rat saliva after a bite has been reported.157 The patient was subsequently proved to be allergic to the saliva (presumably to saliva proteins) and not to other portions of the rat. The bite produced lymphangitic swelling and itching that subsided within 24 hours. Two cases of anaphylaxis after dwarf hamster bites have also been reported.241

PSYCHIATRIC CONSEQUENCES OF ANIMAL ATTACKS Victims of traumatic or life-threatening events may develop posttraumatic stress disorder (PTSD). This syndrome has been recognized by the authors as a result of wild animal attack, and is rarely reported in the scientific literature.108 After physical recovery from an attack, the victim may be plagued by recurrent nightmares and flashbacks of the event and may have an aversion to outdoor travel. Violent and multiple attacks or those associated with deep bites have a higher probability of causing PTSD symptoms.262 Critical incident stress debriefing and post-trauma intervention counseling may be important aspects of care for victims of animal attack.108 PTSD has been described among children who are victims of dog bites.262 In a 2004 study, 12 of 27 pediatric patients developed either complete or partial PTSD as a result of dog bites.262 1111

CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

TABLE 56-4  Wound Management and Tetanus Prophylaxis

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Wild Animal Attacks Neither the annual number of wild animal bites nor the base human population at risk can be reliably estimated, especially when the human population to be considered is only that exposed to a wild animal or in a wilderness setting. The world supports approximately 5500 species of mammals, 10,000 species of birds, and 9000 species of reptiles. The actual number of wild animals in the world is estimated to be in the billions. Many people who suffer relatively minor injuries caused by wild animals do not seek medical attention unless infection or another complication occurs or they fear exposure to rabies. If the injury is minor, patients are generally treated, released, and unrecorded. The following sections consider published data and speciesspecific information to discuss the prevention of attacks and care for human victims of attacks.

CANINES There are approximately 35 species of wild canines, and they are present on every continent except Antarctica. Dingoes, found in Australia, are technically not wild canids, but they are descended from dogs. Coyotes Coyotes (Canis latrans) have not only survived the onslaught of civilization in the United States but have thrived and multiplied. Perhaps as a result, more and more coyote attacks on people have been reported, even in urban areas such as Los Angeles.16,64,177 Most of these incidents occurred in Southern California near a suburban–wildland interface. One study done in 1982 was intended to show the coyote density at such a location. Traps were set for the animals within a one-half mile radius of a particular residence, and 55 coyotes were trapped during an 80-day period.176 Between 2004 and 2007, 541 coyotes were removed on average from Illinois; 312 were from the Chicago area alone. It is estimated that there are 1250 coyotes in the suburban area surrounding Washington, DC.311 Between 1998 and 2003, there were 41 coyote attacks on humans in California, and most were unprovoked; it appears that nonrabid coyotes are becoming more aggressive with humans.79 Rabies is less prevalent among coyotes and foxes with the advent of an oral rabies vaccine for these species.295 Attack incidents are typically preceded by a sequence of increasingly bold coyote behaviors. These may include nighttime coyote attacks on pets; sightings of coyotes in neighborhoods at night; sightings of coyotes during the morning and evening hours; attacks on pets during daylight hours; attacks on pets on leashes; chasing of joggers and bicyclists; and midday sightings of coyotes in the vicinities of children’s playgrounds318 (Figure 56-2, online). Since the 1970s, more than 100 coyote attacks on humans have been recorded in Southern California, with one-half of these incidents involving children who are 10 years old or younger.79 There is one well-documented fatality of a child in 1981, who, despite being rescued by her father, died of blood loss and a broken neck.79 A 5-year-old boy in Middletown, New Jersey (about 64.4  km [40 miles] from New York City) was bitten by a coyote and required 46 stitches to his head.311 A 19-year-old woman was killed by two coyotes (likely coyote– wolf hybrids) in Nova Scotia, Canada while hiking on a trail in October 2009; the woman died of blood loss from multiple bite injuries, and, although one of the animals was wounded, neither coyote was captured.157 The safe environment provided by a wildlife-loving public, which rarely displays aggression toward coyotes, is considered a major contributing factor to the increasing numbers of attacks.79 There has been an increase in reports of coyote attacks in national parks by animals that are subsequently captured and found to be disease free.64 A coyote bite should be treated as a dog bite with respect to antibiotic choice and closure issues; if the animal cannot be captured and examined, rabies prophylaxis should be undertaken. Coyotes have been identified as the reservoir for the human pathogen Bartonella vinsonii sub sp. berkhoffii.80 1112

FIGURE 56-3  Yellowstone wolves. (Courtesy Rick McIntyre.)

Wolves The gray wolf (Canis lupus), also known as the timber wolf, is the largest wild member of the Canidae family (Figure 56-3). There are an estimated 7000 to 11,200 gray wolves in Alaska and more than 5000 in the lower 48 states. Worldwide, the wolf population is estimated at 200,000 in 57 countries.106 Wildlife experts suggest that attacking wolves are habituated to humans and human food sources. However, most unhabituated wolves are traditionally timid. Historically the majority of predatory attacks occurred during the summer months, and victims were predominantly women and children. Predatory attacks by wolves against humans tend to occur in clusters, indicating that human killing is not normal wolf behavior but rather specialized behavior that single wolves or packs develop and maintain until they are killed.335 Throughout Europe and Asia, wolves have well-documented histories of cunning behavior, pack attacks, and human killing.209 In one Indian state, 100 children were injured and 122 killed between 1980 and 1986.274 Between 1840 and 1861, Russia reported 273 nonrabid wolf attacks, resulting in the deaths of 169 children and 7 adults.194 North America has fewer verified cases, although recent research indicates 80 events in Alaska and Canada during which wolves closely approached or attacked people (there were 39 cases of aggression by apparently healthy wolves and 29 cases of fearless behavior by nonaggressive wolves).208,224 Five wolf attacks on humans occurred within a 12-year period in Algonquin Provincial Park in Ontario, Canada, and a kayaker was pulled from his sleeping bag by wolves in British Columbia, Canada.208 In 2005, a hiker in Northern Canada was eaten by wolves, although he likely died of other causes.121,145 Most recently, in March 2010, a woman was killed by wolves in Alaska in what is thought to be the first known fatal attack by wolves in the United States in modern times.235 Villagers in the area had noted increasing aggression from local wolves preceding the attack; wolves are the only large predator in the region, and had been entering the villages at night and frequenting the edges of settlements. A substantial number of attacks by rabid wolves in Iran over a 10-year period provided the clinical population upon which the human diploid cell vaccine for rabies was tested.24 The reintroduction of wolves to wild habitat in the Yellowstone ecosystem and Idaho in 1995 has resulted in the successful proliferation of many new wolves. However, there has not yet been a negative human interaction since their release.158 Comparison of victims of fatal attacks by domestic dogs and wild wolf packs reveals distinct differences in bite-mark patterns; the necks and faces of domestic dog attack victims were the primary sites of injury, whereas a wolf-pack victim was spared damage to the neck but had facial tissue destroyed postmortem. Most punctures are found on the ventral aspect of victims of domestic canine attacks as opposed to dorsal punctures among victims of wild or feral canines. Wild canine bites involve

Foxes Most human attacks by foxes are inflicted by rabid animals; fox bites have caused eyelid lacerations among children who are sleeping in tents and leg punctures among adults.195,313,327 One child died of rabies from fox bites despite appropriate PEP.313 A rabid gray fox bit several people during a single afternoon in 2008 in Arizona.14 Foxes can cause more puncture wounds than other canines, making their bites more prone to infection. Oral vaccination of fox populations has led to a decline in the number of rabid animals.295 Hyenas Hyenas have tremendously strong jaws, with a bite force of 1000 psi, and can leave teeth marks in forged steel (Figure 56-4). They have been known to amputate limbs and behead small children.210 The hyena frequently attacks humans in Africa, and, in certain areas in which locals leave dead or dying people in the bush for predators to eat, hyenas become accustomed to the taste of human flesh. Hyenas forage around campsites and villages, and are wary of awake people. During the summer months, when Africans sleep outside of their huts, many are assaulted with one clean, massive bite that removes the face or the entire head. Young children have been dragged from their huts while sleeping when a family member leaves briefly without latching the door, and it is common for the hyena to injure or amputate the thumb of a sleeping victim as it drags the victim (by the thumb) to a more convenient place for consumption.2 Campers are frequently bitten on the face or limbs while they sleep at night, particularly if they have left food nearby. Victims usually survive but are massively disfigured. In some parts of Africa, the hyena is a more consistent maneater than the leopard or lion. Other Canines In Australia, during a 5-year period, dingoes that had been habituated to people were responsible for 224 attacks on humans that required medical treatment and for several fatal attacks on children.272 However, dingoes are disappearing from Australia quickly183 and in general pose little threat to humans. Jackals are found in Africa, Southeast Europe, and Asia. Jackal attacks are typically only from rabid animals. In Sri Lanka in 2007, one village reported four different attacks by a jackal that was acting abnormally.281 In many areas of the developing world, the main concern with jackals is transmission of rabies to domestic dogs. Two other canines that traditionally hunt in packs are the cape hunting dog of Africa and the Indian “devil dog.” Although both are feared in their respective environments, typically they do not deliberately attack humans.

FIGURE 56-4  African hyena. (Courtesy Kappa Meadows, MD.)

FELINES Adult cats have 30 permanent teeth, arranged in rows of 16 upper and 14 lower. The upper teeth overlap the lower, resulting in an overbite; this helps the animal lock its teeth into prey and exert twisting and tearing forces. The feline bite is much shorter and more rounded, and their incisors are narrower and sharper compared with the bite and teeth of a canine. Big cats typically attack from behind and bite the neck and occiput of their prey in an attempt to maneuver their canine teeth between the victim’s cervical vertebrae and into the spinal cord.95,282,333 The goal of rapidly paralyzing the prey is also accomplished by a violent shake of the cat’s head, which fractures the cervical spine. In a study of fatalities from jaguar attack, 77% of victims were bitten on the nape of the neck, and one-half of the bites were made to the base of the skull.95 In 20% of cases, the killing bite was to the head, with at least one canine piercing the skull or ear canal. Cheetahs prefer to attack the throats of their prey, crushing the larynx and strangling the victim; this method is also used by lions and leopards.209 In addition, big cats claw their prey and produce deep, parallel, incised wounds. Several victims have died of exsanguination without evidence of strangulation or cervical spine injury.95,282 Because of the growing propensity for people in developed countries to keep exotic animals as pets or raise them for profit for hunting purposes, injuries by big cats can occur anywhere. Wound care is the same as for other species, with special attention paid to evaluation for major internal injury. In particular, observe for penetration of deep structures of the cranium and neck, and rule out injuries of the cervical spine and deep cervical vessels (see Box 56-5).95 One victim with an apparently trivial puncture wound after a bite to the neck from a pet cougar was discharged from the emergency department.190 Within hours, her voice was hoarse; on return, she recalled that the cougar had shaken her in its jaws when it bit her, and air was found in the prevertebral and retropharyngeal spaces on radiographic examination. If a big cat is encountered in the wild, humans should not run but instead stand their ground; running will provoke an instinctive response from the cat to chase. Humans should make themselves look as large as possible, such as by raising arms and jackets over the head. Shouting and acting aggressively may deter an attack. Humans should not turn their backs or crouch when confronted by a big cat. However, as with other large animals, fighting back once an attack has begun may cause a cat to abandon the attack.85 Like domestic cats, big cats usually carry Pasteurella as normal flora. Because of the deep penetration of their large teeth, Pasteurella septic arthritis, meningitis, and other serious deep infections can occur.143 Cat-scratch disease (Bartonella henselae), which is common with domestic cats, may also be transmitted by wild cats; it has been isolated in puma and bobcat populations in the Americas.90 Tigers Tigers (Panthera tigris) are members of the Felidae family, and the largest of the four big cats in the genus Panthera. They are territorial and solitary animals that need large areas of habitat to support prey demands. This—as well as the fact that they are endemic to some of Earth’s most populated areas—can lead to increased opportunities for major conflict with humans. One hundred years ago, the tiger population in India was as high as 40,000. A 2008 government census report estimated the tiger population at 1411, down from 3642 in 2002, largely as a result of diminishing habitat and poaching. Tigers are a major threat to human life in the cats’ native regions.222 Although the number of tigers in the world is dwindling rapidly, historically they have been the number one animal killer of humans (see Table 56-2). Nonetheless, man-killing almost invariably results from stress (e.g., wounds, old age) or lack of natural prey and habitat that forces the animal to prey on humans. A tiger subsisting solely on human meat would have to kill approximately 60 adults per year; documented cases in selected regions have approached this rate over periods of up to 8 years. 1113

CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

characteristic crushed and macerated tissue and should be debrided carefully. Other treatment should follow the same guidelines as for victims of domestic canine attack. It is speculated that most wounds are attributable to the dominant animals of a pack. Differences in bite-mark patterns may be attributed to differences in genetics, training, breeding, socialization, and impetus of attack between wolves and dogs.344

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 56-5  African lion. (Courtesy Cary Breidenthal, RN.)

Unlike leopards, tigers rarely enter human settlements, preferring to remain on the outskirts. Maneating tigers in India between 1906 and 1941 ate an estimated 125 persons each, and one had killed 436 persons. However, compared with lions, tigers are not thought to become exclusive man-eaters; rather, they are opportunistic man-eaters in lieu of plentiful natural prey, and tiger biologists hypothesize that these animals have become unafraid of man.222 Over the last five centuries, an estimated 1 million people have been eaten by tigers. During the nineteenth century, the tigers’ toll in India averaged 2000 victims per year. From 1930 to 1940, the annual number never dropped below 1300. During the late 1940s, this rate dropped to 800 per year, where it remains. In other regions, rapid habitat loss as a result of climate change has caused an increase in tiger attacks in the Sundarban Islands of Northern India. In this region, seven fisherman were reported to have been killed by tigers during the first half of 2008.125 Adult tigers are so powerful that their human victims are often killed instantly. It is not unusual for a limb to be severed with a single bite,117,205 and a tiger’s swiping blow to the human head can cause skull fracture.270 Like many big cats, tigers typically strike without warning from behind, biting the head and neck and often shaking the head violently so that it severs the victim’s spinal cord.193 Lions The lion (Panthera leo) is grouped with the four big cats of the genus Panthera (Figure 56-5). Despite their appearance and reputation, lions are not as feared or respected by experienced hunters as are tigers (Figure 56-6). Lions are primarily scavengers, making fewer original kills than hyenas do. Conversion to maneating has been blamed on drought, famine, and human epidemics in which large numbers of corpses are abandoned in the bush. Although some consideration has been given to the theory that infirm lions are more prone to maneating behavior and although tooth decay may explain some

FIGURE 56-6  Lion. (Courtesy Kappa Meadows, MD.)

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FIGURE 56-7  Lion attack victim. This African victim was rescued by bystanders as his head was in the lion’s mouth. His only injury was a degloving scalp laceration. (Courtesy Harold P. Adolph, MD.)

incidents, prey depletion in human-dominated areas is a likelier cause of lion predation on humans.256 In addition, there is an historic predator–prey relationship between Panthera and primate genus members, which suggests that maneating behavior is neither unusual nor aberrant.261 Lion attacks tend to cluster during harvest times and during periods when prey is scarce.254 Wounded or sorely provoked animals, usually in dense brush (Figure 56-7), kill the majority of hunters who succumb to lions. American and Tanzanian scientists report that maneating behavior in rural areas of Tanzania increased from 1990 to 2005. At least 563 villagers were attacked and many eaten over this period.254 Lions are estimated to eat 300 to 500 Africans per year, and rank second to tigers among man-eaters. During the late 1930s and early 1940s, three generations of a single pride in Tanzania were credited with between 1500 and 2000 human kills. A protected population of 250 Asiatic lions in India has attacked 193 humans, killing 28 between 1977 and 1991; biologists credit drought and lion baiting for tourist shows for this carnage.283 Lions that become man-eaters and subsist exclusively on human flesh require approximately 40 victims per year to stay alive. They usually kill instantly with one bite to the head or neck or with a swipe of the paw, which can break an ox’s neck. Lions have tremendous strength, and can easily carry a human victim for a mile without rest. A threatening gesture or shout may repel a lion, although a lioness guarding her cubs is more likely to attack. Experienced hunters find that, when a charging lion is faced head on and confronted, it will often turn tail and run. An intended victim who flees is more likely to be attacked. Many victims who survive the initial mauling die later of infection. Persons who have survived attacks state that it is unwise to struggle and that the cat should be allowed to chew on an arm or another extremity; with luck, it will lose interest and leave. Although most lions in captivity become passive and dull, circus and zoo lions periodically kill attendants; many such deaths have occurred when keepers accidentally have backed into or trod upon an animal. Leopards Leopards are the smallest of the four big cats in the genus Panthera (Figure 56-8). Like the other big cats, leopards suffer from a loss of habitat and hunting pressure that have reduced their range. Originally inhabiting wild land from Korea through Africa, leopards now exist primarily in sub-Saharan Africa, with isolated pockets across the Asian subcontinent. However, leopard numbers still top all others in the genus Panthera. Most attacking leopards have been previously wounded or attacked by a dog; when wounded, trapped, or cornered, a leopard is unpredictable and ruthless, attacking the first person within striking distance. Unmolested and in normal health, the leopard is a shy and nervous animal with a marked fear of humans. Unlike a lion or tiger, the leopard relies on fast claw work and biting. Like the jaguar, the leopard may go for the neck (in an effort to sever the spinal cord) or attempt disemboweling by raking at the victim’s abdomen with its claws. The leopard

seems inclined to retreat when much resistance is offered; the chance of surviving a leopard attack is higher than the chance of surviving a lion or tiger attack. There is a documented report of a man armed only with a screwdriver who fought and killed an attacking leopard.198,199 Before the era of antibiotics, threefourths of people mauled by leopards died from wound infection; however, modern morbidity from these attacks is estimated to be less than 10%.25,92 Mauling by leopards is much more common than killing; estimated casualties are 400 per year, mostly in Africa. The leopard does not often turn into a man-eater; when it does, it attacks mainly children or sick adults. In the state of Bihar in India, leopards ate 300 people between 1959 and 1960.92 The maneating leopard of Rudraprayag in India killed 150 people between 1918 and 1926. Becoming increasingly bold, it eventually took its prey by banging down doors, leaping through windows, or clawing its way through the walls of mud huts. The Panar leopard killed more than 400 people after injury by a poacher made it unable to hunt normal prey.169 Like maneating lions, maneating leopards completely change their normal hunting patterns when the prey becomes exclusively human. Jaguars The jaguar is last of the four big cats in the genus Panthera and the only one native to the Americas; it is not known to be a man-eater. However, attacks do occur. In February 2007, a zookeeper in the United States was mauled to death by a jaguar.227 In January 2009, a Maryland zoo worker at a private zoo was badly mauled.139 There have also been undocumented reports of jaguar attacks in the jungles of South and Central America. The jaguar has an exceptionally powerful bite, even relative to other big cats. It employs a variation of the deep throat bite and suffocation technique employed by other Panthera. Using its canine teeth, it pierces directly through the temporal bones of the skull between the ears of its prey, piercing the brain.124 Cougars The North American cougar (Puma concolor), also called mountain lion or puma, is a clever and shy cat. It is the most widely distributed large animal on the American continent, and the second biggest cat in the Western hemisphere (after the jaguar), although it is more closely related to smaller cats. Cougars are encroaching with increasing frequency into populated areas of the western United States; this is probably because of human expansion into the wilderness and an increased population of protected cougars.192 The current cougar population in Oregon is estimated to be more than 5700,249 and the U.S. population of cougars is estimated at 16,000.321 Humans live, exercise, or picnic in cougar country with increasing frequency.309 Thus, modern suburban dwellers (who are typically ignorant of wild animal behavior) are now in regular close contact with cougars in their homes and parks, whether they know it or not. In North America between 1890 and 2004, there were 88 confirmed cougar attacks on humans, resulting in 48 nonfatal

Bobcats The North American bobcat (Lynx rufus), found throughout the United States, is probably named for its short tail, which is only 15.3 or 17.8 cm (6 or 7 inches) long. Its natural range extends from Canada to Northern Mexico, and expands in more northern latitudes. The bobcat has long legs, large paws, can weigh up to 13.6 kg (30 lbs), and is equipped to kill animals as large as deer. Although it is unusual, bobcats occasionally attack humans. In most cases, the bobcat is rabid and unusually aggressive. In 2000, a Minnesota woman reported suffering puncture wounds to her hand and arm that were consistent with the bites of a bobcat. Another woman was the victim of a witnessed bobcat attack in Big Bend National Park.44 In this case, although experts believed that the animal was behaving normally, the victim was empirically treated for rabies exposure. A hunter sustained injury to the eye and ocular adnexa requiring surgical repair after a bobcat attack.173 Two people were attacked by a rabid bobcat in 2008 in Arizona while hiking in the mountains, suffering puncture wounds and scratches; the bobcat was described as unusually aggressive, and pursued the couple up a hill.132 A man in Florida reported being attacked by a rabid bobcat on his front porch, where he was clawed and bitten until he managed to strangle the animal.215

PRIMATES The Primates order is divided into two main groups: the prosimians, which have characteristics most like those of the earliest primates, and the simians, which is comprised of monkeys and apes. Simians are further divided into the New World monkeys of South and Central America and the Old World monkeys of Africa and Southeastern Asia (Figures 56-10 and 56-11; Figure 56-11, online).

FIGURE 56-9  Victim of cougar predation and fatal mauling. (Courtesy Ben Galloway, MD.)

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FIGURE 56-8  Leopard. (Courtesy Kappa Meadows, MD.)

injuries and 20 human deaths.13 More people have been attacked since 1975 than during the entire previous century,5,21,131 and most attacks occurred in the Western United States and Canada. Throughout the United States, cougars ranked sixteenth in recent years as an animal-related cause of deaths, just behind jellyfish and goats.275 In California, no attacks occurred from 1925 until 1986, when two children were attacked in a regional park in Southern California,190 and the first cougar attack in 34 years occurred in New Mexico in 2008.239 Victims jogging and biking may evoke a predatory response. Young animals that are forced out by adults and must find their own territory are the most frequent attackers of humans,192 and children tend to be the preferred victims: 64% of attacks and 86% of fatalities involve children.35,182,186 There has been only one alleged report of a cougar as a primary man-eater, but cougars commonly consume victims of their attacks (Figure 56-9).32,282 The cougar hunts like a domestic cat: crouching, slinking, sprinting, pouncing, and then breaking the neck of the prey. Neck, head, and spinal injuries are common and sometimes fatal. Like many potentially dangerous wild animals, the cougar can often be scared off by the victim’s aggressive behavior, even after the attack has begun.170 In 2002, a man fought off and killed an attacking cougar with a 7.5-cm (3-inch) pocketknife.328

PART 6  ANIMALS, INSECTS, AND ZOONOSES

The number of humans owning monkeys as pets has increased, although many owners do not appreciate the danger such a pet can pose. Even the most docile pet monkey has wild animal tendencies and instincts and can attack without warning. According to People for the Ethical Treatment of Animals, there were 450 incidents involving primates that were kept as pets or in circuses between 1990 and 1992. These incidents resulted in two human deaths and more than 140 human injuries.

HERBIVORES AND UNGULATES

FIGURE 56-10  Monkeys groom each other at Swayambhunath, a holy temple complex in Kathmandu, Nepal. Every year, tourists are bitten by monkeys who mingle in crowds begging for food. (Courtesy Luanne Freer, MD.)

Monkeys and other primates inflict vicious bites that virtually always become infected, despite use of prophylactic antibiotics.154 Although in developed countries human–primate conflict is a problem limited to laboratory workers, in tropical developing countries, large apes (e.g., baboons) are both at large and often aggressive. Weighing up to 40.8 kg (90 lbs), a large baboon can be dangerous and lethal, particularly when the animal has frequent contact with humans and loses fear of them. There are multiple reports of baboon attacks in South Africa against visitors, typically when the baboon is foraging for food.61 There have been numerous recent reports of packs of wild monkeys driven out of the jungle by hunger, attacking humans who get in the way of food sources.278,285,307 Feral macaque populations have been reported in regions of Texas and Florida.252 Monkeys often bite hands and have been known to amputate parts of fingers. A literature review revealed 132 cases of simian bites in which Bacteroides, Fusobacterium species, and Eikenella corrodens were isolated from some of the wounds.154 Three victims of simian bites with infected wounds grew diverse bacteria, including β-hemolytic streptococci, enterococci, Staphylococcus epidermidis, and Enterobacteriaceae.154 At the present time, simian bites should be considered high risk and treated in the same manner as human bites. Old World macaque monkeys (i.e., rhesus macaque, cynomolgus, and other Asiatic macaque monkeys) are often infected with simian herpes virus (B virus). Transmission to humans is rare, but the risk is real, especially for animal control and laboratory workers.114,240 As with rabies, local wound treatment may be important; of 61 persons bitten by probably infectious monkeys who received wound cleansing with cetrimide and iodine solution, none became infected.320 The mortality rate for B virus is 80% without treatment; through 2002, there were 26 documented cases of B virus infection in humans and 16 deaths. Twenty of the victims developed some degree of encephalitis. The most recently documented case occurred in 2008 and involved a woman who was bitten by a vervet monkey in the Democratic Republic of the Congo in Africa (see Chapter 59).244,331 The wild gorilla, despite its reputation and appearance, is shy and avoids humans. Although it may charge in defense, it seldom attacks, and can be easily confronted and forced to retreat. When a gorilla attacks, it typically takes one bite and runs. In Africa, gorillas are responsible for two or three attacks per year, none of which is fatal, and few of which are severe. Chimpanzees occasionally attack humans, but usually only if provoked or cornered. Rare instances of chimpanzees eating children and women have been reported. The baboon is responsible for one to two attacks per year, almost all in South Africa; these are usually by pets. Occasionally, maneating has been reported. The incidence of hunting and meat eating by these animals has increased over the last century, perhaps paralleling the evolution of humans into hunters and meat eaters.92 1116

Wild Swine Wild pigs are more likely to inflict injury than their domestic counterparts. With a population of over one-half million roaming the French countryside, wild pigs cause crop loss and occasionally gore and bite humans.213 A typical wild boar attack can result in multiple penetrating injuries to the lower part of the body caused by the boar’s tusks (Figure 56-12, online). In an unusual incident, an Indian laborer was gored from behind by a boar, which then returned and attacked his head while he was on the ground; the man died of severe craniofacial injuries.216,292 Domestic pigs can easily become feral, and such populations often revert to the behavior and appearance of a wild boar. In the United States, feral pigs—some weighing up to 181.4 kg (400 lbs) with 10.2-cm (4-inch) tusks and prolific breeding qualities (i.e., some litters of up to 19 have been reported)—are experiencing explosive population growth. More than 1.5 million wild swine roam the state of Texas, and motor vehicle collisions as well as attacks on humans are increasing.54 As of 2008, it was estimated that the population of 4 million feral hogs caused approximately $800 million worth of property damage per year in the United States.51 Swine wounds should be treated as high risk for development of infection, warranting broad-spectrum prophylactic antibiotics (perhaps parenterally) and close follow up if the victim is not admitted to a hospital. African Buffalo Known as one of the “big five” (i.e., the five most difficult African animals to hunt on foot: buffalo, lion, elephant, black rhino and leopard), African buffalo (Syncerus caffer) gore and kill more than 200 people each year. The unprovoked African buffalo usually does not attack. However, when provoked (i.e., shot or cornered), it charges, is difficult to avoid or stop, and can hook the victim 3 m (10 feet) into the air with its horns (Figure 56-13). Buffalo that charge humans are usually old solitary bulls that have left the safety of the large herds, most often because of wounds from poachers’ snares or spears, or from lion attacks. The buffalo is also wily and intelligent; wounded buffalo may lie in wait for trackers, or may double around and come up behind hunters on the trail, often with fatal consequences for the humans (Figure 56-14, online). One hunter was treed by a buffalo but could not get his feet high enough to keep them

FIGURE 56-13  African water buffalo with calf. (Courtesy Cary Breidenthal, RN.)

American Bison Brought back from the brink of extinction, a free-ranging herd of North American bison (Bison bison) with a fluctuating population of 2300 to 4500 now lives on land in and around Yellowstone National Park and is responsible for an average of three tourist injuries per year.237 Fifty-six injuries and three deaths were documented from 1975 to 1993 in Yellowstone as a result of bison–human interaction.97 Despite warnings to avoid approaching these animals any closer than 7.6 m (25 feet), most attacks involve close human approaches to obtain photographs. The mechanism of injury in bison attack is usually penetrating injury, with punctures from goring by horns and blunt injury caused by being tossed in the air and falling or being butted by the animal’s massive head (Figure 56-15). Goring injuries most frequently involve the buttocks or posterior thighs as the victim turns away from the bison to flee (Figure 56-16).97 Gored abdomens and evisceration have also been reported. Despite the inevitable contamination of these deep punctures, wound infection is rare if careful operative irrigation and debridement with closure are combined with broad-spectrum prophylactic antibiotics. Cephalosporins were used in most cases in one series of reported injuries.97 Elephants The elephant (Proboscidea elephantidae) can be one of the most dangerous wild animals and was, until recently, probably the greatest killer of hunters. It is the largest land animal (Figure 56-17), and there are three living species: African forest, African bush, and Asian (Elephas maximus). The annual human death toll related to these animals in Central Africa is probably between 200 and 500.92 Most injuries occur when humans accidentally approach elephants too closely, which the animals interpret as a threat. However, elephants turn rogue from time to time and deliberately attack and kill humans (Figure 56-18, online). As

FIGURE 56-15  American bison. (Courtesy Luanne Freer, MD.)

FIGURE 56-16  Wound from bison goring. (Courtesy Karen Hansen.)

humans and elephants compete for the same space and humans despoil and devastate forests, conflicts increase (Figure 56-19, online). A few rare stories suggest that elephants may actually be maneaters. One of these instances occurred in 1944 at the Zurich Zoo. Elephants that are captive in zoos and circuses may cause deaths while temporarily deranged. Since 1990, captive elephants have killed 39 humans and injured more than 100 worldwide.259 In 2007, a domesticated elephant in Vietnam gored his two handlers to death after they forced him to work without eating.171 Some experts theorize that elephants are capable of vindictive motivation for attack.179,296 In Africa, groups of young elephants have attacked villages in what is thought to be revenge for the destruction of their society by massive hunting done during the 1970s and 1980s.172 India is home to most of the world’s 40,000 Indian elephants (sub sp. Elephas maximus indicus), which reside throughout the subcontinent. In the Indian state of Jharkhand, 300 people were killed by elephants between 2000 and 2004, and, in Assam, 239 people have been killed since 2001.179,296 Elephants kill about 50 people each year in Sri Lanka. Such encounters force some families to sleep in trees, and elephants in one area with a human population of only 25,000 kill at least four people a year.18 In 2004, 22 people were killed in Assam by rogue elephants that repeatedly trampled homes and ate local crops. Reportedly, the elephants were also seeking rice beer, for which they had developed a taste.17 Elephant attacks have become so common that a new statistical category known as human–elephant conflict has been created by elephant researchers.296 Elephants kill by trampling, goring with the tusks, or striking and throwing with the trunk. After the victim has been run over or skewered with the tusks, the elephant then crushes him or her by kneeling (Figure 56-20). Elephants have been known to use weapons during their attacks: a villager who retreated safely up a baobab tree was hit by a tree branch that a bull elephant

FIGURE 56-17  African elephant. (Courtesy Kappa Meadows, MD.)

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clear of the animal; the buffalo repeatedly hooked the man’s feet with his horns, eventually cutting them so that the hunter bled to death while still hanging in the tree. In another anecdotal series, a single buffalo injured several humans in one day; all of the wounds were impaling injuries through the anus.2 When the victim is prostrate, the buffalo gores into the ground with its horns and the heavy horny boss across its forehead and then whips its head from side to side, disemboweling the victim with the sharp horn tips. The horns are always covered with mud, so goring wounds may be heavily contaminated. However, victims who do not have major traumatic injuries generally do well.291 Water buffalo were once a common wild animal on the Indian subcontinent and in Southeast Asia, but are primarily domesticated work animals in these regions today. Domesticated animals pose little threat to humans, but are still capable of attack if provoked. A water buffalo attacked and gored a man to death in Australia in 2005, the first recorded death from a water buffalo in 12 years in that country.317 The buffalo had been acting strangely for several weeks, charging people and entering towns, and was thought to be stressed because of drought in the region.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 56-20  Asian elephant. (Courtesy Luanne Freer, MD.)

had picked up in its trunk and used as a club. Elephants frequently rip the victim’s body apart and scatter the pieces, later covering them with grass and branches. Another elephant tactic is to toss a victim into the trees or straight over his or her back; a number of victims have survived this experience. Some hunters pursued by elephants have diverted them by throwing off items of clothing. Hippopotami The hippopotamus (Hippopotamus amphibius) is a frequent killer in Africa (Figure 56-21). Its placid appearance in zoos belies its activity and personality in the wild; they are ill tempered at best, and have been known to attack crocodiles. A hippopotamus can run at speeds of up to 72.4 km/hr (45 mph) on land. It will attack boats and people in the water if it feels trapped (e.g., between a boat and deep water) or if its calf is threatened. Hippopotami graze on land and habitually run along established narrow tracks back to the river, mostly at night but also in the day. They are not known to change course when challenged, and humans who make the mistake of staying in their tracks may be trampled. With its large canine teeth, a hippopotamus can chop canoes (and the people in them) in half, as it does several times a year on the Zambezi River in Zimbabwe. Surviving a hippopotamus attack is uncommon. Injuries are typically very extensive and can include significant crush injuries to internal organs and other tissues as well as long bone fractures.120,207,265 Moose and Elk Moose (Alces alces) are large and potentially aggressive animals, especially during fall rutting and spring calving seasons. When moose are fed by humans, they become more aggressive when food is no longer available.8 Moose consider dogs predatory and will attack and kill them without other obvious provocation. If

FIGURE 56-21  Hippopotami. (Courtesy Kappa Meadows, MD.)

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FIGURE 56-22  Toddler victim of a moose attack. (Courtesy Luanne Freer, MD.)

the rump hairs are raised, ears laid back, or the moose is licking its lips, it is likely to charge. The subject of the attack should get behind a large solid object for protection. If knocked to the ground by a moose, a victim should roll into a ball, protecting his or her head with the hands and arms, and remaining still until the moose leaves.8 In 1995, a man was killed by a moose in urban Alaska when he approached a cow with a calf who had been harassed by students throwing snowballs.238 Most human injuries caused by moose result from mooserelated motor vehicle collisions, which are quite hazardous in New England and Sweden.46,129 In a New England report, it was stated that an average of two persons per year are seriously injured when their vehicle strikes a moose, usually after dark; 70% of those injured have head and facial injuries, and 26% have cervical spine injuries.129 The mortality rate in this series was 9%, and morbidity declined with the use of seat belts and rear seat location. Each year in British Columbia, it is estimated that three people are killed and an additional 368 injured in wildlife collisions (i.e., deer, moose, and elk); 17,200 animals are killed by these collisions as well312 (Figure 56-22). Similar to moose, bull elk may attack humans during rutting season, and cows may attack by butting and stomping when protecting their young.257 A study done in Michigan from 2002 to 2005 showed a less than 1% prevalence of Mycobacterium bovis in elk.245 Elk can also be carriers of Brucella abortus, which can be transmitted through direct contact with infected animals.279 Deer The deer population continues to grow in parts of the United States. As a reservoir of the tick that are vectors, deer may be credited with the increasing incidence of human Lyme disease.232 Block Island, a 17.7-km2 (11-mile2) island off of Rhode Island, reintroduced one buck and four does to its area in 1968, and had a herd of more than 1000 animals and 45 recorded cases of Lyme disease among residents as of 1997.232 Residents also report having been attacked by deer in their own yards. Deer rarely attack humans, but deer–motor vehicle collisions are quite common in densely populated areas. About 1.5 million deer–vehicle collisions happen each year in the United States, according to the National Highway Traffic Safety Administration93; those accidents cause about 150 deaths and $1.1 billion in property damage. More than 21,000 collisions occurred in Finland in one year, with the majority of events occurring during the first hour after sunset.164 One deer jumped through a window of a law office and injured an attorney,20 and another buck in rut carried a man in its antlers for 45 minutes, then pinned the man on the ground until he was rescued.39 A startled buck gored a child when the boy was feeding the animal; the antler penetrated the child’s axilla, lacerated his pulmonary artery, and caused death by exsanguination.128 Deer may bite, and, like other ungulates, may carry Pasteurella as oral flora. Female deer bite other deer when fighting. Males bite when testosterone levels are low; at these times, antlers are soft and pain sensitive, and cannot be used as weapons. Foreleg kicks are more common, because the

Rhinoceri The black rhinoceros has been represented as one of the meanest animals in Africa because it charges any moving object, including trains. A click of a camera, gentle movement, or scent is enough to induce a charge. Because the rhinoceros has poor eyesight but excellent hearing, it may well be running toward sounds to investigate them. Contrary to the popular belief that because of its nearsightedness it can be easily sidestepped, the rhinoceros can turn on a dime.91 At the end of its charge, it usually hooks right and left with its horns, and is generally satisfied with tossing the victim high (i.e., 3.7 m [12 feet]) in the air. However, like so many large wild animals, it probably does not desire confrontation. Rhinoceri often flee after they have identified a sound as originating from something dangerous (e.g., a human), and persons who have fallen while running from a charge have been investigated with a few typical snorts and then ignored. However, severe injuries can result if the human fails to get out of the way of a rhinoceros. Black rhinoceri in Africa kill a handful of people each year.120 As with the hippopotamus, injuries and death may have more to do with being in the path of a very large and fastmoving object than with the animal’s malicious intent. The white rhinoceros is typically docile; its attacks on humans are extremely rare. Tapirs The tapir (Tapirus terrestris) lives in the rainforests of South America, Central America, and Mexico. The female reaches a length of up to 2 m (6.6 feet) and a height of up to 1 m (3.3 feet), and weighs up to 200 kg (441 lbs). Tapirs are herbivorous and generally docile. They seek refuge in brush when threatened or submerge themselves in water until the threat is gone; however, they may defend themselves by biting with their powerful jaws and teeth. A tapir bit off the arm of a zookeeper in 1998 who came between the usually docile animal and its calf,114,180 and a man died of exsanguination from arm and neck lacerations after a tapir attack in Brazil.163,338 The Environmental Minister of Costa Rica sustained a tapir bite in Corcovado National Park in 2006; this attack also involved a female defending its calf.276 Other Wild Herbivores Other wild species, such as the giraffe, may turn rogue, but this is exceedingly rare. The black wildebeest has killed one or two zookeepers, as have the spiral-horned kudo and bushbuck. Other antelopes have killed or wounded hunters or zookeepers with their sharp horns. Zebras are known to bite tourists who approach too closely.319

BEARS Bears are among the most feared and powerful predators on Earth, yet the incidence of bear attacks on humans is small compared with other animals discussed in this chapter. However, the scientific literature about bear behavior and human interactions is more plentiful than that about, for example, tiger or alligator attacks. Chapter 57 is devoted to a discussion on bear attacks (Figure 56-23, online).

In remote areas of Australia, the odds of hitting a kangaroo are so high that residents fit their vehicles with “roo bars” to deflect kangaroos off of the front of the vehicle.4 In 2004, there were several unprovoked kangaroo attacks in Australia, which led to speculation about a rabies-like disease affecting marsupials; however, there is no published evidence to support this theory. The only well-documented kangaroo attack resulting in a fatality was in 1936, when a hunter was killed trying to separate his dogs from a fight with a kangaroo. Erratic kangaroo behavior may also result from extreme thirst and hunger.336 Kangaroos attack using a combination of kicking and trampling with their powerful hind legs. They are also capable of delivering slashing wounds with their feet.

LARGE BIRDS Ostriches (Struthio camelus) are responsible for one to two deaths per year, mostly in Africa, where they are raised commercially19 (Figure 56-24, online). Most of the fatal attacks involve kicks to the head and abdomen. Disembowelment, eye injuries, and esophageal perforations have all been reported.83,189,234 The ostrich (Figure 56-25) can kick only forward, but when it does, a sharp toenail flicks out like a switchblade and can penetrate the abdomen. Because the ostrich can easily outrun a human being, the only protection is to lie prone to protect against disembowelment and to cover the neck to protect against pecks. Eventually, the ostrich loses interest and allows the victim to escape. The cassowary, which is common in New Guinea, can easily disembowel a hunter with a single kick from its long, sharp toe claws. Birds of paradise have been found to secrete venom on their feathers, although cases of human toxicity from this have not been reported and the phenomenon is little studied. The emu is a flightless bird native to Australia that may weigh 45.4 to 68 kg (100 to 150 lbs). It is usually docile, but when cornered or frightened may lacerate a human handler by kicking.185

RACCOONS Raccoons (Procyon lotor) are medium-sized animals native to North America that adapt well to a wide range of changing habitats. The raccoon is at home as much in urban settings as in deciduous forest ranges, and can be found across the United States. A population was established as a game animal in Germany during the mid-20th century, and is now well established in several northern European countries.337 As raccoons expand their range to include urban settings, conflict with humans will increase. Raccoons are on occasion kept as pets. In 2009, a young boy was bitten by an immature raccoon housed in a box.217 Raccoons tend to be opportunistic hunters, and keeping food and garbage cleaned up and stored properly can eliminate potential encounters. Of the 6940 documented animal rabies cases reported in the United States in 2006, 2615 (37.7%) were in raccoons,47 which represents the highest carrier rate for rabies.196 In the United

KANGAROO Kangaroos (family Macropodidae) are the largest living marsupials in the world, weighing up to 79.4 kg (175 lbs). They use their tails for balance when they jump, and can leap almost 9.1 m (30 feet) forward and 2.4 m (8 feet) high. They are active in the evening and at night, when groups of kangaroos, called mobs, forage on grasses and other plants. A university study from New South Wales reported that kangaroos account for 60% of all animal-related automobile crashes in Australia resulting in fatalities and for 40% of automobile–animal accidents resulting in injuries.224 From 1996 to 2006, there were 2100 kangaroo–vehicle collisions and 13 human deaths from kangaroo–vehicle incidents.

FIGURE 56-25  Ostrich. (Courtesy Kappa Meadows, MD.)

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deer stands on its back legs. Because deer have a dental pad rather than upper incisors, bites are rarely serious and are usually directed at the arms or back, which are normally well covered by clothing. These bites are usually single nips.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

States, large raccoon rabies epizootics in New England and the middle Atlantic states are spreading, and most rabies-positive animals are captured near private homes.298,340 In 2003, raccoon variant rabies caused a human death in the United States, although the route of transmission was unclear, because there was no bite.70 Because rabies is so common in raccoons, rabies PEP should be strongly considered for victims of attack or unusual close contact. Some other important diseases associated with raccoons are leptospirosis, listeriosis, tetanus, and tularemia.212 Raccoons are the definitive host of Baylisascaris procyonis, a zoonotic nematode parasite that may cause larva migrans syndromes in humans.353

PORCUPINES Porcupines are a member of the order Rodentia, further divided into New World species (12 identified) and Old World species (11 identified). They are rarely reported to bite, but their quills may become embedded in the skin of humans. Quills are released on contact, or can be dropped out when the porcupine shakes its body, but cannot be projected at attackers. Because of the structure of quills, they not only embed themselves and are extremely difficult to extract, but can migrate as much as 25.4 cm (10 inches) under the skin. The average porcupine has 30,000 quills, which range from less than 2.5 cm (1 inch) to 10.2 cm (4 inches) in length. The quills are barbed, and their cores are spongy; if they are not removed from a “quilled” victim immediately, they absorb body fluid and expand, causing them to flare farther outward. Thus, each movement of the victim’s muscles or body helps a quill embed deeper. Anecdotally, such migration has led to internal organ damage and death in humans. Quilled dogs have suffered a variety of illnesses, including brain penetration as a result of migration105 (Figure 56-26). Infection seldom results, because quills have mild antiseptic properties, presumably to protect the porcupines, which sometimes impale themselves. No medical reports of appropriate human treatment or complications of porcupine quill injuries exist, although anecdotal reports of human tetanus from porcupine quill puncture have come from Africa.2 Most veterinarians remove quills from animals by simple extraction; the same technique is probably sufficient in humans after local anesthesia and disinfection of the skin.

COATIS The ring-tailed coati, Nasua nasua, is widely distributed in the Americas. It is a social animal whose omnivorous diet includes insects, fruits, and small vertebrates. There is only one published report in the medical literature describing coati attack; two children in their home were injured by a startled coati, causing skin lesions from deep scratches and bites45 (Figures 56-27 and 56-28).

FIGURE 56-26  Domestic dog impaled with porcupine quills. (Courtesy Luanne Freer, MD.)

1120

FIGURE 56-27  Coati bite. (Courtesy Luanne Freer, MD.)

QUOKKAS The quokka is one of the smallest members of the wallaby family, which resides in Western Australia. The quokka typically only bites humans who attempt to feed or pet it. Bites usually occur on the finger or hand. On Rottnest Island, Australia, quokka have been known to steal food after breaking into homes. The island’s infirmary reported 60 quokka bites in 2006.119 Despite the presence of mixed coliform bacteria in quokka mouth cultures, the incidence of bite-wound infection in this series was zero.221

OPOSSUMS The American opossum (Didelphis virginiana) is a non-native species that has adapted to urban living and presents difficulties for animal control agencies. It inflicts bite injuries both when hunted for food and when accidentally provoked while handled in captivity. Opossums compromise a major reservoir of endemic typhus in Los Angeles County in California.101 Aerobically cultured organisms from the mouths of seven wild opossums included streptococci, coagulase-positive and coagulase-negative staphylococci, Aeromonas species, Citrobacter freundii, Eikenella corrodens, and Escherichia coli.175

SKUNKS Skunks are small mammals belonging to the family Mephitidae, order Carnivora. They are capable of secreting a strong, foulsmelling odor. A skunk’s most frequent means of defense is spraying the secretions of its anal sac. A skunk that is ready to

FIGURE 56-28  Coati. (Courtesy Luanne Freer, MD.)

BATS Bats are mammals in the order Chiroptera. There are about 1100 species worldwide, which comprises 20% of all classified mammal species.345 Bats carry a large number of zoonotic pathogens, including rabies, severe acute respiratory syndrome, and possibly Ebola viruses.148 Less than 1% of all bats carry rabies. However, the few cases of rabies reported in the United States each year not caused by dogs are usually caused by bats.220 Bats infected with rabies are clumsy and have difficulty flying, making it more likely they will come into contact with humans. Vampire bats are a vector of rabies in Central and South America; 177 cases were reported from 1980 to 1990, with 27 of these cases in Brazil.30 Sometimes small “epidemics” of bites occur in isolated villages in the jungle, as in one outbreak of 26 bat bites in Honoropois, Brazil; all victims were treated with rabies prophylaxis, and no clinical human rabies was reported.30 In 2004, a rabies outbreak from vampire bats occurred in Columbia, resulting in 14 human deaths.324 Such clusters of attacks may be triggered by human destruction of wild or domestic hosts of the bats (e.g., pigs).219 Vampire bats feed at night on animal blood, including that of humans, by making an incision in the skin to lap up the blood from the victims’ earlobes, forehead, fingers, or toes. One bat can eat a maximum of 1 oz of blood per night. A cave of 1000 bats needs 15 gallons of blood each night, which amounts to more than 5750 gallons per year.91 Protection against vampire bats is effectively achieved with the use of mosquito nets. Insectivorous bats (e.g., free-tailed bats) are noteworthy for the nearly undetectable bite wounds that they leave on their victims.147 All bats should be considered high risk for rabies, and contact, even with captive “pet” bats, should be avoided. The known pathogenesis of rabies and available data suggest that nearly all cases of human rabies attributable to bats were transmitted by bat bites that were minimized or unrecognized by the victims. Non-bite transmission of rabies is very rare, and aerosol transmission has never been well documented in the natural environment.147 Some situations mandating rabies prophylaxis are rather bizarre and reveal more about human nature than about rabies or bats. For example, rabies prophylaxis was initiated after a patient dunked a dead bat in his beer, chewed on the bat’s ear, and then drank the beer.115 In a similar case, prophylaxis was needed when a miner swallowed a live bat on a bet.42 Most bats have small teeth that cannot penetrate human skin, so the risk of bacterial wound infection is low.

States secretes a protein venom from its maxillary venom glands and injects it with the lower incisors. The venom may cause edema, a few days of burning sensation, and pain that lasts up to 2 weeks.78 No specific antivenin is available, and treatment is symptomatic. No bites from this species have been reported since the 1930s. A similar venom is possessed by the European water shrew (Neomys fidiens) and the primitive Cuban insectivore (Solenodon paradoxus).56 Documented bites from these animals are exceedingly rare. A second type of venomous mammal is the male platypus (Ornithorhynchus anatinus), which injects venom from a hollow spur in its hind leg. This venom resembles viperine snake venom and causes local pain, edema, and lymphangitis.56 The pain can be excruciating and unresponsive to intravenous narcotics. Regional nerve block has been reported to be effective in combination with limb immobilization.131 Localized edema also occurs; however, no specific treatment is available, and the exact pathophysiology is unknown. Functional recovery may be delayed for up to 3 months. The echidna or spiny anteater possesses a similar spur and venom, but envenomation has not been reported.137

LARGE REPTILES (See Chapters 54 and 55) Historically, the Nile crocodile (Crocodylus niloticus) has accounted for 1000 human deaths per year in Africa91 (Figure 56-29, online). Most attacks take place in the water, where crocodiles are accustomed to scavenging for dead, sick, and deformed human infants tossed into the water to be disposed of by these reptiles. The crocodile has tremendous grip strength and locks this grip by slotting two lower teeth into holes in the upper jaw. When a crocodile is unable to drag the victim completely underwater, it may grasp a limb and then spin over until the limb is detached. During a 10-year period in Australia, there were 16 attacks and 4 fatalities caused by crocodiles; most victims were swimming or wading at night, and alcohol ingestion was present in one-half of them.226 Wound infections with Aeromonas hydrophila, Pseudomonas pseudomallei, and Proteus, Enterococcus, and Clostridium spp. were reported in 6 of 11 survivors in this series.226 In Malawi, over a period of 4 years, 60 victims were admitted to hospitals after injury by crocodiles; 40% had serious injuries resulting in permanent deformity, and one person died from sepsis.326 The American alligator (Alligator mississippiensis) is thriving in the southern United States, and its habitat is so greatly threatened by human expansion that incidents of alligators appearing in suburban backyards and swimming pools are now common (Figure 56-30). Attacks on children and pets are increasing, with

VENOMOUS MAMMALS Only two types of venomous mammals are known. The shorttailed shrew (Blarina brevicauda) of the northeastern United

FIGURE 56-30  Alligator. (Courtesy Stuart Coleman.)

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spray directs its hindquarters toward the enemy, with its feet firmly planted and tail straight in the air, often stamping the front feet in warning. The spray is accurate to 4 m (13 feet), and, contrary to popular belief, can be discharged when the animal is lifted by its tail.113,339 Skunk musk causes skin irritation, keratoconjunctivitis, temporary blindness, nausea, and occasionally convulsions and loss of consciousness.137 The chief component of the musk is butyl mercaptan; this can be neutralized by strong oxidizing agents, such as sodium hypochlorite in a 5.25% solution (household bleach) further diluted 1 : 5 or 1 : 10 in water. The chlorine forms odorless sulfate or sulfone compounds by oxidizing the mercaptan and breaking the sulfur free from the carbon chain. This solution can be cleansed with tincture of green soap and followed by a dilute bleach rinse. Other effective means of eliminating skunk odor include Summer’s Eve Douche or a mixture of 1 quart of 3% hydrogen peroxide, 0.25 cup of baking soda, and 1 teaspoon of liquid soap. Tomato juice is not an effective means of removing skunk odor. The CDC recorded 1494 cases of rabies in skunks in the United States in 2006; this was 21.5% of reported cases in all species.47,73 Skunks bite readily when captured, but, in one series, only 21 bites were reported for the entire United States for a 10-year period.110

PART 6  ANIMALS, INSECTS, AND ZOONOSES

127 attacks and five deaths reported in Florida from 1973 to 1990.174 Between 2001 and 2007, there were 13 alligator-caused deaths in the United States (mostly in Florida). All of the attacks involved some level of predation.136 The alligator causes crushing injuries to the torso and open extremity fractures, and may roll underwater with the victim, resulting in drowning. Blunt trauma may result from a strike by the animal’s massive tail. Prevention of alligator attacks includes avoiding touching or feeding the animal and not swimming at feeding time (dusk) with a dog or in waters with heavy vegetation.97 Komodo dragons (Varanus komodoensis), native to Indonesia, have also suffered from habitat and prey depletion. Members of the monitor lizard family, Komodo dragons have sharp teeth built for tearing and a venomous bite containing several different toxic proteins. Their bite is not designed for crushing; in fact, its force is similar to that of a house cat.29 The venom causes inhibition of blood clotting, paralysis, and hypotension leading to shock and loss of consciousness in bitten prey.6,141 With the discovery of venom action, the previous assumption that bacteria found in the dragon’s saliva and teeth cause death has been disproved. However, the saliva of the dragon, given its primary food source of carrion, predisposes its bite to contain diverse bacteria, including Escherichia coli, Staphylococcus sp., Providencia spp., Proteus morgani, and Proteus mirabilis.229 Up to 57 different strains of bacteria have been identified in a Komodo dragon’s saliva, including resistant strains of four usually susceptible pathogens.229 Probably because they are fed a cleaner diet, captive animals have cleaner mouths. Komodo dragons are apex predators that hunt game using stealth, ambush, and a keen sense of smell. Komodo dragon attacks on humans are rare, but have been increasing over the past decade. Reports of dragon-related injuries and deaths date back to the 1940s, and five people have been killed by dragons since 1974. The animals are considered especially dangerous to children. In 2007, a Komodo dragon attacked an 8-year-old boy on Komodo Island; the boy died of massive bleeding.22 Locals blamed the attack on the suspension of goat sacrifices, claiming that the hungry dragons wandered into settlements in search of food. In 2009, two Komodo dragons killed a fisherman after he fell out of a tree and was then left bleeding badly from bites to his hands, body, legs, and neck.5 A well-publicized incident involving a publisher occurred in 2001 at the Los Angeles Zoo in California, when the man was invited into a Komodo dragon exhibit and was bitten on the foot.31

MARINE MAMMALS Marine mammals account for about 120 different species of animals and include cetaceans (whales, dolphins), sirenians (manatees), pinnipeds (true seals and walruses), and mustelidaens (otters). Polar bears (see Chapter 57) are sometimes considered marine mammals as well, because they spend most of their lives on pack ice; however, this section only considers seals, walruses, and otters. One survey revealed that 54% of workers in contact with marine mammals reported experiencing at least one injury or illness (mostly cuts, scrapes, bites, and rashes).323 Eleven percent reported developing seal finger, which is discussed later in this chapter. Injury occurred in 52% of these individuals while they were handling the animals or animal tissue. Of these injuries, 36% were severe and included deep wounds and fractures. In another survey of 483 marine mammal workers, 50% suffered an injury caused by a marine mammal, and 23% developed a skin rash.181 Marine mammal work-related illnesses commonly reported by survey participants included seal finger, conjunctivitis, viral dermatitis, bacterial dermatitis, and nonspecific contact dermatitis. Severe illness was less commonly reported and included tuberculosis, leptospirosis, and brucellosis. Traumatic injury included deep wounds (77), bites (38), wounds requiring sutures (26), and fractures (Figure 56-31, online). Marine mammals carry many of the pathogens associated with food-borne gastroenteritis, such as Escherichia coli, Salmonella, and Listeria, although there are no documented cases of 1122

transmission to humans. Like other wildlife, seals and sea lions can shed the protozoan Giardia lamblia in their feces. In rare cases, marine mammals have been infected with rabies virus or Mycobacterium tuberculosis. From 1972 to 1977, five researchers were diagnosed with leptospirosis after working with California sea lions.300 The organism most likely responsible for seal finger is Mycoplasma phocacerebrale. Seal finger (see Chapter 79) is a condition that has been frequently reported by seal researchers and handlers. Although seal finger is usually treated effectively with tetracycline, serious sequelae, including septicemia, have been reported.181,322 In 1998, a calicivirus (i.e., the San Miguel sea lion virus) was isolated from blisters on the hands and feet of a laboratory worker.325 Sealpox is a cutaneous condition caused by parapoxvirus that usually affects seal handlers who have been bitten by infected harbor or grey seals.325 In 1987, two researchers developed cutaneous lesions consistent with sealpox after working with grey harbor seals.323 Seals Pinnipeds are comprised of true seals, earless seals, and walruses. Attacks on humans are rare. Grey harbor seals have pointed sharp teeth for tearing and grasping, and often use their back teeth for crushing shells. In 2005, a woman was trying to help a seal back into the water when it bit off her nose.288 In San Francisco, California, in 2006, the Aquatic Park reported 14 separate biting incidents, all attributed to the same baby harbor seal. On average, 10 seal bites per year are reported in the United States277 (Figure 56-32, online). The much larger leopard seals of the Antarctic are apex predators, weighing up to 500 kg (1102.3 lbs) with canine teeth that are 2.5 cm (1 inch) long. Attacks on humans are rare. In 1985, an explorer reported having been bitten twice by a leopard seal as it tried to drag him into the sea; in 2003, a leopard seal killed a researcher when she was pulled underwater and drowned.65,253 Ernest Shackleton described a leopard seal attack that occurred during his ill-fated Antarctic expedition.253 Walruses Walruses (Odobenus rosmarus) are large marine mammals with a discontinuous circumpolar distribution in the Arctic Ocean. The most prominent physical features of the walrus are long tusks (actually elongated canines) that are present in both genders and can reach a length of 1 m (3.3 feet). They have few other teeth, and use the tusks to rake the ocean bottom for food.41 A fullgrown bull can weigh 1814.4 kg (2 tons) and challenge a polar bear. Few human attacks have been documented as a result of both geographic isolation and the walrus’ generally shy nature. The rare human conflict usually involves an injured or provoked animal. Sea Lions Sea lions (family Otariidae) have four large canine teeth with smaller incisors and cone-shaped teeth. A sea lion’s teeth are designed for grasping and tearing rather than chewing. Sea lions tend to flee if possible, but they are capable of delivering powerful bites when threatened. Although sea lions are not typically aggressive, a series of attacks was reported in San Francisco Bay in California in 2006, when 14 people were bitten. In 2004, a sea lion pulled a fisherman from his boat, but he was able to escape unharmed.341 Elephant Seals Elephant seals (genus Mirounga) are very large mammals that can move surprisingly fast on land. Attacks on humans are rare and in most cases provoked (e.g., when the seal is surprised or approached too closely). Northern (Mirounga angustirostris) and southern (Mirounga leonina) species are both found in the Pacific region. Elephant seals have large incisors and are capable of breaking bones with even a small bite.223 In 2007, a series of attacks were attributed to one bull elephant seal in the San Francisco Bay Area of California; the animal bit a surfer, a kayaker, and a pitbull dog.223 As is the case with other marine mammals, seal finger is a potential complication of an elephant seal bite.34

River Otters The first recorded biting of a human by a river otter was in 1998 in Minnesota. In 2004, a family of three was attacked while swimming in calm river water near Belden, California.166 A 12-year-old boy was suddenly attacked both above and below the water by a river otter, and was bitten and scratched over much of his body. The otter then attacked the child’s mother and father when they arrived to help, and the attack was described as “vicious and unrelenting” despite many attempts by the three to strike and repel the animal. State game officials were unable to locate or capture the animal. The victims’ sutured lacerations healed without incident after prophylactic treatment with amoxicillin– clavulanate, and they received rabies PEP (Figure 56-33). The CDC has recorded 24 rabies cases in river otters, and wildlife experts suppose that, as a result of low population densities and a semi-aquatic existence, otters probably have limited opportunities to contract diseases from other species. Otters travel along rivers while denning, allowing contact with raccoons, which carry a rabies strain that is enzootic in raccoon populations.289

Domestic Animal Attacks Most animal bites are from domestic dogs and cats. The great majority of bites (approximately 80% to 90%) are inflicted by dogs,160 and approximately 1 in every 775 persons seeks emergency care for dog bites each year.332 In 2001, an estimated 368,245 people were treated in U.S. hospitals for nonfatal dogbite–related injuries.75 Domestic cats account for about 5% to 15% of treated bites, although some studies report a figure as high as 25%.160,218,351 The bite location and affected populations vary by animal. Most dog bites occur on the extremities. Facial bites are more common among children, and up to two-thirds of cat bites are on the upper extremities, especially the hand.149,303 A comprehensive study that evaluated 50 patients with dog bites and 57 patients with cat bites identified a median of five bacterial isolates per culture (see Box 56-8).314 Pasteurella species were the most common pathogens found in bites of both dogs (50%) and cats (75%).314 The association of Pasteurella with infections of rapid onset was confirmed. Streptococcus, Staphylococcus, Moraxella, Corynebacterium, and Neisseria were the next most frequent aerobic isolates. Eikenella corrodens, usually associated with human bite infections, was found in only one cat and one dog bite wound. Capnocytophaga species and Weeksella zoohelcum, both of which can cause invasive sepsis, were uncommon in this study and may be opportunistic pathogens. Fusobacterium, Bacteroides, Porphyromonas, and Prevotella were common anaerobic isolates.27

DOGS Dogs are the only species whose bites have been well studied in large numbers. Although they have been domesticated for at

CATS Domestic cats that become feral are an increasing problem in the United States as the population of strays grows and opportunities increase for exposure to wild vectors of rabies. Cats now account for 50% of animal control calls, which has led to proposals for leash and licensing laws for cats. Cats have a weaker biting force than do dogs, but possess sharp, slender teeth, often producing deep puncture wounds. Their bites are associated with a 15% to 80% infection rate314 and a higher incidence of osteomyelitis and septic arthritis compared with dog bites. Cat bites frequently introduce two risk factors for infection: hand location and increased depth of puncture. Other risk factors in cat bites associated with wound infections include older victims, longer delay to emergency department treatment, wound inflicted by a pet rather than a stray, wound care at home, and more severe wounds.111 Cat-scratch disease is an uncommon disease; 90% of cases are caused by scratches from domestic cats, although it has also been reported in one big-cat attack victim.100,190 The average incubation period is 3 to 10 days. The characteristic feature is regional lymphadenitis, which usually involves the lymph nodes of the arm or leg. In most cases, clinical diagnosis is based on finding three of the following four criteria:100 1. Single or regional lymphadenopathy without obvious signs of cutaneous or throat infection 2. Contact with a cat (usually an immature one) 3. Detection of an inoculation site 4. A positive skin test for cat-scratch disease Detailed information about the diagnosis and treatment of this disease is found in Chapter 59. Because the hands and lower extremities are common sites of injury and wounds may be deep and penetrating, most cat 1123

CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

FIGURE 56-33  Victim of a river otter attack. (Courtesy Jill Hanna, MD.)

least 12,000 years, dogs retain many of their wild instincts (e.g., territoriality in a guard dog). Dogs who are less than 1 year old are responsible for the highest incidence of bites.75 The incidence of biting increases substantially during the summer months. The increased susceptibility of children results from their smaller size, relative inability to defend themselves, interest in animals, and unintentional abuse of animals. Wounds from dog attacks may comprise a mixture of biting, clawing, and crushing forces. An adult dog can exert 200 to 300 psi of pressure.11 As a result, deeper tissues may also be injured. Treatment may naturally focus on the crush component of the wound, but the penetrating component may cause the most morbidity. The dog may move and shake its head during the attack, further tearing tissue. Snorting, grunting, or wound manipulation by the biting animal may force air into the tissues. In addition to infectious organisms, foreign debris and teeth may be deposited. During a severe attack, the dog may eat tissue and blood or scavenge on an unconscious or intoxicated victim.159,268 Dog bites to the genitalia have been reported, rarely resulting in orchiectomy.118,155 Dog attacks kill 10 to 20 people in the United States annually,332 and the majority of those killed are children.284 Forty-nine states reported dog-related fatalities, with Alaska reporting the highest death rate from dog attacks. The number of dog-related deaths appears to be increasing.202 Worldwide, dogs are responsible for about 50% of animalrelated injuries to travelers.144 A study done in Thailand of adult travelers at the international airport reported that 1.3% had been bitten by a dog.263 In Africa, there are more people than dogs living in cities compared with villages, and in Asia, there are more dogs than people in cities compared with villages.191 This would suggest that one is more likely to be bitten by a dog while traveling in rural Africa or urban Asia. Risk factors for increased biting propensity include male dog gender and unneutered status. Many dogs that seriously wound or kill humans have long histories of aggressive behavior. Strategies that reduce biting risk include education of owners and the public, selection of dogs, and training, care, and socialization (see Box 56-2).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

bites are considered to be high risk for infection. Such wounds should prompt administration of prophylactic antibiotics (see Box 56-6). Superficial cat bites and scratches elsewhere on the body are not high risk and should receive standard wound care without antibiotic coverage.

RODENTS Rodents do not tend to bite unless severely provoked; their bites are usually small and do not cause much disability. The exact number of rodents in the world is unknown, but they probably number in the hundreds of millions. A 2007 U.S. pet ownership survey showed the following ownership per 1000 households: 1060 ferrets, 1239 hamsters, 1004 guinea pigs, 431 gerbils, and 949 other rodents.10 Despite these numbers, rodent bites account for only 1.7% to 10% of animal bites brought to medical attention.248 Rodent bites are infrequent, seldom cause any problems for the victim, and often occur among lower socioeconomic groups without good access to medical attention. Other populations at risk include laboratory workers who handle rodents used in research. Insufficient data exist to determine any differences in outcomes between wild and domestic rodent bites. Rats, Mice, and Other Small Rodents Rat bites have an infection rate of 2% to 10%, even without treatment, and the rate is usually on the low end of this spectrum.248 Other than bites inflicted by laboratory animals, the vast majority occur in poor communities while the victim is sleeping and involve the face and neck, usually of infants or physically or mentally disabled adults.247,248 There were 415 reported rat bites in New York City between 1986 and 1994.87 Sometimes these can be severe; a week-old infant was bitten around the eyes by a rat, resulting in perforations of the globe, an estimated vascular loss of 55% of red blood cell mass (with an initial hematocrit value of 20%), and eventual blindness.236 Despite the rat’s reputation for spreading disease, however, infection did not occur. Similar bites in infants have resulted in loss of more than threefourths of the eyelids.352 The bacteriology of a rat bite is similar to other animal species; the various systemic diseases transmitted by rats are discussed in Chapters 59 and 60. Sporotrichosis has been reported; this widely distributed saprophyte is found on various plants, in the soil, and on many animals.140 Although rodents occasionally become infected with rabies, they seldom secrete this virus in saliva; therefore, they inflict extremely low-risk bites with regard to the transmission of the disease. However, local epidemics can occur, as documented in the 1980s among rodents and lagomorphs on the east coast of the United States.233 During that epidemic, woodchucks constituted 80% of all rabid animals; the remainder were squirrels, beavers, rabbits (lagomorphs, not rodents), and one rat. Some of these rabid animals were very aggressive; a woodchuck attacked and knocked down an elderly woman in her garden, biting her repeatedly. Rabies was isolated from the buccal cavity of the woodchuck in question. A reasonable current recommendation is that a biting wild rat in the United States should be caught and examined for rabies, and rabies PEP should be initiated only if the rabies test is positive; rabies PEP is probably appropriate for bites from uncaptured rodents inflicted outside of the United States and Canada.248 A case has been reported of a cowpoxvirus–like infection transmitted by a probable rat bite.342 Rodents are believed to be the natural reservoir of the cowpox virus. Rat-bite fever is an acute illness caused by Streptobacillus moniliformis or Spirillum minus, which are part of the normal oral flora of rodents, including squirrels. It may also result from bites of wild and domestic carnivores, such as weasels, dogs, cats, and pigs, which may have become infected when hunting rats and mice.290 Carrier rates among wild rats vary from 50% to 100%.330 Fewer than 100 cases have been reported in the North American literature, and rat-bite fever is not a reportable disease in the United States.330 Although relatively rare, cases can occur in any setting, and can easily be fatal, particularly when the proper diagnosis is not suspected.100,287,330 Further information is found in Chapter 59. 1124

Plague is caused by the bacterium Yersinia pestis. Wild plague is endemic in many parts of the world, chiefly among rats, mice, moles, marmots, squirrels, hares, cats, and mongeese. One of the larger areas of endemic plague is the western United States, where voles, field mice, ground squirrels, prairie dogs, and pack rats carry the infection. Between 1971 and 1999, there was an average of 13 cases of plague per year in that area of the country, but only 2 cases were reported in 2001; however, worldwide, there were 2861 cases reported by 10 countries.103 The infection is usually transmitted to humans by the bites of arthropods that infest infected animals. Handling infected animals allows Yersinia pestis to enter cuts and abrasions, as seen among veterinarians and hunters who skin and clean infected rabbits.72 Transmission by bite or scratch has never been reported. The disease is mentioned here because of its historic significance and the frequency of occurrence among wild animals. Further information is found in Chapter 59. Tularemia represents various syndromes caused by Francisella tularensis. This bacterium normally parasitizes about 100 different mammals and arthropods, most commonly cottontail rabbits, rodents, hares, moles, beavers, muskrats, squirrels, rats, and mice. The primary mode of transmission to humans is via a bloodsucking arthropod (e.g., a tick) or by skin or eye inoculation resulting from skinning, dressing, or handling diseased animals. Other routes of infection include ingestion of water that has been contaminated by urine or feces and inhalation of dust. Infections after bites or scratches from dogs, cats, skunks, coyotes, foxes, and hogs have been reported, although these are rare.273 The disease is an occupational hazard of hunters, butchers, cooks, campers, and laboratory technicians. Humans are quite susceptible, and, although tularemia was removed from the national notifiable disease list in 1995, 105 cases were reported in 1997 in the United States.76 More information is found in Chapter 59. Rabbits Rabbits are a common household pet. They are not true rodents but rather part of the Lagomorpha order and more closely related to horses. Rabbits cannot see in front of their noses, so they may bite a hand that is placed there. They also nip as a means of communication, although such behavior on the part of the rabbit can be interpreted as aggression. Biting is uncommon, but rabbits can inflict painful scratches with their rear limbs when restrained.168 Pasteurella multocida from scratches may cause cutaneous infection in humans.167 Other diseases to which rabbits are susceptible, such as salmonellosis, yersiniosis, and tularemia, are rare. Direct zoonotic transmission of Yersinia pseudotuberculosis from domestic rabbits has been documented.138 More commonly, some external parasites of the rabbit, including fur mite acariasis (Cheyletiella) and dermatophytosis (Trichophyton), may be transmitted to humans.167 Ferrets The two species of ferret in the United States are the common ferret Mustela putorius furo, which is sold as a domestic pet, and the wild black-footed ferret Mustela nigripes, which is an endangered species. The pet ferret was domesticated from the wild European polecat, and was first introduced into the United States during the late 19th century. Ferrets are kept in increasing numbers as domestic pets, especially by urban apartment dwellers (Figure 56-34). Ferrets were bred to hunt and kill small game and rodents in their burrows, and are particularly attracted to suckling animals, possibly because of the scent of milk. The animals have 34 teeth and sharp claws on all four feet. Severe injuries caused by ferrets are not common. When they occur, an infant is often the victim, and is typically sleeping or in a crib. The face, ears, and nose may be mutilated.12 Scratches, lacerations, and puncture wounds are seen, and the ferret may chew on a victim (e.g., a baby’s ear). The neck is also a common target. In a comprehensive review of 452 ferret attacks over 10 years, virtually all unprovoked attacks were on the faces of unattended infants.98 Most victims were less than 3 years old and were attacked while sleeping or lying down. Several injuries were severe, and one child died. Bites were usually multiple, and

FIGURE 56-34  Pet ferret. (Courtesy Luanne Freer, MD.)

sometimes the ferret’s jaws had to be pried open or the ferret had to be killed to secure release.255 Nearly all provoked incidents involve neglect, abuse, or roughhousing with the ferret that it likely perceived as an attack; some of the animals involved in these incidents were ferret–polecat hybrid crosses.37 Ferrets are unusually adept at escaping from cages and enclosures, guaranteeing that they will occasionally be loose unsupervised in the house and also that they can escape to the wild, where they may be exposed to endemic rabies. In one study, 4% of biting ferrets were found to be positive for rabies virus.98 Ferrets are now classified in the same category as cats and dogs (rather than as wild terrestrial carnivores) with regard to rabies pathogenesis and viral shedding patterns. They may be confined and observed for 10 days rather than being routinely euthanized after biting. An effective rabies vaccine for ferrets, IMRAB-3, has been available since 1990, although it requires annual vaccination. Little is known about infection rates or bacteriology in ferretinflicted wounds, although unusual species such as Mycobacterium bovis have been observed.184 Initial treatment should be the same as it is for dog bites.

DOMESTIC HERBIVORES AND UNGULATES From 1992 to 2000, there were averages of 40 deaths and 12,400 nonfatal injuries and illnesses related to animals in the United States annually. Most of these incidents involved domestic farm animals.82,228 Between 1990 and 1993, horses were the second leading cause of farm-related injuries.280 Farm animals cause a disproportionate number of injuries relative to other animals, especially among youth; 6438 on-farm injuries occurred among young victims in 1998. Approximately 41% of those injured were less than 10 years old; 37% of incidents involved horses, and 31% involved cattle. Most of the cattle-related injuries were work related, whereas horse-related injuries were mainly nonoccupational.301 One out of every five youth injuries that occurs on farms in the United States is animal related.301 A Wisconsin study showed that, for injuries requiring hospital admission, farm animals were the cause of 40% of the injuries. The study also revealed that the types of injuries caused by farm animals include those to the head, upper extremities, maxilla, legs, and thoracoabdominal region.94 A study of youth on farms in Australia indicated that 86% reported working with farm animals and in 44% of injuries among this population, the injury was caused by a farm animal. In addition, 72% of youths surveyed perceived working with animals as the most dangerous activity on the farm.82 Little is known about incidence of wound infection after herbivore bite, but the infection rate after camel bites may be as high as 86%.203 Species of Actinobacillus lignieresii, Actinobacillus suis, and Pasteurella multocida have been isolated from infected horse and sheep bites.38,258 Most domestic herbivores carry Pasteurella, and most are given frequent and regular doses of different antibiotics, especially in their feed, leading to

Horses and Donkeys The horse (Figure 56-35) is inclined to both bite and kick, but most horse-related injuries follow a fall during riding activities. More accidents occur per hour riding horses than during motorcycling.88 Young females are most often injured by falls,57 and head injuries cause the majority of deaths.165 Appropriate helmets and footwear help to reduce the severity of injuries. A report of a series of horse- and cow-related injuries found a high correlation of occult craniofacial and torso injuries when field assessment documents the presence of upper extremity injury.243 Falls from horses typically result in head and upper extremity injuries; the most common injuries are fractures, lacerations, and contusions.67 From 1992 to 1994, 109 traumatic brain injuries caused by falls from horses were reported in Oklahoma; these included 3 deaths.71 Twenty-three other traumatic brain injuries resulted from horse-caused injury but were not associated with riding; 21 of these traumatic brain injuries resulted from a direct kick to the head.71 Horse bites are common but usually do not cause severe injuries. The occlusal surfaces of both the horse’s lower and upper incisors are flattened. However, most male horses possess canines that may be used to grab onto a mare’s neck during mounting. The soft-tissue contusions inflicted by a horse can be substantial, but, in a series of 24 horse bites, 21 healed uneventfully.122 Bites can still produce significant injury, including muscle rupture and fat necrosis, with no external wound. Horses also have a propensity for biting human nipples, which are at the same height as a horse’s mouth. Horse kicks from the rear legs can be extremely powerful and cause severe blunt trauma, including cardiac rupture50 and massive pulmonary embolism.267 Donkeys also bite, and death has been reported from fat embolism caused by fractures after a donkey bite.48 Cattle Cattle are usually docile, but can inflict a variety of injuries. Serious bites are infrequent, because these animals possess neither upper incisors nor canines. A cow typically weighs 635 kg (1400 lbs), and a bull can exceed 1360.8 kg (3000 lbs). Accidental treading on the human victim or butting can cause major crush injuries and fractures. Farm animals in Wisconsin kill about six people each year.59 One hospital in rural Wisconsin treated an average of 22 persons per year for horse and cattle injuries, most of which were inflicted by a kick or another assault. In addition, domestic cattle can become infected with rabies (Figure 56-36, online).

FIGURE 56-35  Domestic horses disagreeing about something. (Courtesy Gary Matthews.)

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CHAPTER 56  Bites and Injuries Inflicted by Wild and Domestic Animals

antibiotic resistance of bite wound organisms.269 Pasteurella caballi has been isolated from a horse bite wound.127 Staphylococcus hyicus subsp. hyicus, a well-known cause of disease in many animals, has been reported as a human wound pathogen after a donkey bite.251 Bites from horses, donkeys, cattle, sheep, camels, deer, and most other herbivores are treated with the same antibiotics as are bites from dogs, cats, and humans (see Box 56-6).

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Cattle horn injuries or gorings (Figure 56-37) present typical and unique damage patterns. The horns are used in an inward hooking motion to butt and fling the victim, or the horn tip can be used for goring. Goring injuries seen in bullfighting typically involve the perineum and thigh; they tend to be deep and sometimes fatal. By contrast, bull horn injuries from domestic cattle involve a sweeping arc at the level of the bull’s head, which is at the level of the human abdomen. The semicircular motion of the horn often produces a relatively superficial laceration that leaves deeper structures of the abdomen intact. In one series of 29 cases in which the peritoneum was breached, which usually produced a prolapse of bowel or omentum, 27 laparotomies demonstrated no additional injuries; in only a few cases was the bowel itself damaged.293 The wound infection rate in this series was high (54%), probably as a result of delayed treatment. There were 108 cattle-related deaths in the United States between 2003 and 2007. Twenty-one deaths from working with domestic cattle were reported between 2003 and 2008 in the four U.S. states that accounted for 16% of all cattle operations in the United States. Ten of these fatalities involved attacks by bulls, six were attacks by individual cows, and five involved multiple cattle. In seven attacks, the bull or cow was known to have exhibited past aggressive behavior, and one-third of the deaths occurred in March and April. The victims’ most common activities at the time of death were working with and treating cattle in enclosed spaces (e.g., pens, chutes) and moving or sorting cattle in pens, barns, or pastures. In 16 of the cases, the animal was deemed to have purposefully struck the victim; five other deaths were caused by being crushed against a stationary object or struck by a gate. All but one death resulted from blunt force trauma to the chest, head, or both.69 Bulls should be approached only with a protective device (e.g., heavy stick) and a preplanned exit strategy. A ring in the bull’s nose gives a victim something to hang onto beside the horns and a way to yank the bull’s nose up, which may stop the attack. Dehorning the bull will not eliminate the potential for crushing. If struck by a bull or cow, the victim should not attempt to stand, because this will provoke being thrown to the ground again, but should try to crawl to safety. Children must be educated about the risks of large animals and kept away from them whenever possible. Camels In regions in which camels are used for domestic or agricultural purposes, bite injuries are quite common.203 Although herbivores and usually docile, camels are much more likely to bite in the winter rutting season, and bite fatalities have been reported. Camels have 34 teeth, including large backward-inclined upper canines or tushes (Figure 56-38). The lower tushes are placed relatively forward, and the resultant mouth grip is very effective. Jerking movements of the head result in severe tissue damage and limb avulsion, and rarely can break the human victim’s neck. The forearm is often injured, and bites to the face are well documented.66,246,299 Virtually all camel bites are single.286 Injury or

FIGURE 56-37  Domestic bull goring victim. (Courtesy Luanne Freer, MD.)

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FIGURE 56-38  Camel and its owner/trainer in Marrakech, Morocco. (Courtesy Luanne Freer, MD.)

death can also occur if the camel presses the victim to the ground and crushes him or her after gripping the person in its jaws.203 Domestic Swine Bites from domestic swine are rare; however, when pigs attack, they can be aggressive and inflict deep goring or bite injuries, often on the posterior thigh as the pig approaches from behind.28,242 Pigs have a reputation for inflicting bites that are at high risk for infection, and care should include thorough wound exploration and debridement. The usual wide range of bacterial pathogens is reported, including Pasteurella aerogenes, Pasteurella multocida, Bacteroides, Proteus, Actinobacillus suis,126,161 and hemolytic streptococci, including Streptococcus milleri.28 Unusual gram-negative bacteria, such as Flavobacterium group IIb, have been isolated, as has Mycoplasma.42,231 Both of these organisms are resistant to amoxicillin–clavulanate, so the addition of ciprofloxacin is recommended as prophylaxis for a serious pig bite wound.231

BIRDS Birds may be kept as domestic pets or on farms, and can be responsible for serious injuries. On farms, rooster attacks, often by male fowl defending their territory, are well documented. Children, especially infants, are particularly vulnerable to attack. Rooster injuries have included serious clawing of the face and a fractured skull.271 In one report, a rooster spur was retained in a wound, resulting in chronic infection.99 Septic arthritis was reported in a child after a bite from a domestic fowl.178

Medicolegal Considerations In some cities and regions, animal bites must be reported to public health authorities. Reporting suspected exposure to rabies is mandatory in most regions, and failure to report could become the basis for legal action. Reporting often leads to examination of the offending animal by public health authorities and sometimes to quarantine or destruction of the animal. Reporting animal bites also improves data collection and statistical evidence regarding the problem. Although most wild animals by definition do not have an owner, some exotic species are kept as “pets.” An owner’s failure to meet local regulations regarding licensure and vaccination can lead to legal action. In addition, the victim may seek compensation from the owner of the animal, with the result being that the health care provided and the victim’s medical record will be reviewed in court. The injury may be related to the victim’s employment, generating worker’s compensation or other insurance claims. Therefore, injuries and their circumstances should be documented as fully as possible, with line drawings or photographs added to the medical record whenever possible. In a recent tragic example in Connecticut, a woman was attacked by a friend’s pet chimpanzee. Her injuries required 7 hours of

extensive surgery, and the patient is predicted to have permanent disabilities. Her family has filed litigation against the owner of the chimpanzee.15 Certain types of animal bites, particularly those of the hand, are prone to infection and can lead to permanent litigationassociated complications. A complete medical record is the best protection against such issues as well as to address the more

ordinary matter of malpractice claims made against the health care provider.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 57 

Bear Behavior and Attacks LUANNE FREER AND STEVEN P. FRENCH

Bears are among the most widely distributed animals in the world. At least one of the eight bear species currently exists in Asia, Europe, North and South America, and the Arctic (Table 57-1). Bears in Africa became extinct several million years ago. Australia and Antarctica are the only continents where bears have never existed. The koala bear of Australia is a marsupial and not a true bear. Bears occupy a wide variety of habitats, including tropical forests, polar ice sheets, swamps, barren ground tundra, bamboo jungles, alpine meadows, and coniferous and deciduous forests. Their range extends from sea level up to about 6100 m (20,000 feet). Bears are carnivores. Although some bear species practice specialized feeding in response to their habitat, all bears are omnivores and retain the ability to feed on a variety of food types, including vegetation, insects, and meat. Modern bears have larger brains than did their extinct ancestors,34,47 and the relative brain size of bears is larger than that of other carnivores.22 This greater brain size probably resulted from a need to increase sensory and perceptual capacities for locating an omnivore food base with both seasonal and annual variations in distribution and abundance.10,15,40 The larger brain size reflected the increased intelligence required by bears to develop a complex foraging strategy. Increased intelligence also allowed them to develop individual behavior, shaped by both experience and memory. Thus they possess a wide variety of behaviors and have TABLE 57-1  Distribution of Bear Species Common Name Panda bear Spectacled bear Sloth bear

Scientific Name

Distribution

Ailuropoda melanoleuca Tremarctos ornatus Melursus ursinus

Eastern rim of China’s Tibetan Plateau Andes Mountains in South America Nepal, Bangladesh, Bhutan, northern India, Sri Lanka Southern Asia from Pakistan across northern India and into China and southeast Asia; separate populations in eastern Russia, Korea, Taiwan, and Japan Borneo, Burma, Java, Malaysia, Sumatra, Thailand Alaska, Canada, most of lower 48 states Eurasia, Alaska, Canada, northern Rocky Mountain states (including Wyoming, Montana, Idaho, and Washington) Arctic circle (circumpolar)

Asiatic black bear

Ursus thibetanus

Sun bear

Helarctos malayanus Ursus americanus

American black bear Brown bear

Polar bear

Ursus arctos

Ursus maritimus

been described as playful, lazy, doleful, entertaining, intelligent, caring, powerful, aggressive, terrifying, and vicious.53 The image of bears as “man-eaters” ignites our fear of them. Human injury and deaths from natural phenomena, especially wild animal attacks, are sensationalized. Bear attacks are rare, but the psychological impact of widespread media coverage inflates the perception of their frequency and significance.13,37 Every bear attack is traditionally referred to as a mauling, regardless of the extent of injuries. This term contributes to the emotional response regarding such attacks and leads to “bearanoia” in many people who visit bear country. This fear of bears may affect how people use wilderness areas that have bear populations and how they view the conservation of bears and their habitat. Better understanding of bears and their behavior helps reduce bear attacks, assists physicians in treating bear attack victims, and promotes the conservation of bears.

North American Bears Grizzly bears (Ursus arctos horribilis) are larger and more heavily built than most other ursids, with adults weighing 147 to 386 kg (325 to 850 lb) (Figure 57-1).5 Polar bears (Ursus maritimus) are similar in size and weight but are more elongated in shape (Figure 57-2). Black bears (Ursus americanus) (Figure 57-3) have the same general shape of grizzly bears but are generally smaller than both polar and grizzly bears. Weights for black bears range from 64 to 136 kg (140 to 300 lb) for adult females and 113 to 295 kg (250 to 650 lb) for adult males. Dentition in these three species is bunodont and reflects their omnivorous diet, although polar bears are the most carnivorous of the three (Figure 57-4). Their canine teeth are sturdy and can reach a length of 7 cm (2.75 inches). Their legs are of approximately equal length and taper to large, plantigrade feet. The foreclaws of a grizzly bear are heavier, longer, and straighter than those of a black bear and can reach a length of 8.75 cm

FIGURE 57-1  Grizzly bear. (Courtesy Marilynn G. French.)

For online-only figures, please go to www.expertconsult.com

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FIGURE 57-5  Grizzly paw with claws. (Courtesy Marilynn G. French.)

FIGURE 57-2  Polar bear. (Courtesy Steven D. Evans.)

FIGURE 57-3  American black bear. (Courtesy Marilynn G. French.)

FIGURE 57-6  Alaskan coastal brown bear, demonstrating muscular back hump. (Courtesy Luanne Freer.)

FIGURE 57-4  Grizzly skull, demonstrating canine teeth. (Courtesy Marilynn G. French.)

FIGURE 57-7  Silhouette of brown bear, demonstrating hump and “dished” face. (Courtesy Timothy Floyd.)

(3.5 inches) measured along the external curvature (Figure 57-5).54 A large, muscular hump overlies the scapulae of grizzly bears, giving additional strength to the forelimbs for digging (Figure 57-6). The face of a brown bear tends to be more dish shaped (concaved) than that of a black bear (Figure 57-7). The physical strength of bears is tremendous, and they can run at speeds up to 65 km/hr (40 mph) over irregular terrain. They have a keen sense of hearing and an even keener sense of smell. Their eyesight has been described as poor,28 although many field researchers believe that bears can see as well as humans and are especially adept at detecting movement. Evidence also suggests that grizzly bears have good night vision.20

Grizzly and black bears hibernate for about 5 months during the winter, an evolutionary adaptation to reduced food availability. The hibernation of polar bears is slightly different, as their primary food (seals) is available during the winter.44 Adult male polar bears tend to hibernate for short periods each winter in response to severe storms, whereas pregnant females have more extended hibernation. During the active (nondenning) season, all bear species wander throughout a general home range in search of seasonal foods. The guard hairs on brown bears can be lighter in color and lend a “grizzled” appearance. Black bears can be many colors, ranging from white to black, cinnamon, brown, or “blue.”16

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The grizzly bear symbolizes wilderness in North America (Figure 57-8). In certain respects, “grizzlies” define the “wild” in wilderness. They range from Alaska down through western Canada and into the lower 48 states in remnant populations located in relatively undeveloped federal lands, primarily in the northern Rocky Mountains. Attacks by grizzly bears are relatively rare and sporadic. A total of 162 bear-inflicted injuries (including deaths) were reported from 1900 through 1985 in Canadian and North American national parks.28,29 In the Canadian province of Alberta, there were 29 documented serious or fatal injuries caused by grizzly bears during the period of 1960 through 1998.31 From 1980 to 1994, 21 grizzly bear attacks, including two deaths, occurred in Yellowstone National Park.27 During the following decade, one or two people were injured by grizzly bears in Yellowstone each year, with no recorded deaths. In Alaska, the number of people injured by grizzly bears has increased in recent times, most likely as a result of increased recreational use of grizzly habitat.41,50 Calculation of an accurate injury rate remains elusive. Earlier records were incomplete, and it has always been difficult to define and quantify those at risk. Injury rates are based on total visitation days to the national parks in Canada and the northern United States.29 The average number of grizzly bear–inflicted injuries is 1 in 2,260,276 visitors to these parks combined, with a high of 1 in 317,700 visitors in Kluane National Park and a low of 1 per 6,693,859 visitors in Banff. During this same period, the grizzly bear–inflicted injury rate for Yellowstone National Park was 1 in 1,543,287 visitors, and for Glacier National Park it was 1 in 848,180 visitors. Not every visitor to a national park is exposed to the same risk of being attacked by a grizzly bear. To obtain an injury rate that more accurately reflects the risk for visitors with higher and more uniform exposure, the incidents among registered backcountry users have been reported. However, this method provides an inaccurate injury index because some parks do not register backcountry use and others generally underestimate it. Also, significant and perhaps most backcountry use (and therefore exposure) is by unregistered day hikers. The number of bear attacks (both black and grizzly) increases in months when more people seek recreation in grizzly country. For national parks, the incidence of bear attacks increases during the peak tourist season, July and August. For surrounding national forests, another peak occurs during hunting season, September to November. With more people seeking recreation in bear country, greater opportunity exists for human–bear encounters. Native peoples and grizzly bears occupied the same land for thousands of years in North America in what was probably a neutral coexistence, as neither had a profound influence on the other. However, the European expansion into the West after

FIGURE 57-8  Grizzly bear encounters have become popular events for wildlife photographers. (Courtesy Timothy Floyd.)

CHAPTER 57  Bear Behavior and Attacks

GRIZZLY BEARS

FIGURE 57-9  When surprised at close quarters, grizzly bears, who have the potential to do much more harm, often inflict relatively minor injuries and then flee. This victim of a bear attack stumbled upon a surprised bear who was trapped by fire lines. (Courtesy Luanne Freer.)

Lewis and Clark’s expedition in the early 1800s tipped the scales heavily in favor of humans, both in sheer numbers and in technology, such as guns, traps, and poisons. Bears were killed in large numbers, out of fear and hatred and to protect life and property. Most of their original habitat was occupied by either people or livestock or was dramatically altered by ranching and agricultural development. Selection pressures that began with European expansion into the grizzly bears’ habitat have probably been altering their behavior. Since that early period and even today in protected areas such as national parks, aggressive bears have been removed at a higher rate than nonaggressive bears. Bears that were curious about humans and human developments and those that did not readily flee the presence of humans were also removed at a higher rate. Therefore, bears that avoided humans survived at a higher rate than other bears and probably passed that trait on to their offspring through genes and learning. A built-in safety factor exists for people entering grizzly country, because the vast majority of bears now avoid a confrontation if given the opportunity, which probably explains why grizzly bear attacks on humans are so rare. Unfortunately, the available information on grizzly attacks does not always yield an accurate account of the cause-and-effect relationship. The specific sequence of events is not always known and is subjectively reconstructed, although case histories reveal certain patterns. A sudden and close encounter with a grizzly bear is the primary event leading to human injury. From 1980 to 1994, of 21 people injured by grizzlies in Yellowstone National Park,27 18 resulted from people surprising a grizzly at close quarters. These attacks were often brief, and the bear generally left the area soon after the attack. Although injuries were typically described as a mauling, they were generally much less severe than the bear had the potential to inflict (Figure 57-9), and victims were rarely killed. This suggests that the bear’s behavior in response to a close encounter was to remove a perceived threat. A close encounter with a female with cubs is considered more dangerous, as she is considered to be more aggressive in defense of her young (Figure 57-10). Evidence to support this hypothesis is strong. Females with young represent about 20% of a bear population but account for more than 80% of the bears that injure humans. Another explanation, however, is that females with young are more likely to be active during daylight hours when humans are active, whereas males are active primarily in the predawn hours and after dusk.20 1129

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 57-10  Brown bear sows with cubs are notoriously aggressive in protection of their young. (Courtesy Luanne Freer.)

Grizzly bear attacks sometimes occur near a carcass on which the bear has been feeding. The bears may be more aggressive under these circumstances in defense of the carcass. Grizzly bears of all ages and either gender, however, may readily exit when they sense people approaching.20 When a grizzly bear injures someone near a carcass, the precipitating event may simply be a close encounter with a preoccupied bear. Another class of attacks results from provocation, most often when a grizzly bear is wounded with a gun. Once the bear is injured, its behavioral response is no longer to remove a threat but to fight for its life. These attacks tend to be more prolonged and aggressive, resulting in more severe injuries than those resulting from a close encounter. Provoked bear attacks can result from direct harassment by aggressive photographers (Figure 57-11). Although such incidences are rare, these attacks tend to resemble the response of an injured bear rather than one responding to a close encounter. The injuries tend to be more severe, and a disproportionate number of photographers are killed. Up to 1985, at least 10 photographers were injured, 1 fatally, and from 1986 to 1992, at least 4 were injured, 2 fatally.28 Most people attacked by grizzly bears are injured but not killed; the intent of the bear is simply to remove a perceived threat, not to prey on the individual (Figure 57-12). From 1900 to 1979, 19 human deaths resulted from grizzly attacks documented in the national parks in North America, and 22 deaths occurred in Alaska outside the parks.28,37 A Wikipedia file tracking human deaths in North America from grizzly bear attacks cites 12 deaths in the 10-year period from May 2000 through May 2010; all of these citations are verifiable, but it is possible that this list is not a complete one.58 Some were victims of defensive attacks; however, some deaths were probably the result of predatory attacks. It is important to ask why grizzlies do not prey on

FIGURE 57-12  Hunter attacked by grizzly bear. (Courtesy Luanne Freer.)

humans more often. As a potential prey species, humans are predictable and abundant, easy to catch and kill, and easy for a grizzly to consume. Historic evidence suggests that grizzly bears did not routinely prey on humans except in unusual circumstances. In 1860, a smallpox epidemic struck a small band of Stonie Indians (Assiniboin tribe) camped in the Yarrow Creek drainage in Alberta, Canada.51 Grizzlies began scavenging on the dead left on the ground as the tribe moved to the next drainage. Grizzlies followed them to their next encampment and began preying on survivors. For years, the Indians avoided this area for fear of being eaten by grizzlies that had “learned” to prey on humans. Since about 1900, when reasonably accurate records were first kept, predatory attacks on humans by grizzly bears generally have been rare, sporadic, and isolated events.5 However, a disturbing trend has begun in recent times. Between 1967 and 1986, 12 deaths were inflicted by grizzly bears in Banff, Glacier, and Yellowstone National Parks. In each case, the bear was conditioned to humans’ food (regularly seeking out and obtaining it) or habituated to human presence (not readily fleeing). Nine of the victims were partially consumed, and eight deaths were classified as predatory events.28 During this same period, however, many bears with these same behavioral traits did not prey on humans. Conditioned and habituated behavior may predispose some grizzlies to prey on humans under certain but still not understood circumstances. The relationship between conditioning and habituation appears strong but is not conclusive. The bear involved was not always known, and the terms conditioned and habituation are both borrowed from learning theory and have never been precisely defined by wildlife biologists. This potential relationship, however, has significantly influenced grizzly bear management. Currently, the primary thrust is to prevent bears from obtaining human foods and from routinely being around people and human developments. Grizzly bears may also mistakenly perceive a person as one of their normal prey species. Five such incidents have been documented. Two victims were killed by grizzly bears while making prey calls to lure in other predators. Two victims were attacked while field-dressing a game animal, and the fifth was attacked while carrying the hide of a deer draped over his shoulder. Clearly, persons should not look, smell, or sound like a prey species when in grizzly country.

BLACK BEARS

FIGURE 57-11  Photographers dangerously close to bears in the wild. (Courtesy Luanne Freer.)

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Black bears are the most numerous and widely distributed of all North American bears (Figure 57-13). They occur in more than 30 of the lower 48 states, from Maine to Florida and from California to Washington. Recently, a black bear was recovered in Nebraska, where none had been seen in more than 100 years, adding to the growing numbers of large carnivores reoccupying previously native territory in the Great Plains.32 They also occur throughout Canada and Alaska, extending up to the tree line below the Arctic Circle. They are well adapted to an arboreal habitat and prefer to eat vegetation, carrion, and mast (nuts,

Bears on Other Continents FIGURE 57-13  Black bear. (Courtesy Timothy Floyd.)

acorns), with small mammals and insects accounting for less than 5% of the diet.16 Black bears have been filmed fishing in southeast Alaska4 and observed by the author doing the same in Yellowstone National Park, evidence of their ability to adapt to available food sources.18,19 Between 1960 and 1980, more than 500 people were injured by black bears, but at least 90% of these episodes resulted in minor scratches or bites inflicted by bears that were either conditioned to human foods or habituated to human presence.28 The number of victims of black bear attacks has declined significantly during the past 25 years, in large part because of the aggressive bear management in and around national parks that discourages the feeding of black bears and removes those bears that seek out human foods. Injuries as a result of close encounters are extremely rare, and in contrast to female grizzly (brown) bears, female black bears display little aggression in defense of their young and rarely cause injury. They have short, sharp radial claws better adapted for climbing trees than for attacking humans. They often retreat rather than attack, even in defense; thus, hunters using dogs can “tree” black bears.16 Whereas grizzly (brown) bears sometimes prey on humans at night, black bears occasionally prey on humans during the daytime. In North America, from 1900 through the present, at least 45 people were killed by black bears, with predation considered the motivation in many cases. In many instances, attacks occurred in remote areas outside park boundaries; experts conclude that neither conditioning nor habituation was a major factor. In recent years, black bears attempted to prey or preyed on humans; some attacks occurred at night while the victims were asleep. In one case, the bear broke into a camper and pulled the victim out, and in another case the bear entered a wooden teepee (“wickiup”) and dragged the victim out by her foot.46 In most attacks, the black bears were driven away by aggressive actions by the victims and their companions, such as yelling and throwing objects.

The available data on attacks by bears on other continents are much less complete than those for North American bears. In Europe, the brown bear has coexisted with humans much longer than those in North America. (In some parts of North America, the brown bear is called a grizzly bear, but they are genetically the same species.) As a result, its behavior is less aggressive and more like that of black bears. Numbers of European brown bears are extremely low; the animals are highly cryptic and nocturnal and thus are rarely seen or encountered. In Turkey, more than two-thirds of close encounters between brown bears and humans resulted in no harm to bear or human, and bear attacks were rare and only occasionally led to nonfatal injuries.1 Human injury by brown bears in Europe was nearly nonexistent until 2004, when a rabid brown bear killed two and injured six persons in Romania.3 The brown bears in the former Soviet Union live in vast, relatively undeveloped areas and appear to have aggressive responses against humans similar to those of North American brown bears. Many human injuries from brown bear attacks, including deaths, may be related to bears injured by sport hunters.9 The panda bear (Ailuropoda melanoleuca), commonly known as the giant panda (Figure 57-15, online), lives in the temperate climate of the bamboo jungles distributed along the eastern rim of China’s Tibetan Plateau. It is one of the most recognized bears in the world, with a distinctive white and black coloration. It is a relatively poor climber but will climb trees on occasion to avoid danger. During winter months, the panda bear migrates to lower elevations where food remains plentiful, thus avoiding the need to hibernate.

Polar Bears Polar bears are distributed in a circumpolar fashion around the Arctic Circle and subsist almost exclusively on a diet of seals (see Figure 57-2). In winter, these bears feed primarily while foraging on ice-covered polar seas. Some southern populations live on land during the summer in a state of waking hibernation and starvation. Polar bear–inflicted injuries are much less frequent than those by grizzly (brown) or black bears, primarily because of their remote and harsh environment with relatively little human intrusion. From 1973 to 1987, three people were injured (one fatally) in Norway,23 and from 1965 to 1985, 20 people were injured (six fatally) by polar bears in Canada.29 In 2009, a polar

FIGURE 57-14  A woman jumped into the polar bear exhibit at a zoo in Germany, and was fortunately rescued, although she suffered significantly from the bear’s attack. (Courtesy B.Z./WENN.com.)

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bear attacked a woman at the Berlin Zoo after she climbed a fence and jumped into its habitat during feeding time; the attack and rescue were broadcast on television and the internet (Figure 57-14).11 The number of injuries in the wild would probably be much higher except that most people in polar bear habitat are armed, and in the majority of aggressive encounters the bear is killed before causing injury. Polar bear–inflicted injuries have been classified into two general categories. The major one is predation, primarily by subadult and adult males. In these instances, five of the six victims who died were probably killed instantly. The other category is injury by adult females thought to be defending their young. These episodes are typically brief and nonfatal, which supports the theory that the bear is removing a perceived threat. In more than 90% of aggressive encounters with polar bears, an attractant, such as food, garbage, or carcasses, was considered contributory.29

PART 6  ANIMALS, INSECTS, AND ZOONOSES

The panda bear is primarily a vegetarian. About 99% of its diet consists of stalks, leaves, and shoots of only two bamboo species.52 The panda has an enlarged wrist bone that serves as an opposable digit, much like a thumb. This evolutionary adaptation enables the panda to efficiently hold and strip bamboo stalks. Because bamboo is a poor-quality food, the panda must compensate by eating large amounts. Each day it feeds up to 12 hours. The panda bear is shy and reclusive, representing a minimal threat to human safety in the wild. The spectacled bear (Tremarctos ornatus) lives in the tropical climates of the Andes Mountains along the northwest border of South America. It is one of two bear species that live below the equator. The spectacled bear has a distinctive white coloration around its eyes. It is an excellent climber and spends most of its time in trees eating fruit. It often builds nests and rests in trees as well. Because its source of nutrition is abundant year-round, it does not hibernate. Spectacled bears are relatively small and shy. Encounters have been described as extremely rare, and usually pose very little threat to human safety. A recently published survey of Columbian government officials reported 66 attacks or depredation by Andean bears, which was explained by the authors to be due to recent increases in the level of human activities in that region.36 The sloth bear (Melursus ursinus) lives in the subtropical forests of Nepal, Bangladesh, Bhutan, India, and Sri Lanka (Figure 57-16, online). It has a disheveled appearance because of its long, shaggy fur coat. In some of its range, the sloth bear coexists with elephants, wild boars, leopards, tigers, greater onehorned rhinos, and Asiatic black bears. The sloth bear is a special type of insectivore, termed myrmecophagous, because it feeds primarily on ants and termites. It is uniquely adapted for this feeding behavior. Without the two upper incisors and with an elongated and raised hard palate, mobile lips, and nearly naked snout, the sloth bear can blow away dust to expose termites and create a strong sucking force to feed. It can dig out insect burrows with its long claws, and its coat protects it from insect stings. After the Russian brown bear, the sloth bear may be the most dangerous bear species in Europe or Asia. Approximately one person is seriously injured or killed by a sloth bear in Chitwan National Park in Nepal each year.21 In the remote regions of western Nepal, at least one villager is seriously injured by a sloth bear every other year. Most of these injuries are the result of a close encounter, and the victims receive wounds to the head and neck. No predatory behavior has been reported. In the North Bilaspur Forest of India, 137 attacks by sloth bears (including 11 fatalities) occurred between April 1998 and December 2000. Most (54%) incidents took place during the monsoon season, and 45% in early morning. Victims suffered multiple injuries in most cases (52%), but solitary injuries to leg (25%), hand (12%), and head (8%) regions were also recorded.2 The aggression of the sloth bear is rated between that of the American black bear and grizzly bear. Sloth bear researchers in Nepal work exclusively while riding elephants because of their concern about attacks from rhinos, sloth bears, and tigers, in that order.35 Asiatic black bears (Ursus thibetanus), also known as Tibetan black bears or Himalayan black bears, occupy the broad-leafed forests throughout a large portion of south Asia, from Pakistan across northern India and into China and Southeast Asia (Figure 57-17). Separate populations also occur in eastern Russia, Korea, Taiwan, and Japan. Some of their range overlaps with those of brown bears, sloth bears, and sun bears. The Asiatic black bear is sometimes called the “moon bear” or the “white-breasted bear” because of the crescent-shaped white coloration on its chest. The Asiatic black bear is a dietary generalist and feeds on a wide variety of plants, insects, and animal matter. It is a good climber and often forages and rests in trees. Unlike pandas and spectacled bears, these bears hibernate during the winter months. They are hunted extensively for illegal trade of bear parts and have been declared a threatened species; as such, they rarely come into human contact. A recent decrease in natural habitat has, however, increased the chances of bear–human interaction, resulting in human injury (Figure 57-18). One report documented five cases in 1 year of serious injuries requiring hospitalization.56 1132

FIGURE 57-17  Asiatic black bear. (Courtesy Marilynn G. French.)

FIGURE 57-18  Himalayan black bear injured a Bhutanese farmer, who disturbed the bear feeding on a calf. The patient sustained an open fracture/dislocation of the knee and multiple lacerations. (Courtesy Sam Baker.)

In Kashmir, India, between 1990 and 2007, 417 cases of Asiatic black bear attack were recorded. The victims involved tended to be young to middle-aged (96.8% of cases) and predominantly male (80.33%). Incidence of attack was highest during July to November (76.82%), and most of the attacks (97%) occurred during daytime hours. The face (80.57%) was the most common part of the body injured (Figure 57-19), followed by the head (54.67%), and the mortality rate was 2.39%.48 Another source quoted approximately 150 bear reports per year to tertiary care hospitals in Kashmir, a state with a population of 5.4 million.12

FIGURE 57-19  Extensive facial injury after Himalayan black bear attack. (From Rasool A, Wani AH, Darzi MA, et al: Incidence and pattern of bear maul injuries in Kashmir, Injury 41:116, 2010.)

Bear Attacks

The Essentials for Traveling in Bear Country http://www.wildlife.alaska.gov/index.cfm?adfg=bears.bearfax If You Encounter a Bear? http://www.nps.gov/archive/glac/resources/bears2.htm#Encounter Encountering a Bear http://fwp.mt.gov/recreation/safety/wildlife/bears/ bearEncounter.html What If I See a Black Bear? http://fwp.mt.gov/recreation/safety/wildlife/bears/ bearEncounter.html

FIGURE 57-20  Sun bear. (Courtesy Marilynn G. French.)

The sun bear (Helarctos malayanus) is the smallest of all bear species, rarely weighing more than 45 kg (100 lb) (Figure 57-20). It occupies tropical regions in Borneo, Burma, Java, Malaysia, Sumatra, and Thailand. As with the spectacled bear, the sun bear is equatorial because part of its range extends below the equator. It has a white to cream-colored, horseshoe-shaped marking on its chest, providing its common name. In some localities it is called the honey bear. It has a long slender tongue, an adaptation for extracting honey from beehives. Its claws are long and more sharply curved than those of other bears, enabling it to be a proficient tree climber, where it can easily hang upside down from a branch. The sun bear is rarely seen and represents almost no threat to humans.

Prevention and Risk Reduction Much literature about safety in bear country involves attack victims.13,28,29,37,41 Such information is gathered from victims who are generally unfamiliar with bear behavior and whose interpretations of the events reflect their cultural biases. Also, victims often become instant media celebrities. In several cases, the circumstances surrounding the attack changed significantly with each telling, usually reducing the victim’s culpability. Because of potential litigation, some victims have told their stories only through an attorney. Caution must be used when compiling and analyzing such “data.” Recommendations for avoiding bear attacks have been drawn primarily from what attack victims did “wrong.” Because most people who live, work, and regularly vacation in bear country are never injured, it is equally important to understand what they have done “right.” Unlike bear attack victims, these people have successfully navigated grizzly country without being injured. Although this information is not as readily available as attack records, it is critical to our knowledge of grizzly–human interactions. Box 57-1 lists website resources for how to prevent bear attacks. From 1900 to 1985, 115 human injuries were reported from black, polar, and grizzly bear attacks in Alaska, but only two victims were natives.41 This strongly suggests that the behavior of people is important in determining how to coexist with bears safely. Safety in bear country involves four levels of interaction: (1) avoiding an encounter, (2) reducing the chances of being attacked after an encounter, (3) reducing the severity of injuries received if attacked, and (4) reducing the chances of becoming prey to a bear.

Spray More Effective Than Guns Against Bears http://www.bear.org/website/bear-pages/pepper-spray.html

ridge. Foghorns have been used successfully in Alaska; “bear bells” may not be sufficiently loud (Figure 57-21). 2. Remain alert in bear country and be aware that the terrain and environment may hamper a bear’s ability to detect a human by sight, smell, or sound. The terrain and environment may also hamper your ability to see or hear a bear before it discovers you. An “upwind bear” is more likely to be surprised, as is one in heavy forestation or near loud rushing water, in the rain, or in fog.16 Avoid ripened berry patches, streams with spawning fish, and elk calving grounds.16 A flock of ravens may indicate carrion and the presence of feeding bears. 3. Always use good judgment to avoid a potentially dangerous situation. If fresh bear signs are seen, such as tracks (Figure 57-22), droppings, tree scratchings (Figure 57-23),

FIGURE 57-21  One hopes not to find bear bells within or on bear scat. (Courtesy Timothy Floyd.)

AVOIDING AN ENCOUNTER The following actions can significantly reduce the chances of having a close encounter with a bear: 1. Make noise so that the bear knows a person is present. This requires only casual conversation to prevent startling a bear at close range. The voice may have to be amplified somewhat while traveling along a noisy stream or a windy

FIGURE 57-22  Bear prints. (Courtesy Timothy Floyd.)

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BOX 57-1  Website Resources for How to Prevent

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 57-25  Yawning behavior may indicate agitation in a bear. (Courtesy Timothy Floyd.)

FIGURE 57-23  Tree scratchings from bear claws. (Courtesy Timothy Floyd.)

or a carcass (or even scavenger activity indicating that a carcass may be nearby), consider that a bear is in the vicinity and take an alternate route. If the bear is seen first, slowly and quietly retreat to safety; consider aborting the trip or taking an alternate route. Do not approach bears, or any wild animals, too closely for a better view or photograph. Bears in bear–bear confrontations (Figure 57-24) demonstrate signs of aggression and annoyance. These include standing or turning in profile to appear larger and intimidating, vocal hissing and jaw popping, “yawning” (Figure 57-25), and head swinging (Figure 57-26).16

AVOID PROVOKING AN ATTACK Again, the best way to avoid bear-inflicted injuries is simply to avoid surprising a bear in a close encounter situation. Although no set of responses is guaranteed to prevent injury in a close encounter, the following generalizations may be useful: 1. Allow the bear to know you are human and not a prey species. Step away from any visual obstruction to allow the bear to see you fully. Any attempt to hide at this point will only confuse the bear, which may approach closer to

identify you, thus creating an encounter at an even closer distance. It is probably best to talk in a calm voice to allow the bear to identify you as a human. 2. Although remaining calm is difficult, do not make sudden movements or yell out, particularly with a grizzly bear. The bear may view this as an aggressive action and deal with it by an aggressive response. 3. Do not stare directly at the bear. Look to the side or stand sideways to the bear. Standing your ground is important in determining the bear’s response.54 This posture tells the bear you are willing to defend yourself if necessary, and it may prevent further aggressive behavior. 4. Do not consider climbing a tree or running away. Not only is it impossible to outrun a bear, but running may prevent the bear from correctly identifying a human and may initiate a charge. Once a bear charges, you cannot locate a climbable tree and achieve a safe height fast enough. Attempting to climb a tree may also prevent the bear from correctly identifying you as a human. Therefore, the best defense during a charge is to stand quietly and nonaggressively, and allow the bear to identify you as human and not a prey species. In most cases, the bear aborts the charge after a close encounter without making contact or causing injury. At this point you should leave the area, retreating in the direction opposite to that taken by the bear. If a bear continues to charge, however, resulting in physical contact, your actions should depend on the species, and information from bear attack victims is useful.

REDUCING THE SEVERITY AND EXTENT OF INJURIES If attacked by a bear, a victim can take several important steps to minimize injury. The actions taken immediately before, during,

FIGURE 57-24  Brown bears spar for a prime fishing spot. (Courtesy Luanne Freer.)

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FIGURE 57-26  Head-swinging behavior in a polar bear. (Courtesy Timothy Floyd.)

and after an attack will most likely influence the type and severity of the injuries. Humans are rarely killed during an attack precipitated by a surprise close encounter, even though bears could do so easily and quickly. During these attacks, grizzlies are only trying to remove what they perceive as a threat, and their intent is to use only as much force as necessary. When interacting with others of their species, grizzly bears are head oriented, and they usually direct their aggression toward humans in the same manner— toward the head and neck. Therefore, the general rules to follow during a grizzly attack are to “help” the bear remove the perceived threat and to protect vital body parts, as follows: 1. Do not run, try to climb a tree, fight, or scream. 2. Drop to the ground and protect the head and neck by interlocking the hands behind the head (ear level) and flexing the head forward, either in the fetal position or flat on the ground face down (Figures 57-27 and 57-28). Use elbows to cover the face if the bear turns you over. 3. Do not hold out a forearm or hand to ward off the attack. Bears can readily cause significant neurovascular injuries to these structures. 4. Never try to look at the bear during an attack because it could expose you to serious facial injuries. 5. After the attack, stay down until you are sure the bear has completely left the area. This is extremely important. Victims who have gotten up before the bear has left after the first attack generally received more severe injuries during the second one. 6. When you believe the bear has left the area, peek around while moving as little as possible, try to determine which way the bear went, evaluate options, and then leave the area.

FIGURE 57-28  Prone position to defend against a bear attack. (Courtesy Marilynn G. French.)

PREVENTING PREDATORY BEHAVIOR The most important way to reduce the chance of being preyed on by a bear is to avoid anything that may attract a bear to the campsite while the occupants are sleeping, as follows: 1. Avoid camping along bear travel corridors or at seasonal feeding sites. 2. Avoid campsites littered with human refuse. 3. Use proper food storage to render human food unavailable to bears. Bear-resistant food storage containers are often provided at designated campsites in bear country (Figure 57-29). 4. Reduce food odors by cooking and eating at a site away from the sleeping area. Do not sleep in clothes worn when cooking and eating. 5. Do not leave garbage or food buried or poured into the ground at the campsite. This can cause problems for future campers at this site. This website lists different manufacturers of bear-proof storage and garbage cans: http://www. state.nj.us/dep/fgw/bearcont.htm The chance of a bear entering a campsite to prey on humans is small, but everyone in the camp should be familiar with a contingency plan. Everyone should know the area, even in the dark, and be aware of potential escape options, such as climbable trees or rocky ledges. Everyone should sleep in a tent because it offers a boundary of protection and may deter an inquisitive bear from walking directly to the campers. Although no study has proved its effectiveness, some people build a brush barrier around the tent to prevent a bear from readily approaching it.

FIGURE 57-29  Standard government-issued bear-resistant food container. (Courtesy Marilynn G. French.)

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CHAPTER 57  Bear Behavior and Attacks

FIGURE 57-27  Curling into the fetal position to defend against a bear attack. (Courtesy Marilynn G. French.)

In a close encounter situation, attack victims who immediately protected themselves and did not try to resist typically received minor injuries that could be treated on an outpatient basis. Victims who tried to run or fight the bear and those who left after the initial attack but before the bear had left the area typically received more severe injuries that required multiple surgical procedures, resulting in permanent cosmetic or functional disabilities. If the attack is by a black bear, a different set of guidelines should be followed. Black bear aggression should be countered with aggression, such as shouting, yelling, throwing rocks or sticks, or whatever means are available. The victim should never lie down in a protective, submissive position because black bears are more likely to prey on humans they encounter at close range than are grizzly bears. The data on polar bears are less complete but suggest that attacks by females with offspring are behavioral responses similar to those of grizzly females with offspring. The attacks are defensive, brief, and result in nonlethal injuries. In addition, the bear typically leaves shortly after the incident. If a polar bear is alone, however, a person should assume it is a male, whose behavioral response is more likely predatory, and should use any aggressive response available.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Sleeping bags should be kept at least partially unzipped to facilitate a quick exit. In several instances, a victim trapped inside a sleeping bag has been dragged away from a campsite by a bear. Each tent should be equipped with a flashlight. Pepper spray is useful, as well as a firearm, unless prohibited in that area. Again, a bear that enters a tent or picks up a sleeping camper is trying to prey on that person, so all available defenses should be used. The behavior of a predatory bear is different from that of a bear responding to a close encounter. During a close encounter, a bear’s response is driven by a defensive reaction, which can be aggressive and injurious. In contrast, the behavior of a predatory bear is driven by the desire for food. The bear is not looking for a confrontation or fight but rather a victim to drag from camp, usually only a few hundred feet, and to consume. Predatory grizzly and black bears rarely kill their victims before consuming them. They concentrate on soft tissue or visceral consumption, and the victims frequently remain alive for an hour or more. Therefore a quick, aggressive, and unified response by companions may save the victim’s life. Surprisingly, yelling, throwing rocks, or striking the bear with a stick has been effective in driving the bear away from its victim. Approaching a predatory bear in the dark while it is feeding on a human is risky, but it is probably the victim’s only chance for survival. In contrast, the victim of a predatory attack by a polar bear is typically killed instantaneously, so prevention of such attacks is the only chance for survival. In all predatory attacks by polar bears, all defensive measures must be considered, including guns where permitted.

SPECIAL CONSIDERATIONS Menstruation.  In August 1967, two women were killed in separate events on the same night by different grizzly bears in Glacier National Park. The postmortem examination showed that one had been menstruating. The assumption that menstruation may be a precipitating factor in bear attacks has unfortunately become solidly ingrained into popular opinion. Hysterical coverage by the media enhanced this misconception, and the scientific question was left unanswered by both scientists and government officials.6 A study of polar bear response to menstrual odors was published in 1983.14 Although it was not designed to adequately test the hypothesis that menstruating women were more likely to be either attacked or preyed on by bears, the press came to this conclusion. The Interagency Grizzly Bear Committee then printed an ambivalent caution in the government’s official grizzly bear pamphlet (“Bear Us in Mind”) that said, “Women may choose to stay out of bear country during their menstrual period.” Fortunately, this has since been removed from the pamphlet, because no scientific evidence suggests that menstrual odors precipitate grizzly bear attacks. The attack mentioned previously is the only serious attack on a menstruating woman that has been documented in North America, and even the official investigating team at that time concluded that menstruation did not appear to have played a major role.28 Black bear researchers in North America report no evidence of black bears attacking or being attracted to menstruating women.49 Furthermore, no evidence links menstruation to any of the 21 grizzly bear attacks in Yellowstone National Park from 1980 to 1994.26,27

grizzly bears were sprayed in the face at close range when they charged the researchers (who were outside the cage). Under these controlled conditions, red pepper spray was found to be highly effective in deterring a charging grizzly bear. Pepper spray (5% to 10% capsicum oleoresin) is commercially available as personal protection against aggressive animals. The effectiveness of pepper spray used in the field against aggressive bears has been difficult to assess. It has been used in too few cases to draw firm conclusions. Also, it is impossible to conduct scientific studies testing its effectiveness under these conditions. By 1985, pepper spray was used in the field against aggressive black and grizzly bears in 66 documented cases.30 In general, it appeared more effective in deterring bears that charged after a close encounter than against food-conditioned bears in search of food. During the 1990s, however, most professional outfitters and guides in the northern Rocky Mountains began carrying pepper spray to deter aggressive grizzly bears, preferring spray over firearms. Although data are limited to anecdotal reports, pepper spray can be an effective and nonlethal alternative to repel aggressive grizzly bears, perhaps even more effective than firearms. Carrying pepper spray, however, is not a substitute for knowledge of bear safety and good judgment to avoid aggressive encounters. If carried, spray must always be readily available, either in a belt-mounted holster or on a chest strap. It should be test-fired, and the user should practice drawing and firing it regularly (Figure 57-30). Despite a manufacturer’s claim that pepper spray has an effective range of 9 m (30 feet), the effective range under field conditions is significantly less when there are headwinds or crosswinds. Preliminary field experience indicates that the oil-based pepper spray is more effective than the water-based spray. The author recommends a pepper spray that contains 10% capsicum oleoresin, has 2 million Scoville heat units, and comes in a 15-oz pressurized aerosol container. Unfortunately, people have used pepper spray in the same way they use mosquito spray. Despite its obnoxious and caustic smell, some sprayed it on themselves, as well as their tent, their sleeping bags, and the ground around their campsite. Once the aerosol has been released, the capsicum begins to lose its potency, and soon the active ingredient dissipates. At this point, bears may investigate the smell of pepper. Pepper spray so used thus becomes a bear attractant rather than a deterrent. One manufacturer of pepper spray (UDAP Industries, http://www. udap.com) provides a detailed instructional pamphlet on its proper use. Pepper spray should be aimed toward a charging bear and discharged when the bear is within 6 to 9 m (20 to 30 feet). The person should continue spraying until the bear has stopped its charge, keeping the sprayer aimed at the bear in case it charges again. This continues until the bear has left the area. If the pepper spray is depleted, the best defense if the bear attacks is to lie down, cover the face, and offer little or no resistance. Again, there is no guarantee that pepper spray (or anything) will prevent injury by an aggressive bear.

Sexual Activity.  A common concern among backcountry users is that sexual activity may attract bears and make them more aggressive toward campers. As with menstruation, these fears are based on hysteria and folklore. No anecdotal or scientific evidence supports this hypothesis. Pepper Spray.  Because of the desire for protection against aggressive bears, several methods were investigated for backcountry users. In the late 1970s and early 1980s, several compounds were tested for effectiveness in deterring grizzly bear attacks. The most effective method was an aerosol spray containing capsicum oleoresin, a derivative of red pepper. Captive 1136

FIGURE 57-30  Discharging a canister of pepper spray. (Courtesy Marilynn G. French.)

FIGURE 57-31  Cranial vault of a bear. (Courtesy Timothy Floyd.)

If pepper spray is accidentally discharged into a person’s face, it stimulates facial nociceptors and causes eyelid, ocular, and facial muscle spasms, which may result in temporary blindness. The victim should not rub the eyes (to avoid corneal abrasions) and should irrigate the eyes and skin vigorously with water for at least 15 minutes. Intraoral burning may be relieved by swishing and spitting milk or another casein-containing food product.16 Firearms.  Many people consider carrying firearms for protection when they enter bear country. Guns can be useful in some situations. However, the target area to kill a grizzly with a shot to the head is only about 30 cm2 (12 inches2). The cranial vault is narrow and sloped caudally (Figure 57-31). A bear initiating a charge from a distance of about 45 to 55 m (50 to 60 yards) will take only 4 to 5 seconds to reach its victim. Unless a proficient marksman, a person is unlikely to access a weapon, release the safety, aim accurately, fire, and hit a small target in a brief time under incredible emotional stress. Also, even if a shot could be fired, it probably would only wound the bear. Wounding a charging bear changes its behavior and may make its attack even more aggressive. Because of these factors, pepper spray should be considered as a nonlethal alternative to guns, especially when traveling in places where loaded guns are not permitted, such as national parks. According to most U.S. and Canadian wildlife agencies, the most effective firearms against grizzly bear attacks are a 12-gauge 3-inch magnum shotgun with 1-oz slugs and a 30-06 rifle with a 200-grain bullet. A pistol is not considered to be an effective weapon against a charging grizzly. A large-caliber pistol, such as a 44-caliber magnum, can be used as a point-blank weapon to kill a bear attempting to prey. The effective ranges of a pistol and pepper spray are about the same, but it is easier to hit a moving target with pepper spray because of its shotgun-like aerosol pattern. Dogs.  In most national parks, dogs are not permitted in backcountry settings. Unfortunately, rare and questionable accounts report a dog stirring up a grizzly, then running back to its owner with the bear in pursuit. Most outfitters, guides, and hunters, however, report positive experiences with dogs in grizzly country. Their dogs are generally well trained and have been raised in wilderness environments. Most of these dogs can effectively deter grizzly and black bears from coming into a camp. Although no study has been conducted on the use of untrained dogs to deter aggressive bears, most people who spend considerable time in grizzly country use their dogs for this purpose. Horses.  For individuals concerned about an aggressive bear encounter, another option is the use of horses. No one has been injured by a grizzly or black bear while riding a horse. Horses that frequently travel in bear country are the best to use, because they generally do not react unpredictably and endanger the rider when they encounter bears. Although horses may protect against aggressive grizzly encounters, riders may still be injured by the

Hunter Safety.  Many people participate in sport hunting in bear country each year. Some are hunting for bears, but most hunt for other game species. For hunters of bears, the risks are obvious. Bear hunters intentionally break bear safety rules to close in on their prey. The most dangerous situation, however, is after they shoot and injure a bear. They have an ethical obligation to track the wounded animal and kill it, but this is when most bear hunters are injured. This confirms that guns are not completely effective in preventing bear injury. An injured bear may take refuge in heavy cover, then charge when the hunter is at close range. With little time, a surprised hunter often cannot fire a lethal round, and even when shot, the bear can continue its attack and cause significant injury before it dies. Hunters of other game species in bear country are at significant risk of close encounter and injury. Beside violating bear safety rules, they frequently become preoccupied with the stalk and forget they may encounter a bear. During the 1990s, more than one-half the people injured by grizzly bears in the Yellowstone ecosystem were elk hunters. Some injuries occurred during the stalk, but other factors contributed. Grizzly bears in this ecosystem have learned the association between gunfire and available food. After an elk or other game (moose, deer, bighorn sheep) has been killed, hunters field-dress their kills and leave edible remains (gut piles) on the ground. In several cases, bears approached the kill site before the hunters completed this process. In other cases, an elk or animal was field-dressed late in the evening and then hung in a nearby tree. When the hunters returned the next morning, they encountered a grizzly bear that had claimed the gut pile or the carcass. Hunters must assume that under these circumstances, at least one grizzly bear will be at the site, and they must approach cautiously, preferably on horseback. Bow hunting represents another high-risk activity. In most states, bow hunters are not allowed to carry a firearm as a backup weapon. They also tend to violate bear safety rules to set up a shot. Elk hunters blow an artificial elk call (a bugle or a cow call) to lure in bull elk. This also alerts grizzly bears that prey on adult male elk (bulls) during the breeding season. For protection, bow hunters should (1) hunt from a tree-stand, which provides some protection from grizzly bears, who are poor tree climbers, and (2) carry pepper spray and be prepared to use it.

Bear-Induced Injuries Bear-inflicted injuries range from minor, treated on an outpatient basis, to complex, requiring hospitalization and surgery, typically resulting in significant cosmetic and functional disability. In this regard, bear attacks are similar to most other animal attacks, particularly those inflicted by large animals. The character of such injuries is determined in part by the three main sources: teeth, claws, and paws. The teeth of bears, especially the canines, are large and sturdy. Although the teeth are not particularly sharp, the power of the jaw muscles allows the teeth to penetrate deeply into soft tissues and fracture facial bones and bones of the hand and forearm with ease. The trauma characteristically results from punctures, with shearing, tearing, and crushing forces (Figure 57-32). The claws are another important source of trauma (Figure 57-33). Although the claws on the front pads can be as long as human fingers, they are not particularly sharp on grizzly and polar bears. The bear’s shoulders, however, provide the force and speed that allow claws to cause significant soft tissue damage in a scraping maneuver that results in deep, parallel gashes. Because black bear claws are sharper and more curved, the cuts tend to have sharper, less ragged edges. The bear paw is capable of delivering a powerful force, resulting in significant blunt trauma, particularly to the head and neck, rib cage, and abdominal cavity, especially solid organ rupture. Therefore, victims of bear attacks should be evaluated for occult blunt trauma. 1137

CHAPTER 57  Bear Behavior and Attacks

horse. People are seriously injured or killed in horse accidents each year in the northern Rocky Mountains.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 57-32  Bite wound injuries typical of a bear attack. (Courtesy Luanne Freer.)

Several victims of a bear attack were further injured when a companion accidentally shot them while trying to kill the attacking bear.25 Others were injured when they fell out of a tree while escaping a bear; some sustained long-bone fractures. At least two persons in North America have been killed by such falls, and in both incidents the bear did not attack the victims once they fell to the ground.

Wound Management The specifics of initial wound treatment are determined in part by the available medical equipment and the location in which the victim is first received. Stabilization of the victim remains the primary objective. All victims of bear attacks should be considered to have major trauma and should be transported to the most appropriate facility after stabilization. By the time most bear attack victims reach medical care, their injuries are relatively old. Bear-inflicted injuries are often occult, producing greater deep structure involvement and tissue necrosis than initially expected. Internal injuries from either direct penetration (claws, teeth) or blunt trauma are common. Neurovascular injuries must be considered with trauma to the extremities, and neurosensory and cosmetic injuries are common with trauma to the face.

Antibiotic Therapy There are only a few published studies concerning the oral flora of black or grizzly bears.17,24,45 The bacterial spectrum of black and grizzly bears appear similar to that of dogs, although anaerobes, common in human, dog, and cat bites, have not been reported. In the few case reports available,38,39,50 many victims

received antimicrobial administration prior to hospitalization and prior to wound cultures. Nonetheless, there is no evidence that bear attack victims develop rare or unusual septic complications from unknown pathogens, with the exception of a single reported case of an atypical mycobacterial infection after a brown bear bite in Finland.39 The use of antibiotics shortly after the injury but before clinical evidence of infection remains controversial. The usual risk factors should be assessed (Box 57-2).7 However, the blunt trauma, deep punctures, and shearing-and-tearing forces that are typical of bear attacks create significant tissue ischemia and necrosis that are not apparent on initial examination. In one study, nearly 50% of bear

BOX 57-2  Animal Bite Risk Factors High Risk Location Hand, wrist, or foot Scalp or face in infants Through-and-through bite of cheek Bites over vital structures (e.g., artery, nerve) Bites over a major joint Type of Wound Puncture Tissue crushing that cannot be debrided Victim Characteristics Older than 50 years Asplenic Chronic alcoholic Altered immune status Diabetic Peripheral vascular insufficiency Chronic corticosteroid therapy Prosthetic or diseased cardiac valve Prosthetic or seriously diseased joint Low Risk Location Face, scalp, ears, or mouth Self-bite of buccal mucosa Type of Wound Large, clean lacerations that can be cleansed Partial-thickness lacerations and abrasions

FIGURE 57-33  Claw markings from a bear attack. (Courtesy Luanne Freer.)

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Victim Characteristics Younger than 50 years Good medical health

attack victims (four of nine) developed clinical infections.50 Therefore, antimicrobial prophylaxis should be considered for all bear-inflicted wounds pending culture results and before clinical evidence of infection. Before culture results are available, victims of bear attacks should be treated with broad-spectrum agents to cover Staphylococcus aureus and gram-negative rods in addition to anaerobes. However, adequate wound debridement and cleansing are the primary means of reducing the infection rate. Antibiotics should be administered parenterally for at least 3 days after wounding and for at least 2 days after each debridement.16

Rabies Although rare, rabies has been documented in black bears in the Canadian provinces of Alberta, Ontario, Quebec, and Northwest Territories,57 and cases have been reported in the U.S. states of Maryland, Pennsylvania, Arizona, and New Jersey.8,33,42 Scientists suggest a possible link between the timing of rabies infection (early in the season) and hibernation, proposing that the bears may

have been bitten by rabid animals while they hibernated or that the stress of coming out of hibernation could have induced latent virus from an exposure prior to hibernation. A rabid polar bear in Canada remains the only documented case reported in polar bears.55 A rabid brown bear killed two men and injured six others in Brasov, central Romania in 2004.3 There are no reports of clinical rabies in North American brown bears, but rabies-neutralizing antibody was documented in one brown bear;43 the positive titer is thought to have resulted from ingestion of an oral wildlife rabies vaccine and not from infection with rabies virus. Although rabies in bears is exceedingly rare, the Centers for Disease Control and Prevention (CDC) recommends rabies immunization for victims attacked by wild carnivores. Therefore, all victims of bear attacks should receive the standard informed-consent discussion of the risks and benefits of rabies immunization.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 58 



Alligator and Crocodile Attacks BENJAMIN B. CONSTANCE

Crocodilians have inundated cultural media from traditional folklore to modern television.25 In addition to their fearful appearance, they are one of the few animal species that will attack and kill humans.20 Evidence can be found in paleontologic references that crocodilians preyed on human ancestors.7 Crocodilians have been feared and worshiped in ancient societies such as the Australian Aborigines, Iban people of northern Borneo, Cambodian villages, ancient Egyptians, and Native Americans.3 Following World War II, alligators were increasingly hunted, and because of a decline in numbers, were listed in 1967 on the endangered species list. Following federal protection, they were removed from the list in 1987; alligator populations in the southern United States have since increased.15 Many populations of crocodilians, however, have not fully recovered. With rising human inhabitation around coastal zones of Australia and the southern United States, human–crocodilian interactions are likely to increase.5 Crocodiles, alligators, and caimans are all parts of the reptilian order Crocodylia, comprising a total of 23 species separated into three families: Alligatoridae (with 8 species, including alligators and caimans), Crocodylidae (14 species, including the crocodiles), and Gavialidae (including the Indian gharial) (Figure 58-1).3 Crocodilians date to the time of the dinosaurs and are one of the oldest living members of the reptile family. Alligators and caimans belong to the same crocodilian order, and both have shorter, wider snouts than do crocodiles.8 When an alligator or caiman is seen with a closed mouth, its upper jaw hides the fourth, lower tooth. Some species of caimans have bony ridges, called spectacles, between the eyes.8 Three such species of crocodilians (genus Crocodylus) and alligators (genus Alligator) exist in the United States, two native and one foreign.28 The American alligator (Alligator mississippiensis [Figure 58-2, A]) is the most common species and found in most southern states, including Florida, Georgia, South Carolina, North Carolina, Louisiana, Alabama, Arkansas, Mississippi, Texas, Oklahoma, and likely Tennessee (Figure 58-3). The American crocodile (Crocodylus acutus [Figure 58-2, B]) is found only in south Florida. The non-native caiman (Caiman crocidilus [Figure 58-2, C ]) is becoming increasingly established in south Florida.16 Worldwide, crocodilian habitats include southern United States, Central and South America, sub-Saharan Africa, India, Sri

Lanka, southern China, the Malay Archipelago, Palau, the Solomon Islands, and northern Australia (Figure 58-4). Larger species of crocodiles include the saltwater and Nile crocodiles. These are notoriously the most dangerous, reportedly killing hundreds of people every year in Africa and Southeast Asia.5

Characteristics, Lifestyle, and Habits The crocodile family dates back 225 million years to the Mesozoic Era. Crocodilians evolved, along with modern birds, from a group of animals known as thecodonts. Crocodilians can live in captivity up to 66 years of age, with most living up to 50 years of age in the wild.8 Crocodilians vary in size, but in general males are larger than are females, with the most growth occurring during the first two years of life. For example, the American alligator reaches a maximum adult size of 4.5 m (14.8 feet) and the American crocodile 6 m (19.7 feet). The common caiman reaches 2.8 m (9.3 feet). The notorious Nile crocodile reaches 5.5 m (18 feet) and the saltwater crocodile 7 m (23 feet) (Table 58-1).8 Breeding season is typically late May or early June, with females laying clutches of 30 to 50 eggs. Their diet is predominantly carnivorous, and includes fish, snails, birds, small mammals, frogs, and crustaceans. Crocodilians, like all reptiles, are ectothermic (cold-blooded). They rely on their environment for body temperature, and as a result, their activity level depends greatly on the time of day. In hot climates, crocodiles keep cool during much of the day by staying underwater, before they move onto land during the night. They may remain submerged for more than an hour. They may also be found in mud burrows close to the water’s edge as they lay their eggs or retreat from the water during colder months. Special adaptations make them superior predators in the water environment, preferring slow moving water to preserve their sense of smell when submerged. Crocodilians in cool climates bask in the sun to stay warm.8 Crocodilians may also rest with the mouth open, using the thin skin inside the mouth as a radiator to increase cooling. Crocodilians are largely nocturnal creatures, using their characteristic slit-like eyes to make use of more light than does a round pupil.8 A third eyelid helps protect their eyes while they swim underwater, making them more effective hunters in murky

For online-only figures, please go to www.expertconsult.com

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PART 6  ANIMALS, INSECTS, AND ZOONOSES

Crocodylia

Alligatoridae

Caiman

Gavialidae

Crocodylidae

Alligator

FIGURE 58-1  The order Crocodylia is broken into 3 families: Alligatoridae, including alligators and caimans; Crocodylidae; and Gavialidae, which includes the gharial.

C

B

A

FIGURE 58-2  Three species of Crocodylia live in the Americas. A, The American alligator (Alligator mississippiensis). B, The American crocodile (Crocodylus acutus). C, The caiman (Caiman crocidilus). (A Courtesy Brad Weinert; B courtesy Gerard Caddick and Terra Incognita; C courtesy George Hertner.) TABLE 58-1  Crocodilian Lengths by Species Species and Latin Name

FIGURE 58-3  Map of crocodile- and alligator-inhabited regions of the United States.

American alligator (Alligator mississippiensis) American crocodile (Crocodylus acutus) Australian freshwater crocodile (Crocodylus johnsoni) Black caiman (Melanosuchus niger) Common caiman (Caiman crocodilus) Nile crocodile (Crocodylus niloticus) Saltwater crocodile (Crocodylus porosus)

4.5 m (14.8 feet) 6 m (19.7 feet) 3 m (10 feet) 4.6-6 m (15-19.7 feet) 2.8 m (9.3 feet) 5.5 m (18 feet) 7 m (23 feet)

Data from Dudley K: Alligators and crocodiles, Calgary, 1998, Weigl Educational Publishers Limited.

Alligator sinensis Alligator mississippiensis Crocodiles

Alligators and Caimans

FIGURE 58-4  Map of crocodile- and alligator-inhabited regions of the world.

1140

Maximum Adult Male Size

100 90 Temperature (°F)

80 70 60 50 40 30 20 10

Attacks Most crocodilian attacks occur “out of the blue” as the attacking animal utilizes a sudden burst of speed and the advantage of surprise.6 An adult crocodile can devour prey much larger in size than a human. According to one report, the stomach of an Australian estuarine crocodile contained the remains of an aborigine and a 4-gallon drum containing two blankets. The crocodile can travel in water at a speed of 32 km/hr (20 mph) and can charge a short distance over land at 24 to 48 km/hr (15 to 30 mph). The enormous jaws and canine teeth can bite with sufficient force to sever an outboard boat propeller. Feeding in freshwater rivers and adjacent land has introduced them to cows, horses, and humans, who are attacked when they cross rivers, catch fish, draw water, or work in the fields.27 Alligators residing in lakes and ponds associated with golf courses, parks, and tourist attractions have attacked humans in the United States.25 A study in the United States analyzing crocodilian attacks between 1928 and 2009 identified that 567 adverse encounters and 24 deaths had been reported. It is estimated that these events are largely underreported, and may not be representative of notably higher incidence in other countries. Most fatalities are reported in Florida, followed by Texas, Georgia, and South Carolina.16 Severe injuries described as life or limb threatening represented only 11.8% of cases. Attacks in most instances were only a single bite (81%). Victims were more likely to be males (85.4%) and adults 18 years of age or older (78.6%).16 Most injuries were classified as lacerations and punctures to the arms, forearms, hands, fingers, legs, and thighs. Most injuries occurred while handling alligators, followed by wading or swimming, typically occurring in deep (>1 m) water, followed by shallow water, and within 1 m from shore.16 Most attacks occurred between the months of May and August and during the afternoon hours to twilight (Figure 58-5). Of the attacks in this study, 33% were felt

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Au ly Se gus t pt em b O er ct ob N ov er em D ec ber em be r

Saltwater crocodilians are generally larger and more aggressive than are freshwater crocodilians. They are more active at night and during the summer months but are opportunistic feeders and will pursue a meal when one becomes available. Larger crocodilians have been known to attack larger prey such as pigs, cattle, buffalo, horses, and humans. In addition to shallow and deep water, attacks have been witnessed on beaches and riverbanks. Crocodilians have peg-like teeth well adapted for catching and holding onto prey. However, the teeth are not well suited for chewing, so most prey is killed and allowed to rot, which makes it easier to swallow.28 Once captured, prey is often completely neutralized by being crushed by the attacker’s powerful jaws. Larger prey animals are often attacked at the lower extremities, throwing them off balance prior to their being dragging into the water and drowned. Once overtaken, smaller animals are swallowed whole. Violent thrashing of the crocodilian head from side to side dismembers larger prey. Further attempts of separating smaller pieces are accomplished by rolling the prey over and over underwater, the so-called “death roll.”28 As a result, victims of crocodilian attacks are generally severely disfigured with significant crush injuries.20

Ja

Feeding and Predation Habits

ar

y

0

Alligator attacks Temperature Breeding season FIGURE 58-5  Distribution of alligator attacks and temperature by month.

to be provoked, with the majority of instances stemming from the victim trying to handle the alligator or trying to rescue another human or animal victim. The majority (54.8%) of cases were felt to be unprovoked. In a series of 16 crocodile attacks reported from the Northern Territory of Australia, four fatalities involved transection of the torso or decapitation.19 Most attacks (fatal and nonfatal) were on persons swimming or wading in shallow water. A later study analyzing 62 definite, unprovoked attacks by wild saltwater crocodiles between 1971 and 2004 showed that 27.4% of attacks were fatal, with increasing numbers of attacks in recent years. Fatal injuries were equally likely to be during the day or night; however, nonfatal injuries occurred predominantly during the day (76.7%).3 Most attacks occurred in the wet-warm season during the months of November to April, with 51.6% of all annual attacks occurring during this time period. Most fatal attacks involved saltwater crocodiles greater than 4 m (13 feet) in length. Similar to U.S. studies, the majority of victims were male (75%), with an average age of 31.2 years.3 In riverine areas of Tanzania, crocodiles are a considerable health hazard. In the Korogwe District from 1990 to 1994, 51 human and 49 crocodile deaths were reported. The attacks are attributed to increased waste products in the water, which reduces the crocodiles’ primary food supply. In addition, “tamed” crocodiles are not hunted because of local superstitions and fear of reprisal by witchcraft.25 A study of attacks in Malawi noted that 60 patients were injured during a 4-month period.27 Twentyfour (40%) of the victims had significant injuries, including permanent deformity and one death from sepsis. Smaller crocodilians generally bite only once, but one-third of attacks may involve repeated bites.15 Crocodilians greater than 2.5 m (8 feet) in length more commonly cause serious and repeated attacks, likely attributed to chasing or feeding behavior.15 Even though external injuries may appear to be only minor lacerations, underlying significant crush injuries often exist (Figures 58-6 to 58-8; Figures 58-7 and 58-8, online).14

First Aid Crocodilian bites can produce large crush injuries, punctures, and lacerations. Polymicrobial infections have been found to commonly cause serious deformity, sepsis, and even death.12 Evaluation of every crocodilian attack victim should begin with evaluation of airway, breathing, and circulation. Although it is tempting to direct one’s attention to obvious bite wounds, more severe and life-threatening injuries, such as solid organ 1141

CHAPTER 58  Alligator and Crocodile Attacks

water. Watertight nostrils on the distal end of their long snouts allow an impeccable sense of smell, even when the majority of the body is completely submerged under water. Crocodilians have roughly 28 to 32 teeth in the lower jaw and 30 to 40 teeth in the upper jaw. These teeth are excellent for grabbing and tearing, but cannot be used for chewing. Thus, crocodilians must tear their prey into pieces before swallowing them. Broken teeth are replaced by new teeth growing under exiting teeth, in a manner analogous to that of sharks.8 The jaws of the American alligator were noted in one study to produce the biting force of 1000  kg (2.2 tons).3 This is enough force to crush large bones and shells. Opposing muscles used to open these massive jaws, however, are quite weak and easily kept closed by human arms, as depicted by popular television and alligator tourist shows.

PART 6  ANIMALS, INSECTS, AND ZOONOSES FIGURE 58-6  Superficial lacerations and bruises were all that were noted on this victim of a black caiman (Melanosuchus niger) attack in the Amazon region of Brazil. An underlying, severe femur fracture was noted on autopsy. (Courtesy Vidal Haddad Jr.)

laceration, may exist that are less apparent. Once the airway has been secured, breathing assessed, and bleeding controlled, the patient should be completely examined from head to toe in order to discover other injuries. Basics of wound management consist of hemostasis, fracture stabilization, analgesia, thorough decontamination, and debridement1,13 (Box 58-1). Wounds should be copiously irrigated with clean water or sterile normal saline. Early analgesia will help facilitate patient comfort and debridement. If a patient is unlikely to receive hospital care shortly following an injury, empiric antibiotic therapy with a fluoroquinolone or cephalosporin should be initiated because culturing of fresh wounds immediately following injury has not demonstrated useful in antibiotic selection.10 Bony injuries or significant bleeding should prompt the application of splints to prevent further neurovascular injury and blood loss, improve pain control, and aid in transportation of the patient. Clean dressings should be applied to all open wounds.

Hospital Management Patients presenting to a hospital following crocodilian attack should receive a complete trauma evaluation, starting with an assessment of the airway, breathing, and circulation. Patients with severe injuries or unstable vital signs should be placed on a cardiac monitor, be given supplemental oxygen, and have intravenous (IV) access obtained. Nontrauma receiving facilities might

BOX 58-1  Summary Recommendations for Empiric

consider early consultation with a trauma center, with local goals of care directed toward stabilization, analgesia, antibiotic administration, and wound irrigation prior to transfer to a higher level of care. Early analgesia should be initiated, preferably with parenteral narcotics. In cases of severe deformity and pain not relieved by opiate analgesics, brachial plexus nerve blocks have been successfully used for wounds to the upper extremity.4 Small wounds may be anesthetized with local infiltration and nerve blocks. Severe cases with deep tissue destruction or multiple sites of injury may require general anesthesia to facilitate operative washout and debridement. Initial evaluation of crocodilian attack wounds should include radiographs to assess for underlying fractures or tooth fragments. Further imaging with computed tomography (CT) may be warranted for further evaluation or operative planning. Patients with injuries to the head and neck, loss of consciousness, or severe scalp injuries should receive a CT scan to assess for intracranial or bony skull injury. Injuries in close proximity to a joint should be considered open until proved otherwise, with orthopedic consultation for possible exploration and washout. Areas concerning for compartment syndrome with associated symptoms of increased pain, tense compartments, and/or decreased signs of circulation or temperature should be evaluated with tissue manometry. Compartments with measured pressures >30 mm Hg should be referred for orthopedic evaluation and possible fasciotomy.18 Tetanus prophylaxis and an appropriate broad-spectrum antibiotic, such as a fluoroquinolone or cephalosporin, must be considered. After exploration, irrigation, and debridement, bite wounds should preferably be left open because they are typically crush wounds or deep lacerations with significant bacterial contamination and surrounding soft tissue trauma.26 Cosmetically sensitive areas should be copiously irrigated and referred for delayed closure after 5 days of antibiotic therapy.26 Patients with severe trauma or infection should be admitted for further evaluation and management. Only minor wounds and patients with excellent plans for follow-up should be managed on an outpatient basis. Injuries causing significant trauma to the hands, face, and genitalia may require specialty surgical consultation. Crocodilian attacks should be reported to local authorities or land management bureau agents to facilitate nuisance animal tracking and relocation, as well as compilation of accurate statistics for prevention programs.

Microbiology and Antimicrobials In a study of the oral flora of Alligator mississippiensis, more than 38 species of bacteria and 20 species of fungi were identified by culture techniques (Box 58-2).9 Prophylactic antibiotic therapy should be initiated to accomplish broad-spectrum coverage against gram-negative species, especially Aeromonas, anaerobes, and normal skin flora.9 The current recommendation is to give a fluoroquinolone, such as ciprofloxacin 400 mg IV every 12 hours or 500 mg orally every 12 hours, or a third-generation

Treatment of Crocodilian Attack

• • • • •

Analgesia and/or regional anesthesia Hemostasis Obtain wound cultures prior to irrigation Aggressive debridement and irrigation Empiric antibiotic coverage with a fluoroquinolone or third-generation cephalosporin • If cephalosporin allergic, may also consider trimethoprimsulfamethoxazole or carbapenem • In wounds presenting with hemorrhagic bullae or necrosis, Vibrio species should be considered and the wound treated with surgical drainage and doxycycline, fluoroquinolone, carbapenem, or other appropriate antibiotic • Patients who develop cellulitis or signs of sepsis should be admitted to the hospital and treated aggressively because they carry a higher mortality rate

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BOX 58-2  Bacterial Species Isolated from Crocodilian

Species*

Aerobic Aeromonas hydrophilia Citrobacter freundii Citrobacter diversus Bacteroides oralis Proteus vulgaris Pseudomonas spp. Enterobacter agglomerans Burkholderia pseudomallei *From references 10, 14, 19, 21-23.

Anaerobic Clostridium bifermentans Bacteroides bivius Fusobacterium varium Peptococcus prevotii Clostridium tetani

BOX 58-3  Summary Prevention Recommendations • • • • •

Be cautious around still or slow-moving fresh or brackish water Be cautious of small children or pets Avoid swimming at night and swim only in designated areas Carefully dispose of food scraps Do not feed crocodiles or alligators, and don’t take them as pets • Observe or photograph crocodiles or alligators only at a safe distance, with the ability to rapidly enter a protected shelter or vehicle

cephalosporin, such as ceftriaxone 1 g IV or IM every 24 hours.17 Adults with cephalosporin allergies can be treated with trimethoprim-sulfamethoxazole 8 to 10 mg/kg/day of trimethoprim IV divided every 6 to 12 hours, or 160/800 mg orally twice daily, or a carbapenem such as imipenem/cilastatin 500 mg IV every 6 to 8 hours, for a maximal dose of 50 mg/kg/day.24 There has not been any good study evaluating duration of antibiotic treatment. Soft tissue infections should generally be treated for 7 to 10 days but may require a longer duration of antibiotic therapy for bone or connective tissue involvement. Special attention is given to treating Aeromonas infection, as this can become fulminant and rapidly progress within 24 to 48 hours to cellulitis, bullae formation, local necrosis, and sepsis. There have been case reports of Vibrio vulnificus infections following alligator attacks. V. vulnificus exists in marine and estuarine environments and causes lesions presenting with hemorrhagic bullae or vesicles followed by necrotic ulcers.2,16 These wounds should be surgically drained and treated, at a minimum, with doxycycline in addition to empiric therapy.17 Suspected or established Vibrio or Aeromonas infection should be treated as discussed in Chapter 79.

Prevention The alligator population is increasing in the United States, with nuisance complaints now registered yearly in the thousands (Box 58-3).16 In Florida, the number of nuisance calls related to alligators increased from 4914 in 1987 to 18,307 in 2006.16 These alligators are often moved to other areas or harvested. For example, the Florida Fish and Wildlife Conservation Commission permits the killing of approximately 7000 nuisance alligators each year.11 Persons in the United States traveling to regions inhabited by crocodilian species should exercise extreme caution, especially around the months of May and June, because this is breeding season and roughly 34% of attacks are felt to be defensive in nature.16 Most attacks occur in the deep or shallow regions of slow-moving water or in muddy areas within one meter of shore. Crocodilians are more active during temperatures between 28° and 33° C (82.4° and 91.4° F) and become more dormant below

12.8° C (55° F).28 Crocodilians may quickly become habituated to humans, and travelers should avoid areas where these animals are fed. Caution should be used when traveling with pets because small cats and dogs are natural prey. People should be aware of the locations and activities of small children, and not allow them to approach bodies of water outside of posted swimming areas. Avoid outdoor swimming at dawn or dusk, or during nighttime. Do not throw fish or scraps of food into the water. Do not remove crocodilians from their natural environment or keep one as a pet.

If An Attack Occurs The best way to deal with an attack is to prevent it by being “crocodile wise” and taking steps to avoid an encounter. If an attack does occur, it is important (but perhaps difficult) to remain calm and think clearly. The majority of crocodilian attacks are single bites to an extremity and are nonfatal. Although there is little to no medical literature on surviving crocodilian attacks, there is a wealth of anecdotal suggestions from communities inhabited by crocodilians. The following suggestions are presented based on their relevance to the limited case series of crocodilian attack patterns on humans and general predation habits. In the event of an encounter with an aggressive crocodilian, it is best to run away in a straight line, covering the greatest distance possible away from areas of water. Most fatalities occur in the water, corresponding with their predation habit of the animals drowning their victims. Loud noises and whistles may be helpful in fending off an attack, given the crocodilian’s sensitive hearing. If a bite occurs, most crocodilians will release their prey to gain better purchase or further crush and dismember. This may provide an opportunity to escape. Therefore, the victim of an attack should be prepared to run away at any time. If attacked, avoid the water by any means possible to avoid drowning. In the event of a water attack or being pulled into the water, roll in the same direction as the crocodilian if possible to prevent further injury to an entrapped limb. Crocodilians have a palatal valve in their posterior pharynx that prevents water from pouring into their lungs. This may be disrupted with a foot or hand and may cause the crocodilian to release its grip. It is advised to be aggressive and fight back if an attack is inescapable. Crocodilians have few sensitive areas, but present with their eyes and nostrils on the dorsum of their head. Gouging the eyes or nostrils may result in a release of grip. Attacks by crocodilians on wild prey are generally persistent until escape or death. Therefore, one should only “play dead” if all attempts at escape have been made and further efforts at fighting back are futile.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 59 



Wilderness-Acquired Zoonoses JAMIE R. SHANDRO AND JAMIE G. JENKINS

A zoonosis is an infectious disease that may be transmitted from animals to humans under natural conditions. There are more than 200 zoonotic pathogens, and potential infections vary by animal species (Table 59-1). The risk of acquiring zoonoses increases proportionately with the frequency and intensity of contact with animals. For example, hunters and trappers who handle and are

exposed to the blood, viscera, secretions, and excretions of wild animals are at much greater risk than are recreational campers. Similarly, international travelers who frequent locations with a much higher density of infected animals are at greater risk for infection. The trekker in Nepal is more likely to confront rabies than is the hiker in California. With the current ease of

For online-only figures, please go to www.expertconsult.com

1143

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 59-1  Animals and Some Associated

Zoonoses

Animals

Associated Zoonoses

Dogs

Rabies, echinococcal diseases, erlichiosis (via ticks), Pasteurella, Campylobacter, Toxocara, leptospirosis Sheep Anthrax, brucellosis, echinococcal disease, melioidosis Cattle Anthrax, brucellosis, Salmonella, Taenia tapeworms, variant Creutzfeldt–Jakob disease Goats Anthrax, brucellosis, melioidosis Horses Anthrax, glanders, Hendra virus, Coxiella (Q fever) Cats Bartonella infections (cat-scratch disease, bacillary angiomatosis), Pasteurella, Capnocytophaga, Toxoplasma, tularemia, cowpox Swine Brucellosis, influenza, melioidosis, Nipah virus, cysticercosis, trichinellosis Rodents Hantavirus, leptospirosis, rat-bite fever, plague, tularemia, monkeypox, cowpox, Salmonella typhimurium, rickettsial diseases Wild mammals Leptospirosis, rabies, Giardia (raccoon, skunk, etc.) Rabbits Tularemia, babesiosis Birds Avian influenza, psittacosis, Salmonella, West Nile virus Monkeys Rabies, herpes B, filoviruses, hepatitis, tuberculosis, parasitic infections, flaviviruses (yellow fever), chikungunya

international travel, travelers are increasingly exposed to a wider range of animals and potential zoonoses. This chapter emphasizes diseases in which wildlife plays a significant role in transmission to humans. Rabies is discussed in a separate chapter, as are the majority of arthropod and mosquitoborne diseases. Zoonoses acquired primarily from domestic animals that also have a minor reservoir in wildlife are mentioned briefly; standard texts of veterinary public health133,241,261 and infectious disease118,170 provide further discussion of zoonoses acquired from laboratory or exotic animals.

Anthrax Anthrax is a traditionally zoonotic disease that has come to the forefront most recently as a result of bioterrorism. It still deserves attention as a disease acquired through exposure to animals. Anthrax has afflicted men and beasts for centuries.263 The word anthrax comes from the Greek word anthrakites for coal, referring to the black eschar seen in cutaneous anthrax. Anthrax is believed to have been one of the Egyptian plagues that affected cattle at the time of Moses.84 Virgil described clinical anthrax as the murrain of Noricum in his works on agriculture, The Georgics: “The pelts of diseased animals were useless, and neither water or fire could cleanse the taint from their flesh. The sheepmen could not shear the fleece, which was riddled with disease and corruption, nor did they dare even to touch the rotting strands. If anyone wore garments made from tainted wool, his limbs were soon attacked by inflamed papules and a foul exudate.”286 The anthrax bacillus was the model first used by Robert Koch in the 1870s in the development of his postulates on the germ theory of disease. In the mid-19th century, anthrax was called woolsorters’ and ragpickers’ disease in England and Germany, because workers contracted the disease from working with hides and fibers contaminated with anthrax spores. In the United States in the early 1900s cutaneous anthrax cases were reported among textile and tannery workers. The decrease in the incidence of disease by the late 20th century is attributed to improved animal hygiene as well as the animal anthrax vaccine, developed by Louis Pasteur in 1881. Because anthrax spores (Figure 59-1) are resistant to heat and drying and may remain dormant for decades, they have long been considered a potential biologic weapon. Germ warfare programs in the Soviet Union during the 1920s and 1930s 1144

FIGURE 59-1  Anthrax spores. (From http://bepast.org/docs/photos/ Anthrax/anthrax%20spores.jpg.)

included development and stockpiling of anthrax spores. The first report of anthrax spores used as a weapon of war was in the 1940s, when the Japanese army used them in Manchuria during the Chinese–Japanese war.127 Japan killed thousands of Chinese in widespread attacks with anthrax, typhoid, and plague in its assault on Manchurian towns and cities. Bacillus anthracis spores were accidentally released at a military facility in Sverdlovsk in 1979, resulting in 66 deaths.187 In 2001, the intentional contamination of U.S. mail with B. anthracis spores turned attention once again to anthrax as an agent of bioterrorism.

BACTERIOLOGY Anthrax is caused by Bacillus anthracis bacteria (Figure 59-2), which are encapsulated nonhemolytic, nonmotile, spore-forming, gram-positive rods that grow well on blood agar. B. anthracis has a polysaccharide cell wall antigen and an anthrax toxin. Anthrax spores are resistant to heat, drying, ultraviolet light, and disinfectants, and they may survive up to decades in soil.292 They are alleged to be destroyed by high heat (140° C [284° F] for 3 hours, or 10 minutes of boiling) but may survive for up to 70 hours in mercuric chloride.116 Infections are initiated by skin, pulmonary, or gastrointestinal (GI) contact with endospores, which are phagocytosed by macrophages and carried to regional lymph nodes.86 Inside macrophages, the spores germinate into vegetative bacteria, which can then rapidly divide and initiate further spread of infection. B. anthracis produces a toxin that is a tripartite polypeptide consisting of a lethal factor, edema factor, and protective antigen. This tripartite toxin stimulates release of tumor necrosis factor alpha, interleukin-1β, and other factors that lead to disruption of water balance and neutrophil function in the body, inhibiting the innate and adaptive immune responses to bacteria. In essence,

FIGURE 59-2  A photomicrograph of Bacillus anthracis bacteria using Gram stain technique. Anthrax is diagnosed by isolating B. anthracis from the blood, skin lesions, or respiratory secretions, or by measuring specific antibodies in the blood of persons with suspected cases. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp.)

EPIDEMIOLOGY Most animals are susceptible to anthrax to some degree, but clinical anthrax is primarily a disease of herbivores, such as sheep, cattle, horses, and goats. Most birds are immune to anthrax, although they may carry it on their talons or beaks. The disease is rarely seen in countries where vaccination of herbivore stock is practiced. Outbreaks among herbivores are thought to occur under environmental conditions that are favorable for bacterial multiplication, such as where the pH is higher than 6.0 and the soil is rich in organic matter.251 Such an outbreak occurred in North Dakota in 2005.8 Anthrax is rare in developed nations with aggressive vaccination of livestock, but it is still problematic in areas of Asia and Africa with sporadic vaccination and significant wildlife reservoirs. Most cases in industrialized nations are seen after exposure to contaminated animal products—for example, goat hair imported from Turkey and Pakistan.319 Shepherds, farmers, and workers in industrial plants with potentially contaminated animal products are at highest risk. The most recent reported case was in 2006 from a person in New York who was exposed to contaminated dust while skinning a hide for a drum; 5 days later he developed inhalational anthrax.116 Even more concerning are anthrax-related bioterrorism events, such as the 2001 mail contamination outbreak in the United States. During this outbreak, 22 people were affected, of which there were 11 cases of inhalational and 11 of cutaneous anthrax. The majority of the people affected were mail workers. The survival rate for inhalational anthrax was 55%.

TRANSMISSION Humans are infected by anthrax through contact with infected animals or animal products, or through a preparation of spores in the case of bioterrorism attacks. Notably, there has been no documented human-to-human transmission of anthrax.86 Transmission occurs through direct contact with spores, ingestion of spores, or inhalation of spores.

PRESENTATION AND SYMPTOMS There are three forms of anthrax infection: cutaneous, inhalational, and gastrointestinal. The forms are defined by the route of entry of spores into the human body as well as by the constellation of manifesting symptoms. Cutaneous anthrax is the most common form, accounting for 90% to 95% of cases, and is most often acquired by close contact with infected animals or their products. The primary skin lesion typically begins 3 to 5 days after exposure as a nondescript, painless, and pruritic papule at an area of the skin with a previous abrasion or wound. This progresses within 1 to 2 days to a vesicle that undergoes necrosis and drying to leave the characteristic black eschar surrounded by edema (Figure 59-3).86 Untreated, the disease can lead to tender regional lymph nodes with eventual spread to the bloodstream. Once in the bloodstream, anthrax can rapidly become systemic. Without treatment, anthrax has a mortality rate of up to 20%.292 With treatment, death is rare (less than 1%). Gastrointestinal anthrax, which is more common outside of the United States, is caused by ingesting B. anthracis spores. These usually are found in putrid meat from infected animals.17 The two forms of gastrointestinal anthrax are oropharyngeal and intestinal, each with an incubation period of 1 to 6 days. Symptoms of oropharyngeal anthrax include fever greater than 39° C (102.2° F), severe sore throat, dysphagia, posterior oropharyngeal ulcers, and regional lymphadenopathy. Oropharyngeal lesions begin as edematous ulcerations that variably progress to ulcerations with central necrosis and then a pseudomembranous covering. The oropharyngeal form of gastrointestinal anthrax is also associated with significant soft tissue neck swelling, which may progress to the point of upper airway obstruction.

FIGURE 59-3  Cutaneous anthrax lesion on the skin of the forearm caused by the bacterium Bacillus anthracis. (From Centers for Disease Control and Prevention Public Health Image Library, http://phil.cdc. gov/Phil/home.asp.)

The intestinal form of gastrointestinal anthrax is characterized by anthrax spore infection of the stomach or bowel wall. Initial symptoms include nausea, vomiting, anorexia, and fever greater than 39° C (102.2° F). Symptoms progress to include severe abdominal pain, hematemesis, and/or watery, melanotic, or bloody diarrhea. Patients can present with symptoms of an acute abdomen or new-onset ascites. Mortality can result from bowel perforation or B. anthracis septicemia. Inhalational anthrax is rare worldwide and is associated most prominently with bioterrorism. Inhalational anthrax has an incubation period of 8 to 10 days after inhalation of spores into the airways.31 Symptoms include insidious flulike onset of malaise, fatigue, fever, nonproductive cough, and myalgia.251 The rapid deterioration that follows includes dyspnea, cyanosis, respiratory failure, meningismus, mediastinal hemorrhage, hypotension secondary to septic shock, and possibly death. Of the three forms of disease, inhalational anthrax has the highest mortality rate (45% with antibiotic treatment and 97% without), followed by gastrointestinal anthrax (40% with antibiotic treatment), and cutaneous anthrax (1% with antibiotic treatment and 10% to 20% without).138,251

DIAGNOSIS Cutaneous anthrax can be diagnosed by culture of cutaneous lesions. Gastrointestinal anthrax can be diagnosed by cultures from oropharyngeal lesions, blood, and ascites. Computed tomography (CT) of the abdomen is likely to show mesenteric adenopathy. Abdominal radiographs show nonspecific bowel gas patterns and do not aid in diagnosis of the disease. Stool culture has also not been shown to be useful in aiding the diagnosis of anthrax. Autopsies of patients dying of gastrointestinal anthrax show hemorrhagic inflammation of the small intestine with lymphadenopathy.292 On entrance to the GI tract, anthrax is known to cause ulcerations that can be seen on autopsy to extend the length of the GI tract, but most commonly are found in the mouth, stomach, and duodenum.17 Patients with inhalational anthrax typically present with a normal to elevated white blood cell count. Chest radiographs typically demonstrate mediastinal widening secondary to hilar adenopathy, and they frequently demonstrate pleural effusions (Figure 59-4).138 A CT scan of the chest, which can be the earliest diagnostic clue and is often pathognomonic for inhalational anthrax, is recommended in any suspected case.105 The Centers for Disease Control and Prevention (CDC) recommends that cultures of blood, sputum, pleural and cerebrospinal fluid (CSF) be obtained for analysis in suspected cases of inhalational anthrax.

TREATMENT Effective treatment of all forms of anthrax requires a high index of suspicion and prompt antibiotic therapy. In the 2001 outbreak of bioterrorism-related anthrax, all isolates were susceptible to 1145

CHAPTER 59  Wilderness-Acquired Zoonoses

this allows the bacteria to proliferate in the body, potentially leading to sepsis and death.116

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Bacillary Angiomatosis

FIGURE 59-4  Anthrax-widened mediastinum. (From Jernigan JA, Stephens DS, Ashford DA, et al: Bioterrorism-related inhalational anthrax: The first 10 cases reported in the United States, Emerg Infect Dis 7:933, 2001.)

ciprofloxacin and doxycycline, as well as to other agents.50 Because B. anthracis has the potential for penicillinase and cephalosporinase activity, ciprofloxacin and doxycycline, rather than penicillin-based antibiotics, are the first line of therapy. For active disease, treatment for cutaneous anthrax is oral ciprofloxacin or doxycycline twice daily for 60 days. In children, the dose is ciprofloxacin 10 to 15 mg/kg/day divided every 12 hours (not to exceed the adult dose of 500 mg every 12 hours), or doxycycline 4.4 mg/kg/day divided every 12 hours (not to exceed the adult dose of 100 mg every 12 hours). If systemic symptoms are present, intravenous treatment should be initiated. If patients are clinically improved, therapy may be changed to amoxicillin 500 mg three times daily for adults or 80 mg/kg/day divided three times daily for children. For inhalational and gastrointestinal anthrax, treatment begins with intravenous therapy of ciprofloxacin or doxycycline as well as one or two additional agents (options include rifampin, chloramphenicol, vancomycin, penicillin, ampicillin, imipenem, clindamycin, and clarithromycin). If symptoms improve, treatment switches to an oral regimen of ciprofloxacin or doxycycline for a total course of 60 days. Treatment is the same during pregnancy; the risk of doxycycline or ciprofloxacin during pregnancy is outweighed by the potential mortality resulting from undertreated anthrax infection. In the event of potential exposure to inhaled anthrax spores, the CDC recommends 60 days of ciprofloxacin or doxycycline in combination with a three-dose regimen (0, 2, 4 weeks) of anthrax vaccine (BioThrax, formerly known as AVA) as an emergency public health intervention. There is no recommended postexposure prophylaxis for exposure to cutaneous anthrax alone.

PREVENTION The first vaccine was created in 1881 by Louis Pasteur in an effort to prove the germ theory of disease.263 In the 1950s, a human anthrax vaccine was created by the Army Chemical Corps. This was replaced by a vaccine licensed in 1970. At first, this vac­ cination was mandatory for all U.S. military personal, but after concerns for vaccine safety arose, refusal followed. Safety was proved, so mandatory vaccination was reinstituted for the military. Vaccinations for the public are still debated. Opponents of routine vaccination argue that most anthrax in the United States is cutaneous and easily treatable with oral antibiotics. The vaccine is given in five injections and immunity is thought to last 2 years; therefore, the vaccine has been judged not suitable for public dispersal.295 According to a study done by Fowler and colleagues, given a 1% risk of anthrax attack each year, it would be more cost effective and safer to give postexposure antibiotics and vaccines than to prevaccinate the entire population.8 People who are at risk for acquiring the disease, including wool handlers, mail officers, and the military, can be inoculated. Prevention of zoonotic anthrax infection largely relies on vaccination of animals and people at risk. Travelers should avoid contact with infected animals and undercooked meat. 1146

Bacillary angiomatosis, first described in 1983 during the early years of the acquired immunodeficiency syndrome (AIDS) epidemic, forced reconsideration of cat-scratch disease (CSD), bartonellosis, and trench fever.265 In the early 1990s, it was determined that organisms of the genus Rochalimaea caused a diverse array of clinical syndromes, including cutaneous bacillary angiomatosis, bacillary peliosis hepatitis, fever with bacteremia (formerly known as Rochalimaea bacteremic syndrome), and CSD. Whether the different clinical syndromes result from subtle differences in the infecting organisms or in the response of the immune system remains unclear. Each of these conditions can be caused by the bacteria now known to be Bartonella (formerly Rochalimaea) henselae and Bartonella quintana, also the agent of trench fever.

EPIDEMIOLOGY Although clinically different from CSD, bacillary angiomatosis is also closely associated with a recent cat scratch or bite. A recent study showed that two-thirds of patients suffering from bacillary angiomatosis had cats with the same genotype of B. henselae.57 The vast majority of victims are human immunodeficiency virus (HIV) positive, usually with CD4 count less than 200 cells/ mm3.188,273 In 34% of cases, this infection was the first one to establish the diagnosis of AIDS in a given patient. AIDS patients with bacillary angiomatosis can die if untreated, but erythromycin is usually effective.21

SYMPTOMS Most cases of bacillary angiomatosis involve cutaneous or subcutaneous lesions. The lesions typically consist of elevated, friable, red granulation tissue that is papular, verrucous, or pedunculated and resembles pyogenic granulomas, numbering a few to thousands (Figure 59-5). They tend to enlarge if left untreated. Deeper subcutaneous nodules with or without overlying tenderness and erythema are seen in about one-half of the victims. These lesions can be nearly indistinguishable from those of Kaposi’s sarcoma and can also coexist in the same patient.21 Similar lesions can occur in other body tissues, with nearly all visceral organs, including the brain, heart, larynx, cervix, and vulva, being vulnerable.21 Visceral lesions may be the first sign of infection; patients often have fever, weight loss, and malaise.76 Hepatic involvement (bacillary peliosis hepatitis) can lead to hepatic failure or even rupture. This usually manifests with GI symptoms (nausea, vomiting, diarrhea, or abdominal distention), fever, chills, and hepatosplenomegaly. Histopathologic examination of liver biopsy specimens reveals dilated capillaries or multiple blood-filled cavernous spaces, some of which can be seen on endoscopy or bronchoscopy.188 Bacillary angiomatosis may cause osteomyelitis, manifesting as an extremely painful focal area of a bone that appears as a lytic lesion on radiographic analysis. This usually occurs on the tibia, radius, or fibula and

FIGURE 59-5  Bacillary angiomatosis. (From http://prn.org/index.php/ complications/article/common_skin_problems_of_HIV_disease.)

DIAGNOSIS B. henselae and B. quintana can be isolated from blood using lysis-centrifugation blood cultures,13 but both species have also been isolated with traditional blood culture systems. Serologic diagnosis can also be made using techniques of indirect fluorescent antibody (FA) testing. Serum samples can be sent (for both B. henselae and B. quintana) to the CDC. A commercially available enzyme immunoassay for detection of IgG antibodies to B. henselae is reportedly 5 to 10 times more sensitive than is the indirect FA test.77 Positive results should be interpreted cautiously, taking into account the clinical context, because the meaning of positive serologic results awaits further evaluation with stricter epidemiologic methods. Diagnosis of bacillary angiomatosis is usually made from clinical features and biopsies of lesions, with characteristic histopathologic findings in tissue sections. Blood cultures should be obtained and incubated for a prolonged period. As more is learned about the growth requirements of the causative organisms, they may become easier to culture directly from skin lesions and lymph nodes. Serologic analysis will become an important means of diagnosis.1

TREATMENT Treatment is with erythromycin. If patients cannot tolerate this therapy, rifampin and doxycycline or trimethoprimsulfamethoxazole (TMP-SMX) should be given. Norfloxacin, gentamicin, and ciprofloxacin are also clinically effective.242 Penicillin and first-generation cephalosporins are not beneficial. Therapy is for a minimum of 6 weeks and may have to continue indefinitely in an immunosuppressed patient. Immunocompromised patients may develop a Jarisch-Herxheimer reaction after the first several doses of antibiotics.273

PREVENTION There is ongoing discussion regarding prevention of bacillary angiomatosis in HIV/AIDS patients. Many HIV/AIDS patients possess cats for companions and in doing so, risk contracting B. henselae. The current recommendation is for these patients to decrease rough play with the animals and make medical caregivers aware that they own a cat.273 There is no vaccine for animals or patients at risk.

Brucellosis Brucellosis is an anthropozoonotic disease with a broad clinical spectrum caused by a number of species of Brucella, a small, gram-negative bacterium (Figure 59-6). Brucellosis fits into the differential diagnosis of fever of unknown origin. Brucellosis usually results from ingestion of contaminated milk or milk products or by direct skin contact. Brucella organisms are carried chiefly by swine, cattle, goats, and sheep and may be recovered from almost all tissues in a sick patient. Most animals used as livestock are susceptible to brucellosis, whereas the occurrence in wild animals is rather small.179

BACTERIOLOGY Brucellae organisms are small, gram-negative, unencapsulated, aerobic, intracellular coccobacilli. The species causing disease in humans include B. abortus, suis, melitensis, and less commonly, B. canis. The bacterium can survive in soil for up to 10 weeks, in goat cheese for up to 180 days (at 4° to 8° C [39.2° to 46.4° F]),

FIGURE 59-6  Electron micrograph of Brucella abortus. (Courtesy Dennis Kunkel Microscopy, Inc.)

and in tap water for up to 60 days. It is, however, very sensitive to heat and most disinfectants, and is entirely killed by pasteurization.

EPIDEMIOLOGY Brucella in domesticated animals tends to be species specific, with Brucella abortus infecting cattle, Brucella melitensis goats, Brucella suis swine, Brucella canis dogs, and Brucella ovis sheep. The disease is found worldwide and has an annual attack rate of approximately 500,000; U.S. cases number less than 200. Significant endemic areas include Mexico, Central and South America, Mediterranean countries, the Arabian Gulf, and India. Most cases of brucellosis in the United States are found in Texas and California, and risk factors for the disease include Hispanic ethnicity, travel to Mexico, and ingestion of unpasteurized dairy products.276 Humans can be infected with Brucellae by ingestion of contaminated food, direct inoculation through cuts and skin abrasions, transplacental transmission, and inhalation of infected aerosols.315 Internationally, most cases are transmitted by ingestion of fresh, nonpasteurized goat cheese and raw goat’s milk. Most human cases are caused by infection with B. melitensis. The disease caused by B. melitensis has a higher attack rate and is more severe, whereas brucellosis caused by B. abortus from cattle produces mild clinical disease and is usually occupationally acquired. A proved case of transmission by dog bite has been reported, and dogs carry their own pathogenic species.215

SYMPTOMS Brucellosis may affect many organ systems, with a wide range of disease severity and acuity.68 Because of this, it can cause fever with vague and varied symptoms, and should be considered as a cause of chronic unexplained fever. The disease can be classified into three forms: acute, subacute, and chronic. In acute brucellosis, the victims complain of headache, weakness, diaphoresis, myalgias, and arthralgias. This is the most common presentation. Anorexia, constipation, and weight loss are often seen in the first 3 to 4 weeks. Physical examination may reveal lymphadenopathy, hepatomegaly, or splenomegaly. Bacteremia in the early stages typically induces lesions of the viscera, bones, and joints; osteomyelitis, particularly spondylitis, is a common complication. Rare but serious complications include endocarditis, neurobrucellosis with meningitis, and hepatic abscess. In subacute, or undulant, brucellosis, symptoms are milder but with more frequent arthritis and orchitis. The clinical picture is more varied, and the diagnosis is considered in any fever of undetermined origin. In the pre-antibiotic era, most patients spontaneously cleared their disease in 6 to 12 months. In chronic brucellosis, symptoms have persisted for more than 1 year. It is rare in children but increasingly common as patients 1147

CHAPTER 59  Wilderness-Acquired Zoonoses

occasionally has a cellulitic tender erythematous plaque overlying the area of concern.12 The organism can also cause bacteremia, even in immunocompetent patients. Bartonella bacteremia is characterized by a prolonged symptom complex of malaise, fatigue, anorexia, weight loss, and fevers that are recurring, with ever-increasing temperatures.19,20 Often no site of focal infection is apparent. The symptoms are usually present for weeks to months before the diagnosis is finally made by isolation of the organism in blood cultures.255

PART 6  ANIMALS, INSECTS, AND ZOONOSES

age. Many describe chronic arthralgias and extra-articular rheumatism. Chronic brucellosis can mimic chronic fatigue syndrome.

DIAGNOSIS Brucellosis is most often diagnosed by serologic testing, including serum agglutination, rose bengal, complement fixation, and enzyme-linked immunosorbent assay (ELISA).164 A polymerase chain reaction (PCR) test is an effective method for detecting brucellosis.178 After acute infection, high titers may persist for 18 months. False-positive results may be caused by Francisella tularensis or Yersinia enterocolitica infection. Isolation of Brucella organisms by blood culture may be used for definitive diagnosis, although the cultures are not always positive. Blood cultures have sensitivities of 50% to 80%. Bone marrow biopsy and culture can be used in patients with clinically suspected brucellosis but negative serologic tests and blood cultures.

TREATMENT Treatment for brucellosis is with doxycycline 100 mg PO twice daily for 6 weeks plus either streptomycin 1 g intramuscularly (IM) daily for the first 14 to 21 days, gentamicin 5 mg/kg/day IM for 7 days, or rifampin 600 to 900 mg PO once daily for 6 weeks.67,128 The role of quinolones has been investigated, particularly in combination with rifampin.3 In pregnancy, treat with rifampin 900 mg daily for 6 weeks, with the addition of TMP-SMX during the second trimester.256 The American Academy of Pediatrics recommends children younger than age 8 years take oral TMP-SMX plus rifampin for 4 to 6 weeks, with gentamicin added for the first 14 days if osteoarticular, neural, or endocarditis manifestations are present. For children aged 8 years and older, antibiotic choices are the same as for adults. Focal disease is generally more difficult to eradicate than is mild diffuse disease. Mortality is low, with only two deaths reported in several thousand cases.103

Cat-Scratch Disease Cat-scratch disease is a disease typically transmitted from a cat through a break in the skin (bite, scratch, lick, or other injury). It is usually self-limited and lasts 6 to 12 weeks. The first reference to the disease was in 1889 in the French literature by Henri Parinaud. The first to recognize the cat as the vector for the disease was Robert Debré at the University of Paris in 1931; however, the disease was not officially reported until 1951. CSD is probably the most common cause of unilateral lymphadenop­ athy in children.259 The current cause of CSD is thought to be the gram-negative bacteria, Bartonella henselae, previously known as Rochalimaea henselae.28

EPIDEMIOLOGY CSD has been reported from all countries and in all races. An estimated 24,000 cases are recognized each year in the United States.174 Most cases are found in the fall and winter months, a seasonality thought to be due to the increase in kitten births in the summer and a subsequent rise in flea infestation.214 Compared with healthy cat-owning control subjects, patients with CSD are more likely to have at least one kitten aged 12 months or younger, to have been scratched or bitten by a kitten, and to have at least one kitten with fleas.318 It has been postulated that the domesticated cat Felis domesticus is the reservoir for the disease and that, as with other Bartonella species, the organisms may be transmitted by fleas and ticks between cats.214

TRANSMISSION About 90% of cases are caused by scratches from cats, but dog and monkey bites, as well as thorns and splinters, have also been implicated in transmission.69 The organism may be on the claws or in the oral cavity of the offending cat. Most cases occur in children, particularly boys, who tend to play more aggressively with domestic animals. 1148

SYMPTOMS The average incubation period is 3 to 10 days. The characteristic feature of CSD is regional lymphadenitis, usually involving lymph nodes of the arm or leg. In one series, 54% of lymphadenopathy occurred in the axilla, with the remainder in the neck.259 Often, only one node is involved. The nodes are often painful and tender, and about 25% suppurate.291 Adenopathy may spread proximally; occasionally, cervical adenopathy is mistaken for Hodgkin’s disease. Inguinal lymphadenopathy misdiagnosed as lymphogranuloma venereum has later found to be due to B. henselae from CSD.244 In most cases, a characteristic raised, erythematous, slightly tender, and nonpruritic papule with a small central vesicle or eschar that resembles an insect bite is seen at the site of primary inoculation. Constitutional symptoms are mild, with approximately two-thirds of patients presenting with fever, which is rarely greater than 38.8° C (102° F). Chills, malaise, anorexia, and nausea are common. Infrequent evanescent morbilliform and pleomorphic skin rashes lasting for 48 hours or less have been reported in less than 5% of patients.244 This typical clinical course occurs in 88% of victims; the remainder seek medical treatment for complications such as encephalopathy, atypical pneumonia, and severe systemic disease. The most common of the atypical forms of presentation is Parinaud’s oculoglandular syndrome, which occurs in about 6% of cases and consists of granulomatous conjunctivitis and an ipsilateral, enlarged, tender preauricular lymph node.175 Serious complications are rare and include encephalitis, seizures, transverse myelitis, osteolytic bone lesions, arthritis, splenic and hepatic abscesses, mediastinal adenopathy, optic neuritis, and thrombocytopenic purpura.27,175,194,208 Although encephalop­ athy is rare, CSD is becoming a more common cause of encephalopathy as other viral infectious diseases disappear; the incidence of CSD-associated neurologic complications now ranks with those of varicella and herpes simplex infections, Lyme disease, Rocky Mountain spotted fever, and Kawasaki disease.34 CSD encephalopathy should enter the differential diagnosis of patients (especially young ones) with unexplained coma, seizures (onehalf of whom may be afebrile) or those with fevers of unknown origin. The prognosis for encephalopathy generally is good and to date there have been rare documented neurologic sequelae in immunocompetent patients.

DIAGNOSIS Results of routine laboratory studies, including urinalysis and complete blood cell count, are usually normal, although mild leukocytosis and/or elevation of ESR may be seen as well. An indirect FA test for B. henselae is commercially available. Immunity is thought to be largely cell mediated.113 An intradermal skin test of 0.1 mL of CSD antigen is positive in approximately 95% of victims, although 10% of the population has a false-positive reaction. In confusing cases, biopsy of lymph nodes can yield characteristic findings of areas of granulomatous change and necrosis with central neutrophilic infiltration, a peripheral zone of histiocytic cells, and an outermost zone infiltrated by small lymphocytes and plasma cells.172 This picture is not diagnostic, however, and is also seen in lymphogranuloma venereum (LGV), histoplasmosis, tularemia, brucellosis, sarcoidosis, and tuberculosis. Thus, lymph node biopsy is most useful to rule out malignancy. Warthin-Starry or Brown-Hopps staining of the nodes or the primary skin lesion usually demonstrates small, pleomorphic bacilli.175 In most cases, clinical diagnosis is based on finding three of four criteria: (1) single or regional lymphadenopathy without obvious signs of cutaneous or throat infection, (2) contact with a cat (usually an immature one), (3) detection of an inoculation site, and (4) a positive skin test.37 The skin test has largely replaced serologic testing for confirmation of the disease.173 The workup should exclude other causes of regional lymphadenopathy, such as tuberculosis, tularemia, LGV, lymphoma, brucellosis, and sporotrichosis.237 In general, only sporotrichosis and LGV demonstrate localized unilateral lymphadenopathy; LGV usually occurs in the groin. Cat scratches are normally

TREATMENT CSD usually resolves spontaneously in weeks to months, although in 2% to 14% of persons (usually adults) the course is prolonged and involves systemic complications.173,175 Systemic CSD in an adult has been successfully treated with gentamicin,161 and in a child, with cefuroxime.114 Clear guidelines for the treatment of CSD do not exist mainly because few randomized controlled trials have been done. A randomized controlled trial with azithromycin for CSD showed significant decrease in volume of lymphadenopathy with treatment.14 In a retrospective series of 71 patients, TMP-SMX was seen to have had good results; this was not the case with other antibiotics.66 The largest study, of 268 patients, was also retrospective and found a response rate of 87% with rifampin, 84% with ciprofloxacin, 73% with intramuscular gentamicin, and 58% with TMP-SMX.173 Antibiotics that were of no benefit included amoxicillin-clavulanate, erythromycin, dicloxacillin, cephalexin, tetracycline, cefaclor, ceftriaxone, and cefotaxime. No sequelae of CSD other than the rare complications mentioned above are known. One recent article showed that one bout of CSD seems to offer lifelong immunity, with recurrences of lymphadenopathy shown only rarely.258 For the majority of immunocompetent patients, many experts recommend withholding antibiotic therapy and reassuring patients that the prognosis is excellent. Other experts recommend antibiotic treatment for all patients with CSD. For isolated lymph node involvement, a 5-day course of azithromycin (10 mg/kg on day 1 [500 mg max], followed by 5 mg/kg/day for 4 days [up to 250 mg/day]) may shorten the duration of disease and possibly prevent complications. For patients intolerant to azithromycin, treat with clarithromycin, rifampin, TMP-SMX, or ciprofloxacin. For patients with severe or prolonged disease, or for im­ munocompromised patients, antibiotic treatment is definitely indicated.

Glanders Although little known in the Western world today, glanders is a classic infectious disease. Its greatest historical impact has been through its effect on cavalry horses during military campaigns, influencing battles from biblical times through World War I. There have been no reported cases in the United States since the 1940s. Theories and disputes about the origin, nature, transmission, and treatment of glanders figured prominently in the development of veterinary science in Europe in the latter half of the 18th century. In 1795, Erik Viborg published an account that is remarkably close to our current understanding of the disease. He demonstrated that equine “farcy,” characterized by cutaneous lymphangitis, and the respiratory form of the disease in horses, classically referred to as glanders, were different manifestations of the same infection. He demonstrated that the disease was transmissible from one horse to another by infectious exudates, and that the causative organism could be carried by fomites and killed by heat. Transmission of glanders from horses to humans was documented in France and Germany during the first three decades of the 19th century. The causative organism was isolated by Loeffler and Schütz, as well as by Bouchard, Capiton, and Charrin in 1882. In 1891, Kalning and Helmann independently discovered mallein, derived from the glanders bacillus. Like tuberculin, mallein was thought to have therapeutic or prophylactic value. This turned out to be erroneous, but mallein provided a means of diagnosing the infection in clinically ill and carrier animals and provided a basis for test and slaughter techniques, which have largely eliminated glanders from most parts of the world.

BACTERIOLOGY The causative organism is Burkholderia mallei, a member of the newly renamed Burkholderia genus, which includes Burkholderia pseudomallei, the cause of melioidosis, and Burkholderia cepacia. It is a gram-negative, nonsporulating, obligately aerobic, and nonmotile bacillus that requires glycerol for optimum growth in vitro.213,260 In 1992, Yabuuchi and co-workers313 proposed that seven species, formerly of the Pseudomonas RNA group II, should be transferred to a new genus, Burkholderia, with B. cepacia as the type species. The genus included Burkholderia caryophylli, Burkholderia gladioli, B. mallei, B. pseudomallei, Ralstonia pickettii, and Ralstonia solanacearum; the latter two species were transferred to the genus Ralstonia.313

EPIDEMIOLOGY Glanders occurs in a few Asian and African countries, such as India, China, Mongolia, Egypt, and Mauritania. It is primarily a disease of horses and spreads most rapidly when large numbers of horses, mules, or donkeys are kept in proximity. Many carnivorous mammals are also susceptible to infection, and outbreaks have occurred when infected horsemeat was fed to lions, tigers, and other wild animals in zoos. Occasionally, infections occur in dogs, cats, sheep, and goats. Although glanders is limited to a few countries, recent literature points out a concern that Burkholderia mallei could be used as a bioterrorism agent.94

TRANSMISSION Humans are usually infected by exposure to sick horses. Infection can occur by inhalation of respiratory droplets or by contact with infected discharges. Human infections have occurred from direct contact in the laboratory and from patients.

SYMPTOMS IN EQUIDS Horses may have unilateral or bilateral mucopurulent nasal discharge. There may be enlargement and induration of lymphatics, with ulceration and discharge, especially involving the legs. Nodules, pustules, and ulcers may be seen on the horse’s skin. The cutaneous form of the disease is often referred to as farcy; the thickened, inflamed lymphatics as farcy pipes; and the enlarged lymph nodes as farcy buds. Horses also have pneumonia, with mild respiratory embarrassment in early stages, and more severe respiratory difficulties and cachexia in later stages. Septicemia with lesions in multiple internal organs can occur. Glanders can run an acute and fulminant course in equids, especially in donkeys and mules, or a more chronic course, more often in horses. The case–fatality rate is high, especially with more virulent strains of the organism.

SYMPTOMS IN HUMANS The incubation period of glanders in humans can be as short as 1 to 5 days. Cases with apparent incubation periods of several months may have represented smoldering, unrecognized infection. The severity of disease can vary from mild to fatal, and the course can be acute and fulminant or chronic. Relapses can occur after quiescent periods of up to 10 years. As in horses, manifestations in humans usually involve the skin and respiratory tract. There may be pustular cutaneous eruptions, thick indurated lymphatics that may ulcerate, mucopurulent discharge from the eyes or nose, pneumonia, and metastatic abscesses in internal organs. Depending on the severity, the patient may have anorexia, fever, weight loss, headache, nausea, diarrhea, or septicemic shock. Lobar pneumonia, bronchopneumonia, or nodular densities may be seen on chest radiographs. Cases recently reported from Southeast Asia have been relatively mild, indicating that the local strain of the organism appears to have moderate pathogenicity for humans. 1149

CHAPTER 59  Wilderness-Acquired Zoonoses

found on the upper extremities. Skin tests, cultures, serologic tests, and biopsies are available for differentiation of these other diseases. The tendency for dissemination is greater in immunocompromised patients, who may develop bacillary angiomatosis, which is discussed in the section on this topic.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

DIAGNOSIS Clinical diagnosis in horses based on symptoms can be confirmed by reaction to mallein with a cutaneous hypersensitivity test. Mallein, a filtrate derived from culture of the organism, is injected into the eyelid of a horse. A positive reaction, read 48 hours later, consists of marked local swelling and purulent conjunctivitis. Several serologic tests are also available. The CF test is often used. A dot-ELISA is a more sensitive test.284 Clinical diagnosis in humans is based on consistent symptoms in an individual exposed to horses in an endemic area. The diagnosis can be confirmed by culture of the organism from lesions or tissues, or by serologic testing, using CF or agglutination tests. Agglutination titers are often detectable by the second week of infection. The CF test is less sensitive but more specific than agglutination. CF tests become positive during the third week of infection.213 Laboratory diagnosis can be made by injection of infected material intraperitoneally into male guinea pigs or hamsters. The animals develop peritonitis that extends into the scrotal sac with severe inflammation known as the Strauss reaction. In acute phases of the disease, abscessation occurs. Later, the inflammatory focus is surrounded by a granulomatous reaction, but central karyorrhexis remains a prominent feature of the lesion. The lungs are the internal organs most typically involved (Figures 59-7 and 59-8; Figure 59-8, online), but septicemic glanders can involve the liver, spleen (Figure 59-9), bone, or brain. With chronic infection, multiple subcutaneous and intramuscular abscesses may develop.

A

TREATMENT Studies indicate that sulfadiazine, 100 mg/kg/day in three divided doses given for 3 weeks, is effective. Treatment with tetracyclines and streptomycin is also recommended.213 The organism is sensitive in vitro to sulfamethizole, sulfathiazole, TMP-SMX, gentamicin, kanamycin, streptomycin, and tetracycline.4 Ciprofloxacin and ofloxacin, but not norfloxacin, were found to be effective in treating experimentally infected guinea pigs and hamsters.15 Therapy should be based on culture and sensitivity testing of isolates and on clinical response to treatment. Acute untreated septicemic cases are almost uniformly fatal within 7 to 10 days.213 The prognosis is better in chronic forms of the disease, which can last for years, but deaths are still likely without adequate treatment.

PREVENTION AND CONTROL The only significant reservoir of infection in nature is equids. If the disease were eradicated in them, it would disappear. National programs should be instituted in enzootic countries to eradicate the infection, by mallein or serologic tests of all horses, donkeys, and mules, followed by slaughter of reactive animals. People

B FIGURE 59-9  Abdominal computed tomographic scans from a patient with glanders. A, Before treatment, multiple hepatic and splenic abscesses (arrows). B, After treatment, nearly complete resolution of the abscesses. (From Srinivasan A, Kraus CN, DeShazer D, et al: Brief report: Glanders in a military research microbiologist, N Engl J Med 345:256, 2001.)

who handle horses in enzootic countries, including trekkers who pack gear into the wilderness on these animals, should be advised of the signs of glanders in equids and warned to avoid contact with sick animals. Glanders can be transmitted from one person to another, so strict infection control should be exercised with suspected infected patients. Personnel should avoid contact with all secretions and respiratory droplets. Transmission is also a risk in the laboratory, so if this organism is being cultured, all work should be done under appropriate microbiologic hoods. Some postulate that Burkholderia mallei could be an agent of bioterrorism in the future.

Leptospirosis

FIGURE 59-7  A bronchus filled with and surrounded by pus in the lung of a horse with glanders. (Hematoxylin and eosin, ×100.)

1150

Leptospirosis is an infectious disease caused by Leptospira interrogans. It can be acquired by animals and humans, usually by exposure to water contaminated with urine of wild or domestic animals. Adolf Weil first described the clinical picture of human leptospirosis in 1886. He described four febrile men with “particularities of an acute infectious illness with spleen tumor, jaundice, and nephritis.” In addition, each had “severe nervous symptoms” and an enlarged liver. All recovered, and three had a biphasic clinical course with fever recurring after an afebrile period of 1 to 7 days. The term Weil’s disease was coined by Goldschmidt in 1887. The carrier status was described in asymptomatic field mice by Ido and co-workers in 1915. Since then, the infection has been recognized both as a disease and as an asymptomatic carrier state in hundreds of animal species.

BACTERIOLOGY Leptospira is a genus in the order Spirochaetales, an order characterized by thin, helical, gram-negative bacteria. More than 170 serovars, or serologically distinct strains of Leptospira, are known. Leptospira organisms are spirochetes with hooked or curved ends, 6 to 20 µm long by 0.1 µm wide (Figure 59-10). They can grow on artificial media containing rabbit serum, such as Fletcher’s semisolid and Stuart’s liquid media, or on media containing albumin and fatty acids, such as Ellinghausen-McCulloughJohnson-Harris (EMJH) medium.267 Because this requires special media, one should notify the laboratory of suspicion for Leptospira when sending cultures. In describing outbreaks with shared epidemiologic or clinical features, several syndromes were ascribed to different serotypes, such as Fort Bragg fever caused by Leptospira autumnalis, swineherd’s disease caused by Leptospira pomona, and Weil’s disease caused by Leptospira icterohaemorrhagiae. Such terms are no longer commonly used because of overlap in the symptoms and epidemiology associated with various Leptospira serotypes.

EPIDEMIOLOGY Leptospirosis is found throughout tropical and temperate areas of the world. It is particularly common in Southeast Asia and parts of Latin America, including some Caribbean islands.97 Approximately 40 to 100 cases were reported annually in the

TRANSMISSION Animals contaminate the environment by shedding organisms in their urine. Most human cases are environmentally acquired by contact with contaminated water or soil. Discovering the original animal source is often difficult. A wet, alkaline environment favors survival of Leptospira, with tropical, unpolluted, nonsaline water providing an optimum environment for infection. Heavy tropical rains increase infection risk by saturating soil, flushing

TABLE 59-2  Animal Reservoirs of Leptospires Isolated from Humans* Serogroup (Serovar)

Domestic Animals

Wildlife

Icterohaemorrhagiae (Icterohaemorrhagiae) Canicola (Canicola) Pomona (Pomona)

Dogs, cattle, swine

Brown rat, house rat, cotton rat, Pacific rat, house mouse, muskrat, gray fox, red fox, opossum, striped skunk, woodchuck, nutria Striped skunk, raccoon, armadillo, mongoose Striped skunk, raccoon, wildcat, opossum, woodchuck, red fox, deer, armadillo

Grippotyphosa (Grippotyphosa) Hebdomidis (Hardjo)

Dogs, cattle, swine Dogs, cattle, swine, goats, sheep, horses Dogs, cattle, swine Cattle

Muskrat, fox squirrel, gray squirrel, bobcat, cottontail rabbit, swamp rabbit, raccoon, striped skunk, red fox, gray fox, vole, opossum None

Modified from Hanson LE: Leptospirosis in domestic animals: The public health perspective, J Am Vet Med Assoc 181:1505, 1982. *Isolated in the United States.

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CHAPTER 59  Wilderness-Acquired Zoonoses

FIGURE 59-10  Scanning electron micrograph (SEM) of a number of Leptospira bacteria atop a 0.1-µm polycarbonate filter. Leptospires are long, thin, motile spirochetes that may be free-living or associated with animal hosts; they survive well in fresh water, soil, and mud in tropical areas. Organisms are antigenically complex, with more than 200 known pathogenic serologic variants. Molecular taxonomic studies at the Centers for Disease Control and Prevention and elsewhere have identified 13 named and four unnamed species of pathogenic leptospires. Although some infected persons have no symptoms at all, leptospirosis can cause a wide range of symptoms, including high fever, severe headache, chills, muscle aches, and vomiting. Patients also may have jaundice (yellow skin and eyes), red eyes, abdominal pain, diarrhea, or a rash. (From Centers for Disease Control and Prevention Public Health Image Library, courtesy Rob Weyant, MD, 1998. http://phil.cdc.gov/ Phil/home.asp. Photo courtesy Janice Carr.)

United States (Figure 59-11, online), most commonly in Hawaii. Active surveillance on Kauai and the east coast of the big island of Hawaii revealed a high incidence, accounting for a large proportion of flulike illness.227 Leptospirosis is no longer a reportable condition, although it remains one of the most common zoonoses in the world and should be suspected in travelers with matching clinical syndromes. In 1996, five of 26 travelers returning from a white-water rafting trip in Costa Rica developed a febrile illness and were found to have leptospirosis.47 In 1998, leptospirosis was implicated in an outbreak of acute febrile illness among athletes from 44 states and seven countries who participated in triathlons (which involve open-water swims in fresh water) in Springfield, Illinois, and Madison, Wisconsin. Eighty-four (11%) of Illinois participants and 20 (5%) of Wisconsin participants were infected, and the diagnosis was confirmed by the CDC.48 In Borneo in 2000, 44% of 138 triathlon participants contracted leptospirosis.51 An outbreak was observed among German strawberry farmers in 2007, with the highest attack rates among workers who either worked in the rain with wounds on their hands or had rodent contact.81 These reports highlight the potential risk to those with occupational, avocational, or recreational (including travel) exposure to contaminated fresh water. Leptospirosis is a zoonosis in which certain serovars tend to have host specificity (Table 59-2). Dogs are usually associated with L. icterohaemorrhagiae and L. canicola, and swine and cattle are more frequently infected with L. pomona and L. grippotyphosa, although all four of these serovars or serotypes have been isolated from each host species. The major reservoir for Leptospira infections for humans and domestic animals is wildlife, principally wild mammals, although the organism has also been isolated from frogs and snakes, and serologically positive fish and turtles have been found.171 Leptospirosis may be asymptomatic in animals, as is usually the case in wild animals, including rodents. Animals that acquire clinical disease have fever, appear depressed, lose appetite, may become jaundiced, develop hemorrhages on mucous membranes, and in late stages of the disease may have renal failure.126 In cattle, leptospirosis can cause stillbirths, hemoglobinuria, and thickened yellowish or blood-tinged milk. Leptospires have been isolated from the milk of cattle and goats. A theoretic risk exists that leptospirosis could be transmitted by consuming such milk. Pasteurization should destroy organisms. Stillbirths or delivery of weak piglets is a common sign of leptospirosis in swine. Cats are rarely affected by leptospirosis. They may be resistant to the disease because they are frequently exposed to infection through catching mice and other rodents. Leptospirosis has been suspected as a cause of recurrent uveitis in horses. This is of more interest in comparative pathology than in public health, because horses infrequently transmit the infection to humans.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

leptospires into surface water, and drawing rodents and other small mammals into swampy areas. Infection can also be acquired by contact with infected animal blood and tissues. Factors strongly associated with acquiring leptospirosis in Hawaii include household use of rainwater catchment systems and the presence of skin cuts at the presumed time of exposure.227 Leptospirosis is an occupational problem for veterinary, agricultural, sewer, slaughterhouse, laboratory, and military personnel.96,129,227 Dairy farmers are at risk in milking parlors, probably through exposure to cow’s urine.7,137 Leptospirosis poses an avocational risk for hunters, trappers, hikers, and persons who swim in fresh water, such as ponds and streams that may be contaminated with infected urine. It is acquired by ingestion or by entry through abraded skin or through the mucous membranes of the eyes and mouth.

SYMPTOMS The incubation period for leptospirosis is usually 7 to 12 days (range, 1 to 26 days).226 The disease is classically biphasic, although it may manifest with a variable clinical course.139,216 The primary stage lasts 4 to 7 days and is characterized by organisms in blood, CSF, and various body tissues. During the initial phase, more than one-half of victims have sudden onset of fever, chills, severe malaise, myalgias, headache, lymph node enlargement, and conjunctival injection, usually without exudate. Nausea, vomiting, and abdominal pain may occur. A nonproductive cough is common. The initial clinical differential diagnosis is broad and includes meningitis, hepatitis, influenza, encephalitis, and viral illness. The rickettsioses, typhoid fever, brucellosis, relapsing fever, toxoplasmosis, dengue fever, malaria, yellow fever, septicemia, Kawasaki syndrome, and toxic shock syndrome are also differential diagnoses.129 The conjunctival injection seen in many cases of leptospirosis is not typical of many other diseases, and may help narrow the differential. The primary stage is usually followed by an afebrile period of 1 to 2 days. The onset of the second stage coincides with development of immunoglobulin M (IgM) antibodies. The organisms usually cannot be cultured from blood or CSF during this phase but can be isolated from urine for weeks or months. During the second stage, the victim may have fever, but the temperature is lower than in the primary stage. Headache is persistent, severe, and unresponsive to analgesics. It often heralds the onset of meningitis, one of the common complications of the secondary stage. Myalgias, abdominal pain, nausea, and vomiting can occur in the second as well as in the primary stage. In addition to the conjunctival injection seen in the primary stage, uveitis (iridocyclitis) can be seen in the secondary stage. This can cause longterm ocular damage.253 Occasionally, pharyngitis and a macular, purpuric, or ecchymotic rash occur (Figure 59-12). Rarely, endocarditis or myocarditis occurs. In a clinical study of leptospirosis in Barbados, cardiac arrhythmias and myocarditis occurred in 18% and pericarditis in 6% of patients.88 Splenic enlargement develops in approximately 20% of patients in the second stage. Hepatomegaly is sometimes found, especially if the patient is icteric. Jaundice is a serious prognostic sign. Mortality in cases with jaundice exceeds 15% but is rare in anicteric cases. Mortality depends on the patient’s prior condition and is higher in older individuals than in young adults, with an overall case fatality rate of approximately 5%. Death can occur from hemorrhagic manifestations as a result of vasculitis, renal or hepatic failure, cardiogenic shock, or myocarditis.

FIGURE 59-12  Hemorrhagic macular rash in a patient with leptospirosis. (Courtesy University of Massachusetts Medical School.)

Definitive diagnosis of leptospirosis can be made by culture of the organism on Fletcher’s, Stuart’s, EMJH,267 or Tween 80– albumin medium. Blood and CSF should be cultured during the first week of illness; urine should be cultured thereafter. The likelihood of obtaining a positive culture is greatly diminished once antibiotics have been given. Oxalated blood samples can be sent to the laboratory for culture because the organisms can remain viable in oxalated blood for up to 11 days. Some physicians have relied on darkfield examination for identification of the organisms, but this method is not considered reliable. Artifacts such as fibrin are readily mistaken for leptospires. The spirochetes can be demonstrated in tissue sections with silver stains (Figure 59-13). Leptospirosis can be diagnosed serologically by demonstrating a fourfold rise in antibody titer.289 The commercially available macroscopic slide agglutination test, using killed organisms of multiple serovars, or the CF test is useful for screening purposes. The macroscopic agglutination test may become positive within the first week of illness and can persist for several months. CF antibodies are detectable between days 10 and 21. Acute and

DIAGNOSIS Laboratory findings in leptospirosis include moderate leukocytosis, usually caused by an increase in neutrophils, elevated erythrocyte sedimentation rate, and, less commonly, thrombocytopenia. Elevated bilirubin level (up to 65 mg/dL, mainly direct bilirubin), greatly increased serum creatine kinase level (often five times normal), and a less-than-fivefold increase in aspartate transaminase suggest the diagnosis. An elevated blood urea nitrogen level is a common finding. Serum amylase concentration may also be elevated. 1152

FIGURE 59-13  Leptospira icterohaemorrhagiae in the kidney of an experimentally infected dog. The organisms are indicated by arrows. (Warthin-Starry silver stain, ×1000.)

TREATMENT Treatment of leptospirosis with antibiotics is most effective when begun during the first week of illness, preferably within 4 days of symptom onset. Although antibiotics were thought to have little value after this time, more recent studies indicate that they may still have some usefulness.294 The treatment of choice is doxycycline 100 mg orally twice a day for 7 days.182 Alternative antibiotics include tetracycline 2 g/day orally in three or four divided doses, or penicillin G 3 million units/day parenterally. Amoxicillin, third-generation cephalosporins, and macrolides could also be used. Doxycycline and tetracycline should not be given to pregnant women or to children younger than age 9 years. A Jarisch–Herxheimer reaction may occur after treatment. This is a response to release of endotoxins, usually occurring within 2 to 6 hours after initiating therapy, with sudden onset of fever, chills, malaise, headache, and tachycardia. The reaction typically resolves spontaneously within 24 hours. Other than antibiotic treatment, therapy for leptospirosis is supportive, including fluid therapy, dialysis for renal failure,142 and transfusion for hemorrhagic complications. Recovery from leptospirosis apparently leaves serovar-specific immunity. Individuals can become infected with other serovars. Assuming that the infection and hemorrhagic complications can be controlled, the long-term prognosis after successful treatment is good. Renal and hepatic function usually return, but headache and ocular damage may persist.253

PREVENTION Prevention of human leptospirosis is based on avoiding infected animal tissues and areas contaminated by animal urine, blood, or tissue. Individuals who are at particularly high risk should be educated about prevention and encouraged to wear protective clothing, such as rubber gloves, when handling infective material. Swimming in freshwater ponds and streams likely to be heavily contaminated by urine from livestock or wildlife should be discouraged. Doxycycline 200 mg once a week effectively prevented infection in U.S. soldiers training in Panama.270 Such prophylactic treatment could be given to individuals at unusually high risk. Although Leptospira vaccines have been experimentally produced for human use, no product is approved and commercially available in the United States. Vaccines are available for animals. Immunization of domestic animals has primarily a veterinary benefit, in that the animals are protected from clinical disease. Immunity lasts about 6 months, but immunization does not guarantee that the animal cannot become infected. Several human cases have been traced to immunized dogs that apparently were still able to shed organisms.98 Since then, some veterinary vaccines have been shown experimentally to reduce the renal carrier state.144

Melioidosis Melioidosis is an infection caused by the bacterium Burkholderia (formerly Pseudomonas) pseudomallei, which lives freely in soil and water.313 Disease is spread from the environment to both humans and other animals. The causative agent and disease

process in humans were first described by Whitmore and Krishnaswami298 in Rangoon, Burma in 1912.160

BACTERIOLOGY B. pseudomallei is a bipolar, gram-negative, aerobic rod approximately 0.5 to 1 µm in width and 3 to 5 µm in length. It grows readily on standard laboratory media at 37° C (98.6° F). After 48 to 72 hours of growth, distinctive wrinkled colonies with a “daisy head” appearance are formed. These give off a pungent, putrefactive odor.159 The organism is oxidase positive and nonpyocyanogenic. It is resistant to colistin and gentamicin in vitro.121 In 1992, Yabuuchi and co-workers proposed that seven species, formerly of Pseudomonas RNA group II, should be transferred to a new genus, Burkholderia, with B. cepacia as the type species.313

TRANSMISSION AND EPIDEMIOLOGY Melioidosis is a saprozoonosis transmitted to animals and humans from the environment; transmission does not generally occur between living organisms. Rare cases of transmission from sheep to humans in Australia have been described.59 There is a single case of presumed transmission by the venereal route.183 Disease is reported much more often in adults than in children. Most cases of melioidosis have been reported in areas between 20 degrees north and 20 degrees south of the equator.120 A majority of cases have been reported from Southeast Asia and tropical Australia. The most heavily endemic areas include Myanmar (Burma), Malaysia, Vietnam, Singapore, Cambodia, Thailand, Java, Borneo, New Guinea, and northern Australia. Occasional human and animal cases have been reported from Central India, Sri Lanka, Niger, Madagascar, Ecuador, Panama, Aruba, and Mexico. Cases from the western hemisphere have been reviewed.11 Melioidosis is rare in the United States; most cases are in travelers or visitors, such as two cases in Florida in 2005 that were traced to recent travel from Honduras.54 Melioidosis is endemic to northern Australia, and manifests seasonally. B. pseudomallei survives during Australia’s dry season in the clay layer of the soil, 25 to 30 cm below the surface, and can be brought to the surface and distributed by water seeping through this layer during the wet season.121 Clinical and subclinical infections occur in a variety of animals, most often sheep, goats, and swine. Infections in animals offer no direct threat to human health but are epidemiologic indicators that the organism is in a given geographic area.120 Transmission is thought to occur by direct percutaneous inoculation through wounds contaminated with soil or water, by ingestion, or by inhalation of infective droplets. A high incidence of pulmonary melioidosis in helicopter crew members in Vietnam was ascribed to inhalation of dust and aerosols raised by the helicopters operating in highly endemic areas.120

SYMPTOMS Most human infections are asymptomatic, as indicated by the high prevalence of seropositivity without clinical disease within endemic areas. Active disease is most likely to be seen in individuals with predisposing conditions, particularly diabetes mellitus, alcoholism, neoplasms, malnutrition, and various forms of immunodeficiency. Clinical disease can occur in acute, subacute, or chronic forms. The lungs are the organs most frequently involved. Pulmonary melioidosis can mimic tuberculosis in that the upper lobes are most frequently involved, cough is productive, sputum often contains blood, and patients complain of chest pain and fever (Figure 59-14). However, calcifications in the lungs and hilar lymph nodes typically seen in tuberculosis are rarely seen with melioidosis. An entire lobe or major segment of a lobe may be consolidated, and multiple pulmonary abscesses may be scattered in the lung parenchyma. Septicemia can develop in the acute form of the disease and may mimic other forms of gram-negative sepsis in its manifestations. Multiple abscesses can form in skin, lungs, liver, spleen, kidneys, and bone, but the CNS is rarely involved. Without treatment, the case–fatality rate exceeds 90%. 1153

CHAPTER 59  Wilderness-Acquired Zoonoses

convalescent sera should be tested 2 weeks apart because falsepositive reactions can occur in single samples. Specific serologic diagnosis of the serovar of infection can be made with the microscopic agglutination test (MAT), which uses live organisms but is available in relatively few reference laboratories. A genus-specific MAT employs a single, broadly reactive antigen.293 An IgM-specific, dot-ELISA is comparable with the MAT in its ability to detect recent exposure to leptospires and is rapid and simpler.204 Latex agglutination and indirect hemagglutination have high specificity and sensitivity and are especially useful early in the infection.207 A urine dipstick is available as a rapid screening test for the diagnosis of leptospirosis; if positive, a serum specimen can be sent to a reference laboratory for the MAT for confirmation.246

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A

B

C

FIGURE 59-14  Subacute melioidosis with thin-walled cavities in the right upper lobe of the lung simulating tuberculosis in an American soldier serving in Vietnam. Sputum cultures were positive for Burkholderia pseudomallei and negative for acid-fast bacilli. The patient had a fever; cough with purulent, blood-streaked sputum; chest pain; and weight loss. Posteroanterior view of the chest (A) and anteroposterior (AP) tomogram of the right upper lobe (B) show two thin-walled cavities with virtually no surrounding inflammatory reaction in the posterior segment of the right upper lobe. AP tomogram of the right upper lobe (C) obtained 3 weeks later shows slight diminution in size of the lower, more medial cavity, which has merged with the larger cavity above it. The patient was treated with tetracycline for 2 months with subsequent clearing of his cavitary melioidosis. The subacute or subclinical forms of melioidosis must be considered in the differential diagnosis of thin-walled lung cavities in addition to other entities, such as tuberculosis, coccidioidomycosis, and bullae. (From Palmer PES, Reeder MM, editors: The imaging of tropical diseases: With epidemiological, pathological and clinical correlation, Berlin, 2000, Springer. Reprinted with permission from Springer Science and Business Media.)

In the subacute and chronic forms of disease, abscesses can form in internal organs and may drain through sinus tracts. Melioidosis has been referred to as a “medical time bomb” because infection can lie dormant for months or years, only to become manifest when resistance is lowered. An incubation period as long as 26 years has been reported.180 The infection should be suspected in anyone with a compatible clinical picture, including fever of unknown origin, who has resided in or visited an endemic area.

DIAGNOSIS The only definitive diagnostic procedure is culture of the organism from blood, bone marrow, sputum, pus, or infected tissue. Several serologic tests are available but are not reliable, because many individuals from endemic areas have antibodies to the organism without any evidence of clinical disease. An indirect hemagglutination antibody titer of 1 : 40 or greater is considered compatible with infection, as is a CF titer of 1 : 10 or greater. Rising titers by IgM indirect FA are probably the best immunologic indication of infection. No pathognomonic lesions are seen histologically. The abscesses consist of central areas of necrosis without unique or distinctive features that would permit definitive histopathologic diagnosis.

TREATMENT All cases of melioidosis should be treated with antibiotics. Initial treatment with 10 to 14 days of intravenous (IV) ceftazidime298 has reduced mortality in disseminated septicemic melioidosis to 35% to 40%.159 After parenteral treatment for at least 10 days during which there is clinical improvement, a combination antibiotic oral regimen for 12 to 20 weeks is recommended for a complete course of treatment. Current recommendations include high-dose TMP-SMX (8 mg/kg trimethoprim–40 mg/kg sulfamethoxazole up to two double-strength tablets [320 mg/1600 mg] twice daily) with or without doxycycline (2.5 mg/kg up to 100 mg twice daily). It is sometimes recommended to add folic acid (0.4 mg PO daily) to the TMP-SMX regimen due to folic acid antagonism from this medication. For children younger than age 9 years or pregnant women, recommended treatment is 1154

amoxicillin-clavulanate extended-release twice daily for 20 weeks. Even with compliance, relapse rate is up to 10%. In vitro sensitivity tests do not always correlate with clinical response to antibiotics. Therapy must be given at sufficient dosage and duration to avoid recurrence of infection and emergence of resistant organisms.

PREVENTION AND CONTROL In the field, prevention consists of avoiding ingestion or inhalation of potentially infective soil or water. Wounds, burns, and other injuries should be thoroughly cleaned to avoid infection through contamination. Reasonable care and precautions should be taken in handling purulent drainage of blood, sputum, and other materials from patients with melioidosis.

Rat-Bite Fever Rat-bite fever, also known as Sodoku and Haverhill fever, has been present for more than 2000 years. Long known in the Indian subcontinent, the first clinical report in the United States was in 1839, but the pathogen was unknown until isolated from a ratbitten man by Schottmuller in 1914 and identified as Streptothrix muris ratti. It was renamed in 1925 to Streptobacillus moniliformis. In 1926, an outbreak in the milk supply in Haverhill, Massachusetts, led to the name Haverhill fever. Originally thought to be a different bacterium, it was named Haverhillia multiformis, but was later found to have the same DNA. The second bacterium causing rat-bite fever was originally discovered in the early 19th century and named Sporozoa muris. It was renamed in 1924 to Spirillum minus. It is also referred to as Sodoku (so, “rat”; doku, “poison”). The rat-bite fever pathogens Streptobacillus moniliformis and Spirillum minus cause two distinct syndromes.

EPIDEMIOLOGY Streptobacillus moniliformis and Spirillum minus are parts of the normal oral flora of rodents, including squirrels. Rat-bite fever may also result from bites by wild and domestic carnivores, such as weasels, dogs, cats, and pigs, which may have been infected when hunting rats and mice.250 Carrier rates among wild rats vary from 0% to 50%.23,268 Fewer than 70 cases have been reported in

7 to 10 days, followed by an oral course.268 Effective alternatives for penicillin-allergic patients are doxycycline (intravenous or oral) or tetracycline, 30 mg/kg/day PO in four divided doses, or streptomycin, 15 mg/kg/day IM in two divided doses. Erythromycin is not effective. Complications such as endocarditis should be treated with high-dose IV potassium penicillin G, 10 to 20 million units a day, as well as streptomycin or gentamicin.220 The organism has both a bacillary and a cell wall–deficient L phase, which is thought to account for some of the antibiotic failures. The bacterial phase responds to penicillin, streptomycin, and tetracycline, whereas the L phase is resistant to penicillin.

STREPTOBACILLARY TYPE

Mainly found in Asia, spirillar rat-bite fever is caused by Spirillum minus, a gram-negative, tightly coiled, spirillar microorganism. It is usually transmitted by infected wild rats, although cats have also been implicated. The general setting of socioeconomic deprivation in which this disease occurs is the same as in the streptobacillary form; cases in laboratory animals are unusual. The incubation period is 7 to 28 days, during which the bite lesion often heals.117

Streptobacillary rat-bite fever (Haverhill fever) is caused by S. moniliformis, an aerobic, nonmotile, gram-negative bacillus. The onset of symptoms usually occurs within a week of the bite, but the incubation period may extend to several weeks, during which time the original wound usually heals completely. A bite need not be present, because the disease can also be transmitted by contaminated food, milk, or water.100 S. moniliformis has also been transmitted by simply playing with pet rats, without history of bite or injury.222

SYMPTOMS Although many rats may become colonized with S. moniliformis, few show symptoms of the disease. Initial symptoms in infected humans include fever, chills, migratory arthralgias, cough, malaise, headache, and, less frequently, local lymphadenitis and septic arthritis (which in rare cases can be a presenting symptom).78 These are followed by nonpruritic morbilliform or petechial rash, which frequently involves the palms and soles. Migratory polyarthritis develops in approximately 50% of victims and may last several years. Generalized lymphadenitis may be present; splenomegaly and hepatomegaly are rare.268 Rare complications include pericarditis, endocarditis, pericardial effusions, bronchopneumonia, pneumonitis, periarteritis nodosa, volvulus, and septicemia.90,150

DIAGNOSIS The Venereal Disease Research Laboratories (VDRL) test shows a false-positive result for 25% of victims. Leukocytosis with left shift is common, and agglutinating antibodies for the bacillus appear during the course of the disease. On autopsy, interstitial pneumonia, fibrinous endocarditis, mononuclear meningitis, hepatosplenomegaly, and mononuclear cell infiltrates in regional lymph nodes have been found.249 Culture of the bacteria is difficult because the commercial aerobic blood culture anticoagulant (Liquoid) inhibits growth of the bacteria. Anaerobic cultures may show growth because this anticoagulant is not added. Panmede (a papin digest of ox-liver) supplemented into a brain– heart infusion of cysteine broth in an anaerobic culture media has shown promise for culturing the bacteria.252 When a history of animal bite is lacking, differential diagnosis must include rickettsial and viral infections. Fever and rash may suggest meningococcemia, but meningeal signs are lacking in rat-bite fever. Definitive diagnosis requires demonstration of rising antibody titers or culture of the bacillus from the blood, joint fluid, pustules, or the original bite location. This can make diagnosis difficult. Typically, identification by culture requires experienced laboratory workers who seek the organism.

TREATMENT Untreated, the disease runs a course of several weeks; prolongation of symptoms should raise the suspicion for endocarditis. Mortality in untreated persons is 13%, with most deaths caused by endocarditis and pneumonia. The disease can be fulminant. Two previously healthy adults died within 3 to 6 days after exposure to rats,123 and an infant bitten by a wild rat died 4 days after the bite.249 The treatment of choice is IV or IM penicillin for

SPIRILLAR TYPE

SYMPTOMS After the incubation period there can be exacerbation of the original wound with local development of pain, erythema, purplish discoloration, and swelling. An ulcer may develop, followed by chills, fever, lymphadenitis, and dark-red macular rash. Myalgias are common, but arthritis is absent, which helps in the differentiation from streptobacillary fever. Leukocytosis and a false-positive VDRL test are often present. The disease is episodic and relapsing, with a 24- to 72-hour cycle. The differential diagnosis includes rickettsial and viral diseases when the history of animal bite is not present. In addition to the absence of arthritis, manifestations at the bite site (usually involving lymphadenitis, and still present when systemic illness occurs) are more pronounced than with the streptobacillary variety and the fever and illness are relapsing in nature.268

DIAGNOSIS AND TREATMENT Definitive diagnosis rests on demonstrating the presence of S. minus in a darkfield preparation of exudate from an infected site. The patient’s blood can be inoculated into mice, which may be tested for subsequent infection. The mortality from untreated disease is considerably lower than that from streptobacillary fever. The untreated course spans several months. Antibiotic therapy is the same as for streptobacillary fever.104,117

Plague Plague, a bacterial disease caused by Yersinia pestis and transmitted by the bites of infected fleas, has occurred in explosive epidemics. Probable epidemics of plague occurred during the Peloponnesian War, as described by Thucydides, in approximately 400 BC. It ravaged the Roman Empire and western Europe during the age of Justinian and continued through the 7th century. The best-known and most devastating epidemic started in 1348. Known as the Black Death, the infection spread from Asia throughout western Europe, killing one-third of the population (Figure 59-15, online).107 Having gained notoriety from three major pandemics that killed hundreds of millions of people, plague is now a concern for bioterrorism. Plague is a category A agent of bioterrorism and is a reportable disease under the International Sanitary Regulations.162 The first person to microscopically characterize the disease was Yersin during the third plague pandemic in the late 19th century after the port of Hong Kong became ravaged by the disease. The rodents escaping from that pandemic spread the highly virulent Y. pestis orientalis into North and South America.300 Plague is carried by various rodent reservoir hosts and transmitted by rodent fleas. Most of the outbreaks in Europe have been ascribed to importation of plague from enzootic foci in Asia, by ships bringing infected rats and people to port cities. A matter 1155

CHAPTER 59  Wilderness-Acquired Zoonoses

North America, with at least one-half caused by S. moniliformis in laboratory workers. Rat-bite fever is not a reportable disease; therefore, these numbers are likely underestimated. At least 10%, and up to 100%, of rats are nasopharyngeal carriers of Streptobaccillus.6,44,117 Risk of infection after a rat bite appears to be 10%, with 13% mortality if untreated. Victims of disease caused by S. minus are primarily children of lower socioeconomic groups exposed to poor sanitation and heavy rodent populations.184 Demographics of the disease are shifting; rat-bite fever is now being seen in pet owners and people who work in pet stores. Rare cases can occur in any setting and can easily be fatal, particularly when the proper diagnosis is not suspected.53

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Actual size

FIGURE 59-16  A Norway rat (Rattus norvegicus) in a corn storage bin in Kansas City, Missouri. R. norvegicus is known to be a reservoir of bubonic plague (transmitted to man by the bite of a flea or other insect), endemic typhus fever, rat-bite fever, and a few other dreaded diseases. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp.)

FIGURE 59-18  Male Xenopsylla cheopis (Oriental rat flea) engorged with blood. This flea is the primary vector of plague in most large plague epidemics in Asia, Africa, and South America. Both male and female fleas can transmit the infection. (From http://www.cdc.gov/ ncidod/dvbid/plague/index.htm.)

EPIDEMIOLOGY

Y. pestis is a gram-negative, nonmotile, nonsporulating rod with a bipolar, or “safety-pin,” appearance in smears stained with Giemsa or Wayson stain (Figure 59-17).36 The appearance is somewhat variable by Gram technique. Most standard bacteriologic media support the growth of the organism aerobically or under facultative anaerobic conditions. Optimal in vitro growth occurs at 28° C (82.4° F), at which temperature colonies become visible on plain agar in approximately 48 hours. Virulence factors encoded by the bacterial chromosome include surface capsular material that is antiphagocytic, the ability to synthesize purines even if phagocytosed, resistance to complement mediated lysis,162 and a surface component needed for iron uptake. Virulence factors mediated by a plasmid include dependence on environmental calcium for growth at 37° C (98.6° F) and production of v and w167 antigens. The relationship between calcium dependence and virulence is under investigation.107

The epidemiology of plague is complex. Various fleas can transmit the infection between reservoir rodent hosts and humans. In major epidemics, the prominent carriers were the tropical rat flea (Xenopsylla cheopis) (Figure 59-18) and the black rat (R. rattus), although many other flea and rat species are known to transmit the plague. Children and males have a slight preponderance for the disease.32 Smoldering foci of infection are maintained in nature in wild rodents and their fleas. In the United States, enzootic (maintenance) hosts include deer mice (Peromyscus maniculatus) and various voles (Microtus species). Epizootic (amplifying) hosts include the prairie dog (Cynomys species) (Figure 59-19) and ground squirrel (Spermophilus species). Other rodents and lagomorphs that maintain infection include chipmunks (Eutamias species), marmots (Marmota species), wood rats (Neotoma species), rabbits (Sylvilagus species), and hares (Lepus species).209 Conditions that provide adequate food and shelter for plaguesusceptible rodents put humans at increased risk for acquiring the disease.46 Plague season tends to run from February through August in North America and is related to the presence and prevalence of the vectors and the hosts.32 Enzootic foci of plague remain in parts of Asia, Africa, and South America,33,209 as well as in the western United States. In 2003 the WHO received reports from nine countries with more than 2000 cases of the plague, resulting in 182 deaths, most of which were from Africa.305 The Democratic Republic of the Congo, Mongolia, and parts of China are known to have endemic plague with outbreaks causing widespread public health concerns in regions with no accessible health care.307

FIGURE 59-17  Wayson stain of Yersinia pestis. Note the characteristic “safety pin” appearance of the bacteria. (From http://www.cdc.gov/ ncidod/dvbid/plague/wayson.htm.)

FIGURE 59-19  Thrombus in a vein in the subcutis of a prairie dog naturally infected with plague. Many organisms (fine stippling) are present in the thrombus. (Hematoxylin and eosin, ×1000.)

of considerable historical and epidemiologic interest is how and why the various epidemics eventually subsided. Theories include development of mutant bacteria; changes in patterns of shipping, building, and hygiene; replacement of Rattus rattus by Rattus norvegicus (in the case of the Black Death) (Figure 59-16); and development of immunity in animals and humans.89

BACTERIOLOGY

1156

TRANSMISSION Plague is normally a flea-borne disease of rodents, although other animals, including humans, can become infected. Humans are generally infected by the bite of an infected flea; however, direct contact with and percutaneous inoculation of Y. pestis organisms can lead to disease. Rarely, inhaled infective droplets cause pulmonary plague; human-to-human transmission can occur and is a threat in developing countries and in the United States. In 1997 an outbreak occurred in Madagascar that affected 18 persons with eight deaths. These cases were attributed to a healer sucking bacteremic blood out of an infected patient and subsequently developing pneumonic plague.32

The black rat is highly susceptible to plague and dies with severe septicemia. The concentration of organisms in the rat’s blood ensures infection of the biting flea. When the rat dies, the flea leaves to seek other hosts. This cycle is unusual in that the infection kills the reservoir host and the vector, but the nature of the infection in the flea and rat guarantees further transmission and survival of the microorganism. The bacteria multiply so extensively in the X. cheopis flea that they block its proventriculus, or foregut. The flea cannot feed effectively, becomes ravenously hungry, and regurgitates large numbers of bacilli when it bites. There are multiple theories as to the survival of the bacteria during periods between outbreaks. The most popular hypothesis is that Y. pestis can persist by maintaining a benign relationship within adapted rodents or fleas.93 Another hypothesis is that it may be able to survive in the soil for limited periods of time within the carcasses of infected animals.300

SYMPTOMS The three most common forms of plague are bubonic, pneumonic, and septicemic. Less common forms are meningeal, pharyngeal, and ophthalmic. In the most common form, bubonic plague, buboes develop. These are greatly enlarged and very tender lymph nodes proximal to the point of percutaneous entry, such as a flea bite or a cut infected by handling infected tissues. Inguinal nodes are most often involved because fleas usually bite on the legs. Skinning an infected animal or handling its tissues often results in axillary buboes. Frequently, cervical, hilar, or mesenteric lymph nodes are enlarged. The incubation period for bubonic plague is usually 2 to 6 days but can be up to 10 days before clinically apparent infection is present.32 In mild or early stages of infection, seeding of the blood occurs intermittently, causing a low sensitivity to blood culture testing. Later, if disease becomes severe, all blood cultures are positive. Victims usually have high fever, chills, severe malaise, headache, and myalgias. Toxicity, cardiovascular collapse with shock, and hemorrhagic phenomena may occur. Blackened hemorrhagic skin lesions gave rise to its being called the Black Death during the pandemic of the 14th century. Victims with bacteremia and significant symptoms but no buboes are considered to have septicemic plague. Such cases may be difficult to diagnose unless the physician suspects plague on the basis of epidemiology. As with other forms of gramnegative sepsis, victims have fever, chills, malaise, headache, and GI symptoms such as nausea, vomiting, and diarrhea. The disease can result in cardiovascular collapse. Thrombosis (see Figure 59-19) and disseminated intravascular coagulopathy may be present. Untreated septicemic plague progresses to pulmonary involvement and death. However, transmissible pneumonic infection is estimated to occur in only 5% of patients with septicemic plague, because victims die before alveolar pneumonitis and the potential for spread of droplets. Pneumonic plague can result from inhalation of droplets from another pneumonic patient or by pulmonary seeding from the blood. Pneumonic plague runs an acute and fulminant course and is almost uniformly fatal if not treated. The incubation period is 2 to 3 days and disease is characterized by the sudden onset of fever, cough, bloody sputum, headache, and shaking chills. Radiographs reveal progressive consolidation of pneumonic patches in the lungs, often with pleural effusion (Figure 59-22). Patients are usually critically ill by the time they are symptomatic from the disease.162 Of 71 cases of plague reported in New Mexico between 1980 and 1984, 18 were septicemic.135 The victims were significantly older and more likely to die than those with bubonic plague. The white blood cell counts in the New Mexican septicemic cases were low, normal, or elevated (range, 3000 to 68,700/mm3), but all patients had relative or absolute neutrophilia with a left shift. Bacteria were demonstrable on direct blood smears in 3 of 17 septicemic patients. Plague is most common in persons younger than age 40 years, perhaps because of their greater outdoor activity, but the risk of the septicemic form increases in individuals older than age 40 years. Among patients with septicemic 1157

CHAPTER 59  Wilderness-Acquired Zoonoses

The major enzootic states in the United States are New Mexico, Arizona, California, Colorado, Oregon, Nevada, and Utah. From 1944 through 1993, 362 cases of human plague were reported in the United States; approximately 90% of these occurred in Arizona, California, Colorado, and New Mexico with the highest amount coming from California (Figure 59-20, online). Seven confirmed cases of human plague were reported in 1995 (three in New Mexico, two in California, one in Arizona, and one in Oregon). Five of the seven cases were bubonic, one was septicemic, and one a fatal pneumonic case.167 In 2005, the WHO reported that human plague can cause severe disease with a case–fatality ratio of 30% to 60% if left untreated.305 In many foreign areas, the exact species of rodents and fleas involved in transmission and maintenance are not known. However, it is known that the distribution of the plague is linked to the geographic distribution of its natural foci.305 Vietnam is the only country considered a threat for the international introduction of plague (Figure 59-21, online). Carnivorous mammals can acquire plague by ingesting infected rodents or by being bitten by their fleas. Dogs usually do not become very ill with plague, but cats can acquire severe, often fatal, forms of infection, resembling syndromes seen in humans. Bubonic plague in cats is usually manifested as severe submandibular lymphadenopathy. Cats can also acquire pneumonic plague, characterized by a subacute febrile course with cough and respiratory distress. Cats can transmit plague to humans by bite or by respiratory droplets, or by carrying fleas to people. Plague is an occupational risk for veterinarians who handle sick cats or their tissues.141,218 Although dogs are usually not as severely affected as cats, at least one human case was associated with a dog that apparently died of plague.221 Dogs may be significantly involved in the epidemiology of plague in Tanzania, as reservoirs of vector fleas or bacterial infection.145 In the United States, one person acquired plague while skinning an infected coyote38 and two while skinning bobcats.41 Other carnivores, such as skunks, badgers, and raccoons, have been found with antibody to the plague bacillus and presumably were exposed while hunting infected rodents. Exposure to infected rabbits, their fleas, or both has been associated with human plague.36 Plague is not generally recognized as a disease of farm animals in modern times, but a recent report ascribed one outbreak of plague in a Libyan village to contact with a sick camel and another to contact with two goats.60 In the United States, the major epidemiologic factor associated with acquiring plague is living in a rural or suburban area where the enzootic disease occurs. People who hike, camp, or perform field studies in such areas are subject to this disease. Its diagnosis should be considered in anyone with a compatible history who has recently been in an enzootic area. More recently, a fundamental question in disease ecology has arisen in relation to plague: What happens to the pathogens in between the periods of epidemics that allows the disease to persist? A group of researchers at Stanford University looked into just this in a set of prairie dogs and found that grasshopper mice carry the fleas during interepizootic periods as alternate hosts. The grasshopper mice show heterogeneity to mortality, allowing for periods of quiescence between outbreaks as well as transmission between groups of prairie dogs that are relatively dispersed. This is the first time the theory of percolation-threshold phenomenon with alternate hosts as the key element determining outbreaks has been shown.225

PART 6  ANIMALS, INSECTS, AND ZOONOSES FIGURE 59-22  Pneumonic plague. (From http://er1.org/docs/photos/ Plague/pneumonic%20plague.jpg.)

plague, mortality was greater in younger patients, perhaps because of greater delay in diagnosis and decreased likelihood that they would receive antibiotic therapy on an empiric basis.135 Abdominal pain was present in nearly 40% of the patients in New Mexico. Hepatosplenomegaly occurs in plague and may be a source of abdominal pain, but it was not found in the patients reported in this series. The presence of abdominal symptoms in plague should be emphasized because the disease could be mistaken for other forms of GI illness. A review of the 71 plague cases in New Mexico from 1980 to 1984 revealed that GI symptoms occurred in 57% of patients, with vomiting (39%) the most frequent symptom. Nausea (34%), diarrhea (28%), and abdominal pain (17%) were also observed.134 Plague should be suspected in patients who have various combinations of lymphadenopathy, high fever, malaise, tachycardia, tachypnea, hypotension, and abdominal symptoms and who have come from an endemic area. If the suspicion is reasonable, antibiotic therapy should be instituted immediately. Treatment should not be delayed to await laboratory confirmation of the diagnosis. Rare forms of plague include pharyngeal, meningeal, and ophthalmic. Pharyngeal and ophthalmic plague can be acquired by exposure to droplets expelled by a pneumonic patient. Endophthalmitis can also be secondary to septicemia. Meningitis is acquired by direct seeding while the patient is bacteremic.

DIAGNOSIS Definitive diagnosis is based on culture of the organism from sputum, transtracheal aspirate, blood, or aspirates of buboes. The cultures require a minimum of 4 days for growth. The best staining technique to demonstrate bipolar morphology of the organism is the Giemsa or Wayson technique. Direct FA stain of aspirates and smears provides a reasonably rapid diagnostic technique (Figure 59-23). Although crossreactions with Yersinia pseudotuberculosis have been recorded and occasional strains of the plague bacillus do not stain well with FA, a positive FA test in a patient with a compatible epidemiologic and clinical picture is a reasonable basis for making a diagnosis of plague and instituting therapy. ELISA tests are also used and provide rapid diagnosis, and PCR has shown to be reproducible and highly sensitive; however, neither test lends to ease of use in remote situations.307 Material from buboes should be obtained by fine-needle aspiration rather than excision or incision and drainage. This reduces risks of transmission to medical personnel and of iatrogenic septicemia.

treated immediately without awaiting definitive laboratory studies. The best available drug is gentamicin 5 mg/kg IV/IM qd or 2 mg/ kg loading dose followed by 1.7 mg/kg IV/IM tid for 10 days. A less preferred alternative is doxycycline, loading dose 200 mg IV; thereafter, 100 mg IV bid for 10 days.305 Aminoglycosides penetrate poorly into the CSF and therefore are not recommended for use in persons with meningeal plague.307 Because streptomycin is not readily available in all pharmacies, current recommendations include a 10-day course of gentamicin (not in children or pregnancy), doxycycline, chloramphenicol, or TMP-SMX. A randomized controlled trial in Tanzania demonstrated good efficacy of a 7-day course of either doxycycline (100 mg PO or IV twice daily) or gentamicin (2.5 mg/ kg IM twice daily) as single-agent therapy for plague.195 If the agent chosen is chloramphenicol, it is administered in a loading dose of 25 mg/kg orally, up to 3 g total, followed by 50 to 75 mg/kg/day orally in four divided doses for 10 to 14 days. If the patient does not tolerate oral therapy, chloramphenicol can be given intravenously, 25 mg/kg as a loading dose followed by 60 mg/kg in four divided doses every 6 hours until oral therapy is tolerated. It is preferable to use chloramphenicol in the event of meningitis or endophthalmitis because of good penetration into affected tissues. Use of chloramphenicol is decreasing due to severe adverse effects, including bone marrow suppression, aplastic anaemia and “grey baby” syndrome.307 Whichever drug combination is selected, antibiotic therapy should be given for at least 10 days, or for 3 or 4 days after clinical recovery. Trimethoprim-sulfamethoxazole (320 mg of trimethoprim and 1600 mg of sulfamethoxazole) twice a day for 10 to 17 days was found effective in treating plague.2 Recent literature shows that sulfonamides should be used in the treatment of bubonic plague only.305,307 Infants born to plague-infected mothers may have congenital infection. They can be treated with kanamycin, 15 mg/kg/day IV/IM in four divided doses every 6 hours, or streptomycin, 10 to 20 mg/kg/day in four divided doses every 6 hours. Some experts recommend treatment of children with TMP-SMX, 4 mg/ kg of the trimethoprim component twice daily for 7 to 10 days. The recent discovery of a multidrug-resistant strain of Y. pestis in Madagascar is of concern.106 Resistance to all first-line antibiotics, to the principal treatment alternatives, and to prophylactic drugs was mediated by a transferable plasmid. However, these isolates were susceptible to cephalosporins, quinolones, and trimethoprim. The greatest risk of contagion is by aerosol transmission from patients with the pneumonic form of plague. All persons with suspected plague should be placed in strict quarantine and isolation for a minimum of 48 hours of specific antibiotic treatment. If no respiratory signs develop within 48 hours, wound and skin precautions will suffice for the remainder of the hospitalization. Patients with plague pneumonia or pharyngitis should be kept under strict respiratory quarantine for at least 4 days of antibiotic

TREATMENT Widespread use of antibiotics in the 1940s allowed for adequate treatment of plague.307 Patients with suspected plague should be 1158

FIGURE 59-23  Yersinia pestis seen on direct fluorescent antibody testing. (Courtesy Centers for Disease Control and Prevention.)

PROPHYLAXIS Household contacts and individuals exposed to patients with pneumonic plague should be prophylactically treated with antibiotics. Tetracycline, 500 mg orally every 6 hours for 6 days, can be given to adults. Trimethoprim-sulfamethoxazole can be given to children younger than age 8 years and to most pregnant women. Streptomycin, chloramphenicol, and sulfadiazine are alternative prophylactic medications, given in therapeutic doses for 1 week to 10 days. Household contacts of individuals with bubonic plague do not have to be treated prophylactically. They should have their temperature recorded twice daily, and if it exceeds 37.7° C (99.86° F) orally, they should report immediately to a physician for evaluation. Careful surveillance is indicated for persons who have had face-to-face contact with patients with pneumonic plague. Their well-being should be confirmed daily. The incubation period for primary pneumonic plague is 1 to 3 days and for pharyngeal plague 3 to 6 days. Precautionary follow-up observation of contacts should be maintained throughout this time. All cases of suspected or confirmed plague should be reported to the state health department.

PREVENTION Residents and visitors to plague-endemic areas should be advised of the risks of infection. They should avoid contact with rodents and other possible animal reservoirs of infection that are found sick or dead in the wild. Disposable plastic or rubber gloves should be worn when skinning or dressing a possibly infected animal. Cats and dogs should be kept indoors, leashed, or otherwise restrained. Owners of pets that have access to wild rodent populations must maintain flea control. Veterinary personnel working on animals that could have plague should follow strict infection control procedures. Health departments in enzootic areas should maintain surveillance for plague in local reservoir species. At times of increased plague activity, insecticide sprays and powders can be applied to rodent burrows. Ectoparasite control is essential before any attempt is made to kill the rodents, because killing the rodents without control of their ectoparasites causes fleas to seek other hosts, including dogs, cats, and people. A killed bacterial vaccine is available in the United States but is rarely used. Its application is limited to persons who have intensive, usually occupational, exposure to the infection. Many of these people prefer to rely on sanitation, protective clothing, and prophylactic or therapeutic treatment rather than use the vaccine, because it has short-term (6- to 12-month) efficacy and has a significant incidence of side effects, such as fever, malaise, and pain at the site of injection.42 Clinical and epidemiologic assistance for problems relating to plague can be obtained from the Bacterial Disease Branch, Centers for Disease Control and Prevention, 800-232-4636.

Tularemia Tularemia was first described in 1837 by Homma Soken, a Japanese physician who wrote of a febrile illness with generalized

lymphadenopathy in persons who had eaten infected rabbit meat. In 1911, McCoy described a disease resembling plague in California ground squirrels. In the following year, McCoy and Chapin isolated the organism from rodents in Tulare County, California; this geographic site gave rise to the name of the disease. Edward Francis did much of the landmark bacteriologic and clinical investigation, and the genus of the causative organism, Francisella, is named after him. The role of ticks as vectors of the disease was discovered by Parker and Spencer in 1924. In 1929, they described transovarial transmission of the bacterium in ticks.

BACTERIOLOGY Francisella tularensis is a nonmotile, gram-negative coccobacillus measuring 0.2 by 0.3 to 0.7 µm. It must be grown aerobically on a medium containing cysteine or other sulfhydryl compounds. The organism is best grown on glucose cysteine agar with thiamine, or on cysteine glucose blood agar. The organism has also been isolated in thioglycollate broth, charcoal yeast extract, and Thayer–Martin agar. Two varieties of the organism are recognized in North America. Type A, F. tularensis tularensis, can ferment glycerol and has citrulline ureidase activity. Type B, F. tularensis holarctica, does not ferment glycerol and does not have citrulline ureidase activity. Type A generally causes more severe disease than does type B. Type B is found in streams, ponds, lakes, and rivers in Europe, Asia, and North America and is often recovered from water voles, muskrats, and beavers.308 Type A is more frequently recovered from rabbits and various bloodsucking arthropods. The two varieties sometimes share an ecologic niche.176

EPIDEMIOLOGY The CDC reports a 2 : 1 male-to-female incidence of tularemia, thought to be due to increased outdoors activities and contact with animals by males. The disease is also more common in the summer months among children. Anyone involved in outdoor activities is at risk in endemic areas.56 The reported incidence of tularemia has been steadily decreasing in the United States since its peak at 2291 cases in 1939 (Figure 59-24, online). Other tickborne infections, such as Rocky Mountain spotted fever and Lyme disease, have increased. Most cases of tularemia in the United States have been reported from the South and Midwest, particularly Arkansas, Missouri, Massachusetts, Oklahoma, South Dakota, and Kansas.56 The disease is also widespread in Europe, Canada, the Middle East, Russia, and Japan. Transmission by ticks and other arthropods usually occurs in the spring and summer. Transmission from rabbits most often occurs during the fall and winter hunting seasons. Nearly 200 cases are reported from the United States every year, and although this is a reportable disease, it is likely that the actual number is higher, because the empiric use of antibiotics may have aborted undiagnosed cases.

TRANSMISSION Before 1950, most reported cases of tularemia were associated with direct contact with rabbits. Tularemia is now most frequently transmitted by ticks.25 Many different species of ticks are potential or proven vectors. A common vector in the United States is the dog tick, Dermacentor variabilis. The lone star tick, Amblyomma americanum, is the main vector in the southern United States. In the Czech Republic and Austria, D. reticulatus ticks are the main vectors of tularemia, whereas in the former USSR, the vector is mosquitoes (Aedes, Culex, and Anopheles) and the Ixodes species of tick.91 Because the infection can be transmitted transovarially, ticks are an important natural reservoir. Ticks may transmit the bacteria through their feces, as the organism has not been isolated from their salivary glands. Deerflies and other biting flies may also be suitable vectors.148 In the United States, the second most common source of human infection is rabbits. The infection can be acquired by skinning, eviscerating, or handling the tissues of infected rabbits or by eating improperly cooked infected meat or contaminated vegetables.200 Transmission can also occur by direct contact with or ingestion of infected 1159

CHAPTER 59  Wilderness-Acquired Zoonoses

treatment, until the pharyngeal culture is negative for the organism or respiratory signs abate. Contact personnel should wear gloves, gowns, masks, and eye protection. Strong266 dramatically illustrated effective protective clothing during a pneumonic plague epidemic in Manchuria in 1911. The greatest risk of acquiring plague from a patient with the septicemic or bubonic form is by inoculation of blood or exudate; therefore, strict needle precautions should be undertaken. Buboes should not be incised and drained. In theory, fleas harbored by a septicemic patient should be capable of transmitting the disease, but the CDC recommendations for control of plague do not cover eradication of fleas from human patients.297 No pesticides have been approved by the U.S. Food and Drug Administration (FDA) for this use. Products effective against lice may have limited effectiveness, because most fleas do not remain long on a human host.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

soil, water, or fomites. Infection can occur by inhalation of dust or water aerosol74 or in the laboratory. Organisms remain viable in mud samples stored as long as 14 weeks, in tap water for 3 months, in dry straw for 6 months, and in salted meat for 31 days.18 Occasional cases of tularemia have been transmitted by cat bite43,212 or by handling infected tissue from animals other than rabbits, such as bear,40 deer,39 beaver, and muskrat.316 There is no evidence for human-to-human transmission.308 Given the low numbers (10 to 50) of bacteria needed to cause disease, in the 1950s the United States evaluated tularemia as a potential biologic weapon, with the idea that it could be aerosolized and cause a severe life-threatening pneumonia in any person who was exposed. According to the CDC, this was never accomplished. Concern remains that it may be developed into a biologic weapon.56

SYMPTOMS Classically, tularemia occurs in one of six clinical presentations: glandular, ulceroglandular, oculoglandular, oropharyngeal, pneumonic, or typhoidal.18,176 Evans and co-workers95 simplified this classification into two major categories: ulceroglandular and typhoidal. Patients are considered to have ulceroglandular tularemia if they have lesions of the skin or mucous membranes (Figure 59-25), with or without associated lymphadenopathy, with affected lymph nodes at least 1 cm (0.4 inch) in diameter. Patients without lesions of the skin or mucous membranes and with lesser enlargement of lymph nodes are considered to have typhoidal tularemia. In this classification, pharyngitis or pneumonia can occur in either the ulceroglandular or the typhoidal form of the disease. The ulceroglandular form accounts for approximately 80% of tularemia cases. The typical skin lesion begins as an erythematous papule or nodule that indurates and ulcerates. It is frequently painful and tender. Ulcers associated with handling infected animals are usually located on the hand, with associated lymphadenopathy found in the epitrochlear or axillary regions. Infections transmitted by tick bites are usually located on the lower extremities, associated with inguinal or femoral lymphadenopathy. Glandular tularemia is characterized by the presence of enlarged, tender lymph nodes without an associated skin lesion. However, the skin lesion may have healed or gone unnoticed before development of lymphadenopathy. In the oculoglandular form, unilateral conjunctivitis occurs with concentration of inflammatory response in and around ulcers and nodular lesions on the conjunctiva, with enlargement of the ipsilateral preauricular lymph node.124 The oculoglandular form constitutes 1% to 2% of tularemia cases. It is thought to be spread to the eye by a finger.262 Gastrointestinal or oropharyngeal tularemia may be acquired by eating foods contaminated with bacteria. The patient often

FIGURE 59-25  Cutaneous tularemia. Thumb with skin ulcer of tularemia. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp. Courtesy Dr. Thomas Sellers, Emory University.)

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presents with ulcerative–exudative stomatitis and pharyngitis with significant cervical lymphadenopathy. Interestingly, lymphadenopathy is usually unilateral.308 The typhoidal form occurs in approximately 10% of tularemia cases. It is characterized by fever, chills, and debility with no noticeably enlarged lymph nodes. As the disease progresses, weight loss may be significant. Hepatosplenomegaly can occur, especially in children.136 Pericarditis occurs rarely.95 Exudative pharyngitis can occur with either the typhoidal or the ulceroglandular form. There is usually associated cervical lymphadenitis. Pneumonia is a fairly common complication of tularemia. The pulmonary infection can be acquired by inhalation of aerosol, usually from stirring up the dirt while farming. Symptoms include fever, cough, chest pain, shortness of breath, production of sputum, hemoptysis, nausea, and vomiting. In the severe form of the disease, it may imitate typhoid fever with pulse-temperature dissociation and mental deterioration.308 Radiographic abnormalities of the chest may be found in patients without pulmonary symptoms. Chest x-ray may reveal infiltrates, most often of the lower lobe, hilar lymphadenopathy, and pleural effusion. Tularemia patients with pneumonia are more likely to be older, less likely to have a known source of infection, and more likely to die than those without pulmonary infection.243 Before the advent of antibiotics, the pulmonary form of tularemia resulted in mortality rates of 30% to 60%. Severe complications of tularemia, such as bacteremia, pneumonia, and rhabdomyolysis, are most likely to be seen in patients with significant underlying disease, such as lymphoma, other forms of cancer, or diabetes.206 According to the WHO, without treatment, mortality rates have been as high as 30% to 60% for the Type A disease. With treatment, mortality rates are 2% to 5% (WHO/CDC).308

DIAGNOSIS Ulceroglandular tularemia can be confused with cat-scratch disease, streptococcal or staphylococcal skin diseases, sporotrichosis, and plague. Typhoidal tularemia can mimic septicemic plague, brucellosis, salmonellosis, typhoid fever, other forms of gram-negative sepsis, and leptospirosis. Tularemic pneumonia can appear similar to other forms of bacterial and nonbacterial pneumonia, including Q fever, psittacosis, Legionnaires’ disease, and tuberculosis.219,243 Oculoglandular tularemia resembles Parinaud’s syndrome (granulomatous conjunctivitis with preauricular lymphadenitis) caused by other bacteria (e.g., Leptothrix species and Mycobacterium tuberculosis), syphilis, and cat-scratch disease.124 The differential diagnosis of oropharyngeal tularemia includes infectious mononucleosis, streptococcal pharyngitis, and plague pharyngitis. The disease most likely to be confused with tularemia is plague, because both diseases occur under similar epidemiologic circumstances and are characterized by similar clinical syndromes.37,254 The bacteria causing plague and tularemia share morphologic and cultural features, but can be differentiated serologically and with appropriate microbiologic techniques. Blood chemistries tend to be normal, but other tests reveal elevated white blood cell (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) levels. The CRP can remain elevated for months after the disease.308 Definitive diagnosis of tularemia is usually based on antibody studies, which are best obtained 10 to 20 days after infection.152,269 The most common test is agglutination, either tube agglutination or microagglutination.232 ELISA is also used for diagnosis. An advantage of ELISA is identification of IgM, IgA, and IgG antibodies. Diagnosis is established serologically by demonstrating a fourfold or greater rise in titer between acute and convalescent sera taken one or more weeks apart. Titers of 80 or greater are generally considered significant in the agglutination test. Values rarely reach that level during the first week of infection, but usually reach or exceed that by day 16 of infection. Agglutinating antibodies remain detectable for 10 to 30 years after infection. IgM, IgA, and IgG antibodies also remain detectable by the ELISA technique for at least 11 years after infection. Because of the long persistence of antibody, single titers cannot be used for definitive diagnosis.

TREATMENT Streptomycin, the drug of choice, should be given in a dosage of 30 to 40 mg/kg/day, in two divided portions IM every 12 hours for 3 days, followed by one-half that dosage for another 4 to 7 days. In 1994 Enderlin and co-workers preformed a meta-analysis of the literature and found that in some patients the antibiotics given to treat tularemia resulted in either relapse of the disease after an apparent cure or treatment failure in which no improvement was seen. The rate of cure for streptomycin is 97%, with no relapses. For gentamicin and tetracycline, respectively, the rates of cure were 86% and 88%; rates of relapse, 6% and 12%; and rates of failure, 8% and 0%.92 The duration of therapy with gentamicin and a delay in its initiation may have affected outcome in severe cases.206 For chloramphenicol and tobramycin, cure rates were 77% and 50%; relapse rates, 21% and 0%; and failure rates, 2% and 33%, respectively. Treatment with imipenem/ cilastatin was successful in one case, and with ciprofloxacin or norfloxacin in six cases; therapy with ceftriaxone was ineffective in eight cases.92

PREVENTION Prevention of tularemia involves avoidance of ectoparasites such as ticks and appropriate hygiene in the handling of infected animal tissues. Insect repellents should be applied when going into areas where ticks, deerflies, and other possible vectors are found. Persons walking in tick-infested brush should wear long pants, with the bottoms of the trouser legs tucked into socks or boot tops. Individuals should check frequently for the presence of ticks while in the field. Ticks should be removed as quickly as possible, preferably with pointed forceps grasping the mouthparts, taking care not to break the mouthparts or to squeeze the body of the tick. Persons handling suspect animals should wear rubber or plastic gloves. Reservoir animals such as rabbits or muskrats that appear ill should not be handled. When it is necessary to handle sick animals, infection control procedures should include the use of gloves, face masks, and disposable gowns. Culturing the organism should be attempted only in laboratories that have appropriate containment facilities for handling such dangerous organisms. Laboratory work with F. tularensis should always be conducted under an appropriate microbiologic hood. Standard halogen-containing phenol or alcohol-based antiseptics can be used for disinfecting surfaces. Although person-to-person transmission is rare, reasonable infection control measures should be taken to reduce exposure to aerosols from patients with oropharyngeal or pneumonic tularemia, and exposure to exudates should be avoided. A live-attenuated vaccine is available as an investigational new drug from the U.S. Army Medical Research Institute for Infectious Diseases at Fort Detrick, Maryland. Physicians using this vaccine must register as collaborative investigators and follow a prescribed protocol in advising the patient, administering the vaccine, and reporting on its use. The vaccine is made available only for those who are at high risk, such as laboratory personnel who frequently work with the organism. The vaccine is effective in preventing the typhoidal form of tularemia228-231 but will not prevent cutaneous lesions from forming at the site of an inoculation. The vaccine, when administered by scarification, induces humoral and cell-mediated immune responses.288

Avian/Swine Influenza Influenza pandemics have occurred throughout history and remain a threat today. Originally, influenza was not a reportable disease. Until discovery of the virus in 1930, the influenza illness was thought to be due to a bacterium now known as

Haemophilus influenzae.278 The pandemic-causing strains of influenza are the most virulent ones and contain variable combinations of avian, swine, and human strains of influenza. The most memorable pandemic was the “Spanish flu” of 1918, which killed more people in 1 year than did the bubonic plague and is thought to have been an adapted swine strain.275 In 2009, the H1N1 swine flu spread around the globe in a pandemic. Influenza swine viruses have also been implicated in minor outbreaks, the largest in 1976 at a military base in Fort Dix, New Jersey, causing one fatality among 13 soldiers. First reported cases of the novel H1N1 were in Mexico in late March of 2009; soon thereafter, it was found in the United States and Canada. By October 2009, H1N1 influenza was reported in more than 200 countries,185 likely due to air travel. The first confirmed human infections by avian influenza H5N1 virus were reported in Hong Kong in 1998; 6 of 18 patients died.317 No additional cases were reported until February 2003, when one of two people infected with avian influenza died in Hong Kong.197 In December 2003, several Asian countries reported an outbreak of avian influenza in poultry, but as of December 2009, transmission to humans had occurred in only Vietnam, Thailand, and Indonesia.55 Although only 32 cases were laboratory-confirmed, the mortality reached 70%. Given the limited ability to track disease in these countries, the probability is high that the number of cases was underreported.274

VIROLOGY Avian influenza H5N1 and swine influenza H1N1 are subtypes belonging to the family orthomyxoviridae, all of which are singlestranded RNA viruses (Figure 59-26). Other subtypes that are known to have caused pandemics include H3N2 and H2N2. Subtype identifiers refer to the specific surface proteins present on the virus. H refers to the type of hemagglutinin protein, of which there are 16 subtypes known, and N refers to the type of neuraminidase protein, of which there are 9 subtypes known. Hemagglutinin primarily facilitates binding to the target cell, whereas neuraminidase allows for the release of progeny virions from infected cells.274 It is prudent here to discuss antigenic drift and antigenic shift. “Antigenic drift” is when, because of poor proofreading of genetic material, errors in transcription and translation occur that result in variants of the original strain. Over time, this leads to strains sufficiently different to evade humoral immunity and cause illness in persons who were infected with the original strain. This is why people are susceptible to the flu every year and retain only partial immunity. The more concerning “antigenic shift” is what is thought to cause pandemic outbreaks of influenza. Antigenic shift is when two or more different viruses infect a host and

FIGURE 59-26  Avian influenza. Colorized transmission electron micrograph of avian influenza A H5N1 viruses (seen in gold) grown in MDCK cells (seen in green). (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp. Courtesy C. Goldsmith, J. Katz, and S. Zaki, 1997.)

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Tularemia can also be definitively diagnosed by isolation and identification of the organism from blood, skin lesions, and lymph node biopsies or aspirates.308 Samples for culture, however, are not routinely taken in suspect cases, and they are not encouraged because of the high frequency of contamination and infective risk to laboratory workers handling this organism in vitro.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

combine genetic information to create a novel strain to which humans have little immunity. The pig is implicated in aiding in this re-assortment of genetic material, because the pig trachea has receptors for both avian and human strains and can support the growth of both viruses.278 It is believed that this antigenic shift is responsible for severe global outbreaks of influenza. The Spanish flu of 1918 had the same subtype H1N1 as did the 2009 swine flu and caused 20 to 50 million deaths worldwide. The more recent H1N1, a likely descendant of the Spanish flu, was feared during its initial outbreak because it was found to be a quadruple reassortment of two swine strains (one of which appears to be related to the 1918 strain), one human strain and one avian strain of influenza.185,278,279 The protein divergence of the novel H1N1 is about 20% to 24% from the seasonal flu.309

EPIDEMIOLOGY Endemic reservoirs for influenza are swine, migratory aquatic wildfowl, and many mammalian and avian species. The current “swine flu” originated in Mexico and is thought to have led to human-to-human spread months before the outbreak was recognized in early March as a novel strain of influenza. It spread quickly to the United States, and by May 2009 was found in a herd of pigs in Alberta, Canada.309 This spread was thought to be due to a farmer who had traveled to Mexico and on returning home had transmitted the virus to the pigs. As of December 2009, deaths worldwide totaled near 10,000 persons, with the majority in Europe and the Americas. This is likely an underestimate because of decreased reporting from countries in Africa. The majority of those infected and hospitalized were in the 18 to 64 years age range. Most deaths have been from severe res­ piratory failure from pneumonia and acute respiratory distress syndrome.309 The highly pathogenic H5N1 avian influenza has been confined to poultry outbreaks in Asia. Transmission to humans of this subtype has been limited to Hong Kong, Vietnam, Indonesia, Thailand, and eastern Europe. Subtype H7N7 occurred in humans, primarily as conjunctivitis, in the Netherlands (2003) and Canada (2004).102,151 One of the 83 infected patients in The Netherlands died. In an effort to control the outbreak, Japan, the European Union, and the United States have banned poultry imports from infected areas. By December 2009, little more than 400 cases of avian influenza were reported to the WHO with nearly 270 deaths, most occurring in Indonesia. The case mortality rate has averaged more than 60%.55 Thankfully, this avian influenza is not easily transmitted from human to human. The majority requiring hospitalization were those with comorbid illnesses, such as diabetes, immunosuppression, asthma, and chronic obstructive pulmonary disease (COPD).309

TRANSMISSION Most H5N1 infections in humans result from contact with infected birds or their contaminated feces. There are, however, several cases of limited human-to-human transmission reported in the literature, the most recent believed to be in Indonesia in 2006 where 8 family members were affected by the illness and 7 died, only one of whom had been exposed to infected poultry.29,55,151,306 Most cases are in people sharing living facilities with the index case. No spread outside of this range has been seen. Novel H1N1 is more easily able to spread quickly from human to human. Because of the genetic similarity of the strains, the entire pandemic likely started from an isolated case.55

SYMPTOMS AND DIAGNOSIS The incubation period for influenza is 2 to 4 days. Infected persons may shed the virus 1 day prior to symptoms onset and for 5 to 7 days after the symptoms have resolved.309 Symptomatology for all influenza viruses have remained constant, with patients typically presenting with a febrile respiratory illness within days of exposure. Myalgias, arthralgias, cough, sore throat, shortness of breath, wheezing, headache, rhinorrhea, and chills are common complaints. GI manifestations, such as nausea, vomiting, and diarrhea, may also occur and have been found to be more 1162

common in patients with swine flu. The majority of swine infected with influenza exhibit symptoms of the flu similar to those in humans.309 Chest radiographs show infiltrates of varying patterns. Laboratory tests may demonstrate hepatic dysfunction, renal insufficiency, or coagulopathy; leukopenia and lymphopenia are common.274 Laboratory testing can be performed on a nasopharyngeal aspirate or swab, preferably within 3 days of onset of symptoms.197 Diagnostic tests available for influenza include viral culture, serology, rapid antigen testing, polymerase chain reaction (PCR), and immunofluorescence. Sensitivity and specificity of these tests vary by the laboratory that performs the test, type of test used, and type of specimen tested. In suspected cases of avian or swine influenza, it is critical to collect specimens for viral culture. Only culture isolates can provide information regarding the specific influenza subtypes and strains.

TREATMENT AND PREVENTION The novel H1N1 virus is resistant to amantadine and rimantadine. As of the writing of this chapter, 39 isolates of H1N1 had been found that were resistant to oseltamivir. Nearly all the patients with resistance recovered fully from the disease. The cases of resistance were not geographically connected.310 There have been no cases reported to the CDC of resistance to zanamivir; therefore, this is the recommended treatment of choice in patients who are found to be resistant to oseltamivir. The CDC recommends treating people with confirmed or suspected influenza who require hospitalization; have progressive, severe, or complicated illness; and those at risk for severe disease (children younger than age 2 years, adults aged 65 years or older, pregnant women or those less than 2 weeks postpartum, and persons with severe medical conditions). Further information can be found on the CDC website.310 The recommended treatment is oseltamivir; for persons older than age 7 years, zanamivir may be used. Peramivir is an antiviral formulated for IV use, and is still in clinical trials. It is being released from the CDC in life-threatening cases of influenza that are found to be unresponsive to oseltamivir and zanamivir.310 Avian influenza H5N1 is susceptible to oseltamivir and zanamivir in vitro. It is resistant to amantadine and rimantadine.274 The H5N1 virus is killed by heat and disinfectants such as alcohol. However, the influenza virus can survive in feces for months. Persons coming into contact with patients suspected of avian or swine influenza should observe strict hand hygiene, and respiratory and contact precautions (including wearing a particulate respirator, gloves, gown, and goggles).52 Persons visiting countries with endemic H5N1 should take extra care if visiting farmland or having exposure to poultry. Persons living with someone diagnosed with H5N1 should immediately be tested for H5N1 and prophylactically treated.

Cowpox and Monkeypox Infections Poxviruses are large DNA viruses that are implicated in a variety of human diseases, including smallpox, monkeypox, cowpox, and molluscum contagiosum. Historically, immunization against smallpox was performed with an injection of vaccinia virus, which resulted in a local skin lesion. As a result, pox infections are rare, because this immunization provided cross-protection against other poxviruses. Now, however, because smallpox has been eradicated and immunization is no longer recommended, cases of monkeypox, cowpox, and catpox may increase.285 Epidemiologic evidence suggests that cowpox is not enzootic in cattle, that the cow has a minor role, that feline cowpox is important as a source of human infection, and that wildlife, principally rodents, are virus reservoirs.16 Although poxvirus infection in the domestic cat has only recently been described, the incidence has increased steadily, and cats are now the most frequently reported hosts of poxvirus in England.285 The infection occurs mostly among hunting cats in the late summer and early autumn; infection in humans is usually reported after close contact with or a scratch from a sick cat, although transmission from rats has also been reported.301 The infection is manifested

as an inflamed vesicular nodule with lymphadenitis, systemic symptoms (e.g., fever), and a rapid but self-limited course, similar to the orf poxvirus carried by sheep, cattle, and goats. This disease has not yet been reported in immunosuppressed persons. No effective treatment is available, but normally the disease is self-limited. Monkeypox is endemic to central and western Africa, with the first reported case in laboratory monkeys in Copenhagen in 1958.287 In 2003, the first community-acquired outbreak of monkeypox occurred in the central United States. There were no fatalities and the reservoir was believed to have been infected prairie dogs. Initial symptoms include fever, headache, lymphadenopathy, myalgias, and malaise. Within days, a maculopapular rash erupts, usually spreading in a centrifugal pattern and progressing through several stages before crusting over and sloughing (Figure 59-27).83 In the United States, the mode of transmission is believed to have been through respiratory droplets or direct contact.83 Diagnosis is based on serum samples and scrapings from lesions. As with cowpox, there is no known effective treatment and the disease is self-limited.

Hantavirus Pulmonary Syndrome

EPIDEMIOLOGY Approximately 150,000 to 200,000 cases of Hantavirus syndromes occur throughout the world each year, with the majority in China.238 Although most cases of HPS have been clustered in the western United States, particularly the Four Corners area (Arizona, New Mexico, Colorado, and Utah), the virus is present across the entire United States as well as the majority of the Americas.196,210 The CDC had confirmed 465 cases of HPS in 32 states by mid2007. From January through May 2007, 5 cases of HPS were confirmed across the country, with 2 cases in the Four Corners region. Overall, 64% of those infected were male and 37% were female.49 The 1993 outbreak in the Four Corners of the United States was thought to be due in part to the El Niño effect, creating a surge in the infected rat population by increasing the food supply.240 Since 1994, the CDC has sponsored continuous monitoring studies of rodent populations at nine sites in Arizona, Colorado, and New Mexico. Spikes in the host population correlate with HPS outbreaks among humans. Hantavirus antibody prevalence in deer mouse populations surveyed since 1994 shows about a 10% baseline prevalence, increasing up to 40% prevalence during rodent population peaks. During the 1993 outbreak, a prevalence of 30% was detected.58 In 2004, the Pan American health organization reported only 95 cases, the majority of those being from the United States and Argentina.49 Many outbreaks have occurred among persons of lower socioeconomic status, thought to be due to the poor living facilities that may favor increased encounters with rodents.

There are reports dating back to the Middle Ages from China and England that describe clinical entities similar to what we now know as Hantavirus. During the Korean conflict in 1951, nearly 3000 United Nations and American soldiers were afflicted by an acute febrile illness with renal failure and shock, with a mortality rate nearing 7%.157 This illness became known as Korean hemorrhagic fever.156,157 In 1978, Lee identified the causative agent, naming it Hantavirus because most cases in the troops developed near a small river called Hantann.157 Until 1993, hemorrhagic infections associated with Hantavirus strains were thought to be limited to Asia and Eastern Europe, and they largely lacked respiratory symptoms. In 1993, an outbreak of severe respiratory illness with high mortality occurred in the southwestern United States. This outbreak was subsequently investigated and described as the Hantavirus pulmonary syndrome (HPS), caused by a novel Hantavirus.87

VIROLOGY Hantaviruses in the Bunyaviridae family are trisegmented RNA viruses with a lipid envelope.240 They cause the hemorrhagic fever with renal disease syndrome (HFRS), as well as Hantavirus cardiopulmonary syndrome (HPS). The genus Hantavirus is composed of two main groups: Old World and New World. Infection with Old World Hantaviruses carries a mortality rate of 1% to 15%, whereas the New World strains carry fatality rates near 50%.191 With the New World Hantaviruses (predominately in the Americas), 30% to 40% of persons infected get the mild form of

FIGURE 59-28  The deer mouse, Peromyscus maniculatus, a Hantavirus carrier that becomes a threat when it enters human habitation in rural and suburban areas. All Hantaviruses known to cause Hantavirus pulmonary syndrome (HPS) are carried by New World rats and mice of the family Muridae, subfamily Sigmodontinae. This subfamily contains at least 430 species, which are widespread in North and South America. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/quicksearch.asp. Courtesy James Gathany.)

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FIGURE 59-27  Monkeypox lesions on the arm and leg of a 4-year-old child in Bondua, Grand Gedeh County, Liberia. This infection was caused by a pox virus of the vaccinia, variola, monkeypox type. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/quicksearch.asp.)

disease and 20% to 30% of those infected get the moderate to severe form of disease. Humans are not part of the natural host range of Hantaviruses. Human infection occurs accidently in those exposed to the virus via inhalation, or by contact with urine, feces, or saliva of infected rodents.191 One exception is the Hantavirus strain “Sout” in Argentina, which has been reported to have sporadic human-to-human transmission.177 The Sin Nombre virus, also known as the Four Corners virus, is the primary Hantavirus causing HPS in the United States, with the deer mouse (Peromyscus maniculatus) as the predominant carrier (Figure 59-28).49 Other small mammals, such as piñon mice, brush mice, and western chipmunks, may also be infected. Wild rodents are also the vectors of Hantaan, Puumala, Prospect Hill, and Seoul viruses, all members of the Hantavirus family. Hantaviruses have been isolated from the lung tissues of bats.146

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TRANSMISSION Hantaviruses appear to have co-evolved with the rodent reservoir host species over many thousands of years, likely leading to the lack of illness in the hosts.238 The host animals shed virus in saliva, urine, and feces for weeks. The greatest shedding of the virus takes place 3 to 8 weeks after infection.49 Human infection probably occurs when infective saliva or excreta are inhaled as aerosols, or when excreta are directly inoculated through the skin or perhaps ingested. Humans have also been infected with Hantavirus via rodent bites. Human-to-human transmission of the Sin Nombre virus in the United States does not appear to occur; however, there has been human-to-human transmission of Hantavirus strains in Chile and Argentina. For this reason, it is considered a potential bioterrorism agent by the CDC.49,177

SYMPTOMS Hantavirus renal syndrome (hemorrhagic fever with renal syndrome, HFRS) consists of five stages that may overlap: febrile, hypotensive, oliguric, diuretic, and convalescent. The onset is sudden, with intense headache, petechial rash, fever, and chills. Around day 4 of disease, hypotension and acute renal failure develop. The mortality of this syndrome is 1% to 40% (depending on the strain), and recovery may take months.238 Hantavirus pulmonary syndrome (HPS) begins with an incubation period of 2 to 18 days, followed by prodrome of fever, myalgia, and variable respiratory symptoms that may include cough and shortness of breath with minimal bronchospasm. Acute respiratory distress rapidly follows, with acute noncardiac pulmonary edema and hypotension within 2 to 15 days.191 Other early-phase symptoms include headache, chills, abdominal pain, nausea, and vomiting. Patients often demonstrate hemoconcentration, thrombocytopenia, leukocytosis, hypoalbuminemia, and lactic acidosis. Rapid deterioration occurs, coincident with marked bilateral pulmonary infiltrates identified on chest radiographic examination (Figure 59-29). One percent of patients experience severe neurologic manifestations, including seizures.191 Fever, hypoxia, and hypotension may culminate in death; survivors usually recover within 5 to 7 days and have few or no sequelae. Autopsies have demonstrated intense pulmonary infiltration, with marked accumulations of Hantavirus antigens in endothelial cells.

DIAGNOSIS The causative agent has been identified by serologic tests, PCR to RNA, and immunohistochemistry (Figure 59-30).48,155 Laboratory evidence of acute Hantavirus infection can be obtained by any of the following tests: IgM antibodies to Hantavirus antigens, fourfold or greater increase in antibody titers to Hantavirus antigens in paired serum specimens, positive immunohistochemical stain for Hantavirus antigen in formalin-fixed tissues (Figure

FIGURE 59-29  Hantavirus pulmonary syndrome (HPS) as shown on chest radiograph. (From http://www.bt.cdc.gov/agent/plague/ trainingmodule/3/12hantavirus.htm.)

59-31), or positive PCR from frozen tissue specimens (usually lungs). ELISA testing for Hantavirus was developed by the CDC and is available only in state health departments.186 Typical clinical laboratory findings include hemoconcentration, neutrophilic leukocytosis, thrombocytopenia and circulating immunoblasts. Any person with a severe and sudden respiratory illness should be suspected to have Hantavirus. CDC screening criteria include febrile illness with temperature higher than 38.3° C (101° F) in a previously healthy person characterized by unexplained adult respiratory distress syndrome or bilateral interstitial pulmonary infiltrates developing within 72 hours of hospitalization, with respiratory compromise requiring supplemental oxygen.49

TREATMENT Treatment is supportive, as no cure has been developed. Previously isolated Old World Hantaviruses have demonstrated in vitro sensitivity to ribavirin, although there has been no demonstrated benefit of ribavarin for the New World strains.67 The CDC has stated that the drug is of no use with HPS and is not available for use under any existing research protocol as of 2004. Intensive care unit management of symptoms is recommended with pressors, avoidance of fluid overload, and possible use of ECMO in the most severe cases. There are studies looking into the use of neutralizing antibodies, as it was noted that patients with the more severe form of the disease had significantly lower antibody titers than did those with less severe forms of the disease.186

PREVENTION According to the CDC, Hantavirus transmission to humans may be epidemiologically associated with planting or harvesting field FIGURE 59-30  Electron micrographs of the Hantavirus virions responsible for causing Hantavirus pulmonary syndrome, or HPS. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp.)

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VIROLOGY Hendra virus is a paramyxovirus that shares 70% to 78% of its nucleotide sequencing with the closely related Nipah virus.61,165,217 Formerly called equine Morbillivirus, Hendra virus was further sequenced and classified as a paramyxovirus after the 1994 outbreak in Australia.119

EPIDEMIOLOGY AND TRANSMISSION FIGURE 59-31  Micrograph depicting an atypical, enlarged lymphocyte found in the blood smear from a patient with Hantavirus pulmonary syndrome (HPS). The laboratory finding of this lymphocyte, combined with a bandemia and dropping platelet count, is characteristic of HPS. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp.)

Outbreaks of Hendra virus have occurred in Australia among horses and humans in close contact. The natural reservoir for Hendra virus is thought to be the fruit bat (Pteropus species), but the mode of transmission to horses is unknown.316 Although the virus is found in a large portion of the fruit bat population, human bat handlers have had no reported cases of the virus.248 The documented human cases of Hendra virus are thought to be acquired through close contact with infected horses.

crops, occupying previously vacant dwellings, disturbing rodentinfested areas while hiking or camping, inhabiting dwellings with indoor rodent populations, or residing in an area with an increasing rodent density. Most persons with HPS who had high-risk exposures are thought to have been infected in and around their homes. Limiting opportunities for domestic exposure is important. Measures to prevent HPS can be divided into four areas (Box 59-1).

SYMPTOMS

Hendra Virus

Definitive diagnosis can be accomplished by viral culture or by ELISA of the CSF and serum samples.

Hendra virus was first described after a September 1994 outbreak of a severe respiratory illness among a group of horses and humans in Queensland, Australia. Of 21 affected horses, 14 died of respiratory failure, and of the two humans affected—a trainer BOX 59-1  Centers for Disease Control and Prevention

Recommendations for Preventing Hantavirus Pulmonary Syndrome

1. Eliminate rodent harborage. a. Keep cooking, eating, and food storage areas clean. b. Cover human food and animal feed. c. Contain and elevate garbage. d. Seal holes and cracks in dwellings to prevent entrance by rodents. e. Clear brush and trash from around homes and outbuildings. 2. Control rodent populations by maintaining snap traps and using rodenticides; in areas where plague occurs, control fleas with insecticides. 3. Safely clean up rodent-infested areas. a. Air out infested spaces before cleanup. b. Spray areas of infestation and all excreta, nesting, and other materials with household disinfectant or 10% bleach solution. Then, clean up, seal in bags, and dispose. c. Avoid sweeping, vacuuming, or stirring dust until the area is thoroughly wet with disinfectant. d. Wear rubber gloves; disinfect gloves before removal, and wash hands afterward. e. In areas where plague occurs, spray insecticide on trapped rodents and nesting materials to prevent fleas from abandoning rodents to find new hosts. 4. Avoid rodents when outdoors. a. Do not disturb rodent droppings or camp or sleep near burrows or areas where trash is present. b. Avoid feeding or handling rodents, even if they appear friendly.

The equine form of Hendra virus manifests as a severe respiratory infection. In humans, clinical symptoms include severe respiratory symptoms as well as meningoencephalitis. Few cases have been described.

DIAGNOSIS

TREATMENT Supportive measures are the mainstay of treatment of Hendra virus infection.

PREVENTION AND CONTROL Early identification of equine cases and quarantine of affected animals is the key to preventing human cases.

Nipah Virus The Nipah virus is a chilling example of emerging zoonotic infections; a highly contagious swine-associated virus with a human mortality rate of 75%.75 The original outbreak of Nipah virus in humans occurred in September 1998 in northern Malaysia and spread to farms south of this original epicenter and into Singapore by June 1999. It is believed that spread within Malaysia resulted from sale of infected pigs.189 In Malaysia, there were 265 reported cases with 105 deaths, and in Singapore there were 11 reported cases with 1 death. The outbreak was contained in Singapore once importation of pigs from Malaysia ceased; in Malaysia, more than 1 million pigs from the outbreak area were destroyed before the illness disappeared.153 The virus derives its name from Kampung Sungai Nipah, the village whose patients supplied the first viral isolates.302 In 2004, an outbreak of 36 patients with Nipah virus occurred in Bangladesh.122 This outbreak was notable for person-to-person transmission and 75% mortality rate.

VIROLOGY The Nipah virus is a paramyxovirus closely related to Hendra virus, a paramyxovirus that caused an outbreak of respiratory disease in horses in Australia.313 Hendra and Nipah viruses are classified under the genus henipavirus.290 Nipah is a single-stranded RNA virus encapsidated into a helical core surrounded by a lipid membrane containing two distinct viral glycoproteins.313 1165

CHAPTER 59  Wilderness-Acquired Zoonoses

and a stable hand—one died of severe interstitial pneumonia.192 In a second and unrelated outbreak 13 months later, a farmer died of severe meningoencephalitis after contact with a horse infected with Hendra virus.202

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TRANSMISSION Nipah virus is transmitted to humans by contact with infected pigs or fresh pig products. In the past, there had been isolated suggestions of animals-to-human transmission or human-tohuman transmission, but this was not confirmed by epidemiologic studies until the 2004 outbreak in Bangladesh that was rapidly spread by human-to-human transmission.63,271,272 There is evidence that fruit bats of the species Pteropus hypomelanus may serve as a host reservoir for Nipah virus, as they do for Hendra virus. Nipah virus has been isolated from the urine of P. hypomelanus on Tioman Island, which is just off the Malaysian coast, and neutralizing antibodies have been detected in two species of fruit bats (P. hypomelanus, P. vampyrus).62,314 If fruit bats serve as the reservoir, it is unclear how transmission then occurs to pigs.

SYMPTOMS Nipah virus infection is characterized by encephalitic symptoms. Onset of symptoms occurs within 2 weeks, and patients present with a wide range of symptoms, ranging from nonspecific fever and headache to rapidly progressive encephalitis.115,158 The largest population with Nipah virus that has been studied was 94 patients in 1999 at the University of Malaya Medical Center in Kuala Lumpur, Malaysia.115 More than one-half of patients had decreased level of consciousness (Glasgow Coma Scale [GCS] score <15) at presentation and signs of brainstem dysfunction, including abnormal doll’s-eye reflex, segmental myoclonus, vasomotor instability, and/or pinpoint pupils. Few cases presented with both neurologic and respiratory symptoms or abnormal chest X-ray. The fatality rate in patients with febrile encephalitis was 32%.

DIAGNOSIS AND TREATMENT Nonspecific laboratory findings include thrombocytopenia, leukopenia, transaminitis, and CSF with either elevated WBC count or elevated protein level, similar to other viral encephalitides.115 Definitive diagnosis can be accomplished by viral culture or by ELISA of CSF and serum samples.302 There is no established treatment other than supportive measures. Survivors of Nipah virus encephalitis commonly have neurologic abnormalities.247

Cysticercosis (Taeniasis) The encysted larvae, or cysticerci, of the tapeworm Taenia solium in the flesh of pigs, known as “measly pork,” were well known to the ancient Greeks. These cysticerci are referred to by Aristotle (384-322 BC), who, in the section on diseases of pigs in his History of Animals, gives an account of “bladders that are like hailstones.”198 These tapeworms have been described throughout the centuries and across the globe.

PARASITOLOGY AND TRANSMISSION Taenia is a genus of cestodes, or tapeworms, belonging to the family Taeniidae.193 The two species causing infection in humans are Taenia solium, the pork tapeworm, and Taenia saginata, the beef tapeworm. Both cause an intestinal form of tapeworm infection. T. solium alone produces the more significant clinical syndrome of cysticercosis, involving neural and other tissues in the human body. Taenia solium The life cycle of T. solium involves pigs and humans (Figure 59-32). Humans are infected by ingesting insufficiently cooked pork containing larval tapeworms, or cysticerci. Ingested cysticerci attach to the small intestine with four muscular suckers and a crown of hooklets. Over the next few days, these worms produce proglottids, or segments, which elongate to form a mature tapeworm that can be several meters in length. These proglottids are gravid and release embryonated eggs. Gravid proglottids or eggs are released in human feces into the environment, where they contaminate water or vegetation and then are ingested by pigs. Once ingested, the eggs become 1166

a six-hooked larval form called an oncosphere, which penetrates the intestinal wall of the pig and migrates via the lymphatic or venous system into tissues to complete the cycle and become a cysticercus. Human cysticercosis develops when humans ingest the embryonated eggs or gravid proglottids that normally infect pigs. The infection is also initiated when humans ingest vegetation or water contaminated with human feces containing T. solium eggs, which may be the most common mode of transmission. It is hypothesized that carriers of T. solium tapeworms can ingest eggs via reverse peristalsis and autoinfection, but this has not been proven. Once ingested, these eggs release oncospheres, which, as in the pig, invade the intestinal mucosa and migrate hematogenously into tissues. Once in the tissues, most commonly brain and muscle, the larval form develops into a cysticercus over 3 to 4 months. These cysticerci may remain viable for several years. Taenia saginata The life cycle of T. saginata involves humans and cattle. Humans ingest larval tapeworms, or cysticerci, from insufficiently cooked beef. Ingested cysticerci attach to the small intestine with four muscular suckers and a crown of hooklets. These worms then produce proglottids, or segments, elongating to form a mature tapeworm that can parasitize the small intestine of a human for as long as 25 years and grow up to 10 m in length (Figure 59-33). The proglottids release eggs, which are released via human feces into the environment. These eggs are ingested by cattle, where they form oncospheres, penetrate the intestinal wall, and migrate to other tissues to form a cysticercus and complete the cycle.

EPIDEMIOLOGY T. solium infection is directly associated with eating undercooked pork. It is prevalent in Africa, India, Southeast Asia, China, Mexico, Central America, and South America. It is seen infrequently in the Middle East. It is important to note that cysticercosis also results from ingestion of water or vegetation contaminated by human feces containing T. solium eggs; therefore, human cysticercosis can occur in populations where pork is not consumed and people are not in close contact with pigs.236 Cysticercosis is estimated to affect 50 million people worldwide, although this may be an underestimate, as many cases are undiagnosed.235 Prevalence is higher in rural areas and areas where pigs are raised; seroprevalence in endemic regions in South America is as high as 25%.110 In the United States, many cases of cysticercosis are seen in immigrants from endemic areas. In one study, 10% of patients in Los Angeles presenting to emergency departments with a seizure had a diagnosis of neurocysticercosis; in New Mexico, it was 6% of patients.201 People can be infected when traveling to endemic areas and by ingesting produce or water contaminated with T. solium eggs. T. saginata occurs worldwide. Its life cycle is perpetuated by humans and cattle.

SYMPTOMS The presentations of intestinal infections caused by T. solium and T. saginata are similar, with mild abdominal discomfort, chronic indigestion, hunger pains, and/or diarrhea. Many patients are asymptomatic and present only after discovering a length of the tapeworm in their feces. The symptoms of cysticercosis are related to the tissues involved. The syndrome is usually classified as either neurocysticercosis or extraneural cysticercosis. Neurocysticercosis, the more common form, is further divided into parenchymal and extraparenchymal neurocysticercosis.35 The more common form of neurocysticercosis is parenchymal. Cysticerci in the brain often locate to the cortex or basal ganglia, and patients most often present with either focal or generalized seizures. Cysts are typically less than 1 cm in diameter. In endemic areas, neurocysticercosis is the most common cause of epilepsy, and the prevalence of epilepsy is higher than in nonendemic areas.108 Other symptoms of parenchymal neurocysticercosis include headaches, nausea, and vomiting and psychiatric

i

Oncospheres hatch, 3 penetrate intestinal wall, and circulate to musculature in pigs or humans

CHAPTER 59  Wilderness-Acquired Zoonoses

Cysticercosis (Taenia spp.)

Cysticercosis Cysticerci may develop in any organ, being more common in subcutaneous tissues as well as in the brain and eyes.

Oncospheres develop into cysticerci in muscles of pigs or humans

Humans acquire the infection by ingesting 4 raw or undercooked meat from infected animal host.

2 Embryonated eggs and/or gravid proglottids ingested by pigs or humans

5 Scolex attaches to intestine

i

d 6

Adults in small intestine

1 i = Infective stage d = Diagnostic stage

Eggs or gravid proglottids in feces and passed into environment

FIGURE 59-32  Cysticercosis is an infection of both humans and pigs with the larval stages of the parasitic cestode, Taenia solium. This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier (1). Pigs and humans become infected by ingesting eggs or gravid proglottids (2). Humans are infected either by ingestion of food contaminated with feces, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine (3), invade the intestinal wall, and migrate to striated muscles, as well as to brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequelae if they localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci (4). Cysts evaginate and attach to the small intestine by their scolices (5). Adult tapeworms develop (2 to 7 m [7 to 23 feet] in length); produce less than 1000 proglottids, each with approximately 50,000 eggs; and reside in the small intestine for years (6). (From http://www.dpd.cdc.gov/dpdx/HTML/Cysticercosis.htm.)

FIGURE 59-33  Adult Taenia saginata tapeworm. Humans become infected by ingesting raw or undercooked infected meat. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years, attaching to and residing in the small intestine. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/home.asp.)

presentations. Over time, parenchymal cysticerci calcify as they degenerate and may serve as foci for the seizures. One complication of parenchymal neurocysticercosis is cysticercal encephalitis, which is caused by an intense immune reaction resulting from a massive number of cysts in the brain parenchyma. This reaction can be spontaneous, or it may be provoked by medical therapy that causes degeneration of a large number of cysts simultaneously. Patients present with fever, headache, vomiting, impaired visual acuity, altered mental status, and even seizures. For unknown reasons, this is more common in children and in young women. Extraparenchymal neurocysticercosis includes subarachnoid cysts, racemose cysticercosis, ventricular cysticercosis, and spinal cysticercosis. Patients with subarachnoid cysts may present with cranial nerve palsies and hydrocephalus because of mass effect and inflammation associated with large cysticerci at the base of the brain. Racemose cysticercosis is an infrequent but serious form of extraparenchymal neurocysticercosis. It is characterized by proliferating lobulated cysts resembling a cluster of grapes that are typically lodged in the ventricular system. The presentation consists of arachnoiditis, basilar meningitis, and hydrocephalus, and is associated with a poor prognosis. 1167

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A more common form of extraparenchymal neurocysticercosis involves the presence of ventricular cysts, free-floating or attached to the choroid plexus. These cysts cause inflammation in the ventricles, and patients present with obstructive hydrocephalus and elevated intracranial pressure. Symptoms include focal neurologic symptoms, seizures, and/or dementia. An atypical presentation of a ventricular cyst is Bruns syndrome, which presents with episodes of sudden loss of consciousness associated with head movements; these episodes are caused by intermittent obstruction from mobile cysts in the fourth ventricle.224 Spinal cysticercosis, in which cysticerci are located in the subarachnoid space or intramedullary region, is less common. These cysts can lead to inflammation and demyelination. Patients present with radicular pain or paresthesias in the affected area. Thoracic lesions are most common. Extraneural cysticercosis may involve muscles, the eye, and subcutaneous tissues. Ocular cysticercosis, which occurs in 1% to 3% of all cases of cysticercosis, can involve the anterior chamber, subretinal space, or vitreous humor.111 These cysticerci can cause inflammation when they degenerate, so a thorough ophthalmologic examination should be performed in patients with cysticercosis prior to starting treatment. Other sites of extraneural cysticercosis include muscles and subcutaneous tissues. Cysticerci in these locations are often asymptomatic but may be seen incidentally as nodules or calcifications on radiographs. Rare cases of cysticerci in cardiac muscle have been reported, with resulting conduction disturbances and cardiomyopathy.24

DIAGNOSIS Stool samples from humans harboring Taenia tapeworms may reveal proglottids and eggs. Eggs are spherical, 30 to 40 µm in diameter, and have a thick radially striated shell. T. solium and T. saginata eggs are identical. Proglottids of T. solium, however, are smaller than those of T. saginata. Diagnostic testing for cysticercosis depends on the clinical presentation. Routine blood counts and hepatic panels are normal in typical patients with cysticercosis. The most sensitive serologic test is an enzyme-linked immunoelectrotransfer blot (EITB) assay, with a sensitivity of 98% and a specificity of 100% for patients with active cysticercosis.112,277 Other serologic tests, including ELISA, CF, radioimmunoassay, and other immunoblots, have been used but are less sensitive and specific. The sensitivity of all tests is lower in patients with inactive cysticercosis or only isolated lesions. The EITB is more sensitive in serum than in CSF.299 As with any antibody test, a positive test does not indicate active infection. A lumbar puncture can be useful in the diagnosis of cysticercosis, although it is not necessary. CSF findings include normal glucose, normal to mildly elevated protein and white blood cell counts, and occasional eosinophilia. Serologic tests can be done on CSF, but they are not as sensitive as are serum serologies. Imaging modalities are useful in diagnosing cysticercosis. Plain films may demonstrate calcified cysticercal lesions (Figure 59-34). CT and magnetic resonance imaging (MRI) are most useful in diagnosing neurocysticercosis. CT findings include nonenhancing hypodense lesions of viable cysts and calcified lesions of old cysts. Degenerating lesions may have some surrounding inflammatory edema. CT may also demonstrate extraparenchymal cysts in the ventricles or subarachnoid space and may demonstrate the resultant hydrocephalus. CT is preferred over MRI for serial examinations to follow progress. MRI is more sensitive than CT in detecting small lesions and extraparenchymal lesions. MRI is also better at characterizing the scolex and evaluating degenerative changes in the parasite. For spinal cord lesions, MRI is the preferred imaging modality. Diagnosis of cysticercosis can also be made on pathology, either by brain biopsy (rarely), or by biopsy of muscle or subcutaneous nodule. Cysticerci are 5 to 10 mm (0.2 to 0.4 inch) in diameter and look like a fluid-filled bladder containing a small larval scolex (Figure 59-35). 1168

FIGURE 59-34  This x-ray reveals cysticercosis of the muscle due to the presence of the cestode Taenia saginata, or beef tapeworm. Humans are the only definitive hosts for Taenia saginata and Taenia solium. Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the environment. (From Centers for Disease Control and Prevention Public Health Image Library. http:// phil.cdc.gov/Phil/home.asp.)

TREATMENT For intestinal involvement of either T. solium or T. saginata, the treatment of choice is praziquantel. For neurocysticercosis, treatment depends on presentation, and consensus guidelines have been developed.109 Treatment options include anticonvulsant therapy, antihelminth therapy with albendazole or praziquantel along with corticosteroids, or surgery. Anticonvulsant therapy is indicated and extremely important for patients who present with seizures and neurocysticercosis. Drugs of choice include phenytoin or carbamazepine. Length of therapy depends on recurrence of seizures. Antihelminth therapy is not always indicated in neurocysticercosis, and data showing any added benefit over symptomatic management alone are conflicting.257 Calcified asymptomatic cysts do not require antihelminth therapy. When it is administered, drugs of choice include albendazole, 15 mg/kg/day for 8

FIGURE 59-35  Cysticercosis in muscle section. Note sucker (arrow) of bladderworm. The fluid-filled cyst contains an inverted scolex.  The worm larva is inverted and as such, the rugose tegument is on  the inside of the bladder. The rugose tegument will become the  adult worm’s body surface. (Courtesy Department of Patho­logy, University of Texas Southwestern Medical Center. http:// pathcuric1.swmed.edu/MicroBiology/LabRef/Parasites/Platyhelminth/ SlideC4.html.)

Echinococcosis (hydatidosis, or hydatid disease) is a parasitic disease found wherever sheep are herded and dogs are in close contact with humans. Sheep were first domesticated in the Neolithic era, and large herds of sheep were present during the Mesolithic era around the Caspian Sea during 5000 to 6000 BC.199 Because dogs have long lived in close quarters with humans, feeding off scraps and offal from livestock and transmitting infection through close contact, echinococcosis is a disease that has very likely been present in human populations since the beginning of humanity. Hydatid disease was well known in ancient times, and there are references to cysts in slaughtered animals in the Babylonian Talmud, by Hippocrates in the 4th century BC, by Arataeus in the 1st century AD, and by Galen in the 2nd century AD.101 Echinococcosis is one of the most broadly spread parasitic zoonoses, with cases occurring in nearly all countries and climates around the world.86

PARASITOLOGY AND TRANSMISSION Echinococcus is a genus of cestodes, or tapeworms, belonging to the family Taeniidae.130 Human echinococcosis is caused by infection with the larval stages of Echinococcus. Several species of Echinococcus are known to cause disease in humans. Echinococcus granulosus causes cystic echinococcosis, the most common form of the disease in humans. Echinococcus multilocularis causes alveolar echinococcosis, accounting for 5% of hepatic hydatid disease. Echinococcus vogeli and Echinococcus oligarthrus very rarely cause echinococcosis in humans. The life cycle of Echinococcus involves a definitive (e.g., a dog) and an intermediate (e.g., a sheep) host. Humans become infected as accidental hosts in this life cycle (Figure 59-36).85 In

PREVENTION AND CONTROL Prevention of infection with T. solium and T. saginata involves good hand washing and hygiene to avoid fecal–oral infection. Prevention of primary infection with T. solium requires cooking pork until the interior of the meat is not pink, or else freezing it to −20° C (−4.0° F) for at least 12 hours. Carriers of T. solium pose a public health risk and need to be identified and properly treated. Every effort must be made to avoid contact between human feces and the vegetation and water near pigs or livestock. 6

1

Scolex attaches to intestine

4 Adult in small intestine

5

2

Protoscolex from cyst

Ingestion of cysts (in organs)

i

Definitive host (dogs and other canidae)

Intermediate host (sheep, goats, swine, etc.)

2

4 4

Ingestion of eggs (in feces)

Embryonated 4 egg in feces 4 4

d

4 3

Hydatid cyst in liver, lungs, etc.

Oncosphere hatches; penetrates intestinal wall

3

i

= Infective stage

d

= Diagnostic stage

FIGURE 59-36  The adult Echinococcus granulosus (3 to 6 mm long) (1) resides in the small intestine of the definitive host (dogs or other canids). Gravid proglottids release eggs (2) that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small intestine and releases an oncosphere (3) that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst (4) that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices (5) evaginate, attach to the intestinal mucosa (6), and develop into adult stages (1) in 32 to 80 days. The same life cycle occurs with Echinococcus multilocularis (1.2 to 3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate hosts are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. For Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs, the intermediate hosts are rodents, and the larval stage (in the liver, lungs, and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs (2), with resulting release of oncospheres in the intestine and development of cysts (4) in various organs. (From http://www.dpd.cdc.gov/dpdx/HTML/ Echinococcosis.htm.)

1169

CHAPTER 59  Wilderness-Acquired Zoonoses

Echinococcosis

days, or praziquantel, 75 to 100 mg/kg given in three divided doses 2 hours apart. Praziquantel shows reduced serum levels in the presence of phenytoin, phenobarbital, or corticosteroids because of cytochrome P-450 induction, so albendazole has a more favorable profile in a patient on anticonvulsants or steroids. Steroids are administered along with antihelminth therapy to decrease adverse effects of an inflammatory response from degenerating cysts resulting from therapy. Drugs of choice include either prednisolone, 1 mg/kg/day, or dexamethasone, 0.1 mg/kg/day starting 2 days prior to treatment and continuing for 4 to 6 days after therapy is completed. Additionally, for intraventricular cysts alone, steroids alone are indicated to decrease the inflammatory response and chance of obstruction. Surgery may be required in the case of obstructive neurocysticercosis. Patients with obstructive hydrocephalus require ventriculoperitoneal shunting. Rarely, patients with intraventricular or subarachnoid cysts may require surgical excision. Extraneural cysticercosis does not require treatment if it is asymptomatic. Patients with extraneural cysticercosis should be evaluated for neurocysticercosis.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

America. E. multilocularis has a number of definitive hosts, including foxes, wolves, dogs, coyotes, and cats. Intermediate hosts are rodents, including voles, muskrats, and housemice. Echinococcus vogeli and Echinococcus oligarthrus E. vogeli and E. oligarthrus occur in Central and South America. The definitive hosts of E. vogeli are wild canids, and the intermediate hosts are rodents. The definitive hosts of E. oligarthrus are wild felids, and the intermediate hosts are rodents.

SYMPTOMS

FIGURE 59-37  Gross pathology of membrane and hydatid daughter cysts from human lung. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/ quicksearch.asp.)

the definitive host, the adult tapeworm inhabits the small intestine. These adult worms differ by species. E. granulosus worms are 2 to 7 mm long and consist of a scolex with hooks and suckers as well as at least three proglottids. E. multilocularis worms are up to 4 mm long with two to six proglottids. Proglottids are segments consisting of both male and female sexual organs that produce eggs, which contain oncospheres. These eggs are 30 to 40 µm in size. The definitive host may harbor thousands of worms, each of which can produce thousands of eggs from the proglottids each day. These eggs are expelled in the feces of the definitive host. Intermediate hosts, and incidentally humans, are infected by ingesting these eggs from the environment. The eggs hatch within the intermediate host and release oncospheres, which then penetrate the intestinal mucosa, enter the blood and lymphatic systems, and migrate to visceral organs. After reaching these organs, most commonly the liver, the oncospheres develop into fluid-filled cysts, which then develop into the metacestode or hydatid cyst. Adult forms, or protoscolices, eventually develop within these hydatid cysts. The adult protoscolices develop into secondary daughter cysts within the intermediate host (Figure 59-37). If infected organs from the intermediate host are ingested by the definitive host, the protoscolices develop into mature worms within the definitive host’s small intestine over a period of 4 to 7 weeks to complete the life cycle. A definitive host is required for development of mature worms and thus the release of infectious eggs into the environment. Adult tapeworms do not develop in the intestines of humans or intermediate hosts; therefore, direct transmission of echinococcosis from human to human does not occur.193

EPIDEMIOLOGY The epidemiology of Echinococcus differs by species: Echinococcus granulosus E. granulosus occurs nearly worldwide, and more frequently in rural, grazing areas where dogs ingest organs from infected animals. Human cystic hydatidosis is a significant public health problem in South and Central America, the Middle East, some sub-Saharan countries, China, and the former Soviet Union. Infection rates are highest in endemic rural areas, with prevalence rates of 2% to 6%.233 The definitive hosts for E. granulosus are dogs and other canids. The intermediate hosts are sheep, although other livestock can occasionally act as intermediate hosts. Human infection results from ingestion of eggs from the environment. These eggs may be ingested via contaminated water or vegetables, or from direct contact with infected dogs through fecal–oral contact, which occurs more commonly in children. Echinococcus multilocularis E. multilocularis occurs in the northern hemisphere, including central Europe and the northern parts of Europe, Asia, and North 1170

Echinococcus granulosus (Cystic Hydatidosis) E. granulosus in humans develops as a unilocular hydatid cyst. This cyst is a slow-growing, space-occupying cystic lesion enclosed by a laminated germinative membrane that produces protoscolices, or tapeworm heads (Figure 59-38). The cyst grows as it slowly accumulates fluid. Spillage of this fluid can result in severe reactions, including anaphylaxis and death, and it can also lead to dissemination of infection from the release of protoscolices.193 Because of the slow growth of the cysts, infections remain silent for many years before causing symptoms. Symptoms depend on the organs involved. The liver is most commonly affected, seen in two-thirds of patients. The lungs are involved in approximately 25% of patients, whereas other organs, including brain, bone, heart, muscle, and kidneys, are rarely involved. Single-organ involvement is found in 85% to 90% of patients, and more than two-thirds of patients have only a single cyst. Hepatic involvement, the most common form of echinococcosis, can involve abdominal pain, an abdominal mass, or biliary ductal obstruction. Mass effect on the portal veins, hepatic veins, and inferior vena cava can result in portal hypertension, venous obstruction, or the Budd–Chiari syndrome. Pulmonary involvement can manifest with cough, dyspnea, chest pain, and hemoptysis. Seizures or elevated intracranial pressure can indicate brain involvement. Bony cysts may present as pathologic fractures; the spine, pelvis, and long bones are most commonly involved. Spontaneous or traumatic rupture of cysts releases toxic fluid into involved areas and can produce fever, urticaria, eosinophilia, and anaphylactic shock. Echinococcus multilocularis (Alveolar Hydatidosis) E. multilocularis infection follows a more aggressive course than does E. granulosus infection. E. multilocularis forms cysts composed of a thin laminar layer without a limiting membrane or germinal layer. These cysts behave like a slowly growing, destructive, polycystic tumor. The lesions are made up of multiple irregular cysts, often with mixed solid and cystic components. This polycystic mass invades and destroys adjacent tissues and can metastasize to distant sites in the body. The primary infection in alveolar hydatidosis is hepatic in nearly all cases, but spread to other organs such as the lungs and brain occurs frequently by direct extension or hematogenous or lymphatic dissemination. Manifesting symptoms include right

FIGURE 59-38  “Hydatid sand.” Fluid aspirated from a hydatid cyst shows multiple protoscolices (approximately 100 µm), each of which has typical hooklets. The protoscolices are normally invaginated (left), and they evaginate (middle, then right) when put in saline. (Image contributed by Georgia Division of Public Health.)

Echinococcus vogeli and Echinococcus oligarthrus E. vogeli and E. oligarthrus cause polycystic hydatid disease affecting the liver and occasionally the lungs. Both are rare causes of hydatid disease in humans.

DIAGNOSIS The diagnosis of echinococcosis relies mainly on findings by ultrasonography or other imaging techniques supported by positive serologic tests. Serology testing should be used prior to invasive methods of diagnosing echinococcosis. In patients with negative serology but suspicious lesions on imaging, fine-needle biopsy via ultrasonographic guidance can be useful for confirmation of the diagnosis. However, precautions must be taken with this procedure to avoid leakage of toxic cystic fluid and to control any allergic reaction that results from this leakage. False-negative serology results occur when the location, integrity, or vitality of the cyst is such that the patient has not mounted an antibody response to the cyst. Intact cysts result in the lowest rate of antibody response. Cysts in bone and the liver are more likely to elicit antibody response than those in the lungs or brain. Patients with calcified or dead cysts are generally seronegative. False-positive serology results may occur in patients with other tapeworm infections, cancer, and chronic immune disorders. Echinococcus granulosus Routine serum tests, such as complete blood count and hepatic panels, may demonstrate mild abnormalities but are not diagnostic. Eosinophilia is uncommon and usually present only if there has been leakage of antigenic material from cysts.99 Serology tests for E. granulosus include ELISA, indirect hemagglutination (IHA), and indirect FA tests, with sensitivity ranging from 60% to 90%. The best sensitivity is obtained by using a combination of tests. These tests have limited usefulness for following the course of disease after treatment; imaging techniques are the modality of choice for monitoring disease progress. Imaging is extremely useful in diagnosing cystic hydatidosis. Although plain radiographs may reveal calcified cysts, ultrasound, CT scanning, and MRI are preferable for diagnosis. Ultrasound has the benefits of being easy to perform and less expensive than CT or MRI, and it is particularly useful for evaluation of intra-abdominal cysts. These cysts most commonly appear as anechoic, smooth, round cysts that look much like benign cysts. Septation can be seen when daughter cysts are present. The “hydatid sand” may be visible on ultrasound imaging. The CT scan is useful for better defining the site, size, and composition of cysts, and is better than ultrasound at detecting extrahepatic cysts. CT is also useful to monitor for recurrence during or after therapy. The sensitivity of CT is cited as 95% to 100%.223 MRI is better than ultrasound for mapping extrahepatic cysts, particularly in the brain.281 However, MRI has little benefit over CT scanning for abdominal or pulmonary hydatid cysts, except for better delineating venous or biliary involvement. Other techniques, such as endoscopic retrograde cholangiopancreatography, are also useful in diagnosing biliary involvement of hydatid disease. Echinococcus multilocularis Nonspecific leukopenia or thrombocytopenia, mild eosinophilia, and nonspecific liver function abnormalities may be detected but are not diagnostic. Hypergammaglobulinemia and elevated serum IgE levels are commonly present. Serology tests in alveolar hydatidosis are much more sensitive than for cystic hydatidosis, with a higher proportion of patients having an antibody response to E. multilocularis. Immunoaffinitypurified E. multilocularis antigens used in ELISA have a

sensitivity of 95%. In alveolar echinococcosis, serial serology is useful for following disease course, given its increased sensitivity. The preferred imaging modalities for alveolar hydatidosis are similar to those for cystic hydatidosis—ultrasound, CT, and MRI. These polycystic lesions typically have irregular borders, central necrosis, and irregular calcifications. They are often difficult to distinguish from a tumor. MRI is useful for delineating obstruction of the inferior vena cava or for brain lesions.

TREATMENT Traditionally, surgery is the most common form of treatment for echinococcosis and results in a 90% cure rate when the cysts are completely excised.168 Cystic hydatidosis is more often curable with surgery than is alveolar hydatidosis, which tends to be more invasive. After surgery, medication may be necessary to keep the cysts from recurring. The drug of choice for treatment of cystic echinococcosis (E. granulosus) is albendazole. Albendazole or mebendazole is the recommended treatment for E. multilocularis infections.143 Not all patients with hydatid disease are surgical candidates. The World Health Organization (WHO) recommendations for hydatid disease list the following contraindications for surgery: patients at the extremes of age, patients in very poor general condition, pregnant women, patients with multiple cysts or cysts that are difficult to access, and patients with dead or completely calcified cysts.303 Patients who are not good candidates for surgery have two options: chemotherapy with albendazole or mebendazole, and a newer treatment, the PAIR (percutaneous aspiration, introduction of a protoscolicidal agent, and reaspiration) procedure.140 The PAIR procedure involves percutaneous puncture of cysts under ultrasound guidance, aspiration of cyst fluid, and injection of a protoscolicidal agent such as hypertonic saline or ethanol into the cyst cavity. The cyst is then reaspirated after 15 minutes. PAIR has been employed primarily for cysts in the liver, although cysts in other sites have been treated in this manner. The WHO currently recommends PAIR for inoperable patients and for patients who refuse surgery. The indications for the PAIR procedure are expanding as experience with this modality grows. With appropriate patient selection, PAIR may be used more widely for initial treatment of echinococcosis.80 PAIR is contraindicated in patients with inaccessible cysts or cysts with a high risk of spillage into the abdominal cavity. It is also contraindicated in inactive cysts and for cysts with biliary communication. Risks of the procedure include spillage of fluid and the resulting allergic reaction, bleeding, infection, chemical sclerosing cholangitis, and biliary fistulas. Treatment with albendazole or mebendazole is recommended prior to and after the procedure to decrease risks and increase success of therapy.

PREVENTION AND CONTROL Prevention and control of echinococcosis involve disrupting the life cycle of the parasite.72 Control measures include eliminating stray dogs and preventing dogs from consuming infected viscera by prohibiting home slaughter of sheep. Control programs are ongoing in Australia, Argentina, Chile, Brazil, Peru, China, Portugal, and many Mediterranean countries. Many of these programs include surveillance testing of dogs for Echinococcus and treating infected dogs with praziquantel. The most successful programs, in Iceland, New Zealand, and Tasmania, relied on regular repeated treatment with praziquantel of all at-risk dogs to eliminate the definitive host carriers of E. granulosus.72 Vaccination against E. granulosus is on the horizon. A vaccine for E. granulosus, the EG95 vaccine, is composed of a purified recombinant protein of the echinococcal oncosphere as well as an adjuvant. It is given as two doses 1 month apart, followed by an annual booster. Initial studies show it affords 95% immunity in sheep and other livestock.71,163 For humans, prevention involves avoiding close contact with dogs and foxes and careful washing of vegetables and fresh produce when in endemic areas. The future may hold vaccination for humans as well. 1171

CHAPTER 59  Wilderness-Acquired Zoonoses

upper quadrant discomfort, malaise, and weight loss, and they most commonly relate to hepatic involvement. Biliary obstruction, portal hypertension, and the Budd-Chiari syndrome can also occur. Alveolar hydatidosis is a more aggressive disease than cystic hydatidosis. Untreated, alveolar hydatidosis has a 10-year survival rate of less than 10% after the onset of symptoms, and a 15-year survival rate of less than 1%.5

PART 6  ANIMALS, INSECTS, AND ZOONOSES

i

= Infective stage

d

= Diagnostic stage

Ingestion of Ingestion of undercooked meat meat scraps (esp. pork) or animals

2 3

5 4

i

d

Pigs

2

FIGURE 59-40  Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) (1) of Trichinella. After exposure to gastric acid and pepsin, the larvae are released (2) from the cysts and invade the small bowel mucosa, where they develop into adult worms (3) (females, 2.2 mm in length; males, 1.2 mm; life­ span in the small bowel, 4 weeks). After 1 week, the females release larvae (4) that migrate to the striated muscles where they encyst (5). Trichinella pseudospiralis, however, does not encyst. Encystment is completed in 4 to 5 weeks, and the encysted larvae may remain viable for several years. Ingestion of the encysted larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining the endemicity of this infection. Carnivorous or omnivorous animals, such as pigs and bears, feed on infected rodents or meat from other animals. Different animal hosts are implicated in the life cycle of the different species of Trichinella. Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat). (From http://www.dpd.cdc.gov/ DPDx/HTML/Trichinellosis.htm.)

1

Encysted larva in striated muscle

1 i

d

3

5 4

1

Carnivorism

i

d

Carnivorism

Larvae released in small intestine 1

2 3

5 4

Rodents Encysted larva in striated muscle

i

d

1

5

Adults in small intestine 1

Larva deposited in mucosa

Trichinellosis

LIFE CYCLE

Trichinellosis is an infection caused by nematodes in the genus Trichinella. In the past, only one species, Trichinella spiralis, was recognized. Isoenzyme and DNA analysis indicate that the genus is polyspecific.211 Eight gene pools, T1 through T8, have been identified. T1 is classic T. spiralis; the principal reservoir is in domestic swine, but some wild animals can also be infected. T2, Trichinella nativa, is found primarily in terrestrial mammals such as the bear, walrus, or fox in Arctic and sub-Arctic regions. Most human infections are caused by T1, and few by T2. Relatively few data are available on how frequently the other species infect people. T3 occurs in bears (Ursidae), and T7 and T8 occur in African Hyenidae and Felidae. Only T4, Trichinella pseudospiralis, can infect mammals and birds. Unless stated otherwise, the rest of this discussion relates to trichinellosis generically and to T. spiralis specifically.

The life cycle of Trichinella organisms is unusual in that every host is necessarily both a definitive host, harboring the adult stage of the parasite, and an intermediate host, harboring the larval stage (Figure 59-40). The infection is acquired by ingestion of larvae encysted in skeletal muscle. The worms mature within a few days in the small intestine. The female burrows into the mucosa and deposits larvae in tissue, starting around the fifth day after infection. Most larvae are deposited within 4 weeks, but they can be produced for as long as 4 months. The larvae enter the circulation and invade skeletal muscle within 7 to 14 days (Figure 59-41). They become encapsulated around day 21 after infection and are then infective for the next host that ingests them.

HISTORICAL ASPECTS The Bible references swine as dirty animals, and some religions advocate not eating pork; it is hypothesized that part of this practice encouraged public health by preventing parasitic infections such as trichinellosis and cysticercosis. Trichinella cysts were first noticed by Paget during an anatomic dissection in 1836, when distinct white lesions were found throughout a muscle specimen. The association between encysted organisms and ingestion of contaminated meat was not made until 1850. In 1862, Friedreich diagnosed and described the first clinical case of acute trichinellosis. Outbreaks in Germany in 1849 and 1865 were associated with mortality rates of 19% and 30%, respectively. Examination of diaphragmatic muscle samples in the United States between 1936 and 1941 revealed Trichinella organisms in one of every six samples tested (16.7%). National reporting of trichinellosis began in 1947. The incidence of this disease has decreased significantly since the passage of legislation (the Federal Swine Health Protection Act of 1980) prohibiting the feeding of raw sewage to swine, aided by the widespread freezing of pork and increasing public awareness of the dangers of eating inadequately cooked pork products (Figure 59-39, online). 1172

FIGURE 59-41  Trichinellosis in a polar bear. A larva is seen within a muscle fiber in the center of the picture. The parasite found in Arctic mammals is highly resistant to freezing and has been given a separate species status, Trichinella nativa. (Hematoxylin and eosin, ×100.)

All carnivorous and omnivorous mammals are susceptible to trichinellosis, but most human infections are acquired by eating raw or undercooked pork. Game animals can harbor the parasite. Trichinellosis was found in 1.3% of black bears in New England.131 It can infect other species of bears, raccoons, opossums, seals, walruses, peccaries, and wild swine. Rodents, such as mice and rats, are commonly infected in nature. Except in certain cultures, these small rodents, unlike their larger cousins, for example, squirrels, woodchucks, muskrats, agoutis, and capybaras, are rarely eaten by people. These larger rodents are primarily herbivorous, but are still an occasional source of human infection. Although experimentally susceptible to trichinellosis, herbivores, such as members of the deer and antelope families, are almost never infected naturally, and consumption of their flesh is not associated with this infection. Some outbreaks of trichinellosis have occurred in people who consumed horseflesh.45 The horses could have been infected by consuming mice, dead or alive, in their feed. Alternatively, larvae passed in the stool of infected rodents could have been ingested in the horses’ grain or hay. Swine that are privately raised and slaughtered are a continuing source of human infections in many areas, including the northeastern United States.10 Bears, walruses, and feral swine have been the principal nondomestic sources of trichinellosis in the United States.181 From 1991 to 1996, three deaths in 230 cases were reported to the CDC (an average of 38 cases per year), including 14 multiple case outbreaks from 31 states and Washington, D.C. Information on the suspected food item was available for 134 (58%) of the 230 reported cases. Pork was implicated in 80 (60%) cases, bear meat in 31 (23%), walrus meat in 13 (10%), and cougar meat in 10 (7%). Sausage was the most frequently implicated pork product (i.e., 57 of the 64 cases for which the form of the pork product was identified).190 Wild boars are a source of infection in Germany.131 Twenty-six cases of trichinellosis reported in the United States from 1975 to 1989 were acquired during foreign travel. Seventeen of these persons had traveled to Mexico or Asia.181

FIGURE 59-42  Clinical appearance of the eyes of a patient with trichinellosis. The patient had periorbital swelling, muscle pain, diarrhea, and 28% eosinophils. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/ quicksearch.asp. Courtesy Dr Thomas Sellers, Emory University.)

and may be life-threatening. Damage to the brain or meninges by migrating larvae can cause encephalitic or meningitic symptoms. A spinal tap may reveal eosinophils in the CSF. The third phase of infection is encystment of the larvae within skeletal muscle, starting about the second or third week after infection. This can cause significant myalgias and stiffness in affected muscle groups. The final phase of infection occurs as the larvae die and become calcified. This is a period of convalescence, which is usually asymptomatic, and typically occurs between 6 and 18 months after infection. In the Inuit population of northeastern Canada, trichinellosis is associated with eating raw walrus, and is characterized by prolonged diarrhea and brief muscle symptoms. High peripheral eosinophilia and high Trichinella antibody titers occur. The disease is probably caused by T. nativa, and at least some cases may be associated with reinfection.166

SYMPTOMS

DIAGNOSIS

The signs and symptoms of trichinellosis are closely related to the activities of the parasite in its life cycle. The severity of disease is directly related to the number of adult and larval worms present. GI symptoms predominate during the first week after ingestion of infected meat. The worms mate and invade the intestinal mucosa during the first 48 hours. The female worm is capable of producing up to 1500 larvae during its lifetime. Larvae are deposited starting on approximately the fifth day after ingestion. This activity results in bowel irritation, with nausea, vomiting, variable diarrhea, and abdominal pain. Fever may occur. These symptoms are often mistaken for various forms of food poisoning. GI symptoms may continue until the females are cleared from the intestinal tract at approximately 4 to 6 weeks after infection. Larval production reaches a peak during the second week after infection. The larvae begin to invade skeletal muscle as early as the seventh day. During larval migration, direct capillary damage occurs, resulting in facial edema, especially involving the periorbital area, which may be accompanied by photophobia, blurred vision, diplopia, and complaints of pain on moving the eyes (Figure 59-42). Splinter hemorrhages may appear in the nail beds, and there may be cutaneous petechiae (Figure 59-43). Hemorrhagic lesions can also occur in the conjunctivae and retinae. Core body temperature may reach 40.5° C (105° F). Eosinophils start to increase in peripheral blood during the second week, often exceeding 20% of the total white blood cell count after the third week of infection. The eosinophil count normalizes from 6 to 12 months after infection. Gastroenteric symptoms may continue during this period, until the females are cleared from the intestinal tract approximately 4 to 6 weeks after infection. During the second phase of infection, migrating larvae can cause pulmonary damage, resulting in cough, dyspnea, and pleuritic pain. There may be hemoptysis. Myocarditis can occur

Larvae are sometimes passed in the stool in the early stages of infection, but this occurs infrequently and inconsistently and cannot be used for diagnosis. Trichinellosis is definitively diagnosed by biopsy of the gastrocnemius muscle or of clinically affected (painful, tender) muscles (Figure 59-44). The larvae are demonstrable in muscle beginning about the seventh day after infection. Diagnosis can also be made serologically, using the bentonite flocculation test (BFT), latex particle agglutination, or countercurrent immunoelectrophoresis. The BFT involves a suspension of aluminum silicate particles (bentonite) to which Trichinella antigen is bound and incubated with dilutions of serum from the patient.

FIGURE 59-43  The parasitic disease trichinellosis is manifested by splinter hemorrhages under the fingernails. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc. gov/Phil/quicksearch.asp. Courtesy Dr Thomas Sellers, MD, Emory University.)

1173

CHAPTER 59  Wilderness-Acquired Zoonoses

EPIDEMIOLOGY AND TRANSMISSION

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Gerstmann–Sträussler–Scheinker (GSS) syndrome, fatal familial insomnia (FFI), kuru, and variant Creutzfeldt-Jakob disease (vCJD). In animals, TSEs include BSE, scrapie, chronic wasting disease, transmissible mink encephalopathy, and feline spongiform encephalopathy. BSE is unique in that it is the only animalrelated TSE believed to lead to a human TSE, vCJD, through consumption of contaminated ruminant products.

HISTORICAL ASPECTS

FIGURE 59-44  Micrograph of developing Trichinella cysts within human muscle tissue. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/ quicksearch.asp.)

All these tests usually do not become positive until 3 to 4 weeks after infection. Newer ELISAs are available that measure reaction by different immunoglobulin classes. Most ELISAs offer greater specificity and sensitivity and become positive earlier than many of the other tests.9,234,283 An ELISA for IgG, using the excretory– secretory antigen of T. spiralis larvae, had specificity and sensitivity of 100% at days 57 and 120 after infection, but was negative at day 23.169 An experimental assay, the dissociated enhanced lanthanide fluoroimmunoassay (DELFIA), can detect as little as 1 ng of antigen per milliliter of serum. Circulating antigen was detected in mice as early as 7 days after infection.149

TREATMENT No satisfactory, safe, and effective drug is available for the elimination of larvae, which are responsible for most of the pathologic changes and symptoms of trichinellosis. Thiabendazole (25 mg/ kg twice a day for 5 days, maximum 3 g/day) is effective against adult worms in the intestine. Its efficacy against larvae is questionable, however, and it can cause serious side effects, such as fever, increased edema, and myocarditis.147 Mebendazole (200 to 400 mg three times a day for 3 days, then 400 to 500 mg three times a day for 10 days) is better tolerated,203 but poor intestinal absorption reduces its use in extraintestinal trichinellosis. Albendazole and flubendazole are well absorbed and may be more effective, but supporting data are scarce. Steroids (e.g., prednisone, 30 to 60 mg/day orally for 10 to 30 days) can be given for relief of severe illness, such as myocarditis caused by migrating larvae or nervous system involvement.147 Dosage and duration of treatment are individually determined by clinical response. Steroids reduce the inflammatory response to larvae but can also interfere with rejection of adult females in the intestine, thus prolonging the period of larva deposition.

PREVENTION Trichinellosis is prevented by cooking meat to an internal temperature of 65.6° to 77° C (150° to 170° F). Most Trichinella larvae are killed by freezing. The time required depends on the thickness of the meat and the freezing temperature. Holding meat at −15° C (5° F) for 20 days, −23.3° C (−10° F) for 10 days, or −28.9° C (−20° F) for 6 days is recommended. Salting, drying, and smoking are not always effective. Note that T. nativa found in Arctic mammals is resistant to freezing.

Bovine Spongiform Encephalopathy and Variant Creutzfeldt–Jakob Disease Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE), a family of fatal degenerative diseases of the nervous system that affect humans and animals. In humans, TSEs include Creutzfeldt–Jakob disease (CJD), 1174

The first diagnosis of BSE was reported by the Central Veterinary Laboratory in Weybridge, England, in December 1986.296 In subsequent years, the number of reported cases rose steadily and the British government initiated a series of escalating preventive measures to combat the epidemic. Incidence peaked in 1992, with 36,680 confirmed cattle cases that year.70 By 2000, fewer than 1500 cases had been reported, reflecting ongoing steady decline.70 In late 1995 and early 1996, CJD began appearing in Great Britain in a very unusual population—young adults. Further investigation revealed significant differences from previously documented CJD cases in histopathology, electroencephalography (EEG) waveforms, and MRI brain signal hyperintensities. These cases were named new variant CJD. Classically, CJD has occurred sporadically without the clustering that occurred with this new variant, which led researchers to search for a new risk factor or cause. Given that the onset of symptoms of CJD after initial exposure can be delayed for up to a decade, the time between confirmation of the first case of BSE and the first case of the new vCJD raised suspicions for a bovineto-human transmission.239 Subsequent studies have demonstrated remarkably similar molecular characteristics, histopathology, and clinical features in BSE and vCJD patients.65,154,245 It is now widely accepted that consumption of BSE-contaminated ruminant products can result in vCJD in humans. Many countries, including the United Kingdom, United States, and Canada, have developed vCJD watch groups aimed at identifying sources as they arise.

BIOLOGY The infectious agent is believed to be an abnormal isoform of the prion protein (PrP), designated PrPSc.64 A prion is an infectious protein that lacks nucleic acids. The human PrP gene is located on the short arm of chromosome 20 and spans 16kb.64 PrPSc is derived, through an aberrant post-translational mechanism, from isoform PrPC, which is found as a membrane-anchored glycoprotein in many cells throughout the body. If the PrPC protein undergoes a conformational change to the partially protease-resistant PrPSc, accumulations in nervous tissue lead to BSE and vCJD. It is hypothesized that PrPSc can catalyze transformation of PrPC to more PrPSc.282

EPIDEMIOLOGY BSE is thought to have been a low-level disease of cattle for many years. It is presumed to have risen in incidence in 1980 when changes in rendering resulted in reduction in tallow extraction (previously done by the use of solvents) and provided higher fat content in the meat. It is thought that when these solvents were no longer being used, it allowed cattle protein supplements to become contaminated with a transmissible agent.73 Ever since the number of BSE cases in cattle in Great Britain reached a peak of 36,680 in 1992, there has been a steady decline to a total of 611 cases in 2003.79 A total of 778 cases of BSE were reported outside the United Kingdom in 2003, including one case in the United States from a cow that was imported from Canada.312 According to the CDC, a total of 219 cases of vCJD have been identified since 1996, including cases in the United Kingdom, France, Italy, Spain, Canada, Ireland, the United States, Portugal, The Netherlands, Japan, and Saudi Arabia. The vast majority of vCJD cases occurred in the United Kingdom. Three of the French cases, two of four Irish cases, two of three U.S. cases, the case from Japan, and the case from Canada are believed to have resulted from exposure during time spent in the United Kingdom.311

The incubation period is variable according to routes of exposure, with iatrogenic cases (cornea grafts, neurosurgical instruments, and dura mater) less than 2 years, and approximately 15 years after peripheral insertion of pituitary hormones. It is unclear how long the incubation period is for ingested products.205 With new-variant CJD, it may be only a year from inoculation until death, depending on the route of exposure.

TRANSMISSION Transmission of prions in BSE and vCJD occurs through ingestion of infected ruminant material, which is assumed to be the cause of the outbreak in the United Kingdom in the late 1980s. This practice was banned in 1988 for public health, and more strict measures were put in place in 1989 because of increasing understanding of the disease. In 1996, after continued outbreaks of the disease, recall of all food containing mammalian meat and bone meal (MBM), including animal feed, was put into place.205 The only tissues outside the central nervous system that have been demonstrated to be infectious are the retina, cornea, trigeminal and paraspinal ganglia, distal ileum, and bone marrow.30 This recovered meat was found in hot dogs, sausages, canned meats, and some luncheon meats. A case report describes five cases of unrelated individuals in Kentucky with vCJD from eating squirrel brains in a cuisine termed Burgoo.22 There is also concern about the transmission of vCJD and the TSE between humans by repeated use of infected surgical instruments and via blood transfusion. A recent study described four patients who acquired the new v CJD from non-leucodepleted blood from a then asymptomatic donor.280 There is no blood test for products of vCJD. In the United Kingdom, patients with known BSE and vCJD are not allowed to donate blood and tissues, but the risk remains for persons accepting blood from donors with an asymptomatic infection.

SYMPTOMS AND DIAGNOSIS The incubation period for BSE is 2 to 8 years. Cattle affected by BSE may display apprehension, incoordination, aggression, hindlimb ataxia, tremor, difficulty rising, and hyperesthesia to sound and touch.82 The animal’s condition gradually deteriorates and it dies in 2 weeks to 6 months.82 Diagnosis can be made by postmortem examination of brain tissue (Figure 59-45). On the horizon is a new test developed by the WHO, where a simple lumbar puncture with cerebrospinal fluid (CSF) testing may allow confirmation of the disease in a human or animal. It is highly sensitive and specific for BSE and is being considered for diagnosis of vCJD as well.125 Variant Creutzfeldt–Jakob disease is a progressive neurologic disorder that, unlike traditional CJD, affects a younger population (average age 29 years as opposed to 65 years) and lasts relatively longer (median 14 months as opposed to 4.5 months).304 Early illness is often accompanied by psychiatric features, including depression and schizophrenia-like psychosis.304 Subsequent

FIGURE 59-45  Micrograph of brain tissue showing the histopathologic changes in the cytoarchitecture found in bovine spongiform encephalopathy (BSE). The vacuoles in the gray matter give the brain of BSEaffected cows a sponge-like appearance in tissue sections. (From Centers for Disease Control and Prevention Public Health Image Library. http://phil.cdc.gov/Phil/quicksearch.asp. Courtesy U.S. Department of Agriculture, Animal and Plant Health Inspection Service. Courtesy Al Jenny, MD.)

neurologic symptoms include ataxia, involuntary movements, lack of coordination, and pain.70 As with BSE, diagnosis can be confirmed only by postmortem histopathologic analysis of the brain, although new CSF tests are on the horizon.

TREATMENT AND PREVENTION There is no treatment for either BSE or vCJD. Prevention is based on public health measures, which have led to a remarkable decline in cases in Great Britain. These measures may include a ban on ruminant-to-ruminant feeding, active surveillance for early detection of BSE, and a ban on importation of cattle and bovine products from countries known to have BSE. The economic implications of an importation ban have made such a measure controversial, although it is nearly universal. There have been attempts to devise a treatment for vCJD and BSE, but little to no progress has been made.26,264 Acknowledgment. We thank Leonard Marcus, Eric L. Weiss, and Daniel Garza for their fine work on previous versions of this chapter.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 60 

Rabies JAMES A. WILKERSON III

Rabies has terrorized humanity since the dawn of civilization, and the menace continues. In industrialized nations where human rabies is rare, animal rabies abounds and humans are protected from infection only by vigorous animal vaccination programs, elimination of stray animals, and postexposure immunization. In developing countries, tens of thousands die each year, and over

ten million endure agonizing anxiety following exposure to a possibly rabid animal.217 In the United States, approximately 23,000 persons receive postexposure prophylaxis each year.70,179 An encounter with this uniformly fatal infection, globally the most common form of viral encephalitis, leaves “a more indelible stamp of horror” than does any other disease.138 1175

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Current Status Globally, rabies is the tenth most frequent cause of death from infectious disease.106 The actual number of deaths is unknown because reporting in the developing countries where this infection is common is unreliable. In Tanzania, the estimated incidence of human rabies mortality was 1499 a year (95% confidence interval 891 to 2238), but the average number of deaths officially recorded was 10.8.73 Most of these countries do not have laboratory facilities capable of establishing a dependable diagnosis.68 The World Health Organization (WHO) currently estimates the number of rabies deaths globally at 40,000 to 70,000 a year, although the median number of 55,000 deaths is widely accepted. That is an average of approximately one death every ten minutes.221 Some, perhaps many, human rabies infections are not diagnosed, even in nations with sophisticated medical systems. This problem was vividly dramatized in 2004 by the rabies deaths of four U.S. organ transplant recipients from a donor whose rabies infection had not been recognized.59,64 Only a few months later, three organ transplant recipients in Germany died of rabies and three others with liver and corneal transplants required postexposure prophylaxis.119 A review has suggested that rabies may be underdiagnosed in the United States because physicians see it so infrequently they do not include it in their differential diagnoses.217 In addition to being undiagnosed, rabies is probably incorrectly diagnosed with considerable frequency. Of 33,000 human rabies deaths reported worldwide in 1997, laboratory confirmation was available for less than 0.5%.68

The Rabies Virus Rabies viruses belong to the group Rhabdoviridae, genus Lyssavirus. Seven genotypes are recognized, but genotype 1 is the only one of major significance. This genotype consists of multiple variants or lineages, each closely linked to a single mammal species such as raccoons, skunks, foxes, mongooses, or various bat species. In the 1980s these variants were distinguished with monoclonal antibodies. Subsequently, analysis of nucleotide substitutions in the rabies genome after reverse transcriptase— polymerase chain reaction (RT-PCR) amplification of the viral RNA has allowed identification of the primary reservoirs for each variant, mapping the geographic distribution of variants, and identification of virus spillover into animals and humans.68,191 In addition, for the past 30 years, the source of many human infections has been identifiable in the absence of a recognizable exposure to rabid animals. The rabies virus is bullet-shaped with one flat end and contains a single strand of RNA, which is made up of approximately 12,000 nucleotides and encodes five proteins. Three of these, the nucleoprotein (N), phosphoprotein (P, M1, or NS), and the large polymerase or transcriptase protein (L), make up the core of the virus. The other two, the matrix protein (M) and the transmembrane glycoprotein (G), form its coat.230 The external surface is studded with perpendicular aggregates of glycoprotein, the G protein that recognizes cell surface receptors and facilitates virus entry into cells.15 The 505-amino-acid G protein is composed of a 44-amino-acid internal or “cytoplasmic” portion, a 22-amino-acid hydrophobic transmembrane portion, and the large external “antigenic” portion.160,231 The complete amino acid sequences of these proteins have been determined for several fixed rabies strains.219 A lipid bilayer is closely associated with the matrix protein, and the two form a clearly defined shell for the virus. The M protein is the smallest of the rabies virus structural proteins, with only 202 amino acids,232 but makes up approximately 25% of the total virion protein. It is in close contact with the core and also interacts with the internal segment (cytoplasmic tail) of the surface G protein. The core of the virus forms a tightly structured helix of 30 to 35 coils that extends end-to-end within the virion. The RNA genome is associated with about 1800 closely packed molecules of the 55 kDa nucleoprotein, which together are known as ribonucleoprotein (RNP). The N protein protects the genome from 1176

Envelope (membrane)

Matrix protein

Glycoprotein

Ribonucleoprotein FIGURE 60-1  Structure of the rabies virus. (Modified http://www.cdc.gov/ncidod/dvrd/rabies/the_virus/virus.htm.)

from

digestion and keeps it in a suitable configuration for transcription. Some 30 to 60 copies of the large (≈190 kDa) transcriptaseassociated L protein and about 950 copies of the smaller (≈38 kDa) P or phosphoprotein are responsible for replication of the viral RNA232 (Figure 60-1).

Rabies in the United States INCIDENCE IN HUMANS The incidence of human rabies in the United States fell dramatically from 23.5 infections per year in the late 1940s to 1.0 infection per year during the 1980s (Table 60-1). However, 27 infections were reported from 1990 through 1999, and 26 have been reported from 2000 to 2002. From 1980 to 1989, seven infections were acquired outside the United States. From 1990 to 1999, five infections were acquired outside the United States, and from 2000 to 2008, six infections were acquired in other countries.* Of the human rabies infections acquired in the United States, one originated from a skunk (1981) and two originated from dogs (1991 and 1994). The two dog infections were associated with the epizootic in coyotes that developed when rabies spread across the Rio Grande River from unvaccinated dogs in Mexico. The remaining 42 infections originated from bats. Of the 18 human rabies infections acquired outside the United States during these 28 years, 17 originated from dogs. Only an infection in 2008 in California was determined to have originated from a Mexican free-tailed bat34 (Table 60-2). Although reliable rabies vaccines and antisera first became available during this 62-year period, extensive vaccination of domestic animals, particularly household pets, and elimination of unrestrained and stray animals are considered primarily responsible for the decline in the human infection rate.53,54,151 Such programs reduced the incidence of laboratory-confirmed rabies in dogs from 6949 in 1947 to 75 in 2008.30 The annual cost for these programs is over $300 million, most of which is borne by pet owners.192 *References 45, 47, 48, 51, 59, 62, 64, 225. TABLE 60-1  Human Rabies Infections in the United

States, 1946 to 2008

Time Period 1946-1949 1950-1959 1960-1969 1970-1979 1980-1989 1990-1999 2000-2008

U.S. Infections*

Cases/Year

Non-U.S. Infections†

94 136 38 17 3 22 20

23.5 13.6 3.8 1.7 0.3 2.2 2.5

0 0 3 6 7 5 6

*Rabies infections acquired within the United States. † Rabies infections acquired outside the United States.

Patient  1  2  3  4  5  6  7  8  9 10 11 12 13 14 15 16 17 18

Age 40 30 12 72 19 13 18 11 69 40 26 32 54 72 41 22 11 16

Gender

Onset of Rabies

Location

8/81 1/83 7/84 9/84 5/85 11/87 1/89 4/92 11/93 6/94 2/96 8/96 9/00 2/01 2/04 10/04 11/06 3/08

AR MA TX CA TX CA OR CA CA FL FL NH NY CA FL CA CA CA

M M F F M M M M M M M F M M M M M M

Exposure Location

Attacking Animal

Mexico Nigeria Laos Guatemala Mexico? Philippines Mexico India Mexico Haiti Mexico Nepal Ghana Philippines Haiti El Salvador Philippines Mexico

Dog Dog Dog* Dog Unknown Dog* Dog* Dog Dog Dog* Dog Dog Dog Dog Dog* Dog* Dog* Bat, Tb*

*No documented exposure; source of infection identified by nucleotide analysis.

RABIES IN WILD TERRESTRIAL ANIMALS In the United States and Canada, a vast reservoir of rabies persists in wild animals.192 During 2008, 49 states and Puerto Rico reported 6841 rabies infections in animals, approximately 93% in wild animals and 7% in domestic animals. However, some states accept only animals responsible for a human or domestic animal incident for rabies testing; others test all submitted specimens. Furthermore, the number of rabid wild animals that die without being detected is estimated to be more than 90% of the total, so the identified infections represent only a small fraction of wild animal rabies.125 Several major rabies epizootics are currently recognized. An epizootic of rabies started in Arctic foxes in northern Canada in the late 1940s and early 1950s and swept southward in the middle and late 1950s to involve red foxes in Alberta, Saskatchewan, Manitoba, Ontario, and Quebec. The epizootic crossed the St Lawrence River in 1961, where it involved red foxes in upper New York State, although currently it appears to be limited to the adjacent Canadian provinces, which are experiencing a lower incidence of fox rabies.11,28,127 The epizootic, which moved westward to involve arctic foxes in Alaska and the Northwest Territories,190 surrounds the North Pole and may cover the largest land area of any observed outbreak28 (Figure 60-2). An outbreak of raccoon rabies started in central Florida in the 1940s and spread at the rate of about 40 km (25 miles) per year, reaching Georgia in the early 1960s and Alabama and South Carolina in the 1970s. In the late 1970s a second outbreak appeared on the Virginia–West Virginia border. That epizootic has now spread north to all of New England; in 1999 it crossed into Canada. It has also spread south to join with the epizootic coming north from Florida in North Carolina.46,68,69 The second outbreak developed when raccoons were translocated from Florida for restocking for hunters. Although the animal suppliers held legal permits and health certificates, inclusion of some rabid animals among the more than 3500 transported raccoons has been documented.118,229 As of 2002 more than 50,000 rabies infections in raccoons had been reported in the United States since 1975. The land mass affected by this epidemic is approximately 1 million km2 (383,000 miles2) and includes the residences of 35% of the United States human population (Figure 60-3). The raccoon epizootic is considered particularly threatening because many raccoons live in densely populated urban and suburban areas.68 However, the only known human rabies infection resulting from this epizootic occurred in 2003.47 The spread of rabies from raccoons to humans appears to have been limited in part because raccoons are large animals and their bites are obvious. To some extent, wellvaccinated dogs and other pets form a barrier between wild animals and humans. Perhaps of greatest significance is the

nonaggressive behavior of rabid raccoons. In 38 rabid raccoon incidents in Florida over a 5-year period, bites were inflicted only when humans or dogs tried to kill or capture raccoons that seemed tame.226 Before the raccoon epizootic, most terrestrial rabies in the United States was in skunks. Human rabies resulting from exposure to a spotted skunk in California was reported in 1826.67 Four epizootics are recognized, one of which is in the province of Quebec, Canada, and New York state and is associated with the fox epizootic in that area. A larger epizootic started in Iowa in 1955. It has spread east to Ohio, west to Montana, north to the Canadian provinces of Manitoba (1959), Saskatchewan (1963), and Alberta (1971), and south to meet with a third epizootic that originated in Texas and has spread to surrounding South Central states, particularly Oklahoma and Arkansas. The fourth epizootic in skunks is located in northern California67 (Figure 60-4). An increase in the number of rabid skunks in the East Coast states has recently occurred, but analysis of these infections indicates they result from raccoon rabies spilling over into skunks and are not indicative of a separate skunk epizootic.103 Screening of rabies virus isolates from the epizootics has disclosed five distinctive patterns. Red foxes and skunks in New York and adjacent Canada present one pattern; raccoons from the Atlantic states present a second. The skunks in the southcentral states present a third, and a fourth is represented only by a small outbreak in gray foxes in Arizona. However, the fifth pattern is found in skunks from the north-central states and from California, in dogs from the Mexico border states, and in a small rabies outbreak in gray foxes in Central Texas189 (Figure 60-5). Rabies in rodents is an intriguing problem. Rodents are the animals of choice for rabies virus isolation in the laboratory; yet rabies in small free-living rodents is rare. One explanation is that rodents may usually be killed rather than simply infected by the bites of rabid animals, but rodents are carrion eaters and can be infected by that source as well. In recent years the largest number of rodent rabies infections has been in large rodents such as woodchucks that have been infected by rabid raccoons. Rabid beavers have attacked and bitten humans in North Carolina. However, no transmission of rabies to humans by rodents has been documented.200

RABIES IN BATS With the exception of Antarctica, rabies in bats is global. In Canada, the United States, parts of South America, Western Europe, and Australia (where rabies in carnivores, particularly dogs and foxes, has been controlled), bats are the most prominent source of human rabies.148 Rabies was diagnosed in insectivorous bats in Brazil in the 1920s and in frugivorous bats in Trinidad during the 1930s, 1177

CHAPTER 60  Rabies

TABLE 60-2  Rabies Deaths in the United States Since 1980 From Infections Contracted Outside the Country

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Rabid foxes

Foxes tested

1

1

3-9

5

2

10-53

10

FIGURE 60-2  Rabid foxes reported in the United States in 2008. ( http://www.cdc.gov/rabies/resources/publications/2008-surveillance/foxes.html.)

although the principal subject of these studies was rabies in hematophagous (“vampire”) bats that was being transmitted to humans. The first definitive diagnosis of rabies in nonhematophagous bats was made in a frugivorous bat that flew into a “chemist’s” shop in Port of Spain, Trinidad, on September 10, 1931. However, the incident that drew widespread attention to bat rabies occurred in Tampa, Florida, on June 23, 1953. The 7-yearold son of a ranch hand was looking for a baseball near some shrubbery when a lactating female yellow bat suddenly flew out of the bushes and bit the boy on the chest, remaining firmly attached until knocked off by the boy’s mother. The ranch owner had heard of rabies in vampire bats in Mexico and insisted the bat be examined for infection. Negri bodies were found in smears of the brain, and the diagnosis was confirmed by mouse inoculation of brain tissue. The boy was given postexposure treatment and did not develop an infection.17,69,219 The publicity given this event led to many more bats being submitted for rabies examination. Subsequently, rabies has been found in bats in every state except Hawaii, as well as in eight Canadian provinces.17,165 In 2008, bat rabies was reported from all 48 of the continental states and the District of Columbia54 (Figure 60-6). The estimated incidence of rabies in bats in the United States is 0.5% to 1.0%; the incidence in bats that appear ill or injured is much higher, 7% to 50%.17,201 Rabies virus variants from bats are species specific rather than geographically specific189 and are distinctly different from those of terrestrial animals in the same locations, including the major terrestrial epizootics. Clearly, little exchange of infection between bats and terrestrial animals takes place, although occasional animals infected with rabies virus strains typical of bats are found. Many large areas of the United States, particularly the Pacific 1178

Northwest and New England (prior to the raccoon epizootic), report rabies in bats but in no other species. Even though cats and foxes catch and eat bats, only 3 of 136 cat and fox rabies isolates over a 2-year period were antigenically similar to bat rabies strains.17,79,189 Approximately 70% of human rabies infections and 75% of cryptic rabies deaths in the United States have been caused by the variant associated with silver-haired and the eastern pipistrelle bats, which are reclusive animals rarely found around human habitation. Infections by variants associated with bats that frequent human dwellings are much less common. Infections in other animals by this variant are also disproportionately very high. These bats are small and their bites are difficult to detect. However, in comparison with other rabies virus variants, the variant associated with these two bats replicates better in fibroblasts and epithelial cells, and replicates better at the low temperature of 34° C (93.2° F). These features indicate this variant is better able to replicate in the peripheral tissues involved by most bites.140

RABIES IN DOMESTIC ANIMALS Since rabies in dogs has been controlled, rabies infections in cats have outnumbered infections in dogs (295 to 75 in 2008).30 A major problem in vaccinating cats is establishing ownership. Farmers value cats for rodent control but do not recognize them as property. Cats wander from farm to farm and contact wild animals with rabies. Capturing feral cats so they can be vaccinated is difficult.42 Rabies is not rare in other domestic animals, including cattle, horses, mules, sheep, and goats (Table 60-4).

CHAPTER 60  Rabies

Rabid raccoons

Raccoons tested 1 10

1 2-4 5-69 70-1541

100

FIGURE 60-3  Rabid raccoons reported in the United States in 2008. ( http://www.cdc.gov/rabies/resources/publications/2008-surveillance/ raccoons.html.)

SOURCES OF HUMAN INFECTION In the late 1940s and 1950s most human rabies in the United States resulted from bites by dogs or cats. Of 146 infections in the years 1946 to 1961 for which a source of exposure could be identified, dogs were responsible for 120 and cats for 9 (88.4%). Foxes (7), skunks (5), and bats (5) were responsible for the rest.53 However, after rabies in domestic animals was controlled, human rabies resulting from bites by pets disappeared. Since 1966, all but 2 of the 19 human rabies infections resulting from exposures to rabid dogs were acquired outside of the United States.53,62,151 Before 1965, the CDC had recorded no human rabies occurring within the United States that had been acquired outside the country.151 However, since then the number of infections acquired outside the United States has been significant: 3 of 15 (20%) between 1965 and 1970, 6 of 23 (26%) in the 1970s, 7 of 10 (70%) in the 1980s, and 18 of the 63 cases (29%) since 1980. Lack of knowledge about the risk for rabies in developing countries has led some travelers to disregard animal encounters and not obtain rabies immunoprophylaxis, but some of these infections have been in children who did not inform their parents of the animal contact. Until the 1980s, identifying the source of a number of human rabies infections in the United States was impossible. For many infected persons no animal exposure incident—even an opportunity for animal exposure—could be identified. An infectious

source could not be found for 84 of 230 (35%) human rabies infections occurring in the United States between 1946 and 1961,151 or for 6 of 38 (16%) human infections between 1960 and 1970.52 Only since the 1980s has monoclonal antibody typing or RT-PCR nucleotide analysis allowed the source of human rabies infections to be determined when no animal exposure incident could be identified.17,79,189 However, such studies have made it unmistakably clear that bats are now the major source of human rabies in the United States. Of the 45 human rabies infections acquired within the United States since 1980, 42 are attributed to bats. A study of human rabies of bat origin in the United States and Canada from 1950 through 2007 identified 56 infections, of which 22 (39%) reported a bite, 9 (16%) had a direct contact but no bite, 6 (11%) found one or more bats in their homes (two in the room in which they slept), and 19 (34%) had no history of a bat contact.76 How the infection is transmitted has been uncertain. In 1956 and 1959, two men died of rabies after exploring Frio Cave near Uvalde, Texas. The walls and ceiling of that cave hold astonishing numbers of bats—300 to 400 per square foot. Neither man had been bitten, and the infections were attributed to aerosol transmission of the rabies virus. Subsequently, when experimental animals of various species were placed in the cave in cages that only allowed the virus to be transmitted as an aerosol, a significant percentage developed rabies.74,75 Additionally, aerosol 1179

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Rabid skunks

Skunks tested 1 5

10

1 2-3 4-29 30-349

FIGURE 60-4  Rabid skunks reported in the United States in 2008. ( http://www.cdc.gov/rabies/resources/publications/2008-surveillance/ skunks.html.)

transmission of rabies to humans has occurred at least twice in laboratories.24,228 The CDC recommends rabies vaccination for spelunkers.56 However, nursery caves such as Frio Cave contain an astounding number of bats. Saliva and urine constantly rain down on anyone entering the cave, and the blanket of guano on the floor ranges from several inches to several feet in thickness. In Frio Cave air circulation is so poor that the bats warm the cave, the air is humidified by their respiration, and the concentration of ammonia from their urine is so high that the cave usually cannot be entered without respirators.74 Similar infections in other caves have not been reported. Unrecognized bites appear to be the source of infection for most individuals who have had no recognized bat encounters. Bat teeth are so small and sharp that a bite may not be felt. Even the recognized bites are not particularly painful, although at least one of the individuals known to have been bitten was intoxicated with ethanol at the time.98 For centuries, South American vampire bats have been reported to bite sleeping victims without awakening them. Limiting human rabies of bat origin is best addressed by informing the public of the risk.165 Reducing the bat population is not an acceptable approach. Significant population reduction would be difficult and, if achieved, would be an ecologic disaster because bats play such a major role in insect control (Table 60-3). The CDC and other institutions now advocate the following measures: • Dwellings should be “bat-proofed” by tightly covering all possible entrances, particularly roof ventilation openings, 1180

with wire screens. Protection from bats in unscreened dwellings or when sleeping outdoors can be achieved with mosquito netting. • Contact with bats must be assiduously avoided, particularly bats that are behaving unusually. Bats are nocturnal and any activity during daylight hours should be considered abnormal. Diseased bats often are unable to fly. • Any person who has contact with a bat, regardless of whether a bite is thought to have been inflicted, should receive postexposure prophylactic therapy unless the bat has been caught and examined for rabies. • Any person, particularly a child, who awakens from sleep and finds a bat in the room should receive postexposure prophylaxis unless the bat has been caught and examined. A number of the recent bat rabies victims have been children who experienced this kind of exposure.

Rabies in Other Countries EPIDEMIOLOGY Rabies is found throughout the world, and although more common in tropical or temperate climates, is by no means limited to those areas. Arctic foxes with rabies have been found in Alaska, Northern Canada, Greenland, Norway’s Svalbard Islands, and much of Siberia. An epizootic in the Thule district of Greenland in 1958 and 1959 resulted in death from rabies of 50% of the sled dogs in that area. More than 1000 dogs in the Egedesminde district died in another epizootic in 1959 and 1960. For

CHAPTER 60  Rabies

Skunk

Skunk Skunk

Skunk

Raccoon

Skunk Fox

Fox Fox

Mongoose FIGURE 60-5  Terrestrial rabies reservoirs in the United States in 2008. ( http://www.cdc.gov/rabies/location/usa/surveillance/wild_animals.html.)

reasons that are not known, transmission of rabies to humans is rare in these areas, even though exposures are common.75 Perhaps the rabies variant is more infective for foxes and dogs. Rabies is not found in a few areas of the world, all of which are landmasses or peninsulas isolated by water. Rabies does not occur in Hawaii (the only state in the United States in which rabies is not found), some of the Caribbean islands, Pacific Oceania (including Australia [although Australian bat lyssavirus is found there] and New Zealand), or Antartica.101,147 The two human genotype 1 rabies infections that have occurred in Australia are thought to have been acquired outside that country24,58,101 (Figure 60-7). Great Britain had been free of rabies since an extensive dog confinement and vaccination program in 1903, although concern about reintroduction of rabies was raised by the Channel Tunnel and the reduction of border controls between members of the European Community.69,202 A 55-year-old Scotsman with a fatal infection in 2002 was the first locally acquired lyssavirus infection on that island in 100 years, but the virus was not of genotype 1.94 Rabies has been endemic in Japan since the 10th century. However, following World War II, members of the U.S. Army Veterinary Corps determined that no reservoir of rabies existed in the wild animal populations of Japan, Taiwan, and the Philippines—perhaps in part because wild animals were hunted for food during the war. Extensive campaigns to eliminate stray dogs (which in some areas of Japan reduced the canine population by 70% to 80%) and to vaccinate those remaining succeeded in eradicating the infection from Japan and Taiwan. Endogenously acquired rabies has not occurred in those islands since the late 1950s.5,191 The success of canine rabies eradication programs depends on the society in which the programs are initiated. Such programs

achieve little success in nations that are predominantly Hindu or Buddhist, because the people do not support elimination of animals that have no apparent owner. They often put out food for stray dogs. In contrast, Malaysia, a peninsula that is predominantly Muslim, has been largely free of rabies since the early 1950s.25 Elimination of stray dogs must be combined with vaccination programs. Dogs that are eliminated because they cannot be associated with human ownership are quickly replaced. The annual turnover of the dog population in developing countries has been found to range between 30% and 40%.31 Vaccination of domestic animals for rabies is limited largely to industrialized nations. In many developing countries, vaccination of animals is considered unaffordable and rabies control resources are expended on postexposure immunoprophylaxis of humans. Even though rabies immunoprophylaxis is administered to 800 to 900 persons per million inhabitants annually in such countries, the human death rate from rabies is still high, an average of nearly five deaths for each 1 million population annually.32 In the United States that death rate would result in approximately 1500 rabies deaths a year. The magnitude of the rabies threat in developing countries is illustrated by the experience in Thailand. Rabies has been of particular interest in that country since Princess Banlusirisarn was bitten by a rabid dog within the palace grounds near Bangkok in 1911 and subsequently died. (No rabies vaccine was available in Thailand, then called Siam, at that time.) The princess’s death was instrumental in establishing the Institute Pasteur of Bangkok in 1913, which was renamed the Queen Saovabha Memorial Institute (QSMI) in 1922. The Institute, a WHO Collaborating Center for Research on Rabies Pathogenesis and Prevention, has been and remains the site of many sophisticated rabies investigations. 1181

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Rabid bats

Bats tested 1

1

10

2-5 6-75 76-1312

100

FIGURE 60-6  Rabid bats reported in the United States in 2008. ( http://www.cdc.gov/rabies/resources/publications/2008-surveillance/bats.html.)

RUSSIA CANADA

Chicago San Francisco Los Angeles

UCC London Paris

New York Washington

Moskow

Istanbul

Beijing CHINA

Tehran Delhi Al-Qâhira Mumbai

Mexico

Kolkata

Seoul Tokyo Shanghai Manila

Lagos Jakarta

Lima

Areas where rabies is known to exist Areas where rabies is known to be absent

São Paolo

Buenos Aires

Rabies status is unknown

FIGURE 60-7  Areas of the world in which rabies is present (orange), areas in which rabies is absent (green), and areas for which information is not available (yellow). (Modified from http://www.nathnac.org/pro/factsjeets/rabies.htm, and http://www.ktl.fi/portal/sip,o/julkaisut/oppaat_ja_kirjat/ matkailijan_terveysopas_old/4_matkailijoiden_rokotukset/1415.)

1182

Within the United States Since 1980

Patient

Age

 1  2  3  4  5  6  7  8  9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45

27 5 20 22 Adult Adult Adult 11 82 44 41 24 42 14 4 13 74 27 42 49 65 64 71 32 29 49 26 47 69 28 13 20 25 66 Adult Adult Adult Adult Adult 15 10 16 10 46 55

Gender Onset Date M F M M F M F F M M M F F M F F M M F M M M M M M M M M M M M M M M M M F M ? F M M F M M

6/81 2/83 9/84 5/90 8/91 8/91 10/91 7/93 11/93 1/94 10/94 11/94 11/94 11/94 3/95 9/95 8/95 9/95 9/96 12/96 12/96 12/96 10/97 10/97 12/98 9/00 10/00 10/00 11/00 3/02 8/02 9/02 3/03 9/03 5/04 5/04 5/04 5/04 5/04 11/04 9/05 5/06 9/06 9/07 11/08

Location

Source

Oklahoma Michigan Pennsylvania Texas Texas Arkansas Georgia New York Texas California West Virginia Alabama Tennessee Texas Washington Connecticut California California Kentucky Montana Montana Washington Texas New Jersey Virginia California Georgia Minnesota Wisconsin California Tennessee Iowa Virginia California Texas Texas Texas Texas Texas Wisconsin Mississippi Texas Indiana Minnesota Missouri

Skunk Bat, Ln/Ps Bat* Bat, Tb Dog* Bat, Ln/Ps Bat, Ln/Ps* Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Tb† Bat, Ln/Ps† Dog† Bat, Msp Bat, Ln/Ps† Bat, Tb† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ef† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Tb† Bat, Tb† Bat, Ln/Ps† Bat, Ln/Ps† Bat, Tb† Bat, Ln/Ps† Bat, Ln/Ps† Raccoon† Bat, Ln/Ps† Bat, Msp Bat/Human‡ Bat/Human‡ Bat/Human‡ Bat/Human‡ Bat, Msp§ Bat¶ Bat, Tb† Bat, Ln/Ps† Bat, Msp Bat, Ln/Ps†

Bat species: Ln/Ps, Lasionycteris noctivagans or Pipistrellus subflavus, silver-haired bat or the eastern pipistrelle bat; Tb, Tadarida brasiliensis, Brazilian (Mexican) free-tailed bat; Ef, Eptesicus fuscus, big brown bat; Msp, species unknown. *No documented exposure; source of infection identified by monoclonal antibodies. † No documented exposure; source of infection identified by RT-PCR. ‡ Infection acquired through organ transplant from individual 35. § Patient survived. ¶ No documented exposure; source of infection based on history of bat exposure.

In the 1990s the Institute’s postexposure rabies clinic treated about 18,000 patients with new animal bites each year—an average of almost 50 new patients a day! Furthermore, these patients were only 28% of the estimated 64,000 Thais who receive postexposure therapy annually, many of whom were residents of rural or remote portions of the country and were treated by local physicians.224 However, the number of human deaths from rabies in Thailand declined from about 400 a year in the 1970s to 70 in 1999, even though dog rabies has not been controlled.68 Other developing nations have similar rabies problems. WHO agencies have estimated that 87 countries and territories with a total population of about 2.4 billion people are afflicted with endemic canine rabies.32

SOURCES OF HUMAN INFECTION Although domestic animals are rarely the sources of human rabies in the United States and other developed countries, in developing countries the vast majority of human rabies—99% by some estimates—is the result of exposure to rabid dogs.33,69,213,219 In Thailand, although rabies has been found in an array of exotic tropical animals, including tigers and leopards, between 1979 and 1985, 90.6% of human infections resulted from dog bites and an additional 6% followed unknown events. The remaining 3.6% followed cat attacks.181 Other animals, particularly bats, transmit rabies. Hematophagous, or “vampire,” bats are a major source of animal and human rabies in South and Central America, the only areas where such bats are found. Their range extends between northern Mexico and northern Argentina—basically between the tropics of Cancer and Capricorn—and fossils indicate vampire bats have inhabited those areas for 2.5 million years.93 These animals consume 20 to 25 mL of blood at a feeding, and although cattle are their preferred food source, a study in Colima, Mexico, found human blood in the stomachs of 15.7% of 70 vampire bats.13 Human rabies of vampire bat origin was first recognized in 1929 in Trinidad when Negri bodies were found in the brains of 17 individuals, mostly school-age children, who died with acute ascending paralysis. Subsequently, small epidemics have been recognized almost every year in that country. Interestingly, almost all of the rabies transmitted by vampire bats in Latin America is paralytic in type rather than furious.215 Human rabies resulting from vampire bat bites has been reported almost every year from Mexico, but was first reported from South America in 1953 when 9 of 43 diamond miners who slept outdoors died of a mysterious illness. Autopsies of five of the miners disclosed rabies. In an outbreak in two rural communities in the Amazon Jungle of Peru during the first four months of 1990, 29 of 636 residents (4.6%) died after a rapidly progressive illness characterized by hydrophobia, fever, and headache. Rabies virus was isolated from the brain of the only individual on whom necropsy was possible. Of the 29 victims, 96% had a history of bat bites, although bats also had bitten 22% of unaffected community members.6 Human infection is not the only major problem resulting from rabies transmitted by vampire bats in Central and South America.

TABLE 60-4  Human Rabies Infections Identified in the United States and Puerto Rico, 2008 Domestic Animals (471) Animal

Total

Cats Dogs Cattle Horses/Mules Sheep/Goats Other (Llamas)

294 (3)* 75 (11)* 59 20 (1)* 12 1

Wild Animals (6369) Percentage 4.3% 1.1% 0.9% 0.44% 0.18% 0.01%

Animal

Total

Percentage

Raccoons Bats Skunks Foxes Mongooses Rodents/Lagomorphs Other

2389 1806 454 294 (42)* 34† 97‡

34.9% 23.2% 6.6% 4.3% 0.61% 0.50% 1.42%

From Blanton JD, Robertson K, Palmer D, Rupprecht CE: Rabies surveillance in the United States during 2008, J Am Vet Med Assoc 235:676, 2009. *Figures in parentheses are from Puerto Rico. † 31 groundhogs, 2 rabbits, and 1 beaver. ‡ 22 bobcats, 20 coyotes, 6 deer, 4 opossums, 1 otter, 1 coati, and 1 cougar.

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CHAPTER 60  Rabies

TABLE 60-3  Human Rabies Infections Contracted

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Migrating epizootics of vampire-bat–transmitted bovine paralytic rabies kill thousands of animals annually; the estimated cost in 1980 was $500 million.6,68 Efforts to control these epizootics have included vaccination of cattle and attempts to limit the vampire bat population by administering anticoagulants, usually warfarin. It is interesting to note that meat is often consumed from cattle slaughtered at the first, virtually pathognomic sign of disease, paralysis of the hindquarters. Even normal appearing animals may have infected brains. Four of 1000 (0.4%) apparently healthy cattle selected at random at the Mexico City slaughterhouse of Ferrería were found to be infected by rabies when investigated with fluorescent antibody staining and animal inoculation of brain tissue. However, no cases of human rabies from this source have been reported.13 Human rabies has resulted from consumption of brain tissue from a rabid dog and a rabid cat in Vietnam.218 Mongooses are the major source of rabies in South Africa and in some Caribbean Islands such as Puerto Rico.14,88 The yellow mongoose is the main reservoir of rabies in South Africa.219 The small Indian mongoose, imported many years ago in an effort to control rodents,107 is an important reservoir and vector of rabies in Cuba, the Dominican Republic, Grenada, Haiti, and Puerto Rico.219 In Grenada, from 1968 to 1984, mongooses accounted for 787 (73%) of 1078 cases of animal rabies on the island. Of 208 human exposures requiring antirabies therapy, mongooses were responsible for 119 (57%). The possibility of eliminating the animals by hunting or trapping appears remote in view of the island’s topography and the animal’s skill at adapting to its surroundings. However, mongooses take oral baits, so oral vaccination appears feasible if an appropriate vaccine can be identified.133 About 20% to 40% of mongooses have naturally acquired anti­ rabies antibodies, possibly from having survived infection.82 At the Canadian International Water and Energy Consultants (CIWEC) Clinic in Kathmandu, Nepal, 51 travelers required immunoprophylaxis following rabies exposure during a 2-year period. Although 36 of these encounters were with dogs, 10 were with monkeys at Swayambhunath, the “Monkey Temple,” a Buddhist shrine popular with tourists. The bites were inflicted when monkeys leaped for food carried by visitors.185 Human-to-human transmission of rabies is rare. Eight documented infections were in individuals who received corneal transplants (two from the same person) from individuals whose neuroparalytic disorder was not recognized as rabies.57,92,111 In 1996, Fekadu and colleagues reported two apparent instances of human-to-human rabies transmission in Ethiopia. A 41-year-old woman, who died of rabies 33 days after her 5-year-old son died of the same infection, had been bitten on a finger by her son. Another 5-year-old boy, who developed rabies 33 days after his mother died of that infection, had been repeatedly kissed on his mouth by his mother, apparently passing infected saliva to him. However, these infections were not confirmed by laboratory studies.90 In July 2004, the CDC reported four cases of human rabies transmitted by organ transplants from a single donor. The male donor was hospitalized in Texas with “severe mental status changes,” a low-grade fever, and neurologic imaging findings indicative of a subarachnoid hemorrhage. That lesion expanded rapidly in the 48 hours after admission and lead to cerebral herniation and death. An autopsy was not performed. Only after the organ recipients’ deaths from rabies was the donor’s history of having been bitten by a bat discovered. The donor’s lungs were transplanted to a male who died of intraoperative complications. The liver and one kidney were transplanted to males, and one kidney was transplanted to a female, all of whom died of rabies 27, 37, and 39 days later. The fourth victim had a liver transplant from another donor, but a segment of iliac artery from the first (rabid) donor was inserted during the procedure. This recipient died of rabies approximately one month after the transplant.59,64 In the same year, three German individuals who had received a lung, a kidney, and a kidney/pancreas transplant from the same individual died of rabies. When the cause of their deaths was recognized, three additional transplant recipients who had received a liver and two corneas were given postexposure prophylaxis and survived. The corneas were removed. The donor 1184

had been scratched by a dog while visiting India and had not received postexposure therapy. The nature of her disease was not recognized until the three transplant recipients died.119 One case of human rabies appears attributable to transplacental infection. However, a number of mothers dying of rabies encephalitis have given birth to healthy babies, presumably because the virus travels through nerves—viremia has never been documented—and cannot reach the placenta or fetus.91,111

Features of Human Rabies MORTALITY Rabies in humans, once it has become clinically apparent, is uniformly fatal. No other infection is so lethal or progresses so rapidly. In the 1970s intensive support allowed three humans with clinical rabies to survive.61,105,159 Three rabies survivors have been reported subsequently. The first five infections were vaccination failures, and four of the five survivors had severe residual neurologic deficits, severe enough to be fatal 34 months later in one person.2,136 The rabies virus was not cultured from any of these patients and at least one may have had a reaction to neuralderived vaccine rather than an actual infection.117 In October 2004, a 15-year-old female in Wisconsin became the first human to survive clinical rabies without vaccination. This young lady, who developed symptoms 1 month after she failed to report a recognized bite by a bat, was admitted to the Medical College of Wisconsin, Milwaukee, 5 days later. On the second hospital day, the CDC confirmed the presence of rabies virus– specific antibody in serum and cerebrospinal fluid. Because she had evidence of an adequate immune response, because brain pathology in humans succumbing to rabies largely reflects secondary complications rather than a clear primary process, and because clinical reports have included the hypothesis that death results from “neurotransmitter imbalance” and autonomic failure, her physicians, with her parents’ approval, elected to treat her with antiexcitatory and antiviral drugs. Rabies vaccine and rabies immune globulin were not administered. Coma was induced with ketamine and midazolam, she was intubated and maintained on a ventilator, and received intravenous ribavirin and amantadine. Ketamine is a dissociative anesthetic, but it is also an N-methyl-D-aspartate (NMDA) antagonist, and the NMDA receptor has been speculated to be one of the rabies virus receptors. Later she also was given benzodiazepines and supplemental barbiturates. She recovered slowly, was removed from isolation on the 31st day, and was discharged from the hospital on the 76th day. Attempts to isolate the rabies virus, detect viral antigens, or identify rabies RNA in two skin biopsies and nine salivary specimens were uniformly unsuccessful. Five months after her initial hospitalization, she was alert and communicative, but had choreoathetosis, dysarthria, and an unsteady gait. Twenty-five months after hospitalization, she continued to have fluctuating dysarthria and gait difficulties, as well as an intermittent sensation of cold feet. She had no difficulties with activities of daily living, including driving. In high school, she took college-level courses in English, physics, and calculus, scored above average on a national college achievement test, graduated in 2007, and planned to attend a local college. She had no problems with peer relations or mood disorders.62,113,227 At the time, hope was held that this therapy might be a breakthrough in the treatment of clinical rabies. However, a number of individuals have subsequently been treated by the same protocol, and none survived.29,110,136 In February 2009, a 17-year-old female, who two months previously had come in contact with flying bats in a Texas cave, where several of the bats had hit her body but she had not detected any bites or scratches, presented to a community hospital emergency department with severe frontal headache of 2 weeks’ duration, photophobia, vomiting, neck pain, dizziness, and paresthesia of her face and forearms. She had intermittent disorientation and a Glasgow Coma Scale score of 14, nuchal rigidity, and fever as high a 38.9° C (102 °F). Her cerebrospinal fluid (CSF) had a white blood cell count of 163/mm3 with 97% lymphocytes. Bacterial cultures of CSF grew no organisms. After 3 days, her symptoms resolved and she was discharged.

INCUBATION PERIOD For many years, some human rabies infections have been thought to follow prolonged incubation periods. In 1987, a 13-year-old boy who had immigrated from the Philippine Islands 6 years earlier died with rabies determined by nucleotide analysis to be of Philippine dog origin. He had not been out of the United States since he arrived.49 The second documented Australian rabies patient, a 10-year-old girl of Vietnamese origin, had experienced no identifiable animal contact since she had left North Vietnam 6 years and 4 months earlier. She had spent some time in Hong Kong, and the virus responsible for her death was of an immunotype found in China, although the brain tissue was partially decomposed and nucleotide sequencing was limited.24,101,120 Joshi and Regmi have reported an individual who had an apparent incubation period of 1100 days (3 years).123 The first documented patient with rabies reported in Australia, a 10-year-old boy who died in 1987, probably resulted from a monkey bite inflicted in northern India 16 months earlier.58 An 18-year-old Mexican man who died in Oregon in 1989 was infected with rabies virus of a strain to which he could not have been exposed for at least 10 months, although no history of any type of exposure could be obtained.52 Even longer incubation periods of 10 years and 19 1 2 years have been reported, but these occurred in areas where rabies is endemic and a second exposure in the intervening period could not be ruled out.189 Confirmation of such prolonged incubation periods was achieved in three immigrants into the United States from the Philippines, Laos, and Mexico. Nucleotide analysis disclosed rabies viral amino acid compositions essentially identical to the patterns from rabies viruses isolated from dogs in their native countries and unlike rabies viruses found in the United States. These individuals had been in the United States for 6 years, 4 years, and 11 months before the onset of clinical disease.189,192

In 2004, a 22-year-old man from El Salvador who had been in Los Angeles for 15 months died of rabies that, by nucleotide analysis, was typical of rabies viruses found in dogs in El Salvador and unlike viruses found in the United States.126 Such prolonged incubation periods may explain the inability to recall any animal exposure by some patients. However, the possibility that in the past rabies infections resulted from an unrecognized source, such as an undetected bite by a bat, cannot be dismissed. Almost 99% of human rabies infections clinically manifest in less than 1 year, typically 2 to 12 weeks.15,24,92 The median incubation period in the United States for persons diagnosed between 1960 and 1990 was 24 days for those 15 years old and younger, but 43.5 days in people older than 15. Fixed (laboratory) strains of virus tend to produce shorter incubation periods than do wild or “street” strains. In 1960 in Brazil, 60 people were injected with vaccine that had been inadequately inactivated. Sixteen developed rabies, and the incubation periods ranged from 4 to 16 days.92 The size of the viral inoculum clearly influences the incubation period. Experimental animals injected with large numbers of viruses develop clinical infections significantly faster than do those receiving small inocula. Small inocula resulted in greater central nervous system histologic damage and more widespread infection outside the central nervous system, particularly in salivary glands.87

PATHOGENESIS OF CENTRAL NERVOUS SYSTEM INFECTION Immediately after a bite (or investigational injection), rabies virus can be identified at the site with fluorescent antibodies and remains near the wound or injection site for hours to weeks, depending on the animal species. Viral antigen can be demonstrated in muscle, and viral particles budding into the sarcoplasmic reticulum and from the sarcolemma have been demonstrated by electron microscopy.67 The virus appears to enter both motor and sensory nerves, probably through motor endplates and neuromuscular spindles.12,177 Passage of the virus through peripheral nerves was demonstrated in 1887 when rats80 and rabbits81 were protected from rabies following injections of the virus in their hind legs by sectioning the sciatic nerve. After entry into peripheral nerves, the virus travels at a rate of about 5 to 10 mm per hour to neuronal cell bodies such as dorsal root ganglia.15,67 Replication can begin at this site, and prolonged ensconcement at this site has been suggested as one explanation for prolonged incubation periods.177 Upon reaching the CNS, the virus is widely disseminated with extreme rapidity, almost simultaneously with entry, but the manner in which the virus disseminates throughout the CNS is not known. Viremia has not been documented. Plasma membrane budding from infected to uninfected neurons and dissemination through intercellular spaces or cerebrospinal fluid have been suggested. Clusters of viral particles at neuromuscular junctions, reduction of viral infectivity by nicotinic acetylcholine receptor competitors, and other data suggest that the virus recognizes cholinergic binding sites and perhaps enters peripheral and central nerve fibers through those sites. The large numbers of muscle cholinergic binding sites in foxes, which are exquisitely sensitive to rabies, and the small number of such sites in opossums, which are highly resistant to rabies, support this hypothesis and possibly explain the mechanism of sensitivity or resistance.15 The glycoprotein that coats the viral particle is a major determinant of neuroinvasiveness, and alteration of this protein can markedly alter the kinetics of CNS viral spread.12 Viruses can be isolated from cerebrospinal fluid—a significant antibody concentration in this fluid is considered diagnostic of CNS rabies infection—and spread by this route could be quite fast.183 Additionally, rabies virions have been identified in intercellular spaces in the CNS by electron microscopy. Rabies antigen can be found in essentially all parts of the CNS and, although limited mostly to neurons, can also be found in oligodendrocytes.115 1185

CHAPTER 60  Rabies

Six days later she presented to another hospital with photophobia, vomiting, and muscle pain. Her CSF had a protein of 160 mg/dL (normal is 15 to 60 mg/dL) and a WBC count of 185/mm3 (normal is <5/mm3), of which 95% were lymphocytes and the rest macrophages. She was transferred to a tertiary care children’s hospital. Initially she had decreased strength of the left lower and upper extremities, but that resolved. Four days later she reported loss of sensation and strength of the right extremities and her vomiting increased. A lumbar puncture demonstrated increased intracranial pressure. The history of bat exposure was elicited that day. The following day, serum and CSF, saliva, and nuchal skin samples were submitted to the CDC for rabies testing. No rabies virus antigens or RNA could be identified in the skin or saliva, but four serum and CSF specimens contained rabies virus antibodies. Serum immunoglobulin G (IgG) reactivity increased to a peak dilution of 1 : 8192 and immunoglobulin M (IgM) to 1 : 32. The CSF IgG was positive to a dilution of 1 : 32. After the initial results of testing were confirmed, the young woman received one dose of rabies vaccine and 1500 units of human rabies immune globulin. To avoid potentiating the immune response, more vaccine was not given. She was managed supportively, never required intensive care, and was discharged 16 days later after her symptoms had resolved. Twelve days later she returned to the emergency department with headache and vomiting, which resolved after a lumbar puncture. Her CSF pressure was still elevated. Subsequently, she has not returned for follow-up. Testing for evidence of 30 other causative agents of encephalitis or aseptic meningitis was uniformly negative. Her illness has been classified as presumptive abortive human rabies.60 Other than the 15-year-old girl from Wisconsin and the 17-year-old from Texas who received only a single dose of vaccine, no person who has not been vaccinated has survived clinically evident rabies. (Subclinical human infections probably occur, as discussed later.) The clinical phase of rabies encephalitis rarely lasts more than a few days to a few weeks, and infected persons are severely incapacitated.3,92 The catastrophe of rabies is compounded by the young ages of many of its victims; 40% to 50% are 15 years old or younger.92

PART 6  ANIMALS, INSECTS, AND ZOONOSES

The rabies virus can infect a wide variety of cells in culture; no explanation for its localization to neurons in vivo has been found.124 After wide CNS involvement, the virus passes centrifugally through neural axoplasm to a wide variety of tissues, including salivary glands, corneas, and skin of the head and neck, sites at which identification of the virus may aid in the diagnosis of clinical illnesses. The route of spread to the periphery was demonstrated over 90 years ago, when Bartarelli sectioned nerves to salivary glands and found that the glands subsequently did not contain rabies virus.22 Even within the salivary gland, the virus appears to spread by neural networks and not between adjacent epithelial cells.67 An element of immunopathology is produced by disseminated rabies infection. Among persons exposed to rabies, those immunized with early vaccines who subsequently developed infections did so more rapidly than did unvaccinated individuals, a phenomenon termed “early death.” Experimental confirmation of this feature has been achieved by injecting mice with a lethal quantity of rabies virus and immunosuppressing a portion of them. The immunosuppressed animals survived 20% to 25% longer than unsuppressed animals, but their survivals were shortened to those of the control animals when they were injected with antirabies antibody. Additionally, cytolytic T cells appear to be a significant component of the protective response to rabies virus. Avirulent strains of rabies virus induce rabies specific cytolytic T cells, but virulent strains do not.145 Pathologic alterations in the CNS infected by rabies are surprisingly mild, unless supportive care has kept the patient alive for several weeks, which allows much more extensive, necrotic lesions to develop.165,177 Leptomeningeal congestion is the only grossly visible change typically found. Mild edema may be present if the patient has been hypoxic. Pressure grooves are rare. The meninges may be cloudy if severely inflamed.155 Typical histologic features are perivascular cuffing by mononuclear inflammatory cells, microscopic collections of reactive glial cells known as Babes nodules (named for the man who first described them in 18927), and areas of neuronal degeneration and neuronophagia. Some leptomeningeal inflammation is usually present. Spongiform degeneration similar to that found in prion diseases has been described in animals, particularly in skunks.67 Van Gehuchten and Nelis described a striking proliferation of the capsular cells surrounding ganglionic neurons that pushed these cells apart and separated them by a dense cellular layer. The neurons also contained degenerative changes. Subsequent studies have found the Van Gehuchten–Nelis changes to be present in almost everyone dying with rabies—and to be a much more consistent and reliable diagnostic feature than are viral inclusions.204,205 Negri bodies are the best-known histologic feature of rabies and were the first viral inclusions to be found (Figure 60-8). Negri described these cytoplasmic inclusions in 1903 and considered them parasites that caused the disease.146 Entirely independently, Bosc described identical inclusions in two separate papers

FIGURE 60-8  Negri bodies (arrow) in the cytoplasm of neurons in the hippocampus of a dog. (Hematoxylin and eosin, ×1000.) (Courtesy Mérieux Institute, Inc.)

1186

published the same year, but he is rarely recognized.34,35 Negri bodies are eosinophilic cytoplasmic inclusions. Some contain a small, basophilic inner body, or innerkörperchen, and are known as lyssa bodies. They are found almost entirely within neurons; although most common in Ammon’s horn and Purkinje cells of the cerebellum, they may be seen in any part of the central nervous system, particularly in humans. Inclusions may be seen in other tissues, such as the salivary gland, skin, cornea, and pancreas, as well, but are not seen in the ependyma and choroid plexus. The appearance of the inclusion bodies varies in different animal species, and uninfected animals such as cats commonly contain cytoplasmic inclusions that easily could be confused with rabies bodies.195 By electron microscopy, three types of bodies have been identified: one composed of a granular matrix of viral protein and typical virus particles, a second composed of matrix and tubular structures, and a third composed of matrix alone. Invaginations of cytoplasm into the inclusion give rise to the innerkörperchen, indicating that Negri bodies and lyssa bodies are both diagnostic of rabies.155

CLINICAL FEATURES “Although the clinical features of classical rabies are said to be too well known to require description, few clinicians practicing outside the tropical endemic zone have ever seen the disease, and the rare cases presenting in Europe and North America are often misdiagnosed.”215 Pain, paresthesias, or symptoms such as burning, itching, or numbness at the site of the bite or in the bitten limb are the most common early symptoms. Paresthesias may result from proliferation of rabies virus in the spinal cord at the level at which the nerves enter from the bite site.92 In Thailand, this initial symptom often takes the form of severe itching that can lead to frenzied scratching and extensive excoriations.215 This symptom is so well known among the Thai people, and animal bites are so common in that country, that any cause of itching or dysesthesia, even contact dermatitis, can lead to anxiety months to years after an animal exposure.224 Systemic symptoms usually develop later and are largely nonspecific. Local symptoms may not appear at all. One-third or less of all patients initially have symptoms that suggest the etiology of their infection to physicians who do not commonly encounter the disease. Complaints include malaise, chills, fever, or fatigue. Symptoms that suggest an upper respiratory infection are common and include sore throat, cough, and dyspnea. Gastrointestinal symptoms include anorexia, dysphagia, nausea and vomiting, abdominal pain, and diarrhea. Headache, vertigo, irritability, or anxiety and apprehension suggest CNS involvement. However, even advanced rabies often has nonspecific features.53,151 Hypoventilation and hypoxia are common during the prodrome and early acute neurologic phase, and the cause is not understood. Cardiac involvement is common and is manifested by tachycardia out of proportion to the fever; hypotension, congestive failure, or even cardiac arrest may ensue.92 Two clinical forms of human rabies are recognized. The furious, encephalitic, or agitated form that is associated with periodic episodes of hyperactivity, restlessness, or agitation is considered most typical. This form of rabies is characterized by periodic opisthotonic spasms or convulsions, particularly in response to tactile, auditory, visual, or olfactory stimuli (aerophobia and hydrophobia). Episodes of disorientation, sometimes with hallucinations or violent behavior, often alternate with periods of lucidity, which can be particularly horrifying because the patient recognizes the nature of his or her illness. The terror associated with hydrophobia has been labeled “powerful but indescribable.” Episodes of priapism, increased libido, insomnia, nightmares, and depression may suggest a psychiatric disorder. Patients maintained with supportive therapy progressively deteriorate, become comatose, lose peripheral nerve function, lose brainstem function, and die.92,215 Hydrophobia has been described in only 32% of recent U.S. patients,92 although one recent U.S. rabies victim, an 11-year-old boy, was so afraid of water he would not even take a bath.50

SUBCLINICAL RABIES Although clinical rabies in humans is a uniformly lethal infection with only six (perhaps seven) recognized exceptions, subclinical infections probably occur. Low titers of rabies virus neutralizing antibodies have been found in Canadian Inuit hunters and their wives, as well as in unimmunized students and faculty members of a veterinary medical school.116 In Nigeria, 28.6% of 158 healthy humans who had no history of exposure to rabies or of any antirabies prophylaxis were found to have serum-neutralizing antibodies against rabies. (Antibodies against Mokola virus [genotype 3] and Lagos bat virus [genotype 2] also were found in 7.5% and 2.5% of these individuals.) The investigators suggested that these individuals had been infected, but the infection had been halted before the virus had entered nerves. An attenuated strain of rabies virus also has been suggested as the cause of such antibodies, but an as-yetunidentified virus of the Lyssa group, or even some other crossreacting infectious agent, could be responsible.150 Among 48 family members of Peruvians who died following rabid vampire bat bites in 1990, seven had antirabies antibody levels that ranged from 0.14 to 0.66 international units. These antibodies could not be related to exposure to bats, exposure to other animals, or to other epidemiologic events.6 Some animals, including dogs, have significant amounts of nonspecific virus-neutralizing antibodies in their sera. Up to 20% of raccoons in Virginia and Florida180,229 and 20% to 40% of mongooses on Grenada have antirabies antibodies, which may be evidence of nonfatal infections.82 Up to 80% of bats in crowded nurseries may have rabies antibodies.17 The only finding considered diagnostic of prior rabies infection is antibodies in cerebrospinal fluid.85,86 Even clinical rabies is not always fatal in animals. Pasteur observed that some dogs recovered from early symptoms of rabies and subsequently could not be infected by rabies virus injections.153 Recoveries from infections that produced paralysis have been described in two dogs;89 recovery from clinical rabies has also been described in mice, donkeys, bats,13 and pigs.16

UNDIAGNOSED RABIES Clearly, many rabies infections are not diagnosed in developing countries. The possibility that in industrialized countries a number of human rabies infections are not diagnosed and the true incidence of this infection is higher than reported is suggested by several considerations. The clinical manifestations usually are nonspecific, and many infections are diagnosed late in the course of their illness as the result of testing for any identifiable cause of encephalitis, or subsequently by autopsy examination of the central nervous system. Of the 38 human rabies infections in the United States in the 1960s and 1970s, 8 (21%) were diagnosed after death. Subsequently, the percentage of infections diagnosed postmortem has been higher.52,217 In recent years in the United States, most individuals with rabies have no recognized exposure to potentially infective animals, yet an account of animal exposure often is the only stimulus for laboratory identification of rabies as the cause of the encephalitis.52 The significance of undiagnosed human rabies is uncertain. When the diagnosis is made, members of the patient’s family and all health care personnel who have had a significant exposure to the patient are given postexposure immunoprophylaxis. However, human-to-human transmission of rabies has been reported only following tissue or organ transplantation, except in two individuals in Ethiopia.90

LABORATORY DIAGNOSIS OF RABIES Conventional laboratory procedures are not helpful in establishing a diagnosis of rabies. Cerebrospinal fluid protein and leukocyte counts may be modestly elevated, but these changes are nonspecific. Currently available techniques for a definitive laboratory diagnosis of rabies usually are nondiagnostic in the early days of infection and become useful only a week or more after the onset 1187

CHAPTER 60  Rabies

Experienced observers in Thailand have described hydrophobia as a violent, jerky contraction of the diaphragm and accessory muscles of inspiration that is triggered by attempts to swallow liquids and by other stimuli. Usually it is not associated with neck or throat pain or with laryngopharyngeal spasms. It has been likened to respiratory myoclonus (Leeuwenhoek’s disease). When patients lapse into coma, hydrophobia is typically converted into cluster breathing with long apneic periods.215 The variability of the clinical manifestations of rabies may result from heterogeneity in wild or “street” rabies viral populations (as contrasted with “fixed” viral strains maintained in laboratories), even in the viruses infecting a single animal. Rabies viruses isolated from a boy who died after being bitten by a fox and propagated by intracerebral inoculation of white mice produced three distinctly different forms of disease in the mice.102 The second clinical form of rabies, the paralytic, dumb, or Guillain-Barré–like form, is characterized by progressive paralysis without an initial furious phase. Even though the paralytic form of the disease does not appear to be as familiar to some health care providers, 20% to 30% of human rabies victims present in this manner.3,224 Other animals also have furious or dumb rabies presentations.148 Paralytic rabies is more common after rabid vampire bat bites, in persons injected with fixed virus strains, and in persons who have received postexposure vaccination.92 Distinction from Guillain-Barré syndrome may be difficult, although individuals with that disorder usually do not have urinary incontinence, which is common in rabies-infected persons.116 Individual case reports make clear that every patient is different. The most common misdiagnoses are psychiatric or laryngopharyngeal disorders.116 Physicians at QSMI, who have vast clinical experience, consider inspiratory spasms to be the most reliable clinical sign of rabies, particularly in comatose patients, regardless of whether the disease was initially furious or paralytic. Such respirations also have been described as rapid, irregular, or jerky, termed apneustic. In addition, most of the QSMI patients have myoedema, particularly in the region of the chest, deltoid muscles, and thighs.219,224 However, this phenomenon, a brief, unpropagated, localized muscle contraction that appears in response to percussion with a tendon hammer, has not been confirmed as an important sign of paralytic rabies.116 Because the signs and symptoms are so nonspecific and often are rather mild at onset, many patients with rabies are not hospitalized the first time they are seen by a physician. (Two patients who died in the United States, one between 1960 and 1980 [the year of death was not stated] and the second in 2008, were never hospitalized.32) When admitted, most patients have a fever, which may be mild, but commonly is above 39.4° C (103° F). Of the 38 individuals who died of rabies in the United States between 1960 and 1980, 24 (63%) had difficulty swallowing, but only onehalf of those had definite hydrophobia or aerophobia; 27 (72%) manifested excitement or agitation, 24 (63%) had paralysis or weakness, and 12 (32%) had hypersalivation. Dysesthesias at the exposure site were described by 19 (79%) of the 24 individuals who had an identifiable bite or similar exposure.3 Of the 28 patients diagnosed before death, 26 had a history of an animal exposure. Only four of eight patients diagnosed after death had this history. All 12 patients with hydrophobia were diagnosed before death.3 The duration of illness for patients not given supportive care averages 7.3 days and ranges from 2 to 23 days. For patients who are given supportive care, the average duration of illness is 25.3 days, with a range of 7 to 133 days.3,195 “The following [therapeutic] measures have … been tried in clinical rabies, but without any evidence of effectiveness: administration of vidarabine; multisite intradermal vaccination with cell-culture vaccine; administration of α-interferon and rabies immunoglobulin by intravenous as well as intrathecal routes; and administration of anti-thymocyte globulin, high doses of steroids, inosine pranobex, ribavirin and the antibody-binding fragment of immunoglobulin G.”219 In a recent review of the management of rabies in humans, a combination of some specific therapies was suggested. The authors point out that essentially no individuals with clinical rabies survive, and the best therapy often is palliative.117

PART 6  ANIMALS, INSECTS, AND ZOONOSES

of illness. The diagnosis of rabies should be confirmed as early as possible so that the number of persons exposed to the infection can be limited and therapy for those exposed can be initiated promptly. In industrialized nations, the number of persons exposed to a hospitalized rabies patient can number in the hundreds.163,200 If rabies is suspected, a complete set of samples should be collected for testing by all currently available diagnostic procedures. Consultation is available from the CDC 24 hours a day, seven days a week, and should be obtained (877-554-4625; http://www.cdc.gov/rabies/). However, samples taken antemortem cannot definitively rule out rabies. If infection is seriously suspected, repeated sampling is needed.200 Samples can be transported overnight to the CDC or to state laboratories. The rabies virus is systemically disseminated shortly after central nervous system infection and often can be detected with labeled antibodies or by RNA extraction. Currently, detection of rabies RNA in saliva after RT-PCR amplification appears to be the most reliable procedure. Saliva should be collected with a sterile eyedropper or pipette and placed in a small sterile container that can be sealed securely. No preservative or other material should be added. Tracheal aspirates and sputum are not suitable for diagnostic testing. A 5- or 6-mm punch biopsy of hair-bearing skin with at least 10 hair follicles from the nape of the neck is commonly used for immunohistochemical staining for rabies virus. The specimen should be placed on sterile gauze, moistened with sterile water or saline, and placed in a sealed container with no other fixative or preservative. At least 0.5 mL of serum (not whole blood) is needed to test for antibodies by immunofluorescence and virus neutralization. If no vaccine or rabies immune serum has been administered, the presence of antibodies is diagnostic and testing for CSF antibodies is not needed. At least a similar volume of CSF is needed for antibody studies. Rabies virus can sometimes be found in imprints from the cornea, although this procedure is uncommonly used now. An ophthalmologist should prepare the smears after consultation with the rabies testing laboratory to avoid damaging the cornea. RT-PCR with nucleotide analysis and immunostaining are used to identify the viral antigens. Brain biopsies should not be routinely performed because human rabies is so rare in industrialized countries and no effective treatment is available. If a biopsy is performed to rule out another condition, it can also be examined for rabies.200 Rabies virus often can be isolated from body fluids, particularly saliva and cerebrospinal fluid. The murine neuroblastoma cells used for isolation of rabies are more susceptible to that virus than any other cell line tested, and culture on such cells can usually provide a diagnosis within 24 hours. Mouse inoculation may take 15 to 30 days, although the time can be shortened by sacrificing mice starting 5 days after inoculation and examining the brains with fluorescent antibodies.195,219 In industrialized nations, facilities for such studies can be found in local, state, and national public health laboratories. In developing countries, they often are unavailable.

RABIES IN ATTACKING ANIMALS Before 1903, the diagnosis of rabies in attacking animals was based entirely on the clinical features of the disease or on the presence of unusual material in the stomach of an animal that evidenced bizarre behavior. The dog that attacked Joseph Meister, the first recipient of Pasteur’s antirabies vaccine, was diagnosed as rabid because it had hay, straw, and wood in its stomach.8 In that year, Negri and Bosch described the typical neuronal cytoplasmic inclusions, and for many years the laboratory diagnosis of rabies in animals depended on the detection of such bodies. However, only 60% to 80% of infected animals have identifiable inclusions.199 Typical inclusion bodies are scarce in Arctic foxes, for instance.75 Immunofluorescent detection of rabies antigen in smears of cerebral tissues, which was introduced in 1958 and became widely used in the early 1960s,99 is far more reliable in experienced hands (Figure 60-9). Comprehensive analyses of the 1188

FIGURE 60-9  Fluorescence-labeled, rabies-specific antibody staining of a smear from the brain of a rabid Canadian fox. (×400.) (Courtesy Centers for Disease Control and Prevention.)

performance on survey examinations established that in major U.S. public health laboratories, the sensitivity of fluorescent antibody examination is nearly 100%. Fluorescent antibodies are used to identify rabies antigen in tissue culture (see later) because the rabies virus produces few cytopathogenic changes. The major shortcoming of the procedure is its reduced sensitivity for rabies antigen in decomposed brain tissue. Some investigators have concluded that failure to identify rabies antigen with fluorescent antibodies in partially decomposed brain tissue cannot justify withholding postexposure therapy for exposed individuals.199 A procedure to confirm negative diagnoses is essential. Rabies diagnosis by intracerebral mouse inoculation was introduced in 1935 and demonstrated that only 85% to 95% of rabies infections could be identified by examination for inclusion bodies alone.193 Eventually, most laboratories, even those in developing countries, adopted adult or suckling mouse inoculation. Tissue-culture inoculation began with inoculation of chick embryo cells in 1942.195 Currently, tissue-culture isolation on mouse neuroblastoma cells is used, is far faster, and is also the most sensitive technique for confirming negative immunofluorescence examination results, at least in laboratories with suitable facilities and appropriate personnel.36,174,195 The rabies virus does not produce cytopathic changes in tissue culture, and fluorescent labeled antibodies must be used to diagnose the infection.

Postexposure Rabies Therapy Postexposure treatment for humans consists of reducing the viral inoculum by cleansing the wound as thoroughly as possible, administering antiserum to help control viral reduplication and spread (passive immunization), and administering rabies vaccine to establish immunity to the virus before signs of infection appear (active immunization). “Rabies vaccination is a race between the active immunity induced by vaccination and the natural course of infection.”208

IDENTIFYING EXPOSURE Exposure to rabies is divided into bite and nonbite categories. A bite is considered a significant exposure if it penetrates the skin. Scratches that break the skin are also considered significant exposures because the claws could be contaminated by saliva. Unprovoked attacks are more likely to have been inflicted by a rabid animal than are provoked attacks, but determining whether a dog or cat bite has been provoked is frequently difficult. Bites that occur while feeding or handling apparently healthy animals are generally regarded as unprovoked, but some animals, particularly dogs, may bite anyone walking by or riding a bicycle. Nonbite exposure consists of contamination of cutaneous wounds—including scratches, abrasions, and weeping skin rashes—with saliva, cerebrospinal fluid, or brain tissue from a rabid animal. If the material is dry, it is considered noninfectious.37 Contamination with urine from a rabid animal or person is not considered an exposure, even though rabies viruses have been isolated from kidneys and urine. A laboratory technician cut by a broken specimen container was given postexposure therapy.68

immediately, except when the exposure has occurred in a part of the continental United States known to be free of rabies and the results of immunofluorescent testing are to be available within 48 hours. If the animal is captured, it should be killed and its head shipped to a qualified laboratory immediately. The signs of rabies in wild animals, including wolf hybrids, are not consistent enough or sufficiently well known for a 10-day observation period to reliably determine whether the animal was rabid.56 Small rodents (squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, and mice) and rabbits are rarely found to be infected with rabies and have not been known to produce rabies in humans. ACIP recommends that local health officials be consulted following a bite by a rodent or rabbit.56

INITIAL WOUND MANAGEMENT Immediate and thorough cleansing of bite wounds with soapy water to reduce the viral inoculum is an essential and highly effective component of postexposure therapy. Fishbein, former Chief of the Viral and Rickettsial Zoonoses Branch of the CDC, has stated, “Local treatment is perhaps the single most effective means of preventing rabies.” He also has said, “In some groups exposed to a single rabid animal and many laboratory investigations, local wound care alone has been found to be as or more important than vaccine alone.”92 Vodopija has declared, “Washing the wound with soap and water or with other substances that are lethal to rabies virus may be crucial for survival, irrespective of subsequent immunization.”210 Fangtao, who has had extensive experience with rabies in China, asserts, “The protective effect of each (wound care, immune globulin, and vaccine) should be considered equivalent.”83 Neglect of the wound or inadequate wound care has resulted in rabies in individuals who received ideal immunotherapy.24,56 Many experimental studies have shown that the duration of the incubation period following rabies exposure is inversely proportional to the size of the viral inoculum—a large inoculum produces generalized infection in a much shorter time than does a small inoculum.67 If rabies vaccine is to induce immunity before infection appears, it must have sufficient time. Following a severe rabies exposure, such as a bite about the head or neck, or multiple bites, a major reduction in the number of virus organisms introduced may be essential to allow time for immunization. In experimental studies, the best results have been obtained by thoroughly cleaning the wound with soap and water and then irrigating it with a virucidal agent such as povidone–iodine or a 1% solution of benzalkonium chloride (Zephiran). Soap neutralizes benzalkonium chloride and must be completely rinsed from the wound before it is irrigated with the detergent. With deep wounds, only virucidal substances, such as benzalkonium chloride or povidone–iodine, have been found to be effective. If neither of these agents is available, 70% alcohol (ethanol) or iodine, either tincture or aqueous solution, can be instilled in the wound. The best cleansing agent that can be obtained immediately must be used.37,219 If these measures are painful, which is often the case when they are carried out with appropriate vigor, the area can be anesthetized with a local anesthetic. This vital procedure is often neglected, particularly in developing countries. In a study of 250 patients with rabies seen at the Sassoon Hospital in Pune, India (the eighth-largest city in India with a population over 3.5 million), the wound had been washed with soap and water for only nine patients.184 Appropriate measures to prevent bacterial infection, including antibiotics if indicated, and tetanus prophylaxis should also be instituted.37,173 The WHO Expert Committee and others recommend that bites not be sutured.37,43,56,219

RABIES IMMUNE GLOBULIN Although proposed and investigated by Babes and colleagues over a century ago,9 the benefit of hyperimmune serum immediately after rabies exposure was established only about 55 years ago. The most dramatic study was initiated by Koprowski and carried out in Iran in 1954. Twenty-nine persons were bitten by a single rabid wolf. Thirteen individuals with bites about the head 1189

CHAPTER 60  Rabies

It is important to note that the rabies virus passes through intact mucous membranes, and that any mucous membrane contact, particularly membranes of the oral cavity or conjunctiva, with saliva or other infectious material from a possibly rabid animal is considered an exposure. Exposure of medical personnel or family members caring for patients with rabies is a significant problem. High-risk contact is defined as a percutaneous (through needlestick or open wound) or mucous membrane contact with saliva, cerebrospinal fluid, or brain tissue. Such contact is considered essentially the same as bite and nonbite exposures to rabid animals. Individuals who have had a high-risk contact should receive postexposure immunoprophylaxis. However, routine infection isolation procedures, including respiratory precautions, minimize the risk for medical personnel caring for patients with rabies.37 Individuals who have not had a high-risk contact do not need postexposure immunoprophylaxis, although such treatment is sometimes administered to allay anxiety. In areas where canine rabies is not enzootic, which includes all of the United States except for the area along the border with Mexico (particularly southern Texas), a healthy domestic dog or cat that bites a person should be confined and observed for 10 days, particularly if the animal has been previously vaccinated. A veterinarian should evaluate any illness during confinement. If rabies is suspected, the animal should be humanely killed and its head should be shipped to a qualified laboratory.56 The head must be refrigerated during shipping. Examinations for rabies cannot be reliably performed on decomposed brain tissues.200 Such confinement and observation were judged safe for exposures to ferrets in 1998. Scientific evidence that the same quarantine period would be adequate for wolf hybrids does not exist, because studies of pathogenesis and virus shedding have not been performed. Hybrids that bite humans should be euthanized immediately, and their heads should be shipped to reliable laboratories.148 The significance of the laboratory’s qualifications was emphasized by the death from rabies of a U.S. citizen in 1981 after he was bitten by a dog in Mexico. The dog’s head was shipped to a Mexican laboratory, where it was examined with Sellers’ stain instead of a fluorescent antibody technique. Because no evidence of rabies was found with this less-sensitive technique, he was not given postexposure therapy.152 In a Thai investigation, 13 of 404 rabid animals diagnosed with fluorescent antibodies did not have Negri bodies identifiable with Sellers’ stain.187 Any stray or unwanted animal should be killed immediately and its head submitted for rabies examination. Euthanasia does not have to be delayed for further development of the infection in an attacking animal for a reliable diagnosis to be made.200 No one in the United States has died of rabies when the attacking dog or cat has been healthy after 10 days of observation.189 However, dogs injected with an Ethiopian strain of rabies virus excreted virus in the saliva up to 13 days before signs of disease were observed,88 and dogs that have recovered from experimental rabies excrete virus in saliva for as long as 6 months after recovery.91 If an attacking dog or cat is rabid or is suspected to be rabid, postexposure therapy should be initiated at once. However, a reliable determination of the presence or absence of rabies in animals can usually be completed in less than 1 day.200 If the dog or cat escapes and is not suspected to be rabid, the Advisory Committee on Immunization Practices (ACIP) of the U.S. Department of Health and Human Services recommends that local public health officials be consulted.56 In a study of postexposure therapy practices in the emergency departments of a number of university hospitals from all parts of the United States, the most frequent inappropriate administration of therapy was for animals that could be observed for 10 days. The most common failure to administer postexposure therapy was for animals that could not be observed. The investigators emphasized that physicians often failed to use the expert consultative services available 24 hours a day from their local health departments or the CDC.141 In the United States, any exposure to a skunk, raccoon, bat, fox, or other carnivore, including bears and cougars, should be considered a rabies exposure. Treatment should be initiated

PART 6  ANIMALS, INSECTS, AND ZOONOSES

were treated with antiserum and neurally derived vaccine; only one died. Five individuals with similar bites received vaccine alone; three died.19,20,22 Similar results were demonstrated in China with a much more effective cell-culture vaccine by Lin and associates, who suggested that immune serum might be effective because it stops virus from entering susceptible cells (nerves).84 The need for immune serum with human diploid cell vaccine (HDCV) has been demonstrated by the death from rabies in a 29-year-old female U.S. citizen in Rwanda who received prompt therapy with HDCV but not with hyperimmune serum.77 Measurements of the antibody response to earlier rabies vaccines demonstrated that immune serum reacted with the vaccine and limited the antibody response in the first 7 to 10 days of administration. These data were considered evidence of passive immunity that was essential for early control of the rabies virus, particularly when the viral inoculum was large and the incubation period before the development of clinical rabies was likely to be short.19 However, with contemporary cell-culture vaccines that have a concentration of 2.5 international units/mL, such inhibition of the serum-neutralizing antibody response is not seen.210 The only rabies immune globulin licensed for use in the United States is human rabies immune globulin (HRIG), which is prepared by cold ethanol fractionation from plasma from hyperimmunized human donors and is virtually free of significant side effects.225 In developing countries, immune serum is rarely administered because it is expensive or is unavailable. Only about one-third of the immune serum required for rabies postexposure therapy is being produced. Travelers who have received postexposure therapy usually are not given immune serum unless they know enough about rabies postexposure prophylaxis to demand its administration. When immune serum is given, it is usually of equine origin, which costs only about 10% as much as does HRIG.223 However, contemporary highly purified equine rabies immune globulin (ERIG) is not associated with the 15% to 46% incidence of serum sickness typical of older equine antirabies serum.43 In 3575 individuals treated at the QSMI, ERIG from Pasteur Vaccins of France, Sclavo of Italy, and the Swiss Serum and Vaccine Institute produced allergic reactions in 0.87%, 3.58%, and 6.19% of the recipients, respectively. The reactions were uniformly mild and lasted less than a week with appropriate therapy. Only 9 of the 66 patients with reactions required steroid therapy; the remainder were satisfactorily treated with analgesics and antihistamines. ERIG is also produced in developing countries, but the purification procedures and potency criteria have not been published, and these products may be associated with a higher incidence of adverse reactions. At QSMI, an initial intradermal injection of horse serum is administered, and individuals who present with sensitivity are treated with HRIG. One 17-year-old male did not react to the intradermal injection, but with subsequent injections he had an anaphylactic reaction that was successfully treated with epinephrine, hydrocortisone, and chlorpheniramine.223,225 Equine F(ab′)2 fragment rabies immunoglobulin is also used. In a study of 7660 patients in the Philippines, of 151 patients with laboratory-confirmed exposure, two died of rabies: a 4-yearold girl who had multiple deep lacerations on the nape, neck, and shoulders, and an 8-year-old boy who only received postexposure prophylaxis on the day of exposure. Local adverse reactions were documented in 35 individuals (0.46%); systemic adverse reactions were documented in 104 individuals (1.36%). Only two subjects had documented local adverse reactions within 30 minutes of immunization, and 11 individuals with systemic adverse reactions were documented to be having possible allergic reactions.162 The dose of immune globulin is 20 international units/kg for HRIG or 40 international units/kg for ERIG. Larger-thanrecommended doses should not be administered because the immune globulin neutralizes vaccine given simultaneously. Immune globulin should be administered as soon after exposure as possible but is clearly beneficial when administered within 7 days. In view of the long incubation period for some human 1190

rabies infections, immune globulin administration may be advisable regardless of the interval following exposure. Currently, all agencies recommend injection of as much immune globulin as possible around the bite site.219,225 For bites on the fingers and similar locations where only a limited amount of globulin can be injected locally, the remainder should be injected intramuscularly.37 For individuals with multiple bites, which is common with rabid dog attacks in developing countries, the immune globulin may have to be diluted with saline to achieve uniform injections. The syringe used to inject immune globulin must not be used to inject vaccine, which would be inactivated by residual antiserum.

RABIES VACCINES Louis Pasteur revolutionized rabies therapy—and all of medicine— on July 7, 1885, when he began administering rabies vaccine to Joseph Meister, a 9-year-old boy who had been bitten 14 times by a dog that was killed and diagnosed as rabid because its stomach contained hay, straw, and fragments of wood.209,211 Although the rabies diagnosis in this animal may be suspect, and the boy may not have developed a clinical infection, Pasteur in 1886 observed only a single failure in a series of 688 treatments, many of whom must have been exposed to rabid animals and would have been expected to die without therapy.7 Meister’s only employment as an adult was as a security guard for the Pasteur Institute.193 Pasteur’s first rabies vaccine was produced from rabid rabbit spinal cords that were allowed to dry to attenuate the virus. After 15 days, the cords were noninfectious, so the first injections were made with 14-day-old spinal cords, and subsequent injections were made with cords that had been dried for shorter times.197,208 Roux and Callmette demonstrated that desiccated rabbit spinal cords retained appropriate virulence when preserved in glycerin, which greatly facilitated the production and storage of such vaccine.44,171 Although other vaccines were soon developed, the Pasteur rabbit spinal cord vaccine was administered at the Pasteur Institute of Paris as recently as 1953.208 Subsequently, similar vaccines have been prepared in brain tissues from various animals, particularly goats and sheep, containing virus killed with formaldehyde, phenol, or βpropiolactone.108,197 These preparations are collectively known as Semple or neural tissue vaccines, and Semple’s introduction of such vaccines in 1911 was a significant advance. In 1955, Fuenzalida and Palacios in Chile introduced the use of suckling mice less than 3 days old for the preparation of neurally derived vaccines. Such animals have little cerebral myelin and are thought to yield a product that contains less myelin basic protein. Currently, animals no older than 1 day are used. In Thailand, this vaccine has been found to be as poorly immunogenic and to be associated with as many side effects as are other similar vaccines,95,219,224 but other investigators have found the incidence of neural reactions to be lower.209 At the present time, neural tissue vaccines are still employed for a large percentage of all postexposure rabies therapy worldwide because they are inexpensive. Of 50 million doses of rabies vaccine administered worldwide each year, 20 million are still neural tissue vaccines.39 Such animal brain vaccines have been described as the crudest biologic material administered to man. These vaccines have low immunogenicity, and as many as fifteen 5-mL injections of a 5% to 10% suspension of brain tissue are required to produce satisfactory antibody titers. Intense local reactions are common, and many patients abscond from treatment.39 In Taiwan between 1952 and 1955, 55% of individuals who began rabies vaccination failed to complete treatment.214 In one study, 20 of 681 persons bitten by dogs proved to be rabid refused therapy because they had witnessed the side effects of vaccination in other villagers. Nine (45%) died of clinically diagnosed rabies. Another 62 persons received Semple vaccine, even though the dogs to which they were exposed were not rabid, presumably because the results of testing the dogs were not accepted as valid.187 The potency of these vaccines is highly variable. Some batches are known to have been ineffective. After 15 years of observations, the Pasteur Institute of Iran, a branch of the Pasteur Institute in Paris and a WHO Collaborating Center for Reference and

Because so many problems were associated with Semple vaccines, a safer vaccine was developed with viruses grown in duck embryos. This vaccine was not as immunogenic as contemporary vaccines, and 14 to 23 injections were required to produce satisfactory antibody titers. In addition, this vaccine also had a significant incidence of adverse side effects. Reactions to duck embryo vaccine in one retrospective analysis of 424,000 persons consisted of 22 cases of anaphylaxis, 4 cases of transverse myelitis, 5 cases of cranial neuropathy, 2 cases of nonfatal encephalopathy, and 2 cases of fatal encephalopathy that may actually have been fatal rabies infections.172 Immunization with vaccine grown on duck embryos has failed to prevent rabies, but for many of the failures a prolonged interval separated the exposure and immunoprophylaxis.2

HUMAN VACCINATION Postexposure prevention of human rabies by immunization is unique in the therapy of infectious diseases and is possible only because the moment of exposure can be vividly remembered and the incubation period is relatively long. For 30 years, the recommended procedure for producing active immunity in the United States has consisted of five vaccine injections into the deltoid muscle of 1.0 mL of vaccine on days 0, 3, 7, 14, and 28 after animal exposure. This schedule is known as the “Essen scheme” in recognition of the contributions of Ernst Kuwert of the Essen Institute of Medical Virology and Immunology.209 Immunoprophylaxis is most effective when begun within 24 hours of exposure, but the average delay following animal exposure in the United States and in Nepal has been 5 days.185 Since the incubation period for rabies may be prolonged, no upper limit can be set for the time after a potential rabies exposure at which postexposure vaccine therapy should be given.24,219 In 2010, a number of investigators and the ACIP, after a review of rabies virus pathogenesis, experimental animal models, human immunogenicity studies, prophylaxis effectiveness in humans, documented failures of prophylaxis in humans, and vaccine safety, recommended that postexposure vaccination be reduced to four injections given on days 0, 3, 7, and 14.65 A detailed review of the evidence supporting a 4-dose schedule for human PEP had been previously published.176 The recommendations for wound irrigation and passive immunization with immune globulin remain unchanged. Three vaccine injections are still recommended for preexposure vaccination, and two injections are needed after a rabies exposure for previously immunized individuals. Immunocompromised individuals should still receive five injections and should be tested

TABLE 60-5  Babes’ 1912 Estimates of Mortality Among Unvaccinated Persons Exposed to Animals Assumed to

be Rabid

Attacking Animal

Location of Exposure

Type of Exposure

Wolf Cat Dog Dog or cat Wolf Wolf Cat Dog Wolf or cat Dog Wolf Wolf, cat, or Wolf, cat, or Wolf Wolf, cat, or Wolf, cat, or Wolf, cat, or Wolf, cat, or Wolf, cat, or

Face Face Face Other part of head Neck or arm Face Face Face Fingers or hand Fingers or hand Trunk or legs Face Hands Face Trunk or legs Hands or exposed skin Clothing covered skin Recent wounds in contact with saliva Wounds older than 24 hours in contact with saliva

Bites, multiple, severe Bites, multiple, severe Bites, multiple, severe Bites, multiple, severe Bites, multiple, severe Bite, single Bite, single Bite, single Bites, severe Bites, severe Bites, severe Bites, superficial Bites, superficial Scratches Bites, severe, through clothes Bleeding superficial wound Bleeding superficial wound — —

dog dog dog dog dog dog dog

Likelihood of Mortality (%) 80-100 70 60 50 40 40 40 30 20 15 15 10 5 5 3 2 0.5 0.1 0.0

Babes V: Traité de la rage. Paris: Bailliere et Fils, 81, 1912 cited by Baer.11

1191

CHAPTER 60  Rabies

Research in Rabies, concluded that rabies vaccines prepared in animal brains were totally ineffectual for preventing rabies in individuals bitten about the head or neck who would be expected to develop encephalitis within a short time after exposure.21 Pasteur observed that his treatment was not always successful, particularly after bites around the face.193 In Bangkok, 11% of a group of patients who died of rabies encephalitis had received complete courses of the vaccine starting soon after they were bitten.207 The vaccine appears to be beneficial for less severe exposures.206 Since the time of Pasteur, the failure of immunoprophy­ lactically treated persons to develop clinical rabies has been attributed to the vaccine, and some of these individuals produced antirabies antibodies. However, many, perhaps most, individuals attacked by rabid animals do not develop clinical rabies. In fact, humans are considered to have a low susceptibility to rabies.85 Citing the 1912 studies of Babes, which now could not be repeated, Baer has emphasized that only about 15% of individuals bitten by rabid dogs and not vaccinated develop rabies10,177 (Table 60-5). The absence of rabies infection in many individuals treated with Semple vaccine undoubtedly is a reflection of failure to transmit the infection by attacking animals and not of vaccine effectiveness. The neuroparalytic reactions associated with Semple rabies vaccines are the most serious neurologic complications that follow any vaccination109 and were reported only 4 years after Pasteur introduced his vaccine.21 Remlinger reported 26 cases between 1888 and 1905.164 Even dogs vaccinated with this product developed anorexia, as well as “depression, nervous symptoms, a morbid desire to bite,” or even paresis of the hind limbs.41 Of the patients receiving such vaccines, 15% develop electroencephalographic abnormalities, and 5% develop measurable antibodies against brain tissue. About one-fourth of the severe neurologic reactions are fatal, and an additional one-third cause permanent damage.14,19,147 An incidence of neuroparalytic reactions of approximately 1 in 1200 patients seems to be generally accepted, but much higher rates of 1 : 400, 1 : 220,95 1 : 142,187 or even ten times higher at 1 : 120 have been reported.196 Probably the most accurate evaluation of the frequency of such complications is that the incidence is not known. The countries that have a high incidence of rabies, which are the countries that use neural-derived vaccines for postexposure therapy, also have very poor or no programs for reporting complications.197 Recently, the specter of transmission to humans of spongiform encephalopathies caused by prions from infected sheep by neural tissue vaccines derived from sheep brains has been raised.39

PART 6  ANIMALS, INSECTS, AND ZOONOSES

afterward to determine whether they have developed a protective antibody response. The report warned that manufacturers of the vaccine do not plan to change the recommendation in the package insert. An alternative treatment schedule, termed the 2-1-1 regimen, was first developed in Yugoslavia. On day 0, two 1-mL doses of vaccine are injected into the left and right deltoid muscles. Additional 1-mL injections are given on days 7 and 21. This schedule was originally intended for use only after severe exposures when the incubation period could be expected to be short. However, in a number of countries it is used routinely because it produces antibody levels just as high as does the Essen scheme and only three clinic visits are required.210 The only rabies vaccines licensed for use in the United States are prepared from viruses grown in cell cultures and inactivated with β-propiolactone. HDCV, the first to be licensed and the gold standard against which other vaccines are compared, was made possible by the development of the WI 38 cell line of diploid human fibroblasts by Hayflick and Moorhead and by adaptation of the Pitman-Moore strain of rabies virus to growth in such cells by Wiktor, Plotkin, and Koprowski at the Wistar Institute in Philadelphia.193,209 The virus used to prepare this vaccine was originally isolated in 1882 by Pasteur from a cow bitten by a rabid dog and was maintained by serial passage in rabbit brain before it was adapted to cell culture.178,209 The HDCV available in the United States is produced in cultures of human diploid cells by Sanofi Pasteur. This vaccine was introduced in December 1974 and was licensed for general use in the United States on June 9, 1980.63 A single-dose vial containing lyophilized vaccine that is reconstituted in the vial to a final volume of 1.0 mL, Imovax Rabies is licensed for postexposure and pre­ exposure intramuscular vaccination. The unreconstituted vial must be refrigerated; it cannot be carried into remote areas in first-aid kits. Because HDCV is expensive and cannot be produced in sufficient quantities to supply worldwide demands, a number of cell-culture vaccines have been developed. These vaccines, when produced according to accepted standards, are all considered equally effective.37 These vaccines are far more immunogenic than are earlier products, and protective antibody levels are routinely achieved with only four or five injections.56,208 A protective level is defined as either an antibody concentration that will completely neutralize rabies viruses at a dilution of 1 : 5 as determined by the rapid fluorescent focus inhibition test, or 0.5 international units/mL. These vaccines are so effective that measurement of postvaccination antibody levels is recommended only for individuals who are immunodeficient as the result of disease or therapy. The effectiveness of HDCV was dramatically demonstrated during 1975 and 1976 in Iran by complete prevention of rabies in 45 persons attacked by dogs or wolves subsequently proved to be rabid.19 Between 1980 and 1982, all 511 individuals bitten by rabid animals in the United States and treated with five doses of HDCV—and with HRIG—survived. In the United States, two other cell-cultured vaccines have been licensed. Rabies Vaccine Absorbed (RVA) was prepared from viruses grown on fetal rhesus lung diploid cell cultures, concentrated by adsorption to aluminum phosphate, and produced in a liquid form. RVA was licensed on March 19, 1988. It has been used to vaccinate humans allergic to HDCV but has been unavailable for a number of years.179 At least in part because the raccoon rabies epizootic had increased consumption of rabies vaccine so dramatically, the Food and Drug Administration (FDA) licensed purified chick embryo vaccine (PCEV) in October 1997. This vaccine (RabAvert) has been widely used worldwide. It is thought to produce fewer allergic reactions because it does not contain human albumin altered by β-propiolactone. All three preparations are considered equally efficacious and safe for postexposure therapy and preexposure intramuscular vaccination.56 WHO has approved HDCV and PCEV, as well as purified Vero-cell rabies vaccine (PVRV or Verorab), which is widely used in developing countries. This vaccine is produced in continuous culture and is less expensive to produce, but has not been licensed for use in the United States or Canada.220,222 1192

In its 1992 Eighth Report, the WHO Expert Committee on Rabies made the remarkable statement, “Prompt and thorough cleansing of the wound, and administration of purified equine or human rabies immunoglobulins and cell-culture rabies vaccine immediately after exposure virtually guarantee complete protection. … Pregnancy and infancy are never contraindications to post-exposure rabies vaccination.”219 Although some antigens, particularly surface glycoprotein antigens, vary widely in different viral strains, standard vaccines have provided effective protection against all wild, or “street,” rabies viruses. These vaccines also appear to be effective against other lyssaviruses, except Mokola and Lagos bat virus, although no alternative vaccines are available.217,219 Occasional failures with cell-culture vaccines have been reported, but in essentially every instance, treatment has not been administered correctly. Many of the individuals did not receive immune globulin.37,147,219 Some have had the vaccine injected into gluteal muscles, which is thought to be the cause of these failures.14,37,55,56,109 Hepatitis B vaccine gluteal injections have been found to be less consistently effective than injections in the deltoid.14 All injections of rabies vaccine must be made in the deltoid muscle, or in the quadriceps muscle for small children. Approximately 18,000 persons receive preexposure vaccination and an additional 23,000 receive postexposure immunoprophylaxis each year in the United States, but reactions of any type are very uncommon.30 Reactions following HDCV administration during the first 46 months of use (and reported to the CDC) occurred in 108 individuals, a rate of 11 per 10,000 vaccinees. Few patients required hospitalization, and no fatal reactions were reported. Of these reactions, nine (1/10,000) were immediate hypersensitivity reactions that occurred within minutes to hours after injection and were characterized by bronchospasm, laryngeal edema, and generalized pruritic rash, urticaria, or angioedema. All nine reactions followed postexposure immunization of unvaccinated persons or preexposure vaccination. Eighty-seven delayed reactions appeared 2 to 21 days after injection and were characterized by a generalized pruritic rash or urticaria. Some of the individuals also had arthralgias, arthritis, angioedema, nausea, vomiting, fever, and malaise. Twelve reactions were classified as indeterminate. Unlike the immediate reactions, 81 (93%) of the delayed reactions followed booster injections for individuals who had been vaccinated previously. Most patients improved in 2 to 3 days when treated with antihistamines, but a few required systemic corticosteroids and epinephrine.63 The reactions are attributed to β-propiolactone–altered albumen in the vaccine.170 HDCV vaccine that is free of β-propiolactone was developed by Connaught Laboratories but was not licensed in the United States.27 PCEV and RVA are not made with albumin. Further rabies booster immunizations are not recommended for individuals who have had this type of reaction, but exposure to rabies should be treated in the usual manner.63 Neurologic reactions following HDCV administration have been extremely rare. After millions of vaccinations worldwide, three Guillain-Barré type paralytic reactions have been described, and all three individuals recovered. Other neurologic disorders have occurred at the time of vaccination, but a definite causal relationship has not been established.27,170

IMMUNOCOMPROMISED INDIVIDUALS Immunosuppression as the result of therapy such as corticosteroids, chemotherapy, antimalarials, or other agents, or as the result of illness, particularly human immunodeficiency virus (HIV) infection, may interfere with the immune response to vaccines. If the condition is transient, preexposure vaccination can be postponed until therapy has been completed. If delaying therapy is not feasible, a rabies antibody titer should be obtained after vaccination has been completed even though such determinations are not needed for individuals who are not immunocompromised. If antibody levels are not high enough to be protective, ACIP recommends that individuals who do not seroconvert should be managed in consultation with their physician and appropriate public health officials.137 Immunocompromised

Preexposure Vaccination Preexposure vaccination can be achieved with three deltoid or quadriceps intramuscular injections of 1.0 mL of cell culture vaccine on days 0, 7, and 21 or 28. Preexposure vaccination with 0.1 mL of HDCV injected intradermally on the same schedule was approved by the FDA in April 1987. However, intradermal vaccination does not result in antibody levels as high as those produced by intramuscular injections, and antibodies do not last as long. Some investigators have recommended that only intramuscular injections should be administered.39 In the United States, the question is moot because the raccoon epizootic on the East Coast has increased vaccine utilization so much that syringes with 0.1 mL of the vaccine are not being produced. After a rabid animal bite, previously vaccinated individuals need only intramuscular injections of 1.0 mL of cell-culture vaccine on days 0 and 3. Immune serum is not needed, a major consideration for travelers in developing countries where immune serum may not be available. The additional two injections are essential. Fatal rabies encephalitis developed in a 23-year-old female Peace Corps Volunteer in Kenya who had previously been vaccinated for rabies, but did not report a bite by a pet puppy too young to have been vaccinated and did not receive postexposure therapy.151 Chloroquine interferes with the response to rabies vaccine; vaccination should be completed before malarial chemoprophylaxis with chloroquine is begun. Whether other agents used for malarial chemoprophylaxis interfere with the response to rabies vaccine has not been ascertained.39 ACIP divides individuals for whom preexposure vaccination is recommended into three groups. Group one consists of workers in rabies laboratories and others who may unknowingly be exposed to rabies, for whom vaccination followed by evaluation of antibody titers every 6 months is advised. Boosters are needed if antibody concentrations fall below a titer of ≥1 : 5 by the rapid fluorescent focus inhibition test, or ≥0.5 international units/mL. Group two includes spelunkers, veterinarians in areas where rabies is endemic, animal control workers, and fish and game wardens, for whom vaccination followed by serologic testing or a booster every 2 years is recommended. Group three consists of veterinarians and animal control workers in areas of low rabies endemicity, travelers to foreign rabies-epizootic areas who are staying 30 days or more, and veterinary students, for whom vaccination but no subsequent serologic testing or boosters is advised. Vaccination is not recommended for the United States population at large.56

In 1990, investigators at the CIWEC Clinic in Nepal found the incidence of animal exposure requiring immunoprophylaxis in travelers to be quite low, approximately 1 in 123,000 days (337 years). They disagreed with the recommendation that travelers to foreign rabies epizootic areas staying 30 days or more be vaccinated, because the cost of immunization is high and because the incidence of allergic reactions to booster immunizations is significant.185 However, investigators from the QSMI in Bangkok subsequently surveyed 1882 departing English-speaking travelers in the Bangkok air terminal and determined that 1.2% had been bitten by a dog and 8.7% had been licked by a dog during their stay. These investigators recommended that all travelers be routinely vaccinated for rabies and that the vaccine be inoculated intramuscularly. The CIWEC Clinic now recommends that most travelers to Nepal be preimmunized.158 In a review of immunizations for travelers published in the New England Journal of Medicine, the authors state, “Optimal postexposure prophylaxis against rabies (including rabies immune globulin and tissue-culture–derived vaccines) is often unavailable in many developing countries. Vaccination against rabies before travel should be considered for long-term travelers to the developing world, those who will have unavoidable direct contact with animals, those who may be unable to receive timely postexposure prophylaxis, and those (such as young children) who may be unable to report possible exposure.”182 (emphasis added ) Several of the recent American victims of rabies acquired outside the United States, and the only genotype 1 rabies victims in Australia, were children who, perhaps in fear of punishment, did not tell their parents about bites they had received. The problem of protecting children, who run the highest risk for animal bites, may not be widely recognized.170 Children who cannot understand the hazard of rabies in developing countries probably should be routinely vaccinated; they must also be closely observed so that postexposure booster vaccination can be administered. The effectiveness of preexposure vaccination is documented by the fact that no one residing in the United States who has received preexposure vaccination with a modern cell-culture vaccine has contracted rabies.37 In June 2007, Sanofi Pasteur began renovating its rabies vaccine production facility in France to maintain compliance with the requirements of the U.S. FDA and the French regulatory body, Agence Française de Sécurité Sanitaire des Produits de Santé (AFSSAPS). The company had accumulated a store of rabies vaccine that it thought would last through the renovation, but estimates of demand proved low. As a result, vaccine for preexposure vaccination became unavailable. In 2008 the shortage of vaccine was one of the considerations leading to changing the recommendations for postexposure therapy to four doses instead of five. Renovations are now complete and the facility is operational. Limits on vaccine for preexposure vaccination were lifted in August 2009.

Rabies Therapy in Developing Countries Rabies therapy in developing countries must be modified by financial considerations. The cost for such therapy for a typical laborer could be devastating.187 At least four different measures have been taken to reduce the costs of postexposure rabies therapy and increase the availability of reliable cell-culture vaccines. The simplest has been the transfer of cell-culture vaccine manufacturing technology to developing countries, but in spite of support by WHO and other agencies, progress has been slow. Local manufacturers in Latin America and Asia are producing Vero-cell rabies vaccine “copies” and primary hamster kidney cell rabies vaccines. Because some of these vaccines do not adhere to the strict standards imposed by the FDA or the European Pharmacopeia, they are less expensive to produce. The substitution of ERIG for HRIG, which results in a 90% cost savings, already has been discussed. A third approach has been the use of small-volume intradermal vaccine injections instead of larger-volume intramuscular 1193

CHAPTER 60  Rabies

persons must be particularly careful to avoid rabies exposure, even avoiding travel to areas where rabies is endemic. In one investigation of the response to vaccination, normal controls, asymptomatic individuals with HIV infection, and symptomatic persons with HIV infection were given a 5-dose simulated postexposure vaccination. Seroconversion occurred in 100% of the controls, 76% of the asymptomatic patients, and 57% of the symptomatic patients. However, rabies virus–neutralizing antibodies could not be detected in 40% of the symptomatic individuals with CD4+ T-cell counts below 400/µL.38 However, in another investigation, 18 individuals with CD4+ cell counts less than 200/µL and 9 individuals with CD4+ counts above 200/µL received eight 0.1-mL intradermal inoculations of PCEV each day on days 0, 3, 7, 14, and 30. By day 14, all patients in both groups had protective rabies-neutralizing antibody concentrations. No significant differences between the two groups developed in the following year.186 Thirty HIV-infected adults who had been treated for almost 4 years with highly active anti-retroviral therapy (HAART) and had median CD4+ T-cell counts of 537/µL received two rabies vaccinations within 3 months. The HIV-infected subjects had lower antibody levels than did normal controls, but the levels were protective. Five years after the vaccination, 63% of the HIVinfected individuals still had protective antibody levels.97 No documented failures of rabies postexposure vaccination in HIV-infected individuals have been reported.56

PART 6  ANIMALS, INSECTS, AND ZOONOSES

injections. The Warrells, Phanuphak, and their co-workers at QSMI pioneered the use of intradermal vaccination for postexposure immunoprophylaxis because a smaller volume of vaccine would be required. The regimen developed by the Warrells consisted of intradermal injections of 0.1  mL of HDCV at eight different sites on postbite day 0, injections at four sites on day 7, and injections at one site on days 28 and 90, which reduced the vaccine expense to 30% of the cost of five 1.0  mL intramuscular injections.216,224 Phanuphak intradermally injected 0.1  mL of PVRV at two sites on days 0, 3, and 14, and at one site on days 30 and 90. This regimen reduced the expense for PVRV, which is already much less expensive than HDCV, by an additional 68%.156,157 One hundred Thai patients, who had injuries severe enough to produce active bleeding inflicted by animals proved rabid by fluorescent antibody testing, were treated according to the schedule developed by Phanuphak and his colleagues in a prospective study. This procedure is now known as the Thai Red Cross intradermal postexposure rabies treatment schedule, or TRC-ID. All were uniformly protected from rabies. Since 1987, the TRC-ID regimen has been routinely used for postexposure therapy of over 1000 patients a month at QSMI, with only one failure, a 53-year-old alcoholic with cirrhosis who did not report for treatment until 6 days after his exposure.71 An anticipated problem with intradermal injections was the inadvertent subcutaneous injection of part or all of the vaccine. This has not been a problem at QSMI, but the staff of that institution is highly experienced.71 Nonetheless, deliberate subcutaneous injections have been found to produce antibody titers just as high as intradermal injections.157 The fourth measure has been development of reliable nonhuman cell-culture vaccines. Production of HDCV is characterized by “a demanding technology, low virus yield, and enormously high production costs per unit of vaccine.”210 It is not suitable for large-scale human rabies prevention. A variety of nonhuman cell cultures have been used to produce rabies vaccines: primary cell cultures (hamster kidney, dog kidney, or chick embryo fibroblast), diploid cell lines (human or rhesus monkey), and continuous cell lines (Vero and baby hamster kidney cells). Those made according to FDA standards are considered as effective as HDCV for postexposure immunoprophylaxis and for intramuscular preexposure vaccination.26,56,210 PVRV is produced in cultures of kidney cells from African green monkeys by Sanofi Pasteur in France and by other agencies and is extensively used at QSMI and in other institutions.71,104,224 This vaccine can be prepared in continuous cell lines cultured in suspension on microcarrier beads in biofermenters with a capacity of up to 1000 liters, which makes possible the production of vaccine on an industrial scale at greatly reduced cost.194,209,215 The nonhuman cell-culture vaccines are less satisfactory than HDCV in one respect. Approximately one-third of recipients reported pain at the injection site, and two-thirds of vaccinees given PVRV boosters developed local erythema. About 5% to 10% of recipients had systemic reactions such as fever, headache, malaise, or urticaria.209 In terms of safety and antigenicity, HDCV and the vaccines grown in other cell cultures are identical.

only 6.7% knew that the risk for rabies was significant and 40.1% considered it moderate or low. The danger of dog bites appeared well known, but the risk for scratches (0.7%) and licks (10%) was not known. The danger of cat, fox, monkey, and bat bites was not well known. Only one-half of the travelers knew about preexposure vaccination, and 57.6% of the travelers going to rabies-endemic countries presented to travel clinics too close to their travel departure for vaccination to be completed. Imme­ diate washing of bite wounds was described by only 3% of those questioned, although 21.3% mentioned disinfection with antiseptics.1 Information about rabies is not widely disseminated in developing countries. Travelers must know about this hazard before they depart. According to World Health Organization estimates, 99% of rabies infections are the result of dog bites.139 However, monkeys are a significant threat around some of the temples in parts of Asia, such as the Swayambhunath and Pashupati temples in Nepal. Most monkey bites result from attempts to snatch food carried or being eaten by travelers, which visitors to temples must avoid.72,181 Among foreign travelers in Nepal treated at the CIWEC Clinic, dog bites accounted for only about 75% of reported exposures, and monkeys inflicted 20% of the bites.185 In areas where canine rabies is endemic, which includes essentially all of Latin America and Africa and most of Asia, postexposure treatment should be initiated immediately following a bite by a dog or cat, but can be terminated if the animal remains healthy during a 10-day observation period. The vaccination status of the biting animal must be ignored. Vaccines used for animals in developing countries are not as reliable as those used in the United States, and fatal rabies has been reported in U.S. citizens and in others who were bitten by “vaccinated” dogs in developing countries and did not obtain prompt postexposure therapy.58,225 In the United States, rare rabies infections are found in dogs or cats that have been vaccinated.144 In developing countries, except for those few areas where rabies does not occur, all attacking animals should be considered rabid if they escape.

Rabies Considerations for Travelers

In developing countries, immune serum is rarely administered, because it is expensive or is unavailable. Only about one-third of the immune serum required for rabies postexposure therapy worldwide is being produced. In many areas it cannot be obtained. Even in areas where immune serum is available, travelers who receive postexposure therapy often are not given immune serum. Investigators in France found that of 261 travelers exposed to rabies, only 24% were given immune globulin. Of the travelers who did not receive immune globulin, 43% received a first dose of vaccine more than 7 days after return and before presenting to a clinic in their home country.96 As discussed earlier, when immune serum is given, it is usually of equine origin, the cost of which is only about 10% of the cost of HRIG. If immune globulin is not available for immediate administration, it may be given through day 7 following the administration of the first dose of a tissue culture vaccine.

Rabies is a definite risk for travelers, as illustrated by the 32-yearold female American traveler who was bitten on the hand while petting a stray dog in Kathmandu, Nepal. She missed at least three opportunities to obtain treatment in Nepal, Thailand, and Australia, as well as any number of opportunities after returning to the United States, and died of rabies 75 days later.23 Of the 63 human rabies infections in the United States since 1980, 18 were acquired in other countries, although most of those infections were in immigrants. The United Kingdom, which has been free of rabies since 1919, encountered 23 rabies infections acquired outside the British Isles from 1946 to 2005. Sixteen originated in the Indian subcontinent. From 1981 to 2005, four of the nine rabies infections diagnosed in Germany were acquired elsewhere.119 Probably the major problem in preventing rabies in travelers is their uninformed status. In a study of 300 French travelers, 1194

WOUND CLEANSING Because wound cleansing is such a vital element of postexposure therapy, travelers should be prepared to carry out this procedure in an optimum manner. The best soap to use is a liquid antibacterial preparation; if this is not available, soap of some type can usually be obtained. More important, virucidal agents like povidone–iodine (Betadine) are rarely available unless the traveler’s group had an unusually well-stocked firstaid kit. Travelers could carry a 3- or 4-oz bottle of one of these agents, and it should be reserved solely for cleansing animal bites, not for routine scrapes and cuts. Povidone–iodine preparations are easy to keep on hand because they can be stored in plastic bottles.

IMMUNE GLOBULIN

At the present time, neural-tissue vaccines are still employed for a large percentage of all postexposure rabies therapy worldwide because they are considered inexpensive. Travelers must not allow themselves to be treated with neural-tissue vaccines. Cellculture vaccines can be obtained in most developing countries, although travel to a major city may be required to obtain them.

PREEXPOSURE VACCINATION If postexposure immunization is going to be effective, it must be available on an urgent basis and must include access to contemporary tissue-culture vaccines and either HRIG or purified ERIG. Although access to prompt postexposure care may be available in major cities, it cannot be found in rural or wilderness areas where rabies is endemic. In determining whether preexposure vaccination (discussed earlier) should be administered, travelers and travel medicine consultants must consider the location, the purpose and duration of the trip, lifestyle, activities, and access to health care or repatriation. Investigators at the CIWEC clinic in Kathmandu, Nepal, have found that trekkers do not have a greater risk for being exposed to rabies. However, canine rabies exists in popular trekking areas, and trekkers and participants in similar activities are much farther from medical care than are individuals who remain in cities. For trekkers and climbers in the Mt Everest area of Nepal, it can take days to get to the site of the aircraft landing strip, and additional days elapse before good weather allows aircraft to land. Furthermore, aircraft landings and takeoffs from this site are usually filled to capacity, so an unscheduled traveler may have difficulty boarding a departing flight. WHO recommends that individuals who spend a lot of time outdoors, particularly in rural areas, receive preexposure vaccination.221

CHILDREN Children are considered to be at higher risk for rabies exposure for several reasons: their small stature makes extensive bites more likely, bites occur higher on the trunk or on the face, children are attracted to animals, and they may be less likely to report an exposure for fear of punishment.181 Preverbal children cannot report such events. Children must be carefully monitored and not allowed to play with dogs (even puppies) or cats in rabiesendemic areas. In children, the dose of vaccine for preexposure immunization or postexposure therapy is the same as that for adults: 1.0 mL injected intramuscularly. Only the dose of immune globulin for postexposure treatment is based on body weight.

OBTAINING MEDICAL CARE In foreign countries, American embassies and consulates are reliable sources of help. The U.S. Department of State’s Bureau of Consular Affairs website states, “If an American citizen becomes seriously ill or injured abroad, a U.S. consular officer can assist in locating appropriate medical services and informing family or friends. If necessary, a consular officer can also assist in the transfer of funds from the United States.” The website provides important information in case of emergencies and crises abroad, including the telephone number to contact the State Department’s overseas American Citizens Services (from outside the United States, 202-501-4444).203 Travelers should obtain travel insurance before going to other countries. Medicare does not cover the cost of medical treatment outside the United States; other insurance agencies have varying policies. Payment for unplanned transport back to the United States usually is covered only by travel insurance.

Other Lyssaviruses With RT-PCR amplification and nucleotide analysis, seven rabies virus genotypes have been recognized. Genotypes other than genotype 1 cause very few human infections. (Genotype 2, Lagos bat virus, has not produced a recognized human infection.)

However, these additional genotypes are a source of considerable concern, particularly in Europe where bats infected by genotypes 5 and 6 are common. Treatment of humans infected by viruses of these genotypes with the immune serum and vaccine used for genotype 1 appears to be effective, with the exceptions of genotypes 2 and 3. These two genotypes are so different from the others that specific antisera can be prepared for them; identification of the other genotypes is based almost entirely on nucleotide sequence analyses. True vaccine failure occurs when animals vaccinated with rabies vaccines are exposed to Mokola and Lagos bat viruses.68,94,116,188,217 Therefore genotypes 2 and 3 have been classified as phylogroup 2, and the other genotypes have been lumped into phylogroup 1. • Genotype 1 contains the viral strains that produce almost all recognized infections in humans and terrestrial mammals, many bat infections, and the fixed viral strains found in laboratories. • Genotype 2 (Lagos bat virus) was first isolated from fruiteating (frugivorous) bats on Lagos Island, Nigeria, in 1956. It is not known to infect humans, but it is found in bats and cats in Africa. • Genotype 3 (Mokola virus) was isolated from mice in the Mokola district of Ibadan, Nigeria, in 1968. In 1971, it was recovered from a 6-year-old girl who had a nonlethal infection that was not clinically typical of rabies. Subsequently, a lethal human infection more typical of rabies has been recognized. This virus is found in shrews and cats in Africa. • Genotype 4 (Duvenhage) was isolated in 1970 from a 31-year-old man with that name who died of the infection in Pretoria, South Africa, following a bite on the lip by a bat. It is found in insect-eating (insectivorous) bats in Africa. • Genotype 5 (European bat lyssavirus—EBLV—types 1a and 1b) has produced lethal infection in two Russian girls, a 15-year-old bitten on her finger by a bat and an 11-year-old bitten by a bat on her lip. This virus is found in insectivorous bats in much of Europe. • Genotype 6 (EBLV types 2a and 2b) has produced lethal infections in two people, a 30-year-old male zoologist in Finland and a 55-year-old male bat handler in Scotland. It is also found in insectivorous bats throughout most of Europe. • Genotype 7 (Australian bat lyssavirus—ABLV) was isolated from a 39-year-old female in 1996 and a 37-year-old female in 1998 after both had died in Australia of rabies-like illnesses. It is found in insectivorous and frugivorous bats (flying foxes) in Australia. Bats with antibodies to this virus have also been found in the Philippine Islands. Four other distinct lyssaviruses have been isolated in recent years. An application has been submitted to the International Committee on Virus Taxonomy to have them declared distinct species, although some investigators think they should be considered distinct genotypes. • The aravan virus (ARAV) was isolated from the lesser mouse-eared bat in Kyrgyzstan in 1991.4 • The khujand virus (KHUV) was isolated from the whiskered bat in Tajikistan in 2001. • The irkut virus (IRKV) was isolated from the greater tubenosed bat in Russia (East Siberia) in 2002. • The west Caucasian bat virus (WCBV) was isolated from the Schreiber’s bent-winged bat in Russia (west Caucasus) in 2002. Bats with antibodies to this virus have been found in Kenya.129 No human infections by these viruses have been identified. Bats with antibodies to irkut, aravan, and khujand viruses, as well as the Australian bat lyssavirus (genotype 7) have been found in Thailand.135 These viruses are pathogenic for laboratory mice, hamsters, and bats by intracranial and intramuscular injection routes, except for WCBV, which is pathogenic for mice only by the intracranial route. WCBV has been found to be pathogenic for nonhuman primates by both routes. All produce acute progressive fatal encephalitis essentially identical to rabies. All produce intracytoplasmic inclusions (Negri bodies).When groups of nine Syrian hamsters were treated with various vaccines and challenged with injections of the different viruses, the results shown in Table 60-6 were obtained.131 Genome sequencing of 1195

CHAPTER 60  Rabies

VACCINE

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 60-6  Results of Lyssaviruses Injections

Human diploid cell vaccine Veterinary vaccine Recombinant vaccine Unvaccinated controls

WCBV

ARAV

IRKV

KHUV

4/9*

5/9

6/9

8/9

9/9

2/9

9/9

8/9

9/9

9/9

1/9

4/9

5/9

9/9

9/9

2/9 0/9 0/9 1/9 p < 0.01 p < 0.01 p < 0.001 p < 0.001

Rabies

0/9

*Numerator indicates the number of survivors.

the N, P, and G genes has indicated that the aravan, khujand, and irkut viruses are related to genotypes 4, 5, and 6, and these viruses manifest as a solid phylogroup of Old World bat lyssaviruses. The west Caucasian bat virus is more divergent than are any of the other genotypes, with only limited relatedness to genotypes 2 and 3.128,130

Current Rabies Developments RABIES ERADICATION IN WILD ANIMALS Attempts to destroy wild animals that provide a reservoir for rabies have been made, but these pursuits are expensive and largely ineffective, with the possible exception of a program to eliminate striped skunks in Alberta, Canada. Even if such attempts were cost-effective, the consequences are considered unacceptable—increased populations of animals that had been prey (e.g., rodents) for the destroyed animals.169,219 Eradication of rabies in wild animal populations by oral vaccination was first suggested by Baer, and a program using baits distributed by aircraft was initiated in Canada in the early 1980s. Foxes were the targets of the early studies because they are particularly susceptible to rabies, and an effective oral vaccine could be produced. The most striking successes in vaccinating wild animal populations have been achieved in Western Europe and in Texas. In Europe, the only significant wild reservoir for rabies is the red fox. A wave of fox rabies began on the Polish-Russian border after World War II and swept over most of central Europe.28 The increased incidence of rabies in this species, and an economically distressing rise in the number of secondary rabies infections in livestock, principally sheep and cattle, led to efforts to control that source of infection. After extensive trials to demonstrate its safety, particularly for humans, vaccination of foxes was achieved with an oral attenuated– live-virus vaccine, starting in 1978 in areas of Switzerland, and later in parts of Germany. The vaccine first was placed in capsules attached to chicken heads. Subsequently, a specially designed bait of fishmeal and fat, the “Tübingen fox bait,” was developed. The baits included tetracycline as a marker, and fluorescence microscopy of mandible or canine tooth sections from foxes that were subsequently killed or found dead was used to determine the number of animals that had been immunized. Because dentine is deposited daily, the date of bait uptake could be calculated by counting the increment (von Ebner) lines between the pulp cavity and the tetracycline deposit.121,122,212 Baits were uniformly distributed throughout the test areas by hand or by helicopter. Immunization campaigns were carried out in the spring and fall, the latter particularly to vaccinate young foxes that could not take the baits during the spring. Follow-up studies of tetracycline labeling indicated that 75% to 80% of the foxes had consumed the vaccine, an adequate number to interrupt the spread of infection within the fox population. The attenuated live virus used for the initial vaccinations in Switzerland and Germany retains pathogenicity for rodents and can revert to virulence. In addition, this attenuated virus cannot be used in North America because it is pathogenic for striped skunks and ineffective for raccoons. Starting in 1990, a 1196

vaccinia-rabies recombinant vaccine that expressed the G glycoprotein was used in Belgium and France.40,219 In the areas where the vaccine has been distributed, genotype 1 rabies has largely been eradicated in all terrestrial animals, not just foxes.147 The incidence of rabies in livestock reported from the Belgium test area has fallen from more than 80 cases a year to none.40,226 As a result of this program, Finland and The Netherlands were declared free of terrestrial rabies in 1991, Italy in 1997, Switzerland in 1998, France in 2000, Belgium and Luxembourg in 2001, and the Czech Republic in 2004. Bats in those countries are infected with lyssaviruses of genotypes 5 and 6, and these infections have not been controlled. An epizootic of rabies in raccoon dogs, which apparently had originated in the USSR, was detected in southern Finland, and in the autumn of 1988 a field trial of oral immunization of these dogs and foxes was initiated. Rabies was eliminated from these populations within 12 months.219 An epizootic of rabies in coyotes in southern Texas originated in unvaccinated Mexican dogs that crossed the Rio Grande River. The epizootic spread to domestic dogs and resulted in two human rabies infections and over 2000 postexposure treatments. Control by dropping baits containing oral rabies recombinant vaccine from aircraft has grown to the largest aerial vaccination program ever attempted (2.6 million vaccine/bait units over a 42,000 square mile region during 1997). The rabies baits contain markers such as tetracycline. In 1997, 87% of coyotes manifested tetracycline fluorescence, more than enough of the population to stop the epizootic, which has disappeared. In 2001, only one infection by the dog/coyote rabies variant was found; in 2002 none was encountered.127 A similar program has been used in Ohio to stop the spread of the raccoon rabies epizootic from Pennsylvania on the state’s eastern border. Rare human vaccinia infections have been attributed to contact with the recombinant vaccine baits.175 Although such programs are expensive, they are considered less costly than the alternatives: treating humans, diagnosing animals, vaccinating domestic animals, compensating farmers for culling infected livestock, culling wild foxes, and paying the salaries of individuals who carry out these alternatives.40,147 Additionally, once rabies has been eliminated in a geographic area, it can be kept out by establishing buffer zones in which oral vaccination campaigns are carried out regularly. Vaccination campaigns for the entire area can be carried out less frequently or possibly eliminated entirely.219 In North America, control of rabies in wild animals is much more complex because this infection is enzootic in a variety of animals: skunks, raccoons, foxes, and bats. These animals vary considerably in their sensitivity to different strains of the rabies virus and vaccines prepared from those strains, they respond differently to the rabies virus sachet, and they have widely differing ranges (9.5, 2.5, 1.5, 0.8, and 0.037 km2 for coyotes, raccoons, red foxes, striped skunks, and mongooses). Furthermore, these animals have widely varying population densities, and they prefer different habitats.132 Even though North America contains vast sparsely populated areas, many of the animals live in urban areas. A 60-km2 (23.1-mile2) area of Toronto with a perimeter of 28 km (17.4 miles), in which 252,000 humans lived, also had a population of approximately 1540 skunks, 3510 raccoons, and 70 red foxes from 1987 to 1991.168 The entire city of Toronto is estimated to have a red fox population of approximately 1000 animals.167 A program to trap, vaccinate by injection, and release animals in this area was effective and cost $27,000 to $69,000 (Canadian) a year. That sum was considerably less than the $100,000 (Canadian) spent annually to treat humans exposed to rabid animals in Toronto.168 Although these programs control rabies in the target species, the ecologic effects of increasing the animal population by eliminating a significant cause of mortality are almost entirely unknown.28,212

VACCINE DEVELOPMENTS Killed virus vaccines are currently used for human and most domestic animal vaccinations. Attenuated live virus vaccines have

The rabies matrix (M) protein plays an important role in assembly and budding of progeny viruses. M gene–deficient viruses failed to generate progeny viruses, and mice inoculated intracerebrally developed no signs of disease. Intramuscular injection of these viruses induced formation of neutralizing antibodies. Intranasal installation resulted in almost the same antibody response.114 In a comparison of M gene–deficient and P gene–deficient viruses as vaccines, the M gene–deficient virus induced a more rapid response and a four-fold higher virusneutralizing antibody response in rhesus macaques than did a commercial vaccine. The authors concluded that the M gene– deleted vaccine has the potential for replacing current pre- and postexposure rabies vaccines.66 Transgenic maize has been employed to produce rabies G protein. The amount of G protein produced was approximately 1% of the total soluble plant protein. Transformed kernels were given orally to mice. When challenged 90 days later with a lethal dose of a vampire rabies virus, the edible vaccine had induced viral neutralizing antibodies that protected mice 100%.134 Transgenic tomatoes have been employed to produce fulllength rabies nucleoprotein genes. When injected intraperi­ toneally or administered orally, a protein extract induced the production of antibodies. However, the intraperitoneal injections were only partially protective and the oral injections were not protective.154

REPLACEMENTS FOR RABIES IMMUNE GLOBULIN DNA recombinant technology has been used to express three human rabies virus–neutralizing monoclonal antibodies in a rhabdovirus vector. Growth of the recombinant in cell culture produced high yields of three monoclonal antibodies that differed in epitope recognition. A “cocktail” of these antibodies neutralized several fixed and street rabies viruses. Mice and hamsters treated with this cocktail after infection with a lethal dose of rabies virus were protected. The protection was comparable with that provided by human rabies immune globulin. Notably, such cocktails could help compensate for inadequate production of rabies immune globulin that now prevails in developing nations.143,161 A number of such products have been developed, and they have been used to treat humans.18,100 However, industrial production and widespread use of such products has yet to be initiated.

SIMPLER LABORATORY TESTS FOR RABIES In countries where rabies infection is endemic, funds and infrastructure often are insufficient to allow employment of the direct fluorescent test, which is the “gold standard.” Therefore efforts are being made to develop simpler laboratory procedures for rabies testing. An example is the immunochromatographic test kit, which is both simple and rapid and does not need a cold chain for transportation or sophisticated training for personnel. The kit with two monoclonal antibodies has achieved a sensitivity of 93.2% but had a specificity of 100%.149

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

1197

CHAPTER 60  Rabies

been used only to vaccinate animals. The first vaccine used to orally vaccinate wild red foxes in Europe was an attenuated live virus vaccine. Subunit vaccines contain only one of the viral structural proteins. Since these vaccines contain only an antigenic portion of the virus and not the entire organism, they can induce immunity but are incapable of producing infection. The rabies-vaccinia recombinant vaccine that produces only the G surface protein of the rabies virus has proved to be noninfective, immunogenic, and very effective for vaccinating foxes in Europe.219 However, this recombinant vaccine cannot be used for humans because much of the world’s population has been vaccinated with vaccinia to prevent smallpox, and vaccinia can produce disseminated infections in humans.40 Some orthopoxviruses cannot completely replicate in mammalian cells and therefore cannot produce infections, but they can abortively replicate, so that proteins expressed by the virus are presented to the immune system. A recombinant with canarypox virus that expresses the G glycoprotein has been developed at Sanofi Pasteur; it has been found to be safe and effectively produces a neutralizing antibody response in a variety of animals and humans. This vaccine is currently licensed for vaccinating cats in the United States.39 Orthopox vectoring may permit incorporation of several antigens, such as measles, mumps, rubella, rabies, and pertussis, in a single vaccine, which would greatly facilitate and reduce the cost of human immunization.219 Adenoviruses replicate on mucosal surfaces and could be ideal vectors for oral and intranasal vaccines. Recombinant human adenovirus type 5, into which complementary DNA for glycoprotein (G protein) has been inserted, has been shown to elicit protective levels of neutralizing antibodies in skunks and foxes when administered orally. Deleted replication-defective recombinants have produced high titers of rabies virus– neutralizing antibody in dogs and have provided 100% protection against a lethal rabies challenge in mice. A vaccine containing an adenovirus recombinant that expressed G protein was protective for dogs when injected subcutaneously. These developments appear to hold promise for development of an oral vaccine for dogs.78,112,198 During August 2006 and 2007, baits containing this adenovirus recombinant were aerially distributed in Southwest Ontario, Canada, and successfully immunized raccoons and skunks.166 DNA vaccines based on plasmid vectors expressing the rabies G protein offer promise because they are easy to construct, manipulate, and produce. Such vaccines have produced high titers of virus-neutralizing antibody in mice, dogs, and nonhuman primates. They appear to be effective in much younger animals. In a field trial, a DNA vaccine injected into dogs’ ears with a jet injector was far more efficient for inducing long-lasting high titers of virus-neutralizing antibodies than was cell-culture vaccine.18 DNA vaccines have not proved as effective for postexposure therapy, because the antibody response to such vaccines is slow. Efforts to accelerate the antibody response appear to be effective.39,78 Incomplete rabies viruses that cannot replicate have been investigated as rabies vaccines. One of these experimental viruses lacks the P, or phosphoprotein, gene. (The P and L genes are responsible for viral replication.) The P gene–deficient virus is apathogenic in mice, even when inoculated intracranially. It induced a high titer of virus-neutralizing antibody and protected the mice from lethal challenges with rabies virus.142

CHAPTER 61 

Emergency Veterinary Medicine MURRAY E. FOWLER

Trek personnel, their packs and supplies are usually transported by all-terrain motorized vehicles, helicopters, and fixed-wing aircraft to remote locations around the world. It may seem that animal transport is no longer a consideration. This is, in fact, a false premise. The wilderness experience often involves animals other than humans. Such domestic animals as horses, mules, burros, llamas, elephants, camels, oxen, and yaks may be used for packing or pulling supplies, relieving hikers of this burden. Horses and mules are also ridden by trekkers. Dogs may accompany owners into the wilderness as companions, as trackers of game, or in the Arctic and Antarctic as primary draft animals. A cat may accompany a trek as a mascot or as a companion animal. Any of these animals may become injured or fatigued or may fall ill with a variety of ailments that require emergency treatment and management by trek personnel.

Wild Animal Encounters Observation of wild animals in their natural habitat enhances the wilderness experience, but encounters between wild animals and animals accompanying the trekkers may be less than pleasant. Healthy wild animals usually try to avoid humans, but this may not carry over to domestic animals. Medical and paramedical personnel who may be called to render emergency medical care or assist in the rescue of injured or diseased humans or support animals should recognize that wild animals may be involved. Experienced trekkers can usually recognize when they are intruding into an animal’s domain. Unfortunately, some people lack a sense of courtesy for animals. When trekkers in the wilderness behave as if they are entering the home of a human friend, they show appreciation for the rights of wild animals and have less risk for injury or illness to themselves or their support animals. Understanding the biology and normal behavior of wild animals known to live in the wilderness areas to be visited enhances enjoyment and diminishes exposure to potentially dangerous situations. Others who may be at risk are wildlife biologists, hunters, and people who choose to live in remote areas. Hunters come into intimate contact with wild animals as they pursue, dress, and eat game. Plant scientists, paleontologists, geologists, and other non– animal scientists may inadvertently encounter wild animals. Wildanimal biologists conducting field investigations may capture or immobilize wild animals to collect data. Such individuals are at potential risk for injury or disease, not only as a result of wild animal contact but also from tranquilizing drugs and the firearms used to administer the drugs.

WHY AND WHEN WILD ANIMALS ARE DANGEROUS Few wild animals deliberately stalk humans, but they may stalk support animals. Most wild animals fear humans and, given an opportunity, avoid human contact. Injuries to humans caused by wild animals are usually the result of judgment errors (such as approaching too closely), ill-advised handling of diseased wild animals, or unlucky exposure to highly aggressive or protective animals (see Chapter 51). Such animals may be natural predators seeking food, prey species fearful for their lives or the lives of their young, or diseased and irrational animals (such as those with rabies). Attacks on support animals usually occur at night or when humans are absent. Animals are most likely to respond adversely if startled from sleep or if their flight distance is violated. Flight distance is that distance at which, if approached by an enemy, an animal will 1198

either fight (attack) or flee. The distance is species specific and regionally specific, and it may become greater if animals in the area have been recently hunted. Flight distance may be greater for a person walking or carrying a gun than for a person riding on horseback or in a vehicle. Animals that find themselves cornered occasionally attack or risk injury trying to escape. Any animal may attack if its offspring are in danger. With any large animal, accidental or intentional positioning between a mother and her infant invites attack. Equal danger exists for a person who comes between a territorial male and one or more females. Many wild animals are territorial. Males and females may establish feeding, breeding, and home territories. An animal may share feeding territories with other members of the same species or with different species, but home territories may be defended against any intruder, including humans. Injuries have been inflicted on hunters who approached a recently shot animal, believing it to be dead, only to have the animal revive explosively in a final Herculean effort to fight or flee.

INJURY PREVENTION Humans should not fraternize with wild animals. Food scraps should not be left to tempt wild animals closer for photographs. Any wild animal that will allow touching is a spoiled park animal or is diseased. Neither type should be hand fed. Travelers in the wild should be observant for animal signs (such as feces, tracks, trails, and resting areas) and should respect the behavioral characteristics of animals. Knowledge of the biology and habits of local animals obviates most avoidable close encounters and dangerous situations.

DEALING WITH AN ATTACK Wild animal attacks on support animals usually occur when the animal is tied on a picket line or staked out for grazing. The animal may injure itself trying to escape the attack or may be bitten and mauled by its attacker. In one example, a frightened llama broke loose from a stake, but the lead rope suddenly caught between rocks and the animal’s cervical spine was fractured by the abrupt stop. Wounds inflicted on humans may be lacerations, contusions, punctures, or abrasions. Specific therapies are addressed in Chapter 21.

Support Animals Expedition leaders and participants should consider the wellbeing of support animals and understand their physical capabilities with regard to maximal load, speed, and endurance. Humans should also be able to recognize signs of exertional stress, which is more likely to occur in horses that are ridden than in packhorses that are led. A horse can generally match or exceed the physical endurance of a hiker, but adverse metabolic conditions may develop in horses pushed beyond their limits of endurance. The syndrome that arises from excessive exercise depends on intensity and duration, degree of prior conditioning, and nutritional status. Mules, donkeys, and llamas are less prone than horses to developing these problems, because they usually refuse to be pushed to extremes of exertion. The animal best suited to the terrain, climate, and task to be performed should be selected. Horses, mules, burros (donkeys), and llamas are traditional beasts of burden in North America, wherever sufficient forage and water are available. Each animal

For online-only figures, please go to www.expertconsult.com

Body Weight Animal Horse Mule Donkey Llama Dog Camel Elephant Yak Ox

kg 360-540 275-540 136-275 136-200 9-45 400-550 2300-3700 1000 499-1361

lb 800-1200 600-1200 300-600 300-450 20-100 880-1200 5000-8000 2200 1000-3000

Heart Rate (beats/min)

Respiratory Rate (breaths/min)

28-40 28-40 28-40 60-90 65-120 40-50 25-35 55-80 55-80

10-14 10-14 10-14 10-30 15-30 5-12 4-6 10-30 10-30

*Body Temperature

Weight Carried by Well-Conditioned Animal

°C

°F

kg

lb

37.2-38.0 37.2-38.0 37.2-38.0 37.2-38.7 37.5-38.6 36.4-42.0 36.0-37.0 37.8-39.2 37.8-39.2

99.0-100.5 99.0-100.5 99.0-100.5 99.0-101.8 99.5-102.5 97.5-107.6 97.5-99.0 100.0-102.5 100.0-102.5

110-136 82-136 40-82 34-50 3-14 225 900 235 235

240-300 180-300 90-180 75-110 6-30 500 2000 550 550

*Sustained trekking for 24 to 40 km (15 to 25 miles) per day on moderately difficult trails. The weight includes tack. Animals in training should be expected to carry only one-half to two-thirds of this weight.

has both admirable and undesirable qualities. Horses are usually the largest and can carry the heaviest loads. Mules and burros tend to be more difficult for novices to handle. Llamas have become popular support animals with backpackers in North America. The llama requires less feed, can subsist better on sparse native forages, and is less damaging to the environment than is the horse. No animal should be used on a trek unless at least one member of the party has considerable experience in handling and caring for the chosen animal. In South America, the llama is the beast of burden. Adventurers traveling into rugged and remote areas above 3000 m (9843 feet) will probably use llamas for support. Dogs are necessary draft animals for winter travel in the Arctic and Antarctic. Some hikers place small packs on dogs to carry light items or food for the dog. In other regions, dogs function more as companions. Cats must be placed in an appropriate carrying container, such as an airline shipping container, during transport, because a cat walking on its own would not be able to keep up. Many expeditions are mounted in countries unfamiliar to both leaders and participants. In various parts of Asia, the horse is replaced by the elephant, water buffalo, yaks, oxen, or Bactrian camel. In North Africa, the Middle East, and Australia, the dromedary camel carries the load. In Australia, horses and llamas may be used as well. Each species has specialized requirements for handling, packing, and health care. Expedition physicians may be asked to treat the ailments of support animals. Basic medical training provides the foundation necessary to diagnose and treat many conditions that may be encountered on the trail. This chapter provides an overview and specific anatomic and therapeutic information for some common problems. If in doubt, expedition members should handle an ailing support animal as if it were a human. When support animals carry all or part of the load, there is often capacity for a more sophisticated emergency medical kit to be carried.

PRE-TRIP ANIMAL HEALTH CONSIDERATIONS Treks involving support animals are carried out worldwide. Often, animals are supplied by a person or firm specializing in a given type of animal. The animals may be leased directly to the trek leader, or a handler may be contracted to supply and care for the animals. In either case, it is the responsibility of the trek leader to ensure that the animals meet the requirements necessary for the trek. This is particularly true in foreign countries. The author accompanied a trek in the high Andes in Peru. The trek leader had made arrangements for a certain number of llamas to carry the gear. The requested number of llamas was present, but many were small, thin, and immature. Most of the animals had never carried a pack before and bucked and kicked every time they were turned loose with the pack on. The trek leader had failed to specify details on what was necessary to control the animals. Any trek leader who is not animal savvy should ask for help from someone with animal handling or veterinary experience.

Topics that should be covered include conditioning, foot care, and required immunoprophylaxis. In North America, health certificates are required for travel and entry into the state or province of destination and possibly any intervening states to be traversed. Regulations are extremely variable, so inquiries should be made at least 4 weeks before departure. It is recommended that each animal receive a physical examination by a qualified veterinarian before an extended trip. Conditioning is as important for trek animals as it is for human participants. Training should be in terrain similar to that expected on the trek, with special attention given to toughening the footpads of llamas and dogs by appropriate exercise. The expected terrain to be encountered on the trek should be communicated to the animal supplier well in advance of the trek. Immature animals should not be taken on expeditions. Dogs should be at least 1 year old. Llamas and horses should be older than 3 years. Well-conditioned and trained horses, mules, burros, and dogs can carry approximately 30% of their body weight. Llamas usually carry only 25% of their body weight (Table 61-1). Frequently, arrangements are made to contract for support animal service from suppliers in the trek locale. Persons providing these services do not always understand the trek requirements and may supply animals that are poorly shod, unconditioned, poorly trained, or otherwise unsuitable for the needs of trek participants. Trek leaders must clearly stipulate specifications well in advance of the trek and be adamant about compliance. Horses, Mules, and Donkeys A tetanus booster should have been given within the past year. Vaccination against rabies is appropriate if the trek itinerary includes travel in an endemic area. Encephalomyelitis vaccine should be used in endemic areas, especially during the insect seasons of summer and fall. Internal parasite levels should be evaluated by fecal flotation and appropriate medication given to reduce the parasite burden. The feet should be trimmed and shod properly at least 2 weeks and not more than 4 weeks before a trek begins. Sole pads should be affixed if sharp rocky terrain is expected. Extra shoes for fore and hind feet of the different-sized horses should be carried, along with the appropriate nails and hammer to reattach a shoe, should one be cast. Selecting the breed of horse for a trek may depend on the experience and horsemanship of the trekkers. Horses for riding should be selected for gentleness, ease of mounting, and conformation that fosters a smooth gait and comfortable ride. Correct conformation includes angulation of the joints and a long, sloping pastern that provide good cushioning when a foot strikes the ground. Certain breeds are well known for this, including the Tennessee walking horse and the Missouri fox-trotter. Arabian horses are known for their stamina and endurance but may be high strung and require more expertise on the part of the rider than do other breeds. Thoroughbred or thoroughbred crosses are excellent if they are not flighty or too tall (16 hands or 1.6 meters [64 inches] or more). Quarter horses are also good trail horses unless they have short, upright pasterns that make for a jolting 1199

CHAPTER 61  Emergency Veterinary Medicine

TABLE 61-1  Vital Statistics of Trek Animals

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Poll

Withers

Back Rump

Muzzle Hip Shoulder

Stifle (human knee) Elbow Point of hock Hock (tarsus, human ankle) Accessory carpal bone

Pastern Hoof

Knee (carpus, human wrist) Hind cannon Cannon bone Fetlock Fetlock Pastern P-1 Pastern P-2 P-3

P-1 P-2

FIGURE 61-1  Anatomic sites of the horse.

ride (Figure 61-1). Often, there are more differences within a given breed of horse than between breeds. Avoid typical riding-academy horses that have to be prodded to a gait faster than a slow walk. The same poor conformation that produces a rough ride may also foster trauma to joints and ligaments, which can lead to lameness and unsoundness. Trek leaders are not likely to have a significant choice in animals used as packers. It is important to have sound horses that are properly trained and that are conditioned to accommodate packs. Llamas Llamas should have been given a tetanus toxoid booster within the past 6 months. Other basic immunizations should include Clostridium perfringens toxoid, types C and D, within the past 6 months, and vaccinations against leptospirosis and rabies, if entering an endemic area. Toenails should have been trimmed within the previous 2 months. Internal parasitism is debilitating in llamas. Ova levels should be checked, but usually treatment with an anthelmintic (ivermectin, 0.2 mg/kg subcutaneously, or fenbendazole, 5 mg/ kg orally) is desirable within the previous 2 months. Camels Camels are commonly the beasts of burden for baggage and people in the desert regions of Australia, the Middle East, North Africa, and parts of Asia and Southeast Asia. Camels are excellent trek animals but are considered stubborn, obstreperous, and difficult companions by persons who do not understand them. Trekkers should not use camels unless a qualified handler accompanies the trek. Although camels are domestic animals and quite docile when trained properly, everyone on a camel excursion should be able to recognize their offensive and defensive behaviors. They can kick forward, backward, and to the side. A dromedary camel can scratch its ear with a hind foot, so be aware of the arc of the limb. Camels also bite. They have formidable canine teeth that can inflict considerable damage. Camels, like llamas, are known to spit when they are angry. The spit is composed of regurgitated, foul-smelling stomach contents. Camels that are used to carry people or baggage are trained to lie down for boarding and loading. This is also the position that the cameleer should use to inspect for external parasites, administer injections, collect blood, or administer intravenous medication. Camels should be vaccinated for enterotoxemia (Clostridium perfringens, types C and D), leptospirosis, and melioidosis in endemic areas. Internal parasites of special concern include whipworms (Trichuris) and sarcoptic mange (Sarcoptes scabiei). 1200

FIGURE 61-2  Oxen.

Oxen, Yaks, and Water Buffalo An ox is a castrated male of any breed of cattle that has been trained to work as part of a team, having been paired at a young age (Figure 61-2). Castrated males are more docile and grow larger than do intact males; thus they are able to carry or pull heavier loads. Oxen were the mainstay for agriculture and for transporting people and goods in North America before establishment of the transcontinental railroad in 1869. They are still used for these purposes in many places in the world where access to mechanized agriculture is limited. The yak is the primary draft animal for native people living at high elevations in Central Asia and China (Figure 61-3). Yaks and their handlers are frequently employed by trekkers in these locales. The water buffalo is the beast of burden in wet environments (marshes, rice fields, jungles) of Southeast Asia. The pre-trip care of oxen, yaks, and water buffalos is essentially the same. It is difficult to generalize about immunizations because there are significant regional differences in infectious and parasitic diseases. These animals should receive the general vaccines administered to them in their native countries. If there are known endemic infectious diseases, for which there are vaccines, in the region where the trek will take place, arrangements should be made to have vaccination completed at least a month before the trek. Routine evaluation for parasites and necessary therapies should likewise be done at least 2 weeks before a trek.

FIGURE 61-3  A yak.

Asian elephants have been used for carrying loads, harvesting timber, carrying people, and engaging in warfare since antiquity (Figure 61-4, online). They are also used as beasts of burden for wilderness treks in forested areas of Southeast Asia, India, and southern China. Elephants are often considered to be domestic animals, whereas in reality they are wild animals that respond to taming and training to produce reliable beasts of burden that are useful for many tasks. Elephants should only be used under the care and guidance of a skilled handler, called a mahut or ozzie. Elephants should be immunized against tetanus (toxoid) and in endemic areas against rabies using a killed vaccine. Parasites may be important regionally. Dogs Dogs are routinely immunized against canine distemper, parvovirus, Bordetella (if they will be exposed to other canines), canine adenovirus, leptospirosis, and rabies. Dogs should be on a heartworm preventative medication if traveling in a mosquito endemic area. Vaccinations should be current. It should be noted that the leptospirosis vaccine does not protect against all serovars of this disease, so caution should still be taken when animals will be drinking standing water that could carry this disease. A check should be made for internal parasites and fleas so that appropriate action may be taken. Although dog fleas do not permanently infest humans, they bite and may cause mild to severe local dermal reactions in sensitive individuals. There are several good products, such as pyrethin-containing dusting powder, that can be used to treat or prevent flea infestations and that can be supplied by a veterinarian (who will know the most current and effective products) prior to an outing. It should be noted that it is unlikely that the fleas involved in the sylvatic plague cycle will infest a dog (they do, however, infest prairie dogs). Because external parasites, particularly ticks, can be carriers of multiple diseases, a flea and tick preventative (e.g., Frontline with methoprene, or Frontline Plus with fipronil) is also highly recommended and can be purchased from a veterinarian prior to the trip. Cats Like other animals on a trek, cats should have a pre-trip physical examination, with special emphasis on fleas in the hair coat and evidence for internal parasites, such as Toxoplasma gondii oocysts or ascarid (e.g., Toxascaris leonina and Toxocara cati) ova, in the feces. Vaccinations, including protection against rhinotracheitis, feline calicivirus, and feline panleukopenia, should be current. Rabies vaccination should be current. Although housecats may be vaccinated against other agents, these are the only diseases that are of significance to trekkers.

REST Support animals require less sleep than do human trekkers. Horses can sleep while standing because they have a special locking mechanism of the tendons and ligaments of the limbs. Horses may also lie in sternal or lateral recumbency. Llamas, elephants, and camels usually rest in a sternal position but may also assume lateral recumbency. Llamas enjoy taking a dust bath by rolling in dirt soon after packs are removed. A few may even try to roll with the pack in place. Elephants enjoy a water bath when available.

WATERING AND FEEDING All animals require daily access to potable water. It is not practical to filter or disinfect water for large animals, but this may be considered in extremely filthy conditions. Dogs may be susceptible to giardiasis, and theoretically, it is desirable to provide filtered water for them. However, preventing a free-running dog from drinking from a stream or lake is virtually impossible. Heavily mineralized or silted water may be as unpalatable for animals as for humans and may cause similar gastrointestinal upsets. The basic fluid requirement for a horse or other large trek animal is approximately 40  mL (1.5  oz)/kg/day, or 18  L (5  gal)

for a 450-kg (1000-lb) horse. With work and heavy sweating, the requirement may be tripled. Horses sweat profusely and should be given the opportunity to drink along the trail. Llamas and burros may require one-third less water than a horse. However, although they tolerate dehydration better than do other species, they function better if well hydrated. Some llamas refuse to drink until evening. The camel is noted for its ability to tolerate a number of days (2 to 7) without drinking water. A 450-kg (1000-lb) camel may lose 25% of its body weight via dehydration. That amounts to 114 kg (250 lb). A 114-kg (250-lb) water loss would equal approximately 114 L (30 gal) of water. The camel is unique in that it can drink, at one time, sufficient water to replace the loss without disastrous effects. A human being would be close to death at a 12% loss of body weight caused by dehydration and could not be orally rehydrated all at once. Feeding Horses, Mules, and Burros Horses consume approximately 2% of their body weight daily (or 9 kg [20 lb] of total feed for a 450-kg [1000-lb] horse). When the animals are working hard, one-third of this amount should be concentrates (grains such as rolled oats, barley, or cracked corn; or mixed grains and molasses in loose or pellet form). If forage is unavailable, alfalfa pellets should be carried. Animals should become accustomed to eating pellets before the journey begins. Concentrates should be reduced on days when the animals are not working. Feeding Llamas Llamas require only 1.0% to 2% of their body weight in food daily. Given the opportunity, llamas will graze and browse to satisfy their requirements. Many packers carry a supplement mixture consisting of one-half alfalfa pellets and one-half grain mix (the same as for horses), used as required. Some llamas are reluctant and must be trained to eat pellets or grain. Training should take place at home, before the trek. Feeding Oxen, Yaks, and Water Buffalos These animals are grazers and are able to subsist on native grasses better than can horses. Seasonal availability of forage should be considered during the planning stage of a trek. If necessary, supplements should be carried as part of the trek supplies. Concentrates (such as a mixture of corn, oats, and barley; or omnivore pellets such as those fed to zoo ungulates) should suffice. Pelleted alfalfa is also compact and easy to feed and carry. Trek animals should become accustomed to eating the supplement before the trek begins. Time must be allocated during daylight hours for these animals to graze if they are to subsist on native forages. Numerous wild plants and trees contain chemicals that may make the plant unpalatable or even toxic. If the trek animals are in their native habitat, they may be able to discern toxic plants. More often, a person knowledgeable about the plant life in the area should scout out the intended area for undesirable plants. If supplements are to be fed, this should take place before hungry animals are turned loose to graze. Animals may be tethered to a stake or a picket line in an area intended for grazing. Some handlers rely on hobbles, but the author has had personal experiences with animals learning to cope with hobbles and traveling some distance away from a campground. Feeding Elephants Trek leaders must rely on the elephant handler to know what is required for elephants. Elephants are both grazers and browsers. Given suitable foliage in an area, they will forage adequately if given time to feed. Feeding Dogs and Cats A dog should be accustomed to high-quality dry dog food. Many sled dogs are on a raw diet. The quantity fed should increase by one-half when the dog is exercising. A cat should be accustomed to eating dry cat food. Avoid feeding scraps from trekker’s food. 1201

CHAPTER 61  Emergency Veterinary Medicine

Elephants

PART 6  ANIMALS, INSECTS, AND ZOONOSES

FIGURE 61-5  Sequence of steps to create a halter tie.

FIGURE 61-6  Temporary rope halters.

EMERGENCY RESTRAINT

Llamas

It is assumed that one or (preferably) more persons on the trek are acquainted with the general care and handling of any domestic species involved in the expedition. Methods of haltering and leading are specific for each animal. Securing animals at night may require hobbling or tethering. Skill and experience are necessary to accomplish this without risking injury to the animal or handler. Animal handlers should be able to examine and clean the feet and hoofs of their charges. All people who deal with the animals should know how to create a halter tie (Figure 61-5) so that a safe and secure tie can be made at rest stops or whenever an animal is to be tethered. Knowledge of temporary rope halter construction is desirable in the event of loss or breakage of halters (Figure 61-6).11

Pack llamas are usually docile. Although most allow their feet to be lifted for inspection or treatment, some try to lie down. One or two people should stand on the side opposite the limb being lifted, or the llama should be placed next to a tree or large rock to prevent the animal from moving away. The limb should be firmly grasped. It may be necessary to provide semisupport to the body if the animal tries to lie down.12 If a llama refuses to get up, the rear limbs may be pulled out behind it. If it still refuses to rise, an injury or illness that inhibits rising should be suspected. Only rarely does a llama “spit” against an annoyance. The spit is actually stomach contents, the foul odor of which remains until thoroughly washed off. Spitting is usually directed toward other llamas to express displeasure, but handlers may be caught in the crossfire. If a llama becomes irritated during an examination or treatment procedure, spitting can be controlled by draping a cloth over the nose and tucking the top around the nose piece

Horses, Mules, and Burros Large animals may inflict serious or lethal injuries on people. When in pain or panicked, they may not respond even to their customary handlers. If a horse is down and entangled in rope, wire, or bushes, it should be approached from its back and its head held down until it can be extricated. The handler should stay out of the reach of both fore and hind limbs.11 A horse’s defensive and offensive actions are to strike with the forelimbs, kick forward and backward with the rear limbs, and bite. The safest place to stand is close to the left shoulder. A person examining the feet and legs of a standing horse should keep his or her head above the lower body line to avoid having the horse reach forward with a rear limb and striking it. Additional restraint for painful procedures may be accomplished by grasping one or both ears of the horse. The method of “earing” a horse is as follows: Stand at the left shoulder and grasp the halter or lead rope with the left hand. Place the right hand palm-down with the fingers together and the thumb extended, on the top of the neck. Slide the hand up the neck until the thumb and fingers surround the base of the ear (Figure 61-7). Squeeze tightly, but do not twist the ear. The horse usually tries to pull away as the ear is grasped. Be prepared to move with the horse while maintaining a firm grip. 1202

FIGURE 61-7  Earing a horse.

Camels A knowledgeable and experienced handler should be in charge of camels. Restraint procedures should be left to him or her except in emergencies. Camels used for trekking should be trained to be led and to kush (lie down) for ease of loading baggage and people. Sturdy halters and lead ropes should be supplied for each camel. Persons without experience with camels must appreciate that camels are capable of kicking or striking with all four limbs. The lack of a hind flank fold frees the limb to swing in an extended arc. Keep in mind that a camel is able to scratch its ear with a hind foot. It also has a formidable array of canine teeth and is capable of opening the mouth widely to bite. Known biters should be kept muzzled except when eating. An unhappy camel may exhibit its displeasure by regurgitating stomach contents (called spitting) on a person. Most examination and treatment procedures should be carried out with a camel in the kushed position. Camels may be ridden or packed with equipment and supplies. When ridden, they are usually guided by voice commands or touching with a goad or whip. A single lead rope is either attached to a halter or to a wooden peg inserted through the lateral side of the nostril. Camels are usually secured at night by tethering to a picket line or a stake. The tether may be attached to a sturdy halter or by a hobble on one front ankle. The method employed will depend upon the area of the world where the camel is being used and according to the culture of the camel handler.

CHAPTER 61  Emergency Veterinary Medicine

of the halter. Llamas also dislike the odor of stomach contents on their noses. Llamas can be “eared” in a manner similar to that used for horses.11

FIGURE 61-9  Placing a muzzle on a dog.

Tie the forelimbs together and the hindlimbs together; then stretch them forward and backward.

Oxen, Yaks, and Water Buffalos These animals are usually docile and easy to handle. They should be trained (usually from the time they are juveniles) to respond to voice commands or touching with a goad (stick) on a specific area of the body or limbs. Oxen may be driven by a handler walking alongside or by leading. If two animals are yoked together to pull a cart or wagon, the handler walks beside the animal on the left. Oxen are not usually trained to allow a foot to be picked up as would be done with a horse. Any examination or treatment of the bottom of the hoof may necessitate casting the animal (forcing it to lie down). This may be easily accomplished by using a half-hitch method (Figure 61-8). The animal is tied securely by the head to a solid structure (tree, post, fence or large rock) near the ground. The procedure requires the use of a rope 6 to 9 m (20 to 30 feet) long and 1.27 cm (0.5 inches) in diameter. Tie a loose bowline around the neck of the animal. Then place a half hitch behind the forelegs (see Figure 61-8). Place another half hitch over the caudal aspect of the rib cage. Take up all slack in the loops, so that when pulled from behind, the half hitches will not slip caudally but will tighten on the chest wall. One or two persons begin to exert a steady pull on the rope from behind the ox, and should be persistent. If the ox spreads its hind legs and refuses to go down, place a short rope hobble on the hind legs to prevent the straddle. Then renew the pressure. The pressure exerted on the chest will cause the ox to become recumbent.

Dogs and Cats Dogs usually accompany their owners, who are able to handle them under difficult circumstances. If mildly painful medical procedures must be performed, the head and mouth should be secured. The dog’s body can be securely held against the handler’s body by reaching across the back of the dog and grasping the base of the neck while pulling the opposite shoulder with the elbow toward the handler. The other hand should tuck the dog’s head under the handler’s arm. To secure a dog in lateral recumbency, it is vital to control the down-side legs as well as the head to prevent the dog from being able to effectively rise. Alternatively, a muzzle can be constructed from a nylon cord or even a shoelace. A loop should be formed with an overhand knot on one side. The loop is placed over the muzzle of the dog, with the knot on top, and tightened (Figure 61-9). The ends of the loop should be wrapped around the muzzle, crossed beneath the jaw, and tied behind the ears (Figure 61-10). Cat restraint is accomplished by wrapping the cat in a towel. Grasp the cat by the nape of the neck close to the head. Place the cat on an outstretched towel and press down on the back while another person begins to roll one end of the towel over the cat and continues to roll the cat into the towel. A limb may be withdrawn from the towel roll. Chemical immobilization of a cat is easily accomplished using ketamine HCl at a dose of 10 to 20 mg/kg administered intramuscularly or subcutaneously. Intramuscular injections are administered in the paraspinal muscles to either side of the lumbar spine or in the muscles of the upper rear lumb, making note that injecting in the upper rear limb may cause inadvertent sciatic nerve injury. For subcutaneous injections, grasp a fold of skin on the dorsal aspect of the neck just in front of the shoulders. Lift the skin and inject beneath the tented skin.

FIGURE 61-8  Half-hitch method of casting an ox.

FIGURE 61-10  Completed muzzle on a dog.

1203

PART 6  ANIMALS, INSECTS, AND ZOONOSES

CONDITIONS COMMON TO ALL SPECIES

Hyperthermia (Heat Stress, Heat Exhaustion)

Support animals may injure each other or their human handlers, or they may spread disease (such as ringworm or lice). Human injuries are discussed in Chapter 21.

Hyperthermia is elevation of the core body temperature above normal limits. Chapters 10 and 11 discuss hyperthermia in humans, and it is important to recognize that animals associated with a trek may become overheated as well.12,13

Trauma Contusions, abrasions, and lacerations are the most common ailments encountered in support animals. Falls, stumbling on sharp rocks, brushing against branches, and encounters with other animals are frequent causes of injury. Such wounds should be handled like similar human injuries. Hair or wool should be trimmed from the margins of wounds before treatment or suturing to prevent matting with exudate. The skin may be sutured with any suture material suitable for humans. Antibiotics are not necessary unless vital structures, such as synovial or serosal membranes, are exposed. Rope burns may occur in all species, but they are more likely to occur in horses because they tend to struggle against entanglements, and their skin is quickly burned by abrasive action. Therapy is similar to that for human burns. Thermal burns are unlikely unless animals are caught in brush or forest fires. Foot, Hoof, and Nail Problems Foot injuries may incapacitate an animal and possibly the expedition.7,12 The hoof of the horse covers the distal extremity and the third phalanx (P-3). The specialized horn of the hoof and nail is roughly analogous to the human nail. Horses are digitigrade, walking on the tip of P-3 (see Figure 61-1). In llamas, P-2 and P-3 lie in a horizontal plane within the foot, with only P-1 in the vertical position. The nails of the llama and dog are inconsequential in weight bearing, but if torn or contused, become extremely painful. The weight-bearing surface of the horse’s hoof contains the firm sole and more flexible frog, overlying soft fibroelastic tissue called the digital cushion. Dogs have footpads similar to those of llamas. Oxen, yak, and water buffalo may require hoof trimming just as do horses, mules, and donkeys. Oxen are rarely shod with metal shoes, but it is possible. Any trimming of the hooves should be performed at least a month before a trek. The feet, muscles, tendons, and ligaments should be conditioned for the trek by walking on terrain similar to that of the trek. The structures of the foot are subject to contusions, abrasions, lacerations, and penetration by foreign bodies (such as nails, stones, and sticks). Segments of the hoof wall and nail may be avulsed, exposing the sensitive laminae. Infection may invade the foot and undermine the outer layers, with abscess formation. Not all lesions are visible. Stone bruises of the sole or frog of a horse may be evident only when pressure is exerted on the site of the contusion. Foreign body penetrations and abscesses may cause reluctance to place any weight on the limb. The penetrating object may have been withdrawn or still be in place; in either case, a discolored tract leads to the depth of the wound. Erosions and ulcerations of the footpads are common in unconditioned dogs and llamas. Dogs working in ice, snow, mud, and water may suffer from maceration, cracks, erosions, lacerations, and frostbite. Foot and limb trauma is accompanied by varying degrees of lameness (limping). It may be difficult to establish which leg is painful, but the principles are similar to evaluation of such pain in humans, with the obvious differences of two extra limbs to evaluate and the animal’s inability to communicate. Cellulitis may develop on the limbs or body. The signs include heat, swelling, and redness and are the same in all species, as is therapy. Therapy for foot injuries includes providing drainage of infected lesions, disinfection, and protection of exposed sensitive structures. Antibiotics are not indicated for most wounds unless a joint surface is exposed. It may be necessary to bandage the foot to provide protection while in camp and to fashion special shoes or boots to keep an animal functioning on the trail. Special booties are available commercially for dogs, but a temporary moccasin can be constructed from soft leather (such as the leather used by craftspeople to make moccasins) or duct tape. 1204

Etiology.  The primary cause of hyperthermia in pack animals on treks is excessive muscular exertion, especially during periods of high environmental temperatures and high humidity. Animals that struggle for prolonged periods in swampy terrain or in snow or mud may also produce excessive heat. Although high ambient temperature is a contributing factor, excessive muscle exertion in any climate may cause elevation of body temperature. Pack animals may also develop fever as a result of infectious diseases. Dehydration from inadequate supplies of potable water exacerbates the problem. Inadequate physical conditioning is a common problem and contributes to a cumulative heat load. Other contributing factors include lack of salt in the diet, preexisting cardiovascular insufficiency, obesity, and trauma. Clinical Signs.  Signs vary according to species and the stage of hyperthermia, but all affected animals have increased heart and respiratory rates, usually accompanied by open-mouth breathing. Rectal temperatures may vary from 41.1° to 43.3° C (106° to 110° F). Horses, mules, burros, and llamas sweat in the early stages of hyperthermia, but sweating may cease if the animal becomes severely dehydrated. Sweating is evident in horses but imperceptible in llamas, because most sweating in llamas occurs on the ventral abdomen in what is known as the thermal window, where the fibers are less dense and the fiber length is short. Dogs cool themselves by evaporation of respiratory fluids while panting. The mouth is held open, and the tongue lolls from the mouth. The respiratory rate increases from a normal of 30 breaths/min to 200 to 400 breaths/min. Moisture may be observed dripping from the tongue. As dehydration intensifies, salivation and dripping may slow or cease. Dogs that are unable to effectively pant because of an injury or anatomic conformation are at particular risk for this disorder. Special care needs to be taken when bringing brachycephalic (short-nosed) breeds, such as English Bulldogs or pugs, into the wilderness because these dogs all have a significant degree of respiratory compromise. Hyperthermia causes a shift of blood volume from the viscera and muscles to the skin, resulting in hypovolemia and varying degrees of hypotension. Hypotension causes hypoxemia of the brain, resulting in dullness, restlessness, and incoordination. Hypoxemia may lead to convulsions and collapse. The shift of blood from the gastrointestinal tract may cause decreased motility and the potential for ileus and tympany. Signs of colic in horses and llamas (kicking at the belly, looking back at the side, treading, attempting to lie down and roll) may be noted. A 1° C (1.8° F) rise in body temperature requires 10% more oxygen for proper function of the energy systems of the body. When body temperature reaches 41° C (105.8° F), the respiratory system is no longer able to supply sufficient oxygen by normal respiration. Respiratory acidosis and electrolyte imbalances associated with sweating may produce a syndrome similar to septicemia. Hyperthermia may affect most of the organ systems of the body. The severity of the syndrome cannot be assessed in the field. It is important to recognize the conditions that lead to hyperthermia, to watch for early signs of heat stress, and to stop any activity that contributes to the problem. Mules and burros are not likely to become severely affected because they refuse to go on if stressed. Horses may be driven past their endurance and die of thermal stress. As mentioned previously, dogs that cannot pant effectively (particularly the brachycephalic breeds like bulldogs) can develop heat stress easily. Treatment.  Cessation of excessive muscular activity may be all that is necessary if hyperthermia is mild. If streams or lakes are nearby, the animal can be walked into the water and water can be splashed on its underbelly. Contingencies for hyperthermia

External Parasites The order Diptera, class Insecta includes thousands of species that are annoying or parasitic to humans and domestic and wild animals (see Chapter 47). Trek animals suffer in much the same way as do their human companions. Certain destinations are notorious for insect swarms (flies in Australia, mosquitos and gnats in the Arctic summer). Dipterans are also important disseminators of infectious microorganisms. It is sometimes difficult to differentiate venomous from parasitic species. The saliva of hematogenous dipterans may contain a toxin that aids in altering the endothelium of capillaries to induce free flow of blood, which is then ingested by the fly. Many humans are extremely sensitive to bites from certain flies, and some are sensitive to the toxins in the saliva. Animals may also be sensitive to the toxins in the saliva. Even nonbiting species, such as the housefly (Musca domestica) or the face fly (Musca autumnalis), if feeding on lacrimal secretions or open wounds, may produce a local reaction causing blepharitis, conjunctivitis, and keratitis. Biting flies (mosquitos, gnats, and midges) may produce local reactions in animals. An attack by immense numbers of simulid gnats may cause debility and even death in animals. In the Mississippi River Valley, horses and mules were killed by massive attacks of the buffalo gnat (Cnephia pecuarium). Swarms of biting insects may cause alarming behavioral responses in horses, including crowding together, head shaking, tail switching, and running. As a youngster, the author was mowing alfalfa hay using a team of horses. A cloud of simulid gnats descended on them. It was difficult to control the horses from bolting and at the same time protect oneself from the biting insects.9 Bee Stings.  Most of the aculeate Hymenoptera group of insects have a stinger apparatus, used to paralyze prey species or for defense. Most are small or lack the power to thrust the stinger through vertebrate skin and thus are of no consequence in envenoming people or animals. Other species—bees, wasps, yellow jackets, and hornets—inflict, at the least, a transient, painful sting and sometimes kill animals and people. The honey bee (Apis mellifera) is one of two domesticated insect species (the other is the silk worm, Bombyx mori). Native honey bees in tropical Southeast Asia were the original source of the North American domestic honey bee. When early American colonists missed honey as a sweetener, they imported European strains of the honey bee to Jamestown, Virginia, and the bees became known as European honey bees. The aggressive African honey bee, Apis mellifera adamsonii, a native of tropical southern Africa, was introduced into Brazil in 1956 in the hope of improving the local European strain’s ability to cope with warm weather. The bees readily adapted, but swarms escaped and have been moving northward at a rate of 150 to 200 miles per year. They are now found in California. The African honey bee hybridizes with the domestic honey bee, from which it can be distinguished only by apicultural entomologists. A sting from a single insect is not likely to cause a problem in a horse, llama, or dog. The classic anaphylactic response of humans has not been documented in livestock or companion animals. A local reaction consists of a swollen, edematous, and erythematous plaque. A tiny abscess may form at the injection site. Multiple stings may produce numerous urticarial wheals and cause a severe systemic response as a direct toxic effect of the venom. The pain associated with multiple stings may cause excitement or frenzy in a horse, followed by tachycardia, diarrhea, hemoglobinuria, icterus, and prostration. If the stings are on the head, or near the nostrils or mouth, swelling may occlude air passages, causing dyspnea.

Dogs may yelp at the initial sting. Cats are less likely to vocalize. Most victims of single stings are presented to the veterinarian with facial, aural, or periorbital angioedema. If a dog snaps at a bee or wasp and the sting occurs in the oral or pharyngeal cavity, swelling may occlude the passageway, resulting in severe dyspnea. Multiple bee stings may result in cardiovascular and respiratory collapse with death ensuing in minutes. As soon as the injection site has been identified, the area should be inspected for the remains of the stinger. The stinger of the honey bee has retrograde barbs that oppose extraction of the stinger, causing the caudal insect abdomen to be torn away. A honey bee is thus unable to inflict multiple stings, as do wasps and hornets, which do not have barbed stingers. A retained stinger should be removed by the most rapid method available. Tick Bites.  Members of the order Acarina, class Arachnida (ticks, mites, spiders, and scorpions) pose minimal risk for horses and llamas but may incapacitate dogs. Envenomation should be managed as for a human. Ticks are known to transmit a variety of infectious disease agents, including Borrelia burgdorferi (borreliosis, Lyme disease) and Ehrlichia risticii (Potomac horse fever, ehrlichiosis) in horses, but the biggest hazard of tick infestation in trek animals is tick paralysis.9 Tick paralysis occurs in horses, llamas, dogs, and many species of mammals and birds in North America, Europe, Africa, Australia, and Russia. Usually, only female ticks produce the neurotoxin, which localizes in saliva and is injected into the host when the tick takes a blood meal. Numerous species of ticks are known to produce the toxin. Signs may not appear until 5 to 7 days after the tick bite. Initially, there is paresis of the legs, progressing to unsteady gait, knuckling, ataxia, and ultimately, flaccid paralysis of the hind limbs. Loss of motor function ascends cranially, causing paralysis of the forelimbs. Pain perception remains. Even with paralysis of the limbs, the animal is bright and alert and able to eat and drink if feed is placed within reach. Ultimately, paralysis involves the neck, throat, and face, causing difficulties in chewing, swallowing, and breathing. Respiratory failure is the cause of death. This sequence of clinical signs is the only sure method of diagnosis, unless the tick is found. That may be quite difficult on an animal the size of a horse. The differential diagnosis includes encephalitides, head or spinal trauma, and hyperthermia. There is no antidote for the toxin. The offending tick or ticks must be removed, which may produce a dramatic response. Look in the lightly haired areas of the axillary space, perineum, and behind the ears if tick paralysis is suspected. In a hospital situation, the animal should be endotracheally intubated and respiration supported until the effect of the toxin is dissipated. This is not an option in the field. Skunk Odor Removal All carnivores have scent glands contiguous to the anus, but the striped skunk Mephitis mephitis and several other skunks have highly developed glands that produce a powerful and pungent musk. The excretory duct of each gland leads to a papilla located at the mucocutaneous junction just inside the anus. Skunks are capable of accurate ejection of the musk for a distance as far as 3 m (10 feet). The odor may be detected 2.5 km (1.5 miles) downwind. The musk is a complex mixture of organic compounds. Those primarily responsible for the objectionable odor include S-(E)-2-butenyl thioacetate, S-3-methylbutanyl thioacetate, and S-2-quinolenemethyl thiocyanate, all of which are sulfur-containing thiol compounds. In addition to the obvious odor, skunk musk is nauseating to some people and may also cause retching in dogs. If a person or a pet is sprayed in the face, the musk is an irritant that causes conjunctivitis, keratitis, lacrimation, temporary impairment of vision, glossitis, and slobbering and foaming at the mouth. Quick flushing of the face and eyes with copious quantities of cold water restores vision and minimizes persistent irritation. If conjunctivitis persists, instill contact lens solution or a drop of olive oil into the conjunctival sac. The objective of odor removal is to wash away the offending oily liquid and neutralize the compound by oxidizing the thiols to nonodorous sulfonic acid. Simple bathing will not completely eliminate the odor, which is pungent in a remarkably dilute 1205

CHAPTER 61  Emergency Veterinary Medicine

are parts of all plans for capture operations for wildlife translocation and reintroduction projects. Water is carried for cooling, along with intravenous fluids to deal with heat stress. Cold-water enemas are the most effective and rapid way to cool the body of a large animal. Caution should be used when cooling a dog. The dog should be cooled to a rectal temperature of 39.4° C (103° F) within 30 to 60 minutes. Overcooling or cooling too rapidly can lead to fatal complications.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

concentration. The product used to neutralize the thiols depends on the object to be deodorized. Colored clothing may be damaged by bleaches, and some substances should not be used directly on the coat of a dog and certainly not on the skin of a person. One of the most effective oxidizing agents is a dilute solution of household bleach (Clorox); however, this may bleach clothing and hair and is harsh on the skin of people and animals. Dozens of substances have been recommended and testimonies abound as to their effectiveness. Skunk musk is alkaline, so mildly acidic solutions may be at least partially effective and will reduce the pungency of the odor. Tomato juice, white vinegar, and ammonia in water are all touted but may not completely eliminate the odor. A frequently mentioned formula is a combination of hydrogen peroxide (347 mL [1.4 cups] of 3%), water (237 mL [1 cup]), baking soda (sodium bicarbonate, 60 mL [0.25 cup]), and a dish detergent (15 mL [1 tablespoon]). Mix the peroxide with the water, and then add the baking soda and shampoo. Mix and pour into a squirt or spray bottle. This solution may be sprayed onto a dog or a horse, but it should not be sprayed directly into the eyes or nose. It should remain on the coat for 10 minutes while being worked in with a gloved hand. Washable clothing should be washed with a strong soap or heavy-duty detergent. In a permanent camp, items that cannot be washed (shoes, leather goods) may be buried in sandy soil for a few days. The soil will adsorb the odorous chemicals. The following commercial products have been formulated to neutralize the thiols and completely eliminate the skunk odor: • Neutroleum alpha is nontoxic and may be used on clothing and pets. It may be obtained from USDA, Damage Control, PO Box 81886, Lincoln, NE 68501 (phone: 402-434-2340).

• Skunk-Off is nontoxic and nonirritating, even to mucous membranes, and safe to use on pets and clothing. • Odor-Mute is available in granular form and easy to transport. It is nontoxic and may be applied to pets and clothing after it is dissolved in water. • Summer’ Eve douche is an effective product to neutralize skunk spray odor. Check with pet supply shops or small animal veterinary clinics for these commercial products, which are for use on pets or fabric and not recommended for use directly on people. Only the trek physician is qualified to make such a recommendation. However, washing with soap and copious amounts of cold water will wash considerable musk from human skin. Plant Poisoning It is unrealistic to expect to be able to identify all potentially harmful plants in every locale. However, certain highly toxic plants that grow in wilderness areas of the United States should be recognized (Table 61-2) (see Chapters 64 and 65).2,8,12 Cooperative extension offices at federal land grant institutions frequently publish booklets on local poisonous plants. Horses may be less at risk than llamas, because horses are primarily grazers and not likely to eat trees and shrubs. Llamas eat small quantities of almost anything within reach. Animals are not affected by poison oak (Rhus diversiloba) or poison ivy (Rhus toxicodendron). However, horses, dogs, and llamas may transmit the toxic oils of these shrubs to susceptible people via contact with contaminated hair. Few specific antidotes are available for plant poisons. Symptomatic and supportive treatment includes removal of the poisonous material from the gastrointestinal tract by administration of a cathartic (see Table 61-4) or by adsorbing the toxin with a nonspecific substance such as activated charcoal.

TABLE 61-2  Poisonous Plants That May Affect Horses or Llamas on a Trek Common Name

Scientific Name

Poisonous Principal

False hellebore, corn lily Death camas, sandcorn

Veratrum californicum

Alkaloids

Zigadenus species

Alkaloids

Water hemlock

Cicuta douglasii

Resin

Nightshade

Solanum species

Jimson weed

Datura stramonium

Alkaloidal glycoside, solanine Alkaloid, atropine

Tobacco, tree tobacco

Nicotiana species

Alkaloid, nicotine

Lupine, blue bonnet

Lupinus species

Alkaloid

Dogbane, Indian hemp

Apocynum cannabinum

Oleander

Nerium oleander Ricinus communis Rhododendron species

Cardioactive glycoside (similar to digitoxin) Same as for dogbane Ricin, water solution Andromedotoxin glycoside

Castor bean Rhododendron

Signs of Poisoning

Habitat

Species

Therapy*

Vomiting, salivation, convulsions, fast irregular pulse Foaming at mouth, convulsions, ataxia, vomiting, fast weak pulse Frothing at mouth, muscle twitching, convulsions, death in 15 to 30 minutes Vomiting, weakness, groaning

High mountains, meadows

Llama

Symptomatic

Hillsides, fields, meadows, in spring of year

Horse, llama

Symptomatic

Standing or running water, obligate aquatic

Horse, llama

Symptomatic

Ubiquitous

Horse, llama

Symptomatic

Dry mucous membranes, dilated pupils, mania Stimulation of CNS, then depression; sweating, muscle twitching, convulsions CNS depression, dyspnea, muscle twitching, ataxia, frothing, convulsions Dyspnea, cardiac arrhythmias, agonal convulsions, vomiting, diarrhea Same as for dogbane

Waste places

Horse, llama

Parasympathomimetics

Waste places

Horse, llama

Symptomatic

Ubiquitous

Horse, llama

Symptomatic

Ubiquitous

Horse, llama

Symptomatic

Ornamental

Horse, llama

Anaphylactic shock, diarrhea Vomiting, colic, severe depression

Ornamental

Horse, llama

Symptomatic, gastrotomy Treat for shock; fluids

Shrubs in meadows and moist places

Llama

Activated charcoal, time

*In most cases of poisoning from ingestion of poisonous plants, no specific antidote exists. Victims are treated symptomatically. The critical factor is to empty the digestive tract of the plant material with cathartics, parasympathomimetic stimulation, and enemas. Activated charcoal, given orally, may be of value.

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An abrasion, laceration, or penetrating wound of the cornea is serious, especially in a field situation. Dust and other foreign bodies within the conjunctival sac require prompt removal to avoid more serious injury to the cornea. Management of eye problems in animals is the same as that for humans, with the added difficulty of restraint for examination and therapy. Lightning Strike Lightning strike is a potential hazard in the wilderness (see Chapter 3).10,13 Animals with high head carriage, such as horses and llamas, are especially at risk, whether they are standing or recumbent. Animals, like people, may survive a lightning strike, but frequently a strike is lethal. Unless the strike is witnessed, it may be difficult to make a diagnosis, but the following signs may be noted: depression, blindness, nystagmus, paralysis of the hind limbs, and temporary unconsciousness. Linear singe marks are definitive if present, but lightning may kill an animal without producing burns. One llama was struck while recumbent in an open pasture. When the body was moved, the green grass had been singed where the llama had been lying. A single lightning strike may kill more than one animal, especially if a group has congregated under a tree for shelter. Lightning may kill so quickly that feed is still in the mouth of grazing animals. During an electrical storm, animals on the trek should be positioned in the safest environment possible, away from tall trees and exposed hills. Llamas can be encouraged to lie down in a small ravine or a depression, or against a rock face, with the head tied close to the ground. A picket line stake may be used for the tie-down. Avoid tying an animal to a tree; however, using a small bush for a tie-down may be safe. Horses are more difficult to deal with because it is impossible to get them to lie down unless they are specially trained to do so. Get them into a ravine, or a depressed area, or near a rock face. If an animal is struck and still alive, only time will determine the degree of damage done to the nervous system and other vital organs. If the strike is witnessed and the heart has stopped beating, chest compression (cardiac massage) may be performed if it is determined that it is safe for a human to be in the open. With the animal in lateral recumbency, pull the forelimb as far cranially as possible and press on the chest wall just caudal to the triceps muscle. Cardiac massage may be required for a number of minutes. Snakebite Venomous snakes are found in most wilderness areas of the world, except the Arctic and Antarctic.9,12 Trek leaders should be aware of the species of snakes that may be encountered on the trek and should instruct all personnel on how to deal with a bite in a human or animal. In the United States, the venomous snakes most likely to be encountered are pit vipers, the most ubiquitous of which are rattlesnakes of the species Crotalus. Other members of the North American pit viper group include the copperhead, Agkistrodon contortrix, and the water moccasin, Agkistrodon piscivorus. Llamas and, to a lesser extent, young horses are curious animals and may stick their noses out to investigate strange animals in their area. Thus it is not uncommon for an animal to be struck on the nose. Leg bites may occur in any animal. The main clinical sign of venom injection is pronounced swelling in the area of the bite, beginning 1 to 3 hours after the bite. The most serious consequence of being bitten on the nose is swelling that occludes the nostrils, making it virtually impossible for horses and llamas to breathe. Dogs are not obligate nasal breathers, but the effects of a bite may be more severe in them than in the larger animals. A rattlesnake bite on the nose is an emergency. The trek first-aid kit should contain a 10-cm length of a 1-cm– diameter flexible plastic tube. The first step in managing snakebite on the nose is to insert this into a nostril before any swelling occurs, to prevent occlusion of the nostril and provide a passageway for air. The tube cannot be inserted after swelling has developed. If swelling has already developed, the life-saving procedure is a tracheotomy.

DO NOT attempt to cut the skin and suck out the venom with your mouth. This procedure is not effective. For pit viper envenomation, the only specific treatment is administration of antivenom. Freeze-dried antivenom in vials can be carried in the first-aid kit. The product used for animals is the same as that used for humans. One to three vials should be administered intravenously once signs of envenomation have appeared. Choke Choke in humans refers to lodging of food or other objects in the larynx or trachea, a life-threatening emergency. In animals, the term usually refers to lodging of food or other objects in the esophagus.12,14 The signs of choke may be alarming, but an animal rarely dies from it unless feed is regurgitated and inhaled into the lungs. As a preliminary step, animals should be accustomed to any supplemental feed to be used on the trek. Choke is most often caused by overly rapid ingestion of pellets or grain, so a preventive measure is to slow down ingestion. This can be accomplished by placing rock pebbles in the feed container. Llamas and horses are too fastidious in their eating habits to consume such objects, so they separate the rocks from the feed and thus take longer to eat. Metallic or wooden objects are rarely swallowed. Retching is the principal sign of choke, as the animal attempts to dislodge the mass. Choked animals are able to breathe, but they are clearly in distress. Saliva may flow from the mouth and the victim may cough up particles of the feed. It may be possible to feel a mass on the left side of the neck if the obstruction occurs in the cervical area. Peristaltic waves may be observed moving up and down the left side of the neck. The mass may lodge anywhere along the course of the esophagus, but generally it lies within the chest and is not visible externally. Water may be offered, but feed should be withheld until the problem has corrected itself. Palpate along the lower neck to determine whether a bulge is present. If so, gently massage it to determine whether it can be moved. Sometimes, moderate exercise may cause the object to move toward the stomach. In some cases, passage of a stomach tube and application of gentle pressure may push the mass into the stomach. Medication (intra­ venous acepromazine [0.05 mg/kg] or xylazine [0.05 to 0.25 mg/ kg]) may be necessary to relax esophageal spasm. Drowning Llamas, horses, elephants, and dogs are able to swim, but circumstances may cause submersion in water and inhalation of water into the lungs.13 A heavy fleece would be a serious detriment to a llama in water over its head. Floods may trap and drown animals. The primary problem is to extricate the animal from its predicament, which may be extremely difficult with a large llama or a horse. It is necessary to act quickly (in less than 5 minutes) to prevent death. If the animal is to revive, water must be drained from the lungs. Place the llama on its right side with the body slanted downward to the neck and head so that water can flow out. There is a risk for producing stomach regurgitation in this position, but the need to remove water from the lungs must take precedence, even though this is a desperation maneuver at best. If immersion lasted for more than 2 to 3 minutes, the heart may have stopped, making cardiac massage necessary. The action must be continued until the victim responds or is declared dead. It is highly unlikely that resuscitation will be successful for an animal that has been under water for more than 5 minutes, regardless of the water temperature. Wound Dressing and Bandaging The principles of wound dressing are basically the same as those for humans.13 Cotton or a coarse bandage should not be placed directly on the wound, if possible. A nonadherent 4 × 4-inch gauze compress or an absorbent hydrogel pad is the best material to place against the wound. A padding layer or absorbent layer to collect fluids should be next. Finally, a surface or protective bandage should be applied to hold the padding in place. 1207

CHAPTER 61  Emergency Veterinary Medicine

Eye Injuries

PART 6  ANIMALS, INSECTS, AND ZOONOSES

A variety of bandage materials are suitable. Coban or Vetrap (bandage tape) is the most satisfactory bandage material because it is porous, sticks to itself, and is flexible, fitting to uneven surfaces. Other products, such as Elastikon (elastic tape) or rolled gauze bandages, are also excellent. Duct tape is satisfactory, but care should be taken to avoid wrapping it too tightly, because the tape has no extensibility and may become a tourniquet. Placement of a smooth bandage is an art. Once the anchor roll is in place, firm but uniform pressure should be applied as the bandage unrolls. Joints require special attention. Bandaging should be done in a figure-8 pattern to provide uniform pressure over a variably shaped surface. Avoid pressure over the point of the hock and the accessory carpal bone (back of the carpus) (see Figure 61-1). The foot also requires special consideration. When dressing a foot wound, make certain that the spaces between the digits of dogs or llamas are padded with cotton. The easiest bandage to apply is a Vetrap elastic bandage that conforms to the odd shape. If a severe foot wound occurs while trekking in the back country, additional protection may be necessary to allow the animal to continue on the journey. The author carries a sheet of pliable leather of the type used to construct moccasins. The dressed foot is placed in the center of the sheet, and then the leather is gathered up around the pastern and held in place by duct tape or another bandage, roughly forming a boot shape. Another method is to use a rolled-gauze bandage. After dressing the foot, make a wrap around the pastern, leaving a tail of gauze approximately 15 cm (6 inches) long. The tail is used as a fulcrum to change the direction of the bandage as the digits are covered. Limb Bandages and Splints for Dogs.  Fortunately, dogs can generally ambulate very well on three legs and can usually transport themselves with one leg injured. However, there are times when it is very helpful to be able to immobilize and protect a limb until appropriate veterinary care can be provided. In general, fractures of the humerus and femur should not be bandaged or splinted. The bones cannot be adequately immobilized and the bandage or splint results in more weight distracting the fracture. Fracture or dislocations below the elbow or knee, particularly if they are unstable or open, can be splinted or bandaged to prevent contamination or further trauma, as well as for comfort. When applying rigid casts or splints, try to avoid extending into the axilla and groin because these are common areas for rub sores to develop. When bandaging a dog’s limbs, it is important to continue the bandage all the way down to the toes. If this is not done, the portion of the limb below the bandage will often swell considerably. Tail tip injuries can be difficult to treat because it is difficult to keep bandages in place and vigorous movements of the tail encourage hemorrhage and can result in repeated trauma. The tail can be protected by a rigid or semi-rigid splint, such as a syringe casing that covers the tail tip, and is secured with tape that incorporates tail hair between tape layers to minimize slippage. Cardiopulmonary Resuscitation* Rescue breathing is rarely required for an animal on a trek, except in the case of a lightning strike or drowning. The procedure is different from that employed in humans, because mouthto-mouth breathing cannot be performed on an adult llama or horse. A llama or horse should be placed in lateral recumbency, preferably on the right side. Stand at the animal’s withers (top of the shoulder) and reach across the body to grasp and lift the arch of the rib cage. This maneuver flattens the diaphragm and expands the chest, producing inspiration. Do not press in this same area to force expiration, because this will put pressure on the stomach and possibly cause regurgitation. Instead, press over the heart area just above the elbow and caudal to the muscles of the upper limb. The rate for the horse or llama is 10 to 15 breaths/min. *References 12, 13.

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Cardiac massage may be performed by placing the llama or horse on its right side. Have an assistant pull the upper foreleg forward and press the chest in the area vacated by pulling the leg forward. Kneel next to the bottom of the chest. Position the heels of both hands against the chest approximately 15 cm (6 inches) above the sternum, with the fingers directed toward the spine. Press firmly with the arms held straight and release quickly. Repeat the movement every second. After 15 compressions, check for a pulse in the saphenous artery on the medial aspect of the stifle in a llama, or listen for the heartbeat with a stethoscope. After 15 heart compressions, administer five cycles of rescue breathing, as described previously. It is futile to continue cardiac massage if no oxygen is available to the heart or the general circulation. Massage must be continued until a heartbeat returns and the victim begins to breathe, or when signs indicate that the victim is dead (pupils dilated, no response to touching the cornea). Dogs, as opposed to humans, very rarely arrest for primarily cardiac conditions. Cardiopulmonary arrest can occur secondary to vagal and respiratory conditions, so hypoxia, hypotension, and acidosis are often present at the time of arrest.3 For these reasons, ventiliatory support is definitely appropriate in a canine cardiopulmonary resuscitation effort. This is ideally accomplished with an endotracheal tube, although “mouth to nose” ventilation may be attempted by positioning the rescuer’s mouth around the nose of the closed-mouth dog and administering rescue breaths through the nares. Respiratory rate should be 10 to 24 breaths/ min, with a higher rate for small dogs and a lower one for large dogs. For cardiac compression in medium to large breed dogs, the dog should be in lateral recumbency on the ground. The rescuer kneels on the dorsal (spine) side of the dog and delivers compressions similar to human CPR, with the hands over the widest part of the chest and an ideal rate of 120 compressions per minute. The chest diameter should be decreased by 25% to 33% per compression with a 1:1 ratio of compression to relaxation.3 For smaller dogs, dorsal recumbency (back down position) may be used or the hands can be used to compress the thorax just behind the elbows, depending on the size and conformation of the dog. West Nile Viral Encephalitis Trekkers must be aware of newly emerging diseases that may affect the animals that accompany the trek. West Nile virus disease (WNVD) has become an important consideration because of its explosive spread in the United States and other countries in the New World. WNVD is new to North America (1999) but has been present in Africa and other parts of the Old World for decades. It is a mosquito-borne viral meningomyeloencephalitis with a broad host range that includes humans, horses, camelids, and a large number of bird species. The entire host range is unknown. The virus is an arbovirus that is closely related to the viruses that cause St. Louis encephalitis, Japanese encephalitis, and Murray Valley encephalitis.1 Transmission is via mosquito bites (Culex, Aedes, and Anopheles species) and possibly other blood-sucking insects. The disease has become endemic and is spreading throughout the United States. The incubation period in horses, llamas, and humans is 6 to 10 days. Most infections are subclinical in horses and humans, but 10% of affected individuals develop fever and the encephalitic signs of depression, ataxia, and paresis, particularly of the hind limbs. More advanced signs include head shaking, incessant chewing, paralysis of the lower lip or tongue, severe ataxia, ascending paralysis, and terminal recumbency.1 WNVD is similar to dozens of diseases affecting the central nervous system, including rabies, other encephalitides, head trauma, lead poisoning, water deprivation (dehydration, salt poisoning), brain abscess, and plant poisoning. A definitive diagnosis usually cannot be achieved while on trek, so prophylaxis is the only effective management modality. Two vaccines (West Nile–Innovator, killed [Fort Dodge], and Recombitek, live [Merial]) are approved for use in horses in the United States and have also been used in camelids. If a trek is planned for an area where WNVD is endemic and when

Anthrax Unfortunately, bioterrorism is a potential reality in many countries of the world. People and the animals on a trek may be exposed to some of these agents. Anthrax is a disease that is high on this list and could affect horses, llamas, camels, and elephants. Anthrax is endemic in many places in North America and throughout the world. It is a highly infectious bacterial disease of most domestic mammals, many species of wild mammals, and people. It is caused by the endospore-forming, nonmotile, grampositive rod Bacillus anthracis. The spores may remain in the soil for many decades. Horses, camels, llamas, and elephants with anthrax present with acute septicemia of sudden onset, fever, rapidly progressive debility, respiratory distress, and disorientation. Death may occur within a few hours. In less acute cases, bloody fluid may exude from any body orifice and swellings may appear in various parts of the body, accompanied by limb and perineal edema. The differential diagnosis includes any disease that produces acute septicemia, such as salmonellosis or plague. Oleander (Nerium oleander) poisoning also appears similar.12 A live-spore vaccine (Sternovac) is used in livestock and wild animals. Although B. anthracis is sensitive to many antibiotics, therapy is rarely successful because toxemia is the primary manifestation of the disease in animals. Disaster and Emergency Management A wilderness trek may be engulfed by a natural disaster, a sudden ecologic phenomenon that causes much suffering or loss10 (see Chapter 86). Just as attitude may be the key to human survival in a disaster situation, it is no less important when dealing with animals. Advance planning and preparation are essential. Safety and protection of people take precedence over the needs of animals. However, animals should not be neglected. The following disaster situations may involve animals. Ice Storm.  An ice storm is rain that freezes immediately on striking the ground or foliage. The unique climatic circumstances that produce this phenomenon may last only a few minutes or hours, but the consequences can be great. People and animals may have extreme difficulty walking and may fall and injure themselves. On an equine endurance trail ride, a late-spring freezing rain and snow storm halted a group of horses on the summit of a small mountain peak. Lightning accompanied the storm. The horses were frightened by the thunder and lightning and milled around. Frozen rain and snow accumulated within the shoes on the bottoms of the feet, producing a “horse on ice skates.” There was little direct danger from the lightning, because the peak was covered by radio and television repeater towers with lightning rods attached, but there were anxious moments until the storm abated and the horses’ feet could be cleaned out. Fire.  Fire is an ever-present risk in forests and shrubbed areas (see Chapter 12). Trek leaders should have a plan ready for human evacuation to safety, as well as how to deal with the trek animals. In brush and forest fires, wind is an important factor. Crown fires (flames racing through the tops of trees in a forest) are particularly troublesome. Do not try to outrun a fire burning up a slope. The heat generated by the fire rises and preheats the area above the fire, setting up ideal conditions for rapid spread. In some instances, a hillside may seem to explode into flames because of the extensive preheating. When llamas were caught in an advancing brush fire, they were herded into a bare ground area. In another situation, the llamas were simply turned loose to fend for themselves. Owners remarked that the animals adjusted quite well, without panic. When owners returned to their animals, they found them hungry and thirsty, but without evidence of smoke inhalation or eye

damage. Llama fiber does not burn readily, but it smolders, and in some animals burn spots were noted in the fleece. At one ranch, the only serious problem was burns on the foot pads, presumably caused by animals stepping on hot coals. No one was able to observe how the animals avoided the flames, but both adults and young animals did so. No abortions or premature births occurred as a result of stress. In a fire situation, horses should be turned loose or ridden to a safe place. Flooding.  Animals accompanying trekkers in wilderness areas may become involved in flood conditions when they are tethered near streams that are known to generate flash floods, or when unexpectedly heavy storms cause overflowing banks of streams and rivers. A dam may burst, causing a sudden discharge of tremendous amounts of stored water. Animals are at the same risk as humans. Dry streambeds in many desert areas are prime candidates for flash floods that may be generated miles away, so they should be avoided as campsites. Animals should not be tethered in such locations. Trek leaders should be aware of dams along streams, especially Earth-filled dams. Heavy storms may erode a dam or fill a reservoir behind it beyond its capacity. A llama owner in Idaho watched as a wall of water filled a gorge more than 100 feet deep and nearly engulfed his home, barns, llamas, and farm from a burst dam a few mile upstream. Horses, llamas, and dogs can all swim but may not be able to cope with the currents generated during a flood.

DISORDERS UNIQUE TO HORSES, MULES, AND DONKEYS Common trail disorders encountered in horses, mules, and donkeys may be classified as traumatic, metabolic, or digestive. Laminitis Acute and chronic forms of laminitis (or founder) are possible, but only the acute equine form is likely to be seen in trek animals.4,14 Horses with the chronic form should be excluded in the pre-trip physical examination. Llamas and elephants also have laminae that attach their toenails to the third phalanx, but horses, with their enclosed hoof and complex laminar anatomy, are predisposed to laminitis. Recognizing and minimizing the effects of predisposing factors are the focus of this presentation. Etiology.  Trauma is the most likely cause of inflammation of the foot in the trek horse. Horses should have been trained in a terrain similar to that expected on the trek. However, even a trained horse occasionally encounters an excessively rocky path that traumatizes its feet, especially if the rider is unwise and fails to slow the pace when negotiating the trail. Leather or synthetic pads worn under the shoe may offer some protection, but new pads may be chewed off the foot by rocky trails after less than 80 km (50 miles). Other predisposing factors include ingestion of lush pasture or grain overload and the metabolic stress associated with dehydration or overexertion. Endotoxemia associated with gastrointestinal disorders (severe colic) or septicemia may cause laminitis, but the primary disease is of greater concern to trek personnel. Whatever the predisposing factor, inflammation in the confines of an inflexible hoof causes swelling and malperfusion at the capillary level, and malperfusion causes arteriovenous shunting. Excessive ingestion of cold water, especially when the horse is overheated, may also precipitate laminitis. Clinical Signs.  Laminitis usually develops on both forefeet, but hind feet may also be affected in severe cases. The horse shifts its center of gravity to the hind limbs to minimize pressure on the forefeet, standing with the hind limbs forward under the body and the forelimbs extended in front of the body (camped forward in front), as seen in Figure 61-11. The feet are warm or hot to palpation, and there is a pounding digital artery pulse. The horse is reluctant to move. 1209

CHAPTER 61  Emergency Veterinary Medicine

mosquitos are prevalent, trek horses and llamas should be vaccinated (two injections, 1 month apart). When trek managers contract for animals, they should ensure that the animals have been properly immunized.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Clinical Signs.  Hot and tender swellings are the primary signs of acute saddle sores. The hair or epidermis may be rubbed off. General sensitivity over the back is usually caused by muscle soreness. Evidence of previous sores includes white hairs in spots over the withers or saddle bed, scars that may or may not be haired over, thickening of the dermis, and alopecia with or without swelling.

FIGURE 61-11  Stance of a horse with laminitis: front and hind legs are extended forward.

Management.  Preventing or minimizing the causes of laminitis is vitally important. Once clinical signs occur, the objectives of treatment are to eliminate the predisposing factors, decrease inflammation, and maintain or reestablish blood flow to the laminae. If laminitis is the result of a digestive upset, it is imperative to administer a cathartic (Epsom salts [magnesium sulfate], 1 kg [2.0 lb] in 4 L of water via nasogastric tube). Phenylbutazone (Butazolidin, 6 mg/kg daily, intravenously) should always be administered to relieve pain so the horse will move. Acepromazine maleate (0.04 mg/kg every 6 hours, intramuscularly) is used as a vasodilator to enhance blood flow to the laminae. If available, heparin (60 units/kg subcutaneously) helps to prevent platelet aggregation and thrombus formation. In acute laminitis, the feet are warm or hot, so the inclination is to soak the feet in cold water. However, this is contraindicated, because the object is to increase circulation to the foot, not to inhibit it. It is now thought that mild exercise is an important aid in preventing damage to the laminae. The horse should be exercised slowly on soft ground for 10 to 15 minutes every hour for 12 to 24 hours, and then exercise should be stopped. Even slow walking may be quite painful. A low volar nerve block relieves pain and inhibits vascular constriction within the foot. This is accomplished by palpating the pulsating artery on the posterior lateral aspect of the fetlock (Figure 61-12). The nerve lies posterior to the artery. With a 20- to 22-gauge needle, 3 mL of 2% lidocaine is injected over each nerve. It may be necessary to repeat nerve blocks two or three times daily for several days. Corticosteroids are contraindicated. Saddle, Cinch, and Rigging Sores Saddle sores are contusions, abrasions, or ulcerations of the skin and subcutis caused by friction or point pressure from the saddle, cinch, or rigging. Etiology.  Improperly fitted or maintained tack causes poorly distributed pressure, which is the primary cause of saddle sores. A saddle tree may fit a horse properly at the beginning of a training period but become unsatisfactory after the horse has trimmed down. Spot pressure causes local ischemia. If pressure is prolonged, the capillary bed may be damaged. When the pressure is released rapidly, blood rushes into the blanched site, and extravasation may occur, causing swelling and pain. If the lesion is rested and treated as inflamed tissue, complete healing may occur. However, if the saddle is reapplied, it overlies a lump that is subject to abrasion. The injury can extend through the dermis, resulting in severe ulceration. Cinch and rigging sores are usually caused by friction, leading to blister formation. 1210

Treatment.  Prevention is better than treatment. Toughening the backs of trail horses is a major job of the trainer. Proper pads or blankets must be selected for each horse. On arrival at a rest area, the girth should be slowly loosened at intervals of 10 to 15 minutes to prevent rapid flow of blood into ischemic areas. Once a sore has developed, the horse must be rested or the tack changed to eliminate pressure or friction on the lesion. Holes are often cut in pads to accommodate a saddle sore, but spot pressure at the ring edge may be as detrimental as the original cause of the saddle sore. Riders must keep tack cleaned and in good repair. When the saddle is removed, cold water poured over the back for 15 minutes may minimize swelling. Myopathy Exertional myopathies of horses vary from simple muscle soreness, through the tying-up syndrome (similar to a charley horse in humans), to paralytic myoglobinuria (rhabdomyolysis, azoturia).6,14 Etiology.  Muscle integrity and function depend on proper mobilization and use of energy. Conditioned muscles may function vigorously for extended periods, but if either energy mobilization or use is accelerated to the extreme, mild to severe muscle necrosis may occur. Clinical Signs.  Mild muscle soreness is characterized by alterations in gait that indicate muscle weakness. As severity increases, the gait becomes progressively altered until the horse is in obvious pain and is reluctant to move. The horse has an anxious expression and may sweat excessively. Affected muscles are painful to palpation and may be swollen. Skin temperature over the muscle may be elevated. Muscle spasms may occur but not consistently. Myoglobinuria is observed grossly in moderate to severe cases and should be considered prima facie evidence for stopping and resting or treating the horse.

B

F

A

B

CD E F

H H

G

FIGURE 61-12  Diagram of the anatomy of the equine fetlock. A, Skin. B, Flexor tendons. C, Volar nerve. D, Palmar digital artery. E, Digital vein. F, Suspensory ligament. G, Sesamoid bone. H, Metacarpal bone (cannon).

Dehydration Etiology.  Fluid and electrolyte imbalances6,12,13 play a major role in all metabolic medical problems that develop in the horse as a result of exertional stress. The degree of dehydration is directly related to the amount of fluid lost through evaporative cooling (sweat), which in turn is related to the amount and rate of work performed and to ambient temperatures and humidity. The horse must have an adequate amount (38 to 57 L [10 to 15 gal]) of water each day during a trek. The more strenuous the activity, the more fluids are required. Mules, and especially donkeys, are adapted to coping with mild dehydration. Clinical Signs.  Signs of mild dehydration (3% loss of body weight) are low urine output, dry mouth, and mild loss of skin elasticity. Moderate dehydration (5% loss of body weight) is characterized by marked loss of skin elasticity. The eyes become sunken. Blood pressure may fall as a result of decreased plasma volume. Weakness, fever, and weak pulse may be observed. Sweating is not possible, even with elevated body temperature. Marked dehydration (10% loss of body weight) may involve circulatory failure from decreased plasma volume. Treatment.  During 3 hours of hard work, a 450-kg (about a 1000-lb) horse may lose as much as 38 L (10 gal) of fluid. If this degree of dehydration is not corrected quickly, death may result. The horse should be allowed to drink along the trail if water is available. Small amounts of cool, but not cold, water should be offered. If the horse refuses to drink, gastric intubation may be indicated. Fluid is also absorbed from the colon; thus enemas of water (10 to 20 L [2.6 to 5.3 gal]) are effective in rehydration. Electrolyte replacement is encouraged, but for the usual case of dehydration, this is not critical. Packaged electrolytes are available in veterinary supply shops. Heat stress usually accompanies dehydration, so cooling (such as shade or a water bath) is important. Administration of intravenous fluids, if available, is routine therapy. Camels are uniquely adapted to desert conditions. They are able to survive a week without water. Optimally, a camel, like horses and llamas, should be watered daily. Camels do not store water but conserve it because of a diurnal fluctuation of body temperature, from a normal of 37° C (98.6° F) up to 42° C (107.6°F). The body acts as a heat-sink during the heat of the day, thus conserving vital water that would otherwise be lost through evaporative cooling. During the cool desert night, the heat is dissipated by conduction. Camels can concentrate urine to a syrup consistency to avoid water loss through urine. Fecal pellets are passed that are dry enough to be used for fuel immediately after defecation. The camel can tolerate a 25% reduction in body weight from dehydration, and after such severe dehydration is able to drink sufficient water at one session to rehydrate. The shape of the camel erythrocyte is elliptical, allowing circulation despite significant hemoconcentration. This elliptical shape allows the cell volume to expand 250% without hemolysis when rehydration occurs. Exhausted Horse Syndrome The term exhausted horse syndrome (EHS) was coined to describe a complex metabolic syndrome occurring when horses are pushed beyond endurance limits.6,14 The syndrome has no precise characterization, because the initiating mechanism varies with the

prevailing conditions. The development of EHS depends on the condition and training of the horse, the pace set by the rider, the terrain traversed, and climatic factors such as temperature, wind, and humidity. Clinical Signs.  There is a composite picture, but the individual horse may show only a few signs. The severely affected horse is depressed and exhibits lethargic movements, holding its head low. The eyes are expressionless. Facial grimacing creates an anxious expression that may progress to a pained expression if colic or muscle spasms accompany the syndrome. The horse takes no interest in its surroundings. Anorexia is typical, and frequently the horse has no inclination to drink, even though dehydrated. The corneas appear glazed. Body temperature is usually elevated and may reach 41° C (106° F). The horse does not cool properly. Usually, body temperature continues to rise. Temperature measured rectally may be inaccurate in the exhausted horse, because the anal sphincter loses tone and allows air to enter the rectum. Cardiovascular and respiratory systems are markedly affected by endurance riding. Heart and respiratory rates are elevated. The rates depend on the prior condition of the horse, pace, length of action, and amount of work performed in climbing or walking on soft footing. Heart rates of 150 beats/min are not uncommon after a grueling climb. With 10 to 15 minutes of rest, the heart rate of a conditioned horse should drop below 60 beats/min, whereas in the exhausted horse, tachycardia and tachypnea may persist. The exhausted horse may have a respiratory rate faster than the heart rate. Respiration under these circumstances is shallow and inefficient. Additional cardiopulmonary signs may include synchronous diaphragmatic flutter, arrhythmias, murmurs, and visible jugular pulses. Auscultation of the thorax may reveal moist rales and, in extreme cases, frank pulmonary edema. Severe dehydration is the most consistent sign of EHS. Loss of skin elasticity, sunken eyeballs, and dry mouth and mucous membranes reflect a 7% to 10% loss of body weight, after a loss of 30 to 40 L (8 to 10.5 gal) of fluid. Serious electrolyte and acid–base imbalances are associated with dehydration. Alkalosis is common. Muscular manifestations of EHS include fatigue, trembling, spasm, stiffness, muscles painful to palpation, and rarely, exertional rhabdomyolysis (stiff gait, excessive sweating, high respiratory rate, and firm and painful muscles of the back and rump). Horses suffering from EHS are prone to colic, which also may occur independently. When colic accompanies EHS, it is of the spasmodic type, with diminished or absent borborygmus. Treatment.  Rest, rehydration, and electrolyte supplementation are the keys to recovery. If the horse is drinking and will take electrolytes in the water, the effect is nearly as beneficial as the administration of intravenous fluids. Packaged electrolyte powders can be carried. If the horse is hyperthermic, shows evidence of shock, and refuses to drink, more drastic steps must be taken. The horse may require 40 to 50 L (10.5 to 13.2 gal) of fluid. Beside intravenous fluid (80 mL/kg/hr) administration, gastric intubation may be employed to give fluids orally. Enemas are also effective, because fluid is absorbed from the colon (it is essentially impossible to instill water into the rectum too rapidly or in too great a volume as long as the fluid is allowed to be pushed out by peristaltic activity). Synchronous Diaphragmatic Flutter Synchronous diaphragmatic flutter (SDF) is a clinical sign observed in endurance horses while on long-distance rides, and it may be seen on an expedition.4,6,14 It is defined as spasmodic contraction of the diaphragm synchronous with the heartbeat. It is not life threatening per se, but indicates mild to serious metabolic conditions that may be, or may become, life threatening. Overexertion with excessive sweating produces metabolic alterations. The development of SDF at any point on a trek should be ample reason to prevent the horse from going further until the metabolic alteration is resolved. 1211

CHAPTER 61  Emergency Veterinary Medicine

Treatment.  Rest is paramount in all cases. A rider may have difficulty differentiating the pain associated with myopathy from that seen with colic until the horse is allowed to lie down, looks at its own side, or kicks at its own belly. It is disastrous to force the severely myopathic horse to walk, as is done with a suspected case of colic. If there is doubt, the horse should not be exercised. Horses in inaccessible locations should not be walked out until all possible recovery has taken place. Horses with mild muscle soreness may improve if walked slowly, but rest from ride exertion is the primary recommended therapy.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

Although acute exertional stress is characterized by acidemia, SDF is associated with alkalemia. Electrolyte imbalances may also be involved. Experimental work seems to indicate that hypocalcemia, hypokalemia, and alkalosis act in concert (or, less likely, individually) to cause equine SDF. Clinical Signs.  SDF may develop after 32 to 48 km (20 to 30 miles) of riding. There is no gender, age, or breed predilection. The primary sign is spasmodic contraction in the flank area. The “thump” is easily felt by light palpation in the flank area. Auscultation of the heart while holding a hand over the dorsocaudal rib area can reveal that diaphragmatic contraction is synchronous with the heartbeat. SDF may be the only clinical sign noted, or it may be seen as part of EHS. The degree of thumping may vary from a barely perceptible quiver to a contraction that seems to rock the horse’s body and is observable from a distance. The flutter may be continuous or intermittent, especially in degree. Treatment.  Rest and rehydration are required. Colic* Colic is the clinical manifestation of abdominal pain, usually the result of a gastrointestinal disorder. It may also arise from the urinary system or peritoneum. The condition is most commonly seen in horses, but may be seen in all animals. Types of colic in horses are numerous because of the unique and complex anatomy of the equine digestive system (Figure 61-13, online). The colon and caecum are voluminous in the horse, but there are narrow areas where impactions may form. The ileum enters the colon near the pelvic inlet. Etiology.  Colic may be produced by gastric tympany, intestinal obstruction, or hyperspasticity. The most likely inciting causes on a trek are overeating of nonregular forages, ingestion of poisonous plants, or exhaustion. One illustrative tale is of a commercial packer who hobbled a pack string of horses to graze in a meadow for a noon rest stop. Two hours later, when it was time to begin the afternoon trek, two of the horses were colicky. In checking the meadow, the packer saw many plants of death camas (Zygadenus species), some of which had been eaten. The colic was sufficiently severe to require a layover at the meadow for the rest of the day. Clinical Signs.  Horses express colic by looking back at one side, stamping the feet, getting up and down, rolling, and pressing the head against trees or rocks. The pulse rate may exceed 100 beats/min, and the pain may be severe. The conjunctival membranes are congested and cyanotic. Treatment.  Only superficial emergency measures are discussed. Treatment is variable, depending on the anatomic location of the obstruction or spasm. Mild obstructions may be relieved by hydration and administration of a cathartic. Cold-water enemas may stimulate sluggish intestinal peristalsis and relieve impaction of the terminal small colon. Pain and spasms may be relieved by administration of flunixin meglumine (Banamine), 0.6 mg/kg intramuscularly twice a day. Walking the horse may prevent it from lying down and rolling, which may result in torsion of the intestine.

MEDICAL PROBLEMS UNIQUE TO PACK LLAMAS Most of the medical problems in llamas12,13 have been considered earlier, under headings of disorders common to all animals. Llamas are hardy animals and unlikely to allow themselves to be pushed to exhaustion. If fatigued, they simply lie down and refuse to rise. They will not tolerate excessive loads. An appropriate load for a well-trained and conditioned large llama is 45 kg (100 lb).

*Reference 14.

1212

Plant poisoning is more likely in llamas than in horses, but such incidents are rare. Rope burns from entanglement in tethers are less likely than in horses. The llama is less excitable, and if it becomes entangled, it usually lies quietly until help arrives. North American venomous snakes pose minimal threat to large animals. However, llamas are curious and may be bitten on the nose while investigating the strange animal. Nose bites from rattlesnakes are especially hazardous to llamas, because local swelling may occlude the nostrils (see Snakebite, earlier). Llamas are primarily obligate nasal breathers, so dyspnea and suffocation may ensue. Rattlesnake bites of the limbs cause edema and in severe cases, local tissue necrosis and ulceration. Many cases are diagnosed as trauma unless the bite is observed. The signs of snakebite in llamas are essentially the same as in horses.9,12 Therapy for a nose bite may require tracheotomy (in the upper one-third of the neck; the surgical approach is similar in all species) and insertion of an improvised tube to allow breathing. Edema may persist for 2 to 3 days. If the bite is observed and progressive swelling noted, a small tube (1 cm [just under 0.5 inch] in diameter) can be inserted 15 cm [about 6 inches] into the ventral meatus of the nasal passage and sutured to the nares. An alternative improvisation is to insert a woman’s small hollow plastic hair curler into the nostril. Swelling occurs around the tube or curler, but patency of the nasal passage is maintained.

MEDICAL PROBLEMS IN CAMELS Camel Pox Camel pox is the most common infectious disease of camels in their native countries. Pox has not occurred in the feral camels of Australia. Etiology.  Camel pox is caused by Orthopoxvirus cameli and is unique to camels. It is related to vaccinia, cow pox, and monkey pox. It is transmitted by contact through abraded skin or mechanically by flies. Clinical Signs.  In mild cases, signs may be limited to typical pox pustules on the nostrils, eyelids, and oral and nasal mucous membranes without systemic signs. More severe infection may produce lesions over the entire body and within the respiratory tract. Management.  There is no treatment once lesions have formed. An effective vaccine is now available and should be given at least a month before a trek into an endemic area. Trypanosomiasis Camels are subject to many species of parasites, but the only one likely to be encountered while on a trek is trypanosomiasis, caused by protozoan parasites in the genus Trypanosoma. Trypanosoma evansii is the etiologic agent for surra, a serious disease in India, the Middle East, Africa, Asia, and Southeast Asia. Clinical Signs.  In acute cases, the parasites may be observed in circulating blood. Signs may include fever, progressive anemia, depression, weakness, ventral edema, emaciation, secondary pneumonia, and death. Management.  There are therapeutic agents used to treat these parasitisms; however, it is more important to have a pre-trip physical examination performed that includes a hemogram, which provides information on anemia.

MEDICAL PROBLEMS IN OXEN, YAKS, AND WATER BUFFALOS These animals are subject to the diseases common to other large animals that may be used on a trek.

MEDICAL PROBLEMS IN ELEPHANTS The primary concern for elephants is damaged feet. Toenails, soles, and pads must be properly groomed and the feet checked daily, or more frequently, for stones, slivers, and traumatic lesions.

When dealing with injured dogs, it is imperative to remember that these animals are predators capable of causing grave injury to people. Dogs that would ordinarily be very tractable and trustworthy can inflict serious wounds on their owners when in a fight with another animal, injured, scared, or in pain. Deydration Etiology.  Dehydration is of definite concern in dogs. Although dogs do not sweat, evaporative fluid loss from panting is significant, particularly in dry weather. Clinical Signs.  Hydration status can be estimated by touching a finger to the gums, which should be pink and moist, not tacky. Another method of evaluation is by lifting up the loose skin over the shoulder blades and then letting it drop. The skin should slide back rapidly to its normal position in a well-hydrated animal; if it does not, suspect dehydration. Since skin elasticity decreases with age, examiners must take the animal’s age into account. It is prudent to establish the baseline normal situation for animals prior to the expedition by feeling the gums and checking skin status in the non-dehydrated condition, so that a change in status can be appreciated. Management.  Prevention is obviously the best treatment for dehydration. Most dogs can keep up with fluid losses through oral intake if provided with adequate water supplies and the opportunity to drink. However, in some cases, dehydration can still occur. Search dogs will perform their duties with enormous dedication and vigor in spite of becoming dehydrated, so they may need to be pre-hydrated with crystalloid, particularly when their activities are carried out in a hot and humid environment. Fluid There are several ways to administer necessary fluid to a dog, depending on the clinical situation. The fluid types used in dogs are the same as those in people, and include crystalloids such as lactated Ringer’s solution (LRS) or normal saline. The “shock dose” that is approximately equal to the animal’s blood volume is 90  mL/kg of crystalloid in the dog. This is not generally given as a single bolus, but administered titrated to effect. There are several methods of fluid administration. The best method is intravenously through a cephalic or lateral saphenous catheter. Fluids can also be given subcutaneously, except in cases of severe dehydration where they will not be absorbed, such as in very cold weather where they could contribute to frostbite. For subcutaneous administration, the skin can be tented up and a needle placed in the subcutaneous space. In this method, the amount of fluid given per site is generally 10 to 20  mL/kg and is limited by patient comfort. Fluids given subcutaneously are absorbed over 4 to 8 hours. In very small or young dogs, fluid may also be given by intraosseous catheter. Spinal Trauma The vast majority of spinal trauma in dogs is caused by vehicular accidents (when the animals are struck by cars). Because of the size and strength of the neck muscles in relationship to the head, cervical spinal injuries are less common than are thoracolumbar injuries. Thus, immobilization of the head and neck after trauma in dogs is less of a priority than in humans. Spinal cord injury results in varying degrees of paresis or paralysis depending on the nature of trauma. The most important factor affecting longterm prognosis is whether the dog retains sensation in the hind legs for thoracolumbar injuries, or in all four legs for cervical injuries. When evaluating pain sensation, the toes should be pinched firmly just behind the toenails with fingernails or even with an instrument such as a hemostat. It is important to remember that withdrawing the foot is a reflex and does not by itself indicate that the dog has sensation in the toes. The dog must vocalize or look up at the rescuer and acknowledge that it feels the painful stimulus. If pain sensation has been lost in a dog with a spinal cord injury, the prognosis if very guarded for return to

function, although some dogs will do well in a cart. Dogs with suspected spinal cord injuries should be immobilized as best possible and transported for veterinary care. Poisoning While dogs rarely eat enough of poisonous plants to cause problems, there are many toxins present in the outdoors that they may encounter, including eating the medications (and recreational drugs) of their owners. Unless the substance is caustic or a petroleum product, if there is a high suspicion that a dog had ingested a toxin at a toxic dose, vomiting should be induced. Apomorphine tablets crushed and placed into the conjunctival sac is the ideal method to induce vomiting; 1 to 2  mL/ kg of household (3%) hydrogen peroxide or a few tablespoons of salt can act as gastric irritants and cause vomiting. Because salt and hydrogen peroxide are gastric irritants, there can be side effects to these methods. Several animal poison control hotlines are available to consult for a fee and can be very valuable. These include American Society for the Prevention of Cruelty to Animals (ASPCA) Poison Control Center (888-4264435); PROSAR International Animal Poison Center (888-2328870); and Pet Poison Helpline (800-213-1680). The best thing to do is to carry a phone number for a veterinarian willing to be available to take a telephone call for advice during your expedition. • Ethylene Glycol:  This is found in automobile antifreeze and windshield wiper fluids. It is sweet, so dogs like the taste. The minimum lethal dose is 4.4 to 6.6 mg/kg. • Grape and Raisin Toxicity:  This is not dose related and is a cause of renal failure in some dogs. • Lead Toxicosis:  In a wilderness setting, this occurs most commonly from ingestion of lead fishing weights, because most shotgun pellets used to hunt birds no longer contain lead. Clinical signs include GI upset and neurologic dysfunction. • Strychnine:  Strychnine is used as coyote bait and can be eaten by dogs. It causes tetanic seizures. Sled Dogs Sled dogs undergo unique training and have things asked of them that are far beyond tasks expected of most other domestic dogs. One of the problems most frequently encountered in sled dogs in a race situation is hemorrhagic colitis. This has been associated with multiple possible causative microbes, such as Campylobacter and Salmonella, some of which are zoonotic. However, the common causal factor seems to be the extreme physiologic demands of racing. Treatment is with metronidazole (10 to 15 mg/ kg PO BID) and supportive care. Sled dogs are also prone to carpal (wrist) injuries because of punching through the top snow crust. These injuries generally resolve with rest. Sled dogs are prone to foot injuries; most racing dogs wear preventive booties for this reason. Feet and booties should be inspected regularly. Although dehydration is a concern in sled dogs because of the evaporative loss from panting, it important to remember that subcutaneous fluid should not be given because of the increased risk of frostbite. In a severe cold weather situation, all necessary supplemental fluid should be given intravenously. Laryngeal Paralysis Etiology.  This disease occurs in older medium and large breed dogs, particularly Labrador retrievers. The problem occurs because of degeneration of the recurrent laryngeal nerve that innervates the intrinsic muscles of the larynx. There is mounting evidence that for many dogs, this problem is one part of a generalized, slowly progressive, peripheral neuropathy. Clinical Signs.  This slowly progressive disease manifests as respiratory stridor with increased respiratory noise and effort, particularly during the inspiratory phase. Many afflicted dogs have a greater-than-normal hoarse bark because they are unable to close the glottis to initiate the normal bark. As the dog attempts to inspire, negative pressure generated in the airway apposes the arytenoid cartilages and closes the glottis. The harder the dog works to breathe, the more difficult breathing 1213

CHAPTER 61  Emergency Veterinary Medicine

PROBLEMS UNIQUE TO DOGS

PART 6  ANIMALS, INSECTS, AND ZOONOSES

becomes. Dogs with laryngeal paralysis can become hypoxic, but the disease is more commonly life threatening because the dogs are unable to thermoregulate effectively by panting. In a vicious cycle, the hotter the dogs become, the harder they work to breathe, and the more heat they generate. Because they cannot dissipate this heat, heat stroke can result. Many afflicted dogs do well when relaxed and in a cool environment, but the stress of outdoor activity, particularly in warm weather, can precipitate a crisis. Because this is a disease that affects breeds commonly favored by outdoors persons, it is important to take preventive measures in any dog suspected. Treatment.  Treatment in the field involves preventing and managing heat and other stresses. Dogs should be kept cool and calm. Exercise should be avoided and every effort should be made to keep the dog from becoming overheated or excited. Sedation can be used if available. If the dog is in a critical situation, endotracheal intubation or tracheostomy can be performed, although this is rarely feasible in the field. Gastric Dilatation and Volvulus or “Bloat” Etiology.  Gastric dilatation and volvulus (GDV) occurs most commonly in older, large and giant breed dogs, particularly deepchest breeds such as Great Danes. In this condition, the stomach twists around such that both the esophagus and pyloric outflow become occluded. The stomach distends with gas and stretches until it severely impedes blood flow with resultant physiologic abnormalities and possible gastric necrosis. This condition can be fatal within 6 hours of onset if untreated and mortality rates are high even with appropriate treatment. Mortality is almost 100% without treatment. Clinical Signs.  Dogs with this condition are unable to swallow or to vomit. They will attempt to vomit and often bring up recently swallowed saliva that looks like uncooked egg whites. Their abdomen becomes progressively distended and tympanitic as the stomach fills up with gas. They will become weak and shocky as the condition worsens. Treatment.  Definitive surgical treatment is needed to resolve this problem. All haste should be made in taking the animal to a veterinary facility. While the animal is being transported, passing an orogastric tube is ideal to decompress the stomach. However, this can be very difficult, even with an anesthetized dog and proper equipment. One way to relieve gaseous distension is to perform trocharization with a large bore needle, or preferably a large bore over-the-needle catheter that is less likely to lacerate the stomach as it decompresses. This procedure should only be attempted in situations where veterinary care is not immediately available, because of risk of lacerating abdominal organs. The needle or catheter is inserted about a hands’ width behind the last rib in the center of the lateral body wall. The operator will hear and smell gas escaping if trocharization is successful. This can repeated multiple times if necessary while the animal is being transported. Porcupine Quills When dogs are brought into porcupine country, the risk for an encounter is great. Some dogs fail to learn from experience and are repeatedly quilled. The dog must have physical contact with the porcupine for the tail to introduce the quills. The muzzle and face are the usual sites of penetration, and a dog can be blinded by perforation of the eyeball. The quills must be removed physically. A pair of pliers should be included in trek supplies and equipment. The process is painful; sedation with diazepam is indicated. The quill should not be broken because the retrograde barbs on the quill foster migration and abscess formation. Grass Awns Numerous species of grass, such as foxtail grass, have awns with barbs that may become attached to the dog’s hair coat or lodged in the external ear canal, nasal passage, conjunctival sac, or interdigital space. Dogs that must travel at the time of year 1214

when plants are mature and the awns are easily dislodged from the seed head should be inspected frequently for awns in these sites. Signs depend on the location of the foreign body. When it is within the ear canal, the dog paws at its ear and shakes its head. The head may be held tilted. Exudate may flow from the ear. Awns in the nostril cause sneezing and nasal exudate. Awns in the conjunctival sac cause lacrimation, photophobia, and corneal edema and ulceration, and the dog paws at the eye. Awn penetration between the digits and at other locations through the skin is more difficult to diagnose because the awn may be at some distance from the fistula. Awns must be removed physically. Sedation, topical anesthesia, or both may be necessary. Although topical ophthalmic anesthetics are desirable in the eye, lidocaine may be used in an emergency. A pair of small alligator forceps is most suitable for reaching into otherwise inaccessible places. An otoscope may be necessary to visualize awns in the nostril or ear canal. Instillation of an antiseptic or antibiotic ointment is desirable after removal of the awn. Stinging Nettle Poisoning Stinging nettle (Urtica species) is common along streams and lakes in wilderness areas.13 Humans vary in sensitivity when the plants accidentally contact exposed skin. Leaves and stems are covered by harsh hairs, some of which have a tiny ball tip that breaks off just before penetration. The specialized hairs are hollow. A base gland produces histamines and acetylcholine, which are injected into the victim. Short-haired dogs that move through patches of stinging nettle are at risk for poisoning from the cumulative effect of thousands of minute injections of acetylcholine. Weakness, dyspnea, muscle tremors (characteristic of the action of acetylcholine on peripheral nerves) and even death have been reported in a few hunting dogs with massive exposure. Parasympathomimetic effects include salivation, diarrhea, tachycardia, and pupillary dilation. Atropine sulfate (0.04  mg/kg) subcutaneously is a specific treatment, although it may not be effective. Antihistamines such as diphenhydramine (2  mg/kg PO or SQ) may be of clinical benefit. Harness Sores Improperly fitted harnesses on sled dogs may produce the same type of friction lesions that occur in horses or llamas.

DISEASES UNIQUE TO CATS Basic medical care for a cat is similar to that for a dog. Fleas are mentioned because of the usual close contact of a cat with its owner or other people on the trek. Many people are sensitive to flea bites. Cats should be treated to kill fleas before the trek begins, but they may acquire fleas from other cats they encounter or from rodents. Constipation (obstipation) is a sign associated with many diseases. On a trip, a cat may respond negatively to a change in diet. If the cat is habituated to defecating in a litter box, it may be necessary to train the cat to use soil before taking it along on a trek. Signs of constipation include anorexia, lethargy, tenesmus, and frequent unsuccessful attempts to defecate. Severe cases of constipation may be treated with cool-water enemas and handled in much the same way as a constipated person. Hairballs Ingestion of hair during self-grooming is a frequent cause of gastric irritation and obstruction in cats. The prominent clinical sign is vomiting, commonly with hair found in the vomitus. Hairballs may exit the stomach and cause obstruction farther along the gastrointestinal tract. The usual management of hairballs is to place a commercial lubricant laxative on the paw of the cat, which it will lick off and ingest. The common ingredients in such commercial products are white petrolatum, cod liver oil, corn syrup, malt syrup, and light mineral oil. Typical commercial products are Laxatone, Cat Lax, Lax-aire and Laxa Stat, which are obtained in pet shops and veterinary clinics. These medications may also be used for mild constipation in cats and dogs.

Support animals may escape from any type of restraint and run away or simply wander off. More commonly, animals are tied with improper knots, or poor-quality snaps and halters are used that break when the slightest pressure is applied. A trekker may tie an animal to a shrub, bush, or branch that can be pulled up or broken off with a slight tug. Animals that are frightened by predators or other wild animals wandering into an area where they are tied may bolt and exert tremendous pressure on tethers, picket lines, stakes, or branches. Hobbling is a common technique that allows horses and mules to graze. Trek leaders must know the habits of individual animals when hobbled. One horse may accept having the front feet hobbled together and graze peacefully, taking only the short steps possible. Another horse may learn how to gallop with the front feet hobbled. The author once had to track a pair of packhorses for 5 miles to recapture them. They were heading home, and the only thing that stopped them was a stream they could not negotiate with the hobbles on. Some horses must be hobbled with three restrained legs. Even experienced trekkers (such as commercial packers) may become overconfident and place misguided faith in an animal’s willingness to stand quietly without wandering away. The trekker may leave just a lead rope or ground tie dragging on the ground. The animal may become frightened or bored and wander off. The author is aware of a llama carrying a full pack that wandered off and was missing (pack and all) for a full month. Contrary to popular belief, not all llamas are social, so they may not return to a herd that is securely tethered. Llamas, like horses and dogs, have homing instincts and may set off toward where they presume home to be located. Steps to Take in the Event of an Escape If a breakaway is observed, members of the party should not further frighten the animal by rushing at it. It should be given a chance to settle down and return to the group. The handlers can move around the animal to block obvious escape routes but should not try to chase it. All of these animals can run faster than a human. If the escapee has an animal buddy in the group or a favorite person, the animal buddy can be used as “bait” or the favorite person can make an approach. A favorite treat in camp can be used to entice the animal back to the fold. If an animal is discovered missing, an analysis of the situation to determine what caused the escape is needed. Was it frightened? Did it break tack? Is it dragging a log, branch, or rope? Is there evidence that other animals were nearby? Is blood or hair strewn about? In what direction did it probably go? Generally, animals return toward the direction from which they have come. Frightened animals or those escaping at night may not adhere to any rule. A search for tracks can be made, but llamas may not leave much of a track, particularly in rocky terrain. Scanning the surroundings may result in a sighting of the animal. It may be in the vicinity of camp, resting under a tree or in a clump of bushes. The search should be conducted in a planned fashion, using all persons possible. Unless tracks direct otherwise, the trail back toward a trailhead should be searched first. From firsthand experience, the author can attest to the desirability of taking another animal, preferably a buddy of the escapee, along on the search. Even though the animal is sighted, it may not be caught unless a second animal is there to bait it. Vantage points should be used, and searchers should consider where they themselves might have gone under the circumstances. Lush meadows or other areas where desirable feed may exist should be checked. Fellow hikers, and ultimately the Forest Service or other regulatory agencies, should be alerted about the missing animal.

MEDICATION PROCEDURES A list of medications and indications for their use is provided in Tables 61-3 and 61-4. In the horse, intramuscular injections are given in the neck or rump. Subcutaneous injections are given by lifting a fold of skin just cranial to the scapula. Intravenous injections are given in the jugular vein, which is easily

A

CHAPTER 61  Emergency Veterinary Medicine

ESCAPE OF SUPPORT ANIMALS

B

D

E

A B

A

C

FIGURE 61-14  Diagrams of medication sites in the horse, llama, and dog. A, Subcutaneous. B, Intramuscular. C, Cephalic vein for intravenous. D, Jugular vein. E, Site for low volar nerve block.

distended along the jugular groove on the ventral aspect of the neck (Figure 61-14). In the llama, intramuscular injections are given in the relatively hairless area at the back of the upper rear leg, by standing against the body in front of the rear limb while facing the rear and reaching around the back of the animal to give the injection. Subcutaneous injections are given in the relatively hairless area of the caudal abdomen, just in front of the rear limb, or by lifting a fold of skin just cranial to the scapula. It is difficult for an inexperienced individual to locate the jugular vein for intravenous administration in the llama. Intramuscular or subcutaneous routes are recommended. In camels, intramuscular injections are given in the triceps muscle or the upper hind leg when the camel is in a kushed position. The jugular vein may be distended for intravenous administration. In oxen, intramuscular injections are given as in camels. Intravenous injections are easily given in the distended jugular vein. In elephants, intramuscular injections are given in the triceps muscle or upper hind leg. Subcutaneous injections are difficult in elephants because of their thick skin. Intravenous medication is administered into the veins on the back side of the ear. In the dog and cat, intramuscular injections may be administered in the triceps muscles caudal to the shoulder, paraspinal muscles on either side of the lumbar spine, or muscle masses on the upper rear limb. Subcutaneous injections are made by lifting a fold of loose skin on the neck near the withers. Intravenous administration is via the jugular vein or the cephalic vein (Figure 61-15). For the latter, an assistant grasps the limb at the elbow to occlude the vein, which courses on the dorsal aspect of the forearm. The vein is more visible if the hair is wetted down with water.

EUTHANASIA Euthanasia may become necessary in the event of injury or illness that cannot be corrected or when there is little likelihood of removing the animal to a location where remedial action can be taken. Horses, mules, donkeys, camels, llamas, and oxen cannot 1215

PART 6  ANIMALS, INSECTS, AND ZOONOSES

TABLE 61-3  Medications for Dogs* Generic Name

Trade Name (Company)

Concentration in Vial

Route of Administration

Acepromazine maleate Amoxicillin

Prom Ace (Fort Dodge) Generic

10 mg/mL or tabs Tabs

IM, SQ, PO

Ampicillin sodium Apomorphine

Generic Generic

Aspirin-buffered and enteric coated preferred Atropine sulfate

Generic

Dog

Indication and notes Tranquilizer

PO

0.05-0.22 mg/kg IM, SQ or 0.5-2.2 mg/kg PO 10-20 mg/kg q 12 hr

— Tabs, injectable

IM IM or crushed tab placed in conjunctival sac PO with food

10-30 mg/kg q 6-8 hr 0.04 mg/kg IV, 0.08 mg/ kg IM or 0.25 mg/kg in conjunctival sac 10-25 mg/kg q 12 hr

Generic

2 mg/mL

IM, SQ

0.04 mg/kg

Azithromycin

Zithromax (Pfizer)

PO

5-10 mg/kg QD for 3-5 d

Cephalexin

Generic, Keflex

PO

22 mg/kg BID-TID

Infections, skin

Charcoal (activated)

Generic

Concentration varies with reconstitution 250 mg and 500 mg capsules —

Infections and Lyme disease Infection For induction of emesis. Rinse conjunctiva after emesis occurs Canine specific NSAIDs safer and more effective. Inhibits platelet function Bradycardia, antidote for blue-green algae or muscarinic mushroom intoxication Infections

PO

Toxin adsorbent

Ciprofloxacin Clindamycin

Tabs Tabs

PO PO

Diazepam

Generic Antirobe, Cleocin, generic Generic

1-4 g/kg as slurry with water 10-20 mg/kg QD 5-11 mg/kg q 12 hr

5 mg/mL

IV, per rectum, intranasal

Diphenhydramine

Generic

Tabs, injectable

PO, SQ

Doxycycline

Generic

Tabs

PO

Famotidine Hydromorphone Lidocaine

Pepcid Generic Generic

Tabs, injectable Injectable 2%

PO,SQ, IM IM, IV, SQ

Metronidazole

Flagyl (pharmacia)

Tabs

PO

3-5 mg/kg q 12 hr (infection), 10 mg/kg q 24 hr (Lyme disease) 0.5 mg/kg q 12 hr 0.05-0.2 mg/kg q 2-6 hr As needed; do not exceed 8 mg/kg total dose 15 mg/kg q 12 hr

Misoprostol

Cytotec (Pfizer)

Tabs

PO

1-5 mcg/kg q 8-12 hr

Morphine

Generic

IM, SQ, IV

0.5-2 mg/kg IM, SQ, 0.1-0.2 IV q 4 hr

Nitenpyram

Capstar, Program

Oral, injectable variable concentrations Tabs

PO

Give per label directions

Omeprazole Oxycodone

Prilosec Generic

Tabs Tabs

PO PO

0.5-1.0 mg/kg q 24 hr 0.1-0.2 mg/kg q 6-8 hr

Prednisone Trimethoprim/ sulfamethoxazole Tramadol

Generic Tribrissen (Schering-Plough) Ultram (Ortho-McNeil)

Tabs Tabs

PO PO

0.5-1 mg/kg q 12-24 hr 15-30 mg/kg q 12 hr

Antibacterial, antiprotozoal and amebicidal agent Gastric ulcers, abortifacient Can have histamine release particularly with IV injection Very safe, effective, over-the-counter flea adulticide. Will not treat larvae or eggs Gastric ulcers Pain, sedation (not well studied in canines) Anti-inflammatory Infection

Tabs

PO

2-4 mg/kg q 8 hr

Analgesic

0.2-1 mg/kg IV, 2 mg/kg per rectum or intranasal for status epilepticus 2-4 mg/kg q 8 hr

Infections Infections, abscesses, oral infections Sedation or anti-epileptic

Allergic reactions, motion sickness Infection, Lyme disease, ehrlichiosis, Rocky Mountain spotted fever Decrease gastric acidity Pain control, sedation Local anesthesia

IM, Intramuscular; IV, intravenous; PO, oral; q, daily; QD, once daily; BID, twice daily; QID, 4 times daily; SQ, subcutaneous; TID, 3 times daily. *Most veterinary-specific drugs not listed. See your veterinarian.

be carried out of a wilderness area manually, but large animals may be airlifted out of the wilderness by helicopter with the animal in a special sling. However, this may be quite expensive. Dogs may be placed in an improvised stretcher and carried out. Indications for euthanasia include compound and comminuted fractures of long bones, falling or sliding into inaccessible places from which the animal is unable to extricate itself or trek participants are unable to aid the animal, lacerations exposing 1216

abdominal or thoracic organs (such as wild animal attacks or ramming tree branches into the body), head injuries resulting in persistent convulsions or coma, and protracted colicky pain unrelieved by analgesics or mild catharsis, usually associated with a pulse rate greater than 100 beats/min, rolling, and congested conjunctival membranes. The expedition may carry a bottle of euthanasia solution (toxic barbiturates), which must be given intravenously or

Dosage and Interval

Trade Name (Company)

Concentration in Vial

Route of Administration

Horse

Llama

Dog

Indication

10 mg/mL

IV, IM

0.04-0.1 mg/kg

Not indicated

0.05-0.22 mL/kg

Tranquilizer

Ampicillin sodium

Prom Ace (Fort Dodge) Generic

—

IM

Generic Benza Pen (Pfizer)

2 mg/mL 150,000 units/ mL

IM, SQ IM

25 mg/kg q 6 hr 0.04 mg/kg 40,000 units/kg q5d

Charcoal (activated) Dexamethasone

Generic

—

PO

60-250 g

10-25 mg/kg TID 0.04 mg/kg 5000-15,000 units/kg q2d 100 g

Infection

Atropine sulfate Benzathine penicillin G

10-50 mg/kg QID 0.04 mg/kg Not recommended

3-5 g

Toxins

Azium (ScheringPlough) Generic

2 mg/mL

IM

2-4 mg/kg

1-2 mg/kg

4 mg/kg q 8 hr

Shock

5 mg/mL

IV, IM

0.05-0.1 mg/kg

2-5 mg/kg

Sedation

Generic (Bayer) Panacur (Hoechst Roussel) Banamine (ScheringPlough) Ivomec (Merck AGVET) Vetelar (Pfizer) Generic

1 : 1000, 1 mg/ mL —

IV, IM

0.1-0.4 mg/kg

0.1-0.5 mg/kg

Anaphylaxis

PO

5-20 mg/kg

0.2-0.4 mg/ kg 0.1-0.5 mg/ kg 10-15 mg/kg single dose

50 mg/kg

Parasites

—

IM

1.0 mg/kg daily

1.0 mg/kg daily

0.3 mg/kg daily

Colic pain, inflammation

—

PO, SQ

Parasites

IV, IM

0.2 mg/kg single dose 2-5 mg/kg As needed

Not indicated

100 mg/mL 2%

0.2 mg/kg single dose 2.0 mg/kg As needed

Not indicated As needed

Carmilax (Pfizer) Generic Butazolidin (ScheringPlough) Tribrissen (ScheringPlough) Rompun (Bayer) T-61 (Taylor)

361 g/lb

PO

—

—

— 200 mg/mL 1-g tablet

PO IV, PO

8-25 g 15 mg/kg q 8 hr

Cathartic Pain, inflammation

24%

IV, SQ

20-100 g 1-2 g/450 kg, 2-4 g/450 kg daily 2 mg/kg BID

10-20 g total dose Not indicated 2-4 mg/kg daily

Anesthesia Local anesthesia Cathartic

2 mg/kg bid q 12 hr

2.2 mg/kg

Infection

100 mg/mL

IV, IM

0.5-1.0 mg/kg

1.1 mg/kg

Sedation

—

IV

40 mL total dose

0.25-0.5 mg/ kg 25 mL total dose

0.3 mL/kg

Euthanasia

Generic Name Acepromazine maleate

Diazepam Epinephrine Fenbendazole Flunixen meglumine Ivermectin Ketamine Lidocaine Magnesium oxide Magnesium sulfate Phenylbutazone Trimethoprim/ sulfamethoxazole Xylazine Euthanasia solution

Stinging nettle Infection

BID, Twice daily; IM, intramuscular; IV, intravenous; PO, oral; q, every; QID, 4 times daily; SQ, subcutaneous; TID, 3 times daily.

intraperitoneally (see Table 61-4). If firearms are carried, a properly placed bullet to the head produces a fast and humane death. For placement, the shooter stands in front of the animal’s head and draws an imaginary line from the medial canthus of each eye to the base of the opposite ear. The shot should be aimed where those lines cross and approximately perpendicular

to the contour of the forehead (Figure 61-16). The tip of the barrel should be no more than 6 inches from the head. A heavy blow to the head at the same location is equally effective. The blow may be administered with the blunt edge of a singlebladed ax or hatchet. A large rock held in the hand may also be used. A less desirable but sometimes expedient

FIGURE 61-15  Holding a dog for administration of intravenous medication.

FIGURE 61-16  Location for euthanasia blow or shot.

1217

CHAPTER 61  Emergency Veterinary Medicine

TABLE 61-4  Medications for Trek Animals

PART 6  ANIMALS, INSECTS, AND ZOONOSES

method is to sever the jugular vein to allow exsanguination. This would probably be used on an animal that is already unconscious. Elephants are more difficult to euthanize. The usual landmarks for placement of a bullet in most mammals cannot be used because the brain is surrounded by a complex of sinuses. Small caliber bullets are unable to penetrate the bones of the head. The most appropriate method for elephant euthanasia is intravenous administration of a concentrated solution of potassium chloride (KCl). Powdered KCl is readily available from chemical companies or a pharmacy without a prescription. It need not be medical grade, and sterility is not necessary. A saturated solution is prepared by adding 180 g of KCl to 600 mL of hot water, which provides 0.3 g/mL of solution. The dose required to stop the heart is 44 mg/kg (20 mg/lb). For a 3000-kg (6600-lb) elephant, it would require 440 mL of the 0.3 g/mL saturated solution. In practice, the solution is administered in excess, so it would be appropriate to make a double quantity of KCl solution to account for possible spillage. This method of euthanasia is suitable for any large domestic or wild animal.

MISCELLANEOUS INFORMATION Some vital statistics for support animals are provided in Table 61-1. Equipment and supplies for support animals, their levels of priority, and sources are provided in Box 61-1, Table 61-5, and Appendix A. The rectal body temperature of an animal is assessed by inserting a digital clinical thermometer (lubricated with water or spittle) through the anus with a slight twisting motion. The use of the same thermometer for humans and animals is generally aesthetically unacceptable, even though the thermometer may be cleansed and disinfected between uses.

BOX 61-1  Equipment and Supplies for Animals* 1.  Sterile pack Needle forceps Thumb forceps Scissors Scalpel handle and blades Hemostats (2) 2.  Alligator forceps 3.  Suture material (Vicryl), swaged needles, 4 packets, various sizes (0 to 4-0) 4.  Gauze sponges, 4 × 4-inch (100) 5.  Roll cotton, 1 lb 6.  Vetrap bandages, 3-inch, 6 rolls 7.  Syringes, plastic, 12-mL (6) 8.  Needles, 22- to 18-gauge (20) 9.  Tubing Silastic, 1-cm outside diameter, 10 cm (4 inches) long, for endotracheal tube Plastic flexible stomach tube, 1-cm inside diameter, 100 cm (40 inches) long 10.  Funnel, plastic, to fit into stomach tube 11.  Hose, garden, 20 cm (8 inches), to serve as a speculum for passage of the stomach tube 12.  Hoof knife 13.  Hammer 14.  Pliers 15.  Horseshoes and nails 16.  Pliable sheet of leather 17.  Heavy needle and thread 18.  Otoscope 19.  Stomach pump *Table 61-5 addresses the priorities for horses, llamas, and dogs.

1218

TABLE 61-5  Priorities of Emergency Supplies for

Trek Animals*

Supplies Primary Horses Llamas Dogs

1, 3-10, 12-15 1, 3, 4, 6-12, 14 1, 2, 4, 6-8, 14, 16, 17

Secondary 19 19 18

*Numbers refer to supplies as numbered in Box 61-1.

TRANSPORTING ANIMALS TO AND FROM THE TRAILHEAD Dogs Dogs are easily transported in the fiberglass carrying cages commonly used by dog owners and for airline shipment.12,13 Appropriate opportunities for exercise and relieving themselves should be provided. Whether food and water should be provided depends on the duration of the journey and on other conditions such as ambient temperature. A journey of longer than 12 hours would require at least water. Horses Horses may be transported in horse trailers or trucks.12,13 Each animal should have been trained to enter and leave the conveyance with ease. The conveyance should be covered to prevent insects and flying debris from striking animals in the face or eyes. Legs should be wrapped to support the lower limb tendons, joints, and ligaments. Someone on the trek staff must know how to attend to these animals. Llamas, Camels, and Oxen Llamas are often moved from one location to another, and they generally travel well.12,13 The majority lie down soon after the beginning of a journey and remain recumbent while moving. However, traveling is stressful for most llamas, whether or not they exhibit overt signs of stress. They do not need to be tied within a truck or trailer. In fact, it may be hazardous to do so. At least two fatalities have been associated with trailering tied llamas. One tied llama became entangled in a lead rope that was too long, and it suffocated. In the second accident, the llama was tied in a trailer constructed with a horizontal bar across the front, at a height corresponding to the midcervical region on the llama. The llama was tied with a rope over the bar. At the destination, the llama was found dead, partially hanging from the bar. At necropsy, a massive hematoma was located in the pharynx, which obstructed the glottis. Apparently, the llama had bumped against the horizontal bar at some point in the journey, rupturing a vessel in the pharynx. As the llama pulled back on the rope and halter, the mouth was forced shut so that blood in the pharynx could not flow out the mouth or nostrils. Llamas are small enough and adaptable enough to be moved in numerous types of vehicles, including private vans, pickup trucks, livestock trucks, trailers, and commercial vans. Vehicle and trailer licenses must be current. If animals are insured, establish whether there is coverage for transportation; if not, explore the possibility of acquiring trip insurance. Llamas should be accustomed to the vehicle in which they are to travel. Certainly, this should include halter training and practice leading them into the vehicle or a similar conveyance. Vehicles and trailers should receive routine maintenance (brakes, tires, batteries, lights) before the trip. It is particularly vital to ascertain that exhaust fumes do not flow past the heads of the llamas. Climatic conditions must be considered. More than one llama has died as a result of heat stress while being trailered. Most trek animals are not shipped by air, but it may be advisable to adopt the criterion used by most airlines: they refuse to carry live animals if daytime temperatures reach over 29.4° C (85° F) anywhere that the plane lands. Use caution when transporting in hot weather. Road conditions should be investigated, including

Moving A Recumbent Llama.  Moving a recumbent llama12,13 may be accomplished using the following technique. A plastic

or canvas tarp that is longer than the length of the animal may be rolled up on one side and placed next to the animal that has been moved into the sternal position (Figure 61-17). Allow the animal to resume lateral recumbency so that the tarp can be unrolled beneath the llama. Do not roll the animal on its back onto the tarp; rolling may cause regurgitation and possibly aspiration pneumonia. Rather, partially roll the animal from lateral to sternal recumbency and push the roll under it. Then both sides of the tarp may be rolled up to form a hand-hold for those who will lift and carry the animal. The head and forequarters should be kept higher than the hindquarters to avoid passive regurgitation. For llamas, it may be appropriate to rig a temporary sling inside a trailer or truck using a large bath towel or piece of canvas. Cut four leg holes, corresponding to the distance between the legs of the llama. Gently lift a forelimb and insert the foot through one hole; repeat with the other forelimb, and then repeat with the hind limbs. Fasten a small rope to each corner by first folding the corner of the towel over a small rock (about 2.5  cm [1 inch] in diameter), and then tie a slipknot around the cloth and the rock and pull it tight. The ropes may then be tied to the side of the trailer or partition. The feet should remain on the floor of the trailer, and a person should ride beside the animal. Elephants are usually moved in special trucks or trailers and then walked to an appropriate trailhead.

FIELD EVACUATION OF INJURED ANIMALS Field evacuation of injured or seriously sick trek members by helicopter has become a viable option for all but the most remote wilderness expeditions. Cost is not an important factor in evacuating humans, but it may have to be considered in animal evacuations. Dogs may be taken into the cabin of a helicopter. Llamas and horses must be slung beneath the helicopter. A sling for a short journey of a llama may be fashioned with four rope loops, all brought together over the back of the llama (Figure 61-18). A sling for a horse may be constructed from a rope (Figure 61-19).11 The diameter and length of the rope used depends on the size of the animal. A 15-m, 1.3-cm (50-foot, 0.5-inch) nylon

1

2

3

4 FIGURE 61-17  Using a tarp to lift a llama.

1219

CHAPTER 61  Emergency Veterinary Medicine

any construction detours that may cause delays. Storms should be anticipated. Some trailers have a small ramp leading up to the floor of the trailer for loading and unloading. Others require that the animal step up to load. Llamas prefer to step up rather than walk up a ramp. It is unwise to pull or push a llama into a step-up trailer. A leg may slip beneath the floor of the trailer and be fractured if the animal lunges forward. Appropriate training before loading would obviate problems of this nature. Trailer flooring must be considered. Although llamas are surefooted and can generally walk on smooth surfaces, a bare floor in a trailer, whether it is metal or wood, is not appropriate. Rubber mats or indoor/outdoor carpeting are most desirable because they ensure adequate footing, provide insulation from both heat and cold, and are softer to lie on. Straw is often used, but although it may provide insulation in cold weather (and absorbs urine), it does not provide adequate footing. It is unwise to use straw for bedding on long journeys, especially if no feed is supplied. Hungry or bored animals may eat the straw, and if unaccustomed to it, may develop digestive upsets. Sand may be used, but wood shavings or sawdust become embedded in the fiber coat and are difficult to remove. Llamas may be trained to use different water containers, including a flowing stream or pool. If the animal is not familiar with a variety of water sources, water it with a plastic or metal bucket for a few days before beginning a trip. Animals may be reluctant to drink sufficient new-source water, which in hot weather may be disastrous. The odor or taste of new water may be disguised by pre-training the animal to drink water containing two drops of vanilla extract or oil of eucalyptus. New water can then be similarly treated. Llamas may be unwilling to defecate or urinate in a strange environment. A periodic opportunity should be provided for them by stopping for a rest so that they may stand or, if feasible, be off-loaded. It may be desirable to carry a container of dung, so that at a rest stop or at the destination, a few pellets may be spread in an appropriate spot and the llama led to investigate them.

tail, up over the back and underneath all the ropes on the back. Take all slack out of the ropes and complete the sling by doubling the running ends back and tying with a halter tie. An attempt should be made to place the lifting site over the approximate center of gravity of the animal (just behind the withers). However, even if this is not done, the animal can still be lifted, because each leg is in its own loop sling. The animal cannot slip out of the sling. A more elaborate sling is available commercially and has been used in numerous large animal rescue operations (Figures 61-20 and 61-21, online). It is not possible to move a recumbent elephant without special cranes and vehicles. The speeds of support animals are listed in Table 61-6.

PART 6  ANIMALS, INSECTS, AND ZOONOSES

X

Y

APPENDIX A 

SOURCES OF VETERINARY DRUGS FOR EXPEDITIONS FIGURE 61-18  Diagram of a rope sling for a llama.

climbing rope is suitable to lift a 450-kg (1000-lb) horse. First, double the rope; then form a loose neck loop using a bowline knot. Slip the loop over the head and position the loop with the knot at the base of the chest. Bring the running segments between the front legs and back through the corresponding side of the neck loop. Cross the ropes over the back; then bring the ropes between the hind legs. Be certain not to cross ropes underneath the animal. The ropes should pass on either side of the

Bayer Corporation PO Box 390 Shawnee Mission, KS 66201 Fort Dodge Laboratories PO Box 518 Fort Dodge, IA 50501 Hoechst Roussel Vet Route 202-206 Box 2500 Somerville, NJ 08876-1258 Pfizer Animal Health 235 East 42nd St New York, NY 10017

3

1

2

4 FIGURE 61-19  Placement of a rope sling on a horse.

1220

Animal

Walk, Reasonable Terrain on Trails

Horse, riding Horse, packing Mule Donkey Ox, yak, water buffalo Camel Llama Elephant Dog† Human

4.0-5.0 3.0-4.0 4.0-5.0 3.0-4.0 2.0-3.0 4.0-5.0 3.0-4.0 3.0-5.0 3.0-4.0 3.0-4.0

Walk, Difficult Terrain 1.0-3.0 0.5-2.0 0.5-2.0 0.5-2.0 0.5-2.0 1.0-2.0 2.0-3.0 0.5-2.0 2.0-3.0 0.5-2.0

Brisk Walk Short Distance, Reasonable Terrain

Moderate Fast Gait

9/0-11.0 — 8.0-9.0 — — 8.0-9.0 Rarely used when packing 6.0-8.0 <10.0 5.0-6.0

Trot Rarely used Trot Trot Rarely used Pace Pace Amble Trot Jog

*To convert miles per hour to kilometers per hour, multiply mph by 1.61. To convert miles per hour to meters per second, divide mph by 2.23. † Depends on the size of the dog

Schering Plough Animal Health Corp. (merged with Merck) 10488 So. 136th St. Omaha Nebraska, 68138 Taylor Pharmaceutical Co. Decatur, IL 62525

Acknowledgment.  The contribution of S. Christopher Ralphs, DVM, MS, DaCVS, to this chapter is greatly appreciated.

Wyeth-Ayerst Pharmaceuticals 555 Lancaster Ave. St Davids, PA 19087

Complete references used in this text are available online at www.expertconsult.com.

REFERENCES

1221

CHAPTER 61  Emergency Veterinary Medicine

TABLE 61-6  Speed of Trek Animals (miles per hour, mph*)

CHAPTER 62

Seasonal and Acute Allergic Reactions NARESH J. PATEL

Allergic rhinitis is the most common atopic disease. Although the prevalence varies by region, it is estimated that nearly 25% of the population may be affected.8 It is the second most prevalent chronic condition in the United States, outranked only by hypertension.72 Allergic rhinitis may be classified as seasonal (commonly referred to as hay fever) or perennial. The seasonal form is caused by aeroallergens released from the pollens of windpollinated plants, which include trees, grasses, and weeds. Perennial symptoms are commonly the result of exposure to house dust mites, domestic pets, cockroaches, and mold. In temperate climates, sufferers of perennial allergic rhinitis with a seasonal component often experience worsening symptoms during the warmer months because of the additional burden of seasonal allergens. Although anaphylaxis is not as common as allergic rhinitis, it represents the most severe form of allergic reaction and can lead to a serious, including fatal, outcome if not treated promptly. The exact prevalence of anaphylaxis is not known. Based on extrapolation from data, the estimated risk for anaphylaxis per person in the United States is 1% to 3%.79 Anaphylactic reactions are probably underrecognized and underreported, particularly in cases of unexplained death. In one study, elevated tryptase levels, which are often found during acute anaphylaxis, were found in 13% of 68 patients postmortem.62 Foods and medications are the most common causes of anaphylaxis. Each year, approximately 40 deaths in the United States are attributed to anaphylaxis resulting from bee stings.2

Allergic Rhinitis Allergic rhinitis is a chronic immunoglobulin E–mediated (IgEmediated) inflammatory disease of the nasal mucosa. It is the most common atopic disease, and for reasons not yet clear, its prevalence is increasing worldwide. The economic impact of allergic rhinitis is impressive. In 2002, the total direct and indirect costs were $7.3 billion and $4.2 billion, respectively.61 Indirect costs were mainly attributed to work or school absenteeism. In the United States, allergic rhinitis is responsible for 3.5 million lost work days and 2 million lost school days.61 The disease usually manifests in early childhood or adolescence and peaks in the second or third decade of life. The disease does not appear to favor any gender, ethnic group, or race. The most important risk factor for development of allergic rhinitis is a family history of atopy, especially with early onset of disease. In comparison with the general population, the risk is 30% greater if one parent or sibling is atopic, and 50% greater if both parents are affected.47 On the other hand, lack of complete concordance for atopy in identical twins emphasizes the importance of environmental factors in disease development.4 Allergic rhinitis, like other atopic conditions such as asthma and atopic dermatitis, tends to cluster in families.

PATHOPHYSIOLOGY The two important components in the pathogenesis of allergic rhinitis are the acute allergic reaction and late inflammatory events. Type I immediate hypersensitivity reaction accounts for most of the acute clinical manifestations of allergic rhinitis, and cells such as eosinophils, basophils, and T lymphocytes play important roles in late inflammatory events. Production of allergen-specific IgE (sensitization) antibodies forms the 1224

underlying basis of immediate hypersensitivity; atopy is defined as the genetic predisposition to develop allergen-specific IgE antibodies. The sensitization process requires a cooperative effort between CD4 T lymphocytes and B lymphocytes (Figure 62-1). It begins with presentation of an allergen to CD4 T lymphocytes by antigen-presenting cells (e.g., macrophages) in the context of a major histocompatibility complex. Cytokines released from CD4 T lymphocytes as a result of this interaction cause differentiation of B lymphocytes into immunoglobulin-secreting plasma cells. This differentiation leads to isotype switching (production of specific antibody types) within the plasma cells. For example, release of cytokine interleukin IL-4 or IL-13 from T lymphocytes promotes IgE switching.14 Once allergen-specific IgE antibody is produced, subsequent exposure and allergen binding to the IgE molecule on the surface of mast cells result in cross-linking of the IgE molecule. Consequently, mast cells or basophils degranulate and release preformed and newly synthesized mediators. The prototype preformed mediator is histamine, and the newly synthesized mediators include those of the arachidonic acid pathway (leukotrienes, prostaglandins, and platelet-activating factor), neuropeptides (e.g., substance P), and cytokines (e.g., IL-4, IL-5). Release of chemical mediators has various pathologic and clinical consequences. Sneezing and itching result from histamine stimulation of its receptors on sensory nerve endings. Rhinorrhea results from increased vascular permeability produced by all the mediators, and leukotrienes and prostaglandins are believed to play major roles in nasal congestion.74 Our knowledge of the pathophysiology of allergic rhinitis has been greatly enhanced by nasal challenge studies.26 It is now known that the allergic reaction consists of an early phase, characterized by mast-cell or basophil degranulation, and a late phase, which occurs 4 to 6 hours after the early phase (see Figure 62-1). The hallmark of the late-phase reaction is an influx of inflammatory cells, such as eosinophils, basophils, and T lymphocytes.3 For example, basophils cause further histamine release, and T lymphocytes release additional cytokines that enhance IgE production (via IL-4) and eosinophil activation (via IL-5). As a result of further inflammatory activity by these cells, there is recrudescence of symptoms many hours after the initial allergen exposure. Leukotrienes, prostaglandins, and cytokines released in the earlyphase reaction play an important role in recruiting the late-phase cellular components to the inflammatory site. Although inhaled corticosteroids block both the early- and late-phase reactions, systemic corticosteroids block only the late-phase reaction.

ALLERGENS Airborne allergens are the primary etiologic agents of allergic rhinitis. Although many potential allergenic proteins exist, relatively few are clinically important and even fewer have been isolated and characterized. Allergens are low-molecular-weight proteins or glycoproteins capable of eliciting a type I immediate hypersensitivity reaction (production of IgE antibodies). Allergens can be conveniently divided into those that exist in the outdoor environment and those that exist in the indoor environment. In the outdoors, pollens of trees, grasses, and weeds, and certain fungi (e.g., Alternaria and Cladosporium species) most commonly provoke symptoms. Pollen-sensitive individuals typically experience seasonal rhinitis in predictable time intervals from one season to the next. Although fungi are more ubiquitous in nature and do not have the distinct seasons that pollens have,

Phase 2 Clinical disease Early inflammation

Allergen

Antigenpresenting cell

Late inflammation

Allergen IgE antibodies

Processed allergen

B cell

CD4 T cell

Late-phase reaction

Cellular infiltration

Mast cell Eosinophils Mediator Basophils release Monocytes Nerves Lymphocytes Blood

Resolution

Hyperresponsiveness

Complications

Priming

? Irreversible disease

vessels Glands Plasma cell

CHAPTER 62  Seasonal and Acute Allergic Reactions

Phase 1 Sensitization

IgE antibodies

Sneezing Rhinorrhea Congestion

FIGURE 62-1  The natural history of allergic rhinitis (a simplified schematic). During phase 1, the individual becomes sensitized to an allergen. During phase 2, clinical disease develops. An overwhelming majority of individuals have an early response on re-exposure to the allergen. The activation of mast cells and release of mediators dominate the early response. After the early response, most individuals have cellular infiltration of the nasal mucosa, causing late inflammatory events, including the spontaneous recurrence of release of mediators (late-phase reaction), hyperresponsiveness to irritants, and increased responsiveness to the allergen (priming). Circles indicate the heterogeneity of these late inflammatory events. Inflammation can resolve spontaneously, cause a complication, or lead to an irreversible form of chronic rhinitis. (From Naclerio R: Allergic rhinitis, N Engl J Med 325:860, 1991.)

both outdoor and indoor fungi thrive in moist and humid environments. Therefore in temperate climates, fungi counts start to rise in spring, with a peak in mid- to late summer. Indoor allergens include fungi, furred animals, cockroaches, and dust mites. Unlike outdoor allergens, which typically cause seasonal symptoms, indoor allergens often cause perennial symptoms. However, the symptoms are less drastic in nature, often making diagnosis more difficult. Pollens.  Pollination in higher-order plants consists of transfer of the male gametophyte to the female gametophyte. In this process, pollen grains serve as vectors for male gametophytes. Of the different types of pollen-producing plants, flowering plants (including trees, grasses, and weeds) are the most important from an allergic standpoint. Flowering plants may be divided into those that rely on animal vectors (e.g., insects) for pollination (termed entomophilous) and those that depend on the wind (termed anemophilous). In general, only anemophilous plants (including trees, grasses, and weeds) cause allergic symptoms.67 Pollens of entomophilous plants do not achieve high airborne concentrations. In temperate climates, pollination of trees, grasses, and weeds occurs in predictable time intervals in a given region. Therefore it is important to know the relevant local botany and respective pollination seasons (Table 62-1 and Figure 62-2). As shown in Figure 62-2, tree pollination marks the onset of allergy season in most parts of North America. It begins as early as mid-January in the Southwest or early April in the Northeast, and it terminates between early and late May. Trees of allergenic significance in various regions are listed in Table 62-1. Grass pollen, with its worldwide distribution, is a significant source of allergen exposure and a major cause of allergic rhinitis in sensitive individuals. In frost-free areas of North America, grass pollen may be present year-round, whereas in temperate climates, grass pollination peaks between mid-May and mid-July. Important grass types are rye, timothy, Kentucky bluegrass, orchard, Johnson, and Bermuda. Unlike ragweed and tree pollen allergens, grass pollen allergens show extensive cross-reactivity among different species, and allergic individuals are generally sensitive to many of these species. Weeds represent the final pollen producers of the season, typically generating pollen from mid-August through mid-October. Although a variety of weeds

cause regionally significant allergies, ragweed is found in most parts of North America. Fungi.  Numerous allergenic fungi are responsible for both seasonal and perennial symptoms. The three most important classes of allergic fungi are zygomycetes (e.g., Rhizopus, Mucor), basidiomycetes (e.g., rust, smut, Ganoderma), and ascomycetes (e.g., Cladosporium, Penicillium, Aspergillus, Alternaria, Epicoccum). Trees

Northeast Northwest Mid-Atlantic Southwest Southeast Midwest

Grasses

Northeast Northwest Mid-Atlantic Southwest Southeast Midwest

Weeds

Northeast Northwest Mid-Atlantic Southwest Southeast Midwest

Jan

Feb

Mar

Apr

May

Jun

Jul

Aug

Sep

Oct

Nov

Dec

FIGURE 62-2  Pollen seasons by region in the continental United States. (From Sicherer SH, Eggleston PA: Environmental allergens. In Lieberman P, Anderson JA, editors: Allergic diseases: Diagnosis and treatment, Totowa, NJ, 1997, Humana.)

1225

PART 7  PLANTS

TABLE 62-1  Selected Trees, Grasses, and Weeds of Allergenic Significance* Region (States)

Trees

Grasses

Weeds

Region (States)

Trees

Grasses

Weeds

Northeast (ME, NH, VT, NY, PA, NJ, MA, RI, CT)

Birch Elm Maple Poplar Oak Birch Elm Maple Hickory Oak Ash Elm Maple Willow Box Elder Alder Birch Maple Oak Walnut Elm Oak Box Elder Willow Maple

Orchard Timothy June Sweet vernal Bluegrass Orchard Timothy Bluegrass June Bermuda Orchard Timothy Bluegrass June

Sheep sorrel Plantain Russian thistle Giant ragweed Short ragweed Plantain Dock Sage Short ragweed Giant ragweed Plantain Dock Russian thistle Short ragweed Giant ragweed

Rocky Mountains (ID, WY, CO, UT, western MT) South (FL, GA, AL, TX, AR, southern MO)

Timothy Orchard Fescue Redtop June Bermuda Orchard Timothy Saltgrass

Sagebrush Russian thistle Short ragweed Giant ragweed

Timothy Bluegrass Fescue Rye Redtop Timothy Orchard Bluegrass Bermuda Redtop

Dock Plantain Russian thistle Nettle Sagebrush Marsh-elder Russian thistle Western hemp Short ragweed Giant ragweed

Cedar Elm Ash Birch Oak Cedar Elm Mulberry Poplar Oak Cedar Ash Mulberry Oak Olive Ash Walnut Elm Oak Olive

Mid-Atlantic (DE, MC, DC, VA, NC, SC) North Central (OH, KY, WI, MI, IA, WI, northern MO, IL, IN, TN) Pacific Northwest (WA, NV, OR, northern CA) Plains (NE, MN, eastern MT, Dakotas)

Southwest (western TX, NM, AZ) Southern California

Bermuda Johnson

Bermuda Saltgrass Brome

Dock Pigweed Russian thistle Giant ragweed Short ragweed Sagebrush Russian thistle Saltbush Kochia Short ragweed Nettle Bur ragweed Russian thistle Sage Western ragweed

From Sicherer SH, Eggleston PA: Environmental allergens. In Lieberman P, Anderson JA, editors: Allergic diseases: Diagnosis and treatment, Totowa, NJ, 1997, Humana. *Plants are listed in the order of bloom for each region. Grasses are listed by prevalence in each region.

Among the outdoor fungi, Cladosporium and Alternaria are the most abundant and cause significant symptoms in sensitive individuals. Although fungi can survive in various climates, they grow best in warm, humid environments. The peak fungal season in many areas is in mid- to late summer and fall, with a marked reduction after the first frost in temperate climates. Fungi levels may rise in spring, when decaying vegetation is uncovered after the snow has melted. Common outdoor sources of fungal growth are leaves, moist debris, and soil; therefore outdoor activities, such as raking, farming, and mowing, significantly increase exposure. Dust Mites.  Dust mites are microscopic arachnids that are close relatives of ticks and spiders. They feed on human epidermal scales and, like fungi, prefer a warm, humid environment. Dust mites are the most common indoor allergens and can cause significant perennial symptoms in sensitive individuals. Although there is no good correlation between exposure level and degree of rhinitis symptoms, a level of 10 µg/g of dust is considered a risk factor for development of acute asthma symptoms.53 Common indoor sources of dust mite exposure include mattresses, pillows, blankets, upholstery, and stuffed toys. Dust mites may proliferate in sleeping bags stored in humid environments (e.g., damp basements). Animals.  Animals, especially cats, can be highly allergenic and in sensitized individuals can cause significant symptoms. Cats and dogs are the most common pets in the United States, with more than one-third to one-half of all homes housing at least one cat or dog.64 Birds, rabbits, hamsters, guinea pigs, rats, and mice are some other potentially allergenic pets. The major allergens of the cat and the dog are found in their saliva and sebaceous glands. The cat allergen can remain a potential source of allergy months after the removal of the cat, because of its light, sticky qualities. Outdoors, inhalation of the emanations of moths, locusts, beetles, and flies may cause allergic symptoms. Residents of the area around western Lake Erie may experience allergic symptoms caused by the mayfly.76 Finally, the cockroach is potentially allergenic and is frequently encountered in heavily infested, crowded, or multifamily dwellings. 1226

FUNCTIONS OF THE NOSE The main functions of the nose—to warm, humidify, and filter air—are possible because of turbulent airflow resulting from increased surface area provided by the three turbinates (superior, middle, and inferior) on each side. The nose’s functions are mainly controlled by the underlying neurovascular system. Blood supply to the nose is via the ophthalmic (branch of the internal carotid) and internal maxillary (branch of the external carotid) arteries. Neural innervations include the sensory (via the trigeminal nerve, which is responsible for the sneezing reflex) and autonomic (parasympathetic and sympathetic) nervous systems. Nasal congestion is proportionally related to the amount of blood pooling in the cavernous sinusoids (located within the turbinates) and to the degree of mucosal edema. Sinusoid filling and emptying are controlled by the autonomic nervous system. Vasodilatory parasympathetic stimulation allows the sinusoid reservoir to fill via opening and closing of capillary and postcapillary venule sphincters, respectively. Conversely, sympathetic stimulation contracts the capillary sphincter and relaxes the postcapillary venule sphincter, allowing the reservoir to empty. In most people, cyclic swelling and shrinking of the turbinates between the two sides of the nose is inherent. This nasal cycle, which is approximately 1 to 4 hours in length, results from alternating sympathetic discharge and is responsible for the sensation of alternating unilateral nasal blockage experienced by allergic rhinitis sufferers.22 Another major function of the nose is olfaction. The olfactory area is located at the roof of the nasal cavity above the middle turbinate. Significant turbinate edema can lead to poor ventilation of this area and associated hyposmia, which is common among allergic rhinitis sufferers.

CLINICAL EVALUATION A thorough, careful history is crucial in evaluation of allergic rhinitis and is often helpful in determining whether or not an individual is allergic. Allergy testing is used to confirm the underlying clinical suspicion. Symptoms of allergic rhinitis can range from intermittently mild to incapacitating, such as during peak

Allergy Testing Because of the temporal correlation of symptoms with a particular season, diagnosis of seasonal allergic rhinitis can often be made clinically without the need for testing. However, given the ambiguity of various allergen exposures in perennial rhinitis, allergy testing is generally recommended. Allergy testing may be performed either by skin testing or by the radioallergosorbent test (RAST). In skin testing, which is widely accepted and more sensitive,30 minute quantities of specific allergens are introduced under the skin, and a positive response depends on allergenspecific release of histamine. In the RAST, evidence of allergenspecific IgE is determined using the patient’s serum. Given its lesser sensitivity, greater cost, and longer turnaround time for results, RAST is typically used in special circumstances only, such as for patients with severe eczema or dermatographism, in whom skin testing might be difficult to interpret. Testing can pinpoint specific allergen sensitivities, which can be useful in providing allergen avoidance measures. Allergy testing must be performed if immunotherapy is being considered. Differential Diagnosis Given the significant and overlapping symptoms of various rhinitis conditions, the differential diagnosis of rhinitis must be considered during the initial evaluation (Box 62-1). Rhinitis can be classified as acute or chronic. The most common cause of acute rhinitis is a viral infection, and allergic rhinitis may be confused with viral rhinitis. However, unlike the symptoms of allergic rhinitis, those of viral rhinitis usually do not persist longer than 2 weeks unless superseding sinusitis develops. A foreign body or trauma also can cause acute rhinitis. Unilateral symptoms are the hallmark of foreign body obstruction. The differential diagnosis of chronic nonallergic rhinitis is broad. Nonallergic rhinitis with eosinophilia syndrome (NARES)

BOX 62-1  Differential Diagnosis of Rhinitis

CHAPTER 62  Seasonal and Acute Allergic Reactions

pollen season. The hallmark of allergic rhinitis is temporal correlation of symptoms with allergen exposure.46 The most common symptoms of allergic rhinitis—sneezing, nasal congestion, rhinorrhea, and pruritus of the nose and eyes—are nonspecific. Itching and sneezing are the most distinctive complaints associated with allergic rhinitis,47 whereas nasal congestion seems to be more prominent in perennial rhinitis than in seasonal rhinitis. In some individuals, ocular symptoms predominate over nasal symptoms. Allergic rhinitis sufferers often experience the priming effect (an increase in sensitivity to allergens after repeated exposure) and hyperresponsiveness to nonallergenic environmental stimuli, such as tobacco smoke, strong odors, pollutants, and weather changes.11 Since the time intervals of pollination are predictable in a given season, the timing of symptoms is often helpful in identifying the responsible pollen(s). For example, in the Midwest, ragweed sufferers characteristically start experiencing symptoms in mid-August. Conversely, because any number of allergens may cause symptoms in individuals with perennial rhinitis, determining the specific responsible allergen(s) can be difficult. Other conditions of the upper respiratory tract may mimic allergic rhinitis and must be considered. Complications of allergic rhinitis include sinusitis, otitis media with effusion, and asthma. Additionally, numerous studies have shown that allergic rhinitis may significantly affect quality of life, with effects such as sleep loss, fatigue, poor concentration, reduced productivity, and irritability.28 Although a decline in their quality of life may seem like an obvious clue to the severity of the disease, patients may not be aware of this decline if they have been living with their condition for years and have become accustomed to it.71 As is true for the symptoms described by the patient, many of the signs noted on physical examination are not exclusive to allergic rhinitis. Classically, the nasal mucosa is pale blue and edematous, but this color change is noted in only 60% of sufferers, and many individuals have erythematous mucosa.15 In children, the “allergic salute” (upward nasal rubbing) and “allergic shiners” (dark, puffy circles under the eyes) may be present. Other notable signs include septal deviation, polyps, and an obvious foreign body. If congestion is profound, use of a topical decongestant such as oxymetazoline (Afrin) may improve visualization.

Acute Rhinitis • Upper respiratory tract infection • Foreign body • Trauma Chronic Rhinitis • Allergic • Nonallergic • NARES (non-allergic rhinitis with eosinophilia syndrome) • Chronic sinusitis • Systemic diseases • Vasculitis • Wegener’s granulomatosis • Churg-Strauss syndrome • Cystic fibrosis • Sarcoidosis • Hypothyroidism • Rhinitis medicamentosa • Medications • Calcium channel clockers • ACE inhibitors • β-blockers • Mechanical-anatomic obstruction • Nasal polyps • Foreign body • Tumor • Septal deviation • Adenoid hypertrophy • Gustatory rhinitis • Atrophic rhinitis • Rhinitis of pregnancy • Cerebrospinal fluid leak • Vasomotor (idiopathic) rhinitis

is characterized by (1) symptoms similar to allergic rhinitis, (2) eosinophilia on nasal smear, and (3) a negative skin test.27 Chronic sinusitis, which can occur as a complication of allergic rhinitis, commonly causes nasal congestion, sinus pressure, postnasal drip, cough, and diminished senses of smell and taste. Symptoms of chronic sinusitis, unlike those of acute sinusitis, are subtle and may require radiologic evaluation, preferably computed tomography. Systemic diseases, such as vasculitis and cystic fibrosis, may cause chronic rhinitis. Rhinitis medicamentosa, which usually results from overuse of topical α-adrenergic vasoconstrictors (e.g., oxymetazoline), is associated with profound nasal congestion caused by rebound effects on withdrawal of the decongestant, usually after 5 to 7 days of topical use. Medications that have been implicated in chronic rhinitis include nonsteroidal antiinflammatory drugs (NSAIDs), angiotensinconverting enzyme inhibitors, and β-blockers. Mechanical and anatomic abnormalities should always be sought on physical examination. Nasal polyps have a pearly, smooth, peeled grape-like appearance and are often bilateral. Nasal polyps may be associated with chronic sinusitis, asthma, and aspirin sensitivity.63 Unilateral symptoms should always heighten suspicion for a foreign body or tumor. Some degree of septal deviation may be found in most people. Therefore, unless symptoms are severe, treatment is unnecessary. In children, adenoid hypertrophy must be considered. Symptoms of gustatory rhinitis are caused by a cholinergic response that occurs after such stimuli as eating, running, and exposure to cold air. Atrophic rhinitis is a rare condition that manifests in older adults as a thick, bilateral, odorous discharge with little nasal congestion.21 Rhinitis of pregnancy should be considered in the pregnant woman with congestion, especially if there is no previous history of rhinitis. Although rare, 1227

PART 7  PLANTS

cerebrospinal fluid (CSF) leak must be considered in anyone with clear rhinorrhea and a history of central nervous system trauma. Testing for the presence of glucose in the nasal mucus is helpful in making the diagnosis. The diagnostic test of choice to detect CSF leak is an assay for a β-2 transferrin level in the nasal mucus.65 Often a diagnosis of exclusion, vasomotor (idiopathic) rhinitis is a common cause of nonallergic rhinitis in adults. Although the term implies a cause relating to vascular or neurologic dysfunction, the mechanism of vasomotor rhinitis is poorly understood. The symptoms of vasomotor rhinitis are frequently obstructive rather than secretory. Therefore nasal congestion and sinus pressure predominate over sneezing and rhinorrhea.39 Individuals with vasomotor rhinitis typically experience perennial symptoms that may be triggered by changes in weather, spicy foods, and irritants, such as smoke, strong scents, and chemicals.

TREATMENT Avoidance of the offending allergens is the first step in the treatment of allergic rhinitis. However, avoidance is often difficult because of the ubiquitous presence of the allergens in the environment or because of an inability to part from a beloved pet. Therefore pharmacologic intervention is often necessary. The optimal treatment plan should be individualized on the basis of symptoms, seasonal patterns, and presence of possible comorbid conditions. The ideal medication is efficacious, cost effective, and compliance friendly, with minimal side effects. Furthermore, based on the pathophysiology of allergic rhinitis, the best therapeutic agent is one that effectively addresses both early- and late-phase reactions.68 Currently, the main classes of medications available for treatment of allergic rhinitis are antihistamines, decongestants, topical or oral glucocorticoids, anticholinergics, cromolyn sodium, and leukotriene-receptor antagonists. In addition, immunotherapy should be considered in moderately to highly sensitive individuals. Avoidance.  Although it may be difficult to avoid pollen because of its widespread distribution, certain common-sense measures can be taken to decrease exposure. Outdoor activities should be limited or completely avoided on days when pollen counts are high. On any given day, pollen counts typically peak in the late morning to mid-afternoon.77 Limiting activities such as leaf raking, lawn mowing, and farming can reduce exposure to outdoor fungi. Because fungi thrive in moist, humid environments, important indoor control measures include dehumidification, proper ventilation, fungicide use in contaminated areas, and removal of sources of fungal growth. Dust mite exposure can be reduced by several methods, including covering mattresses and pillows with allergen-proof encasings, frequently washing of bedding in hot water, and removing carpeting or treating it with denaturing chemicals. Complete removal of the offending animal from the environment is the best treatment for animal allergy. However, this option is often not exercised. If the pet stays in the home environment, then bathing the pet at regular intervals and keeping it out of the bedroom may be helpful. Use of high-efficiency particulate air (HEPA) filters has been shown to be beneficial in removing animal allergens from the environment.12 Antihistamines and Decongestants.  Antihistamines have been used for 50 years and are considered by many to be the first line of therapy in the treatment of allergic rhinitis.54 They are most effective against seasonal rhinitis in which sneezing, itching, rhinorrhea, and watery eyes are the most prominent symptoms. However, only 33% to 50% of seasonal allergic rhinitis sufferers obtain complete relief with antihistamine therapy alone.7 Antihistamines have little or no effect on nasal congestion because of the minor role of histamine in the pathophysiology of congestion. For this reason, antihistamines are usually inadequate for treatment of perennial rhinitis, in which nasal congestion is often a predominant symptom. Antihistamines act by occupying H1 receptors on cells and thereby blocking histamine binding. Older- and newergeneration antihistamines are equally effective. However, the 1228

TABLE 62-2  Newer-Generation Antihistamines Dosage Chemical Name

Trade Name

Adult

Cetirizine

Zyrtec

10 mg daily

Levocetirizine

Xyzal

5 mg daily

Loratadine

Claritin

10 mg daily

Desloratadine

Clarinex

5 mg daily

Fexofenadine

Allegra

Azelastine

Astepro

Olopatadine

Patanase

60 mg BID to 180 mg daily 2 sprays per nostril, BID 2 sprays per nostril, BID

Children (<12 years)

Minimum Age

2.5-10 mg daily 1.25-2.5 mg daily 2.5-10 mg daily 1.0-2.5 mg daily 30 mg BID

6 mo

1 spray per nostril, BID 1 spray per nostril, BID

12 yr

6 mo 2 yr 6 mo 2 yr

6 yr

*BID, Twice a day.

newer-generation antihistamines have gained tremendous popularity because their use is associated with a much lower incidence of sedation and fewer anticholinergic side effects. Commonly used older-generation antihistamines, most of which are available over the counter, are chlorpheniramine, diphenhydramine, brompheniramine, clemastine, and hydroxyzine. The duration of action of brompheniramine and diphenhydramine is 6 to 10 hours, whereas those of chlorpheniramine and hydroxyzine are 24 and 36 hours, respectively. Although sedation is a well-known side effect of the older-generation antihistamines, many patients are unaware of its effects on cognitive functions44 and impairment in driving performance.50 Newer-generation antihistamines are used widely and have been shown to be safe, effective, and well tolerated.29 Moreover, newer-generation antihistamines are more specific in their actions and do not have anticholinergic or anti–α-adrenergic activity. Seven newer-generation antihistamines, including five oral and two intranasal, are currently available (Table 62-2). With the exception of azelastine, olopatadine, and certain formulations of fexofenadine, these medications are given once daily. All seven are approved for use in children; cetirizine, levocetirizine, and desloratadine are approved for those as young as 6 months of age. Azelastine and olopatadine are the only H1 receptor antagonists available in a nasal spray formulation. Studies have shown that both azelastine and olopatadine are safe and effective in relieving most allergic rhinitis symptoms, including nasal congestion.5,34 Although all antihistamines have a relatively rapid onset of action and may be used as needed, they are most effective if either taken before exposure (e.g., before pollen season begins) or used on a regular basis. In some individuals, addition of a decongestant to the antihistamine may be helpful. Decongestants act by stimulating α-adrenergic receptors and thereby reducing blood supply to the sinusoids. Most are short acting (4 to 6 hours) and available over the counter with or without antihistamine combination. Pseudoephedrine is the most commonly used decongestant. Fexofenadine, desloratadine, loratadine, and cetirizine are available in combination with a decongestant. Insomnia and irritability are the most common side effects of decongestants, although individual tolerance varies widely. Individuals with hypertension, glaucoma, or cardiac arrhythmias should use decongestants cautiously or, preferably, not at all. Topical decongestants (e.g., oxymetazoline) have a fast onset of action (within minutes) and therefore provide rapid relief of symptoms. Because of the risk for rhinitis medicamentosa, topical decongestant use should be limited to no more than 3 to 5 days.

Generic Name

Trade Name

Recommended Dose (each nostril)

Beclomethasone Budesonide Flunisolide Fluticasone propionate Fluticasone furoate Mometasone Triamcinolone Ciclesonide

Beconase AQ Rhinocort Aqua Nasarel Flonase Veramyst Nasonex Nasacort AQ Omnaris

1-2 sprays BID 1-4 sprays daily 2 sprays BID 1-2 sprays daily 1-2 sprays daily 1-2 sprays daily 1-2 sprays daily 1-2 sprays daily

Amount Per Spray (mcg) 42 32 29 50 27.5 50 55 50

Minimum Age (years) 6 6 6 4 2 2 2 6

BID, Twice a day. *All preparations are aqueous based.

Nasal Corticosteroids.  Nasal corticosteroids are the gold standard of treatment for allergic rhinitis. Numerous well-designed studies have shown that nasal corticosteroids are superior to antihistamines and cromolyn sodium.6,9 With the exception of ocular symptoms, nasal corticosteroids are effective in controlling all symptoms of allergic rhinitis. Nasal corticosteroids are often the first line of therapy for patients with perennial rhinitis. Corticosteroids control the rate of protein synthesis by either inducing or suppressing gene transcription within the cell.33 The inhibitory effect of all corticosteroids on the late-phase reaction is well established, but studies have shown that nasal corticosteroids, unlike their oral counterparts, also inhibit the early-phase reaction.1 Several preparations of nasal corticosteroids are currently available (Table 62-3). All are equally effective; hence selection is based on convenience, cost, and delivery system. All nasal corticosteroids are in aqueous form and administered either once or twice a day. Because of their relatively slow onset of action, the maximal benefit of nasal corticosteroids may not be realized until 1 to 3 weeks after the initiation of therapy. For individuals with seasonal rhinitis, it is best to start nasal corticosteroid therapy shortly before the onset of pollen season. There is no role for regular use of oral corticosteroids in the treatment of allergic rhinitis. However, a short course (7 to 10 days) of oral corticosteroids may be appropriate when symptoms are severe, such as during peak pollen season. In addition to providing quicker relief, oral corticosteroids may facilitate improved delivery of nasal corticosteroids to the nasal mucosa. The most common side effects of nasal corticosteroids are local irritation and bleeding, reported in approximately 10% and 2% of patients, respectively.43 The incidence of side effects is higher during winter months because of drier conditions. Although rare, nasal septal perforation has been reported with use of nasal corticosteroids.60 If significant septal ulceration and crust formation are noted, therapy should be discontinued for a few days and nasal hygiene with saline spray should be instituted. Long-term studies have shown no evidence of mucosal atrophy associated with the use of nasal corticosteroids.45 Because of the rapid metabolism of nasal steroids, hypothalamic-pituitaryadrenal axis suppression is generally not a problem. Therefore risk for systemic side effects is low. Leukotriene-Receptor Antagonists.  Leukotriene-receptor anta­ gonists (LTRAs), which were previously indicated only for asthma, are now approved for use in allergic rhinitis. Cysteinyl leuko­ trienes, which are products of the arachidonic acid pathway, are important mediators of the allergic inflammatory effects. The leukotrienes cause nasal congestion that results from vasodilation. Because leukotrienes play a major role in the pathophysiology of nasal congestion, the LTRAs may significantly reduce nasal congestion.32 Additionally, they cause mucus production and therefore rhinorrhea. Various studies have demonstrated that leukotriene levels are increased in nasal lavage in both seasonal and perennial allergic rhinitis.66 LTRAs block binding of cysteinyl leukotrienes to the CYS-LT1 receptor in the respiratory tract. Several studies have compared the effects of LTRAs with those of antihistamines and nasal corticosteroids. In one study comparing the LTRA montelukast with loratadine, both were found equally effective in alleviating nasal symptoms.52 However, in a

different study comparing montelukast with the nasal corticosteroid fluticasone propionate, montelukast was significantly less effective than fluticasone propionate in relieving nasal symptoms.40 The effectiveness of combining LTRAs and antihistamines have also been studied. One study showed that the combination of montelukast with loratadine was more effective than either agent alone.43 However, other studies have refuted this finding.48 In conclusion, the studies of LTRAs in allergic rhinitis show that they perform as well as antihistamines, but not as well as nasal corticosteroids. Montelukast, zafirlukast, and zileuton are three currently available oral LTRAs. However, only montelukast is approved for use in both allergic rhinitis and asthma. The other two LTRAs are approved only for use in asthma. The recommended dosage of montelukast for adults and adolescents 15 years of age and older is 10 mg at bedtime. Pediatric dosing is 5 mg and 4 mg at bedtime for ages 6 to 14 years and 6 months to 5 years, respectively. In general, LTRAs appear to be well tolerated. Occasional liver toxicity has been reported with zafirlukast55 and zileuton, but not with montelukast. Other Medications.  Other classes of medications available for treatment of allergic rhinitis are cromolyn sodium and nasal anticholinergic drugs. Although much less potent than nasal corticosteroids, cromolyn is very safe. Its mechanism of action is not completely understood, but it is believed to inhibit mast cell degranulation. For optimal relief, it requires regular use and frequent dosing (three to four times daily). It is useful as a prophylactic treatment before a known exposure, such as visiting someone with a cat. If rhinorrhea is the predominant symptom, use of a nasal anticholinergic, such as ipratropium, may be beneficial. An additional side benefit of ipratropium may be reduction of postnasal drip. The recommended dosage of ipratropium is one to two sprays in each nostril two to four times a day. The main side effect of intranasal ipratropium is nasal dryness. Immunotherapy.  Allergen immunotherapy is a form of immunomodulation in which a state of tolerance is achieved by injecting gradually increasing amounts of allergen extracts into a sensitized person. Although the precise mechanisms of immunotherapy are unknown, several immunologic changes have been observed, including induction of allergen-specific IgG “blocking antibodies,” decreases in allergen-specific IgE, modulation of mast cell or basophil function, and increases in suppressor T cells (CD8).19 The efficacy of immunotherapy in patients with allergic rhinitis has been well established in numerous studies.16,42 Most individuals who receive immunotherapy for allergic rhinitis obtain a variable degree of relief, enabling better symptom control with less medication. Immunotherapy should be considered in individuals who respond poorly to medical therapy and in indiv­ iduals who experience significant side effects to medications. Additionally, consideration may be given if allergen avoidance is not possible. In immunotherapy, weekly injections of allergens at escalating dosages are administered until a maintenance dosage is reached, generally within 4 to 6 months. Thereafter, one or more injections are given monthly, depending on the number of allergen sensitivities. Although there are no data 1229

CHAPTER 62  Seasonal and Acute Allergic Reactions

TABLE 62-3  Nasal Corticosteroids*

PART 7  PLANTS

regarding optimal duration of immunotherapy, the general recommendations are from 3 to 5 years.75 The most common adverse reactions of immunotherapy are local, consisting of erythema, edema, and pruritus at the site of injection. The risk for systemic reaction is approximately 0.1% to 1% per injection.23 Manifestations of a systemic reaction are variable and may include urticaria, flushing, rhinitis, bronchospasm, laryngospasm, abdominal cramping, and hypotension. The risk for systemic reactions is much greater in individuals with poorly controlled asthma. Therefore immunotherapy is generally not recommended in asthmatics with a forced expiratory volume in 1 second (FEV1) of less than 70% of predicted. Because most systemic reactions occur within 20 to 30 minutes after injection, recipients should be observed in the physician’s office for this time period. Some practitioners require patients to carry epinephrine (e.g., EpiPen, Twinject) to self-treat reactions that may occur after leaving the physician’s office.

Anaphylaxis Anaphylaxis is a systemic life-threatening allergic reaction resulting from IgE-mediated mast-cell and basophil degranulation. It is the most severe form of type I hypersensitivity reaction, and clinical manifestations may occur in various end organs, including the skin, upper respiratory tract, lower respiratory tract, gastrointestinal tract, and cardiovascular system. An anaphylactoid reaction is non-IgE antibody mediated but may be clinically indistinguishable from anaphylaxis (Box 62-2). Mechanisms of anaphylactoid reactions include direct release of mediators from mast cells and basophils (e.g., caused by opiates, radiocontrast material), disturbances in arachidonic acid metabolism (e.g., caused by NSAIDs),17 and complement activation (e.g., caused by transfusion reactions).

ETIOLOGY The various causes of anaphylaxis can be categorized into those that are IgE antibody mediated and those that are non-IgE antibody mediated (see Box 62-2). Foods were the most frequent causative agents of anaphylaxis in one series of 179 subjects spanning 3.5 years, accounting for 36% of episodes.78 Egg, cow’s milk, wheat, soybean, peanut, tree nuts (e.g., hazelnut, walnut, cashew, almond), fish, and shellfish (e.g., shrimp, lobster, crab) account for more than 90% of all food-related anaphylactic reactions. In children, peanuts are probably the most frequent cause of food-induced anaphylaxis.59 Individuals may accidentally

BOX 62-2  Classification of Anaphylactic and

Anaphylactoid Reactions

Anaphylaxis (IgE Antibody Mediated) • Food • Drugs (penicillin, cephalosporins, insulin, sometimes aspirin and other NSAIDs) • Insect stings and bites • Other (exposure to antivenom or aquatic proteins) Anaphylactoid (Non-IgE Antibody Mediated) • Direct stimulation of mast cells • Drugs (opiates, vancomycin) • Radiocontrast material • Disturbances in arachidonic acid metabolism • Aspirin and other NSAIDs • Physical stimuli (exercise, cold) • Idiopathic • Complement activation • Transfusion reactions • Immunoglobulin IgE, Immunoglobulin E; NSAIDs, nonsteroidal antiinflammatory drugs.

1230

ingest the allergenic food when it is disguised in cooking preparations or hidden by misleading labeling or contamination during the preparation process. Drugs, especially antibiotics, may cause an anaphylactic or an anaphylactoid reaction. Penicillin and its derivatives are most often implicated, with reactions occurring in between 1 and 5 of every 10,000 courses of treatment.25 Opiates and vancomycin cause drug reactions by directly degranulating mast cells and basophils, so prior sensitization is not required. Aspirin and other NSAIDs can provoke allergic reactions that are either IgE or non-IgE antibody mediated, depending on the presence or absence of underlying asthma or cutaneous diseases (e.g., chronic urticaria). In the presence of asthma and chronic urticaria, disturbance in arachidonic acid metabolism is the predominant mechanism. Aspirin and other NSAIDs inhibit the cyclooxygenase pathway, leading to rapid synthesis of the lipoxygenase pathway products,36 especially leukotrienes, which are important mediators of inflammation. Important outdoor-related causes of anaphylaxis are envenomation (e.g., bee sting), contact with aquatic proteins, and antivenom therapy (e.g., for snakebite). The estimated incidence of insect sting anaphylaxis in the general population is 0.3% to 3%.56 Bee sting anaphylactic reactions are especially common in individuals younger than 20 years but are more likely to be fatal in older adults. In general, children’s reactions are milder (e.g., urticaria only) than are those of adults. Individuals who experience a sting-related anaphylactic reaction have a 50% to 60% risk for suffering anaphylaxis after subsequent insect stings.56 The offending insects vary depending on geographic location. In the United States, yellow jackets cause the most allergic reactions, whereas in Europe, honey bees and wasps cause the majority of insect sting–related reactions. Although rare, anaphylaxis can result from bites inflicted by certain insects (e.g., the kissing bug Triatoma protracta, the deer fly Chrysops discalis,24 and ticks).10 Physical stimuli may provoke anaphylactoid reactions. In exercise-induced reactions, symptoms typically arise after 5 minutes of moderate to heavy exercise, resolving within 30 minutes to 4 hours after exercise cessation.73 About 50% of affected individuals are atopic, and most engage in regular vigorous exercise. A coinciding factor, such as ingestion of an allergenic food (e.g., shellfish)41,51 or NSAID, may be necessary to induce this type of reaction—that is, exercise only or ingestion of the food only does not cause the reaction. In a cholinergic reaction, symptoms occur after exercise and after passive exposure to heat (e.g., hot showers, sweating, and anxiety). In coldinduced reactions, symptoms occur after exposure to a cold stimulus, such as being outside on a cold day, holding a cold object, or eating a cold food. Recurrent anaphylaxis without identifiable cause is known as idiopathic anaphylaxis. Although all the target organs of anaphylaxis may be affected, idiopathic anaphylaxis most commonly causes urticaria or angioedema, or both. The diagnosis of idiopathic anaphylaxis is one of exclusion. Individuals who suffer frequent episodes are less likely to undergo remission. Short-term treatment is the same as that for anaphylaxis resulting from other causes. Depending on the frequency of attacks, long-term treatment may require regular use of oral corticosteroids. Complement activation plays a key role in anaphylactoid reactions resulting from the transfusion of blood products and immunoglobulins. Transfusion of an incompatible blood type can lead to cytotoxic anaphylactoid reactions if complement-fixing antibodies to formed elements of blood, such as red cells, white cells, and platelets, are present. In γ-globulin–related anaphylactoid reactions, immune complex aggregation occurs when antigen–antibody complexes activate complement.

PATHOPHYSIOLOGY Unlike the local pathologic and clinical manifestations of allergic rhinitis, the clinical consequences of type I immediate hypersensitivity in anaphylaxis are systemic. Histamine is the most important mediator and is responsible for most of the clinical manifestations. Important effects of histamine include

CLINICAL FEATURES AND DIAGNOSIS Clinical manifestations of anaphylaxis may occur in various end organs, including the skin (urticaria, angioedema, and flushing), upper respiratory tract (rhinitis, stridor, and hoarseness), lower respiratory tract (wheezing, bronchospasm, and cough), gastrointestinal tract (abdominal pain, diarrhea, and vomiting), and cardiovascular system (tachycardia, hypotension, and shock). Urticaria and angioedema are by far the most common manifestations, occurring in 83% to 90% of individuals with anaphylaxis.31 The second most common manifestations are respiratory tract symptoms, followed by dizziness or syncope and gastrointestinal symptoms. Cardiovascular collapse with shock can occur rapidly, without any other antecedent symptoms. Most anaphylactic reactions occur soon (within 5 minutes to 2 hours) after exposure to an inciting agent, but other patterns are possible. In bimodal anaphylaxis, symptoms begin within minutes of exposure; after transient clinical improvement, the allergic reaction returns 1 to 8 hours later.70 Protracted anaphylaxis can begin suddenly or gradually, but the clinical manifestations are prolonged, sometimes requiring hours or even days of intense resuscitation. Generally, the more rapid the onset, the more severe the episode.37 Fatalities usually result from airway obstruction or cardiovascular collapse, or both. Plasma histamine and serum tryptase can be helpful in making the diagnosis of anaphylaxis, because both may be elevated during an acute episode. The best time to measure plasma histamine is between 10 minutes and 1 hour after the onset of symptoms, whereas the best time to measure serum tryptase is between 1 and 2 hours after the onset of symptoms.35

TREATMENT Anaphylaxis is a medical emergency requiring prompt recognition and treatment. Treatment depends on the severity of the reaction and the organ system (or systems) involved. For mild anaphylactic or anaphylactoid reactions limited to the skin, antihistamines alone are effective. Individuals with cutaneous reactions should be monitored closely for signs of respiratory or cardiovascular compromise; manifestations beyond the skin require more aggressive measures, such as administration of fluids, bronchodilators, and epinephrine. Short-term management of anaphylaxis is detailed in Box 62-3.69 Because most fatalities occur as a result of delayed treatment,18 the importance of prompt administration of epinephrine cannot be overemphasized. Intravenous epinephrine may be administered if the reaction is life threatening and if the patient does not respond to subcutaneous epinephrine. However,

BOX 62-3  Treatment of Anaphylaxis General Measures • Place the individual in Trendelenburg’s position. • Establish and maintain the airway. (If necessary, perform cricothyrotomy.) • Administer oxygen as needed. • Place a venous tourniquet above the reaction site (e.g., insect sting) to decrease systemic absorption of the antigen. • Obtain intravenous access and infuse a volume expander (colloid-containing solution or normal saline) to achieve a systolic blood pressure of 90 mm Hg in an adult. Epinephrine Use and Treatment of Hypotension • Administer aqueous epinephrine, 1 : 1000, 0.3-0.5 mL (0.3-0.5) intramuscularly in the deltoid region. The epinephrine dosage for children is 0.01 mL/kg. Repeat once or twice as necessary at 15- to 20-minute intervals to control the signs and symptoms. • If the reaction is life threatening and if the patient does not respond to intramuscular epinephrine, administer epinephrine intravenously. Mix 0.1 mL (0.1 mg) of 1 : 1000 aqueous epinephrine in 10 mL of normal saline (final dilution, 1 : 100,000) and infuse over 10 minutes. If hypotension persists, a continuous epinephrine infusion may be started by adding 1 mL (1 mg) of 1 : 1000 epinephrine to 250 mL of normal saline, creating a concentration of 4 mcg/mL. Infuse this solution at a rate of 1 mcg/min (15 mini drops/min). The rate of infusion can be increased to 4-5 mcg/min if the clinical response is inadequate. In children and infants, the starting dosage is 0.1 mcg/kg/min, up to maximum of 1.5 mcg/kg/min. Intravenous epinephrine should be used with caution in persons older than 35. • If epinephrine and fluids are ineffective, intravenous dopamine infusion should be initiated. Mix 400 mg of dopamine in 500 mL of D5W (800 mcg/mL) and infuse at a rate of 2-20 mcg/ kg/min. The rate should be titrated using the blood pressure as a guide. Norepinephrine, a potent vasopressor, can be used to treat severe hypotension that is unresponsive to the administration of epinephrine, fluids, and dopamine. Mix 4 mg of norepinephrine in 1000 mL of D5W (4 mcg/mL) and infuse at a rate of 0.5-1 mcg/kg/min. • In a refractory case in which the individual is not responsive to epinephrine (e.g., an individual on a β-blocker medication), administer glucagon 1-5 mg intravenously over 2 minutes. If necessary, a continuous infusion of 1 mg in 1000 mL of D5W (1 mcg/mL) should be started at a rate of 5-15 mcg/ minute. Treatment of Bronchospasm • Administer a β2-agonist (albuterol, metaproterenol, pirbuterol, or terbutaline) via nebulization as required for bronchospasm that is not relieved by epinephrine. • Continuous nebulization may be required if bronchospasm persists. Antihistamines and Corticosteroids • Administer diphenhydramine 25-50 mg (1 mg/kg in children) intravenously over 3 minutes intramuscularly, or orally when the reaction is not severe. Addition of cimetidine 300 mg intravenously over 5 minutes may reverse refractory anaphylactic shock caused by the blockade of both H1 and H2 receptors. Transient hypotension, bradycardia, and arrhythmias have been reported after rapid intravenous administration of cimetidine. • Most authorities advocate the use of glucocorticoids to decrease the likelihood of a late-phase reaction. The standard therapy is either hydrocortisone 200-300 mg intravenously, or in milder cases, prednisone 30-60 mg orally.

intravenous epinephrine should be used with caution in persons older than 35 years. Aerosolized aqueous epinephrine can prevent upper airway edema but is inadequate to abort systemic anaphylaxis.13 Use of over-the-counter epinephrine inhalation aerosol bronchodilators (e.g., Primatene Mist) is generally not recommended because of its lack of adrenergic specificity (i.e., 1231

CHAPTER 62  Seasonal and Acute Allergic Reactions

vasodilation, increased vascular permeability, smooth muscle contraction, stimulation of nerve endings, and glandular secretion. These effects lead to various clinical manifestations, including flushing, urticaria or angioedema, hypotension or shock, wheezing, laryngospasm, abdominal cramping, and diarrhea. Arachidonic acid metabolites, such as prostaglandins, thromboxane A2, and platelet-activating factor, also are released from mast cells and basophils, causing airway smooth muscle contraction, increased vascular permeability, goblet and mucosal gland secretion, and peripheral vasodilation. Platelet-activating factor also contracts smooth muscle and enhances vascular permeability. A late-phase reaction may occur many hours after the initial event. Nitric oxide (NO), a by-product of inflammation, has been found to be increased during anaphylaxis.57 NO has the potential to be both protective and damaging in anaphylaxis. It relaxes bronchial smooth muscle while dilating vascular smooth muscle. Therefore its effects on smooth muscle can improve bronchospasm while worsening hypotension. The overall effects of NO are adversarial. In both animals and humans, NO synthesis inhibitor exerts a beneficial effect in shock.37 The role of NO in the production of anaphylactic reaction has been questioned. In a study of 77 patients with acute allergic reactions, no correlation was found between NO levels and plasma histamine or serum tryptase.38 In addition, NO levels were no higher in patients with hypotension.

it is non-β2 selective) and its extremely short half-life. These agents should also be used with caution in individuals with a history of coronary artery disease and arrhythmias. Repletion of intravascular volume is a mainstay of treatment for hypotension. A large volume of fluid may be necessary and should be given rapidly in either colloid or crystalloid form. Vasopressor drugs may be needed to treat hypotension if the response to subcutaneous epinephrine and fluids is inadequate. Dopamine is often the initial drug of choice. Norepinephrine, a potent vasopressor, can be used to treat severe hypotension that is unresponsive to epinephrine, dopamine, and fluids. Glucagon may be necessary to treat refractory hypotension (e.g., patients on β-blocker medications) that is resistant to standard therapeutic regimens.80 Glucagon is the drug of choice for patients on β-blocker medications.20 Medical antishock trousers have been used successfully to treat refractory hypotension associated with anaphylaxis.49 For prominent wheezing, intermittent or continuous use (depending on severity) of an aerosolized β2-agonist is recommended. Although antihistamines are only adjunctive therapy to epinephrine, they can relieve symptoms dramatically. Combining an H1 antihistamine and an H2 antihistamine may be more effective than administering either alone.58 Most authorities recommend the use of glucocorticoids to decrease the likelihood of a late-phase reaction. Because the symptoms can recur after the initial anaphylactic event, patients should be observed for 2 to 24 hours after

TABLE 62-4  Select Kits of Self-Injecting

Epinephrine

Brand Name

Company

EpiPen EpiPen Jr. Twinject Twinject Jr.

Dey Laboratories Dey Laboratories Shionogi Pharma Shionogi Pharma

Dose (mg)

Doses Per Unit

0.3 0.15 0.3 0.15

1 1 2 2

being stabilized, depending on the severity of the episode. Any individual with severe respiratory or cardiac compromise should be hospitalized. Persons at risk for anaphylaxis should carry a device allowing self-injection of epinephrine (Table 62-4) at all times and should wear a medical information bracelet or carry a medical information card. Finally, it is important to identify the precipitating agent for anaphylaxis so that preventive measures can be taken to reduce the risk for future reactions.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 63 

Plant-Induced Dermatitis  JOSHUA D. SHOFNER AND ALEXA B. KIMBALL

Cutaneous exposure to plants may cause a wide array of skin problems. Plant-induced dermatitis can manifest in multiple fashions, including weeping eczematous patches and plaques, vesicles and bullae, fine scaly patches, or any combination of the above. Because the end result may be a generic response to injury, dermatitis is often an easy clinical diagnosis to make. However, determining the type of dermatitis with which the patient is afflicted can be difficult and frustrating. Acute care providers are often the first individuals to encounter and treat severe plant-induced dermatitis, so the ability to make a rapid and accurate diagnosis is crucial. There are numerous subtypes of dermatitis: contact (irritant or allergic), photoallergic, nummular, asteatotic, stasis, seborrheic, atopic, and dyshidrotic. Dermatitis can manifest acutely with vesicles and bullae or can manifest in a chronic form with lichenification and hyperpigmentation. The acute nature of dermatitis is often itchy and uncomfortable, leading patients to seek emergency care. The history and physical examination are of the utmost importance in determining causality. A morphologic approach to the physical examination is a high-yield method for generating the appropriate differential diagnosis. Is the rash linear in nature? This often implies an external contactant. Is the rash in sun-exposed areas? This implies a photosensitive dermatitis. In addition, the symptoms of the rash are important. Irritant reactions tend to decrescendo in severity, being the worst at presentation and gradually improving over time, whereas those that are allergic tend to crescendo, then decrescendo. They gradually build over 1 to 21 days to peak intensity, then slowly improve. There are many clinical mimics of plant-induced dermatitis, including drug hypersensitivity reactions, connective tissue disease, superficial fungal infections, urticaria, and cutaneous T-cell lymphoma. If a patient has persistent dermatitis that lasts 1232

longer than a month, a biopsy is often indicated to help differentiate possible mimickers. A pathologic review of the biopsy specimen will help rule out other conditions and lead to appropriate therapy. The subset of dermatitis discussed in this chapter is plantinduced dermatitis. Plant-induced dermatitis can be caused by contact with a wide variety of plants. Thousands of species of plants have been reported to cause dermatitis. The specific effects that each of these plants has on the skin have not been fully determined or described. The majority of medical literature regarding plant-induced dermatitis is anecdotal and has not been confirmed by independent observers. Few large-scale studies of the effects of plants have been performed. The exception to that is the Toxicodendron (poison ivy/oak/sumac) species of plants, owing to their ubiquitous nature. The most common injury to skin caused by plants is a simple scratch, laceration, or puncture wound. This can lead to either bacterial or fungal infection. Plant-induced dermatitis reactions can be further subclassified into numerous groups. These include irritant contact dermatitis, allergic contact dermatitis, phototoxic dermatitis, and photoallergic dermatitis. Plants can also cause contact urticaria and foreign-body reactions.

Irritant Contact Dermatitis A wide variety of plants cause irritant contact dermatitis, or nonallergic inflammation of the skin caused by direct contact with the offending plant. Most of these rashes are mild and self-limited, typically involving 1% to 2% body surface area. Irritant contact dermatitis causes transient redness and pruritus of the contacted skin. The spectrum of reactions ranges from linear scratch marks to weeping ulcerated red scaly plaques, the latter of which may be difficult to link to the originating plant.

For online-only figures, please go to www.expertconsult.com

CHAPTER 63  Plant-Induced Dermatitis

FIGURE 63-1  The spiny thorns of the rose bush. (Courtesy USDANRCS PLANTS Database; Herman DE, et al: North Dakota tree handbook, USDA NRCS ND State Soil Conservation Committee, Bismarck, ND, 1996, NDSU Extension and Western Area Power Administration.)

The most common cause of plant-induced contact dermatitis is irritant in nature. Irritant contact dermatitis can be further subdivided into traumatic (mechanical) and chemical causes. Most plants have the potential to cause traumatic skin injury. Whether it is a thorn from a hawthorn tree, a cut from a sharp leaf edge, or scratches from briars, human skin is ill prepared to protect itself from such insults (Figure 63-1). Any foreign body embedded in the skin can cause a granulomatous reaction pattern. Some plants are more prone to causing this type of inflammatory reaction. Plants with thorns and barbs (Figure 63-2) are the most likely culprits. Rose thorns and cactus spines are common offenders. Cacti are indigenous to the southwestern United States. They are popular as houseplants and can be grown indoors with proper care. Therefore, cactus injuries can be seen in a wide variety of locales.109 The initial contact and acute injury may lead to chronic granulomatous inflammatory eruption, which typically takes 4 to 8 weeks to develop. It is the lag time that may make the diagnosis difficult. Clinically, the rash consists of erythematous and indurated papules, plaques, and nodules. The lesions are often grouped and localized, which is a clue to the diagnosis. Cactus spines may also penetrate so deeply into the skin that they cause pseudotumors of bone.101 The prickly pear (Opuntia ficus-indica) is found in North and Central America, as well as around the Mediterranean Sea. It is a member of the Cactaceae family. The fruit is covered with glochids. A unique example of mechanical trauma is from a glochid. Glochids are modified leaves that appear as tufts of barbed spines or hairs found on Opuntia species of cacti (Figure 63-3). They have sharp tips that penetrate skin and cause irritation by disrupting the epidermis. They are very loosely held to

FIGURE 63-3  Prickly pear cactus. (Courtesy Jon Sullivan.)

the cactus, release with the slightest touch, are quite irritating to skin, and cause variable amounts of discomfort and itching. They have a tendency to break off from the cactus and work their way onto the skin, causing a granulomatous reaction that may resemble scabetic nodules.101 They can also implant into the conjunctiva.125 Glochids are present year-round and cause dermatitis in all seasons. Similarly, penetrating injuries from a variety of cactus species, including the Echinopsis, have been reported throughout the southwestern United States. Typical injuries manifest on the extremities as inflammatory papules. In rare cases, the cactus spines can penetrate into bone and soft tissue spaces and cause an inflammatory arthritis. Appropriate footwear and clothing, including gloves, are of utmost importance when encountering plants that can cause mechanical skin trauma. Treatment is to remove the spines from the skin. This is best done mechanically with a forceps under bright illumination and magnification if necessary (Figure 63-4).91,125 When biopsies are performed of the chronic (4 weeks after initial injury) inflammatory papules that are caused by cacti glochid implantation, a granulomatous reaction pattern is found.75 Multiple multinucleated giant cells, histiocytes, granulomas, and organic plant material can be seen histologically

FIGURE 63-2  Many plants (including these from Peru) have evolved thorns and spines in self-defense. (Courtesy Paul S. Auerbach.)

1233

PART 7  PLANTS FIGURE 63-4  Penetrating cactus spine injury to mediastinum of child. (From O’Neill PJ, Sinha M, McArthur RA, et al: Penetrating cactus spine injury to the mediastinum of a child, J Pediatr Surg 43:e33, 2008.)

under polarized light sources. Occasionally, a traumatic injury may implant one or more microbes. When performing a biopsy, one should also perform a tissue culture for bacteria, mycobacterium, and fungal species. This is especially true in cases with pustular morphologies. Initial treatment should be prompt extraction of the cactus spines. The smaller the spine, the more difficult the removal.75 This is a particular problem when encountering injuries from the beaver tail cactus (Figure 63-5), which has very small glochids that can be quite difficult to remove. Many methods of removal have been employed to remove the spines. Tweezers are often the first line of removal, and various gels, glue, tape, and facial masks have been tried.81 The best method is mechanical removal with a small forceps or fine needle. Once removal is accomplished, a topical corticosteroid can be employed. A midpotency

FIGURE 63-5  Beaver tail cactus. (Courtesy Eric Lewis.)

1234

topical corticosteroid, such as triamcinolone acetonide (Aristocort, Kenalog) 0.1% cream or ointment, is often all that is needed. Most granulomatous reactions resolve within 2 to 4 months.35 Often, the removal is unsuccessful, and the glochids work their way to the surface over a period of months to years. Supportive care with cool compresses with aluminum acetate solution 1 : 40 in water used as soak, compress, or wet dressing is very helpful. Administering pain medication and initiating prompt therapy for any co-infection are integral parts of the overall treatment plan. Infections may also be inoculated into the skin from mechanical plant injury. The most well known is Sporothrix schenckii fungal infection occurring after a prick or puncture from a rose thorn. S. schenckii is a common dimorphic fungus found in organic material. The characteristic lymphangitic spread is easily recognized (Figure 63-6). Typically, an ulcerating nodule develops at the site of inoculation; then over the next 3 weeks, on average (3 days to 12 weeks), nodules develop along the draining lymphatic channels. The nodules eventually ulcerate, and patients develop chronic lymphangitis. First-line therapy is either saturated solution of potassium iodide or itraconazole.85 There are many other infections caused by traumatic implantation of bacteria, fungus, and algae into skin or underlying subcutaneous tissues (Box 63-1). Another common problem, is direct implantation of plant organic material into the skin, causing a foreign-body reaction, such as that seen with a splinter. The goals in treatment are to remove the foreign material promptly and treat infections with the appropriate antimicrobial agent. Wood dust can also cause an eczematous dermatitis of either the irritant or allergic type. The victims are nearly always woodworkers who have been exposed repeatedly. Allergic contact dermatitis occasionally develops. Rarely, an erythema multiformelike configuration is noted.48 Respiratory hypersensitivity, including asthma, to wood dusts is well documented.111 Solid wood has very rarely been reported to cause dermatitis.116 Table 63-1 lists the most commonly reported woods to cause contact dermatitis. Dermatitis from woods is almost entirely seen in an occupational setting. Treatment includes avoidance of the offending agents and use of ultra-potent topical steroids such as clobetasol 0.05% ointment twice daily to the affected areas for up to 2 weeks. The most common form of plant-induced irritant contact dermatitis is from plant-derived chemicals. Acids, enzymes, isothiocyanates, phorbol esters, calcium oxalate, and alcohols cause these reactions. The chemicals are directly toxic to the skin, and work by altering the inherent pH balance, dissolving the protective lipids of the stratum corneum, and denaturing skin proteins. They require direct contact of the plant material with the epidermis. Many factors can modify irritant reactions. The most important variables are duration of skin contact, concentration of the irritant, and underlying skin integrity and thickness.8 Concentration of the irritant chemical in the plant will be at different levels in the stem, petals, roots, and leaves. Levels of the irritant also fluctuate at different times of the year, so it would not be

FIGURE 63-6  The characteristic red nodules seen indicating lymphangitic spread of Sporothrix schenckii.

TABLE 63-1  Sampling of Wood Trees That Cause

Bacterial • Staphylococcus aureus • Clostridium tetani

Common Name

Botanical Name

African black walnut African blackwood Bolivian rosewood Brazilian box tree Cocobolo Cordia East Indian rosewood Ebony Honduran mahogany Iroko Litre Macassar ebony Mahogany Milo wood Obeche Padauk Pao ferro Perupok Pine Redwood Sapele wood Silky oak Sucupira Tali wood Teak Walnut White ash Zebrawood

Mansonia altissima Dalbergia melanoxylon Machaerium acutifolium Aspidosperma species Dalbergia retusa Cordia goeldiana Dalbergia latifolia Diospyros celebica Swietenia macrophylla Chlorophora excelsa Lithrea caustica Diospyros celebica Khaya species Thespesia populnea Triplochiton scleroxylon Pterocarpus dalbergiodes Machaerium scleroxylum Lophopetalum dubicum Pinus species Sequioa sempervirens Entandrophragma cylindricum Grevillea robusta Bowdichia nitida Erythrophleum guineense Tectona grandis Juglans nigra Fraxinus americanus Astronium fraxinifolium

Plant Injury

Chromomycosis • Fonsecaea pedrosoi • Phialophora compacta • Phialophora verrucosa • Cladosporium carrionii • Rhinocladiella aquaspersa Phaeohyphomycosis • Exophiala jeanselmei • Wangiella dermatitidis Mycetoma • Madurella mycetomatis • Actinomadura madurae • Actinomadura pelletieri • Nocardia brasiliensis • Nocardia cavae • Nocardia asteroids • Streptomyces somaliensis • Madurella grisea • Leptosphaeria senegalensis • Petriellidium boydii • Aspergillus nidulans

Contact Dermatitis

Protothecosis • Prototheca wickerhamii

Data from references 2, 3, 24, 25, 49, 50, 70, and 97.

Mycobacterial • Mycobacterium kanasii • Mycobacterium marinum • Mycobacterium ulcerans

Central and South America, but about 40 species live in the southern United States. They typically appear as low-lying shrubs. Some plants, such as those listed in Table 63-3, contain proteolytic enzymes, which cause skin irritation when contacted in sufficiently high concentrations. Plants such as Mucuna pruriens (cowhage) contain a proteolytic enzyme—mucunain—that causes

Other Fungal • Blastomyces dermatitidis • Sporothrix schenckii • Histoplasma capsulatum Data from references 67, 88, 123.

uncommon for someone to have a reaction in the summer months from contacting the leaves of an irritating plant and not have the same reaction when touching the stem in winter. Plants in the spurge (Euphorbiaceae) family exude a milky sap when traumatized. This sap contains a chemical mixture of irritating diterpenes and phorbol esters.42 After skin contact, the reactions can vary from mild stinging and burning to erythema, vesiculation, and bulla formation. Blister formation occurs typically within 24 hours. Eczematous weeping plaques can also be seen in the first 24 hours. Reactions can last for 2 to 3 weeks. The spurge family is a large family of plants with more than 7000 described members. These plants are found predominantly in tropical climates; in the United States, they can be found mainly in Florida and the southwestern states. Some well-known members of the Euphorbiaceae family include the croton plant, wolfsmilk, manchineel tree, and snow-on-the-mountain. Figure 63-7 demonstrates three of these commonly irritating plants. Table 63-2 is a list of the most common Euphorbiaceae. Plants of the genus Croton are also members of the spurge family. These tropical plants are the source of croton oil. This oil had been used in the past as a purgative and for many medicinal remedies. The plants contain a mixture of phorbol esters and diterpenes in their leaves, stems, and seeds.18 These esters can cause immediate blistering of the skin, as well as a weeping eczematous eruption. These plants are found mostly in

TABLE 63-2  Common Members of the

Euphorbiaceae Family

Common Name

Botanical Name

Poinsettia Candelabra cactus Caper spurge Chinese tallow Crown-of-thorns Cypress spurge Manchineel tree Pencil tree Petty spurge Sandbox tree Snow-on-the-mountain Sun spurge Wolfsmilk

Euphorbia pulcherrima Euphorbia lactea Euphorbia lathyrus Sapium sebiferum Euphorbia splendens Euphorbia cyparissias Hippomane mancinella Euphorbia tirucalli Euphorbia peplus Hura crepitans Euphorbia marginata Euphorbia helioscopia Euphorbia purpurea

Data from Asilian A, Faghihi G: Severe irritant contact dermatitis from cypress spurge, Contact Dermatitis 51:37, 2004; and Lovell CR: Irritant plants. In Lovell CR, editor: Plants and the skin, Oxford, 1993, Blackwell Scientific Publications, pp 42-95.

TABLE 63-3  Common Plants with Irritant Enzymes Common Name

Botanical Name

Proteolytic Enzyme

Cowhage Crownflower Pineapple Papaya Fig tree

Mucuna pruriens Calotropis species Ananas comosus Carica papaya Ficus carica

Mucunain Mudarin Bromelin Papain Ficin

1235

CHAPTER 63  Plant-Induced Dermatitis

BOX 63-1  Infections Associated with Mechanical

PART 7  PLANTS

FIGURE 63-7  Common plants that induce irritant phytophotodermatitis. A, Snow-onthe-mountain. B, Wolfsmilk. C, Croton bush. (C courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)

A

C

B

intense itching immediately on contact. Its seed pods are covered with tiny stinging hairs called trichomes. Trichomes contain high concentrations of mucunain. This enzyme has been used for decades by practical jokers in its dried form as itch powder. Recently, medical researchers have made use of the irritant enzyme found in papaya. Papain is a proteolytic enzyme that is used in a number of commercial wound dressings to aid in degradation of necrotic tissue and aid in wound healing.98 Calcium oxalate is a common skin irritant. Calcium oxalate in plants is found in a crystalline needle-like form called raphides. It is present in many plants, including dumb cane, rhubarb, agave, daffodils, and hyacinths, in irritating concentrations. Dumb cane (Dieffenbachia species) is a common houseplant well known to cause irritant skin and mucous membrane reactions (Figure 63-8).29 The common name arises from the effect it has on those unlucky enough to chew its leaves, which release calcium oxalate. Calcium oxalate causes irritation, swelling, salivation, pain, and blistering of mucous membranes. In an extreme case, the afflicted person is unable to speak normally, owing to involvement of the mucous membranes.126 When the sap of this plant contacts the eye, conjunctival swelling and corneal ulcers may occur.82 Raphides are also found in Agave species. Irritant contact dermatitis has been reported in tequila distillery workers, who are in frequent contact with Agave tequilana.104 Purpuric and irritant reactions have been reported to occur after exposure to the sap of Agave americana.25,100 Immediate burning on exposure is characteristic of calcium oxalate toxicity. Daffodils and hyacinths are among the many other species containing calcium oxalate, which is found in its highest concentration in the bulb.114 Agricultural workers who gather these bulbs and flowers are at highest risk for irritant dermatitis, typically on the distal extremities where they came into contact with the plant.59 The family Solanaceae contains the peppers. These plant species contain several capsaicinoids, the most common of which is capsaicin. Capsaicin is a chemical compound that can cause skin and mucous membrane burning, itching, and in severe cases, vesiculation and bulla formation. Specialized cells of the plant’s placenta produce capsaicin. Capsaicin binds to receptors on neurons and causes release of substance P from primary sensory neurons. With repeated applications, capsaicin causes depletion of substance P and desensitizes the neuron. This effect is used in clinical practice with topical application of capsaicincontaining compounds to skin in areas of chronic pain, such as for postherpetic neuralgia. 1236

Brassicaceae (Cruciferae) is a large family of plants that causes irritant contact dermatitis. More than 3500 species live in temperate regions of the world.31 Its members include horseradish (Armoracia rusticana), black mustard (Brassica nigra), and white mustard (Sinapis alba) (Figure 63-9). These plants contain glucosinolates, which are converted to isothiocyanate, which causes irritant dermatitis.78 This reaction is catalyzed by the enzyme myrosinase. Substrate interacts with the enzyme after the plant is crushed, as in chewing.31 Contact with these plants can cause a wide range of cutaneous reactions, including burning sensation, pain, red patches, and blister formation. The Ranunculaceae family includes buttercups and Old Man’s Beard (Figure 63-10). Table 63-4 lists a small sampling of plants in this family reported to cause irritant contact dermatitis.

FIGURE 63-8  Diffenbachia species.

Ranunculaceae

Common Name

Botanical Name

American prairie crocus Buttercup Christmas rose Meadow rue Pasque flower Pilewort Staves-acre Traveler’s joy Windflower Wolfsbane

Pulsatilla patens Ranunculus species Helleborus niger Thalictrum foliosum Pulsatilla vulgaris Ranunculus ficaria Delphinium species Clematis vitalba Anemone nemorosa Aconitum napellus

TABLE 63-5  Plants Causing Irritant Phytocontact

Dermatitis and Their Primary Irritant Chemicals

FIGURE 63-9  White mustard plant. (Courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)

Protoanemonin is considered the primary irritant toxin in this group of plants. Reactions from these plants tend to be mild and rarely cause people to seek medical care. Table 63-5 includes plants and plant families that cause irritant phytocontact dermatitis and lists their primary irritant substance.70,114 It is currently believed that both irritation and contact sensitization are mediated by epidermally derived cytokines. Tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), macrophage inflammatory protein-2 (MIP-2), and granulocyte-macrophage colony-stimulating factor (GM-CSF) are produced and secreted into tissue in response to both allergens and irritants. However, a number of other proteins are released only by allergenic stimulation. In irritant contact dermatitis, the chemical irritant (which is usually an acid, alkali, surfactant, solvent, oxidant, enzyme or toxin) damages the keratinocyte. This damage is highly dependent on the concentration of the irritant. No sensitization or elicitation phase occurs, as is seen in allergic contact dermatitis,

A

Common Name

Botanical Name

Irritant Chemical

Agave Black mustard Buttercup Coral plant Cowhage Croton Daffodils Dumb cane Hyacinths Manchineel tree

Agave americana Brassica nigra Ranunculus bulbosus Jatropha Mucuna pruriens Croton tiglium Amaryllidaceae family Dieffenbachia species Liliaceae family Hippomane mancinella Podophyllium peltatum Euphorbia tirucalli Opuntia species Euphorbiaceae family

Calcium oxalate Isothiocyanates Protoanemonin Thioglycoside Proteolytic enzymes Phorbol esters Calcium oxalate Calcium oxalate Calcium oxalate Phorbol esters

May apple Pencil tree Prickly pear Spurges Mustard, radish, etc. Buttercups, pilewort Common caper Peppers Spider plant

Cruciferae (Brassicaceae) family Ranunculaceae Capparidaceae family (e.g., Capparis spinosa) Solanaceae family Cleomaceae family (e.g., Cleome species)

Podophyllin resin Triterpene alcohols Spines Shorbol and diterpene esters Isothiocyanates Protoanemonin Isothiocyanates Capsaicin Isiothiocyanates

Data from High WA: Agave contact dermatitis, Am J Contact Dermat 14:213, 2003; and Ricks MR, Vogel PS, Elston DM, et al: Purpuric agave dermatitis, J Am Acad Dermatol 40:356, 1999.

B

FIGURE 63-10  Plants of the family Ranunculaceae. A, Buttercup. B, Old Man’s Beard. (B courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)

1237

CHAPTER 63  Plant-Induced Dermatitis

TABLE 63-4  Irritant Plants in the Family

PART 7  PLANTS

which is a key discerning feature between the two types of plantinduced contact dermatitis. The damaged keratinocyte activates phospholipase A2. This in turn cleaves arachidonic acid and diacylglyceride (DAG) from the cell membrane. The arachidonic acid is converted into various prostaglandins and leukotrienes. Prostaglandins and leukotrienes cause endothelial cells to dilate and become leaky, resulting in edema. They also act on mast cells to release histamine and are chemoattractants for lymphocytes and neutrophils. Further recruitment of lymphocytes and neutrophils is facilitated by expression of intercellular adhesion molecule-1 (ICAM-1) by keratinocytes.79 The DAG causes upregulation of genes for cytokines such as interleukin-1 (IL-1) and GM-CSF. These proteins then act to stimulate T cells and neutrophils. All these inflammatory cells and release of various cytokines and vasoactive substances lead to the clinical findings in irritant contact dermatitis. This is a continuing area of investigation.102,127

TREATMENT Treatment of primary irritant dermatitis requires multiple steps. The victim must be removed from exposure to the irritant chemicals. Gentle cleansing of the wound with antibacterial soap, applying cool compresses, and watching for infection are essential. Antihistamines, such as hydroxyzine, 10 to 25 mg administered orally 4 times daily, or diphenhydramine, 25 mg orally 2 to 4 times daily, can help with itching. The sedating antihistamines tend to work better than the newer nonsedating types (fexofenadine, loratadine, and desloratadine), although some patients respond well to the nonsedating forms. Topical mediumstrength steroids, such as triamcinolone 0.1% cream, may be applied twice a day to the affected areas for up to 2 weeks without risk for atrophy. Clobetasol 0.05% cream or ointment (an ultrapotent topical steroid) can also be used in severe cases. In the case of topical medium-strength and ultrapotent topical steroids, care should be taken to avoid application in the groin, axillae, and face. Typical application regimens are twice daily for 1 to 2 weeks. Cool compresses with aluminum acetate solution (Domeboro, Burow’s solution) diluted 1 : 40 in water are very helpful in soothing pruritus and exudative skin irritation. Dermatitis generally heals in less than 7 days if no complications develop and if tissue damage is minimal. If the patient is unable to be removed from the source of irritation, no medicine, cream, or soak will alleviate the problem. People are sometimes forced to change occupations or hobbies, or at the very least modify their environment.

Allergic Contact Dermatitis Allergic contact dermatitis is a type IV delayed hypersensitivity reaction. This form of contact allergy is far more common than is contact urticaria. The most common acute presentation is linearly arranged eczematous, edematous patches and plaques with varying amounts of vesiculation and bulla eruption. Occasionally, the eruption is widespread. If the face is involved, there can be severe eyelid swelling. Patients are quite distressed by their appearance. In severe cases, they can have systemic symptoms of fever, chills, fatigue, and lethargy. In its more chronic form, as is seen with the Compositae family, allergic contact dermatitis presents with lichenified eczematous plaques in exposed areas.

TOXICODENDRON FAMILY The most common cause of acute allergic contact dermatitis in the United States is from exposure to poison ivy, oak, and sumac plants (Table 63-6). In the past, allergic contact dermatitis caused by poison ivy, oak, or sumac was referred to as Rhus dermatitis. Recent botanical nomenclature places the poison ivy, oak, and sumac plants in the Anacardiaceae family in the genus Toxicodendron. The Rhus genus contains plants that are not known to cause allergic contact dermatitis. Therefore the term “Rhus dermatitis” should be abandoned. Toxicodendron weeds are fastidious. They do not grow in Alaska or Hawaii and do not survive well above 1500 m (5000 feet), in deserts, or in rainforests. They grow best along cool 1238

TABLE 63-6  Toxicodendron Species Common Name

Botanical Name

Western poison oak Eastern poison oak Poison ivy Rydberg’s poison ivy Poison sumac

Toxicodendron Toxicodendron Toxicodendron Toxicodendron Toxicodendron

diversilobum quercifolium radicans rydbergii vernix

streams and lakes and luxuriate if it is also sunny and hot. They are found in every state of the continental United States. The plants have different configurations in different regions, but generally, poison ivy grows east of the Rockies, poison oak grows west of the Rockies, and poison sumac grows best in the southeastern United States. Because avoidance is the best prevention, it is important to learn what the plants look like in a given area (Figure 63-11). Once contaminated with the oil (resin), an average person has 1 to 4 hours to wash it off with soap and water to prevent dermatitis. Poison ivy (T. radicans) grows in moist shady regions east of the Rockies. The plants thrive at sea level and do very poorly above 1500 m (5000 feet). Poison ivy is never found on the west coast of the United States. The leaflets are 10 to 30 cm (4 to 12 inches) long and are found in groups of three. The shape of the leaves is often ovate or obtuse. The leaves can be shiny, smooth, and hairless, or they can be rough, hairy, and velvety (Figure 63-12).12,31 Its characteristic shape has lead to the adage, “Leaves of three, let them be” (Figure 63-13). It is a climbing shrub commonly found growing up the trunks of large trees, with aerial roots that are quite prominent. Poison oak (T. diversilobum) is found in the west coastal states of North America and is given the designation western poison oak. It is a common shrub with multiple stems that form three leaflets. The leaves are larger on plants that grow in shade than on those grown in full or partial sunny conditions. It has many brown aerial roots and clusters of yellow flowers that bloom in the spring.31 The flowers bear cream-colored berries. In the California hills, poison oak grows like a forest, but in cooler, dry climates, it remains isolated in small patches. Poison sumac (T. vernix) is a fast-growing small tree or shrub. Some plants grow as tall as 12 m (40 feet), but the average height is about 4.5 m (15 feet). The plants are found in wet marshy regions of the United States. Its leaves are unique among Toxicodendron species. They are configured as 7 to 13 smooth oval leaflets attached along a central stem.31 The plant forms palecolored fruit. Nonpoisonous sumacs can be recognized by their jagged leaf margins and red berries. All Toxicodendron plants have many interconnected channels that contain sap. When the plant is traumatized and a channel is broken open, the sap is extruded and hardens as a black resin to seal off the damage. This sap is the material that contains the allergen urushiol.31 All parts of the plant contain the urushiol resin (Figure 63-14, online), which is a heavy, nonvolatile oil. In its natural state, the oil is colorless or slightly yellow. Because the oil is virtually invisible, many people fail to understand how they acquired the rash. It is not a vapor, because at 315° C (600° F) in a fire or oven, urushiol splatters like butter. In a camp or forest fire, it attaches to smoke particles and can be carried downwind. The oil also readily coats the fur of animals, which explains why people often get the dermatitis from their outdoor pets. On exposure to air, the oil oxidizes, polymerizes, and turns black. This is a way to recognize the weeds, especially in autumn when the leaves fall off. The amount of urushiol present in poison ivy and poison oak is roughly equal year-round, even when the plants are only sticks without leaves in the winter. As the leaves turn red and start to dry up in the fall, important nutrients, including urushiol, return to the stem and roots through subepidermal resin canals.50 Thus dead leaves that fall to the ground are virtually devoid of urushiol. Urushiol is exposed to skin when a plant that has been injured or bruised releases it to the surface of the leaf, petal, stem, or

C

B

D

CHAPTER 63  Plant-Induced Dermatitis

A

E

FIGURE 63-11  Plants in the Toxicodendron genus. A, Poison ivy. B, Poison ivy growing as a sea of vines. C, Poison oak. D, Poison oak, close up. E, Poison sumac. (C courtesy Paul S. Auerbach.)

root. Clinical effects are usually manifested 24 to 48 hours after contact in a previously sensitized individual; 10 to 14 days after contact in a patient on first exposure. Typically, linear streaking of papulovesicles occurs; edema, weeping, and crusting are also commonly seen (Figure 63-15). A distinct linear nature is often a clue to the diagnosis of allergic contact dermatitis. On occasion, the eruption can appear to be urticarial in nature or can mimic cellulitis. Appearance of black dots on the skin in areas of involvement can be helpful in determining the etiology.65 The black dots represent dried urushiol that has been oxidized by air

A

B

C

D

FIGURE 63-12  A to D, Poison ivy can have various appearances.

(Figure 63-16). Severe itching leading to excoriations nearly always accompanies the rash. This can lead to secondary infection. The antigen is found in the milky sap, which is quickly absorbed into the skin. Thus it is nearly impossible to wash off the sap quickly enough to prevent dermatitis. Once the sap touches the body, it is often spread by inadvertent transfer. This explains why patients often develop eruptions in sites distant from the initial contact with the plant. There are many unique urushiol chemicals. Collectively, they can be called urushioids. Each plant has a different urushioid concentration and composition. Urushioids have a structure that contains a benzene ring with a varying-length carbon side chain. The concentrations of the various urushioids of each plant depend on growing conditions and season, which also affect their antigenic properties. If the side chain is desaturated and longer, this increases the catechols’ antigenicity. Conversely, if there is a substitution on the catechol ring, this reduces antigenicity.79 Addition of an aliphatic

FIGURE 63-13  Close-up views of the characteristic three-leaf pattern of Toxicodendron. (Courtesy Peter Schalock, Massachusetts General Hospital, Boston, Mass.)

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PART 7  PLANTS

A

B

C

FIGURE 63-15  Representation of the linear nature of poison ivy–induced allergic contact dermatitis. A, Knee. B, Hand. C, Finger.

side chain and presence of free phenolic groups also increase antigenicity.114 Poison ivy contains predominantly urushiol III, poison oak contains mostly urushiol I, and poison sumac contains predominantly urushiol II.31,79 If the patient avoids re-exposure, dermatitis resolves within 14 to 21 days in most cases. It is important to diagnose secondary impetiginization because this can lead to cellulitis if not treated with appropriate antibiotics. The most likely pathogens are Staphylococcus aureus and streptococcal species. Hyposensitization therapy has not proved practical or particularly effective and is rarely performed. Patients need to be informed to thoroughly clean clothing, through at least one complete automated hot water wash and rinse cycle with detergent, and to clean any object that may have come in contact with the plant in order to avoid repeat exposure. It is estimated that 50% to 70% of the population is sensitive to the causative antigen, urushiol. The amount of purified urushiol required to elicit a reaction is 2 to 2.5 mg.45 Some people (about 35%) are considered subclinically sensitive because they have negative skin test reactions to 2.5 mg urushiol, but react to higher concentrations, such as 5, 10, and 50 mg.40,45 Clinically, this group is interesting because they invariably did not have poison ivy dermatitis as teenagers and often plucked the weeds with apparent impunity. However, usually in midlife after a bout of weed pulling, a rash spreads explosively. For unknown reasons, they have crossed the line into clinical sensitivity. If

FIGURE 63-16  Poison ivy–induced allergic contact dermatitis after a young woman accidentally pinched some poison ivy leaves behind her knee. Note the central black dots, which represent the dried urushiol.

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patch-tested with dilutions of urushiol, these individuals are often exquisitely sensitive and do not appear to lose their reactivity. The flare-up may last for several weeks, probably because of prior contamination of the home and workplace with urushiol oil. Treatment must be aggressive and more prolonged than usual. A smaller group (10% to 15%) does not react to higher concentrations and cannot be sensitized by 1000 mg. This group was first detected and studied in passive transfer experiments in the 1950s.46 These individuals are considered to be naturally tolerant, but it remains unclear whether they achieved that state by early antigenic exposure or by genetic luck. They have no inherent resistance to contact sensitization with other chemicals and otherwise appear healthy.47 They may hold a clue to the molecular basis for immunologic tolerance. From a practical standpoint, only 10% to 15% of Americans (up to 40 million people) can be categorized as exquisitely sensitive. Generally, these persons seek and need emergency medical care (Figure 63-17). They typically have had prior unpleasant experiences. Within 2 to 6 hours after exposure, swelling is accompanied by an erythematous, intensely pruritic, edematous, vesicular, and ultimately bullous eruption that can be associated with fever, malaise, and prostration (Figure 63-18). This true

FIGURE 63-17  Generalized poison ivy dermatitis.

CHAPTER 63  Plant-Induced Dermatitis

A

C

B

FIGURE 63-18  Severe acute poison oak dermatitis. A, Facial edema. B, Blisters. C, Penile edema. (Courtesy Axel Hoke.)

dermatologic emergency should be treated immediately and vigorously. Extreme susceptibility tends to be familial; if one parent is supersensitive, children are likely to be as well. If both parents are sensitive, the chance of sensitive offspring is about 80%.121 The level of individual sensitivity is not determined by severity of the initial bout of dermatitis, although nearly one-half of patients admit to a memorable bout of dermatitis as a teenager. However, no more than 25% to 35% of victims at age 30 to 40 were stricken within the previous year.40 When these subjects are patch-tested with weak dilutions of urushiol, less than one-half react as might be expected from their history. An individual’s level of reactivity does not change appreciably if he or she is tested monthly over a year; testing at less frequent intervals in very sensitive subjects over 3 to 4 years has shown little or no change in the level of reactivity.45 Repeated mild to moderate bouts of dermatitis maintain the sensitive state, whereas a single severe bout may produce a prolonged period of anergy or refractoriness, not unlike the clinical condition of “hardening” or unresponsiveness, which is well described in the industrial setting.39,40,106 The Anacardiaceae family accounts for most cases of allergic contact dermatitis in the United States. Table 63-7 catalogs the major members of this family and the plants most likely to cause dermatitis. Most individuals who spend a great deal of time outdoors know how to recognize these plants and appropriately avoid them. Figure 63-11 shows poison ivy, oak, and sumac. However, these are not the only plants that need to be considered. Table 63-8 lists some common plants causing allergic contact dermatitis. In patients that have demonstrated allergic contact dermatitis to the Toxicodendron plants, there is a high risk of crossreactivity with a number of other plants, including mango, oil from the cashew nut shell, fruit pulp from ginkgo biloba, Japanese lacquer tree, and India marker ink tree. Mango dermatitis

(Figure 63-19) has been reported to be the leading cause of plant dermatitis in Hawaii.114 Urushiol is found in the plant’s leaves and stems and in its fruit’s skin. Typically, people are exposed to the urushiol when they eat or manipulate the fruit that has yet to be peeled. Facial involvement, particularly of the lips, occurs after biting into a mango that still carries its outer peel. TABLE 63-8  Plants Causing Allergic Contact

Dermatitis

Common Name

Botanical Name

(Various) (Various) (Various) Lichen Liverwort Pine tree Poison ivy Poison oak Poison sumac Primrose Ragweed Tulip

Alstromeria species Compositae species (about 20,000 species) Grevilla species Cladonia, Evernia, and Primelia species Frullania species Pinus species Toxicodendron radicans Toxicodendron diversilobum Toxicodendron vernix Primula obconica Ambrosia species Tulipia species

Data from Marks JG Jr, Elsner P, DeLeo VA: Contact and occupational dermatology, ed 3, St Louis, 2002, Mosby, pp 13-15.

TABLE 63-7  Anacardiaceae Family Common Name

Botanical Name

Brazilian pepper Cashew El litre tree Ginkgo tree Indian marking nut Japanese lacquer Korean lacquer tree Mango Pepeo tree Poison ivy Poison oak

Schinus terebinthifolius Anacardium occidentale Lithraea caustica Ginkgo biloba Semecarpus anacardium Rhus vernicifera Rhus vernicifera stokes Mangifera indica Mauria puberula Toxicodendron radicans and T. rydbergii Toxicodendron diversilobum and T. toxicarium Toxicodendron vernix Metopium toxiferum Anacardium melanorrhoea

Poison sumac Poisonwood Renges tree

Data from Marks JG Jr, Elsner P, DeLeo VA: Contact and occupational dermatology, ed 3, St Louis, 2002, Mosby, pp 13-15.

FIGURE 63-19  Pruritic and eczematous rash 3 days after onset. One week earlier, this 27-year-old man had peeled a mango, become distracted by a telephone call, and rested his left hand on his right leg. Three days later, contact dermatitis became apparent. When much younger, the patient had been sensitized to poison oak and poison ivy; the sap of the mango rind contains oleoresins that cross-react with the oleoresins of poison ivy. The rash resolved after 1 week of treatment with topical corticosteroids. (From Tucker MO, Swan CR: Images in clinical medicine: The mango-poison ivy connection, N Engl J Med 339:235, 1998.)

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PART 7  PLANTS

FIGURE 63-21  Poison ivy on the left, with three leaves, adjacent to the commonly mistaken Virginia creeper with five leaves (bottom and right).

the Virginia creeper. English ivy, Hedra helix, is another plant that is often difficult to differentiate from poison ivy. H. helix has been reported to cause allergic contact dermatitis.128

IMMUNOLOGY OF POISON IVY AND POISON OAK DERMATITIS

FIGURE 63-20  Ginkgo biloba.

The other common area of involvement is the hand after individuals peel the fruit.78 Once peeled, mangos are no longer allergenic. The ginkgo tree, Ginkgo biloba, is commonly found in cities, where the trees thrive. Its characteristic split leaves are easily recognized (Figure 63-20). It has been reported to cause allergic contact dermatitis in joggers who run through debris on sidewalks and roadways containing ginkgo leaves, flowers, and fruit. Multiple plants are similar in appearance to the poison ivy plant and need to be differentiated. Table 63-9 lists some of the more common “imposters” for the poison ivy plant. The Virginia creeper, Parthenocissus quinquefolia, is commonly misidentified as poison ivy. Figure 63-21 shows poison ivy side by side with TABLE 63-9  Imposters of the Poison Ivy Plant Common Name

Botanical Name

Boston ivy English ivy Skunkbush sumac Virginia creeper

Parthenocissus tricuspidata Hedra helix Rhus trilobata Parthenocissus quinquefolia

Data from McGovern TW, LaWarre SR, Brunette C: Is it or isn’t it? Poison ivy look-a-likes, Am J Contact Dermat 11:104, 2000.

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The immunologic mechanism for allergic contact dermatitis is generally felt to be type IV cell-mediated delayed hypersensitivity.41 An initial sensitization phase occurs, followed by an elicitation phase on subsequent exposure. Allergic contact dermatitis is caused by haptens. Haptens are low-molecular-weight compounds, nearly always 500 daltons or less, that exist as unprocessed antigen. They are lipid soluble, allowing them to pass into the stratum corneum.73 Contact allergens are not immunogenic by themselves; they bind to epidermal proteins to generate new antigenic determinants.72 Urushiol from poison ivy is a hapten. Langerhans cells are the main antigenpresenting cells (APCs) in the skin. They are normally in a resting state, with little to no ability to stimulate T cells. In skin, keratinocytes are also part of the immune surveillance system. They respond quickly to every chemical insult, either irritant or allergenic, in antigen-dependent fashion, to produce a variety of cytokines. These function mainly to amplify future inflammatory responses.10,89 Early on, they secrete TNF-α and ICAM.1 Later, they release IL-1, IL-6, IL-8, and IL-10; still later, macrophage chemotactic factor and other cytokines are released.9,53,54,89,95 These may in turn release acute-phase reactants from mast cells and endothelial cells, as seen in irritant responses.10,89 Current research is attempting to identify which keratinocyte cytokines specify the allergic reaction, as distinct from simply injury. Nevertheless, it is known that the catechol molecules of poison oak and poison ivy enter the skin and bind through nucleophilic attack at benzene ring positions 4, 5, and 6 to surface proteins on APCs, which are primarily epidermal Langerhans cells. These cytokines from the keratinocytes cause Langerhans cells to mature and enter into an active state. Active Langerhans cells are then able to recognize and internalize antigens. Langerhans cells are responsible for immunosurveillance. In the sensitization phase, when a hapten such as urushiol is applied to skin, it penetrates the stratum corneum. Urushiol then activates the skin’s innate immune response, leading to upregulation of proinflammatory cytokines and eventual recognition of the antigen by activated APCs. These cells internalize the urushiol by pinocytosis. Proteolytic enzymes in lysosomes then process the urushiol. This processing consists of proteolytic degradation of the protein into smaller antigenic peptides. The antigenic

TREATMENT Systemic corticosteroids are widely accepted as the first line of treatment for moderate to severe disease, especially given early and in large, therapeutic doses. In mild cases, ultrapotent topical steroids alone, such as clobetasol 0.05% ointment twice daily to the affected areas for 2 weeks, may suffice. If the reaction is of less than 2 hours’ duration, intravenous (IV) hydrocortisone (adult dose 100 to 200 mg) or methylprednisolone (adult dose 500 mg to 1 g) can be curative. After a patient has suffered 4 to 6 hours with massive edema, erythema, and pruritus, IV therapy

is highly effective, but it must be followed by more prolonged oral or intramuscular (IM) administration of corticosteroids. Most patients in this category seek help after 8 to 16 hours of discomfort, at which point IV therapy is less effective. In these circumstances, oral prednisone, 1 mg/kg per day for 3 to 4 days followed by a slow taper over 2 to 3 weeks, helps many patients, but the danger lies in a sudden flare-up, which becomes poorly responsive to steroids, at the end of therapy. This more often happens with rapid prednisone tapers. Whenever considering systemic corticosteroids for acute allergic contact dermatitis, the physician should evaluate the patient for active infection, vascular accident, endocrinopathy, or familial history of glaucoma. Side effects from oral corticosteroids include hypertension, increased risk for infection, adrenal insufficiency, glaucoma, cataracts, increased blood glucose, mood changes, osteoporosis, osteonecrosis, edema, weight gain, hypokalemia, peptic ulcer disease, bowel perforation, myopathy, Cushing’s syndrome, adrenal suppression, and stunted growth in adolescents. If dermatitis has been present for more than 24 hours, which is typically the case in clinical practice, the aggressive regimen is less successful. When the onset of dermatitis is delayed for several days and the eruption is mild or moderate, systemic therapy offers less benefit. In the situation of a mildly to moderately sensitive patient with delayed onset, topical corticosteroids are the mainstay of therapy. Typically, an ultrapotent topical steroid, such as clobetasol (Temovate), is used twice daily for no more than 14 days. Table 63-10 lists the most common topical corticosteroids and their classification. Prolonged use of ultrapotent corticosteroids may lead to skin atrophy. The face, axillae, and groin are highly susceptible to atrophy, so use of ultrapotent

TABLE 63-10  Steroid Classification Generic Name Ultrapotent Betamethasone dipropionate Clobetasol propionate Diflorasone diacetate

Trade Name

Preparations Available

Diprolene

0.05% cream ointment 0.05% cream ointment 0.05% cream ointment 0.05% cream ointment

Temovate, Cormax Psorcon

Halobetasol propionate High Potency Amcinonide Desoximetasone

Ultravate

Fluocinonide

Lidex

Halcinonide Medium Potency Betamethasone valerate Fluocinolone acetonide Fluticasone propionate Hydrocortisone butyrate Hydrocortisone valerate Triamcinolone acetonide Low Potency Alclometasone dipropionate Clocortolone pivalate Desonide

Halog

Hydrocortisone acetate

Cyclocort Topicort

Luxiq

or or or or

0.1% cream or ointment 0.25% cream or ointment 0.05% cream or ointment 0.1% cream or ointment

Locoid

0.1% cream or ointment, 0.12% foam 0.025% cream or ointment 0.005% ointment or 0.05% cream 0.1% cream

Westcort

0.2% cream or ointment

Aristocort, Kenalog

0.1% cream or ointment

Aclovate

0.05% cream or ointment 0.1% cream 0.05% cream or ointment 0.5% cream or ointment

Synalar Cutivate

Cloderm DesOwen, Tridesilon Cortaid, Corticaine

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CHAPTER 63  Plant-Induced Dermatitis

peptides that have undergone chemical degradation associate with class II major histocompatibility complex (MHC) molecules and are expressed on the surface of the APCs. The APCs then leave the epidermis and travel to regional lymph nodes, where they present processed antigen on the cell surface in context with a class I MHC molecule to the T-cell receptor complex on a CD8+ T cell, or in context with the class II MHC molecule to the T-cell receptor complex on a CD4+ T cell. Presence or absence of an urushiol-specific T-cell receptor is genetically determined. During early fetal development, the thymus interacts with various T cells. Through gene rearrangements, thousands of unique T-cell receptors are produced that recognize unique antigens. If no T cell is present that recognizes the antigen complex on the APC, no reaction occurs, and the patient does not develop allergic contact dermatitis. To complete the sensitization signal, another surface protein (the B7 antigen) forms a co-stimulatory signal by binding to the CD28 ligand on the T cell. This then activates the T cell, which divides repeatedly to form a clone of urushiol-specific CD8+ and CD4+ cells. These subsequently expand into clones of circulating activated T-effector and T-memory lymphocytes.62,77 In the elicitation phase, upon a new challenge by urushiol, the hapten enters the epidermis and again is internalized by Langerhans cells. It is processed and expressed by the MHC molecules, which then interact with the clone of T cells now specifically ready to interact with this MHC–antigen complex. This leads to the appearance of allergic contact dermatitis, typically within 24 to 72 hours of exposure. Langerhans cells in the skin that interact with T cells secrete IL-1, which stimulates the T cells to secrete IL-2 and express IL-2 receptors, which directly leads to activation, proliferation, and expansion of the T-cell clone. Activated T cells will also secrete IFN-γ, which acts on keratinocytes to express ICAM-1, which allows them to directly interact with T cells.79 Keratinocytes also secrete many cytokines that cause expansion and proliferation of these T cells. The CD8 lymphocytes elicit a cell-mediated cytotoxic immune response at the site of contact characterized by erythema, edema, and vesiculation resulting from destruction of epidermal cells and activation of the dermal vasculature. The clinical reaction is driven by the CD8 cytotoxic, effector T cells. This can be modified by CD4 T cells that may be either TH1 or, more likely, TH2 in nature.62,77 In an individual patient, this determines the severity of dermatitis after exposure to the poisonous weeds. In addition, alternate pathways exist that account for the varying presentations of ACD. An acute eruption can begin within hours of initial exposure. Some have emphasized the presence of basophils in these hyperacute poison oak and poison ivy lesions and have proposed a role for basophil mediators in the pathogenesis of an early-onset acute reaction.37 Others have proposed alternate hyperacute mechanisms involving mast cell degranulation, or a CD4 T-cell– mediated induction of IgE reactivity.61,63 Suppressor pathways to decrease the extent of the above pathways also exist. These mechanisms are poorly understood, but include a number of specific pathways, including elimination of primed dendritic cells by effector CD8 T cells, release of antiinflammatory cytokines, and activation of suppressor T cells.121 These responses are generated to counterbalance or downregulate the type IV hypersensitivity reaction. It is the exposure to antigen through noncutaneous routes that leads to these suppressor pathways or, if there is a massive exposure, to antigen at the sensitization phase.79 The final resulting skin reaction is a balance of sensitization and suppression of these antigenspecific reactions.

PART 7  PLANTS

products should be avoided in these regions. In most mild cases of dermatitis, a medium- to high-potency topical steroid and 15to 30-minute cool compresses three or four times a day with a 1 : 40 dilution of aluminum acetate (Domeboro, Burow’s solution) will suffice. A bath with 1 cup of Aveeno oatmeal per tub of water, in addition to therapy with antihistamines such as hydroxyzine or diphenhydramine, is helpful for the itching. Treatment is usually required for 1 to 2 weeks. In more severe cases with the eyelids, hands, or more than 10% body surface area involvement, a systemic corticosteroid, such as prednisone in a tapering dose starting at 1 mg/kg or triamcinolone (Kenalog) 40 mg IM, is employed, tapering slowly over a course of 2 to 3 weeks to avoid rebound. Antihistamines, such as hydroxyzine, 10 mg given orally four times daily (up to 100 mg per day) or diphenhydramine, 25 mg orally two or three times per day, can be used to suppress itching. Calamine lotion and aluminum acetate compresses also help with the itching. New topical immunomodulators—pimecrolimus (Elidel) 1% cream and tacrolimus (Protopic) 0.03% or 0.1% ointment—offer a noncorticosteroid treatment alternative. There is no risk for atrophy with these two agents. Preliminary studies show them to be helpful in alleviating allergic and irritant contact dermatitides, but expense is often a limiting factor.5,6 Most patients visit a pharmacy looking for over-the-counter (OTC) preparations; usually, they are disappointed. The eruption heals spontaneously in 7 to 10 days, so the most helpful option is an inexpensive agent, such as calamine lotion, which is comforting and helps form a crust. Aluminum acetate (Domeboro, Burow’s solution) 1 : 40 diluted in plain water used as a soak, compress, or wet dressing is helpful, as is a 1% acetic acid wet dressing (white vinegar) in water. The soaks are performed for 15 to 30 minutes at a time and can be repeated as often as necessary. Regardless of the therapy chosen, time is required for healing. Although field workers have mentioned that Aloe vera latex empirically improves wound healing, a major study in contact dermatitis showed that it was ineffective.129 Topical lotions with anesthetics or antihistamines offer no additional benefit and may induce contact sensitization to the chemical additives. Allergic contact dermatitis is a self-healing disease if iatrogenic influences are avoided. Secondary superficial infections may occur in children, during hospitalization, or in cases with prolonged pruritus and scratching. Use of antibacterial soaps usually prevents this complication. As the dermatitis heals and scales form after 10 to 14 days, the patient may note a resurgence of pruritus, which left untreated can lead to subacute lichenoid neurodermatitis (Figure 63-22). Judicious use of almost any steroid cream or ointment, such as triamcinolone acetonide 0.025%, desonide 0.025%, or hydrocortisone 2.5%, helps alleviate symptoms.

PREVENTION Prevention involves a combination of avoidance and destruction of plants. This can be done directly, by educating individuals at risk to recognize and avoid these plants, or indirectly, by wearing protective clothing and gloves when coming into contact with them. Rubber gloves that are the thickness of surgical gloves are inadequate protection because urushiol is able to penetrate through rubber. Vinyl gloves are more protective, as are other plastic gloves. Leather gloves are acceptable. Many herbicides are available to kill the plants. Unfortunately, none is specific to Toxicodendron species. Proper cleaning of clothing is essential. Washing immediately with soap (detergent) and water has been shown to destroy urushiol. A lotion containing the organoclay quaternium-18 bentonite is very effective in preventing this type of dermatitis. If applied before contact with the urushiol resin, it has been proven to decrease poison ivy, oak, and sumac dermatitis by inactivating the resin.80 The best approaches to prophylaxis, based on an intimate understanding of the chemistry of urushiol and the biology of the weeds, are recognition and avoidance.43 When this is not possible, protective clothing that is either disposable or washable should be worn. Wool is the best material to use as a protective 1244

FIGURE 63-22  Resurgence of pruritus, leading to patch of subchronic lichenoid neurodermatitis.

barrier because it binds the allergen readily.31 Clothing should be washed with detergent or, preferably, bleach to inactivate urushiol. Tools and other inanimate objects are best cleaned with a dilute solution of bleach. Bleach rapidly inactivates urushiol, and organic solvents such as alcohol, gasoline, and acetone can extract it from contaminated surfaces. For cleansing the skin after contact, a variety of products are available, some more useful than others. A commercially available solvent is Tecnu, sold over the counter, but this is merely an inexpensive petroleum solvent sold at a high price and should not be used for therapy. An excellent choice is rubbing (isopropyl) alcohol, which should be applied liberally for decontamination and followed by liberal use of water wash-off to avoid spreading the oil on the skin. Care should be taken to limit contact time with the skin, particularly with children, who may be susceptible to transcutaneous alcohol toxicity. Use of soap is inferior to better solvents. The newer topical agent Zanfel has been shown to experimentally decrease urushiolinduced contact dermatitis. It is a mixture of alcohol solubles and anionic surfactants that binds to the urushiol antigen and renders it unable to induce an allergic reaction. If applied soon enough after exposure, it has the potential to decrease urushiol-induced allergic contact dermatitis.34 The idea of using barrier preparations has become popular again, even though in the past, such creams and ointments proved disappointing.92 The current favorite, an organoclay called Ivy-Block, was developed to protect forestry workers against these weeds during national firefighting escapades.44 This approach was confirmed in a multicenter study.80 The lotion can be obtained readily from a pharmacist or by major marketers. Oak-N-Ivy-Armor is a product marketed to be used as a preventative lotion. It actively binds urushiol and keeps it from contacting the skin. Similar topical preventive products include Buji Block and Ongard. Stokogard outdoor cream, composed of a linoleic ester dimer, was removed from the market for lack of U.S. Food and Drug Administration (FDA) approval but is still available in industrial supply houses that are not regulated.93 When the cream is first applied, it has a foul smell (like dead fish), resulting from release of the ester. The odor disappears in about 20 minutes, and the cream acts like a barrier to delay the penetration of urushiol oil. It must be washed off in 4 to 6 hours for protection.

• Artichoke • Black-eyed Susan • Butterweed • Chamomile • Chicory • Chrysanthemum • Cornflower • Daisy • Dahlia • Dandelion • Endive • Feverfew • Goldenrod • Ironweed • Lettuce

• Marigold • Mugwort • Pyrethrum • Ragweed • Ragwort • Sagebrush • Sneezeweed • Stinking mayweed • Sunflower • Tansy • Tarragon • Thistle • Yarrow • Zinnia

patch-testing the patient to various portions of the actual leaf, stem, and petal against appropriate controls. A screening mixture of sesquiterpene lactones is available, but this mixture will miss some relevant allergies to Compositae plants. It is prudent to patch-test the patient with the actual plant that is suspected of causing the allergic reaction. Ragweed (Ambrosia species) is a member of the Compositae family of plants; hence its allergen is a sesquiterpene lactone. Figure 63-24 shows a photo of common ragweed. Ragweed pollen likely contains two individual antigens, one that can cause respiratory ailments, such as asthma or allergic rhinitis, and another that contains sesquiterpene lactones and causes allergic contact dermatitis. Clinically, patients show involvement of the head and neck region and other areas not covered with clothing. The dermatitis is chronic in nature and tends to mimic photocontact dermatitis. In this case, the upper eyelid and submental regions may be involved, which is not the case in photocontact dermatitis. Ambrosia deltoidea is a weed in the Compositae

Data from Marks JG Jr, Elsner P, DeLeo VA: Contact and occupational dermatology, ed 3, St Louis, 2002, Mosby, pp 13-15.

COMPOSITAE FAMILY There are more than 20,000 species of plants in the Compositae family. A brief list of some of the more commonly recognized members appears in Box 63-2. A few highly recognizable members are pictured in Figure 63-23. Compositae species have worldwide distribution. The allergens found in these plants are sesquiterpene lactones. More than 3000 individual sesquiterpene lactones have been identified.32,52 The lactones are made in the trichomes found on the plant’s surface. The allergen is not highly sensitizing; thus individuals typically afflicted have repeated contact with the allergen and are usually involved in daily handling of plants. These people include florists, nursery workers, horticulturists, and produce handlers. Rarely, home gardeners or people who spend a great deal of time outdoors are afflicted. The dermatitis is fairly characteristic across the Compositae family. The clinical scenario is often a chronic lichenified eruption resembling photodermatitis.79 Clues that this is not photodermatitis include involvement of the upper eyelids and the submental region of the neck, areas that are classically spared in true photodermatitis. Definitive diagnosis can be made by

A

B

FIGURE 63-24  Ragweed, Ambrosia species.

C

FIGURE 63-23  Compositae members. A, Dahlia. B, Chrysanthemum. C, Daisy. (C courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)

1245

CHAPTER 63  Plant-Induced Dermatitis

BOX 63-2  Familiar Compositae Species

PART 7  PLANTS

family found in the southwestern United States that has also been reported to cause airborne allergic contact dermatitis. This plant bears little resemblance to the common ragweed.105 Wild feverfew (Parthenium hysterophorus) is a weed in the Compositae family found throughout the Western hemisphere. It is an acute cause of allergic contact dermatitis, although in clinical practice, it most often manifests as chronic lichenified dermatitis in areas chronically exposed to the allergen. It caused epidemic outbreaks of dermatitis in India after it was accidentally transplanted there. It is not a native plant to India and has thrived in its new environment. The epidemics have become so severe that it has been nicknamed the “scourge of India.”79 Peruvian lily (Alstroemeria species) (Figure 63-25) is a very popular cut flower. Its allergen is tuliposide A or α-methyleneγ-butyrolactone. Allergic contact dermatitis to this plant is the most common cause of allergic contact dermatitis in florists. Florists who repeatedly cut the flowers and stems are chronically exposed to the allergen. Subsequently, they have the highest sensitization rate. It is a very rare cause of allergic contact dermatitis in individuals outside of the floral industry. Liverworts (Frullania species) are members of the Jubulaceae family (related to mosses) that commonly live on tree bark. They are small reddish-brown plants found most often in the Pacific Northwest. There are hundreds of species of Frullania plants. Similar to members of the Compositae family, this plant causes chronic lichenified dermatitis that is rarely seen in the acute phase. The allergen is sesquiterpene lactone. Allergic contact dermatitis due to Frullania is a problem among lumberjacks and forest workers, but it may affect any individual who takes a walk in the woods.79 Grevillea banksii and G. robusta have been implicated as causing allergic contact dermatitis. These plants are native to Australia but have been transplanted around the globe. They grow as shrubs and are used in domestic landscaping. The allergen is a resorcinol. Similarly, Dittrichia graveolens (stinkwort) is a weed native to the Mediterranean but has become naturalized initially in Australia and now in the United States and has recently been reported as a cause of allergic contact dermatitis in outdoor workers.117 Allergic contact dermatitis to lichens is seen most often in forestry workers and gardeners. Lichens live worldwide and grow just about anywhere (Figure 63-26). They are composed of algae and fungi that live in a symbiotic relationship. The allergens are usnic acid, atranorin, and evernic acid.79 The clinical picture is very similar to Compositae dermatitis.118 The false heliotrope plant (Phacelia crenulata) is found in the deserts of the southwestern United States. It causes acute allergic contact dermatitis in the direct areas of contact. A linear

FIGURE 63-26  Close-up view of lichen. (Courtesy Peter Schalock, Massachusetts General Hospital, Boston, Mass.)

papulovesicular reaction, not unlike the reaction to Toxicodendron, is usually seen. Two common, easily recognized plants that can cause allergic contact dermatitis are the tulip and primrose. The tulip (Tulipia species) is an early spring flowering plant (Figure 63-27). Its allergen is tuliposide A. Tuliposide A is the same allergen found in Alstroemeria (Peruvian lily, discussed earlier). The allergen has its highest concentration in the epidermis of the bulb, from which originate the clinical findings of “tulip fingers,” a chronic fissured and scaly eczematous rash of the fingertips in people who routinely handle the bulbs (Figure 63-28).56 This is most common in commercial gardeners; occasionally, an avid home gardener is affected. People who are allergic to tulips should avoid Alstroemeria. Primrose (Primula obconica) is a common houseplant reported to cause allergic contact dermatitis in home gardeners

FIGURE 63-27  Tulip, Tulipia species.

FIGURE 63-25  A familiar cut flower, Peruvian lily (Alstroemeria species).

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FIGURE 63-28  Eczematous scaly patches on the fingers of a floral worker.

Fruits • Apple • Carrot • Celery • Parsley • Potato • Tomato Plants • Tulip

Trees • Birch pollen • Western red cedar Vegetables • Chives • Grains • Lettuce • Onion

Spices • Cinnamon • Garlic • Mustard • Rapeseed FIGURE 63-29  Primrose, a common houseplant.

(Figure 63-29). Its allergen is primin (2-methoxy-6-pentyl-1,4benzoquinone). The allergen is found in the highest concentration in the trichomes of the stem and leaves. A genetically altered hybrid has been produced that does not make primin and thus has no potential to induce allergic contact dermatitis. This hybrid is likely responsible for the decrease noted in the incidence of primin-induced allergic contact dermatitis.27 The creosote bush (Larrea species) is found throughout North and South America (Figure 63-30). It is a shrubby bush with leaves covered by a resinous substance. There are a few reports of this resin causing allergic contact dermatitis.71 The Hydrophyllaceae family of plants contains a class of chemicals called phacelioids.99 These substances are related to urushiol and can be potent allergens. However, they do not cross-react with urushiol. The Cineraria hybrid has also been described as a cause of allergic contact dermatitis in the Compositae family.28 Not all cases of Compositae-induced dermatitis are allergic in nature. The glove artichoke (Cynara solumus) has been associated with an irritant vesicobullous reaction affecting the fingertips, although patch-test results have been negative.96 Some patients have even presented with erythrodermic presentations, especially from the P. hysterophorus (wild feverfew) species.2

Contact Urticaria: Immunologic and Nonimmunologic Subtypes Contact urticaria can be classified as immunologically or nonimmunologically induced. The immunologic subtype is due to an

immediate hypersensitivity reaction requiring antibody formation to a particular substance. These type I hypersensitivity reactions show a broad clinical spectrum, from mild skin hives to anaphylaxis. Prick testing and radioallergosorbent test (RAST) testing are of benefit in determining the cause in certain cases. The immunologic form of urticaria depends on the individual patient’s immune activity or hyperactivity. There is no predictable manner to determine to which plants a person may develop a type I reaction. Food handlers and persons otherwise constantly exposed to plant products are likely to be more at risk. Many plant species have been reported to cause contact immunologic urticaria.66,78 Patients typically present with urticarial wheals in the areas of exposure within 1 to 2 hours of handling a particular plant. Occasionally, there is oral involvement with tongue and lip swelling. When there is prominent oral involvement, one must also consider consumed fruit as a cause. Box 63-3 is a partial list of some plants causing contact immunologic urticaria. Atopic individuals have been reported to be at higher risk for type I contact urticaria.78 Nonimmunologic plant contact dermatitis is caused by direct release of urticating substances onto or into the skin. Four main families of plants contain stinging hairs or spines that can cause contact urticaria: Euphorbiaceae, Hydrophyllaceae, Loasaceae, and Urticaceae.78 Most of these plants are found in the tropics, with the exception of stinging nettles, which have a worldwide distribution and are found throughout the United States. Box 63-4 lists some of the more common nettle plants. The most common plant causing contact urticaria is the stinging nettle Urtica dioica (Figure 63-31). Within the Urticaceae family reside other plants capable of producing contact urticaria by means of the nonimmunologic route. Urticarial reactions are typically acute and resolve spontaneously, so the advice of a physician is rarely sought. Persistent paresthesia lasting hours has been reported.83

BOX 63-4  Plants in the Nettle Family

FIGURE 63-30  Leaves of the creosote bush are covered with a resinous substance. (Courtesy Jon Sullivan.)

• Urtica • Urtica • Urtica • Urtica • Urtica • Urtica • Urtica • Urtica

chamaedryoides dioica gracilis ferox membranacea urens pilulifera parviflora

1247

CHAPTER 63  Plant-Induced Dermatitis

BOX 63-3  Plants That Cause Immunologic Urticaria

PART 7  PLANTS FIGURE 63-31  Urtica dioica, or stinging nettle. (Courtesy Peter Schalock, Massachusetts General Hospital, Boston, Mass).

In the case of nonimmunologic urticaria, release of histamine from mast cells with vasodilation and leakage of fluid appears to be an early direct chemical change leading to clinical hives.36,107 The molecular events in mast cell degranulation are thought to be similar to those described for immunogenic urticaria, with certain discrete differences. There is no evidence for a selective membrane receptor, such as the high-affinity immunoglobulin E (IgE) receptor that is now well characterized and required for immunologic degranulation of mast cells.107,112 Instead, a receptorindependent mode of action occurs for all nonimmunologic histamine liberators, acting directly on a pertussis toxin-sensitive G protein to initiate a signal through phospholipase C activation, which degranulates mast cells of their histamine content.86 There does not seem to be a requirement for methylation of the membrane phospholipids. Rather, a high intracellular calcium accumulation must occur, and the reaction is rapidly terminated without delayed mediator release.103 Arachidonic acid metabolites are not formed in any amount.14 Figure 63-32, A and B, shows the stinging nettle plant and a close-up view of its spines. Contact with spines on the plant causes release of biologically active substances from the spines. These include histamine, acetylcholine, 5-hydroxytryptamine (serotonin), leukotriene B4 (LTB4), and leukotriene C4 (LTC4).7,26,33,38 These chemicals lead directly to urticaria. There is no standardized therapy for stinging nettle dermatitis. Often the symptoms resolve in several hours. If pruritus is severe, treatment with the antihistamine diphenhydramine 25 to 50 mg every 6 to 8 hours as needed is indicated. Figure 63-32, C, illustrates the faint urticarial papules seen after contact with the stinging nettle plant. Numerous plants have been associated with release of urticating substances, including chili pepper (Capsicum species) and cowhage (Mucuna pruriens). In the case of chili pepper, the released chemical is capsaicin; with cowhage, it is mucanain.79 The pathogenesis of immunogenic contact urticaria is a variation of immediate type I hypersensitivity. The central cytologic reactor in skin is the mast cell, which has high-affinity IgE receptors in its membrane. An IgE molecule binds to the receptor by its Fc portion, exposing the Fab segments as recognition sites for circulating proteins. When a divalent protein antigen appropriately bridges two IgE molecules, a series of biochemical events transpires that leads to mast cell degranulation. Initially, the plasma membrane is perturbed. Several lipids are phosphorylated and G proteins are activated, which in turn activate phospholipase C to hydrolyze phosphatidylinositol 4,5-bisphosphate (PIP2) and yield two messengers: diacylglycerol (DG) and inositol triphosphate (InsP3).20 InsP3 binds to its receptor on the endoplasmic reticulum, forming a calcium channel to release free calcium ions (Ca2+) into the cytosol.11,15,58,90 Simultaneously, DG activates protein kinase C in the plasma membrane, opening calcium channels and allowing entrance of extracellular Ca2+, which 1248

further loads the cytosol with free Ca2+, an important “messenger” in the stimulus secretion process.74 G proteins interact with and release the nucleotide complexed to protein α-chains, some of which probably inhibit or stimulate cyclic adenosine phosphate and its actions as a second messenger.20,115 The result of the extensive alteration in intracellular milieu is activation of a serine proteinase and exocytosis of mast cell granule contents.36,107 These come in three forms: preformed and rapidly released; preformed, bound to the granule matrix of heparin, and slowly released; and newly formed mediators. In addition, mast cells produce a variety of cytokines, including IL-1, IL-3, IL-4, IL-5, and IL-6; GM-CSF; and TNF-α.113 These cytokines interact with cells and structures, such as endothelium in the skin, to amplify the various inflammatory responses.36,107,113 In acute urticaria, the rapidly released preformed mediators account for most of the signs and symptoms. These mediators include histamine, some chemotactic factors, and arylsulfatase. If the lesions persist or extend, other mediators, such as newly formed leukotrienes, heparin (or heparin fragments), cytokines, and a number of proteases, may be involved in the continuing tissue damage. The sequence of inflammatory events leading to acute urticaria occurs most often in people with an atopic background, especially those with pollen allergies.66 The patients with significant pollen allergies are also at risk for pollen-fruit allergy syndrome, described as a mucosal contact urticaria typically seen when these patients are exposed to Betula pendula (silver birch), Artemisia vulgaris (mugwort) or timothy grass (Phleum pratense).64 Cross-reacting foods include apple, pear, carrot, celery, tomato, cherry, carrot, celery, aniseed, and peach. This group of people, mainly women and especially health care workers, have been found in recent years to be exquisitely sensitive to latex rubber gloves and sensitive to proteins in the natural latex from rubber trees in Asia.22,69,87,108,119 In the past decade, this has increasingly become a problem. There are more than 200 polypeptides produced in natural latex rubber, many of which are contact sensitizers, so that a single antigen is not likely to be identified for a given patient. In the clinical realm, IgE-mediated immediate-type hypersensitivity and thus the potential for anaphylaxis is a disastrous complication. In addition to the polypeptides appearing in natural rubber latex, many are found in a number of plants, particularly those consumed as food. One theory is that the cross-reacting allergens are “defense proteins” with a role to protect the plant from attack by pathogens.68 Whether this is true requires further investigation, but it is also possible that by plant engineering, these allergens may be genetically removed from the foods we consume. In addition to fruit and nuts, mustard has been implicated in anaphylaxis.94 In less severe cases, vesicular, eczematous rashes have been noted within hours of eating mustard or rapeseed, which is used widely in production of vegetable oils and margarine.84 Recent reports have also surfaced describing contact urticaria to raw potato, as well as the Solanaceae and Alliaceae families of plants, which include tomato, green bell pepper, jalapeño, chive, red leaf lettuce, serrano pepper, pasilla pepper, leek, red bell pepper, garlic, and yellow onion. In contrast to urticarial reactions, erythema multiforme–like eruptions are well recognized after contact with bracelets and ornamental necklaces made of exotic woods, such as Dalbergia nigra.48 Erythema multiforme has also been seen after exposure to more common plants, such as poison ivy, primula, and mugwort.48,124 Pathologically, it is theorized that multiforme lesions result from vasculitis caused by deposition of immune complexes in or around the blood vessels. Diagnosis of immunogenic contact urticaria can be confirmed by simple tests. As a useful test, application of the suspected plant product to the antecubital fossa twice a day for several days may reproduce the wheal response. Open and closed patch tests, with examination of test sites in 2 to 6 hours, can be useful, as can more conventional prick, scratch, or scratchchamber tests, in which the results are read in 15 to 20 minutes.66 It is most important to determine whether urtication is immunologic or nonimmunologic in nature, because this helps to quantify the risk for anaphylaxis.51,66 For complete evaluation, an allergist obtains radioallergosorbent tests to quantify

CHAPTER 63  Plant-Induced Dermatitis

A

B

C FIGURE 63-32  A, Stinging nettle. B, Close-up view of the stinging nettle spines. C, Urticarial papules induced after contact with the stinging nettle.

specific IgE in the patient’s serum. More refined serologic tests include crossed radioimmunoelectrophoresis (CRIE) and CRIE inhibition.23 Patients with contact urticaria typically visit the emergency department when an eruption is extensive or extreme or if it is associated with stridor, wheezing, and collapse. Because mast cell degranulation is the central problem, epinephrine is the drug of choice because it stimulates cyclic adenosine monophosphate formation that opposes further degranulation. All patients with a risk for severe urticaria should carry an epinephrine injection (EpiPen) with them at all times. Other supportive treatments for anaphylactic shock, such as albuterol, aminophylline, oxygen, or IV hydrocortisone, may be required once the patient arrives in an emergency department. In less severe cases, antihistamines are valuable. IM or IV diphenhydramine (Benadryl), in an adult dose of 25 to 50 mg, usually stops progression of wheal formation and can be followed by oral hydroxyzine (10 to 25 mg 3 times a day) or cyproheptadine (4 mg 3 times a day) for 2 to 5 days. Pure H1-blockers, such as fexofenadine (60 mg 2 times a day), are also effective and do not depress the central nervous system, although the prescriber must be aware of any unique adverse reactions. It is important to make certain the patient is not inadvertently exposed to hidden parts of the plant on the body, in clothing, or in a towel, blanket, or knapsack. Recrudescence of the urticarial response usually can be traced to con­ tinuing unknown contact with the offending agent. In patients with high risk for urticarial eruptions and airway involvement,

education regarding avoidance of the offending plant is crucial to the maintenance of a symptom-free lifestyle.

PHYTOPHOTODERMATITIS Plants and their components can interact with ultraviolet rays of the sun and produce a clinically distinct entity known as phytophotodermatitis. The two types of phytophotodermatitis are phototoxic and photoallergic. Phototoxic reactions, which appear clinically as an exaggerated sunburn, are analogous to irritant contact dermatitis; photoallergic reactions, which appear eczematous, are analogous to allergic contact dermatitis. Phototoxic reactions are encountered more frequently. They are often recognized by a clinician’s knowledge of offending agents and the morphology of the exanthem. The reactions most commonly appear as linear red patches and plaques with or without edema, but they can be bullous in nature.120 A characteristic finding is postinflammatory hyperpigmentation lasting for months to years. Most of these reactions are likely to go unreported or unrecognized, most often because of their mild nature, but also because it is often difficult to pinpoint the exact cause of the problem. Phototoxic reactions are typically dose dependent and can occur in anyone if sufficient concentrations of ultraviolet light and the toxic plant material are achieved. In general, the wavelength of light needed to induce the most severe reactions is in the ultraviolet A (UVA), 320 to 400 nm, range. 1249

PART 7  PLANTS

For most phototoxic reactions, the plant toxin is a furocoumarin (psoralen). Furocoumarins intercalate into cellular DNA and cause formation of pyrimidine dimers, which interrupt DNA synthesis. This leads to cell damage and the clinical effects. When ultraviolet light interacts with the psoralen molecule, it raises the energy level from the ground to an excited state. When the excited molecule returns to its ground state, energy is released that causes cross-linking of two strands of DNA. This interferes with DNA synthesis and ultimately cell division. This reaction is used to our advantage in treatments such as PUVA (psoralen plus ultraviolet A) light therapy and in extracorporeal photopheresis. PUVA therapies are used for conditions ranging from vitiligo and psoriasis to cutaneous T-cell lymphoma. Extracorporeal photopheresis is a treatment modality wherein a patient is connected by an IV line to a pheresis machine. Blood is first drawn from the patient. Next, leukocytes are isolated and exposed to a photoactive drug (psoralen), followed by exposure of blood to ultraviolet light (UVA). This blood is then returned to the patient. This process causes cross-linking of DNA in the pathogenic T cells and death of these cells. This treatment is used almost exclusively for cutaneous T-cell lymphoma and graft-versus-host disease.

Phytophototoxic Contact Dermatitis Furocoumarins include psoralen, 5-methoxy-psoralen (bergapten), 8-methoxy-psoralen (xanthotoxin), angelicin (isopsoralen), 5-hydroxy-psoralen (bergaptol), 8-hydroxy-psoralen (xanthotoxol), and limettin.13,120 Psoralens are modified furocoumarins. Most of these chemicals are found in four plant families: Apiaceae, Rutaceae, Moraceae, and Leguminosae. Figure 63-33 shows a few examples of these plants. Figure 63-34 shows an example of the dermatitis that can result from exposure. Note the welldemarcated angulated hyperpigmented streaks that are characteristic of the disease. Table 63-11 lists members of the families implicated in phytophototoxic contact dermatitis. Apiaceae, or Umbelliferae, is a well-recognized family that has an umbrella-like configuration to its flowers. In the United States, this family of plants is the most common cause of phytophototoxic dermatitis. The Moraceae and Leguminosae families are rare causes in the United States.114 So-called meadow dermatitis (dermatitis bullosa striata et pratensis) occurs after exposure of wet human skin to psoralencontaining plants during daylight hours.13 The most common offending plants are the yellow-flowered wild meadow parsnip and wild yellow flowered herb.101 Bizarre linear configurations, such as an imprint, are often found on the lower extremities on bare skin after a walk through a field of a psoralen-containing weed. Agriculture field workers and grocery store workers, in particular celery handlers, have been the most frequently reported

A

FIGURE 63-34  Phototoxic dermatitis induced by furocoumarins. (Courtesy Richard A. Johnson, Massachusetts General Hospital, Boston, Mass.)

occupations to have problems with phytophototoxic dermatitis. Another occupation that has reports of phytophototoxic dermatitis is bartending. Lime handling while mixing drinks, if combined with ultraviolet light, may cause this dermatitis.* Berloque (pendant- or drop-like) dermatitis is perfumeinduced phytophotodermatitis. Typically, a patient seeks care for hyperpigmented macules on the head and neck, with no obvious preexisting rash or dermatitis. Unfortunately, the hyperpigmentation can last for years. The original cause of this reaction was the oil of bergamot, which is derived from bergamot oranges and

*References 4, 30, 48, 55, 110, 122.

B

FIGURE 63-33  Phototoxic plants. A, Fig tree. B, Gas plant. (B courtesy Yves Sell, Institute of Botany, Louis Pasteur University, Strasbourg, France.)

1250

TABLE 63-11  Common Members of the

Umbelliferae, Rutaceae, Moraceae, and Leguminosae Families Found to Cause Phototoxic Contact Dermatitis

Common Name Umbelliferae (Apiaceae) Angelica Celery Carrot Cow parsley Cow parsnip Dill False bishop’s weed Fennel Giant hogweed Parsley Parsnip Queen Anne’s lace Spring parsley Moraceae Fig Rutaceae Bergamot lime Berry rue Common rue Gas plant (burning bush) Grapefruit Lemon Lime Mexican lime Mokihana Orange Zabon Leguminosae Babchi (scurf-pea) Citrina

Botanical Name Angelica gigas Apium graveolens dulce Daucus carota Heracleum sphondylium Heracleum lanatum Anethum graveolus Ammi majus Foenialum vulgare Heracleum mantegazzianium Petroselinum crispum Pastinaca sativa Ammi majus Cymopterus watsonii Ficus carica Citrus bergamia Cneoridium dumosum Ruta graveolens Dictamnus albus Citrus paradissi Citrus limon Citrus aurantifolia Citrus aurantifolia Pelea anisata Citrus sinensis Citrus maxima Psoralea corylifolia Coronilla glauca

Data from references 17, 19, 54, 57, 70, and 109.

used in many perfumes. The oil contains a mixture of psoralens, including 5-methoxy-psoralen (5-MOP). Pseudophytophotodermatitis is a reaction that has been reported to occur after prolonged human exposure to celery that has been infected with a psoralen-producing fungus (Sclerotinia sclerotiorum), more commonly known as “pink rot.” This occurs primarily in field workers who are responsible for harvesting the plants.114 Pseudophytodermatitis has been used to describe dermatitis caused by arthropods that live on the plant or chemical agents that have been applied to the plants.114 One common arthropod causing dermatitis is the grain itch mite Pediculoides ventricosus, which can infest straw or hay. Numerous chemicals that are purposefully applied to plants can also cause contact dermatitis.

BOX 63-5  Some Insecticides, Fungicides, and

Herbicides That Cause Irritant Dermatitis (Pseudophytodermatitis)

• Captan • Captofol • Difoltan • Dithiocarbamates • Folpet • Mancozeb (manganese and zinc ethylene-bis-dithiocarbamate) • Maneb (manganese ethylene-bis-dithiocarbamate) • Organophosphates • Paraquat • Phtahan • Randox • Sulfur Data from Craigmill AL, editor: Environmental Toxicology Newsletter, University of California, Davis, 3:1, 1982; and Mark K, Brancaccio RR, Soter NA, et al: Allergic contact and photoallergic contact dermatitis to plants and pesticide allergens, Arch Dermatol 135:67, 1999.

Most commonly these are insecticides, herbicides, or fungicides (Box 63-5). Waxes or azo dyes applied to various fruits and vegetables can also cause pseudophytodermatitis. Azo dyes are synthetic dyes containing the azo group (two connected nitrogen atoms) and are used in many industries, including the food industry.

Phytophotoallergic Contact Dermatitis The phytophotoallergic reaction is exceedingly rare. Clinically, it manifests as an eczematous eruption localized to sun-exposed areas of the body that came into contact with the offending plant. It is likely underrecognized and underreported. Rare case reports are found throughout the literature. The plants reported to cause this reaction are tromso palm (Heracleum laciniatum), feverfew (Parthenium hysterophorus), garlic (Allium sativum), Frullania, and some coumarin (psoralen)–containing plants.* The clinical importance of these reactions is unknown. In the future, better screening methods may increase recognition of these reactions. Until then, only clinicians with access to extended patch-testing series and/or with sufficient suspicion and knowledge will recognize these reactions. *References 3, 16, 21, 60, 76, 78.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 64 

Toxic Plant Ingestions KIMBERLIE A. GRAEME

Over 63,000 plant exposures were reported to 61 American poison control centers in 2008, representing 2.5% of all human toxic exposures reported that year. The most frequently reported exposures were peace lily, pokeweed, philodendron, poison ivy and poinsettia. One death due to plant poisoning, out of 1756

deaths due to poisoning, was reported.34 A review of plant poisonings reported to American poison control centers over an 18-year period (1983 to 2000) revealed 30 fatalities, with seven due to Cicuta species (water hemlock) and five due to Datura species (jimsonweed).152 Most plant exposures are unintentional

For online only figures, please go to www.expertconsult.com

1251

PART 7  PLANTS

and occur in children under the age of 6 years.168 Intentional ingestions are more common in adults, due to suicidal intent or abuse, and are more likely to produce serious poisonings.34,168 Worldwide, Atropa belladonna (deadly nightshade), Hyoscyamus niger (black henbane), Conium maculatum (poison hemlock), Areca catechu (betel nut), Thevetia peruviana (yellow oleander), Nerium oleander (common oleander), Cerbera manghas (sea mango), Veratrum album (hellebore), Aconitum carmichaeli (aconite), Taxus spp. (yew), Colchicum autumnale (autumn crocus), Gloriosa superba (glory lily), Ricinus communis (castor bean), Atractylis gummifera (bird-lime or blue thistle), and Blighia sapida (ackee fruit) also cause significant morbidity and mortality.*

General Considerations Prompt and precise identification of the plant causing toxicity may not be feasible.34 Supportive care takes priority over plant identification. Airway, breathing, and circulation are assessed, including hydration status, end-organ perfusion, and urine output. Oral administration of activated charcoal (1g/kg), up to 50 g, may aid gastrointestinal (GI) decontamination; however, recommendations on when to administer activated charcoal are challenging, because this has not been prospectively studied for most plant ingestions. If a patient is actively vomiting, activated charcoal may or may not contribute to decontamination. If the patient has a depressed mental status or is likely to seize, administration of activated charcoal may result in pulmonary aspiration of charcoal. Opinions on when to administer activated charcoal vary between toxicologists. After emergency care has been provided, a history should include time of ingestion, amount and part of plants ingested, initial symptoms, and time between ingestion and onset of symptoms. Method of preparation (e.g., drying, cooking, boiling) and number of persons who ate the same plant are also important considerations. Plant identification may be aided by communication with poison control center personnel and by Internet searches.12,273,274 Laboratory studies depend on clinical presentation and suspected plant exposure. Complications of poisoning include aspiration pneumonia, rhabdomyolysis, and deep vein thrombosis. Differential diagnosis is initially kept broad so that other illnesses, such as infection and trauma, are not missed. Table 64-1 provides signs and symptoms of toxic plant ingestions.

Plant Toxins The discussion of plant toxins in this chapter is for the most part arranged on the basis of the organ systems primarily affected: central nervous, cardiovascular, GI, renal, endocrine/metabolic, hematopoietic, and/or reproductive system. Some plants contain toxins that injure many organ systems. Mention is also made of the chemical group to which the plants belong based on chemical structure. Most fall into one of the following categories: alkaloids, glycosides, resins, oxalates, or phytotoxins. Alkaloids.  Alkaloids are nitrogen-containing organic compounds that act as bases and form salts with acids. Plant alkaloids are soluble organic acid–alkaloid salts that contain nitrogen in a ring structure that is heterocyclic or aromatic, or both. Alkaloids are generally distributed throughout a given plant, so all ingested parts are toxic. Further subdivision into chemical groups is based on ring structure (Table 64-2).

Resins.  Resins are highly toxic compounds of diverse chemical and plant origin united by the physical characteristics of insolubility in water, absence of nitrogen, and solid or semisolid state on extraction at room temperature. Resins are usually mixed with other compounds, such as volatile or essential oils (oleoresins), gum (gum resins), and sugars (glycoresins). Oxalates.  Oxalates occur naturally in plants as soluble (sodium or potassium) or insoluble (calcium) oxalates or acid oxalates. Oxalates have corrosive effects and bind serum calcium, causing hypocalcemia. Phytotoxins.  Phytotoxins, or toxalbumins, are among the most toxic substances of plant origin. They are composed of large protein molecules that resemble bacterial toxins in structure and in their ability to act as antigens (Figure 64-2, online).

Central Nervous System Toxins ANTICHOLINERGIC PLANTS (TROPANE ALKALOIDS) Plants containing tropane alkaloids (often called belladonna alkaloids) include atropine, hyoscyamine (the levorotatory isomer of atropine), and hyoscine (scopolamine).* Structures of the tropane alkaloids follow: R

H C

CH

CH2 CH3

CH2

CH2 CH3 CH2

N

N O

Tropane

Scopolamine

R

R

CH CH2 CH3

HOOC CH2

CH CH2 CH3 CH2

N

N

Atropine

Cocaine

Tropane alkaloids are found in about 25 genera and 2000 species of plants. Plants causing human toxicity include A. belladonna (deadly nightshade), Mandragora species (mandrake), H. niger (black henbane), Datura species (jimsonweed), and Brugmansia species (angel’s trumpet).† The Solanaceae family includes Solanum and Scopolia carniolica, the source of scopolamine.

Glycosides.  Sugars in the form of acetals are called glycosides. In glycosides, a glycosyl group replaces an alcohol or a hydroxyl group. On hydrolysis, glycosides yield sugars (glycones) and aglycone compounds. The aglycone moiety accounts for most of the toxicity, although the sugar may enhance solubility and absorption (Figure 64-1, online). Glycoside-producing plants include cardioactive, cyanogenic, saponin, anthraquinone, and coumarin glycoside compounds.

Anticholinergic Syndrome.  Toxicity may ensue after ingesting or smoking plant parts.45 The tropane alkaloids competitively inhibit postsynaptic muscarinic receptors, producing the classic anticholinergic syndrome (Figure 64-3 and Box 64-1).104,113,203,209,230 A useful clinical sign of anticholinergic toxicity is lack of perspiration in the axillae. Anticholinergic findings suggestive of poisoning may be remembered using the following mnemonic:209,240 Hot as a hare (or hot as Hades), Blind as a bat, Dry as a bone, Red as a beet, Mad as a hatter.

*References 84, 90, 93, 120, 168, 173, 268, 280.

*References 37, 89, 138, 140, 173, 179, 230, 255. † References 37, 113, 138, 140, 173, 179, 203, 209, 230, 242.

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System Involved Central nervous

†

Syndrome

Common Name

Genus

Signs and Symptoms

Anticholinergic*

Jimsonweed Angel’s trumpet Deadly nightshade Black henbane Mandrake Tobacco Poison hemlock Betel nut Blue cohosh Golden chain tree Kentucky coffee tree Mescal bean bush Morning glory Nutmeg Marijuana Peyote Ibogaine Khat Poppy Yellow jessamine Strychnine Water hemlock Wild wisteria Myrtle-leaved coriaria

Datura Brugmansia Atropa Hyoscyamus Mandrogora Nicotiana Conium Areca Caulophyllum Laburnum Gymnocladus Sophora Ipomoea Myristica Cannabis Lophophora Tabernanthe iboga Cathus Papaver Gelsemium Strychnos Cicuta Securidacea Coriaria

See Box 64-1

Foxglove Common oleander Yellow oleander Squill Sea mango Lily of the valley Ouabain King’s crown Monkshood Hellebore Death camas Rhododendron Azaleas

Digitalis Nerium Thevetia Urginea Cerbera Convallaria Strophanthus Calotropis Aconitum Veratrum Zigadenus Rhododendron Rhododendron

Na+ and Ca+ transport inhibitors

Yew

Taxus

Oral irritants

Philodendron Dumb cane Peace lily Elephant’s ear Giant elephant’s ear

Philodendron Dieffenbachia Spathiphyllum Colocasia Alocasia

Gastrointestinal irritants

Chinaberry tree Nightshade Pokeweed¶

Melia Solanum Phytolacca

Protein synthesis inhibitors

Castor bean Rosary pea Purging nut Black locust Groundsel Gordolobo Tansy ragwort Comfrey Mate Rattlebox

Ricinus Abrus Jatropha Robinia Senecio Senecio Senecio Symphytum Ilex Crotalaria

Oxalates

Rhubarb Sorrel

Rheum Rumex

Other

Aloe Birthwart Djenkol bean Oduvan

Aloe Aristolochia Pithecolobium Cleistanthus

Nicotinic*

Hallucinogenic*

Sedating† Paralyzing‡ Epileptogenic*§

Cardiovascular†

Na+,K+ ATPase inhibitors

Sodium channel openers‡

Oral and gastrointestinal||

Hepatotoxins

Renal

See Box 64-2

Hallucinations

Sedation Weakness Twitching Seizures Hyperreflexia GI distress Altered mental status GI distress Visual changes Altered mental status Dysrhythmias Hypotension Hyperkalemia GI distress Visual disturbances Paresthesias Altered mental status Weakness/paralysis Dysrhythmias Hypotension GI distress Altered mental status Dysrhythmias Widening of QRS Hypotension Hypersalivation Oropharyngeal edema Vesicles Dysphagia Aphonia Airway compromise GI distress Neurologic symptoms Vomiting Foamy diarrhea Dehydration Altered mental status Plasmablasts GI distress Dehydration Elevated liver enzymes Multiorgan failure Venoocclusive disease Hepatomegaly Jaundice

Hypocalemia Tetany Renal failure Renal insufficiency Renal failure

Continued

CHAPTER 64  Toxic Plant Ingestions

TABLE 64-1  Effects of Toxic Plants on Organ Systems

PART 7  PLANTS

TABLE 64-1  Effects of Toxic Plants on Organ Systems—cont’d System Involved

Syndrome

Common Name

Genus

Signs and Symptoms

Hematopoietic

Anticoagulating

Yellow sweet clover Tonka bean Woodruff Autumn crocus Christmas bells Glory lily Podophyllum Fava bean

Melilotus Coumarouna Galium Colchicum Sandersonia Gloriosa Podophyllum Vicia

Bleeding

Ackee fruit Wild yams Cocklebur Bird-lime Ox-eye daisy Licorice

Blighia Dioscorea Xanthium Atractylis Callilepis Glycyrrhiza

Apple seed Cherry pits Peach pits Plum pits Apricot pits

Malus Prunus Prunus Prunus Prunus

Bone marrow inhibitors

Hemolytic

Endocrine and metabolic

Hypoglycemia inducers§

Mineralocorticoid inducers

Cyanogenic

GI distress Dehydration Pancytopenia Weakness Hemolysis Hemoglobinuria Anemia Jaundice Vomiting Seizures Hypoglycemia Metabolic acidosis Liver disease Hypertension Edema Weakness Rhabdomyolysis Hypokalemia GI distress Bitter almond breath Agitation/seizures Coma Metabolic acidosis Dysrhythmias

*Anticholinergic and nicotinic plants can be hallucinogenic and epileptiogenic. † Many plants that affect the central nervous system and cardiovascular system can result in sedation and seizures. ‡ Cardiovascular agents that open sodium channels may also produce weakness or paralysis. § Hypoglycemic agents are also epileptogenic. || The majority of toxic plants cause some GI distress. ¶ Also a hematopoietic poison.

Jimsonweed.  Datura species are generally known as jimsonweed or thorn apple, and Brugmansia species are generally known as angel’s trumpet (Figure 64-4).112,113,263 Young, thin, and tender stems of jimsonweed contain the highest concentration of tropane alkaloids.179 However, the seeds also contain high concentrations

BOX 64-1  Anticholinergic Syndrome Central • CNS excitation • Agitation • Hallucinations • Lethargy • Coma • Respiratory depression • Mumbling speech • Muteness • Undressing behavior • Repetitive picking behavior Peripheral • Tachycardia • Mydriasis • Blurred vision • Inability to accommodate (visually) • Flushed skin • Hyperthermia • Absent bowel sounds • Urinary retention • Dry mucous membranes

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of the alkaloids, and as little as one-half a teaspoonful of seeds may cause death from cardiopulmonary arrest. The word jimsonweed is thought to be derived from Jamestown, Virginia, where British troops reportedly behaved bizarrely after consuming Datura in 1676. D. stramonium has been reportedly used in Haitian zombification rituals.45,67,112,113 Jimsonweed has been used to treat asthma, heralding the current use of ipratropium bromide. Reports of abuse of Datura and Brugmansia as hallucinogens continue to be reported in the United States and Europe.45,113,217,255 Clusters of poisonings among adolescents are typical.* Frequently, a tea of the plant parts is brewed.138 Report of toxicity after using a homemade Datura toothpaste has also been reported.205 A mass poisoning occurred in Botswana after consumption of porridge made from sorghum flour contaminated with seeds of D. stramonium.197 Symptoms may appear within minutes and may last for days.68,203,255 Tachycardia, dry mouth, agitation, nausea, vomiting, incoherence, disorientation, auditory and visual hallucinations, mydriasis, decreased bowel sounds, slurred speech, hyperthermia, flushed skin, urinary retention, and hypertension have been reported.† Blurred vision and photophobia may be secondary to mydriasis. Isolated mydriasis and cycloplegia may be seen, including anisocoria, after topical contact to the eyes.123,130,263 With severe toxicity, seizures, flaccid paralysis, and coma may ensue. Focal neurologic signs and posturing, as well as death, have also been reported.‡ Death may occur as a result of behavioral changes, leading to trauma, drowning, or environmental exposure associated with hyper- or hypothermia.138 Autopsy has revealed edema of the brain and lungs with focal hemorrhages within the alveolar lumens, ischemic lesions

*References 44, 68, 112, 138, 223, 255. † References 45, 68, 138, 203, 209, 223, 255. ‡ References 89, 194, 197, 200, 203, 255.

Alkaloid Type

Alkaloid Structure

Examples

Indole

Ergonovine (ergots) Strychnine Physostigmine (calabar beans) Rauwolfia alkaloids (reserpine)

Isoquinoline

Opium alkaloids Emetine (ipecac)

Pyridine/ piperidine

Nicotine (tobacco) Arecoline (betel nut) Lobeline (Indian tobacco)

Purine

Caffeine Theobromine (cacao)

Quinoline

Cinchona alkaloids (quinidine)

Steroid

Veratrum alkaloids (false hellebore) Aconite (monkshood)

Deadly Nightshade.  Ingestion of A. belladonna is less common than Datura and Brugmansia ingestion. All parts of deadly nightshade contain tropane alkaloids, but the highest concentrations are in the ripe fruit and green leaves; each berry may contain up to 2 mg of atropine. The berries may be mistaken for bilberries (hurtleberries). A family of eight had varying acute exposures to A. belladonna after eating both raw and cooked berries in a pie. The most severely poisoned patient had anticholinergic symptoms, with hypertonia, hyperthermia, respiratory failure, and coma requiring mechanical ventilation. Urine drug screens detected only atropine and not scopolamine, the latter which is present in much smaller quantities.230,242 A review of 49 children with acute deadly nightshade intoxication found that children most commonly demonstrated meaningless speech, tachycardia, mydriasis, and flushing; lethargy and coma were seen in the more severely poisoned children.37 A patient with seasonal chronic ingestion presented with recurrent tachycardia, mydriasis, inability to concentrate, visual hallucinations, delusions, inappropriate laughter, dizziness, and headache.140 Treatment.  Treatment of anticholinergic plant exposure consists primarily of decontamination and supportive care, including airway protection, intravenous (IV) fluids, and vasopressors for hypotension resistant to IV fluids. Hyperthermia should be assessed and treated if significant. Agitation can be treated with careful administration of benzodiazepines. Haloperidol and phenothiazines should not be used because these agents may enhance toxicity. Foley catheterization or nasogastric tube

Atropine (belladonna) Hyoscyamine Hyoscine (scopolamine)

Tropane

CNS NN ACh

M

Sympathetic Diaphoresis Vasoconstriction ↑ Urethral sphincter tone Mydriasis Some diaphoresis Tachycardia Vasodilation Bronchodilation Metabolic effects: ↓ K+ ↓ PO4 ↓ pH ↑ Glucose ↑ WBC ↑ Ketones

M

ACh

α β Epi NE

NE NE

Adrenal medulla

Parasympathetic

ACh NN

ACh NN

ANS

ACh

NN

ACh

M

Miosis Lacrimation Salivation Bronchospasm Bronchorrhea Bradyarrhythmias Urination Increased GI motility

ACh NN Spinal cord

ACh

NM

Skeletal muscle

FIGURE 64-3  Nicotinic and muscarinic receptors of the central nervous system, autonomic nervous system, and peripheral skeletal muscles. Anticholinergic toxins (e.g., tropane alkaloids) antagonize muscarinic receptors, causing confusion, agitation, abnormal movements, hallucinations, and coma centrally, and mydriasis, anhidrosis, tachycardia, urinary retention, and ileus peripherally. Direct nicotinic agonists (e.g., arecoline, coniine, cytisine, lobeline, nicotine) stimulate nicotinic receptors; however, prolonged depolarization at the receptor causes eventual blockade of nicotinic receptors. ACh, Acetylcholine; ANS, Autonomic nervous system; CNS, central nervous system; Epi, epinephrine; M, muscarinic receptor; NE, norepinephrine; NM, nicotinic receptor at skeletal muscle; NN, nicotinic receptor in nervous system.

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CHAPTER 64  Toxic Plant Ingestions

and edema of the heart, and hyperemia of the sinusoidal tracts of the liver.31 Anticholinergic poisoning should be suspected when patients are observed to communicate with imaginary friends with mumbled speech, and to demonstrate repetitive picking behavior.112,242 Symptoms generally begin 30 to 60 minutes after ingestion and continue for 24 to 48 hours, but they may begin within several minutes and persist for several days. Patients are generally amnestic of events during their poisoning. Studies may show leukocytosis, mild transient elevation of liver enzymes, elevated creatine phosphokinase (CPK) levels and other evidence of rhabdomyolysis, and changes on an electrocardiogram (ECG) that are consistent with tachycardia and dysrhythmias.45,68,89,113

TABLE 64-2  Plant Alkaloids and Their Structures

PART 7  PLANTS

A

B

C

D

FIGURE 64-4  Jimsonweed (Datura species) is a bush with trumpet-like flowers (A) and thorny seedpods that contain numerous small kidneyshaped seeds (B). A nickel is shown for size comparison. Angel’s trumpet (Brugmansia species) is a tree (C) with trumpet-like flowers (D). (Courtesy Kimberlie A. Graeme, MD, and Phillip Saba, MD.)

placement may be necessary if there is bladder distention or decreased gut motility, respectively.104,138,140,200,230 Some recommend treating severe central anticholinergic syndrome with carefully titrated physostigmine, which is derived from the calabar bean of Physostigma venenosum. This cholinesterase inhibitor blocks acetylcholine degradation; the resultant accumulation of acetylcholine overcomes the competitive inhibition of atropinic agents, such as those found in jimsonweed. Rapid, though generally transient, reversal of peripheral and central nervous system (CNS) effects can ensue. However, bradycardia, asystole, ventricular arrhythmias, hypotension, bronchospasm, bronchorrhea, and seizures have been reported after rapid IV administration of physostigmine, limiting its routine use. Persons with cardiac conduction abnormalities are particularly susceptible to the cardiac complications. Use of physostigmine generally does not shorten the hospital stay.* Most cases of anticholinergic poisoning can be managed safely and effectively with supportive care alone.240 Consultation with a toxicologist is recommended before using physostigmine. If physostigmine is used, the recipient should be on a cardiac monitor, with pulse oximetry, and a physician at the bedside should slowly administer graduated doses of the drug.36,104,242 *References 44, 104, 138, 200, 209, 223, 242, 255.

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NICOTINIC PLANTS (PYRIDINE AND PIPERIDINE ALKALOIDS) The pyridine–piperidine group contains the major alkaloids nicotine, coniine, lobeline, arecoline, piperine, and isopelletierine. Structures of some pyridine/piperidine alkaloids follow: N

N

CH3 N

Pyridine OCCH2

N

Nicotine CH3CHOH C6H5

C4H5

N Lobeline

CH2

CH2

CH3

Coniine

Nicotine alkaloids are found mainly in the Solanaceae family of plants. Other families containing nicotine alkaloids include Hippocastanaceae (horse chestnut) and Asclepiadaceae (milkweed).

CHAPTER 64  Toxic Plant Ingestions

BOX 64-2  Nicotinic Syndrome Early Stage • Hypertension • Tachycardia • Vomiting • Diarrhea • Muscle fasciculations • Convulsions

FIGURE 64-5  Tree tobacco (Nicotiana glauca).

Tobacco Plants.  Tobacco contains both nicotine and related alkaloids with similar pharmacologic properties, such as the alkaloid anabasine, which is found in Nicotiana glauca (wild tree tobacco) (Figure 64-5). N. glauca has been mistaken for Amaranthus hybridus (marog) and eaten with porridge in South Africa. Ingestion of N. glauca is generally fatal. Anabasine, an isomer of nicotine that appears to be more toxic than nicotine, probably accounts for much of the toxicity of N. glauca, N. debneyi, and N. rotundifolia. Anabasine concentrations can be particularly high in the roots of the plants. Although there are over 60 Nicotiana species, some other more common tobacco family members include N. rustica (Mapacho), N. tabacum (cultivated or common tobacco), N. trigonophylla (desert tobacco) (Figure 64-6), and N. attenuata (coyote tobacco). N. tabacum is the major source of commercial tobacco and contains between 0.5% and 9% nicotine. N. rustica (Mapacho) tends to contain higher concentrations of nicotine than does N. tabacum. Nicotine alkaloids are rapidly absorbed from the oral and GI tracts, the respiratory tract, and the skin. The kidneys excrete nicotine fairly rapidly after biotransformation in the liver and lungs. The half-life is 1 to 2 hours. Although the lethal dose of ingested nicotine is not well established, 2 to 5 mg may cause nausea, and 40 to 60 mg may be lethal in humans. One to two cigarettes, ingested and absorbed, could be lethal in a child.176,180,228,236,247 Nicotinic Syndrome.  Peripherally, acetylcholine is a neurotransmitter for autonomic and somatic motor fibers. It is stored in vesicles within the presynaptic neuron and is released by calcium-dependent exocytosis into the synapse, where it binds to receptors and is eventually degraded by acetylcholinesterase. Acetylcholine can bind to two receptor types, nicotinic and muscarinic. Nicotinic receptors are located on postganglionic autonomic neurons (NN receptors) and at skeletal neuromuscular junctions (NM receptors). Direct nicotinic agonists (e.g., arecoline,

Late Stage • Hypotension • Bradyarrhythmias • Paralysis • Coma

coniine, cytisine, lobeline, nicotine) prolong depolarization at these receptors and eventually cause blockade of nicotinic receptors. Clinical evidence of stimulation followed by blockade is apparent. Hypertension, tachycardia, pallor, vomiting, diarrhea, abdominal pain, salivation, bronchorrhea, tachypnea, muscle fasciculations, spasms, confusion, agitation, tremor, and convulsions (the stimulation) are followed by hypotension, bradyarrhythmias (occasionally asystole), hyporeflexia, paralysis, coma, and respiratory failure (the blockade). When death occurs, it is generally due to respiratory paralysis (Box 64-2; see also Figure 64-3).* Green tobacco sickness is a mild form of nicotine poisoning seen in tobacco-naive field workers with dermal exposure to leaves of green tobacco in wet environments. Nicotine, a watersoluble alkaloid, is absorbed dermally. The syndrome is characterized by weakness, salivation, nausea, vomiting, diarrhea, abdominal cramps, headache, dizziness, visual and hearing disturbances, respiratory depression, and occasionally fluctuations in blood pressure and heart rate. Neuromuscular blockade may result in death. A urinary nicotine metabolite, cotinine, may be helpful diagnostically.15,176,228,247 Lobeline, derived from the Indian tobacco plant Lobelia inflata, is a high-affinity nicotinic ligand. It can cause nicotinelike effects, but is generally less toxic than is nicotine.63 Poison Hemlock.  C. maculatum (poison hemlock) (Figure 64-7), also known as spotted hemlock, California or Nebraska fern, stinkweed, fool’s parsley, and carrot weed, is often mistaken for an edible plant, such as parsley, parsnip, or anise; however, it has a mousy odor and an unpleasant bitter taste, and it burns the mouth and throat. The stem is hollow with purplish to reddish brown spots. Its long taproot is solid and parsnip-like. Although all plant parts are poisonous, the unripe fruit is especially toxic. Poisonings are more common in the spring and summer. Poisoning may also occur after eating birds that have *References 43, 60, 176, 180, 228, 236.

FIGURE 64-6  Nicotiana trigonophylla (desert tobacco) and other Nicotiana species are characterized by narrow tube-like flowers. (Courtesy Kimberlie A. Graeme, MD.)

FIGURE 64-7  Poison hemlock (Conium maculatum).

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PART 7  PLANTS

FIGURE 64-8  Betel nut (Areca catechu). (Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)

consumed poison hemlock. Coniine and γ-coniceine, the principal alkaloids in C. maculatum, are pyridine derivatives similar to nicotine. Coniine is more toxic than is γ-coniceine. The alkaloid is volatile and susceptible to drying and heating.25,152,228,268,274 C. maculatum was used in ancient times for capital punishment and murder. The primary action of the toxic alkaloids is activation and then blockade of nicotinic acetylcholine receptors. Initially, stimulation causes sialorrhea, nausea, vomiting, diarrhea, abdominal cramping, tremor, ataxia, confusion, blurred vision, hypertension and tachycardia, followed by dry mucosae, GI hypotonia, lethargy, weakness, diminished cardiac contraction, hypotension, and bradycardia, as with nicotinic syndrome. Muscles rapidly swell and stiffen, with multifocal necrosis of myocytes and associated muscle pain. Muscle fasciculations may be followed by flaccid paralysis, including respiratory paralysis. Rhabdomyolysis and acute tubular necrosis with renal failure may occur. Elevated CPK and liver function tests (LFTs) may be noted. Death is usually from respiratory failure. Autopsy may reveal congestion of the lungs and liver.* Betel Nut.  Areca catechu (areca palm) (Figure 64-8) produces betel nut, a common masticatory drug in the Far East, Asia, India, and the South Pacific; it is also shipped elsewhere. An estimated 10% to 25% of the world’s population chews “betel quid.” It is generally chewed with slaked lime paste (calcium hydroxide) wrapped in leaves of betel pepper (Piper betel ). known as “quid,” “punsupari,” and “pan masala.” Occasionally, tobacco is added. Quid is sucked in the lateral gingival pocket. Commercially, areca nut is marketed in the form of sweetened areca nut, known as “supari.” A. catechu contains arecoline and guvacoline, which are hydrolyzed to arecaidine and guvacine, respectively. These are strong inhibitors of gamma-aminobutyric acid (GABA) uptake. These arecal alkaloids also are nicotinic and muscarinic. Betel pepper leaves contain betel oil, which contains psychoactive phenols and cadinene. These possess cocaine-like properties. Clinical effects resemble nicotinic syndrome and cholinergic toxicity, including CNS effects (dizziness, euphoria, subjective arousal, altered mental status, hallucinations, psychosis, convulsions), cardiac effects (tachycardia, hypertension, palpitations, arrhythmias, bradycardia, hypotension, chest discomfort, and acute myocardial infarction in susceptible individuals), pulmonary effects (bronchospasm, tachypnea, dyspnea), GI effects (salivation, vomiting, diarrhea), urogenic effects (urinary incontinence), and musculoskeletal effects (weakness and paralysis). Use with calcium salts may result in hypercalcemia, hypokalemia, and metabolic acidosis with renal potassium wasting and renal insufficiency. Betel nut use is also associated with flushing, diaphoresis, warm sensations, red- or orange-stained oral mucosa and saliva, and teeth stained dark brown or black. Precancerous oral lesions may also occur with chronic use.† *References 25, 77, 96, 97, 104, 118, 228, 268, 274. † References 29, 52, 71, 135, 167, 168, 188, 233, 249.

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Blue Cohosh.  Caulophyllum thalictroides is known as blue cohosh or squaw root. All parts of the plant contain the nicotinic alkaloid n-methylcytisine, which is much less potent than nicotine. Teas made from C. thalictroides have been used to induce labor and have resulted in newborn death and perinatal complications of stroke, congestive heart failure, respiratory failure, and circulatory collapse. The infant toxicity is thought to be due to the toxic saponins, caulosaponin and caulophyllosaponin.228 Golden Chain Tree.  All parts of Laburnum anagyroides (golden chain tree) are toxic and contain the nicotinic alkaloids cytisine and n-methylcytisine. Cytisine is a quinolizidine alkaloid but is often classified with the pyridine and piperidine alkaloids. These alkaloids stimulate nicotinic ganglions. The toxins are concentrated in the seeds. Toxicity is generally only mild to moderate; however, an unusual fatality occurred in which 23 seedpods were found in the stomach of an adult at autopsy. Other plants that contain cytisine include Kentucky coffee tree (Gymnocladus dioica), necklace pod sophora (Sophora tomentosa), and mescal bean bush (Sophora secundiflora) (Figure 64-9) (see Hallucinogenic Plants, later). Structures follow:228

NH N

N O

Quinolizidine

Cytisine

Treatment.  Treatment of nicotinic syndromes consists of supportive care with particular attention to airway protection and ventilation. Administration of activated charcoal has been used because it adsorbs nicotine in vitro. However, nicotine and related alkaloids are absorbed rapidly and often produce vomiting, which may limit the usefulness of activated charcoal. These alkaloids may also induce altered mental status, which can increase the risks associated with activated charcoal. Benzodiazepines and barbiturates are given for seizures. Adequate urine output is maintained, with consideration of urine alkalinization. Treating initial excessive adrenergic stimulation with adrenergic antagonists is ill advised because this complicates the nicotinic blockade that typically follows. Symptomatic bradycardia is treated with atropine; hypotension can be treated with IV fluids and inotropic agents if needed. Atropine may also help to treat bronchorrhea.228

HALLUCINOGENIC PLANTS (INDOLES, PHENYLALKYLAMINES) About 90 of the 800,000 known plant species are hallucinogenic. Numerous rituals and religious ceremonies incorporate these plants. Many psychoactive plants are indole derivatives, which

C

B

FIGURE 64-9  Mescal bean bush (Sophora secundiflora) (A) is characterized by bean pods that contain burnt-red seeds (B) and by purple blooms (C). (Courtesy Phillip Saba, MD, and Kimberlie A. Graeme, MD.)

are among the most potent psychoactive compounds in nature and have the following structure:

N H Indole nucleus

Chemical relationships exist among serotonin, psilocybin (Psilocybe species), and D-lysergic acid diethylamide (LSD). LSD is synthesized from ergonovine (or ergometrine), derived from Claviceps purpurea. Striking structural similarities exist between the most potent psychoactive plant compounds and biochemically important neurotransmitters, as follows: NH1

OR

N(CH3)2

HO N H

N H

Serotonin

Psilocybin OH

HO

CHCH2NH2

HO

CH3O

CH2CH2NH2

CH3O OCH3

Norepinephrine

Mescaline

ergotism resulted from repeated ingestion of ergot-contaminated breads. Ergotism has two forms, gangrenous and convulsive. Both begin similarly with a vague illness that may include GI symptoms, progressing to a sensation of ants crawling on the skin, primarily affecting the legs. Hallucinations can occur with both forms. Gangrenous ergotism, a vasospastic disease, was the cause of the ninth-century epidemic disease known as St Anthony’s fire, which consisted of burning limb pain and eventual loss of limb sensation, followed by gangrene and autoamputation of charcoalblack limbs. People migrated to St Anthony’s Order, a society of monks, and began to heal, once they received a diet free of ergot-contaminated grains. Convulsive ergotism is characterized by painful flexion of the fingers and wrists, flexion or extension of the ankles, double vision, altered mental state, hallucinations, and diaphoresis. With progression, the body becomes bent in spasm, appearing to roll up into a ball, or it becomes rigid in extension; this may be followed by seizures.* Morning Glory.  The active component of the naturally occurring hallucinogen found in the seeds of morning glory (Ipomoea violacea) (Figure 64-10) is ergine, or (+)-lysergic acid amide, an indole derivative.112 About 300 seeds, or enough to fill a cupped hand, are equivalent to 200 to 300 mg of LSD, with similar systemic and hallucinatory effects. Ingestion of Hawaiian baby woodrose seeds (Argyrlia nervosa) has similar effects.105 Nutmeg.  Myristica fragrans (Figure 64-11) is used to make the spices nutmeg and mace. Mature rinds of the fruit split, revealing a bright-red, fringed, fleshy coating on the outside of its seed. The coating contains mace, and the seed contains nutmeg. Nutmeg contains myristicin, which has an indole-like structure and is metabolized to amphetamine-like compounds. Other alkylbenzene derivatives, such as safrole and elemicin, are also found *References 40, 41, 45, 80, 118, 264.

R

CH3 N CH3

OH H H

N H Lysergic acid diethylamide

CH3H13

CH3 O CH3

Tetrahydrocannabinol

Ergot.  The ergot alkaloids ergonovine and ergotamine are indole derivatives found in the fungus C. purpurea, which infects rye and other grains. The ergot alkaloids are serotonin agonists. Commercial grains are now inspected for the presence of ergot, and inadvertent poisoning is rare. An outbreak of ergotism occurred in Ethiopia in 1977. In the Middle Ages, epidemics of

FIGURE 64-10  Morning glory (Ipomoea violacea).

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CHAPTER 64  Toxic Plant Ingestions

A

PART 7  PLANTS

A

FIGURE 64-12  Peyote (Lophophora williamsii).

B FIGURE 64-11  Nutmeg (Myristica fragrans). (Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)

in nutmeg. Nutmeg has been abused for its alleged hallucinogenic effects. A person who ingested one grated nutmeg (7 g) had weakness, loss of coordination, vertigo, fainting, nausea, and paresthesias but no hallucinations.238,265 Cannabis.  Cannabis preparations are largely derived from the female Cannabis sativa plant. The primary psychoactive component is δ-9-tetrahydrocannabinol (THC), which is most concentrated in the flowering tops. Marijuana generally contains 0.5% to 5% THC; however, the Sinsemilla and Netherwood varieties may contain up to 20% THC, and hashish and hashish oils have higher concentrations. Cannabinoids can be smoked or ingested. A typical marijuana cigarette contains 0.5 to 1.0 g of cannabis, and the THC delivered varies from 20% to 70%, with a bioavailability of 5% to 24%. As little as 2 mg of available THC produces effects in occasional users.119 Cannabinoids bind to specific cannabinoid receptors in areas of the brain involved with cognition, memory reward, pain perception, and motor coordination. Cannabinoids act as neuromodulators in the release and action of neurotransmitters (e.g., acetylcholine, glutamate).75,119 Endogenous ligands for these receptors are endocannabinoids. The first endocannabinoid identified was anandamide, named after the Sanskrit word ananda, which means “bliss.” Desirable effects include mild mood-altering qualities, euphoria, alteration in perceptions, time distortion, and intensification of ordinary sensory experiences (e.g., gustatory, visual, and auditory sensations). Adverse effects include impairment of short-term memory and attention, mydriasis and slowly reactive pupils, impairment of motor skills and reaction times, nausea, vomiting, and anxiety. Psychotic symptoms have been reported in persons vulnerable to psychosis. Clinically, tachycardia may occur within minutes of THC exposure and may last a few hours. Minor changes in blood pressure may also occur. Exposed toddlers may present with lethargy, slurred speech, ataxia, and shaking.27,119 Peyote.  The hallucinogenic peyote cactus Lophophora williamsii (Figure 64-12) contains alkaloids that are phenylethylamines or isoquinolines rather than indoles. Mescaline (3,4,5-trimethoxyβ-phenylethylamine), the primary psychoactive component of peyote, is structurally similar to the neurotransmitters norepinephrine and epinephrine and to hallucinogenic amphetamines. Pharmacologically, however, mescaline is similar to hallucinogenic indoles. Mescaline may affect the action of norepinephrine and serotonin, evidenced clinically by sympathomimetic effects, followed by marked visual hallucinations. Mescaline produces slight rises in blood pressure and heart rate, tachypnea, 1260

hyperreflexia, mydriasis, ataxia, perspiration, flushing, salivation, and urination. No deaths have been reported from peyote poisoning. Type B botulism was associated with consumption of a ceremonial tea made from peyote that was stored in a jar by members of the Native American Church. Affected members had bilaterally symmetric, flaccid weakness in all extremities, dysphagia, nasal speech, and diplopia.9,126 Mescal Bean Bush.  The mescal bean bush or Texas mountain laurel (Sophora secundiflora) of the pea family (Fabaceae) produces hallucinogenic dark-red beans (mescal beans; see Figure 64-9). The beans contain the toxic alkaloid cytisine, which causes nausea, numbing sensations, hallucinations, unconsciousness, convulsions, and death through respiratory failure. The beans may be boiled in water and the mixture consumed, producing a delirium or “visionary trance.” The origin of mescalism in modern peyote religion is debated. Mescal beans are worn during some peyote ceremonies.9 Tabernanthe iboga.  Tabernanthe iboga contains indole alkaloids, including ibogaine. The root of this plant is used in West Africa to communicate with ancestors, reportedly producing “visions” and “waking dreams.” It produces altered states of consciousness, delusions, hallucinations, mydriasis, tachycardia, tremor, and ataxia. Convulsions and lethal respiratory arrest have also been reported. A man was found dead after ingesting a powdered root bark of T. iboga shrub mixed with sweet concentrated milk. Autopsy revealed pulmonary edema with hemorrhagic alveolitis and vascular congestion.39,151 Khat.  The evergreen khat tree, Catha edulis, grows in East Africa and Arabia (Figure 64-13). Khat is also known as chat, qat, kat, kath, gat, eschat, miraa, murungu, qaad, and jaad. As early as 1237, khat was advocated in Arabic medical literature as a

FIGURE 64-13  Khat (Catha edulis). (Courtesy Daniel Brooks, MD, and Tammy Tyree, NP.)

C

CH

O

CH3

CH3 N H

Methcathinone

C

CH

O

CH3

H N H

Cathinone

CH

CH

OH

CH3

N

CH3 H

Ephedrine

Cathinone in fresh plant material must be extracted by masticating laboriously; this results in gradual absorption. As the leaf wilts, cathinone content decreases and the leaf loses its potency as a psychostimulant. Because only fresh leaves produce the desired stimulatory effects, in the past, khat use was generally limited to countries where khat was produced (e.g., North Yemen, Ethiopia, Kenya); however, khat is now air-freighted to Europe and the United States, with a recent increase in use in upstate New York. Khat is transported damp, rolled in a banana leaf bundle called a marduff. Desirable effects of khat include increased energy and alertness, feelings of increased endurance and self-esteem, enhanced imaginative ability, higher capacity to associate ideas, and euphoria. Cathinone has both positive chronotropic and inotropic effects. Tachycardia, increased blood pressure, tachypnea, and mydriasis are seen. Adverse effects include anorexia, hypomania, insomnia, delusions, paranoid psychosis, aggression, depression, anxiety, hyperthermia, stomatitis, oral lesions/cancers, gastritis, and endocrine disturbances. Khat use has also been associated with vasoconstriction, acute myocardial infarction, leukoencephalopathy and an increased incidence of acute cerebral infarction. Khat is known to be habit forming and has been classified as a substance of abuse by the World Health Organization. Cathinone is a Schedule I controlled substance under federal regulations in the United States.†

ANTICHOLINERGIC PLANTS Henbane (H. niger). jimsonweed (D. stramonium), and mandrake (Mandragora officinarum) contain tropane alkaloids and can produce hallucinations, as discussed earlier. Treatment.  Treatment of patients exposed to hallucinogenic plants is generally supportive. First-line treatment for agitation is generally benzodiazepines.

SEDATING PLANTS (ISOQUINOLINE ALKALOIDS)

Opiate toxicity from poppy seed exposure occurred in a 6-monthold infant given 75 mL of strained milk made with 200 g of poppy seeds in 500 mL milk, resulting in respiratory arrest requiring ventilation. Opiate toxicity has also occurred after ingestion of a boiled poppy plant and after ingestion of spaghetti with poppy seeds. Poppy dependence has also been described. Ingestion of poppy seeds can result in detectable levels of morphine and codeine by urine drug screen testing.146,158,204,262

NEUROMUSCULAR BLOCKING PLANTS (INDOLE ALKALOIDS) Yellow Jasmine.  Gelsemium sempervirens (Carolina or yellow jessamine) is a woody perennial evergreen vine with fragrant yellow flowers. It contains multiple indole alkaloids, including gelsemine, gelseminine, and gelsemoidin. Gelsemine binds to acetylcholine receptors at the neuromuscular junction (peripheral nicotinic acetylcholine receptors) and, to a lesser extent, at muscarinic receptors. A toddler who ate the blossoms of G. sempervirens experienced neuromuscular blockade with ataxia, dysarthria, facial and extremity weakness, bilateral ptosis, and transient coma. The child recovered without sequelae.26

CONVULSANT PLANTS (INDOLES, RESINS) Strychnine.  Strychnine, an indole found in seeds of the tree Strychnos nux-vomica, is a powerful CNS stimulant. Poisoning may also occur after ingestion of rodent poisons containing strychnine, with the use of illicit drugs contaminated with strychnine, or with the use of herbal remedies contaminated with strychnine. Strychnine is especially concentrated in the seeds and roots of the plant. The bark of S. nux-vomica also contains the alkaloid brucine, which is less potent than strychnine, but produces similar toxicity when consumed. Strychnine is a selective, competitive antagonist of glycine, a major inhibitory neurotransmitter, at its postsynaptic receptors in the spinal cord and brainstem. Poisoning produces an excitatory state, with hyperreflexia, hypersensitivity to stimuli, migratory rippling movements of the muscles, twitching, rigidity, and spinal convulsions (generally, flexor spasm of the upper limbs, extensor spasm of the lower limbs, opisthotonic posturing, and spasms of the jaw muscles, all without loss of consciousness or postictal states). Minimal stimulation elicits diffuse muscle contractions. In between spasms, which last from 30 seconds to 2 minutes, muscles become completely relaxed. Respiratory and secondary cardiac failure may ensue during severe convulsions. Treatment consists of supportive care, benzodiazepines, and barbiturates. Chemical paralysis with a nondepolarizing agent, endotracheal intubation, and mechanical ventilation may be required for severely poisoned patients. Hyperthermia, rhabdomyolysis, renal failure, and acidosis may occur secondary to convulsions. These complications often require treatment. Occasionally, death ensues despite aggressive treatment.* Some Strychnos species in Africa contain alkaloids that produce curare-like effects. These alkaloids act through nondepolarizing and competitive mechanisms at the neuromuscular junction, competing with acetylcholine for the receptor, hence blocking nerve-to-muscle transmission. This results in paralysis; however, paralysis is not seen after ingestion of these species, because the toxic alkaloids are not absorbed from the gastrointestinal tract.207

Poppy.  Papaver somniferum flowers are large and white with purple stains at the base of each petal. They yield opium, a complex of more than 20 alkaloids, including morphine, codeine, and papaverine. Morphine was the first plant alkaloid isolated, by pharmacist Friederich Wilhelm Adam Serturner in 1806.117 Seeds of P. somniferum are used in various foods and beverages, including bagels, muffins, pastries, curry sauce, rice, and teas.

Wild Wisteria.  The root of Securidacea longepedunculata (violet tree; wild wisteria) has been used as an intravaginal suicidal poison and an abortifacient. The distilled oil of the root is primarily methyl salicylate (discussed latter with essential oils); however, wild wisteria also contains the alkaloid securinine, a GABA-A receptor antagonist, which produces hyperreflexia, hypertonia, and seizures. Death can result within hours of placing the root intravaginally, and is generally preceded by vomiting, diarrhea, and dehydration.246

*References 3, 5, 7, 39, 42, 128, 190, 193, 201, 258. † References 1, 3, 4, 5, 7, 14, 51, 72, 109, 128, 144, 172, 182, 190, 193, 201.

*References 22, 47, 95, 169, 186, 195, 207, 231, 232, 278.

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CHAPTER 64  Toxic Plant Ingestions

mood-elevating and hunger-suppressing agent. Khat leaves and bark continue to be chewed, with the juice of the masticated plant being swallowed for stimulatory effects. Khat contains cathinone (2-amino-1-phenyl-1-propanone), cathine (norpseudoephedrine), and norephedrine. Cathinone, a phenylalkylamine, is the major psychoactive constituent. Structurally, cathinone is similar to amphetamines, and khat has been referred to as a “natural” amphetamine. Like amphetamines, cathinone is an indirect sympathomimetic, inducing release of dopamine, serotonin, and norepinephrine.* The structures of methcathinone, cathinone, and ephedrine follow:

PART 7  PLANTS

A

B

FIGURE 64-14  Cicuta species have characteristic flowering tops, typical of the Umbelliferae family (A), and roots with air-filled chambers at the ends of hollow stems (B). (Courtesy Steven Curry, MD.)

Water Hemlock.  Water hemlock (Cicuta maculata) is one of the most toxic resin-containing plants. The resin of C. maculata, an unsaturated aliphatic alcohol called cicutoxin, has the following structure: CH2

CH2

CH2

(C

C)2

OH

(CH

CH)3 CH (OH) C3H7

Cicutoxin

Species within the Umbelliferae (also called Apiaceae) family are divided into the Cicuta and Oenanthe genera. Nine subspecies of Cicuta of the Umbelliferae family are poisonous (Figure 64-14). C. virosa is common European water hemlock, whereas C. maculata and C. douglasii are found in North America. Oenanthe crocata, or hemlock water dropwort, is found in Europe and North America. Common names for Cicuta species include cowbane, five-finger root, snake weed, snake root, wild carrot, dead man’s fingers, death-of-man, poison parsnip, wild parsnip, beaver poison, children’s bane, muskrat weed, spotted hemlock, spotted cowbane, musquash root, false parsley, fever root, mock-eel root, wild dill, spotted parsley, and carotte à Moreau. Roots have a parsnip-like or carrot-like odor, and Cicuta species are often mistaken for edible plants, such as water parsnip. These plants have also been mistaken for pignut, sweet flag, wild carrot, wild celery, wild ginseng, and kvanne. Mature roots have air-filled chambers and are found on the ends of hollow stems. All parts of the plant are toxic, but the roots contain the highest concentration of cicutoxin. Ingestion of as little as 2 to 3 cm of the root may be fatal to an adult. The severity of poisoning and time until onset of symptoms is proportional to the amount of plant ingested. The plant is most toxic in the spring. The principal toxins, cicutoxin and oenanthotoxin, contained in these plants act as noncompetitive GABA antagonists in the central nervous system, resulting in unabated neuronal depolarization that manifiests as seizures, including status epilepticus.104,131,152,229 Water hemlock poisoning should be considered in any patient who presents with cholinergic-like poisoning and abrupt onset of seizures. Early symptoms include muscarinic effects and involve primarily the GI tract: abdominal pain, vomiting, and diarrhea. However, marked diaphoresis, salivation, and respiratory distress may also be seen. Nicotinic effects are less prominent (see Figure 64-3). Tachycardia and hypertension or bradycardia and hypotension may be seen. Dysrhythmias may occur. Ataxia, paresthesias, muscle spasms, weakness, and altered mental status have been reported. With severe poisoning, coma and epileptiform seizure activity, or spastic and tonic movements, including opisthotonus without electroencephalographic seizure activity, may occur. Rhabdomyolysis and renal failure have been reported. Deaths may be associated with persistent seizures, 1262

cerebral edema, ventricular fibrillation, pulmonary edema, cardiopulmonary arrest, and disseminated intravascular coagulation. Laboratory abnormalities include metabolic acidosis and elevated CPK and LFTs. Treatment includes securing an airway, ventilation, and treatment of seizures with benzodiazepines and barbiturates. Phenytoin is contraindicated because it is ineffective for seizure control. Anticholinergic agents are not recommended, because these agents do not reduce seizure activity. Continuous EEG monitoring is helpful. Treatment of hypoxia, acidosis, hyperthermia, rhabdomyolysis, and cerebral edema should be provided. Hypotension can be treated with intravenous fluids and vasopressors. Recovery can take up to 4 days, and some patients never completely recover. Although survival has improved with aggressive supportive care, death may still ensue. Autopsies reveal pulmonary and cerebral edema, brain hemorrhages and renal necrosis.104,131,152,229 Myrtle-leaved Coriaria.  Coriaria myrtifolia (also known as myrtle-leaved coriaria, Currier’s sumach, or Redoul sumach) grows in the western Mediterranean area. C. myrtifolia contains coriamyrtin, an analogue of picrotoxin. The toxin is found in high concentrations in the berries, which resemble blackberries. Ingestion of only a few fruits can produce significant toxicity. The leaves are also toxic. Rarely, individuals have become poisoned after eating snails acquired off the plant, after drinking the milk of goats that had been eating the plant, and after consuming honey contaminated by its nectar. The leaves have also been mistakenly eaten when thought to be the leaves of senna (Cassia senna L.). Initially, vomiting, abdominal pain and drunken intoxication are seen. This may be followed by twitching, seizures (including status epilepticus), coma and apnea. Death may occur. Treatment with benzodiazepines and barbiturates should be considered.69 Other Convulsants.  Anticholinergic and nicotinic plants may produce seizures, as discussed earlier. Ingestion of plants that produce hypoglycemia, such as ackee (B. sapida), wild yam (Dioscorea spp.), cocklebur (Xanthium spp.), bird-lime (Atractylis gummifera) and ox-eye daisy (Callilepis laureola) are associated with seizures and discussed later.

Cardiovascular Toxins Cardiovascular toxins found in plants are listed in Box 64-3.

CARDIOTOXINS THAT INHIBIT NA+/K+ ATPASE (CARDIAC GLYCOSIDES) More than 200 naturally occurring cardiac glycosides have been identified. Plant cardiac glycosides are composed of a steroid backbone, an attached five-membered unsaturated lactone ring (six-membered for Helleborus), and either a carbohydrate or sugar moiety in glycosidic linkage. The toxic aglycones are released by acid and enzymatic hydrolysis. The attached sugar

CHAPTER 64  Toxic Plant Ingestions

BOX 64-3  Cardiovascular Toxins Found in Plants Alkaloids • Steroid (e.g., aconite, veratrum alkaloids) • Taxane (e.g., taxines) Glycosides • Cardiac (e.g., lanatosides, oleandrin, thevetin) Resins • Grayanotoxins (e.g., o-acetyl-andromedol)

moiety has no inherent cardiac action but may enhance solubility, absorption, and toxicity of the aglycone moiety. Cardiac glycosides bind to the membrane-bound enzyme Na+,K+ ATPase, increasing intracellular Na+ and Ca2+ levels and automaticity (Figure 64-15).215 Cardiac glycosides are found in Digitalis purpurea (foxglove) (Figure 64-16), Digitalis lanata, N. oleander (common oleander) (Figure 64-17), T. peruviana (yellow oleander) (Figure 64-18), Convallaria majalis (lily of the valley) (Figure 64-19), Urginea maritima (squill or sea onion) (Figure 64-20), U. indica, Cerbera manghas (sea mango), C. odollam (pink-eyed cerbera), Strophanthus gratus (ouabain), Asclepias species (balloon cotton, red-headed cotton-bush milkweeds), Calotropis procera (king’s crown), Carissa spectabilis (wintersweet), C. acokanthera (bushman’s poison), Plumeria rubra (frangipani), Cryptostegia grandifolia (rubber vine), Euonymus europaeus (spindle tree), Cheiranthus, Erysimum (wallflower), and Helleborus niger (henbane).* Foxglove.  D. purpurea grows wild in parts of the United States and is cultivated as a garden ornamental plant. D. purpurea contains only digitoxin, not digoxin. Withering reported the medical use of extracts of D. purpurea based on a recipe for treating “dropsy.”129,192 The leaves have been consumed in a risotto when they were mistaken for borage leaves, and in a salad when mistaken for dandelion leaves.38,189 Toxicity has also been

Cardiac glycoside

3Na+

3Na+

–

Na+/Ca2+

ATPase Na+ 2K+

+ Na+

+ Ca2+ Sarcoplasmic reticulum

Na+ 1 Ca2+

Ca2+

Ca2+ 2+

Ca

Ca2+

+

Actin and myosin

FIGURE 64-15  Cardiac glycosides bind to and inhibit the membranebound enzyme Na+/K+ ATPase in cardiac myocytes (shown), baroreceptor cells, and skeletal muscle cells. Inhibition of Na+/K+ ATPase in cardiac myocytes results in accumulation of intracellular Na+, which results in accumulation of Ca2+ within myocytes via Na+,Ca2+ exchangers. The resultant increase in intracellular Ca2+ stimulates further release of Ca2+ from the sarcoplasmic reticulum. The increased intracellular Ca2+ interacts with troponin C of the actin–myosin complex to cause increased contractions, seen as increased automaticity (e.g., premature ventricular contractions on electrocardiogram). Inhibition of membrane-bound enzyme Na+/K+ ATPase in baroreceptor cells and skeletal muscle cells contributes to increased vagal tone and hyperkalemia, respectively. *References 81, 86, 104, 116, 118, 129, 161, 189, 260.

FIGURE 64-16  Digitalis purpurea (foxglove). (Courtesy Kimberlie A. Graeme, MD.)

reported from consumption of contaminated field water with Digitalis plants growing nearby.189 D. lanata was mistakenly substituted for plantain in herbal products, with resultant human cardiotoxicity.239 D. lanata contains lanatosides A, B, and C, which yield digoxin and digitoxin. Intentional overdoses also occur.157,189 Oleander.  All parts of N. oleander and T. peruviana are toxic, but the seeds contain more glycoside than do other parts of the plant. Yellow oleander (T. peruviana), a native plant of tropical America, grows abundantly in the United States. Ingestion of a couple of seeds of yellow oleander, known as “lucky nuts,” can result in death; however, the number of seeds ingested is a poor guide to the degree of poisoning. Yellow oleander contains the cardiac glycosides thevetin A and B, thevetoxin, neriifolin, peruvoside, ruvoside, and others. It is a popular suicidal agent in Sri Lanka and India. Of patients admitted with T. peruviana poisoning in Sri Lanka, 43% had arrhythmias, many requiring temporary pacing; 6% died shortly after admission. Common oleander (N. oleander), a native plant of the Mediterranean, grows abundantly in the United States. Common oleander contains the principal cardiac glycosides oleandrin and neriine, as well as folinerin and digitoxigenin. Severe toxicity has been reported after consumption of unprocessed common oleander leaves and prepared teas. Chronic toxicity has occurred with criminal intentional poisoning. Topical application of homemade N. oleander solutions onto psoriatic wounds has resulted in toxicity.* Squill.  U. maritima was used by ancient Egyptians and Romans as a diuretic, heart tonic, expectorant, emetic, and rat poison. Squill contains several cardiac glycosides, including scillaren A, glucoscillaren A, scillaridin A, and scilliroside.86,260,271 Sea Mango.  C. manghas (sea mango) is similar to C. odollam (pink-eyed cerbera, yellow-eyed cerbera, suicide tree). This tree grows in India, Vietnam, Cambodia, Sri Lanka, Burma (Myanmar), *References 66, 81, 82, 104, 111, 161, 163, 191, 215, 276.

1263

PART 7  PLANTS

A

A

B B FIGURE 64-17  Nerium oleander (common oleander) plants have white or pink flowers (A) and long, narrow seedpods (B). (Courtesy Kimberlie A. Graeme, MD.)

FIGURE 64-18  Thevetia peruviana (yellow oleander) has yellow flowers (A) with smooth seedpods, known as “lucky nuts,” composed of green flesh surrounding a hard brown seed (B). (Courtesy Kimberlie A. Graeme, MD.)

Madagascar, and Australia. The plant has large white flowers that smell like jasmine. When the fruit is still green, it looks like a small mango. The inner fruit (kernel) is white, but upon exposure to air turns violet, then dark grey, and then black. The crushed, white fleshy kernel is commonly consumed as a suicidal poison in India and Sri Lanka. The seeds are quite toxic. The leaves are less toxic. These plants contain the toxins cerberoside, cerberin, and odollin. After ingestion, death can occur within hours.83,107,168,259 Clinical Presentation.  The onset of symptoms and duration of action are well known for certain glycoside preparations, such as digoxin, digitoxin, and ouabain, but may vary considerably after plant ingestions. For example, oleandrin exhibits protracted binding times to cardiac myocardial tissues.161 Generally, cardiac glycoside toxicity produces nausea, vomiting, diarrhea, abdominal tenderness, visual changes (appearance of yellow and green colors, “halos,” geometric shapes, scintillations, photophobia), mental status changes (disorientation, psychosis, lethargy, stupor, dysarthria, weakness, dizziness, restlessness, seizures), cardiac disturbances (palpitations, premature ventricular beats, bradycardia, atrioventricular block, sinus node block, paroxysmal atrial tachycardia with block, junctional tachycardia, bidirectional ventricular tachycardia, ventricular arrhythmias, myocardial depression with cardiogenic shock, syncope), hyperkalemia, and death. When death occurs, it is generally caused by cardiotoxicity. The 1264

FIGURE 64-19  Lily of the valley (Convallaria majalis). (Courtesy Donald Kunkel, MD.)

B

FIGURE 64-20  Urginea species (squill or sea onion) have broad leaves (A) and a red, underground bulb (some varieties have a white bulb) (B). (Courtesy Kimberlie A. Graeme, MD.)

ECG may reveal nonspecific ST-segment and T-wave changes, similar to digoxin-induced changes.* Serum digoxin levels may be elevated after exposure to plants containing cardiac glycosides, because antibody-based digoxin assays cross-react nonquantitatively with many cardiac glycosides. Digoxin immunoassays predict only the presence of the glycoside, not the degree of toxicity.82,116,161,260 Conversely, the degree of hyperkalemia often correlates with severity of toxicity.82,107 Treatment.  Continuous cardiac monitoring for at least 24 hours is recommended because of the risk for arrhythmias. Cardiac glycoside toxicity from plant ingestions has been successfully treated with a single dose or multiple repeated doses of activated charcoal, cardiac pacing, antiarrhythmic agents, and digoxin-specific Fab fragments (e.g., Digibind and DigiFab). Maintenance of fluid and electrolyte balance is important. Potassium levels should be checked frequently. Correction of hyperkalemia with insulin and dextrose is recommended. Sodium polystyrene sulfonate resin is not recommended because total body hypokalemia may ensue. Theoretically, administration of exogenous calcium could be harmful because of high intracellular calcium concentrations in poisoned myocytes. It is hypothesized that the heart would perform one final contraction without relaxation, a state termed stone heart. Bradyarrhythmias have been managed with atropine and beta-adrenergic agents. However, there is a theoretical risk for increasing tachyarrhythmias, which may be more difficult to treat. Some have advised against the use of atropine and beta-adrenergic agents unless bradycardia is life threatening. Some feel that cardiac pacing is a better alternative, although this may precipitate tachyarrhythmias. Ventricular tachycardia often resists electrical cardioversion, and electrical cardioversion can precipitate ventricular fibrillation or asystole. Therefore electrical cardioversion is reserved for resistant cases. For tachyarrhythmias, lidocaine has been advocated. The role of magnesium is not known, although some have subjectively noted death following yellow oleander poisoning treated with intravenous magnesium. Amiodarone, quinidine, and calcium-channel blockers are contraindicated because they may increase digitalis concentration; beta-blockers are contraindicated because they may worsen heart block. Digoxin-specific Fab antibody fragments may couple to circulating cardiac glycosides and limit binding of cardiac glycosides to Na+,K+ ATPase. Administration of digoxin-specific Fab antibody fragments to reverse cardiotoxicity from plant glycosides has been successful in several animal and human studies. Clinical trials in Sri Lanka revealed that intravenous administration of 1200  mg digoxinspecific antibody fragments reversed life-threatening cardiac arrhythmias and corrected hyperkalemia after yellow oleander poisoning.† *References 78, 111, 163, 189, 215, 239, 276. References 57, 82, 83, 84, 107, 111, 148, 161, 189, 215, 218, 239.

†

CARDIOTOXINS THAT OPEN SODIUM CHANNELS (STEROID ALKALOIDS, RESINS) Steroid alkaloids form principal toxic components of several common cardiotoxic plants: Aconitum species (monkshood, wolfsbane and helmet flower), V. viride (American hellebore, green hellebore), and Zigadenus species (death camas). Aconite is found in Aconitum species, and veratrum alkaloids are found in V. viride, V. nigrum var. japonicum (false hellebore), V. californicum (skunk cabbage), V. album (white hellebore), Z. paniculatus (death camas), Z. venenosus, Z. nuttallii, and Z. gramineus. Aconite.  Aconite poisonings have become more common, because of the use of Aconitum species (A. napellus [monkshood]) (Figure 64-21), A. carmichaeli (chuanwa), A. brachypodium, A. vulparia, and A. kusnezoffii (caowu) in herbal products. Delphinium species (larkspur) demonstrate similar toxicity. All parts of these plants are toxic, with the roots being most toxic. Aconitum species contain diterpenoid-ester alkaloids, particularly aconitine, but also mesaconitine, hypaconitine, and yunaconitine, which are neurotoxins and cardiotoxins. Boiling these plants in water hydrolyzes aconite alkaloids to less toxic benzoylaconine and aconine derivatives. Soaking or boiling, termed decoction, is generally done when these plants are used as herbal medicines. The estimated lethal dose of wild plant is 1 g.* Aconite alkaloids activate voltage-sensitive sodium channels and affect excitable membranes of neural, cardiac, and muscle tissues. Hypaconitine affects sodium channels of the nerve membrane more selectively than does aconitine and is more potent than aconitine and mesaconitine in producing neuromuscular block. These neurotoxins produce conduction block and *References 8, 46, 48, 49, 104, 165, 181.

FIGURE 64-21  Monkshood (Aconitum species).

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CHAPTER 64  Toxic Plant Ingestions

A

PART 7  PLANTS

paralysis through voltage-sensitive sodium channels in axons. In cardiac tissues, prolonged depolarization prevents repolarization of excitable membranes. Enhancement of the transmembrane inward sodium current during the plateau phase of the action potential prolongs repolarization in cardiac myocytes and induces delayed and early after-depolarizations. Delayed afterdepolarizations result in increased automaticity, such as premature ventricular beats. Early after-depolarizations produce lengthening of the QT interval. Hypotension and bradycardia may be induced by activation of the ventromedial nucleus of the hypothalamus.8,46,49,102,165 Symptoms begin within 3 minutes to 6 hours of ingestion and may persist for several days. Nonspecific GI symptoms (nausea, vomiting, diarrhea) are accompanied by neurotoxicity and cardiotoxicity. Visual impairment, dizziness, vertigo, ataxia, paresthesias (e.g., numbness of mouth and extremities), hyporeflexia, weakness, paralysis, coma, restlessness, and convulsions may occur. Cardiac effects are clinically similar to cardiac glycoside toxicity, with enhanced vagal tone, bradycardia, heart block, ectopic beats, supraventricular tachycardia, bundle branch block, junctional escape rhythms, ventricular tachycardia, bifascicular ventricular tachycardia, polymorphic ventricular tachycardia, torsades de pointes, ventricular fibrillation, asystole, and hypotension. Bidirectional ventricular tachycardia, which is generally considered suggestive of cardiac glycoside toxicity, has also been reported with aconite poisoning. Elevated CPK levels, with or without evidence of myocardial infarction, may occur. Hypokalemia, metabolic or respiratory acidosis, respiratory alkalosis, and renal and hepatic impairment may be noted. Occasionally, death ensues, generally from ventricular arrhythmias, such as refractory ventricular fibrillation. Respiratory paralysis may also result in death.* Veratrum Alkaloids.  Veratrum and Zigadenus species belong to the lily family. All parts of these plants are toxic, with the rhizomes being more toxic than the tops. Veratrum species may be found in some sneezing powders and have been accidentally ingested when mistaken for Gentiana lutea (yellow gentian). Gentian wines are usually made from G. lutea. When accidentally made from Veratrum species, these wines can be toxic. V. viride has also been mistaken for skunk cabbage, ramps, and pokeweed (Phytolacca americana), producing toxicity after ingestion. Zigadenus species, also known as foothill camas, death camas, and mountain camas, have been accidentally ingested when mistaken for nontoxic wild onions (Allium macropetalum) and sego lilies (Calochortus nuttallii). Amianthium muscitoxicum and Schoenocaulon officinale (Sabadilla) also contain veratrum alkaloids. Veratrum alkaloids include protoveratrine, veratridine, cevadine, jervine, zygadenine, and zygacine, which are found in the entire plant, although the bulb and flower usually cause toxicity. These alkaloids are extremely toxic and rapidly increase permeability of voltage-sensitive sodium channels in excitable cell membranes. This results in initial depolarization and then subsequent loss of membrane potential. Stimulation of vagal fibers may result in bradycardia and hypotension.† Symptoms generally occur within 30 minutes to 4 hours and generally resolve within 24 to 48 hours, although symptoms may persist for many days. Toxicity is characterized by headache, diaphoresis, salivation, nausea, vomiting, diarrhea, abdominal pain, hypotension, bradycardia, and shock. Syncope, respiratory depression, scotomata, paresthesias, fasciculations, muscle spasticity, hyperreflexia, vertigo, ataxia, dizziness, coma, seizures, and death may also occur. ECG findings may mimic cardiac glycoside toxicity, including repolarization abnormalities (e.g., abnormal T waves and ST segments), sinoatrial and atrioventricular blocks, and prolonged QT intervals.‡ Grayanotoxins.  Resins called grayanotoxins are found in rhododendrons, mountain laurels, and azaleas. They produce toxicity similar to that seen with the steroid alkaloids veratrum and *References 46, 49, 102, 104, 145, 165, 168, 181, 241. † References 94, 104, 108, 114, 132, 206, 213, 227, 273, 280. ‡ References 94, 114, 206, 227, 273, 280.

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aconite. They act by binding to myocardial sodium channels and increasing their permeability and by increasing vagal tone. Grayanotoxins also inhibit cardiac and respiratory actions within the central nervous system. Poisoning may result from ingestion of leaves, flowers, or nectar. Grayanotoxin-contaminated honey, termed “mad honey,” is the most common source. The nectar of Rhododendron species contains the grayanotoxin o-acetylandromedol, formerly andromedotoxin, which is transferred to humans through consumption of honey produced by bees using the plant’s nectar. “Mad honey” was reportedly used as a biologic weapon against the Romans in 67 BC. Poisonings still occur in Asia Minor. “Mad honey” is sometimes taken in hopes of sexual performance enhancement but may result in toxicity. Symptoms include diaphoresis, hypersalivation, nausea, vomiting, bradycardia, arrhythmias (AV blocks, junctional rhythms), chest pain, hypotension, shock, dizziness, syncope, circumoral and extremity paresthesias, incoordination, and muscular weakness. A patient presented with acute myocardial infarction with normal coronary arteries after “mad honey” ingestion.237 Patients generally recover in 1 to 2 days. In Korea, the blossoms of azaleas (R. mucronulatum) are used to make wine, honeyed flower juice, and griddle cakes, with reported toxicity.* Treatment.  Treatment of cardiotoxic steroid alkaloid poisoning is supportive, with attention paid to fluid and electrolyte balance. Atropine for bradycardia and vasopressors for fluid-resistant hypotension are appropriate. Victims may require mechanical ventilation and cardiopulmonary resuscitation. Magnesium may suppress early afterdepolarizations and polymorphic ventricular tachycardia. Lidocaine, procainamide, flecainide, amiodarone, and hemoperfusion have also been used to treat ventricular arrhythmias secondary to aconite poisoning in various case reports. Ventricular dysrhythmias may be resistant to cardioversion and antiarrhythmic agents. Cardiopulmonary bypass, extracorporeal membrane oxygenation, and ventricular assist device placement have been used successfully in the treatment of aconite poisoning.†

OTHER CARDIOTOXINS Taxine Alkaloids.  Taxus species include T. baccata (English yew), T. brevifolia (Western yew), T. cuspidata (Japanese yew), and T. sumatrana (Sumatra or Chinese yew). The toxic alkaloids include taxines A and B. Yew plants also contain nitriles, ephedrine, and irritant oils. All parts of Taxus plants are toxic except the pulp, or aril, which contains very little taxine. The seeds, which are surrounded by the aril, may be toxic if chewed sufficiently to allow absorption of taxine. The plant is most toxic in the winter. Taxine B, believed to be the primary cardiotoxic alkaloid, inhibits both calcium and sodium transport across cell membranes.‡ Most Taxus exposures occur in children, are accidental, and are not associated with significant toxicity. However, serious toxicity and death have occurred after intentional ingestions of Taxus species. The lethal oral dose of yew leaves is 0.6 to 1.3 g/ kg body weight. Although GI toxicity is most common, dizziness, pupil dilation, muscle weakness, altered mental status, and convulsions have also been reported. Severe toxicity is characterized by bradycardias, heart blocks, ventricular tachycardia, ventricular fibrillation, widened QRS complexes, hypotension, and cardiac arrest.§ Brugada syndrome pattern has been noted on the ECG during toxicity; it resolved with recovery.267 Hemolysis with multiorgan failure has been reported.168 Autopsies have revealed dilated cardiac ventricles and congestion of the organs with pronounced cerebral and pulmonary edema. Plant parts are often found in the stomach and small bowel on autopsy. 3,5-Dimethoxyphenol

*References 2, 53, 55, 70, 149, 159, 164, 269. † References 8, 46, 49, 53, 55, 79, 104, 108, 114, 164, 166, 181, 196, 206, 227, 241, 273, 279. ‡ References 99, 154, 162, 168, 210, 211, 257, 266, 267, 275. § References 154, 168, 178, 185, 210, 222, 257, 266, 267, 275.

CHAPTER 64  Toxic Plant Ingestions

B

A

C

FIGURE 64-22  Plants that are oral irritants. Philodendron (A), Dieffenbachia (B), Spathiphyllum (C). (Courtesy Kimberlie A. Graeme, MD.)

demonstrated by gas-chromatography-mass spectrometry of blood or urine is a marker of Taxus poisoning.99,211,272 Reported yew-induced arrhythmias in humans are consistent with arrhythmias induced by blockade of voltage-gated sodium channels. These are described as bradycardia with wide QRS complexes, despite normal electrolytes. Two patients who ingested yew presented with severe cardiotoxicity and a wide QRS complex, which appeared to respond favorably to administration of hypertonic sodium bicarbonate.178,210,222 However, sodium bicarbonate administration did not narrow the widened QRS complex of Taxus-poisoned swine.222 Because there is little risk to administering sodium bicarbonate and possible significant benefit, this treatment should be considered if widened QRS is noted. Lidocaine administration and cardiac pacing have also been reportedly beneficial for treatment of humans poisoned with yew.267

Oral and Gastrointestinal Toxins ORAL IRRITANTS (GLYCOSIDES, OXALATES) Daphne.  Coumarin glycosides produce effects similar to those of irritant glycoalkaloids of the steroid alkaloid group. The plant of significance is daphne (Daphne mezereum), with its fragrant, succulent berries. The widely cultivated daphne represents a significant risk to curious children, for whom only a few ingested berries may be lethal. The fruits contain a coumarin glycoside and a diterpene that irritate mucous membranes, with swelling of the tongue and lips. Blisters form if berries are rubbed on the skin. Severe gastroenteritis with GI bleeding may occur after ingestion. In addition, progressive weakness, paralysis, seizures, and coma may develop. Treatment is supportive. Insoluble Oxalates.  Plant exposures involving Philodendron, Dieffenbachia (dumb cane), Spathiphyllum species (peace lily) (Figure 64-22), Colocasia species (elephant’s ear, common calla) and Brassaia (octopus tree, Queensland umbrella tree) are

frequently reported.153,170,202 In Taiwan, Alocasia macrorrhiza (giant elephant’s ear, taro) commonly produces similar toxicity.168 These plants contain insoluble oxalates arranged in numerous crystalline needles of calcium oxalate (raphides) contained in specialized cells (idioblasts). When stimulated, as by mastication, idioblasts forcefully release raphides that become embedded in exposed tissues, resulting in painful oropharyngeal edema, hypersalivation, vesicle formation, dysphagia, and aphonia. These plants also contain trypsin-like proteases, histamine, and kinin-like substances that may contribute to toxicity.170,254,270 Dieffenbachia is commonly known as dumb cane because of the victim’s inability to speak after chewing the plant. Vesicle, bullae, or ulcer formation of the oral mucous membranes and esophageal erosions may be noted. Respiratory obstruction (resulting from edema) and sudden death have been reported. Treatment is supportive, with special attention to maintaining a patent airway. Severe edema and potential for airway obstruction may warrant intensive care monitoring. After massive ingestions, hypocalcemia and its effects should be anticipated. In a mass food-borne illness in Chicago, victims presented with oral burning and facial edema after lunch in an office cafeteria serving a Chinese vegetable entrée, found to contain raphides.170,202,254,270

GASTROINTESTINAL IRRITANTS (RESINS, ALKALOIDS) Gastrointestinal toxins found in plants are listed in Box 64-4. Chinaberry Trees.  Melia azedarach plants (Figure 64-23) are found throughout the southern United States and Hawaii. The chinaberry tree, also known as China tree, Texas umbrella tree, or white cedar tree, contains tetranortriterpenes (resins) identified as meliatoxins A1, A2, B1, and B2, which are enterotoxic and neurotoxic. The bark contains toosendanin. The exact mechanisms of these toxins have yet to be determined. Gastroenteritis can occur after ingestion of any part of the plant, but typically 1267

PART 7  PLANTS

BOX 64-4  Gastrointestinal Toxins Found in Plants Alkaloids • Amine (e.g., colchicine) • Isoquinoline and quinoline (e.g., emetine in ipecac) • Pyrrolizidine • Steroid (e.g., solanine) Glycosides • Coumarin • Saponin (e.g., phytolaccatoxin) Resins • Cicutoxin • Meliatoxins Phytotoxins • Abrin • Curcin • Ricin

A

B FIGURE 64-23  Chinaberry (Melia azedarach) tree (A) and berries (B). (Courtesy Kimberlie A. Graeme, MD.)

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occurs after the berries are ingested by children. Immature berries are green but turn yellow and wrinkle with age. After ingestion of as little as one berry, severe gastroenteritis may ensue, often with bloody diarrhea. In Chinese medicine, M. azedarach bark has been boiled and drank with resultant dizziness, muscle soreness and weakness, ataxia, areflexia, coma, blurred vision, ptosis, numbness, headache, nausea, vomiting, abdominal discomfort, and diarrhea that can be bloody. Mild elevation of liver enzymes and CPK, as well as hypokalemia and acidosis, have been reported. Symptoms may be rapid in onset or delayed by several hours after ingestion. Death has been reported in children after the ingestion of berries of the African variety of chinaberry tree. Fatalities are generally due to respiratory arrest. Autopsy has revealed cerebral edema, midbrain necrosis, intracranial hemorrhage, pulmonary congestion, gastrointestinal hemorrhage, yellow discoloration of the liver, and congestion of the kidneys. Treatment is supportive, with replacement of fluids and electrolytes. Tachycardia and hypotension generally respond to IV fluids.124,208 Solanum.  The genus Solanum makes up the largest group of steroid alkaloid–containing plants and includes S. tuberosum (potato), S. gracile (wild tomato), S. carolinense (horse nettle), S. pseudocapsicum (Jerusalem cherry), S. dulcamara (woody nightshade), S. americanum (black nightshade), and other nightshade plants. Solanum species are used medicinally in some countries. Solanine, a glycoalkaloid with a steroid-like moiety, has been isolated from more than 1700 different Solanum species. It is found throughout the plants but is most concentrated in unripe fruits. Solanine generally produces gastroenteritis, but bradycardia, weakness, and CNS and respiratory depression may be seen. Treatment is supportive, with replacement of fluids and electrolytes. If hypotension ensues, it generally responds to IV fluids. Atropine may be beneficial if bradycardia develops. Spontaneous recovery usually occurs in 1 to 3 days.44,61,110 Saponin Glycosides (Pokeweed).  Saponin glycosides are found throughout the plant kingdom, for example, in English ivy (Hedera helix), pokeweed (Phytolacca americana), tung tree (Aleurites species), ginseng (Panax ginseng or quinquefolium), and licorice (Glycyrrhiza glabra.)104 Saponins are GI irritants that facilitate their own intestinal absorption. Saponins may induce lysis of erythrocytes, causing hemolytic anemia. In addition, most saponins are found in combination with other toxins, resulting in diverse clinical syndromes. P. americana, or P. decandra, is most commonly known as pokeweed but is also known as Virginia poke, inkberry, pocan, pigeonberry, American cancer-root, garget, red ink, American nightshade, scoke, jalap, and redwood. It may be mistaken for horseradish, parsnip, or Jerusalem artichoke. P. americana has green leaves with red stalks. Berries are green when immature and turn deep purple with maturity. Pokeberries typically leave a purple stain. The root is the most toxic part of the plant. P. americana is ingested intentionally in pokeweed salad and pokeberry teas. When prepared for ingestion, leaves should be parboiled, which entails boiling the leaves first in water that is discarded before boiling the leaves again and rinsing them with fresh water. However, parboiling does not necessarily offer protection against toxicity.104 The saponin glycosides phytolaccatoxin and phytolaccagenin account for the GI injury, which manifests as fulminant gastroenteritis, with vomiting and diarrhea 2 to 4 hours after ingestion. Diarrhea may appear foamy from the sudsing effect of saponin glycosides. Hypotension may follow significant GI fluid losses. Severe ingestions may result in weakness, loss of consciousness, seizures, and respiratory depression.104 P. americana also contains mitogenic, hemagglutinating, and antiviral proteins. Pokeweed mitogen may induce morphologic changes in lymphocytes and plasma cells. An increased number of circulating plasmablasts and proplasmacytes, eosinophilia, and thrombocytopenia can be seen after ingestion or after handling P. americana with broken skin. Treatment for acute toxicity includes fluid replacement for dehydration secondary to GI losses. Airway support may be

B FIGURE 64-24  Castor bean plant (Ricinus communis) (A) contains ricin and is characterized by broad, serrated leaves, with fresh beans encased within a soft, thorny, red seedpod. With age, the seeds and their surrounding seedpod become brown, and the seeds develop hard shells that are difficult to penetrate (B). (Courtesy Phillip Saba, MD, and Kimberlie A. Graeme, MD.)

needed. Seizures should be treated with benzodiazepines. Hematologic changes generally resolve within weeks.104

TOXINS THAT INHIBIT PROTEIN SYNTHESIS (PHYTOTOXINS) Toxalbumins (Ricin, Abrin, Curcin, Robin, Phasin).  Toxalbumins are found in Abrus precatorius (jequirity bean, rosary pea, prayer bead), which contains abrin, R. communis (castor bean) (Figure 64-24, A), which contains ricin, Jatropha curcas (purging nut) and J. multifida, which contain curcin, and Robinia pseudoacacia (black locust), which contains robin and phasin. These toxins inhibit protein synthesis and cause cell death. These toxins are glycoproteins composed of two peptide chains, designated A and B, connected by a disulfide bond (see Figure 64-2). Chain B binds to the cell membrane. The toxin penetrates the cell by endocytosis. Chain A binds irreversibly and inactivates the ribosomes via glycosidase activity, which disrupts protein synthesis and results in cell death. Much of the toxicity is the result of endothelial cell damage, which causes increased capillary permeability, fluid and protein leakage, and edema.* Ricin poisoning results from eating or chewing on the nut or seed. Fresh, immature castor beans are encased within a soft, thorny, red seedpod. With age, the seeds and surrounding seedpod become brown, and the seeds develop hard shells that are difficult to penetrate but can be punctured by teeth (see Figure 64-24, B). The oral lethal dose is estimated to be 1 mg/ kg, theoretically as little as 1 bean in a child and 8 to 10 in an adult. After a latent period of 1 to 6 hours, nausea, vomiting, *References 6, 24, 32, 74, 76, 120, 136, 199, 212.

Treatment.  Treatment is supportive, including fluid and electrolyte replacement. Patients who remain asymptomatic for 4 to 6 hours after ingestion of seeds may be discharged, with instructions to return if symptoms develop. Laboratory follow-up for delayed liver toxicity may be appropriate. Studies indicate that ricin antibody administered intravenously shortly after exposure could be beneficial. Animal studies indicate that vaccination with abrin and ricin toxoids may offer protection against subsequent *References 32, 74, 76, 120, 199, 212.

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CHAPTER 64  Toxic Plant Ingestions

A

diarrhea, hemorrhagic gastritis, abdominal pain, thirst, dehydration, hypotension, coma, hyporeflexia, seizures, respiratory compromise, and shock may occur. Liver disease, with elevated LFTs, is common. Death may occur from dehydration and electrolyte imbalances; convulsions may precede death. Death on the third day or later is usually due to multiorgan failure. Autopsy may reveal GI tract ulcerations, necrosis of the lymph nodes and liver, nephritis, and pulmonary edema.* A discrepancy between the serious toxicity of isolated ricin exposure and the milder toxicity of ingested seeds of R. communis has been recognized. A young adult consumed 10 to 15 seeds of R. communis and experienced severe cramping abdominal pain and vomiting 4 hours after ingestion, without GI bleeding or abdominal guarding. He received IV fluids. By the third day, he had recovered completely. Other cases of oral ingestion of masticated seeds indicate that GI distress may be followed a few days later by elevated liver enzymes or hyperbilirubinemia, followed by complete recovery. In contrast, a Bulgarian broadcaster who was injected with isolated ricin died from severe gastroenteritis and multiorgan failure. Ingested R. communis is much less toxic than is parenteral ricin. The degree of mastication of castor beans may determine the degree of toxicity seen with oral ingestions. Fresh seeds are likely to be more toxic than are aged seeds that are enveloped by a hard coat. Although deaths have been reported with ingestions of a couple of seeds, toxicity is unlikely if mature seeds are swallowed whole. Furthermore, some of the toxin, which is a protein, is very likely digested in the GI tract.6,32,74,76,199 Similarly, deaths have been reported after ingestion of fresh jequirity beans (A. precatorius) if the soft, immature bean is chewed or if the hard shell of the mature bean is penetrated. The estimated human fatal dose of abrin is 0.1 to 1 mcg/kg. One-half of a seed has been reported to cause toxicity in a child, and one chewed bean could be fatal. However, as with castor beans, the mature bean shell is often not penetrated; therefore significant toxicity is not often seen. For example, a 15-month-old child ingested more than 20 jequirity beans with only minor clinical toxicity, including mild hepatomegaly and mild elevation of aspartate aminotransferase (AST).74,93,212 Symptoms generally begin within a few hours. Mild symptoms involve diarrhea alone. More severe symptoms include persistent vomiting, diarrhea, and abdominal pain, with associated hypovolemia and hypokalemia. Hemorrhagic gastritis with bloody diarrhea may ensue. Dehydration may be associated with shock and hepatorenal dysfunction. Severely ill patients may present with hyperthermia, mental status changes, and seizures. Systemic effects may be delayed as inhibition of protein synthesis occurs. Delayed effects may occur 1 to 5 days after ingestion. Terminally, elevated serum LFTs and creatinine levels may be seen, indicating hepatorenal failure. If death occurs, it is generally 3 to 5 days after ingestion and is associated with seizures, tachycardia, GI distress, mucosal changes of the GI tract (including edema and hemorrhage of the Peyer’s patches), focal necrosis and failure of the liver and kidneys, and retinal hemorrhage. Cerebral and pulmonary edema, hypertension, and pancreatitis have also been observed.6,74,93,212 Jatropha species have attractive, sweet-flavored fruit that may entice children. The presentation of toxicity may be mistaken for organophosphate poisoning, with diaphoresis, vomiting, diarrhea, obtundation, and miosis reported in one case. However, mydriasis has also been reported. Other cases have manifested with hemorrhagic gastroenteritis, hypotension, muscle spasm, and hyperpnea, as well. Leukocytosis may be noted.150

PART 7  PLANTS

abrin and ricin challenges, respectively. However, there does not appear to be cross-immunity between abrin and ricin toxoids. Toxoids and antibodies are not readily available.*

HEPATOTOXIC AGENTS Pyrrolizidine Alkaloids.  Plants containing pyrrolizidine alkaloids include Senecio vulgaris (groundsel), S. longilobus (gordolobo), S. jacobaea (tansy ragwort), S. latifolius (Dan’s cabbage or muti), Symphytum officinale (comfrey), Gynura segetum, Ilex paraguanyensis (mate), Heliotropium species, Crotalaria species (rattlebox), Amsinckia intermedia (fiddle neck or tar weed), Baccharius pteronoides, Astragulus lentiginosus, Gnaphalium, Cynoglossum, Echium, Tussilago farfara, and Adenotyles alliariae (alpendost). These plants are consumed in herbal preparations, in breads made with grains that are contaminated with pyrrolizidine-containing weeds (“bread poisoning”), and in teas. For example, Senecio and Crotalaria, which are used to make “bush tea” in Jamaica, have been associated with hepatotoxicity. Less commonly, contaminated animal meat, milk, or honey from exposed animals or bees may be the source of exposure. Pyrrolizidine alkaloids are heterocyclic compounds that act as alkylating agents and are activated in the liver, by cytochrome P450 and mixed-function oxidase systems, to form reactive pyrrolic metabolites that alkylate proteins and DNA, thereby inhibiting protein and nucleic acid synthesis. Toxicity is associated with hepatic venoocclusive disease, hepatomegaly, cirrhosis, and Budd-Chiari syndrome, which is characterized by obstruction of the trunk or large branches of the hepatic vein.100,216,219,243,248 Young victims seem more susceptible than adults. Ingestion of 10 mg of pyrrolizidine alkaloid is probably enough to produce acute or chronic venoocclusive disease. Venoocclusive liver disease is characterized by nonthrombotic occlusion of the central veins of hepatic lobules. Histologic liver findings include central vein dilation, sinusoidal congestion, centrilobular necrosis, and fibrosis. Clinical evidence of intrahepatic portal hypertension may include painful hepatomegaly, ascites, weight gain, and jaundice. Hepatic failure and death may ensue. Neonatal death secondary to hepatotoxicity has been reported after intrauterine exposure to pyrrolizidine alkaloids from an herbal preparation; neonatal ascites, skin edema, hepatomegaly, and anemia were noted. Elevated LFTs and bilirubin, as well as hyponatremia, may be noted. Occasionally, laparoscopic liver biopsy and hepatic and portal decompression are helpful in diagnosis and treatment, respectively. Treatment, including albumin infusions, diuretics, and therapeutic paracentesis, is supportive. N-acetylcysteine may reduce the toxicity. Cirrhosis and portal hypertension may be persistent.† Kava Kava.  Piper methysticum (Kava kava) is used recreationally and medicinally in Polynesia and Micronesia. Traditionally, kava extracts are prepared from kava roots macerated with water or coconut milk. Kava kava is associated with yellowing of the skin and reddening of the eyes, termed kava dermopathy, and may be hepatotoxic.101,171,

Renal Toxins Soluble Oxalates.  Soluble oxalates are found in rhubarb (Rheum rhaponticum) and sorrel (Rumex species) plants. Soluble oxalates are rapidly absorbed via the GI tract. Generalized disturbance of monovalent and divalent cation metabolism occurs. Serum ionized calcium levels may drop rapidly. Weakness, tetany, hypotension, and seizures may develop. Acute renal failure may occur if calcium oxalate precipitates in urine and obstructs the renal tubules.92,225 The structures of oxalates follow: COOH

COOK

COOH

COOH

COONa COONa

Oxalic acid

Potassium oxalate

Sodium oxalate

*References 24, 32, 74, 76, 199, 212. † References 19, 54, 100, 216, 219, 243, 244, 248, 281.

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Sodium bicarbonate lavage should be avoided because of the risk for sodium oxalate formation. IV calcium is recommended for tetany, prolonged QT interval on ECG, or depressed serum ionized calcium. Urine output should be maintained to prevent deposition of calcium oxalate crystals in renal tubules. Other Nephrotoxins.  Aloe spp. contains aloins and aloinosides and can cause parenchymatous nephritis and acute renal failure. Initially, inflammation of the gastrointestinal tract with bloody diarrhea is seen, followed by fluid and electrolyte loss. Arthralgias and palpable purpura followed by hematuria, proteinuria, renal failure, and death were reported in a man who ingested the juice extracted from four to five leaves of Aloe vera (Aloe barbadenis).30,246 Aristolocia clematitis (birthwart) contains aristolochic acid, which is nephrotoxic, producing interstitial nephropathy.246 Pithecolobium lobatum (djenkol bean) poisoning is characterized by nausea, vomiting, spasmodic pain, hematuria, and oliguria, with evidence of urinary obstruction and acute renal failure. A sulfurous odor may be noted on the breath and of the urine. Urine may contain needle-like crystals. Animal studies show acute tubular necrosis.246 Cleistanthus collinus (Vadisaaku, Oduvan) is used as a suicidal and homicidal poison in India. Fresh leaves or the extract of boiled leaves are generally consumed. C. collinus contains diphyllin glycosides, cleistanthins A and B, which are thought to be responsible for the toxicity; however, the mechanisms of action remain to be determined. Toxicity is generally not evident for 3 to 4 days. Distal renal tubular acidosis, with urinary potassium wasting and metabolic acidosis, is seen. Renal failure may ensue. Vomiting, dysrhythmias (including bradycardia), hypotension, hypoxia, acute respiratory distress syndrome (ARDS), altered mental status, and muscle weakness are also reported. Muscle weakness may manifest as dysarthria, dysphagia, pstosis, ocular palsies, and weak neck muscles leading to inability to hold up the head. Coagulopathy, elevated liver enzymes, elevated CPK, hypokalemia, hyponatremia, hyperchloremia, and urinary alkalosis have been noted. Treatment is supportive. Neostigmine and atropine have been advocated in case reports and animal studies. Mortality rates of approximately 30% are reported, despite medical care. Death is usually due to cardiac or respiratory failure.21,62,187,251

Hematopoietic Toxins PLANTS WITH ANTICOAGULANT PROPERTIES (LACTONE GLYCOSIDES) Dipteryx odoratum and Coumarouna (or Dipteryx) oppositofolia (tonka bean) were among the first historically mentioned medical sources of coumarin. Melilotus officinalis (yellow sweet clover, yellow melilot, common melilot), Asperula odorata, and Galium odoratum (woodruff) also contain significant quantities of coumarin. These coumarin-containing products have been consumed in teas. Yellow sweet clover poisoning is caused by dicumarol, a fungal metabolite produced from coumarin substrates in spoiling plants. Dicumarol interferes with the synthesis of vitamin K–dependent coagulation factors, inducing coagulopathy. Generally, this has been a problem in livestock but not humans.155,214,219

TOXINS THAT INHIBIT CELL DIVISION AND BONE MARROW Colchicine.  Colchicine toxicity can occur after ingestion of Sandersonia aurantiaca (Christmas-bells, Chinese lantern lily), Gloriosa superba (glory lily), and, more commonly, C. autumnale, all of the lily family. C. autumnale is commonly known as autumn crocus, wild saffron, meadow saffron, naked lady, naked boy, and son-before-the-father. It can be mistaken for an edible plant, such as leek, wild garlic or Bear’s garlic (Allium ursinum). C. autumnale is found in Europe, North America, and Asia. All parts of the plant contain colchicine, an amine alkaloid, but the highest concentrations are found in the underground bulb. Colchicine binds selectively and reversibly to microtubules, disrupting cell division, cell shape, mobility, and phagocytosis. Cells

Podophyllum.  Podophyllum peltatum is most commonly known as the mayapple, but has also been called American mandrake. Because of this common name, it has been occasionally confused with true mandrake (Mandragora officinarum), an unrelated plant with anticholinergic properties. Toxicity from P. peltatum exposure is caused by the glucoside podophyllotoxin. Dysosma pleiantha also contains podophyllotoxin.168 Acute toxicity after ingestion of P. peltatum may occur after a latent period of several hours, followed by GI distress and associated hypovolemia. Nervous system effects (confusion, delirium, coma, peripheral neuropathy), bone marrow depression, and multiorgan failure may ensue as a result of the antimitotic effect of podophyllotoxin. Treatment is similar to that for colchicine.98

PLANTS THAT INDUCE HEMOLYSIS Fava Beans.  Fava beans (Vicia faba) contain vicine and convicine, two metabolically inactive glycones that may be cleaved by β-glycosidase to produce divicine and isouramil. Divicine and isouramil may account for the hemolytic crisis seen in response to oxidative stress when individuals deficient in glucose-6-phosphate dehydrogenase ingest fava beans. Favism has been reported in infants who ingest breast milk from mothers who have recently ingested fava beans and in fetuses of mothers who have ingested fava beans. Clinically, favism is characterized by hemoglobinuria, anemia, and jaundice. Patients may present with complaints of malaise, weakness, lethargy, nausea, vomiting, headache, and lumbar or abdominal pain. Renal failure may ensue. Supportive care is the mainstay of treatment. Occasionally, transfusions and hemodialysis are needed.58,122,127

*References 33, 35, 64, 84, 103, 106, 142, 147, 168, 224, 246, 277. † References 33, 35, 64, 84, 106, 125, 137, 142, 147, 168, 224, 246, 277. ‡ References 33, 35, 84, 106, 125, 137, 277.

Endocrine and Metabolic Toxins PLANTS THAT INDUCE HYPOGLYCEMIA Ackee Fruit.  B. sapida, or ackee (akee) fruit trees, are indigenous to West Africa but are prevalent in the West Indies, Central America, and southern Florida. Unripe ackee fruit has a closed yellow aril that is toxic. Ripe ackee fruit, with a spontaneously opened red aril, is nontoxic. The seeds contain hypoglycin B and are toxic regardless of the maturation of the aril. Unripe ackee fruit contains hypoglycin A, or L(R,S)-2-amino-3methylenecyclopropylproprionic acid, a water-soluble amino acid that is converted to methylenecyclopropylacetyl-coenzyme A in vivo. Both compounds are hypoglycemic agents; the second is a suicide inhibitor of β-oxidation of fatty acids. Inhibition of fatty acid metabolism results in microvesicular steatosis of the liver, hyperammonemia, metabolic acidosis, and hypoglycemia. Laboratory and histopathologic findings are indistinguishable from those of Reye’s syndrome, but urine shows increased concentrations of glutaric and ethylmalonic acids after hypoglycin A exposure.18,141,175,234 Ackee fruit constitutes a traditional Jamaican breakfast and has been associated with Jamaican vomiting sickness. Ingestion of unripe ackee fruit caused an outbreak epidemic of fatal encephalopathy in West Africa, primarily affecting children ages 2 to 6 years, who experienced vomiting, hypotonia, convulsions, and coma. All children died within 48 hours of the onset of vomiting. Necropsy revealed massive liver steatosis and severe hypoglycemia. Urine concentrations of dicarboxylic acids were elevated. Similarly, an epidemic of over 100 cases occurred in Haiti, associated with vomiting, abdominal pain, loss of consciousness, convulsions, and many deaths. Hypoglycemia was noted. Carnitine derivatives, octanoylcarnitine and hexanoylcarnitine, were noted in the urine, confirming exposure to hypoglycin. Fatal ackee fruit poisoning is more common in children than in adults; adults are more likely to present with self-resolving cholestatic jaundice.141,175,183,234,235 Treatment is largely supportive and consists of securing an airway and administering IV fluids and dextrose. Before hypoglycemia was recognized, mortality rates of symptomatic unripe ackee fruit exposure approached 80%. Frequent glucose and electrolyte measurements with appropriate replacement are essential. Seizures are treated with benzodiazepines and barbiturates, remembering that serum glucose should be assessed in all seizing patients. Theoretically, riboflavin, clofibrate, glycine, methylene blue, and L-carnitine may be beneficial, although their efficacy is not established. Carnitine may facilitate transport of fatty acids into mitochondria and has been used for other toxins (e.g., valproate) that inhibit β-oxidation of fatty acids.18,156,234,235 Wild Yams.  Dioscorea spp. contain dioscorines and dioscines. They are tuberous plants, commonly known as yams, used as a staple food in Africa and Asia. The tubers are usually detoxified in running water, soaking in salt water, boiling for several hours, squeezing out the juice, and roasting. The nondetoxified plant has been used in homicide, suicide, and hunting. Central nervous system irritability with seizures, liver failure, and renal failure are seen. Hypoglycemia is reported.246 Cocklebur.  Cocklebur (Xanthium strumarium and X. spinosum) has a worldwide distribution and can be found along river banks, beaches, and lake shores. The stem is angled with red or black spots. The fruit is hard, brown, and woody; it contains two seeds that taste like sunflower seeds. The seeds and seedlings contain carboxyatractyloside, a sulfonated diterpenoid glycoside. This toxin inhibits oxidative phosphorylation and translocation of ADP and ATP across mitochondrial membranes. Carboxyatractytloside is an analogue of atractyloside, which is found in Callilepis laureola (ox-eye daisy) and Atractylis gummifera (bird-lime, blue thistle), discussed below. Drying of seeds does not diminish the toxicity. Patients present with acute abdominal pain, nausea, vomiting, diaphoresis, palpitations, drowsiness, and dyspnea, followed by respiratory depression. With severe poisoning, seizures, coma, and death may occur. Seizures may be repetitive, frequent, and 1271

CHAPTER 64  Toxic Plant Ingestions

with the highest turnover rates, such as those of the GI mucosa and bone marrow, are affected most severely. Cell arrest in metaphase and abnormal nuclear morphology are seen at autopsy; the clumps of chromatin material seen in the nuclei are called colchicine bodies.* Acute poisoning may occur after a latent period of several hours. Initial GI effects are severe abdominal pain, nausea, vomiting, diarrhea, and hemorrhagic gastroenteritis, which may result in electrolyte abnormalities, volume depletion, acidosis, shock, arrhythmias, and multiorgan failure. Muscular weakness and ascending paralysis may cause respiratory arrest, which may occur with a clear sensorium; however, patients may present comatose or convulsing. Myocardial toxicity, rhabdomyolysis, and pancreatitis have also been reported. Initially, leukocytosis may be seen, but bone marrow depression with pancytopenia may follow and may predispose to hemorrhage and infection. Autopsy reveals hypocellular bone marrow. Autopsy may also reveal diffuse vacuolization in the cytoplasma of hepatocytes and congestion of the liver, kidneys, spleen, lungs, and brain. Occasionally, hemorrhagic edema is seen. Isolated mitotic structures within the epithelium of the colon have also been reported at autopsy. Patients that survive severe toxicity may develop alopecia days to weeks after poisoning.† Because of the severity of poisoning and not infrequent lethal outcomes, aggressive decontamination should be considered. Colchicine-specific Fab antibody fragments have been developed and used with success in France for management of acute poisoning with the drug form of colchicine, but this treatment is not commercially available; therefore treatment is symptomatic and supportive. Pulmonary function tests can be used to monitor respiratory function, assessing for fatigue and progressive ascending paralysis. Assisted ventilation is used as needed. Parenteral analgesics are given cautiously to relieve severe abdominal pain, because colchicine sensitizes patients to CNS depressants. Fluid and electrolyte replacement and occasionally blood component replacement and granulocyte colony-stimulating factor (G-CSF) may be necessary. Maintain adequate urine output and assess for infection.‡

PART 7  PLANTS

difficult to treat. Patients may appear pale or with icterus and may be clammy, without pyrexia. Hepatomegaly and rhabdomyolysis may be noted. Laboratory findings may reveal elevated liver enzymes, elevated BUN and creatinine, hyponatremia, transient hyperglycemia followed by marked hypoglycemia, elevated CPK and CPK-MB, metabolic acidosis, and evidence of a consumption coagulopathy (diminished fibrinogen and prolonged prothrombin time). Electrocardiogram may show ST segment abnormalities. Death may occur within 2 days of ingestion. Autopsy findings include centrilobular hepatic necrosis, renal proximal tubular necrosis, microvascular hemorrhage of the cerebrum and cerebellum, and leukocytic infiltrates in the muscles, pancreas, lungs, and myocardium. Increased vascular permeability is suspected. No antidote is known, and treatment is supportive. Phenylbutazone, a nonsteroidal antiinflammatory drug that is generally unavailable because of its toxicity, has been shown to reduce the cytotoxic effects of carboxyatractyloside in rats.245,261 Bird-Lime/Blue Thistle.  Atractylis gummifera (bird-lime, blue thistle) is found in North Africa and the Mediterranean. It has a sugary taste and has been confused with edible wild artichoke. A. gummifera contains two poisonous glucosides: atractyloside and carboxyatractyloside. The glucosides inhibit oxidative phosphorylation, block transport of ADP at the mitochondrial membrane, and block conversion of ADP to ATP. The toxins inhibit the actions of P450 and b5 cytochromes. Clinically, headache, abdominal pain, vomiting, hematemesis, diarrhea, and dizziness are followed by liver failure, associated with jaundice and hepatitis. Seizures, coma, dysrhythmias, and renal failure may also be seen. Laboratory studies reveal hypoglycemia, metabolic acidosis, uremia, and hyperkalemia. Death is generally from multiorgan system failure. Autopsy reveals lesions, necrosis, and congestion of the liver and kidneys.120,121,245,246,261 Ox-Eye Daisy.  Callilepis laureola (ox-eye daisy, wildemagriet, impila) has been used as a medicinal plant in South Africa. It contains the poisonous glucosides, atractyloside and carboxyatractyloside. Toxicity and treatment are similar to those for cocklebur and bird-lime exposure, as discussed earlier.

PLANTS THAT INTERFERE WITH STEROID METABOLISM Licorice.  Licorice use predates the Babylonian and Egyptian empires. Its genus name, Glycyrrhiza, is derived from the Greek word for sweet root. Adverse effects with chronic ingestion of G. glabra (natural licorice) result from altered steroid metabolism. G. glabra contains glycyrrhizic acid, which is converted to 18-β-glycyrrhetinic acid in the GI tract. Both acids inhibit 11-β-hydroxysteroid dehydrogenase, an enzyme essential to the in vivo conversion of cortisol to cortisone. Excessive local cortisol binds to and activates mineralocorticoid receptors in the kidneys, producing a hypermineralocorticoid syndrome, characterized by water and sodium retention with potassium excretion. Signs and symptoms of chronic ingestion include hypertension, edema, hypokalemia, metabolic alkalosis, headache, paresthesias, weakness, paralysis, tetany, and muscle cramps. Myopathy and myoglobinuria have been reported. Heart failure, arrhythmias (e.g., torsades de pointes, ventricular fibrillation), and cardiac arrest have been attributed to licorice root ingestion. Treatment consists of discontinuing exposure to licorice, maintaining good urine output, and alkalinizing the urine of patients suffering from rhabdomyolysis. Occasionally, potassiumsparing diuretics (e.g., triamterene, spironolactone) are useful. Torsades de pointes may respond to magnesium and potassium infusions.*

CYANOGENIC PLANTS Glycosides that yield hydrocyanic acid on hydrolysis are known as cyanogenic glycosides (see Figure 64-1, online). Cyanogenic *References 20, 87, 91, 115, 139, 177, 246.

1272

glycosides include amygdalin, prunasin, linamarin, lotaustralin, and triglochinin.50 Amygdalin (D-mandelonitrile-β-D-glucoside-6β-glucoside), which is abundant in the Rosaceae family, is the cyanogenic compound found in the seeds of Malus species (apples) and pits of Prunus species, including cherries, peaches, plums, and apricots. Deaths have been reported after ingestion of apricot, apple, cherry, and other fruit seeds.226 Black or wild cherries (Prunus serotina) are considered the most dangerous. Poisonings have resulted from milkshakes that contained apricot kernels and from apricot kernels sold in health food stores as snacks.252 Linseeds (Linum usitatissimum) and cycad seeds (Cycas species) are also cyanogenic.50,220 Cassava (Manihot esculenta) contains the cyanogenic glucoside linamarin, which is rapidly hydrolyzed to acetone cyanohydrin, which breaks down into hydrogen cyanide and acetone.88,221 Both chronic and acute cyanide toxicity have been reported after ingestion of cassava. Chronic ingestion produces an upper motor neuron disease known as Konzo, or tropical spastic paraparesis. Konzo occurs after recurrent consumption of improperly prepared cassava during droughts, in areas where cassava is a staple food, such as in Africa. To remove cyanogens, roots should be soaked; however, when water is scarce, this soaking process is limited.16,17,88 Cyanide combines with and inhibits many enzymes. It possesses great affinity for the ferric iron in cytochrome oxidase of the electron transport chain, accounting for most of its toxicity (Figure 64-25). By combining with cytochrome oxidase, cyanide prevents electron transport, thereby preventing ATP production by oxidative phosphorylation. Metabolic acidosis ensues. Humans detoxify cyanide by transferring sulfane sulfur to cyanide to form thiocyanate. Numerous sulfur sources are most likely acted on by various sulfurtransferases to form the sulfane sulfur needed to convert cyanide to thiocyanate. Administration of exogenous sulfane sulfur, such as sodium thiosulfate, can greatly facilitate this detoxification.59 Clinically, GI distress, bitter almond breath, CNS changes (agitation, anxiety, excitement, weakness, numbness, hypotonia, spasticity, coma, seizures), respiratory changes (hyperpnea, dyspnea, apnea, cyanosis), cardiovascular changes (tachycardia and hypertension followed by bradycardia and hypotension, heart block, ventricular arrhythmias, asystole), and metabolic changes (anion gap metabolic acidosis) are seen. Skin color may be pink or cyanotic, and the partial pressure of oxygen may be normal in cyanide poisoning. ECG may reveal T-on-R phenomenon as a result of progressive shortening of the ST segment. Multiorgan failure and death may occur.59,168,221 Treatment.  Patients with cyanogenic glycoside poisoning may respond to treatment with 100% oxygen and cyanide antidote kits. The traditional antidote kit (Lily cyanide kit) contains amyl nitrite, sodium nitrite (3% solution given intravenously on the basis of hemoglobin and weight; generally, 300 mg in a nonanemic adult), and sodium thiosulfate (12.5 g in an adult). Red blood cell or plasma cyanide levels can be determined; however, treatment should be initiated promptly, without confirmation of exposure, in patients with evidence of toxicity. Cyanide antidote kits are designed to induce methemoglobinemia through nitrite exposure. Cyanide binds preferentially to the ferric ion of methemoglobin rather than to that of cytochrome oxidase in the electron transport chain. Forming methemoglobin limits inhibition of electron transport by cyanide and restores cellular respiration. Sodium thiosulfate in the cyanide kit provides exogenous sulfane sulfur groups that bind to cyanide and form thiocyanate. Recently available in the United States, hydroxocobalamin (Cyanokit) is also used to treat cyanide toxicity. Cyanide combines with hydroxocobalamin to form cyanocobalamin, which is excreted in the urine and bile. Sodium thiosulfate may be given in conjunction with hydroxocobalamin, with theoretical synergistic therapeutic effects. Supportive care, including mechanical ventilation, intravenous fluids, and vasopressors, may be used.59,221,252

Reproductive Toxins Plants used as abortifacients include Ruta chalepensis (ruda), Lycopodium saururus (cola de quirquincho), Petroselinum

Cyt-Fe3+

+

(Cytochrome oxidase)

(2)

Hb-Fe2+

+

(Hemoglobin) (3)

Hb-Fe3+

Na2S2O3 (Sodium thiosulfate)

Cyt-FeCN (Cytochrome oxidase-cyanide complex)

NaNO2

Hb-Fe3+

(Nitrites)

(Methemoglobin)

+

(Methemoglobin)

(4)

HCN (Hydrocyanic acid)

+

Cyt-FeCN

Hb-FeCN

(Cytochrome oxidase–cyanide complex)

(Cyanomethemoglobin)

CN (Cyanide)

Rhodanese SCN– – Oxidase

SCN– (Thiocyanate)

+

+

CHAPTER 64  Toxic Plant Ingestions

(1)

Cyt-Fe3+ (Cytochrome oxidase)

Na2SO3 (Sodium sulfate)

FIGURE 64-25  Principal steps in hydrocyanic acid poisoning and detoxification. 1, Breakdown of cellular respiration resulting from the binding of cyanide to cytochrome oxidase. 2, Conversion of the ferrous (Fe2+) form of hemoglobin to the ferric (Fe3+) form (methemoglobin) via nitrites. 3, Preferential binding of cyanide to methemoglobin, liberating cytochrome oxidase and restoring cellular respiration. 4, Providing exogenous thiosulfate to aid in formation of the less toxic thiocyanate via various sulfurtransferases, such as rhodanese. Thiocyanate is then excreted from the body. The reaction is slowly reversible via the enzyme thiocyanate oxidase, and rebound may occur.

hortense (parsley), Mentha pulegium (pennyroyal), S. longepedunculata (wild wisteria) and T. peruviana (yellow oleander). These plants generally cause significant morbidity and mortality to the women using the plants. Pennyroyal is discussed later. Yellow oleander and wild wisteria were discussed earlier.56,84

Other Toxins OILS Irritant oils, including various mustards (Brassica species), horseradish (Amoracia lapathifolia), and protoanemonin from the buttercup family (Ranunculaceae), induce gastroenteritis. Essential oils, often found in combination with resins (oleoresins), are extracted commercially for use as rubefacients, salves, and liniments. Essential oils include the following. Clove.  The toxic component of clove oil is eugenol. Near fatal hepatic failure has been reported in children ingesting as little as 10 mL of this oil.85 Eucalyptus.  The toxic component of eucalyptus oil is 1,8cineole (eucalyptol), which is derived from leaves of Eucalyptus globulus. Ingestion of eucalyptus oil is associated with diaphoresis, CNS depression (hyporeflexia, weakness, ataxia, slurred speech, agitation, confusion, coma, respiratory depression, convulsions), GI upset (vomiting, diarrhea, abdominal pain), and respiratory effects (bronchospasm, pneumonitis, pulmonary edema). Metabolic acidosis, rhabdomyolysis, hypotension, and death may occur. Fatalities have been reported after ingestion of as little as 3.5 mL and may occur as early as 15 minutes after ingestion. Topical application may also result in significant CNS toxicity. The urine may smell of eucalyptus oil, violets, or freshmown hay.11,65,256 Lavender.  Lavandula species are used to prepare an essential oil that contains linalool and linalyl acetate, and to a lesser extent, lavandulyl acetate and terpinen-4-ol. This oil can cause central nervous system depression and confusion if ingested. The scent of lavender may be noted on the breath.160 Pennyroyal.  Pulegone, a monoterpene, is the primary toxin of pennyroyal oil, which is derived from Hedeoma pulegioides or M. pulegium. Pennyroyal oil also contains several other monoterpenes. Pulegone is oxidized by hepatic cytochrome P450 enzymes to form the toxic metabolite menthofuran and other toxins. Menthofuran induces much of the hepatic and pulmonary

damage. Reactive oxidative metabolites of pulegone and menthofuran bind to target cell proteins and induce cellular damage. M. pulegium use has caused death in women using it as an overthe-counter abortifacient and death in infants given mint teas made with the plant. Hepatic and neurologic injuries are generally seen. Hepatic failure followed by shock, multiorgan failure, and death may occur after ingestion. Neurologic manifestations include dizziness, obtundation, hallucinations, seizures, and cerebral edema. Laboratory studies may reveal elevated LFTs, coagulopathies, and metabolic acidosis. Liver histology at autopsy reveals centrilobular hepatic necrosis or confluent hepatocellular necrosis. Treatment includes fluid and electrolyte replacement as needed. N-Acetylcysteine has been used for treatment because the hepatotoxicity is similar to acetaminophen-induced hepatotoxicity and is associated with glutathione depletion. Animal studies indicate that treatment with cimetidine and disulfiram may be helpful.10,13,152,253 Pine.  Pine oil is a mixture of highly lipophilic hydrocarbons obtained from the distillation of wood from pine trees. It contains the toxin 1-alpha-terpineol. Pine oil may cause skin irritation, as well as acute respiratory irritation and central nervous system depression. Autopsy has revealed hemorrhagic and necrotic lungs.174 Wintergreen.  Methyl salicylate is the methyl ester of salicylic acid, derived from Gaultheria procumbens (wintergreen). Widely used as an antirheumatic agent in the 19th century, it fell into disfavor because of its extreme side effects and availability of the more effective acetylsalicylic acid. Poisoning now occurs most often in children, who are attracted to the color, smell, and flavor of wintergreen oil. As little as 4  mL may result in fatality. Oil of wintergreen is found in herbal products, such as Koong Yick Hung Fa oil, and ingestion has caused significant toxicity. Oil of wintergreen may also produce laryngeal edema. Poisoning is identical to salicylism, including CNS excitation, hyperventilation, hyperthermia, and metabolic acidosis. Treatment is as for salicylism.28,133 Structures of salicylic acid and methyl salicylate follow: COOH

COOCH3 OH

Salicylic acid

OH

Methyl salicylate

1273

PART 7  PLANTS

Wormwood.  Wormwood oil, from the plants Artemisia absinthium and A. pontica, is used to make the emerald green liqueur absinthe, which has been ingested for its psychoanaleptic effect. Absinthe was banned because it produces neurotoxicity. Wormwood oil contains α- and β-thujone. Alpha-thujone is an antagonist at GABAA receptors. Wormwood oil may cause vomiting, vertigo, delirium, hallucinations, convulsions, coma, respiratory arrest, and death.23,73,134,198,250

Elements and Nitrates Many plants absorb or accumulate metallic compounds (selenium, molybdenum, arsenic, lead, cadmium), nitrites, and nitrates. They are generally of little importance in humans but constitute a danger to grazing livestock. However, numerous cases of

methemoglobinemia in infants ingesting vegetables high in nitrate content have been reported. Vegetables cited include spinach, beets, cabbage, and carrots grown in high-nitrate soils. A prepared fennel puree reportedly caused methemoglobinemia in infants. The infants presented with respiratory distress, tachycardia, depressed mental status, and cyanosis. Methemoglobin levels were as high as 65%. Treatment with methylene blue (2 mg/kg IV) was used successfully. The fennel puree was found to have markedly elevated nitrate levels. Nitrates are converted to nitrites in the infant gut, which then induce methemoglobinemia.143,184 Acknowledgments.  I thank Donald Kunkel, George Braitberg, Michele Adler, and Edward Geehr for their contributions to previous editions of this chapter and Phillip Saba, Daniel Brooks, Tammy Tyree, Steven Curry and Donald Kunkel for contributing photographs.

APPENDIX A 

COMMON TOXIC PLANTS Common Name

Genus

Species

Toxin

Toxic Effect

Ackee (Akee) Angel’s trumpet

Blighia Brugmansia

sapida suaveolens

Hypoglycemic Anticholinergic

Apple seeds Apricot pits Autumn crocus Azalea (see Rhododendron) Belladonna (see Deadly nightshade) Bellyache bush Betel nut Black cherry Black locust Black snake root (see Death camas) Blue cohosh Carolina jessamine (aka, yellow jessamine) Cassava (aka, manioc, tapioca) Castor bean Cherry Chinaberry tree Christmas rose

Malus Prunus Colchium

spp. spp. autumnale

Hypoglycin Atropine, hyoscyamine, hyoscine Cyanogenic glycosides Cyanogenic glycosides Colchicine

Jatropha Areca Prunus Robinia

gossypiifolia catechu serotina pseudoacacia

Curcin Arecoline, arecaine Cyanogenic glycoside Robin, robitin (glycoside)

Protein synthesis inhibition Nicotinic Cyanogenic Protein synthesis inhibition

Caulophyllum Gelsemium

thalictroides sempervirens

n-Methylcytisine, saponins Gelsemine, sempervirine

Nicotinic Psychoactive

Manihot Ricinus Prunus Melia Helleborus

esculenta communis spp. azedarach niger

Cyanogenic Protein synthesis inhibition Cyanogenic GI irritant Cardiotoxic

Coca Coral plant Daphne

Erythroxylon Jatropha Daphne

coca multifida mezereum

Day jessamine Deadly nightshade Death camas (aka, black snakeroot) Devil’s trumpet (aka, hairy thorn apple)

Cestrum Atropa Zigadenus Datura

diurnum belladonna spp. metel

Dieffenbachia (aka dumb cane) Elephant ear English bean (see Fava bean) False hellebore (aka, Indian poke) Fava bean

Dieffenbachia Colocasia

spp. antiquorum

Cyanogenic glycoside Ricin Cyanogenic glycoside Meliatoxin Hellebrin, helleborin, helleborein Ecogonine Curcin Dihydroxycoumarin, diterpene mezerein Tropane alkaloids Atropine Zygacine, zygadenine Atropine, hyoscyamine, hyoscine Oxalate, asparagine Oxalates

Veratrum Vicia

spp. faba

Veratrin

Foxglove

Digitalis

purpurea

Glory lily Golden chain (aka, golden rain) Horse bean (see Fava bean) Horse chestnut Hyacinth bean Hydrangea Inkberry (see Pokeweed) Jequirity pea (aka, rosary pea, precatory bean) Jessamine (see Carolina jessamine) Jessamines Jetbead

Gloriosa Laburnum

superba anagyroides

Digitoxin, gitaloxin, gitoxin Colchicine-like alkaloids Cytisine

Cardiotoxic Hemolytic anemia in glucose6-phosphate deficiency Cardiotoxic

Aesculus Dolichos Hydrangea

spp. lablab spp.

Aesculin Cyanogenic glycosides Cyanogenic glycosides

Coumarin glycosides Cyanogenic Cyanogenic

Abrus

precatorius

Abrin

Protein synthesis inhibition

Cestrum Rhodotypos

spp. tetrapetala

Tropane alkaloids Cyanogenic glycosides

Anticholinergic Cyanogenic

1274

Cyanogenic Cyanogenic Hematopoietic

Psychoactive Protein synthesis inhibition Coumarin glycosides Anticholinergic Anticholinergic Cardiotoxic Anticholinergic Oral irritant Oral irritant

Hematopoietic toxicity Nicotinic

Genus

Species

Toxin

Toxic Effect

Jimsonweed

Datura

stramonium

Atropine, hyoscyamine, hyoscine

Anticholinergic

Gymnocladus

dioica

Cytisine

Nicotinic

Convallaria

majalis

Cardiotoxic

Lobelia (aka, Indian tobacco) Mandrake (aka, Satan’s apple)

Lobelia Mandragora

spp. officinarum

Marijuana Mayapple Mescal bean Monkshood (aka, aconite, wolfsbane) Morning glory Mountain laurel

Cannabis Podophyllum Sophora Aconitum Ipomoea Kalmia

sativa peltatum secundiflora spp. violacea latifolia

Narcissus (see Jonquil) Night-blooming jasmine Nutmeg Oleander

Convallotoxin, convallarin, convallamarin Lobelamine, lobeline Hyoscyamine, scopolamine Tetrahydrocannabinol Podophyllotoxin Cytisine Aconitine (+)-Lysergic acid amide Andromedotoxin, arbutin, grayanotoxins

Cestrum Myristica Nerium

spp. fragrans oleander

Anticholinergic Psychoactive Cardiotoxic

Prunus Lophophora Philodendron Jatropha

spp. williamsii spp. curcas

Tropane alkaloids Myristicin Oleandrin, oleandroside, nevioside Cyanogenic glycosides Mescaline, lophophorine Oxalate Curcin

Prunus Conium Phytolacca

spp. maculatum americana

Cyanogenic glycosides Coniine, Coniceine Triterpene saponins

Cyanogenic Nicotinic GI irritant and hematopoietic toxin

Sesbania Rhododendron Rheum Senecio Urginea Ornithogalum

spp. spp. rhabarbarum longilobus maritima umbellatum

Pyrrolizidine alkaloids Grayanotoxins Oxalates Pyrrolizidine alkaloids Cardiac glycosides Cardiac glycosides, amine alkaloids

Hepatotoxic Cardiotoxic Nephrotoxic Hepatotoxic Cardiotoxic Cardiotoxic

Nicotiana Nicotiana Datura

tabacum glauca arborea

Nicotinic Nicotinic Anticholinergic

Cicuta

maculata

Nicotine Anabasine Atropine, hyoscyamine, hyoscine Cicutoxin

Thevetia Taxus

peruviana spp.

Thevetin, thevetoxin Taxine

Cardiotoxic Cardiotoxic

Jonquil (see Daffodil) Kentucky coffee tree Larkspur (see Delphinium) Lily of the valley

Peach pits Peyote Philodendron Physic nut (aka purging nut) Pigeonberry (see Pokeweed) Plum pit Poison hemlock Pokeweed (aka, pokeberry, Virginia poke, scoke, garget, inkberry, caokum, American cancer, cancer jalap) Purging nut (see Physic nut) Rattlepod (aka, scarlet, wisteria tree) Rhododendron (aka, laurel, azalea) Rhubarb Senecio (aka, threadleaf, groundsel) Squill Star of Bethlehem Strawberry bush (see Burning bush) Texas mountain laurel (see mescal bean) Tobacco Tree tobacco Trumpet lily Water hemlock Wild cherry (see Black cherry) Woody nightshade (see Nightshade) Yellow jessamine (see Carolina jessamine) Yellow oleander (aka, lucky nut) Yew

APPENDIX B 

NONTOXIC PLANTS • African violet (Saintpaulia ionantha) • Air plant (Kalanchoe pinnata) • Aluminum plant (Pilea cadierei) • Aralia, false (Dizygotheca elegantissima) • Aralia, Japanese (Fatsia japonica) • Asparagus fern (Asparagus plumosus), berry • Baby’s breath (Gypsophilia paniculata) • Baby’s tears (Helxine [or Soleirolia] soleirolii) • Begonia (Begonia rex) • Bird of paradise* (Strelitzia reginae) • Bird’s nest fern (Asplenium nidus) • Boston fern (Nephrolepsis exaltata bostoniensis) • Bromeliad family • California poppy (Eschscholzia californica)

Nicotinic Anticholinergic Psychoactive Hematopoietic toxicity Psychoactive Cardiotoxic and neurotoxic Psychoactive Cardiotoxic

Cyanogenic Psychoactive Oral irritant Protein synthesis inhibition

Convulsant

• Camellia (Camellia japonica) • Christmas cactus (Schlumbergera bridgesii) • Coffee tree (Coffea arabica) • Coleus • Coral berry* (Aechamea fulgens, Ardisia crispa) • Cornstalk plant (Dracaena fragrans) • Crape myrtle (Lagerstromea indica) • Creeping Charlie* (Pilea nummularifolia) • Crocus* (spring-blooming only) • Croton* (Codiaeum variegatum) • Dahlia • Dandelion (Taraxacum officinale) • Dogwood (Cornus) • Donkey’s tail (Sedum morganianum) • Dragon tree (Dracaena draco, Dracaena marginata) • Easter cactus (Schlumbergera bridgesii) • Easter lily (Lilium longiflorum) • Echeveria: Mexican snowball, painted lady, plush plant 1275

CHAPTER 64  Toxic Plant Ingestions

Common Name

• Emerald ripple (Peperomia caperata) • Fiddleleaf fig (Ficus lyrata) • Fig tree, weeping (Ficus benjamina) • Forget-me-not (Myosotis alpestris, Myosotis sylvatica) • Forsythia • Fuchsia • Gardenia • Geranium* (Pelargonium) • Gloxinia (Sinningia speciosa) • Grape ivy (Cissus rhombifolia) • Hawaiian ti plant (Cordyline terminalis) • Hawthorne (Crataegus), berry • Heavenly bamboo (Nandina domestica), berry • Hibiscus • Honeysuckle berry (Lonicera) • Ice plant • Impatiens walleriana • Jade plant (Crassula argentea) • Jasmine ( Jasminum rex), Madagascar jasmine • Kalanchoe: maternity plant, monkey plant, panda bear plant • Lace plant, Madagascar (Aponogeton senetralis) • Lady, lady’s slipper (Cypripedium, Paphiopedilum) • Lily of the Nile (Agapanthus) • Lipstick plant (Aeschynanthus radicans) • Maidenhair fern (Adiantum) • Marigold, African/American tall (Tagetes) • Moon cactus (Gymnocalycium) • Mother-in-law’s tongue or snake plant (Sansevieria trifasciata) • Mother of pearls (Grapetopetalum paraguayense) • Nandina berry • Natal plum (Carissa grandiflora) • Norfolk Island pine (Araucaria heterophylla) • Old man cactus (Cephalocereus senilis) • Olive tree (Olea europaea) • Orchid (Cattleya, Cymbidium, Oncidium) • Oregon grape (Mahonia aquifolium) • Palm, bamboo (Chamaedorea erumpeus) • Paradise (Howea [or Kentia] forsterana) • Parlor (Chamaedorea [or Kentia] elegans) • Sentry (Howea belmoreana) • Pansy flower (Viola) • Peanut cactus (Chamaecereus sylvestri) • Pellionia • Peony flower (Paeonia) • Peperomia • Petunia • Phlox • Piggyback plant (Tolmiea menziesii) • Pigmy date palm (Phoenix roebelenii) • Pocketbook (Calceolaria herbeohybrida) • Polka dot or freckle face plant (Hypoestes sanguinolenta)

• Prayer plant (Maranta leuconeura) • Pussy willow (Salix discolor) • Pyracantha berry • Queen’s tears (Billbergia nutans) • Rabbit’s foot fern (Davallia fejeensis) • Rainbow plant (Billbergia saundersii) • Raphiolepsis • Rattlesnake plant (Calathea insignis) • Ribbon plant (Dracaena sandriana) • Rock rose (Cistus) • Rosary pearls (Senecio rowleyanus) • Rosary vine (Ceropegia woodii) • Roses (Rosa) • Rubber plant (Ficus elastica) • Schefflera plant (Brassaia [or Schefflera] actinophylia) • Sedum • Sensitive plant (Mimosa pudica) • Silver heart (Peperomia marmorata) • Snake plant or mother-in-law’s tongue (Sansevieria trifasciata) • Snapdragon (Antirrhinum majus) • Spider plant (Anthericum, Chlorophytum comosum) • Staghorn fern (Platycerium bifurcatum) • Starfish flower (Stapelia) • String of beads* (Senecio rowleyanus and Senecio herreianus) • String of hearts (Ceropegia woodii) • Swedish ivy (Plectranthus australis) • Sword fern (Nephrolepsis cordifolia, Nephrolepsis exaltala) • Tahitian bridal veil (Gibasis geniculata, Tripogandra multiflora) • Umbrella tree (Schefflera actinophylla) • Vagabond plant (Vriesea) • Velvet plant, purple (Gynura aurantiaca) • Venus fly trap (Dionaea muscipula) • Violet (Viola) • Wandering Jew (Tradescantia albiflora) • Wandering Jew—red and white (Zebrina pendula) • Wax plant (Hoya exotica) • Yucca • Zebra plant (Aphelandre squarrosa) • Zinnia *This species has not been reported to cause illness, but other species may be toxic. Modified from “Your Guide to Plant Safety,” courtesy San Francisco Bay Area Regional Poison Center.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 65

Toxic Mushroom Ingestions  SANDRA M. SCHNEIDER AND MARK W. DONNELLY Had nature any outcast face? Could she a son condemn? Had nature an Iscariot? That mushroom— it is him. EMILY DICKINSON

Mushrooms are often considered the vermin of the vegetable world, likened to snakes, slugs, and worms. Some are regarded as mystical and others as delicacies. The locations of tasty morels 1276

are passed on from generation to generation, closely guarded from strangers. Each autumn and spring, foragers scour the woods for known delicacies and new ones untried. Some

For online-only figures, please go to www.expertconsult.com

Cap (pileus)

Spores

Annulus

Veil

Universal veil

Stipe

Button

Partial veil

Vulva

A

Immature

Mature

B

Hyphae

FIGURE 65-2  Structural characteristics (A) and life cycle (B) of mushrooms.

mushroom foragers search for “little brown mushrooms,” not for their taste, but to evoke hallucinations. Eating unidentified or misidentified species can be dangerous. In the vast majority of toxic ingestions (perhaps up to 95%), the mushroom was incorrectly identified. More than 40,000 species of fungi are currently described, with a few thousand new ones added each year. Only a few species are toxic. The fungi kingdom contains molds, smuts, rusts, mildews, yeasts, and mushrooms, which are different from plants because they lack chlorophyll. Yeasts are single-cell organisms that divide using budding. Mold is any fungus that grows with thread-like connections and a fuzzy appearance. Mildew, rust, and smut are all fungi related to mushrooms and break down vegetable matter, leaving behind a white, red, or black powder, respectively. Toadstool is often used to describe toxic mushrooms. This chapter differentiates toxic mushrooms by their toxins and scientific names. The body of a fungus is a dense network of branching filaments, or hyphae. The mushroom is the fruiting body of the fungus, containing the spores. The hyphae and mycelia generally occur in an underground network supporting the visible mushroom. Mushrooms often grow in large rings radiating from a central network of mycelia. In the past, these “fairy rings” were thought to have mythical influence (Figure 65-1, online). Recently a fairy ring in northeast Oregon has been found to occupy an area over 10 km2 (3.9 miles2). This ring is thought to be between 2000 and 8000 years old, making it the oldest and largest single organism on the planet. Fungi are largely saprophytic (i.e., growing on decaying vegetable matter), involved with the decomposition of rotting materials, usually wood. They can also be parasitic (i.e., living on another living organism, injuring the host) or symbiotic (i.e., living together with each benefiting).

Some emerge only after significant environmental changes, such as the large quantity of morels that may be found where a forest fire has recently occurred. As a mushroom emerges from the ground, it is covered with a membrane or veil (Figure 65-2). As the mushroom grows (Figure 65-3), the membrane breaks, leaving residual marks known as warts on the cap of the mushroom (Figure 65-4). These warts may remain firmly attached to the mushroom or may remain as only residual spots, depending on the species of mushroom and environmental conditions. The emerging cap takes on a shape consistent with the specific species, ranging from cylindric to convex to funnel shaped. Gills located under the cap contain the spore-producing bodies. Some gills are covered with a second membrane or partial veil, which later pulls away to form an annulus, or ring, midway down the stalk of the mushroom. Gills may be attached firmly to the stalk, sometimes running down the stalk, or only to the cap itself (free gills) (Figure 65-5). Attachment of the gills is an important aid to identification of some poisonous mushrooms, such as Amanita phalloides (Figure 65-6). The stalk (stipe) begins at the cap and ends either underground or in a cup (vulva) (Figure 65-7). A vulva at or just below ground level often is seen in a poisonous species. The stipe is generally located in the center of the cap and may or may not be tapered. The stipes of many poisonous species enlarge below the cap, ending in a bulb. The stipe may have a ringed membrane as evidence that the partial veil formerly protected the gills (Figure 65-8). Spores are produced by spore-forming bodies on the gills and expelled into the air after they mature. Spores vary in size, color, and shape but are usually unicellular. They average 5 to 10 µm in diameter. Spores are useful in identifying mushroom species (Figure 65-9 and Box 65-1). They

FIGURE 65-3  Growth of an Amanita species.

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Warts

PART 7  PLANTS

FIGURE 65-7  Death cap (Amanita phalloides). FIGURE 65-4  Warts on Amanita muscaria. (By Peter Rosbjerg from http://www.flickr.com. Used with permission.)

Attached gills

Free gills

FIGURE 65-8  Typical features of an Amanita mushroom. (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

Notched gills

Decurrent gills

FIGURE 65-5  Mushroom gill types.

can be obtained by cutting the stipe of a fresh specimen close to the gills, then laying the cap gill-side down on white paper for a few hours at room temperature. The initial color seen after removal of the gills is used for identification. With drying, the color may fade or change. Additional information about spores can be acquired by staining with Melzer’s reagent (a solution of iodine and chloral hydrate). Spores that stain blue are called amyloid, indicating the presence of starch (Figure 65-10). This technique may be particularly useful in spore identification from gastric aspirates. Spores of Amanita species are amyloid. Thinlayer chromatography of spores available from a mycology

FIGURE 65-9  Spores from a mushroom. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

laboratory, mushroom farm, or botany department is a more accurate aid to identification. There are many species of mushrooms, including several that are hunted, that have no caps, gills, or stipes. They have developed alternative methods of releasing their spores. The “puffball” mushrooms are well known by the cloud of spores they release through a pore on the top surface of their spherical fruiting BOX 65-1  Obtaining Spore Prints

FIGURE 65-6  Amanita phalloides. (Grüner Knollenblätterpilz). (By Maja Dumat from http://www.flickr.com. Used with permission.)

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1. Obtain a fresh specimen. 2. Cut off stalk close to the gills. 3. Lay cap, gill side down, on white paper for several hours at room temperature. 4. Note color of spores on paper immediately after removal of cap. Drying may alter spore appearance.

CHAPTER 65  Toxic Mushroom Ingestions

FIGURE 65-10  Spore print staining positive for amyloid.

bodies (Figure 65-11). This spore release occurs when the spores are mature and may be initiated by a falling branch, errant placement of a deer’s hoof, or the squeezing fingers of a curious child. Mushrooms are composed of approximately 90% water and 3% proteins and other nitrogen-containing compounds. The remainder is largely carbohydrate, fat, and a few vitamins. Nutritionally unimpressive, mushrooms are consumed in great quantities, primarily for their taste and texture. Wild mushrooms have the additional allure of being free. This is changing in many parts of the northwestern United States, where some species of mushroom have become so profitable that pickers have had to buy commercial permits, and gun battles have erupted over territorial disputes. Of the many varieties of wild mushrooms, few are deadly or cause serious illness. All mushrooms, including toxic ones, are safe to handle without gloves; however, hand washing after handling is strongly recommended. Many experts will even bite off and chew a small piece of mushroom to gather taste information before spitting it out. As in wine tasting, a thorough rinsing is recommended after each taste. Many immigrants fail to realize that the nontoxic mushrooms from their native lands have toxic look-alikes in America. This is particularly true of Southeast Asian immigrants, who are attracted to the large Amanita species. Entire families have been poisoned, with many fatalities. The Russian roulette played by mushroom foragers is statistically safe. Some self-proclaimed experts are simply lucky; occasionally, they are not.

Nontoxic Mushrooms The most common commercially available mushroom in the United States is Agaricus bisporus (Figure 65-12). It is cultivated in abandoned mine shafts and caves. This small white mushroom

FIGURE 65-11  Puffball mushrooms (edible).

FIGURE 65-12  Agaricus bisporus—edible.

with dark gills is often picked before the gills are fully exposed. Although the mushroom is considered nontoxic, hypersensitivity reactions and gastrointestinal symptoms have been reported. In some parts of the United States, close relatives of this common mushroom account for the largest percentage of toxic mushroom cases. Most often it causes gastrointestinal disturbance. Agaricus species may be confused with the deadly Amanita species (Figure 65-13). The popular portobello mushroom is a type of A. bisporus. A. bisporus can also be found in the wild. Nontoxic mushrooms may carry environmental toxins, such as heavy metals and pesticides. Mushrooms with high lead concentrations have been gathered near highways.34 High mercury concentrations are found in mushrooms from industrial sites.87 Many mushrooms fruit among cultivated plants and may contain toxic levels of pesticides. Human toxicity has not been reported. Fungi may cause allergic reactions. Molds that grow in damp locations in buildings have been suspected to cause a variety of patient complaints. They are one cause of the “sick building” syndrome that has resulted in some structures being vacated or demolished when the problem could not be remedied by conventional methods. Acute anaphylaxis from mushroom ingestion is rare, despite the presence of haptens capable of inciting an allergic response.57 More often, symptoms develop from inhalation of spores.74 Victims may present with anaphylaxis or, more commonly, with chronic hypersensitivity pneumonitis. Hypersensitivity reactions are described in workers exposed to cultivation of A. bisporus (the most popular commercially grown mushroom in America)63 and shiitake (Lentinus edodes), the popular Japanese mushroom (Figure 65-14).91 Asthma symptoms developed in nearly 10% of shiitake-exposed workers. In one study, all workers had positive skin and inhalation challenge tests.102 Spore counts correlate with asthma symptoms.

FIGURE 65-13  Amanita rubescens.

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FIGURE 65-14  Shiitake mushroom.

Gastroenteric symptoms after ingestion of mushrooms may not be due to toxins. Bacterial food poisoning may occur in foods that coincidentally contain mushrooms. Small bowel obstruction occurred in a person who consumed 500 g of the edible mushroom Cantharellus cibarius (chanterelle) (Figures 65-15 and 65-16; Figure 65-15, online).36 This was largely a result of poor mastication, because entire mushrooms were recovered from the victim’s intestines. Most wild mushrooms are nontoxic, and many are delicious. Morels (Morchella esculenta or deliciosa (Figure 65-17) are highly prized delicacies. Chanterelles (C. cibarius) (see Figures 65-15 and 65-16; Figure 65-15, online) and several species of Boletus (Figures 65-18 and 65-19; Figure 65-18, online) are particularly tasty. The chicken mushroom (Laetiporus sulphureus) (Figures 65-20 and 65-21; Figure 65-20, online) is often used in place of chicken in Chinese dishes. Extracts of the shiitake mushroom, L. edodes, may have antimalarial properties.121

FIGURE 65-17  Morels (Morchella esculenta).

Gastrointestinal Toxins Most toxic mushrooms fall into the group of gastrointestinal irritants. This large, heterogeneous group of mushrooms causes gastrointestinal distress, consisting of nausea, vomiting, and diarrhea, beginning 1 to 2 hours after ingestion and resolving in 6 to 12 hours. Even A. bisporus, the common cultivated mushroom, may cause brief gastroenteritis in some individuals.103 The mechanism is unknown.

CAUSATIVE MUSHROOMS A large number of unrelated mushrooms cause gastrointestinal symptoms with varying host responses (Box 65-4). Chlorophyllum molybdites (also known as Lepiota morganii) (Figure 65-22) Text continued on page 1285.

Types of Mushroom Toxicity Mushroom toxicity can be classified into several types, which are summarized in Box 65-2. Detailed discussions of each type are presented in the sections that follow. Box 65-3 provides a method for identifying what kind of mushroom may have caused a patient’s illness.

FIGURE 65-19  Boletus luridus. (By Tomasz Przechlewski from http:// www.flickr.com. Used with permission.)

FIGURE 65-16  Cantharellus cibarius (chanterelles). (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

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FIGURE 65-21  Laetiporus sulphureus. (By Carl Mueller from http:// www.flickr.com. Used with permission.)

BOX 65-3  Guide to Mushroom Identification

1. Gastrointestinal irritants 2. Disulfiram-like toxins 3. Neurotoxins Muscarinic Isoxazole derivatives Psilocybin-hallucinogenic 4. Protoplasmic Gyromitrin—hepatotoxic Amatoxin—hepatotoxic Orellanine—nephrotoxic

1. Collect any specimens left at home—preferably uncooked. 2. Collect fresh specimens from gathering site(s). 3. Transport and store mushrooms in paper bags. 4. Spores can be recovered from gastrointestinal fluid. 5. Note initial toxicity and time since ingestion. Note symptoms or lack of symptoms among others ingesting mushrooms. 6. Contact a regional poison information center for assistance in locating an expert in identification. 7. When symptoms are not consistent with identified species, consider that the victim might have ingested another type of mushroom.

BOX 65-4  Mushrooms Reported to Cause Gastrointestinal Irritation Agaricus albolutescens hondensis (Figure 65-23) placomyces silvaticus silvicola xanthodermus (Figure 65-24) Amanita brunnescens (Figure 65-25) chlorinosma flavoconia (Figures 65-26 and 65-27; Figure 65-27, online) flavorubescens (Figure 65-28) frostiana parcivolvata spissa spreta volvata Boletus luridus (see Figure 65-19) pulcherrimus satans sensibilis Chlorophyllum molybdites (Lepiota morganii) (Figure 65-29, online)

torminosus (Figure 65-35) uvidus Lepiota clypeolaria (Figure 65-36) cristata (Figure 65-37) lutea (Figures 65-38 and 65-39) morganii naucina Lycoperdon marginatum subincarnatum Morchella (Figures 65-40 and 65-41; Figure 65-41, online) angusticeps crassipes deliciosa esculenta (Figure 65-42) semilibera (Figure 65-43) Naematoloma (Hypholoma) fasciculare Omphalotus olearius illudens (Figure 65-44) olivascens (Figure 65-45) Paxillus involutus

Entoloma (Rhodophyllus) lividum nidorosum rhodopolium salmoneum (Figure 65-30) strictius vernum

Ramaria (Clavaria) formosa (Figure 65-46) gelantinosa

Cantharellus (Figure 65-31) bonari floccosus kauffmanii

Scleroderma aurantium cepa (Figure 65-49)

Hebeloma crustuliniforme fastibile mesophaeum sinapizans Lactarius chrysorrheus (Figures 65-32 and 65-33; Figure 65-33, online) glaucescens helvus representaneus rufus (Figure 65-34) scrobiculatus

Russula emetica (Figures 65-47 and 65-48; Figure 65-47, online)

Tricholoma album muscarium pardinum pessundatum saponaceum sejunctum sulphureum venenatum Verpa bohemica

CHAPTER 65  Toxic Mushroom Ingestions

BOX 65-2  Types of Mushroom Toxicity

PART 7  PLANTS FIGURE 65-22  Chlorophyllum molybdites (also known as Lepiota morganii) (By Jason Hollinger from http://www.flickr.com. Used with permission.)

FIGURE 65-23  Agaricus hondensis. (By Dan Bennett from http://www. flickr.com. Used with permission.)

FIGURE 65-24  Agaricus xanthodermus. (By Damon W. Smith from http://www.flickr.com. Used with permission.)

FIGURE 65-25  Amanita brunnescens. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

FIGURE 65-26  Amanita flavoconia. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

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FIGURE 65-28  Amanita flavorubescens.

CHAPTER 65  Toxic Mushroom Ingestions FIGURE 65-31  Cantharellus mushroom. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

FIGURE 65-30  Entoloma (Rhodophyllus) salmoneum. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

FIGURE 65-32  Lactarius chrysorrheus. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

1 cm

FIGURE 65-34  Lactarius rufus. (By aSIMULAtor from http://www.flickr. com. Used with permission.)

FIGURE 65-36  Lepiota clypeolaria. (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

FIGURE 65-35  Lactarius torminosus. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

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FIGURE 65-38  Lepiota lutea. (By Lara604 from http://www.flickr.com. Used with permission.) FIGURE 65-37  Lepiota cristata. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

FIGURE 65-39  Lepiota lutea. (By Lara604 from http://www.flickr.com. Used with permission.)

FIGURE 65-40  Morchella sp. (By Damon W. Smith from http://www. flickr.com. Used with permission.)

FIGURE 65-42  Morchella esculenta. (By Jason Sturner from http:// www.flickr.com. Used with permission.)

FIGURE 65-43  Morchella semilibera. (By Jason Sturner from http:// www.flickr.com. Used with permission.)

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FIGURE 65-45  Omphalotus olivascens. (By Nathan Wilson from http:// www.mushroomobserver.org/image/show_image/621 from http:// www.flickr.com. Used with permission.)

FIGURE 65-48  Russula emetica. (By Maja Dumat from http://www. flickr.com. Used with permission.)

is the most frequently ingested toxic mushroom in America. Most persons who ingest C. molybdites confuse it with A. bisporus, which it closely resembles. The common name for C. molybdites, green-spored parasol, describes the characteristics of this summer mushroom. The whitish cap is 10 to 40 cm (3.9 to 15.7 inches), initially smooth and round, and becomes convex with maturity. Tan or brown warts may be present. The gills are free from the stalk, initially white to yellow, and become green with maturity. The stalk is 5 to 25 cm (2 to 9.8 inches) long, smooth, and white. The ring is generally brown on the underside. Spores are green. The mushroom is common in most of eastern and southern North America and in California. In southern California, it is a common lawn mushroom. Another common mushroom causing gastrointestinal symptoms is the jack-o’-lantern (see Figure 65-44). Its botanical classification is not completely settled. Most commonly, it is referred to as Omphalotus illudens (see Figure 65-44), Omphalotus olearius, or Omphalotus olivascens (see Figure 65-45). The mushroom is a bright orange-yellow mushroom with sharpedged gills and often grows in clusters at the base of stumps or on buried roots of deciduous trees. The cap is 4 to 16  cm (1.6 to 6.3 inches) in diameter on a stalk that is 4 to 20  cm (1.6 to 7.9 inches) long. Gills are olive to orange, with white to yellow spores. The mushroom shows characteristic luminescence lasting 40 to 50 hours after collection. Members of this family are found in both eastern and western North America, generally in autumn and early spring. They may be mistaken for the edible species C. cibarius (see Figure 65-15, online). Some European reports have documented hepatic impairment and muscarinic effect following ingestion.110 It is not clear

1 cm FIGURE 65-46  Ramaria (Clavaria) formosa. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

FIGURE 65-49  Scleroderma cepa. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

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FIGURE 65-44  Omphalotus illudens. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

PART 7  PLANTS

TABLE 65-1  Gastrointestinal Irritant Mushrooms

Mistaken for Edible Species

Gastrointestinal Irritant

Edible Species

Agaricus   albolutescens   silvaticus   xanthodermus (see Figure 65-24) Amanita brunnescens (see Figure 65-25)

Agaricus bisporus

Chlorophyllum molybdites (see Figures 65-22 and 65-29; Figure 65-29, online) Entoloma species (see Figure 65-30) Hebeloma crustuliniforme Naematoloma fasciculare

FIGURE 65-50  Amanita caesarea. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

whether the mushroom and its toxins are the same on both sides of the Atlantic. Although the genus Amanita is most famous for its deadly member A. phalloides (see Figure 65-6), the genus also contains tasty nontoxic mushrooms (e.g., Amanita caesarea [Figure 65-50], Amanita calyptrata, and Amanita velosa). Several Amanita species cause gastrointestinal symptoms indistinguishable from those caused by jack-o’-lantern mushrooms or C. molybdites (see Figure 65-29, online). Amanita brunnescens (see Figure 65-25) and Amanita flavorubescens (see Figure 65-28) are frequently listed as containing gastrointestinal toxins, although they are occasionally listed as edible. Both have broad yellowish to brown caps (3 to 15 cm [1.2 to 5.9 inches]) with loosely attached warts. The stalks are 3 to 18 cm (1.2 to 7.1 inches) long, enlarging toward the base with a superior ring. A. brunnescens stains reddish brown when bruised. As with most Amanita, these mushrooms are found in summer or fall associated with hardwoods or conifers. Several members of the genus Agaricus, particularly Agaricus albolutescens, A. silvaticus, and A. xanthodermus (Figure 65-51), can cause gastrointestinal symptoms. They resemble the cultivated mushrooms in grocery stores and are found in meadows and lawns in the summer and autumn. Table 65-1 lists the lookalike toxic and nontoxic mushrooms in this group.

FIGURE 65-51  Agaricus xanthodermus. (By Damon W. Smith from http://www.flickr.com. Used with permission.)

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Paxillus involutus Ramaria formosa (see Figure 65-46) Ramaria gelatinosa Scleroderma aurantium Tricholoma pessundatum Omphalotus olearius (see Figure 65-44)

Amanita flavorubescens (see Figure 65-28) Amanita inaurata (Figure 65-52) Lepiota species (Figure 65-53) Agaricus bisporus (see Figure 65-12) Pluteus cervinus Entoloma abortivum Rozites caperata (Figure 65-54) Armillaria mellea (Figures 65-55 to 65-58) Naematoloma sublateritium Naematoloma capnoides Lactarius species (Figure 65-59) Ramaria species Lycoperdon perlatum (Figure 65-60) Cantharellus cibarius (see Figure 65-16) Laetiporus sulphureus (see Figure 65-21) Armillaria mellea (see Figures 65-55 to 65-58)

TOXINS A variety of toxins have been extracted from these mushrooms, although their structures are poorly described. Most are protein based and heat labile, although toxicity may not be completely eliminated with cooking. In some cases the toxin may be destroyed by heating (temperature and duration vary by species), parboiling, or even preserving in salt. Host response to a toxin

FIGURE 65-52  Amanita inaurata. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

FIGURE 65-54  Rozites caperata. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

FIGURE 65-55  Armillaria mellea. (By Nathan Wilson from http://www. mushroomobserver.org/image/show_image/621 from http://www. flickr.com. Used with permission.)

FIGURE 65-56  Armillaria mellea. (By Maja Dumat from http://www. flickr.com. Used with permission.)

1 cm

FIGURE 65-57  Armillaria mellea. (By Jason Hollinger from flickr.com. Used with permission.)

FIGURE 65-58  Armillaria mellea. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

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1 cm FIGURE 65-53  Lepiota species—some are toxic.

PART 7  PLANTS

BOX 65-5  Treatment of Gastrointestinal Irritant

Mushroom Ingestion

1. Note time since ingestion. If more than 2 hours between ingestion and symptoms, a more serious protoplasmic toxin ingestion may have occurred. Monitor liver transaminases. 2. Provide fluid and electrolytes replacement. 3. Provide antiemetic and antidiarrheal medications as needed.

FIGURE 65-59  Lactarius sp. (By Maja Dumat from http://www.flickr. com. Used with permission.)

varies; some persons can eat such mushrooms without harm, whereas others become quite ill. Some mushrooms also contain hemolysins and toxins that cause hemorrhage and hepatitis in animals.58,106 Human hemolysis has not been reported.58

CLINICAL PRESENTATION Within 1 to 2 hours of ingestion of these mushrooms, nausea, vomiting, intestinal cramping, and diarrhea develop. Stools are usually watery and occasionally bloody with fecal leukocytes. Chills, headaches, and myalgias may occur. Symptoms remit spontaneously in 6 to 12 hours. Most victims require only fluid and electrolytes replacement. A few serious cases reported in the literature have been associated with severe dehydration. In a review of 106 cases, all victims responded well to fluid and electrolyte replacement and occasional antiemetic or antidiarrheal medications.21 Admitted patients were discharged in an average of 2 days. Persons whose symptoms are delayed (beginning 4 hours or more after ingestion) probably have ingested a more toxic mushroom, possibly Amanita, Galerina, Lepiota, or Gyromitra. Those who ingest these more toxic mushrooms present with very severe gastrointestinal distress and may develop hepatic failure. Recent reports of ingestion of jack-o’-lantern mushrooms describe mildly elevated liver transaminases.110 Cases of metabolic acidosis and dehydration, and even death, are attributed to C. molybdites (see Figure 65-22).14,105

antiemetic such as prochlorperazine, 5 mg IV or 10 mg intramuscularly (IM), may prevent further emesis, although there is no evidence for its use. If patients present within 1 hour of ingestion and vomiting has not occurred, activated charcoal (1 g/kg) without cathartic is given orally or through a nasogastric tube. There is no evidence, however, that its use decreases toxicity. Once vomiting starts, charcoal is likely useless. Although antimotility drugs are often given, there is no evidence that they are effective. Most cases are self-limited. Care should be taken not to dismiss early gastrointestinal symptoms when several types of unknown mushrooms have been ingested. Individuals may ingest both gastrointestinal irritant mushrooms and mushrooms containing serious toxins. Persons with prolonged gastroenteritis from unidentified mushrooms should be observed for 24 to 48 hours for development of delayed hepatic damage. Special efforts should be made to identify the ingested mushrooms.

Disulfiram-Like Toxins A fascinating toxicity is caused by some members of the Coprinus genus, known as “inky caps” (Figures 65-61 and 65-62; Figure 65-61, online). Individuals who ingest these mushrooms and subsequently ingest alcohol have symptoms similar to those of an alcohol-disulfiram (Antabuse) reaction.

CAUSATIVE MUSHROOMS Several members of the Coprinus genus may contain disulfiramlike toxins (Box 65-6), but symptoms are most common with Coprinus atramentarius. The mushroom has a 2- to 8-cm (0.8- to 3.1-inch) cylindric cap on a thin 4- to 5-cm (1.6- to 2-inch) stalk. The cap is white or occasionally orange or yellow at the top.

TREATMENT Treatment is largely supportive (Box 65-5) and does not depend on the type of mushroom ingested. Intravenous (IV) fluid and electrolytes replacement may be required. In a severe case, an

FIGURE 65-60  Lycoperdon perlatum. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

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FIGURE 65-62  Coprinus sp. (By Damon W. Smith from http://www. flickr.com. Used with permission.)

BOX 65-7  Treatment of Coprine Toxicity (Disulfiram-

Coprinus (Figure 65-63) atramentarius comatus (see Figures 65-61 and 65-62; Figure 65-61, online) insignis micaceus

1. Generally requires only supportive care. 2. Hypotension responds to fluid or, if necessary, intravenous norepinephrine (2 to 4 mcg/min or 0.05 to 0.1 mcg/kg/min in children, increasing as needed every 5 to 10 minutes). 3. Severe symptomatic supraventricular tachycardia can be controlled with intravenous propranolol (0.5 to 3 mg in adults, or in children 0.01 to 0.02 mg/kg up to a maximum of 1 mg per dose, repeated after 5 to 10 minutes as needed).

to Cause an Alcohol-Disulfiram Reaction

Clitocybe clavipes (Figure 65-64)

The mature cap often develops cracks, which turn up at its margins. The cap blackens as it matures and then liquefies into the “inky cap.” A ring may be present low on the stalk. Spores are black. C. atramentarius grows throughout North America in clusters of three or more in grass or wood debris. It often appears overnight after a rain. Several members of the Coprinus genus, including C. atramentarius, are edible if no alcohol is ingested for the next 72 hours.

Like Toxin)

TOXIN Mushrooms causing a disulfiram reaction contain the toxin coprine, first isolated from the mushroom C. atramentarius in 1975.43 Coprine is distinct from disulfiram and is most likely a derivative of glutamine. It probably is not present in the raw mushroom, but rather a hydrolyte created during cooking.61 Coprine (or its derivative L-aminocyclopropanol) inhibits acetaldehyde dehydrogenase, similar to the action of disulfiram. Acetaldehyde accumulates, leading to flushing, diaphoresis, headache, tachycardia, nausea, and vomiting. Some clinicians believe that coprine is a relatively poor inhibitor of acetaldehyde dehydrogenase and suggest that symptoms result from altered neurotransmitter levels.76

CLINICAL PRESENTATION A history of wild mushroom ingestion within days before symptoms is rarely offered. Ingestion of the mushroom imparts sensitivity to alcohol, which begins 2 to 6 hours after ingestion and may last up to 72 hours. Within 15 to 30 minutes of subsequent alcohol ingestion, the victim experiences severe headache, flushing, and tachycardia. Hyperventilation, shortness of breath, and palpitations may occur. Chest pain and orthostatic hypotension occur in severe cases. Symptoms can be confused with an allergic reaction or acute myocardial infarction. Symptoms resolve spontaneously within 3 to 6 hours.

TREATMENT

FIGURE 65-63  Coprinus sp. (By Jason Hollinger from http://www.flickr. com. Used with permission.)

Supportive and symptomatic treatments are suggested (Box 65-7). Because these symptoms may have other, more severe causes, baseline laboratory tests (blood urea nitrogen [BUN], creatinine, electrolytes, and glucose) should be drawn. Urine output should be monitored. IV fluids should be given to keep urine output at 50  mL/hr (in children 1  mL/kg/hr). Activated charcoal is not beneficial. Charcoal does not adsorb alcohol, and the coprine has already been absorbed by the time the reaction occurs. Hypotension generally responds to IV fluid administration. Severe hypotension refractory to fluid replacement should be treated with norepinephrine (initially 2 to 4  mcg/min; 0.05 to 0.1  mcg/kg/min in children and increased as necessary); norepinephrine stores are depleted in a true disulfiram reaction. Propranolol (0.5 to 3  mg  IV; 0.01 to 0.02  mg/kg  IV up to 1  mg in children) is used for severe symptomatic supraventricular tachycardia. Propranolol may be repeated as needed after 5 to 10 minutes.

Neurologic Toxins MUSCARINE

FIGURE 65-64  Clitocybe mushrooms—some are toxic.

Muscarine was first isolated from the mushroom Amanita muscaria (Figures 65-65 to 65-69; Figures 65-66, 65-68, and 65-69, online) more than 150 years ago. A classic muscarinic reaction includes salivation, lacrimation, urination, diaphoresis, gastrointestinal upset, and emesis (SLUDGE syndrome). Buddhist adepts may have used A. muscaria in the second to ninth centuries to achieve enlightenment.40 1289

CHAPTER 65  Toxic Mushroom Ingestions

BOX 65-6  Mushrooms Suspected of Causing or Reported

PART 7  PLANTS

FIGURE 65-70  Inocybe mushrooms—some are toxic.

FIGURE 65-65  Amanita muscaria. (By Kevin L. Cole from http://www. flickr.com. Used with permission.)

Causative Mushrooms A. muscaria (see Figures 65-65 to 65-69; Figures 65-66, 65-68, and 65-69, online) has a cap 5 to 30 cm (2 to 11.8 inches) in diameter that is scarlet red with white warts. The stalk tapers upward and is white, often hollow, and grows 15 to 20 cm (5.9 to 7.9 inches) in length. It has a prominent vulva and numerous rings. Gills are free and white, as are the spores. The mushrooms grow in eastern North America and throughout much of the western United States, often near Boletus edulis. They grow under hardwoods and conifers from summer to autumn. Potentially toxic amounts of muscarine are found in some Inocybe (Figure 65-70) and Clitocybe mushrooms (Figure 65-71, Box 65-8 and Table 65-2; see also Figure 65-64). Inocybe mushrooms (see Figure 65-70) are small brown mushrooms with conical caps up to 6 cm (2.4 inches) in diameter. Stalks are 2 to 10 cm (0.8 to 3.9 inches) long, covered with fine brown to white hairs. Gills are brown and notched; spores are brown. They are found typically under hardwoods and conifers in the summer and fall. All members of this family are considered poisonous.

FIGURE 65-67  Amanita muscaria. (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

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In contrast, many Clitocybe mushrooms (see Figure 65-64) are edible, but except for Clitocybe nuda and its close relatives, they are not worth pursuing. A few contain muscarine. All Clitocybe mushrooms are whitish-tan to gray mushrooms with caps 15 to 33 mm (0.6 to 1.3 inches) long on hairless stalks 1 to 5 cm (0.4 to 2 inches) long. Gills are decurrent (run down the stalk), and spores are white. They are usually single specimens (not clustered) found on lawns in the summer and fall. Many Inocybe and Clitocybe mushrooms contain larger concentrations of muscarine than does A. muscaria. Other toxins (e.g., ibotenic acid) are present in A. muscaria and contribute to its toxicity. Toxin Muscarine is a quaternary trimethyl ammonium salt of 2-methyl3-oxy-5-(amino) tetrahydrofuran. Muscarine stimulates postganglionic cholinergic receptors (muscarinic receptors), mimicking the action of acetylcholine. Muscarine stimulation of the gastrointestinal tract leads to increased secretory activity, contraction amplitude, and peristalsis. Stimulation of the urinary tract leads to bladder contraction and increased peristalsis of the ureters. Stimulation of secretory tissue leads to salivation and lacrimation. Bronchoconstriction, flushing, and diaphoresis result from additional stimulation of bronchial and vascular tissues. Cardiac effects include reflex tachycardia, or more often bradycardia and decreased atrioventricular conduction. Central nervous system (CNS) effects include headache, ataxia, and visual disturbances. The sensorium is generally not affected (except in ingestion of A. muscaria, which contains other CNS toxins).

FIGURE 65-71  Clitocybe sp. (By Damon W. Smith from http://www. flickr.com. Used with permission.)

Containing Muscarine

Amanita gemmata muscaria (see Figures 65-65 to 65-69; Figures 65-66, 65-68, and 65-69, online) pantherina (Figure 65-72) parcivolvata Boletus calopus luridus pulcherrimus satanas Clitocybe (see Figures 65-64 and 65-71) aurantiaca dealbata nebularis

FIGURE 65-72  Amanita pantherina. (By Maja Dumat from http://www. flickr.com. Used with permission.) 5 mm

Hebeloma crustuliniforme Inocybe (see Figure 65-70) fastigiata geophylla napipes patouillardii pudica Mycena pura (Figure 65-73) Omphalotus (see Figure 65-44) olivascens (see Figure 65-45) olearius illudens (see Figure 65-44)

Clinical Presentation Symptoms develop within 15 to 30 minutes after ingestion of muscarine-containing mushrooms. Typical symptoms include salivation, urination, lacrimation, diarrhea, diaphoresis, abdominal pain, nausea, and emesis. Bradycardia, bronchospasm, and constricted pupils are also noted. Copious bronchial secretions may cause respiratory failure requiring mechanical ventilation. Symptoms remit spontaneously in 6 to 24 hours. In Europe, some deaths are reported from Inocybe patouillardii.61 Although this mushroom is rarely eaten, ingestion carries a mortality rate of 6% to 12%, particularly among persons with preexisting pulmonary or cardiac disease. Most deaths occur within the first 12 hours as a result of respiratory failure or cardiovascular collapse.

FIGURE 65-73  Mycena pura. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

Treatment Treatment is outlined in Box 65-9. Many victims require supportive care with oxygen, suctioning, and IV fluid replacement. Activated charcoal and cathartics are rarely given because of the prominent emesis and diarrhea. Atropine is a muscarine antagonist but should be used only to control secretions or profound bradycardia. It should not be given prophylactically or for nonsymptomatic bradycardia because it may worsen the delirium, ataxia, and hallucinations induced by A. muscaria. Atropine is dosed at 0.01 mg/kg IV for children and 1 mg IV for adults. When secretions are life threatening, that initial dose may be TABLE 65-2  Look-Alikes of Mushrooms Causing

Muscarine Poisoning

Toxic Species

Edible Species

Clitocybe dealbata Inocybe species (see Figure 65-70)

Marasmius oreades (Figure 65-74) Marasmius oreades (see Figure 65-74)

FIGURE 65-74  Marasmius oreades. (By Becky Dewdney-York from http://www.flickr.com. Used with permission.)

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BOX 65-8  Mushrooms Reported or Suspected of

PART 7  PLANTS

BOX 65-9  Treatment of Muscarinic Toxicity 1. Supportive care with oxygen, suctioning, and endotracheal intubation as needed. 2. Fluid and electrolyte replacement. 3. Atropine (if symptoms are life threatening) 0.01 mg/kg intravenously every 5 to 10 minutes until secretions are controlled. There is no upper limit to the dose if secretions are excessive. Atropine may worsen central nervous system effects of some mushrooms such as Amanita muscaria.

BOX 65-10  Mushrooms Reported or Suspected of

Containing Ibotenic Acid, Muscimol, and Related Compounds

Amanita cokeri gemmata muscaria (see Figures 65-65 to 65-69; Figures 65-66, 65-68, and 65-69, online) pantherina (see Figure 65-72) Panaeolus campanulatus Tricholoma muscarium

FIGURE 65-75  Amanita rubescens. (By Danel Solabarrieta from http:// www.flickr.com. Used with permission.)

doubled on subsequent doses. There is no upper limit on the dose of atropine if secretions are severe and potentially life threatening. Symptoms resolve spontaneously within 24 hours.

ISOXAZOLE REACTIONS The isoxazole derivatives ibotenic acid and muscimol produce CNS symptoms, including excitement and alteration in visual perception. Causative Mushrooms Several mushrooms contain ibotenic acid (Box 65-10 and Table 65-3). A. muscaria is described previously. Amanita pantherina (see Figure 65-72) is 5 to 15 cm (2 to 5.9 inches) long with a cap 5 to 15 cm (2 to 5.9 inches) in diameter. The cap is generally white to pink in the young specimen but becomes reddish brown or brown, often darker at the rim, with maturity. Fragments of the universal veil form warts on the cap but may be washed off by rain. The stalk has a distinct ring, with a vulva at the bottom. When the flesh is cut or injured (e.g., by insect larvae), it develops a pinkish tinge. Gills are free and produce white spores. The raw mushroom has little smell and tastes very much like a raw potato. It grows from June to November in woodlands throughout North America. A. muscaria and A. pantherina have been identified for sale in markets in Japan and elsewhere.

Toxin Ibotenic acid is found in the bright red cap of A. muscaria and undergoes decarboxylation during drying to form muscimol, which is more toxic than ibotenic acid. The potency of the cap remains high despite drying. Muscimol is a γ-aminobutyric acid (GABA) receptor agonist.47 Muscimol increases CNS serotonin levels and decreases catecholamine levels. Ibotenic acid resembles GABA and in animals can act as does GABA. Liquid chromatography can identify these compounds.71,108

TABLE 65-3  Look-Alikes of Mushrooms Containing

Isoxazole Toxins

Toxic Species

Edible Species

Amanita muscaria (see Figures 65-65 to 65-69; Figures 65-66, 65-68, and 65-69, online)

Amanita caesarea (see Figure 65-50) Amanita rubescens (see Figure 65-13) Armillaria mellea (see Figures 65-55 to 65-58) Russula species (see Figures 65-47 and 65-48; Figure 65-47, online) Amanita rubescens (Figures 65-75 and 65-76)

Amanita gemmata Amanita pantherina (see Figure 65-72)

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FIGURE 65-76  Amanita rubescens. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

TABLE 65-4  Look-Alikes of Mushrooms Containing

1. Supportive care. 2. Sedation as needed with benzodiazepine (diazepam 2 to 5 mg IV every 10 minutes as needed) or phenobarbital (30 mg IV hourly). 3. If hyperpyrexia occurs (primarily seen in children), consider external cooling.

Toxic Species

Edible Species

Panaeolus foenisecii (see Figure 65-80)

Psathyrella candolleana (see Figure 65-81) Agrocybe pediades Marasmius oreades (see Figure 65-74) Coprinus species (see Figures 65-61 to 65-63; Figure 65-61, online)

Psilocybin Toxin

Psilocybin or Psilocin

Panaeolus species (see Figure 65-80)

IV, Intravenously.

Clinical Presentation Ingestion of 10 mg of A. muscaria produces mild intoxication, dizziness, and ataxia. Ingestion of 15 mg leads to pronounced ataxia and visual disturbances.37,70 Delirium or manic behavior may develop. Physical activity is accelerated, with inability to judge size. Visual hallucinations, seizures, and muscle twitching are common. Some victims complain of residual headache for up to 48 hours. Symptoms begin within 30 minutes of ingestion and generally last 2 hours. Rare fatalities have been reported. Some people have ataxia and paralysis of ocular convergence.37 In rare cases, symptoms last as long as 48 hours, depending on the dosage and individual host effect. There is a case report of psychosis lasting 5 days following ingestion of A. muscaria.11 Ingestion of A. pantherina produces similar symptoms. In severe cases seizures and CNS depression are observed,92 and very rarely, death.80

support and ventilatory assistance should be immediately available. Atropine may worsen the hallucinations, agitation, and delirium associated with isoxazole derivatives and should therefore be withheld unless the secretions or bradycardia are life threatening.

Treatment Treatment consists of supportive care (Box 65-11). Emesis caused by the toxin is unusual. Gastric emptying and charcoal administration are difficult because of CNS disturbances and have no proven effectiveness. Therefore these are not recommended. Appropriate sedation with phenobarbital (30 mg IV hourly in adults, 0.5 mg/kg in children) or diazepam (2 to 5 mg IV repeated every 10 to 15 minutes in adults as needed, 0.1 to 0.3 mg/kg IV in children) is often necessary but requires caution. Phenobarbital or diazepam administered to treat A. muscaria ingestion may lead to unexpected apnea, flaccid paralysis, or both. Airway

Causative Mushrooms The most common hallucinogenic mushrooms are species of the Psilocybe genus (Box 65-12 and Table 65-4), which includes more than 100 species, not all of which cause hallucinations. These are “little brown mushrooms” (LBMs) (Figure 65-82). The cap is 0.5 to 4 cm (0.2 to 1.6 inches) in diameter (depending on the species), is usually smooth, and becomes sticky or slippery when wet. The stalk is slender and 4 to 15 cm (1.6 to 5.9 inches) long. Gills are gray to purple gray; spores are dark, nearly black. The flesh of these mushrooms often turns blue or greenish when bruised or cut. The mushrooms are often mistaken for more poisonous species (e.g., Galerina [Figure 65-83] or Inocybe [see Figure 65-70]). These mushrooms also resemble A. bisporus. Regular grocery store mushrooms laced with lysergic acid

HALLUCINOGENIC MUSHROOMS Perhaps the most sought-after mushrooms are “magic mushrooms,” which are available as whole mushrooms in the wild, and as spores (to grow your own) through mail-order catalogs. These mushrooms have been used for centuries for their hallucinogenic effects. Small stone mushroom icons believed to be 3500 years old were found in Meso-American ruins.61 Honey laced with Psilocybe can be purchased at Dutch coffee shops.

BOX 65-12  Mushrooms Reported or Suspected

of Containing Either Psilocybin or Psilocin   or Both

Amanita citrina (Figures 65-77 and 65-78) porphyria Conocybe cyanopus siligineoides smithii

foenisecii (Figure 65-80) phalaenarum semiovatus sphinctrinus subbalteatus Psathyrella sepulchralis

Naematoloma Popperianum

Psilocybe baeocystis caerulescens caerulipes cyanescens cubensis pelliculosa semilanceata strictipes stuntzii

Panaeolus campanulatus castaneifolius cyanescens fimicola

Stropharia aeruginosa coronilla hornemannii squamosa

Gymnopilus (Figure 65-79) aeruginosus purpuratus spectabilis validipes

FIGURE 65-77  Amanita citrina. (By Tomasz Przechlewski from http:// www.flickr.com. Used with permission.)

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BOX 65-11  Treatment of Isoxazole Toxins or

PART 7  PLANTS FIGURE 65-78  Amanita citrina. (By Tomasz Przechlewski from http:// www.flickr.com. Used with permission.)

diethylamide (LSD) or other hallucinogens are sold on the street as Psilocybe. Hallucinogenic mushrooms grow in a variety of habitats and are found throughout the world. Other mushrooms, including members of the Panaeolus (see Figure 65-80) and Gymnopilus genera (see Figure 65-79), may contain psilocybin. Panaeolus mushrooms are also LBMs about the same size as Psilocybe. Gills are dark gray or black with black spores. They grow on dung throughout the tropics and subtropics of North America. Unlike Psilocybe, their caps do not become sticky or slippery when wet. The hallucinogenic effect and quantity of toxin varies among Panaeolus species. Some Gymnopilus species (e.g., Gymnopilus aeruginosus) contain hallucinogens. These medium-sized mushrooms (cap 5 to 15 cm [2 to 5.9 inches]; stalk 5 to 12 cm [2 to 4.7 inches]) are variable in color (green, yellow, salmon, and red), with yellowish gills and rusty spores. They grow on stumps or sawdust in the Pacific Northwest. Visual hallucinations and ataxia were reported in a person ingesting L. sulphureus (see Figures 65-20 and 65-21; Figure 65-20, online), previously thought to be harmless.2 It is not clear whether this mushroom contained hallucinogenic material or the individual ingested an additional mushroom.

FIGURE 65-79  Gymnopilus mushroom—some are toxic.

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FIGURE 65-80  Panaeolus foenisecii. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

Toxin Psilocybin and its somewhat unstable metabolite psilocin are indole compounds derived from tryptamine. These two toxins were first isolated by Albert Hofmann,45 known as the father of LSD. Chemically the toxins resemble 5-hydroxytryptamine and LSD and have similar effects. They maintain their potency in dried specimens. Psilocybin, as well as LSD, inhibits the firing rate of serotonindependent neurons, particularly at the presynaptic receptors. It induces euphoria, hallucinations, and loss of time sensation. Many of these symptoms are similar to those seen with LSD. Some species contain phenylethylamine, which may be responsible for tachycardia and other adverse reactions.4 In human volunteer studies, peak plasma levels were reached at 105 minutes.42 Clinical Presentation Ingestion of 5 mg of psilocybin (10 mg of fresh Psilocybe cubensis) causes moderate euphoria. Ingestion of 10 mg leads to hallucinations and loss of time sensation. Heightened imagination occurs within 15 to 30 minutes of ingestion. Hallucinations may

FIGURE 65-81  Psathyrella candolleana. (By Jason Hollinger from http://www.flickr.com. Used with permission.)

FIGURE 65-82  Psilocybe caerulipes.

Treatment Recommendations are similar to those for isoxazole toxin (see Box 65-11). Initially the victim should be placed in a quiet supportive environment. Gastric emptying and activated charcoal administration are often impossible and may only enhance hallucinations. These modalities should be considered in victims with very large ingestions who are brought early for treatment. Sedation can be accomplished when necessary with a benzodiazepine (diazepam, 0.1 mg/kg IV in children, or 2 to 5 mg IV in adults, repeated every 5 minutes as needed), phenobarbital (0.5 mg/kg IV in children, 30 mg IV in adults, repeated every 60 minutes as needed), chlorpromazine (50 to 100 mg IM), or haloperidol (5 mg IM). There is no evidence for the use of newer antipsychotic medications. Seizures can be controlled with diazepam in the doses just listed. Hyperpyrexia, seen primarily in children, is best treated with external cooling.

Protoplasmic Poisons GYROMITRA TOXIN

FIGURE 65-83  Galerina marginata. (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

False morels (Gyromitra esculenta [Figure 65-84]) were once thought to be edible. During times of famine in Europe, ingestion of Gyromitra was encouraged.41 Since 1793, these mushrooms have been suspected of causing toxicity and since World War II, have been known to cause hepatic failure, neurologic symptoms, and death. Today they are collected, sold fresh, canned, and exported (“morschels”) in eastern and central Europe (Figure 65-85, online).72 Symptoms appear 4 to 50 hours (usually 5 to 12 hours) after ingestion, with timing similar to that of A. phalloides poisoning. Gyromitra grows primarily in the spring and A. phalloides in the fall. Because of this difference in seasons and their distinct appearance, the identity of the two mushrooms is rarely confused. Causative Mushrooms G. esculenta (Figure 65-86) is approximately 5 to 16 cm (2 to 6.3 inches) in height with a reddish-brown to dark brown, irregularly shaped cap. The cap’s surface is curved and folded, resembling a brain. The stalk is often as thick as the cap. The insides of the cap and stalk are hollow. This mushroom grows in the spring near pines and in sandy soil throughout North America. It is particularly common in Germany, Poland, and other eastern European countries. Mature species, particularly those with cap

FIGURE 65-84  Gyromitra esculenta, which contains the hepatoxin gyromitrin. (From Phillips R: Mushrooms of North America, Boston, 1991, Little, Brown.)

FIGURE 65-86  Gyromitra esculenta. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

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CHAPTER 65  Toxic Mushroom Ingestions

last for 4 to 6 hours. Serious side effects are rarely seen, but fever and seizures have been reported in children.68 Up to 50% of victims have tachycardia and hypertension.81 Ingestion resulting in myocardial infarction has been reported.8 Flashbacks have been reported to occur in some victims for up to 4 months after ingestion.6 Multifocal cerebral demyelination has been reported after ingestion of psilocybin-containing mushrooms.104

PART 7  PLANTS

TABLE 65-5  Look-Alike of Mushrooms Containing

Gyromitrin

Toxic Species

Edible Species

Gyromitra esculenta (see Figure 65-86)

Morchella esculenta (see Figures 65-40 to 65-42; Figure 65-41, online)

decay, may have increased toxicity. These mushrooms may be mistaken for morels, which are considered among the most delicious of wild mushrooms (Table 65-5). Other members of the Gyromitra family contain gyromitrin. None of these mushrooms has been reported to cause toxicity in humans. Toxin Gyromitrin (N-methyl-N-formylhydrazone) was first isolated in 1967. This toxin is moderately volatile and heat sensitive. Cooking the mushrooms thoroughly and discarding the cooking liquid may decrease or eliminate the toxin. Symptoms have occurred despite proper cooking. Once gyromitrin enters the stomach, hydrolysis yields Nmethyl-N-formylhydrazine (MFH), which forms N-methylhydrazine or monomethylhydrazine (MH),72 a component of rocket fuel. MH is a competitive inhibitor of pyridoxal phosphate, which interferes with enzyme systems (including decarboxylases, deaminases, and transaminases) requiring pyridoxine as a cofactor.3 As a result, levels of GABA fall, interfering with neurotransmission.56 It is believed that this decrease in GABA leads to altered mental status, seizures, or both. Recent questions have been raised about this widely accepted theory, because MH may cause seizures without a change in brain GABA levels.67 MFH and MH undergo oxidation in the liver into two highly reactive intermediates: a free methyl radical and an unstable diazonium compound.72 These substances appear to produce local hepatic necrosis by blocking the activity of hepatic cytochrome enzyme systems, glutathione, and other hepatic biomolecules. There are significant concerns about long-term toxicity associated with repeated consumption of this mushroom. Each kilogram of fresh G. esculenta contains 3 to 100 mg gyromitrin. Fresh mushrooms contain 50 to 300 mg of MH per kilogram, and dried mushrooms up to 400 mg/kg. The human median lethal dose (LD50) is suspected to be 20 to 50 mg/kg for adults and 10 to 30 mg/kg for children, or 0.4 to 1 kg of fresh mushrooms for an adult (average 30 mushrooms) and 0.2 to 0.6 kg for a child.72 Clinical Presentation Symptoms are summarized in Box 65-13. They are generally delayed for 4 to 50 (average 5 to 12) hours after ingestion. Initial symptoms include nausea, vomiting, and severe diarrhea. Some victims may have dizziness, weakness, muscle cramps, and loss of muscle coordination. In a severe ingestion, delirium, seizures, and coma are present. Hepatic failure develops over several days after ingestion, although hepatic damage is generally mild. Hypoglycemia, hypovolemia, severe hepatic failure, and death may occur. Symptoms from gyromitrin toxin depend on amount consumed, toxin concentration, nature of the mushrooms, and other host factors. The variability of symptoms after ingestion of gyromitrin mushrooms is much greater than with other mushroom species. Some individuals can consume large quantities of Gyromitra with few or no symptoms. A second meal by the same BOX 65-13  Symptoms of Gyromitrin Toxicity 1. Onset of nausea, vomiting, and diarrhea within 4 to 50 (average 5 to 12) hours. 2. Neurologic symptoms of dizziness, weakness, and loss of muscle coordination. Severe neurologic symptoms include coma, delirium, and seizures. 3. Hepatic failure begins 2 to 4 days after ingestion. Hepatic failure is often associated with hypoglycemia.

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BOX 65-14  Treatment of Gyromitrin Toxicity 1. Activated charcoal if the patient presents within 1 hour of ingestion. Note that most of these patients will be asymptomatic. 2. Fluid and electrolyte replacement as needed. 3. Glucose replacement. Treat hypoglycemia with glucose infusion. 4. Pyridoxine 25 mg/kg up to 20 g/day intravenously to control seizures or coma.5 If significant hepatic failure occurs, transfer to transplant facility.

person may lead to severe toxicity. Repeated consumption may increase the risk for a severe reaction. Several drugs, including isoniazid, hydralazine, and probably MH,16 are metabolized through acetylation of a hydrazine or amino group by the liver. Individuals vary markedly in the rapidity of acetylation. Two major human groups are termed “fast” and “slow” acetylators, respectively, with slow acetylation being an autosomal recessive trait. Slow acetylators in general have greater and more prolonged toxicity after ingestion of these drugs. Similar variation in toxicity in fast and slow acetylators is seen when Gyromitra mushrooms are ingested. Treatment Symptoms develop several hours after ingestion of Gyromitra. Treatment is summarized in Box 65-14. Activated charcoal (1 g/ kg orally or via gastric tube) is of no value if given more than 1 hour after ingestion. At that time, most patients are asymptomatic and unaware that they have ingested a toxic mushroom. Pyridoxine has been useful in victims with neurologic disorders such as seizures and coma from MH toxicity and is of theoretic benefit in patients with gyromitrin toxicity. Persons who ingest G. esculenta and develop significant neurologic symptoms should receive pyridoxine (25 mg/kg IV initial dose, up to 20 g/ day).3,55,119 No evidence indicates that pyridoxine alters the course of hepatic disease. High-dose pyridoxine therapy may cause acute peripheral neuropathies.1 Baseline measurements of liver transaminases (alanine aminotransferase [ALT], aspartate aminotransferase [AST]), prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), BUN, creatinine, complete blood cell count (CBC), platelet count, glucose, and electrolytes should be performed. ALT, AST, PT, PTT, INR, BUN, and creatinine should be monitored at least daily for 3 to 4 days for the development of hepatic failure. Rapid deterioration of liver (ALT or AST >2000 international units, PTT >50 seconds) mandates immediate transfer to a tertiary center with liver transplantation capability. Persons with significant hepatic failure may require monitoring of blood glucose level every 2 to 4 hours and supplemental glucose administration for symptomatic hypoglycemia. No specific antidote or treatment is available for the fulminant hepatic failure. The appropriate timing or necessity of liver transplantation is uncertain. In persons with fulminant hepatic failure from infectious causes, the presence of an abnormal PT (unresponsive to fresh-frozen plasma) and development of hepatorenal syndrome, grade II hepatic encephalopathy, hypoglycemia, and uncorrectable metabolic acidosis are used as signs that transplantation is needed on an emergent basis. Persons with fulminant hepatic failure from toxic ingestion, elevated bilirubin level, and young age are important indicators of a poor prognosis. As discussed later, the model for end-stage liver disease (MELD) score for assessing liver failure provides the best prognostic information. Mortality from gyromitrin poisoning is reported to be 15% to 35%.30

RENAL TOXICITY Although originally thought to be an edible mushroom, Cortinarius orellanus was associated with 81 cases of renal toxicity in the 1950s.39 This led to isolation of the toxin orellanine, which is found in the mushrooms C. orellanus, Cortinarius

FIGURE 65-87  Cortinarius sp. (United States).

speciosissimus, and Cortinarius gentilis. Most cases occur in Europe and Japan. Causative Mushrooms C. orellanus has a small brown to brownish-red smooth cap 30 to 80 cm (12 to 31 inches) in diameter. The stalk is somewhat yellow, often darker closer toward the soil. Gills are orange to rust with rust-colored spores. It grows in deciduous woods, most commonly in sandy soil underneath oaks and birches. It is ubiquitous throughout Europe. Some other species of Cortinarius are found in the United States and may be toxic (Figure 65-87 and Box 65-15). Amanita smithiana, which grows in the Pacific Northwest, has been associated with renal failure in the United States.117 It may be mistaken for Tricholoma magnivelare.115 Amanita proxima in France and Amanita pseudoporphyria in Japan have caused similar symptoms.93 Toxin The two toxins isolated from C. orellanus, orellanine and orelline, are structurally related to paraquat and diquat. Their mechanism of action remains a mystery. These are heat-stable compounds, unaffected by cooking. The toxin appears to cause intense interstitial nephritis with early fibrosis.46 The toxin can be identified with thin-layer chromotography.49 The Amanita species contain aminohexadrienoic acid,93,115 which appears to be responsible for its renal toxicity. Clinical Presentation Persons who ingest these mushrooms are generally asymptomatic for 2 to 20 days. During this latent period, acute renal failure develops. Some persons develop neurologic changes, including paresthesias, taste impairment, and cognitive disorders. Symptoms vary greatly. One case report described 26 soldiers who ate soup made of C. orellanus in nearly identical quantities.10 Acute renal failure developed in 12 victims on or around day 11.10 Eight individuals later recovered normal renal function, whereas four required long-term dialysis or kidney transplantation. The BOX 65-15  Mushrooms Reported as Causing

Renal Failure

Amanita proxima pseudoporphyria smithiana (Figure 65-88) Cortinarius gentilis orellanus

rellanus rubellus speciosissimus splendens venenosus

other 14 soldiers showed no rise in BUN or creatinine levels but developed leukocyturia and hematuria that persisted for more than 1 month. Renal failure reportedly occurs in 30% to 46% of persons who ingest these mushrooms and become ill. Renal function returns in approximately 50% of affected victims. Renal biopsy in patients with orellanine-induced renal failure shows changes in tubular epithelial cells and in actin filaments within their cytoplasm.77 These biopsy changes may persist for up to 3 months.10 Treatment In most persons who ingest nephrotoxic mushrooms, unexplained acute renal failure develops many days later. If a person presents within 1 hour after eating orellanine-containing mushrooms, gastric emptying and activated charcoal administration (1 g/kg orally or via gastric tube) is theoretically indicated to prevent some absorption, decreasing the resultant toxicity. There is no evidence for its use. Early presentation is very rare. Once acute renal failure develops, baseline and repeated monitoring of BUN, creatinine, electrolytes, CBC, differential, and urinalysis should be performed to monitor renal function. Urine output should be monitored, and if it decreases, fluid administration should be used to achieve optimal hydration. Serum potassium, calcium, and magnesium should be monitored closely. If renal failure progresses, the victim should be transferred to a facility for hemodialysis and possible renal transplantation. Renal function may return to normal after months of dialysis dependency.

AMATOXINS The mushrooms that contain amatoxins are responsible for 90% to 95% of fatalities due to mushrooms (Box 65-16 and Table 65-6). A. phalloides is most common in central and eastern Europe; immigrants to the United States may have carried mushroom spores in wood products from eastern Europe. Amanita verna and Amanita virosa are more common in the United States. Toxicity has occurred from cooked or frozen mushrooms and even tea made from Amanita mushrooms.83 Causative Mushrooms Mushrooms reported or suspected of containing amatoxins are listed in Box 65-16. The common names of A. phalloides (Figure 65-89; see also Figures 65-6 and 65-7) and its relatives, A. verna and A. virosa (Figures 65-90 and 65-91), are death cap, death angel, and destroying angel, reflecting their association with fatal outcome. A. phalloides has a white to greenish cap 4 to 16 cm (1.6 to 6.3 inches) in diameter, often with remnants of the veil as warts. The stalk is generally thick, 5 to 18 cm (2 to 7 inches) long, with a large bulb at the base, often with a vulva. A thin ring is usually present on the stalk. Gills are generally free and white to green in color; spores are white. The mushrooms grow under deciduous trees in the autumn. 1297

CHAPTER 65  Toxic Mushroom Ingestions

FIGURE 65-88  Amanita smithiana. (By Heather Gardner-Madras from http://www.flickr.com. Used with permission.)

PART 7  PLANTS

BOX 65-16  Mushrooms Reported or Suspected of

TABLE 65-6  Look-Alikes of Mushrooms Containing

Amanita bisporigera decipiens Jacquetant hygroscopica Coker ocreata ocreata Peck phalloides (see Figures 65-6, 65-7, and 65-89) suballiacea Murr tenuifolia Murr verna virosa (see Figures 65-90 and 65-91)

Toxic Species

Edible Species

Amanita phalloides (see Figures 65-6 and 65-7) Amanita verna Amanita virosa (see Figure 65-90)

Amanita fulva (Figure 65-97)

Containing Amatoxins

Conocybe filaris Galerina autumnalis Smith and Singer (Figures 65-92 and 65-93) badipes Kühn beinrothil fasciculata Hongo helvoliceps marginata marginata Kühner (Figures 65-94 to 65-96; Figures 65-94 and 65-96, online) sulciceps Boedjin unicolor Sing venenata AH Smith Lepiota brunneoincarnata Chodat and Martin brunneolilacea Bon and Boiffard castanea castanea Quelet citrophylla (Berk and Br.) Sacc. clypeolaria (Bull.:Fr.) Kummer (see Figure 65-36) clypeolarioides Rea felina (Pers.:Fr) Karsten fulvella Rea fuscovinacea Moeller and Lange griseovirens Maire heimii Locq. helveola helveola Bres. helveoloides Bon ex Bon and Andary josserandii josserandii Bon and Boiffard kuehneri Huijsm. Ex Hora langei Locq. lilacea Bres. locanensis Espinosa ochraceofulva Orton pseudohelveola Kühner ex Hora pseudolilacea Huijsm. rufescens Lange subincarnata Lange xanthophylla Orton

A. virosa (see Figures 65-90 and 65-91) is more common in the United States. It resembles A. phalloides, but the cap is more yellow or white. A. verna is characteristically white. All grow in deciduous woods. Even mushroom experts have been tempted by the large white mushroom, which is tasty. The fatality rate is 35% in adults and 50% in children. Unfortunately, mushroom gatherers may mistake amatoxin-bearing Amanita species for edible mushrooms (see Table 65-6). 1298

Amatoxin

Lepiota flavovirens Agaricus bisporus (see Figure 65-12)

Some Lepiota mushrooms (see Figure 65-36), including Lepiota castanea and Lepiota josserandii, contain high concentrations of amatoxin. There have been two deaths attributed to L. josserandii in upstate New York. Mushrooms that contain amatoxin may have a positive Meixner test. This test was first described by Wieland118 in 1949 and popularized by Meixner.69 A drop of liquid is expressed from a fresh mushroom onto print-free (ligand-free) newspaper and allowed to dry. A drop of concentrated (10 to 12 N) hydrochloric acid is added. A blue color develops within 1 to 2 minutes in the presence of amatoxins. Control tests on newspaper without mushroom juice and paper containing ligand should be conducted. False-positive results are common and can be elicited by excessive drying temperatures (greater than 63° C [145.4° F]) or exposure to sunlight. The test can detect 2 mcg of α-amatoxin.7 False-positive tests also occur from mushrooms containing psilocybin, terpenes, bufotenin, and other tryptamine compounds.7 Nearly 20% of gilled mushrooms that did not contain amatoxins tested positive in one study.100 A positive test does not identify an amatoxin-containing mushroom, and further identification is necessary. Thin-layer chromatography more accurately identifies the presence of amatoxin and can be done on mushroom liquid, human serum, or urine.86 Radioimmunoassay (RIA) and a recently developed enzyme-linked immunosorbent assay (ELISA) test79 can detect amatoxins in serum or urine. Toxins The mushroom A. phalloides contains two groups of toxins: amatoxins and phallotoxins. Each group contains several toxins. There are now eight identified amatoxins: α-amanitin, β-amanitin, γ-amanitin, ε-amanitin, amanin, amaninamide, amanullinic acid, and amanullin. Of these, α-amanitin is thought to be primarily responsible for human disease. α-Amanitin injected into animals produces hepatic toxicity characteristic of human ingestion of A. phalloides. In dogs, two phases of toxicity are seen. The first is cellular impairment with inhibition of protein and urea synthesis, followed by a second phase of hepatocellular changes, including condensation of nuclear chromatin and foaming of the cytoplasm.66 Phallotoxins include phalloidin, phalloin, phallisin, phallacidin, phallacin, phallisacin, and prophalloin. Phalloidin is the primary phallotoxin. Phallotoxins bind to F-actin, disrupting

FIGURE 65-89  Amanita phalloides—toxic.

CHAPTER 65  Toxic Mushroom Ingestions

FIGURE 65-91  Amanita virosa—toxic.

FIGURE 65-90  Amanita virosa. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

1 cm

FIGURE 65-93  Galerina autumnalis. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

FIGURE 65-92  Galerina autumnalis. (By Jason Hollinger from http:// www.flickr.com. Used with permission.)

FIGURE 65-95  Galerina marginata. (By Tomasz Przechlewski from http://www.flickr.com. Used with permission.)

FIGURE 65-97  Amanita fulva. (By Jason Hollinger from http://www. flickr.com. Used with permission.)

1299

PART 7  PLANTS

plasma membranes and causing massive efflux of calcium and potassium. Phallotoxins cause death in animals within 2 hours but are not believed to play a role in human toxicity.31 Humans may not even absorb these toxins, although they may be responsible for local gastric irritation. A. virosa contains amatoxins and virotoxins. Virotoxins resemble phallotoxin biochemically and also bind F-actin and cause death in animals within a few hours. Six different virotoxins have been isolated, but none is thought to play a role in human Amanita hepatotoxicity. Amatoxins are heat stable and not destroyed by cooking, freezing, or drying. A. phalloides mushrooms stored in a freezer for 7 to 8 months have resulted in death.44 Amatoxins are concentrated in the cap, gills, ring, and stalk. Phallotoxins are more concentrated in the bulb and vulva. The concentration of toxin in a given mushroom depends on environmental factors and soil.18 After ingestion, amatoxins are absorbed from the gut and actively transported into the liver through transport systems shared by bile acids and xenobiotics. They do not appear to cross the placenta.112 α-Amanitin is rapidly cleared from plasma.51 Amatoxins are not protein bound. They bind to ribonucleic acid (RNA) polymerase II and inhibit formation of messenger RNA (mRNA).21 This in turn inhibits transcription, because the reservoir of mRNA is depleted. Amatoxins are excreted into the bile, where they are reabsorbed and once again transported into the liver.12 Interruption of this enterohepatic circulation could be a therapeutic tool. However, by the time clinical symptoms are present, enterohepatic circulation largely is complete, making disruption of the enterohepatic circulation ineffective. Within the liver, α-amanitin may undergo some metabolism through the hepatic cytochrome system. Animal studies suggest that a more toxic metabolite may be produced through this metabolism, although this metabolite has never been isolated.98,99 Nuclear fragmentation and condensation of chromosomal material have been observed within 15 hours of injection.25 Glycogen is rapidly depleted, and fatty degeneration occurs within liver parenchymal cells. Mitochondria become swollen, and microvesicles appear throughout the cytoplasm.25 Direct renal toxicity may occur. Clinical Presentation Symptoms are summarized in Box 65-17. People who ingest the mushroom Amanita phalloides feel well for 4 to 16 hours. Severe nausea, vomiting, abdominal cramps, and diarrhea follow this characteristic latent period. Early complications include fluid and electrolyte imbalance (hypoglycemia, hypokalemia, and elevated BUN due to dehydration). People in whom symptoms develop earlier (between 4 and 10 hours) are more likely to experience severe hepatotoxicity. Over the next 12 to 24 hours, the victim’s gastrointestinal symptoms abate. The second latent period is followed by hepatic failure, which develops between 48 and 72 hours after ingestion in most victims. Hepatic failure may be of varying severity; it is frequently worse in children and depends minimally on the amount of mushroom ingested. Kidney failure can develop as a result of hepatic injury or possibly by direct renal toxicity to the kidneys.35 Children have greater toxicity and higher mortality, perhaps because of the relative quantity of mushrooms ingested or the varying metabolism in young children (differing levels of cytochrome enzymes). Previous experiments showed that ethanol concurrently ingested with A. phalloides decreased hepatotoxicity.27 Therefore decreased toxicity in adults could theoretically

BOX 65-17  Symptoms of Amatoxin Ingestion 1. Delayed onset of nausea, vomiting, and diarrhea 4 to 16 hours after ingestion. 2. Resolution of gastrointestinal symptoms 12 to 24 hours later. 3. Onset of hepatic and occasionally renal failure 48 to 72 hours after ingestion. 4. Coagulopathy and pancreatitis may be seen with the hepatotoxicity.

1300

BOX 65-18  Treatment of Amatoxin Ingestion Established Activated charcoal (1 g/kg orally or via gastric tube) if the ingestion has occurred within 5 hours. Silymarin (silibinin) 20 to 40 mg/kg/day IV, 1.4 to 4.2 g/day orally Experimental Hyperbaric oxygen if available Cimetidine 4 to 10 g IV divided over 48 hours If significant hepatic failure develops, transfer to transplant facility IV, Intravenously.

result from ingestion of ethanol with an Amanita mushroom dinner. More recently, however, ethanol failed to alter hepatotoxicity in an animal model poisoned with α-amanitin, which raises doubts about this explanation for increased toxicity in children.97 In addition to hepatic failure, endocrinopathies can develop, with hypocalcemia, decreased thyroid function, and elevated insulin levels in the presence of hypoglycemia.54 Hypocalcemia may be caused in part by a loss of calcium through diarrhea or by a direct effect on osteoclasts. Renal failure may contribute to hypocalcemia. The thyroid abnormalities probably result from decreased hormone synthesis caused by overwhelming illness and blocked peripheral conversion of thyroxine (T4) to triiodothyronine (T3). Thyroid-stimulating hormone depression may result from decreased synthesis caused by inhibition of RNA polymerase II by amatoxin. Hypothyroidism has not been clinically significant. Hypoglycemia is probably the result of several processes, including impaired hepatic gluconeogenesis, increased insulin release from the initial hyperglycemia, and tissue destruction of the pancreas.28 Bone marrow toxicity with decreased neutrophils, lymphocytes, and platelets has been noted. Disseminated intravascular coagulation and coagulopathies secondary to hepatic dysfunction are common.90 Pancreatitis occurs in up to 50% of patients.28 Hypophosphatemia is particularly common in children, for unknown reasons. Myopathy has been associated with Amanita toxicity.38 Hepatic biopsy shows diffuse and severe steatosis with periportal inflammation and necrosis. Renal biopsy shows acute tubular necrosis with hyaline casts.24 Extremely high levels of hepatic enzymes are seen. Level of liver transaminases are not helpful in predicting the victim’s prognosis. A precipitous drop in liver transaminases, often to normal levels, may occur just before death. Treatment Attempts to treat A. phalloides poisoning have ranged from scientific to purely empiric (Box 65-18). Noting that rabbits were able to eat the A. phalloides mushroom with impunity, clinicians fed ground raw rabbit to victims of Amanita poisoning, without success.109 Hemodialysis was long recommended but now has been shown to be ineffective, because the toxin is rapidly cleared from the plasma. Amatoxin is taken up in liver cells within 5 hours after IV administration.23 In a retrospective study of 205 cases of amatoxin ingestion,28 hemodialysis worsened the prognosis, and charcoal hemoperfusion did not provide any improvement in outcome. Plasmapheresis has been used, but this appears to be ineffective because the toxin is largely intracellular and has caused cellular damage by the time symptoms appear.82 Despite this scientific evidence, the literature continues to report the use of dialysis, hemoperfusion, and plasmapheresis.53 Antigen-binding fragment (Fab) monoclonal antibodies against amatoxin were developed and tested in mice. Although hepatic toxicity was markedly lessened, renal toxicity was 50 times greater than in control animals, possibly due to dissociation of the amatoxin-Fab molecule in the kidneys.22 Previously, thioctic acid and benzylpenicillin were recommended as treatments. Both these treatments are now questioned. In a retrospective study, thioctic acid was more frequently associated in humans with fatal outcome.28 A more recent review

for other causes of fulminant hepatic failure are often applied to this setting. Factors associated with poor prognosis in acetaminophen-induced hepatic damage include metabolic acidosis, PT greater than 50 seconds, and elevated serum creatinine (>2.0 mg/dL).78 The largest study suggests that a person with ALT or AST level greater than 2000 international units, grade II hepatic encephalopathy, or PT greater than 50 seconds is at serious risk for death and should be considered for an emergency liver transplant.21 Persons who met these criteria have survived without transplant.64,88 The MELD score appears to be more effective than the King’s College or Clichy’s criteria for assessing the need for hepatic transplant. There are many online calculators for the MELD score, which uses bilirubin, INR, and creatinine levels.120 A recent report suggests that increased reparative enzymes correlate with hepatic recovery.48 These enzymes, including α-fetoprotein, retinal binding protein, γ-glutamyl transferase, and des-γ-carboxyprothrombin, are thought to be released during the healing phase of liver disease. Because hepatic failure develops rapidly, victims with toxicity due to mushrooms who have significant hepatic dysfunction must be transferred early to a transplantation site. Patients undergoing liver transplantation for fulminant hepatic failure (not caused by A. phalloides) have a 60% to 80% survival rate.20 There are no statistics specifically for victims of mushroom poisoning. In Europe, an extracorporeal liver assistance device (molecular absorbent regenerating system) has been developed and used successfully in four patients.17,50,62,101 Recently a temporary liver transplant was performed on a child and sustained her while her own liver recovered.89 Some persons who survive acute hepatic failure due to Amanita without needing hepatic transplant may have persistent elevation in liver transaminases. In one study of 14 persons with severe Amanita-induced hepatotoxicity, 8 showed persisted elevations in AST and ALT without normalization over a 1-year follow-up period.21 All had biopsy evidence of chronic active hepatitis with positive anti–smooth muscle antibody and cryoglobulins. It is not known whether these persons will have an increased risk for hepatoma or develop more serious complications of chronic active hepatitis. Amatoxin ingestion during pregnancy does not appear to have serious consequences. There are now several reports that suggest amatoxin does not cross the placenta.96,107 A case study of 22 pregnant women poisoned during their pregnancy had similar outcomes to a control group; however, only five ingested mushrooms in their first trimester.107

MISCELLANEOUS REPORTS OF TOXICITY FROM MUSHROOMS Occasional toxicity has been reported with other mushrooms. Erythromelalgia has been reported after ingestion of Clitocybe amoenolens.32,94,95 The mushroom contains the toxin clitidine, which resembles nicotinic acid. Tricholoma equestre or Russula subnigricans ingestion is associated with rhabdomyolysis, respiratory failure, and hepatic and renal dysfunction.5,15,93 Deaths due to acute myocarditis and renal failure have been reported.5

Approach to the Victim of Mushroom Poisoning Four types of individuals develop mushroom toxicity: foragers, children, those seeking hallucinogenic “highs,” and, rarely, victims of attempted homicide. Most victims seek medical care only after symptoms develop. If small children are observed chewing on lawn mushrooms, caregivers should be advised to call the nearest regional poison information center. Persons with agitation, altered perceptions, or frank hallucinations temporally related to mushroom ingestion are probably intoxicated with isoxazole or hallucinogenic mushrooms. Whether the mushrooms are picked accidentally or ingested intentionally, the treatment and clinical course are identical. Persons who develop muscarinic symptoms (salivation, urination, diaphoresis, gastrointestinal upset, and emesis) present such a classic picture that it is rarely confused with any other presentation. Some drugs (e.g., bethanechol) may cause similar symptoms 1301

CHAPTER 65  Toxic Mushroom Ingestions

of patients treated with a variety of antidotes showed benzylpenicillin was more effective than simple supportive care, but less effective than silymarin or antioxidant therapy.20 The authors of that paper suggested abandoning the use of penicillin. However, because silymarin has not been easily available in the United States, some poison centers may still recommend penicillin. If benzylpenicillin is used, the recommended dose is high— 300,000 to 1,000,000 units/kg/day IV. Side effects are significant and include allergy, hyponatremia,19 and granulocytopenia.75 Silymarin is the active component of the milk thistle Silybum marianum. It is an antioxidant that accumulates in the liver.59 Silymarin binds tightly to the plasma membrane, stabilizing it,84,85 and hinders amatoxin from penetrating the cell wall.52,113,114 It is a free radical scavenger,29,65,116 inhibits lipid peroxidation,9,13,29,73 and stimulates RNA polymerase I.116 In both retrospective studies, silymarin has shown promising reductions in mortality.20,26 The intravenous form has recently become available in the United States under the name Legalon. The intravenous dose of silybin dihemisuccinate is 5 mg/kg over 1 hour followed by 20 mg/kg/ day for 6 days or until liver transaminases normalize. The oral preparation (70-mg capsules) is less well studied; dosage recommendation is 1.4 to 4.2 g/day. It is most effective when started within 24 hours of ingestion.33 Gastric decontamination (ipecac, gastric lavage, whole bowel irrigation) is not considered effective. The ingestion is generally many hours old, and the intense vomiting is generally enough to clear the stomach. Although amatoxin has enterohepatic circulation, there are no data that provide support for any therapy designed to disrupt the enterohepatic circulation unless the ingestion is noted within the first few hours.20 Likewise, there are no data to support forced diuresis. The French have used hyperbaric oxygen as a treatment for Amanita toxicity.60 Hyperbaric oxygen has been shown to have efficacy in animal models. Recent animal work has suggested the use of antioxidants. Cimetidine has been shown to be effective in animals98 and has been reportedly used in humans20 (dosage: 4 to 10 g/day IV for adults; pediatric dose not described). Vitamin C and N-acetylcysteine have been used with some success.20,111 Other reported treatments include aucubin and kutkin, both plant derivatives.20 IV normal saline or Ringer’s lactate is needed to replace gastrointestinal fluid losses. Electrolyte losses (particularly potassium) may be significant. BUN, creatinine, CBC with differential, platelet count, electrolytes, glucose, calcium, phosphorus, magnesium, urinalysis, PT, PTT, INR, fibrinogen, amylase, protein, and albumin should be initially measured and repeated at least daily to monitor liver and renal function. Hyperglycemia is common on the first day, but insulin is generally not required. Hypoglycemia occurs after 24 hours and may be severe, requiring IV concentrated glucose. Therefore bedside determinations of glucose level should be performed at least every 6 hours. The patient with liver failure due to Amanita will appear like a patient with any other type of advanced liver disease, with jaundice and asterixis. Hepatic encephalopathy can develop with elevated ammonia level and increased intracranial pressure. Tests of liver damage, including ALT, AST, alkaline phosphatase, ammonia, PT, and PTT, should be repeated at least daily and 2 to 3 times a day if hepatic failure develops. Transaminases that rise rapidly or are in excess of 2000 international units or PTT greater than 50 seconds signal severe toxicity and the need for referral to a transplant center. Once liver failure begins, it is treated the same as any other fulminant hepatitis. Hypoglycemia is common. Supplemental glucose should be readily available. Dietary protein should be limited to 0.5 g/kg/day. There is no need to supply supplemental thiamin or multivitamins. Oral lactulose, 30 to 45 mL every 6 to 8 hours, may reduce hepatic encephalopathy. In patients who do not tolerate lactulose, neomycin 1 g orally 3 times a day can be tried. PT, PTT, and INR should be measured at least twice a day once hepatic failure begins, and vitamin K (100 mg IM), fresh-frozen plasma (2 to 6 units initially), or both should be used to correct abnormalities in coagulation. If hepatic failure progresses, a liver transplant may be required. The timing of the transplant is highly controversial. Criteria used

when taken in overdose. Victims of this variety of mushroom poisoning generally remain mentally clear and should be able to relate an appropriate history. Victims with gastrointestinal symptoms can be divided into those with early and those with delayed presentations. Those with early (within 2 hours of ingestion) gastrointestinal symptoms generally have a benign course, except for persons with a mixed ingestion. Most guidebooks for mushroom hunters recommend eating only one variety of mushroom at a time, but more daring or foolish individuals mix multiple mushrooms and eat them frequently over the day. This makes diagnosis based on time of onset of symptoms difficult. Early onset of gastrointestinal symptoms may mask more significant delayed symptoms. In these cases, identification of ingested mushrooms becomes essential to planning therapy. Accurate botanical identification of the mushroom can be difficult. Only 800 of the 3000 species found in Europe can be identified without a microscope.109 With the popularity of digital imaging, photos of suspicious mushrooms can be sent to poison control centers via e-mail and similarly can be forwarded to mycologists. This may save several hours of travel and may help initiate treatment, if needed, in a more timely fashion. When multiple mushrooms are eaten together, the residual specimens brought from home may not be those causing toxicity. Cooking and refrigeration alter identifying features. Fresh mushroom specimens should be transported in a paper bag rather than in a plastic container to limit the effects of humidity. Finally, precise identification of even a good specimen can be difficult and should be done by an expert. Mycologists can be contacted through a poison control center, university, museum, or commercial mushroom grower. In difficult cases, spores can be obtained from emesis or gastric emptying procedures. Specimens should be refrigerated while awaiting analysis. More specific diagnosis can be made through thin-layer chromatography or RIA techniques. Botanical identification may not match the victim’s symptoms. The victim should be treated according to time of onset of symptoms and condition when examined. Victims with early-onset gastrointestinal symptoms require supportive care with fluid and electrolyte replacement. For those with delayed gastrointestinal symptoms or mixed ingestions containing amatoxin or gyromitrin mushrooms, treatment should begin as soon as possible. Toxic mushrooms can be differentiated by the season (spring: Gyromitra; autumn: Amanita). Persons who have disulfiram-like reactions to alcohol should be questioned about prior mushroom ingestion. This situation is

rarely correctly diagnosed because symptoms are thought to result from panic attacks, alcohol intoxication, or even an allergic reaction. Persons rarely relate their symptoms to the dinner of mushrooms eaten days earlier. Any person with unexplained acute renal failure should be questioned about prior wild mushroom ingestion. Although C. orellanus is more common in Europe and Japan, it is found with increasing frequency in the United States. Because of the long delay before the onset of renal failure (1 to 2 weeks), the history of mushroom ingestion may be missed. Mushroom poisoning cases remain relatively rare in the United States (they are still more common in parts of Europe and Asia), and until recently, up-to-date information was not accessible to the general public except through poison centers. With the plethora of worldwide Internet connections, there are now mushroom experts readily available to answer questions about possible exposures within minutes to hours of contact. The active forager should use well-written field guides in addition to Internet sources and should cross-reference several sources before consuming any unknown mushrooms.

Recommended Field Guides Lincoff G: The Audubon Society field guide to North American mushrooms, New York, 1992, Knopf. Lincoff G: Simon and Schuster’s guide to mushrooms, New York, 1981, Simon and Schuster (European mushrooms). Phillips R: Mushrooms of North America, Boston, 1991, Little, Brown & Company. Miller OK: Mushrooms in North America, New York, 2006, E.P. Dutton.

Recommended Websites http://www.fungaljungal.org http://www.mushroomexpert.com http://www.evergreen.edu/mushrooms http://www.bluewillowpages.com/mushroomexpert/sitemap2. html

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 66 

Ethnobotany: Plant-Derived Medical Therapy KEVIN DAVISON AND RICK MARINELLI

The history of ethnobotany begins before the advent of written records. In all ancient civilizations, plants served as important elements of food, shelter, dyes, ornamentation, religious rituals, and medicines. The term ethnobotany refers to an individual culture’s use of specific plants. Medicinal use of the plant kingdom has been termed herbalism, plant medicine, and natural-based medicine and is called phytomedicine in its current application. The word herb is broadly defined as a nonwoody plant that dies down to the ground after flowering. The most commonly used interpretation, however, is any plant used for 1302

medicinal therapy, nutritional value, food seasoning, or dyeing another substance. The history of the discovery of the medicinal uses of plants by humans remains conjectural. Many scenarios probably occurred. Perhaps, in a prehistoric jungle of South America, a pool of water containing fallen plant material leached out some of the precious medicinal constituents of leaves, flowers, stems, and bark. Tannins, glycosides, sugars, and alkaloids from the bark were infused into the waters. Because of burning fever and severe dehydration, an extremely ill native drank from the pool,

For online-only figures, please go to www.expertconsult.com

Discoveries quickly followed. The bronchodilator and antitussive ephedrine, from the herb Ephedra sinica, was often used in Chinese medicinal formulas for bronchial asthma. The discovery of morphine led to the creation of all the narcotic analgesics. The bark of the cinchona tree was found to contain quinine in 1819, which led to the development of antimalarial drugs. The traditional herbal extract from rhubarb (Rheum spp.) has several active compounds. These compounds mediate many of the pharmacologic effects, such as its purgative action (from sennosides); antibacterial, antifungal, and antitumor activities (from anthraquinones); antiinflammatory and analgesic activities; and improvements of lipid metabolism (from stilbenes). Treatment of leukemias from an extract of Madagascar periwinkle (Catharanthus roseus), known as vincristine, has been highly effective.43 Discoveries in the 19th and 20th centuries included atropine (from belladonna leaves, Atropa belladonna) in 1831, cocaine (from coca leaves, Erythroxylum coca) in 1860, ergotamine (from Claviceps purpurea) in 1918, and tubocurarine in 1935.124 European settlers brought herbal knowledge and their medicinal methods to the Americas. Because of the abundance and wide use of plants on the new continents, they also learned much from the indigenous peoples. The colonists found that conditions afflicting them, such as malaria and scurvy, were treated effectively with herbs by the Native Americans.126 In the 1700s, herbal medicine continued to have popular applications in lay circles, but it was also investigated by the new medical establishment. Although the creation of a small elite group of learned professionals was thought to violate the political and constitutional concepts of the early American democratic movement, the practice of medicine was carried over from England and Scotland during pre-Revolutionary days. Before a professional medical class was established, most illness in America was treated within the family or extended family network. Many concepts were modified in the colonies between 1765, when the first medical school opened, and 1850, when more than 42 schools of medicine had been recognized. The inquiry into Digitalis purpurea (foxglove) by William Withering exemplified the change in perspective from anecdotal folk medicine to a critical examination for specific uses of botanicals from a biochemical point of view. During the early 1800s, the trend was to look at the efficacy of botanicals and their intrinsic value from a more scientific perspective. Several developments delayed the appreciation of herbalism by physicians in the colonies. For instance, Samuel Thomson promoted a system of herbal medicine by proselytizing about his patented method of herbal prescribing, which used many Native American herbs. A central theme in his approach was advocacy of self-prescribing based on the philosophies and herbal prescriptions found in his book, New Guide to Health. The right to sell “family franchises” for use of the Thomsonian method of healing was the basis of a widespread lay movement between 1822 and Thomson’s death in 1843. Thomson adamantly believed that no professional medical class should exist and that democratic medicine was best practiced by laypersons within a Thomsonian “family unit.”40 Although his methods were considered crude and unscientific, he had over 3 million faithful followers in 1839. Founded on ignorance, prejudice, and dogma, the Thomsonian school did little to help physicians accept European and American herbal medicines. European physicians in the Thomsonian movement wished to separate themselves from lay practitioners by creating requirements and standards for the practice of Thomsonian medicine. Thomson was adamantly against this, but a decade after his death, the Thomsonian physicians formed the Eclectic School of Medicine, which attempted to unite “professional physicians,” Thomsonianism, and traditional herbal medicine. Establishment of several Eclectic medical schools was a step toward validating herbal medicine, but it failed to bring herbalism into the mainstream medical establishment. The founding of the American Medical Association and the Flexner Report on medical education in 1910 thoroughly established the modern pharmaceutical industry in the medical education system.40 Because of the availability of pure, active constituents from plant drugs and the synthetic drugs that began to appear on the market toward the end of the 19th century, the prescribing habits of physicians began to change. The sensibility and predictability 1303

CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

and his fever miraculously disappeared. The pond became known for its magical healing powers. If the water held bark from the cinchona tree, the native may have serendipitously discovered quinine. Archaeologic evidence shows that prehistoric humans used plants extensively to treat physical ailments. Instinct and trial and error led to the realization that, for example, cinchona bark controlled intermittent fevers, animals fed ergotized grain aborted their fetuses, and the latex sap from the opium poppy could be eaten to alleviate pain. Innumerable medicinal plant traditions, some originating as far back as 2700 BC, still remain intact. Ethnobotanically, the use of plant-based medicines in a particular culture represented much more than an individual’s efforts to survive. Analyzing the methods and degrees of use of indigenous medicines reveals information about cultural philosophy, ingenuity, and sophistication. The Chinese developed an extensive and elaborate system for prescribing, classifying, and processing herbs that dates back to the third millennium BC. The formulas identified the specific effect of each herb and interactions with other herbs. Less tolerable herbs were blended with those that would counteract undesirable effects. Formulas were custom blended, taking into account a victim’s constitution and the stage of the disease. Some of the ancient knowledge from these writings is being used in contemporary herbal preparations commercially sold as “patent” (readily available in pill form) medicines. Many native tribes of New Guinea, Indonesia, and the Amazon use single-herb formulations to treat nearly all medical conditions, as they did thousands of years ago. In the West, written records dating to the Sumerians accurately describe the medicinal uses of specific plants.110 In the same period of about 3000 years ago, the first Asian written record, the Ben Tsao Gan Mu, was compiled by the Chinese. It listed more than 360 medicinal plants and their classifications, uses, contraindications, and methods of action as perceived at that time. Roman and Greek herbal remedies were described in the writings of Hippocrates and later in those of Galen, providing a pattern for development of the Western medical tradition. Hippocrates was an advocate of using a few simple plant preparations, along with fresh air, rest, and proper diet, to help the body’s own “life force” eliminate problems. In contrast, Galen promoted use of direct intervention to correct the imbalances that cause disease, employing large dosages of complicated mixtures that included animal, plant, and mineral ingredients.124 The earliest European compendium that listed the uses and properties of medicinal plants, De Materia Medica, was written by the Greek physician Dioscorides in the first century AD. He described about 600 plants, and his work remained the authoritative herbal medicinal resource into the 17th century.42 Herbalism was practiced in many different ways during and after the Middle Ages. There were learned traditional herbalists and lay practitioners, as well as wandering herbalists, who professed pagan animism or Christian superstitions that often were more influential in healing than were the herbs’ properties. Little was added to the knowledge of herbalism during this period. After the Middle Ages and invention of the printing press in the 1400s, hundreds of herbal publications were compiled. Most early works were available only in Latin or Greek; it was not until the 15th through 17th centuries that the great age of herbalism was appreciated in English.110 Tides changed in European herbalism when a Swiss pharmacist-physician named Theophrastus Bombastus Von Hohenheim, better known as Paracelsus (1490 to 1541), introduced a new dimension. He advocated chemistry and chemical processing and used mineral salts, acids, and other preparations in medicinal therapies. This was a departure from the plantbased medicinal methods of the past. During the latter part of the 17th century, the predominance of plant medicines slowly eroded. In 1806, Freidrich Serturner, a small-town German pharmacist, became known for his efforts to isolate organic acids from plants in an attempt to find the active ingredient in opium. He discovered organic alkaloids, which became known as the first set of active plant constituents.160 Because of their physiologic activity, the search for plant alkaloids continued into the 20th century.

PART 7  PLANTS

A

B

C

FIGURE 66-1  A, Calendula officinalis. B, Calendula drying and dried in a jar. C, Calendula flower bud. (A and B courtesy Cascade Anderson Geller; C courtesy Jill Stansbury.)

of administering exact dosages were appealing. For example, the pure alkaloid of quinine, rather than a foul-tasting extract of cinchona bark containing variable percentages of quinine and other alkaloids with different physiologic properties, could be prescribed for malaria. Many “crude drugs” were standardized for therapeutic activity. Digitalis, which still retains its status in the United States Pharmacopeia (USP), is one example. Of the 200 plant drugs officially listed in the USP in 1936, about 19% are still official today.160 An estimated 25% of all prescriptions dispensed in community pharmacies between 1959 and 1980 contained ingredients extracted from higher plants. For a significant number of synthetic drugs, natural drug products continue to serve as either models or starting points for synthesis.

Evolution of Phytopharmaceuticals The drive toward patenting and ownership in the pharmaceutical industry has been a strong incentive to research and develop plant-based products. Because a plant cannot be patented, however, little U.S. effort has gone into developing herbal medicines during the past century. The principal active constituents of botanicals are investigated for their biologic activity, but in many cases these are less effective than is the whole crude extract of an herb.124 One problem in the development of the U.S. botanical pharmaceutical industry has been quality control. In addition, lack of standardization plagues plant-based products. Quality control and standardization of crude plant extracts for herbal medicines were virtually nonexistent until recently,124 or we might be using more botanical medicines for common ailments. In Europe and Asia, where pharmaceutical firms have been producing standardized phytopharmaceuticals (plant-based standardized extracts) for decades, research and development have demonstrated that they make economic and medical sense. Europeans use phytopharmaceuticals as part of their mainstream medical practice. In hospitals, they are used primarily as adjuvant therapies. More than 70% of general practitioners in Germany prescribe phytopharmaceuticals, and the public health insurance system pays for most of these prescriptions. The total annual market for phytopharmaceuticals in Germany alone is $1.7 billion. Beginning in 1993, the licensing procedure for German physicians required a knowledge of phytotherapy.142 Production and evaluation of botanical medicines have improved significantly in the past six decades. In crude plant evaluation, modern laboratory analysis can determine the percentage of active constituents, as well as solubility, specific gravity, melting point, optical rotation, and water content. Scientists detect resins, alkaloids, flavonoids, enzymes, essential oils, fats, carbohydrates, and protein content. They can precisely assay using liquid, high-pressure liquid, paper, and thin-layer chromatographies; spectrophotometry; atomic absorption; and magnetic resonance imaging. These methods improve the predictability and therapeutic effectiveness of standardized crude botanical medicines, which are then evaluated for their efficacy in animal studies to determine pharmacologic potency, activity, and toxicity. U.S. and European companies have set strict quality control 1304

guidelines to ensure optimal yields of pharmacoactive constituents, with acceptable levels of impurities, pesticides, residual solvents, and heavy metals, and acceptable bacterial counts. Specific cultivation and harvesting techniques affect the therapeutic value of a given herb, which is related to the amount of active constituents in a specific medicinal plant. Methods of packaging, storage, and transport can dramatically affect the stability of active compounds. Both extracts and concentrates are obtained by adding appropriate solvents to raw herbs, which draws out the active constituents. The most common method is infusion, which is analogous to a tea bag being steeped in hot water to make tea; in this case, water is the solvent. When the water is slowly evaporated, the concentrate contains the active constituents. Pure ethanol is a solvent that is often used effectively to concentrate active herbal constituents. Immersing a high-quality bulk or raw herb in pure ethanol for hours or days, depending on the herb and the part used, and then pressing the solids out, yields an herbal tincture. The alcoholic tincture is diluted with water to yield a 20% alcohol tincture. In another method, a 20% alcohol mixture is the solvent. Fluid extracts can be made by vacuumdistilling some of the alcohol off; this avoids elevating the temperature, which may affect some of the active constituents. Another concentration process, solid extraction, yields a solid or semisolid product that can then be powdered or granulated for administration. Once an extract is produced, qualitative and quantitative analyses can be performed to assist in standardization. The percentage of known active constituents is assayed, to obtain predictable clinical results. An herbal infusion is generally a better source of active compounds than is an air-dried or a sun-dried powdered herb (Figure 66-1), but its action may not be as strong as those of concentrates such as tinctures, solid extracts, and fluid extracts. Potency of an extract can be defined by (1) percentage of active constituents or (2) concentration. Herbalists express concentration as an equivalency: a four-to-one extract is equivalent to or derived from four parts of the crude herb to yield one part extract. This is usually written as “4 : 1 solid extract.” Longer shelf life, greater effectiveness, and higher concentration of active constituents make a more standardized (thus better) product than the raw powdered herb; however, efficacy is difficult to compare. An example of a product that is standardized by the percentage concentration of pharmacoactive glycosides is Ginkgo biloba extract, marketed in Europe under the trade names Tanakan, Rokan, and Tebonin. It is typically standardized as 24% flavonoid glycoside. G. biloba extract has been shown to prevent metabolic and neuronal disturbances of cerebral ischemia and hypoxia in experimental models.93,105 Quality control is addressed for many herbal products when the known clinical effectiveness can be attributed to a specific active constituent. Improved analytic methods and use of highquality herbs (i.e., high in active constituents) helps ensure standardization. In Europe, the dosage is expressed in milligrams of active constituents, a system that favors consistency. The main difference between the infusion or extraction method and chemical isolation or synthesis is that the extracts still contain all the

Herbal Preparations for Clinical and Wilderness Use Botanical preparations can be readily and accurately prescribed for travelers and wilderness enthusiasts who need medical help. Throughout the ages, botanicals have been useful adjunctive therapeutic agents. Knowing which preparations from the natural pharmacopeia can be used and how to use them engenders a sense of integration with the natural environment. Indigenous peoples who depend on the botanical world hold a vast amount of untapped knowledge. Wilderness enthusiasts should help preserve this understanding of the natural world and do what they can to save natural habitats. Further investigation into the plant kingdom for useful medicinal agents will aid in these efforts. Herbal medicines can be prepared by decoction or infusion of bulk or raw herbs, or by making an extract, a concentrate, or a tincture. Infusions are prepared like a standard tea. The soft parts of plants—flowers, stems, and leaves—are placed in a warmed pot. Boiling water is poured over the herb, and the pot is covered to prevent beneficial essential oils from evaporating. The mixture infuses for about 10 minutes and then is strained. The supernatant can be used immediately or refrigerated in an airtight container for as long as 2 days. A standard adult dose of an herbal preparation is 28.3 g (1 oz) of dried herb in 473.2 mL (1 pint) of water, or 1 tablespoon per cup. The amount is doubled if the herb is fresh. Generally, it is best to take infusions hot by the cupful, 3 times daily for a chronic problem and up to every hour or two during an acute illness. To make infusions palatable, many herbalists add licorice, aniseed, or honey. The hard or woody parts of plants, such as bark, seeds, roots, rhizomes, and nuts, have tough cell walls that must be broken down by longer heating before they impart their constituents to water. The herbs can be first broken into small pieces by chopping, crushing, or hammering. Traditionally, a decoction was prepared in an earthen crock reserved especially for making herbal preparations. In the past, herbalists believed that some quality of the medicine was affected by the type of vessel or container in which the brew was prepared. Contemporary practitioners generally recommend the use of stainless steel, ceramic, or enamel and specifically discourage the use of aluminum or other alloyed metal pots. The herb is placed in an appropriate container and covered with cold water. The mixture is brought to a boil, covered, and simmered for 10 to 45 minutes, depending on the type and part of the herb being used. A decoction can be strained, flavored, or sweetened like an infusion, and it is consumed while hot. Modern practitioners use the most efficient and predictable forms of specific herbal medicines. Concentrates in capsule form are most effective and easiest to administer. The standard herbal concentrate found in the marketplace is in a ratio of 4 : 1. Ease of administration and dosing and the predictable clinical effects have made this the industry standard. Herbal tinctures are extracted into a specific percentage of alcohol and can be mixed easily to make formulas tailored to personal circumstances. Formula prescribing is an art, and a combination may be many times more effective than a single herb. Classic formulas for common ailments have been cataloged since the first herbal compendiums were recorded centuries ago. In this chapter, however, the focus is on single herbs and their specific uses, identification, and preparation.

Homeopathic Use of Botanicals Medical pioneer Samuel Hahnemann developed a radically different system of medicine nearly 200 years ago. Homeopathy is derived from the Greek words homoios, which means “similar,” and pathos, which means “disease” or “suffering.” The law of similars states that a substance that causes a set of symptoms in

pharmacologic dosages can be used as a cure for similar symptoms (even if the etiologic agent is different) if that substance is given in a homeopathic dilution. Most homeopathic remedies are prepared from plant, mineral, and animal products. In homeopathic medicine, there is a perfectly matched simillimum (the most effective medicine) if the predominant symptoms of a disease or illness match the symptoms produced when the substance is taken in large dosages by a healthy individual. For example, the herb A. belladonna, which contains atropine, is poisonous. In excessive dosages, the herb causes death; in moderate dosages, it creates hot, feverish states; and in tiny (homeopathic) dosages, it can effectively treat certain types of fevers, viral syndromes, and inflammatory states. A homeopathic dilution is created by taking a prepared tincture (mother tincture) of a botanical or an extract from nonplant sources and diluting it in a sequential or serial method. The difference in a homeopathic dilution is in its methodology. A homeopathic medicine must be succussed (shaken or agitated) mechanically or manually a prescribed number of times between the serial dilutions to be effective. The succussion method originally discovered by Hahnemann is said to “dynamize” the medicine. The succussion method is purported to affect the water molecules, creating a “memory” that the water molecules store in a lattice formation. This is similar to the storage of information on a magnetic disk or tape, except the signature resonance pattern is created from the interaction of the original tincture within the water’s lattice structure. The dilution can range from a 1× potency, which is a decimal dilution of a given ingredient (one part mother tincture per nine parts solute), to a 1 cup (one part mother tincture to 99 parts solute), to an extremely dilute 200c (one part mother tincture per 99 parts solute, serially diluted 200 times). A high-potency dilution (serially diluted more than 30 times in the × potencies and more than 12 times in c potencies) would be taken much less frequently than a low-potency dilution. To make a 30× homeopathic preparation of Arnica montana, one drop of the plant tincture is added to nine drops of pure water, and the mixture is succussed 50 to 100 times. Next, one drop from that solution would be added to nine drops of pure water and again succussed 50 to 100 times. This is repeated 30 times to yield the desired 30× homeopathic remedy. The number refers to the number of succussions and the letter to the ratio of the mother tincture to pure water. The mechanisms by which homeopathy works have yet to be elucidated, even though it has been practiced effectively for several hundred years. In 1900, an estimated 15% of U.S. physicians were prescribing homeopathic remedies.114 Recent studies have shown effective results in clinical trials using homeopathic medicines.31,88,100 Mechanisms of action for many common pharmaceuticals also remain unknown. Many theories in medicine are still based largely on empirical observations rather than on theoretical understanding. One herbal folk remedy for bruises, sprains, strains, and rheumatism in European and Native American medicine is topical application of the plant A. montana (leopard’s bane). Consistent with the homeopathic principle, toxic quantities of the wholeplant extract of arnica produce the same set of symptoms that it is intended to cure when administered internally in a homeopathic dosage or when the tincture or oil is applied topically to the affected area. Arnica is contained in herbal and homeopathic dosages in numerous ointments, salves, and poultices for the treatment of trauma resulting from localized sprains, strains, or contusions. Controlled studies in Germany have shown that effective products for sprains from athletic activity use an ointment that contains homeopathic arnica.171

Topical Application The earliest method of plant administration was topical application. Although many plants contain generalized moistureenhancing properties, some were found to be particularly effective in ameliorating specific acute conditions when applied topically. Two methods are used to apply remedies to the skin. The endermatic method applies medicine on the skin without 1305

CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

synergistic cofactors that enhance the function of the active ingredient. This important aspect of herbal medicine is lost once the active constituent is removed from the whole plant.

PART 7  PLANTS

friction, as when applying a compress to the dermis and epidermis after an abrasion or laceration. The epidermatic method uses friction and is most effective with botanical oils, liniments, ointments, and medicated warm and cold friction rubs, primarily for subdermal contusions and trauma, to effect circulatory changes.54 Topical application of medicinal plants is useful for many conditions, including abrasions, lacerations, burns, insect bites, infections, rashes, and dermatoses. Other applications include contusions, varicosities, joint pain, inflammation, and musculotendinous aches, strains, and sprains. Topical herbal remedies are applied with a poultice, a compress, a fomentation, or an ointment. Probably the most common, the poultice is used to apply a remedy to a skin area with moist heat. A poultice is prepared by bruising or crushing the medicinal parts of the plant to a pulpy mass, and then applying this to the affected area and covering it all with a moist heat source. If dried plants are used (or fresh plants if necessary), the materials are moistened by mixing with a hot, soft, adhesive substance such as moist flour or corn meal. A good way to apply a poultice is to spread the paste or pulp on a hot, wet cloth, which is wrapped around the affected area to help retain moisture and heat. The cloth is moistened with hot water as necessary. With irritant plants, such as those used in a mustard plaster, the paste is kept between two pieces of cloth to prevent direct contact with the skin. After the poultice is removed, the area is washed well with water to remove any residue. A poultice can be used to soothe, to irritate, or to draw impurities from the affected area, depending on which plants are applied. A fomentation is a hot cloth soaked with an herbal infusion or decoction. Fomentations are generally less active than are poultices. A cold compress is used for conditions that require an antiinflammatory cure. A cold, infusion- or decoction-soaked cloth is applied to an area and then removed when the body’s circulation has warmed the cloth to body temperature. The botanicals’ active constituents determine what actions the external applications will impart. For example, a poultice with an astringent herb such as Hamamelis (witch hazel) has an entirely different effect from one made with a strong vasodilator and rubefacient, such as capsicum (cayenne pepper). Ointments are another method of topical administration. Most ointments are made in a base of petroleum jelly, stable vegetable oils, beeswax, or a combination of these. The extract from the desired botanical is suspended within the base to create a stable solid product. Topical botanical products have the same function as do topical pharmaceutical ointments and are used to treat lacerations, abrasions, infections, and insect bites. Other uses for botanical topicals include hemostatic, antiinflammatory, antihistamine, rubefacient, analgesic, emollient, and circulatory stimulant actions. Herbal poultices, compresses, and ointments deliver their active compounds transdermally, as do pharmaceutical topical agents. The first uses of most medicinal plants were probably topical. In contemporary herbology, many of these plants are also used internally. Whole plants containing more than one ingredient with biologic activity generally invoke synergistic action of several components to produce the therapeutic action. Thus most botanicals have multiple applications for therapeutic purposes. Herbalists and homeopaths treat trauma of the skin, muscles, tendons, ligaments, and joint tissue with a topical agent in ointment or poultice form and give the same medicine internally in minute (homeopathic) dosages to enhance the activity, as with concurrent use of arnica ointment and homeopathic arnica. The major precaution in medical botany is to identify toxicity. Some of the most effective topical agents can be toxic if ingested. Most of these plants found in the wild could not be taken in sufficient dosages to be fatal before causing gastrointestinal (GI) upset. A tincture, herbal concentrate, or powdered version of the plant, however, could have deadly potential.

Use of Herbal Medicine in the Wilderness Travelers in the wilderness can choose preprocessed herbal preparations or naturally available plants in the immediate vicinity. A surprisingly large number of minor medical conditions 1306

encountered in an outdoor setting can be treated with plants in that location. North American recreational areas are home to medicinal plants that have been used by Native Americans for centuries. Recreationists in desert, alpine, and river environments can find medicinal plants in abundance. Nearly all plants encountered during an alpine trek in North America have some medicinal property, as do many in tropical and subtropical regions. Considerations for using herbal products in the wilderness are availability, ease of application, incidence of side effects, toxicity, spectrum of applicability, affordability, and effectiveness.

AVAILABILITY AND APPLICATION If a condition can be improved by application of a local botanical growing in the immediate vicinity, the pharmacy is immediately available. Plants may be in season, plentiful, and easily harvested. Finding the appropriate plants can be challenging, however, depending on the location, the season, the traveler’s familiarity with botanicals, and the type of medical condition. During mild seasons and at elevations conducive to plant growth in the continental United States, the chances of finding common plants are good. Otherwise, standardized commercial preparations of these herbs can be carried. These are packaged for long storage life, sanitary and convenient application, and standardization of active ingredients. Hundreds of plants can be applied topically for a variety of conditions. Most of the readily available plants, even if properly identified, require some form of processing for the active constituents to be used fully. Furthermore, expertise in the field requires years of training by a knowledgeable botanist and herbalist. It also requires knowledge of plants’ seasonal variations, ecologic niches, and precise identifications. However, a person who is neither a botanist nor a herbalist can gain a basic understanding of a few plant medicines that have a wide spectrum of applicability and a broad range of geographic distribution.

SIDE EFFECTS AND TOXICITY The American Association of Poison Control Centers annually reports plant ingestion as a significant category of accidental poisoning. In 1997, 5.6% of U.S. poisonings came from plants and mushrooms. Of the substances that were involved in pediatric poisonings, plants were responsible for 7.4% of exposures. Side effects or toxic reactions from botanicals are rare. Among the botanicals covered in this chapter, toxicity is not a major consideration, although anything can be toxic when used excessively or indiscriminately. Many toxic plants produce GI distress, vomiting, or diarrhea before any severe neurologic or cardio­ respiratory derangement. Often, toxic side effects are caused by one substance in a plant. When isolated, minute amounts of an alkaloid may be potentially dangerous, but when ingested in a form modified by other constituents, the altered drug effect allows tolerance of larger amounts of the toxic substance or substances. As is true for any medication, medicinal plants should be applied appropriately, and dosages for internal use should not exceed recommendations. Pregnancy and nursing may be contraindications. Dosages for almost any herb can be found in numerous references.124 Felter54 stated that “as a rule, doses usually administered are far in excess of necessity and it is better to err on the side of insufficient dosage and trust to nature, than to overdose to the present or future harm or danger of the patient.” In general, for the self-harvested herbs presented in this chapter, the dry, crushed, herbal adult dosage should be 1 teaspoon per cup or 8 oz of water; when the fresh herb is used, the amount should be twice that. Although no absolute law exists for administering medicines to children, Cowling’s rule takes the child’s age at the next birthday and divides by 24 to determine what fraction of the adult dosage should be given.54

SPECTRUM OF APPLICABILITY Most herbal medicines that have been cataloged and used historically are specifically indicated for one condition, although additional therapeutic effects have been noted over time. All the

AFFORDABILITY If the herbalist collects plants and processes them personally, the cost is minimal. The purchase price of botanicals depends on the rarity and origin. Some exotic and rare botanicals from Asia and the Amazon rainforest demand a high price on the world market. Panax ginseng has long been regarded by Asian peoples as a prized herbal tonic and can cost hundreds of dollars per root, depending on the size, origin, and age. Panax quinquefolius, or American ginseng, can cost as much as $52 per pound and was valued at $62 million as a cash crop in 1992.18 Many exotic herbal and animal-derived medicines from China have prices as high as those of precious metals. Most of the herbs produced in the continental United States and used for common ailments average 20¢ to 30¢ per dose (equivalent to 1 teaspoon of herbal tincture). Prices are not yet standardized. Quality control for production and supply and demand seem to dictate the cost of the mass-marketed herbal products. The best way to obtain a standardized product with a good quality-to-price ratio is to acquire the product from a botanical company that has been in business for at least 10 years and sells only to licensed health care practitioners.

North American Plant Medicines EPHEDRA (Ephedra species) Description and Habitat.  Common names for ephedra include Brigham Young weed, desert herb, Mormon tea, squaw tea, and teamsters’ tea. Ephedra spp. are shrubs with erect, straw-like branches found in desert or arid regions throughout the world and in the southwestern deserts of the United States. The Chinese ephedra called Ma Huang, E. sinica, is found throughout Asia; Ephedra distacha is found throughout Europe; Ephedra trifurca or Ephedra viridis (desert tea) (Figure 66-2), Ephedra nevadensis (Mormon tea), and Ephedra americana (American ephedra) (Figure 66-3, online) are found in North America; and Ephedra gerardiana (Pakistani ephedra) is found in Pakistan and India. The 0.6- to 2.1-m (2- to 7-foot) shrubs grow on dry, rocky, or sandy soils. The broom-like

FIGURE 66-2  Ephedra viridis. (Courtesy Cascade Anderson Geller.)

shrub has many jointed green stems with two or three small scale-like leaves that grow at the joint of stems and branches (Figure 66-4, online). Pharmacology.  Ephedra is generally used for its alkaloid content, which tends to consist of ephedrine, pseudoephedrine, and norpseudoephedrine. The various species vary significantly in both alkaloid type and content. In E. sinica, the total alkaloid content can be from 3.3% to 20%, with 40% to 90% being ephedrine and the remainder pseudoephedrine.48 The North American varieties, such as Mormon tea (E. nevadensis), are reported to contain no ephedrine. Ephedra’s pharmacology centers on the actions of ephedrine. Ephedrine and pseudoephedrine are used widely in prescription and over-the-counter drugs to treat asthma, hay fever, and rhinitis.62 The central nervous system (CNS) effects of ephedrine are similar to those of epinephrine but are much milder, and the duration of action is much longer. The cardiovascular effects are increased blood pressure, cardiac output, and heart rate. In addition, ephedrine increases brain, heart, and muscle blood flow while decreasing renal and intestinal circulation.62 Relaxation of bronchial, airway, and uterine smooth muscles also occurs.62 Pseudoephedrine has weaker CNS and cardiovascular system actions but has bronchial smooth muscle relaxation effects. Because it has fewer side effects, it is used more often than ephedrine for asthma.62 Pseudoephedrine also demonstrates significant antiinflammatory activity.74,94 Per 100 g, the dry leaf of ephedra is reported to contain 5 g protein, 5810 mg calcium, and 500 mg potassium.48 Native American and European Medicinal Uses.  Ephedra has been used extensively in the West and in Asia for upper respiratory conditions such as asthma, bronchitis, and hay fever. It has also been used to treat edema, arthritis, fever, hypotension, and urticaria.35 It is said to be valuable as a diuretic, febrifuge, and tonic.110 The Navajo Indians applied the dried, crushed, long leaf of ephedra to syphilitic sores, and the Hopi Indians drank a tea from the branches and twigs of a related species for the same condition.165 Other tribes used the ground and roasted root for making bread.48 Mormon tea is a folk remedy for colds, gonorrhea, headache, nephritis, and syphilis.48 Mexicans mix the leaves with tobacco and smoke them for headaches.48 Modern Clinical and Wilderness Applications.  Ephedra has proved to be an effective bronchodilator for treating mild to moderate asthma and hay fever. The common preparations include other herbs that have antitussive and expectorant effects, such as licorice (Glycyrrhiza glabra) and grindelia (Grindelia camporium). Ephedrine promotes weight loss.124 Appetite suppression plays a role, but increased metabolic rate of adipose tissue is the main mechanism.8 The weight reduction effects can be enhanced by up to 60% with the addition of methylxanthine.49 In response to accumulating evidence of adverse affects related to Ephedra, the FDA banned the sale of Ephedracontaining supplements on the retail market. In the wilderness, specifically the desert, the raw herb Mormon tea from E. nevadensis or E. viridis can be useful for hay fever, mild asthma, bronchitis, or upper respiratory infection (URI). These species contain minimal amounts of ephedrine and principally contain pseudoephedrine; thus they can be used without some of the unpleasant side effects of the Asian species. They can also be used for mild fevers associated with influenza or URI. The shrubs are typically found growing on dry, rocky, or sandy slopes. The leaves can be picked fresh or sun dried for 6 to 8 hours and can be prepared as a steeped tea or an infusion. Generally, the dose should be the equivalent volume of 1 teaspoon of dried, crushed stems per 8 oz of water, steeped for 10 minutes. The patient should not exceed a dosage of this amount given 6 times per day. Once harvested, the leaves can be kept for an indefinite period for later use if stored in an airtight container. 1307

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botanicals covered here have multiple uses. Comfrey (Symphytum officinale) may be used as a topical antiinflammatory agent; it also has constituents that are effective for GI conditions when taken internally.110 Aloe vera gel is an excellent topical agent for abrasions and burns; taken internally, the latex portion serves as an effective laxative.110 Calendula officinalis has antimicrobial properties that make it an effective topical dressing for mild infectious conditions, whereas internally it has antipyretic effects.110

PART 7  PLANTS

FIGURE 66-5  Goldenseal (Hydrastis canadensis).

Toxicity.  According to Duke,48 an infusion of ephedra produced a “prompt and extensive contraction of uterine muscle when applied to smooth muscle strips of virgin guinea pig uteri.” Ephedra may also elevate blood pressure. Frequent use may result in nervousness and restlessness. It should be used with caution if the patient has hypertension, heart disease, thyrotoxism, diabetes, or benign prostatic hypertrophy. Ephedra should not be used with antihypertensive or antidepressant medications.

GOLDENSEAL (Hydrastis canadensis) Description and Habitat.  Hydrastis (Figure 66-5) has a perennial root or rhizome that is tortuous, knotty, and creeping. The internal color is bright yellow, with numerous long fibers. The stem is erect, simple, herbaceous, and rounded, from 15 to 30 cm (5.9 to 11.8 inches) in height, becoming purplish and bearing two unequal terminal leaves. The leaves are alternately palmate with three to five lobes, hairy, dark green, and cordate at the base. The flowers, which are evident in early spring, are solitary, terminal, small, and white or rose colored. The plant is a native of eastern North America and cultivated in Oregon and Washington. The parts used are the dried rhizome and roots. Pharmacology.  The alkaloids derived from Hydrastis are hydrastine (1.5% to 4%), berberine (0.5% to 6%), berberastine (2% to 3%), canadine, hydrastinine, and related compounds. Other constituents include meconin, chlorogenic acid, phytosterins, and resins.124 Native American and European Medicinal Uses and Folklore.  Native Americans used Hydrastis extensively as an herbal medicine and clothing dye. The Cherokee Indians used the roots as a wash for local inflammations, as a decoction for general debility and dyspepsia, and to improve appetite. The Iroquois Indians used a decoction of the root for whooping cough, diarrhea, liver trouble, fever, sour stomach, flatulence, pneumonia, and heart trouble.119 Early European uses date back to 1793: in Collections for an Essay Towards a Materia Medica of the United States, Benjamin Smith Barton noted that Hydrastis was useful as an eyewash for conjunctival inflammation and as a bitter tonic. In the pharmacy of the 19th century (1830), goldenseal was listed among the official remedies in the first revision of the New York edition of the USP. It was listed in the USP until 1926 and recognized in the National Formulary until 1955.75 Modern Clinical and Wilderness Applications.  Goldenseal is among the top sellers in the American herbal medicine market. It is used as an antiseptic, hemostatic, diuretic, laxative, tonic, and antiinflammatory for inflammation of the mucous membranes. It has also been recommended for hemorrhoids, nasal congestion, sore mouth and gums, conjunctivitis, external wounds, sores, acne, and ringworm.107 1308

Modern research into the active ingredients berberine and hydrastine has shown why some of the folk applications are effective. The most widely studied component is berberine. This isoquinoline alkaloid has demonstrated antibiotic, immunostimulatory, anticonvulsant, sedative, febrifugal, hypotensive, uterotonic, choleretic, and carminative (promoting the elimination of intestinal gas) activities.124 Berberine has broad-spectrum antibiotic activity. The antimicrobial activity has been demonstrated on protozoa, fungi, and bacteria, both in vitro and in vivo. Anti­ microbial action has been noted against Staphylococcus, Streptococcus, Chlamydia, Corynebacterium diphtheriae, Escherichia coli, Salmonella typhi, Vibrio cholerae, Pseudomonas, Shigella dysenteriae, Entamoeba histolytica, Trichomonas vaginalis, Neisseria gonorrhoeae, Neisseria meningitidis, Treponema pallidum, Giardia lamblia, Leishmania donovani, and Candida albicans.124 Berberine inhibits adherence of bacteria to host cells.151 Active ingredients in the crude botanical may be responsible for the wide-spectrum effectiveness of Hydrastis. The antifungal properties, for example, prevent the overgrowth of Candida that frequently occurs with use of other antibiotic therapies. Other studies have shown the immunostimulatory activity of berberine-containing plants. Berberine increases blood flow through the spleen; improved circulation may augment the immune function of this lymphoid organ.137 Berberine also activates macrophages.99 Historically, berberine-containing plants have been used as febrifuges, and in rat studies they have an antipyretic effect three times as potent as that of aspirin.124 Plants such as goldenseal are very effective in treating acute GI infections. In several clinical studies, berberine has successfully treated acute diarrhea caused by E. coli, S. dysenteriae, Salmonella, Klebsiella, Giardia, and V. cholerae.* Berberine-containing plants, in addition to having antimicrobial properties, influence the enterotoxins produced by offending pathogens.25,152,153 GI illness is a major concern of travelers to areas with questionable sanitation. Both waterborne and food-borne bacterial and protozoal infections are concerns for persons in wilderness and Third World environments. Some experts recommend using a berberine-containing botanical source prophylactically at least 1 week before a visit to questionable areas and for 1 week after return.124 Various eye complaints involving the conjunctivae and surrounding mucous membranes have been effectively treated with forms of berberine extract. Recent studies point to the effectiveness of berberine in treating infection caused by Chlamydia trachomatis. Clinical trials found that a 2% berberine solution compared favorably with sulfacetamide. Although the symptoms resolved more slowly with the berberine extract, the rate of relapse was much lower in the berberine-treated group.10,120 A standardized form of H. canadensis is beneficial for generalized digestive disorders (acute dysentery, gastritis) and for infective, congestive, and inflammatory states (sinusitis, pharyngitis, stomatitis) of mucous membranes. A typical dosage depends on the source and method of the extract. For the previous conditions, the following dosages, 3 times a day, are recommended: dried root or as infusion, 2 to 4 g; tincture (1 : 5), 6 to 12 mL (1.5 to 3 teaspoons); or solid extract (4 : 1 or 10% alkaloid content), 250 to 500 mg. Hydrastis can also be used as a wash or rinse for conjunctivitis, sinusitis, and pharyngitis. Eye drops, nasal lavage, and gargle are applied in a 5% preparation of a 1 : 5 tincture, or 1 to 2 teaspoons of powdered herb in 8 oz of water to create an infusion for application to inflamed mucous membranes. This can be repeated 3 times a day. Toxicity.  Berberine and berberine-containing plants are generally nontoxic. In recommended dosages, berberine-containing plants have not been shown to be toxic in clinical trials. The median lethal dose (LD50) of berberine sulfate in mice is approximately 25 mg/kg, and in dogs, intravenous (IV) dosages up to 45 mg/kg do not produce lethal or gross toxic effects.137 Hydrastis should not be used during pregnancy, and long-term ingestion may interfere with the metabolism of B vitamins. *References 13, 38, 46, 70, 92, 138, 143.

FIGURE 66-6  Arnica montana. (Courtesy Jill Stansbury.)

ARNICA (Arnica montana) Description and Habitat.  Arnica is a perennial plant generally found in mountainous areas of Canada, the northern United States, and Europe. The plant reaches a height of 30 to 60 cm (11.8 to 23.6 inches) and generally contains from one to nine large daisy-like flower heads, which bloom during summer months (Figures 66-6 to 66-8; Figures 66-7 and 66-8, online). Pharmacology.  The flower is used both internally and externally for medicinal effects. The rootstock is used to make commercial preparations for tinctures and oils that are applied topically. The active constituents of the plant drug are flavonoids, volatile oils, and plant pigments (carotenoids).166 Specific constituents include arnicine, formic acid, thymohydroquinone, lobelamine, and lobeline (piperidine alkaloid).31 Native American and European Medicinal Uses and Folklore.  The Catawba Indians administered the tea of arnica roots to treat back pain. In Europe, the flower heads have been used since the 16th century as an application for bruises and strains.164 European arnica was included in the USP from the early 1800s until 1960 and was recognized for its effects on the healing of bruises and sprains. Specific instructions given in the American Dispensory in 1922 listed arnica as effective for “muscular soreness and pain from strain or overexertion; advanced stage of disease, with marked enfeeblement, weak circulation, and impaired spinal innervation; … tensive backache, as if bruised or strained; [and] … headache with tensive, bruised feeling and pain on movement.”54 Arnica in concentrated tincture form has been a popular but not necessarily safe medicine to treat inflammatory swellings and to relieve the soreness of myalgia and the effects of bruises and contusions. Dosages above the therapeutic range cause vagal inhibition when ingested and may cause toxicity if the concentrated tincture is applied topically. Therefore the most common use has been fomentation of the flowers for topical applications in the treatment of strains and sprains. Modern Clinical and Wilderness Applications.  Contemporary use of A. montana is generally limited to topical commercially prepared ointments and salves, in conjunction with internal homeopathic (low-dose) use for the same indications. Although its alkaloid (arnicine) and volatile oil (thymohydroquinone) are both relatively toxic, the actions of these constituents are extremely useful in resolving contusions and soft tissue injury. Most ointments are found to contain a 1× homeopathic dilution of arnica tincture, which is about 4% by volume. Oral dosage is given in homeopathic potencies of 6× to 200c, depending on the severity of the condition. For application in the wilderness, most naturopathic first-aid kits include both the ointment and the oral homeopathic forms of arnica. For direct use of the plant in treating minor sprains and strains, 2 teaspoons of the dried flower tops can be steeped in 1 cup of water for 10 minutes, and the infusion applied in a cold compress to the affected area. This should be repeated each

Toxicity.  Arnica tincture or infusion can be toxic if the concentration is too high. Undiluted tincture should not be used internally or in compress form over an open wound. Vagus nerve inhibition is the primary toxic effect; GI irritation is also noted. Toxic reactions include gastric burning; nausea; vomiting; headache; decreased temperature; dyspnea; cardiovascular collapse; convulsions; motor, sensory, and vagal paralysis; and death.31

GARLIC (Allium sativum) Description and Habitat.  Garlic is a member of the lily family. It is a perennial plant cultivated worldwide (Figure 66-9). The garlic bulb is composed of individual cloves enclosed in a white skin. The medicinal herb is found in the bulb and is used either fresh or dehydrated. Garlic oil, which also has medicinal value, is obtained by steamed distillation of the crushed fresh bulbs.107 Pharmacology.  The medicinal compounds in garlic generally contain sulfur and have been the subject of most research on garlic. Two primary compounds are an odorless chemical called alliin and the enzyme allinase, which begins a cascade of chemical reactions when the garlic clove is cut, crushed, or bruised. Alliin is converted to allicin, which is responsible for the characteristic odor of garlic. Allicin is strongly antibacterial and considered to be the major source of the antimicrobial effects of garlic. Breakdown products of allicin include diallyl sulfide, disulfide, and trisulfide. Heat speeds up the reaction, so cooked garlic and steamed distilled garlic oil contain little or no allicin. About 0.1% to 0.36% of the volatile oils in garlic is composed of sulfurcontaining compounds (e.g., allicin, diallyl sulfide, diallyl trisulfide). These volatile oils are considered to be responsible for most of the pharmacologic properties of garlic. Other constituents of garlic include s-methyl-L-cysteine sulfoxide, protein (16.8% by dry weight), a high concentration of trace minerals (particularly selenium and germanium), vitamins, glucosinolates, and the enzymes alliinase, peroxidase, and myrosinase.124,132 Native American and European Medicinal Uses and Folklore.  Throughout history, garlic has played an important part in

FIGURE 66-9  Garlic blossom (Allium sp.). (Courtesy Cascade Anderson Geller.)

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CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

2 hours in addition to standard first-aid procedures. The infusion lasts a day if refrigerated and a few hours if not; therefore it is best to use a fresh infusion whenever possible. In addition, if available, the oral homeopathic preparation (30× to 200c) should be taken 3 times daily until the swelling is reduced significantly. A topical ointment can be applied every 2 to 3 hours for this condition in place of the compress. According to Weiss,165 arnica is safe and effective for topical contusions and for stimulating granulation and epithelialization. A tablespoon of tincture is added to 500 mL of water, and the gauze compress is then placed on the wound. This stimulates local circulation and acts on the peripheral vasculature. After granulation has occurred, ointments may be applied.

PART 7  PLANTS

medicinal herbology. Clay garlic bulbs dating back to 3750 BC were found in Egypt. Preserved garlic bulbs were discovered in the tomb of Tutankhamen. An entire basket of these bulbs from the tomb of Kha at Thebes is in the Turin Egyptian museum. The Greek historian Herodotus recorded that an enormous amount of money was spent on garlic for the builders of the great pyramids. One of the earliest Sanskrit manuscripts, the Bower manuscript, devotes its entire first section to garlic, describing its legendary origins. It says that garlic keeps in order the three fluids and can cure thinness, weakness of digestion, lassitude, coughs, inflammation of the skin, piles, glandular swellings in the abdomen and enlargement of the spleen, indigestion, constipation, excessive urination, worms, wind in the body (rheumatism), leprosy, epilepsy, and paralysis. Within the traditional medical circles of Greece and Rome, medieval Europe, and the Far East, similar claims may be found. Galen, Dioscorides, and Aristotle extolled garlic as an excellent medicine. Hippocrates recommended garlic as a diuretic; to regulate digestion; to treat bowel pains, inflammations, and infections; and to regulate menstruation. Early Chinese and European herbalists used garlic as a heating and drying agent, and therefore to prevent and cure diseases arising from cold, poisons, excesses of diet and drink, and sluggish metabolism. Pasteur noted garlic’s antimicrobial properties in 1858. Albert Schweitzer used garlic in Africa to treat amebic dysentery. Garlic was also used as an antiseptic to prevent gangrene during both world wars. Modern Clinical and Wilderness Applications.  The pharmacologic effects of garlic are based on its activity as a hypoglycemic and hypolipemic regulating agent,* anticoagulant,† antihypertensive,112,133 antimicrobial,‡ detoxifier of heavy metals,3 and immune system modulator.89 Animal and human studies have substantiated that garlic lowers serum cholesterol and triglyceride levels and increases the amount of high-density lipoproteins. Dietary atherosclerosis was significantly reduced in rabbits fed garlic consistently for weeks; also, an extract of garlic and onions was more effective than clofibrate against hyperlipidemia and subsequent lipid deposition within the aorta.21 After 4 months of feeding rabbits a highcholesterol diet, the average lipid content in the aorta of the control animals rose from 5.95 to 13.75 mg/100 g dry weight. Animals taking clofibrate for 4 months had 7.95 mg, and garlicfed animals 6.23 mg/100 g dry weight of lipid content in the aorta.21 Other studies of experimental atherosclerosis in rabbits support these findings.84,96 Decreased atheromatous lesions seem to be a consistent finding in rabbits fed high-cholesterol diets supplemented with garlic. Of various sulfur-containing amino acids isolated from garlic, s-methylcysteine and s-allylcysteine exert the greatest antilipidemic effects.82 Components of garlic can combine with the sulfhydryl group, the functional part of coenzyme A that is necessary for biosynthesis of fatty acids, cholesterol, triglycerides, and phospholipids. The lipid-lowering effect may best be attributed to inactivation of the sulfhydryl group.9 In vitro and in vivo tests show reduced conversion of acetate into cholesterol by liver tissues.36 Because sulfhydryl groups are involved at all levels of metabolic activity, the impact of garlic could be more extensive. Studies suggest that garlic may lower blood pressure by acting the same way prostaglandin E1 does, by decreasing peripheral vascular resistance.129 As a nutritional supplement, garlic is composed of magnesium, iron, copper, zinc, selenium, calcium, potassium chloride, germanium, sulfur compounds, amino acids, and vitamins A, B1, and C. Garlic increases the body’s capacity to assimilate thiamine by enhancing its absorption. Thiamine is a key part of the co-carboxylase enzyme system, which has beneficial effects on liver cells; this may explain why garlic offers prophylaxis against liver and gallbladder damage. In one study, garlic was shown to *References 7, 9, 14, 20, 22, 26-28, 36, 37, 69, 82, 83, 86-88, 90, 91, 96, 97, 127. † References 6, 19, 24, 25, 29, 60, 85, 111, 125, 139, 148. ‡ References 4, 5, 33, 56, 101, 111, 126, 1, 157.

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protect hepatocytes in tissue culture from the damage of carbon tetrachloride.129 Antioxidant activity has been attributed to garlic and garlic derivatives. The free radical scavenger action of garlic may be explained by its germanium, glutathione, selenium, and zinc content. The last three are key components of the antioxidant enzyme superoxide dismutase and glutathione peroxidase. Animal studies show that feeding garlic oil enhanced physical endurance in normal rats and also reduced the decrease in physical endurance induced by isoproterenol, a synthetic catecholamine that induces necrosis of the myocardium.141 Garlic inhibits platelet aggregation in animals; similar effects can be demonstrated in vitro and in vivo in humans.44,147 An antiplatelet extract of garlic, ajoene, was found to potentiate the antithrombotic effect of antiinflammatory drugs. Under fasting conditions, inhibition of platelet aggregation by garlic or its extracts is dosage related.149 The garlic effect may be linked to inhibition of thromboxane synthesis or to altered properties of the plasma membrane. Methyl (2-propenyl) trisulfide, another component of garlic, is 10 times more potent as an inhibitor of platelet aggregation than diallyl disulfide or trisulfide.6 Thrombocyte aggregation inhibition is enhanced by two other compounds, 2-vinyl-1,3-dithiene and allyl-1,5-hexidienyl-trisulfide.17 Garlic and its juice or oil also enhance fibrinolysis.23 In a double-blind, placebo-controlled trial, cycloalliin, a component of garlic, was given to volunteers and patients after myocardial infarction and significantly increased fibrinolysis 1.5 hours later.52 Chutani and Bordia39 observed that the increase took place 6.5 to 12 hours after garlic intake. Daily garlic ingestion for 1 month generated a 72% to 85% increase in fibrinolysis in patients with ischemic heart disease.136 The pharmacologic versatility of garlic is best reflected by its antiviral, antifungal, antiprotozoan, antiparasitic, and antibacterial activities.* Laymen are credited with being the first to describe the scientific basis for the medicinal use of garlic extract.168 Huddleson and colleagues78 and Cavallito and Bailey34 demonstrated in 1944 that garlic juice and allicin at low concentrations inhibited the growth of Staphylococcus, Streptococcus, Bacillus, Brucella, and Vibrio spp. Recent studies using serial dilutions and filter paper disk techniques have shown that fresh garlic, powdered garlic, and vacuum-dried preparations were effective antibiotic agents against many bacteria, including Staphylococcus aureus, α- and β-hemolytic Streptococcus, E. coli, Proteus vulgaris, Salmonella enteritidis, Citrobacter, and Klebsiella pneumoniae.124 These studies compared the antimicrobial effects of antibiotics, including penicillin, streptomycin, chloramphenicol, erythromycin, and tetracycline, with those of garlic. Beside confirming garlic’s well-known antibacterial effects, studies demonstrated its effectiveness in inhibiting the growth of some antibiotic-resistant bacteria.1,51,144 Garlic has also demonstrated significant antifungal activity against a wide range of fungi.† From a wilderness perspective, inhibition of fungi that can affect the skin (Microsporum, Trichophyton, Epidermophyton, and Candida albicans) can be significant. Garlic juice applied topically is an effective alternative in treating fungal skin diseases.4 Garlic compares well with nystatin, gentian violet, and six other reputed antifungal agents used to treat C. albicans.2,121,131,140 Garlic has long been associated with prophylaxis against influenza virus. In vivo studies with mice revealed that garlic administration protected mice against intranasal inoculation with influenza viruses and enhanced reproduction of neutralizing antibodies after vaccine administration.126 In vitro studies have shown that garlic has antiviral activity against influenza B virus and herpes simplex virus type I.155 Preliminary studies have revealed significant enhancement of natural killer (NK) cell activity in humans administered raw or cold, aged whole-clove garlic preparations daily for 3 weeks.89 The antiviral activity of garlic in humans may be secondary to the direct toxic effect on viruses and enhanced NK cell activity that destroys virus-infected cells. *References 4, 5, 33, 56, 127, 154, 170. † References 2, 4, 58, 79, 118, 121, 131, 140, 160.

CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

Wilderness Medical Applications.  The use of garlic in the outdoor setting can be extensive. Its use as a food should be encouraged despite its odor, particularly in people with elevated cholesterol levels, heart disease, hypertension, diabetes, asthma, fungal infections, respiratory infections, and GI disorders (intestinal parasites, dysentery). A macerated garlic poultice and garlic slices serve as topical agents for fungal infections, ulcerated wounds, pyoderma, and other skin infections. The poultice can be used directly on the dermatologic problem, and as a suppository it can be used to treat vaginitis, particularly infections caused by C. albicans. For this application, one to two fresh chopped cloves can be made into a poultice. This should be kept on the affected site for several hours and changed at least once every 6 hours with a fresh preparation. If the garlic causes epidermal irritation, its use is discontinued. Prophylactic use during the flu season can reduce the incidence of infection. Within the first 48 hours of onset of a flu or upper respiratory infection, one or two cloves can be consumed with a carbohydrate source to prevent stomach irritation. Alternatively, two or three oil-of-garlic capsules can be taken. For persons concerned about the social-segregating aspect, extracts that preserve the allicin content but remain odorless can be used. Toxicity.  For the vast majority of individuals, garlic is nontoxic at usual dosages. However, some people develop allergic contact dermatitis or irritation of the digestive tract. Apparently they are unable to detoxify allicin and other sulfur-containing components. Prolonged consumption of large amounts of raw garlic by rats results in anemia, weight loss, and failure to grow.127

GINGER (Zingiber officinale) Description and Habitat.  Ginger is an upright perennial herb with tuberous rhizomes, from which an aerial stem grows to 1.5 m (4.9 feet) in height. It is native to southern Asia, although it is cultivated in the tropics. Extracts and dried ginger are produced from dried unpeeled ginger; peeled ginger loses much of its essential oil content.159 Pharmacology.  Ginger is composed of a rich variety of nutrients and enzymes. The general composition is starch (50%); protein (9%); lipid (6% to 8%), composed of phosphatidic acid, lecithin, free fatty acids, and triglycerides; protease (up to 2.26%); volatile oils (1% to 4%), the principal components of which are three sesquiterpenes (bisabolene, zingiberene, zingiberol); vitamins, especially niacin and vitamin A; and resins.159 Native American and European Medicinal Use.  Z. officinale (Figures 66-10 and 66-11) is native to southern Asia and tropical Africa. Therefore it did not have a role in the early herbal preparations of European and Native American herbal medicine. Modern Clinical and Wilderness Applications.  Clinical use of ginger for antiinflammatory action, cholesterol-lowering effects, and relief of dizziness and motion sickness is noted in

FIGURE 66-11  Ginger plant with rootstock. (Courtesy Kevin Davison.)

herbal texts.* A choleretic effect (the promotion of bile flow to the gallbladder and small intestine) and the conversion of cholesterol into bile acids are enhanced by ginger ingestion and may be responsible for its overall cholesterol-lowering effect. An early eclectic medical text listed ginger as a local stimulant, sialogogue, diaphoretic, and carminative.54 Powdered ginger in a large quantity of cold water taken before sleep frequently “breaks up” a severe cold, and a hot infusion of ginger tea is a popular remedy for similar use to mitigate the pains of dysmenorrhea.54 Ginger may relieve painful spasmodic contractions of the stomach and intestine. The antiinflammatory action of ginger is thought to be caused by potent inhibition of inflammatory compounds, such as prostaglandins and thromboxanes.98 Ginger is also known to contain strong plant proteases such as bromelain, ficaine, and papain, which may explain some of its antiinflammatory action.159 Ginger has been used historically for major GI complaints. It is generally regarded as an excellent carminative (promoting elimination of intestinal gas) and intestinal spasmolytic.124 One of the most noted uses of ginger in contemporary herbal medicine that applies to wilderness medicine is its action on the symptoms of motion sickness and seasickness.66,67,123 Ginger is also a significant antiemetic. It has long been used for the treatment of nausea and vomiting associated with pregnancy. The efficacy of ginger has been confirmed in hyperemesis gravidarum, a severe form of nausea and vomiting during pregnancy. Ginger root powder at a dosage of 250 mg 4 times a day brought a significant reduction in both the severity of nausea and the number of attacks of vomiting during pregnancy.55 To treat motion sickness and vertigo, two 500-mg capsules of powdered ginger root are eaten 20 to 30 minutes before the precipitating event. The same dose is used for the nausea of pregnancy during the acute attack. The raw ginger root can be grated using 1 teaspoon in 4 oz of water, steeped for 10 minutes, and taken every 30 minutes until the symptoms of motion sickness abate. Toxicity.  There appears to be no toxicity associated with ginger root ingestion.

FIGURE 66-10  Ginger (Zingiber officinale) flower. (Courtesy Kevin Davison.)

*References 54, 55, 66-68, 98, 123, 145, 149, 150, 159.

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PART 7  PLANTS

A

B FIGURE 66-12  A, Comfrey (Symphytum officinale) flower. B, Comfrey (Symphytum officinale) leaf. (A courtesy Cascade Anderson Geller.)

COMFREY (Symphytum officinale) Description and Habitat.  Comfrey (Figure 66-12) is a perennial herb with a stout spreading root that is divisible for propagation. Comfrey grows about 1 m (3.3 feet) high and has coarse, bristly, oblong, lanceolate leaves. The tubular flower can be purplish, blue, white, red, or yellow (see Figure 66-12, A). About 25 Symphytum species are described; they are indigenous to countries around the Mediterranean Sea and in northern Asia. Comfrey is typically found in moist meadows and other wet places in the United States and Europe. Pharmacology.  The chemical constituents of S. officinale roots include carbohydrate, predominantly sucrose; the amino acids serine and asparagine; the phenolic acids chlorogenic acid, caffeic acid, and p-coumaric acid; the alkaloids choline and allantoin; and the pyrrolizidine alkaloids viridiflorine, echinatine, heliosupine, symphytine, echimidine, and lasiocarpine.161 The most concentrated (0.88% to 1.71%) alkaloid, allantoin, is generally credited with comfrey’s beneficial effects. Native American and European Medicinal Uses and Folklore.  In Europe, comfrey is a common perennial grown in the garden for animal fodder. Russian comfrey is often promoted as a medicinal herb for use as a tonic. Comfrey is also cultivated in Japan as a green vegetable, and a tonic made from it has been used in American herbal medicine for hundreds of years.103 Comfrey has long been known as an external agent for rehabilitation of musculoskeletal and orthopedic injuries. Its former 1312

name, bone knit, derives from the external use of poultices of leaves and roots, which were believed to help heal burns, sprains, swellings, and bruises. Comfrey has been claimed to heal gastric ulcers and hemorrhoids, suppress bleeding, and relieve bronchial congestion and inflammation.15 The healing action of a poultice derived from the roots and leaves is probably related to the presence of allantoin, an agent that promotes cell proliferation. The underground parts contain 0.6% to 1.3% allantoin and 4% to 6.5% tannin.32,117 Comfrey extracts applied topically have been reported to heal wounds and bones in about one-half of the normal time. In herbology, a general rule is that if anything is broken, use comfrey.169 Herbalists have also found that the allantoin concentration from a fluid extract of comfrey can increase the rate of wound healing of lacerations sufficiently to avoid the use of sutures.167 In European folklore, comfrey was regarded as an herb having unsurpassed ability to heal any injured or broken tissue. The mucilage (gelatinous mucopolysaccharide) of the comfrey root was named “the great cell proliferator,” helping new flesh and bones to grow. Comfrey was one of the main herbs found in any poultice or fomentation. European herbalists considered comfrey exceptional for coughs and soothing inflamed tissues. Comfrey is effective for treating upper respiratory inflammation and has been used successfully to treat hemorrhagic conditions of the lungs. Modern Clinical and Wilderness Applications.  Comfrey lotions and salves containing 0.5% to 2.5% allantoin have been used for sprains, strains, and contusions. In the 1980s, comfrey became controversial because of potential hepatotoxicity. Members of the family Boraginaceae (Heliotropium, Symphytum) contain a variety of related pyrrolizidine alkaloids reported to cause hepatotoxicity in animals. Although no hepatotoxic episodes from ingestion of comfrey have been reported in humans, the potential exists, so caution is advised when using comfrey for internal consumption.103 Topical use of comfrey products as yet poses no concern for toxicity. As a topical agent after acute trauma such as musculoskeletal injuries, strains and sprains, or contusions, comfrey is an exceptional medicine.16 A prepared gel of comfrey with a standardized allantoin concentration should be carried during travel or camping expeditions in the wilderness. The raw herb can be used if the plant is nearby. The herb is readily identifiable, but it should not be confused with foxglove (Digitalis purpurea) and should be used with caution when taken internally in its raw state. For use in a poultice or compress, the leaves may be picked damp, macerated, and applied topically for up to 24 hours. Toxicity.  Comfrey is not recommended for routine internal ingestion. Animal studies indicate that hepatic damage is an eventual outcome if the herb is consumed over a long period.

ALOE (Aloe vera) Description and Habitat.  The aloe is a perennial plant native to South and East Africa and is also cultivated in the West Indies and other tropical and temperate areas. The leaves, which emerge from a central rosette produced by a central fibrous root, are 30 to 60 cm (11.8 to 23.6 inches) long, narrow, fleshy, and light green with spiny teeth on the margins (Figure 66-13). Aloe is easily cultivated as a houseplant and can be grown in a sunny warm spot with good drainage. The genus Aloe comprises more than 300 species, which are members of the Liliaceae (lily) family. Aloe spp. are perennial succulents native to Africa. They are not cacti and should not be confused with American aloe, the century plant. Pharmacology.  Two important products are derived from aloe: a gel and a latex. Aloe gel is a clear gelatinous material extracted from the mucilaginous cells found in the inner tissue of the leaf (see Figure 66-13). It is obtained by crushing the leaves and straining the mass repeatedly to remove cellular debris. The result is a clear gel, which is the product most frequently used in the health food and cosmetic industries. It is generally devoid of

anthraquinone glycosides. A variety of compounds have been identified in Aloe spp., including polysaccharides, tannins, organic acids, enzymes, vitamins, minerals, saponins, and steroids.103 The bitter yellow latex of aloe contains cathartic anthraquinone glycosides, mostly barbaloin, as the active constituents. The concentrations of the glycosides vary with the type of aloe, ranging from 4% to 25% of aloe in concentration. The watersoluble fraction of aloe is called aloin and is a mixture of active glycosides. Cathartics have been derived from extracts of the latex and can create strong purgative effects by stimulating the large intestine. Native American and European Medicinal Uses and Folklore.  Fresh Aloe vera gel is well known for its domestic medicinal values.63,106,122,130 It has been dubbed the burn plant, the first-aid plant, and the medicine plant. When fresh, the gel relieves thermal burns and sunburns and promotes wound healing. It also has moisturizing and emollient properties. Because of these effects, aloe is widely used as a home remedy. Aloin and other anthraquinone derivatives of aloe are extensively used as active ingredients in laxative preparations. Aloin is also used as an antiobesity preparation.107 Aloe or aloin extracts are also used in sunscreens and other cosmetic preparations, and in drugs for moisturizing, emollient, or wound-healing purposes. In folk medicine, aloe is used for condylomas, warts, abnormal skin growths, and cancers of the lip, anus, breast, larynx, liver, nose, stomach, and uterus.48 Other folklore suggests that parts of the plants be chewed to purify the blood. The pulp is said to possess wound-healing hormonal activities and “biogenic stimulators” and is used for intestinal ailments, sore throat, and ulcers. In India it is used to treat piles and rectal fissures. Slukari hunters in Africa’s Congo basin rubbed their bodies with the gel to eliminate the human scent, making them less likely to disturb prey. During epidemics of influenza, Lesotho natives take a public bath in an infusion of Aloe latifolia.48 Modern Clinical and Wilderness Applications.  Although numerous claims have been made for aloe gel, its most common lay use is in the treatment of minor burns and skin irritations. In 1935, a report described the use of aloe in the treatment of radiation-induced dermatitis.41 This study followed a 5-week course of topical applications of either the whole leaf or the leaf macerated into gel, resulting in complete wound healing after 4 months. In 1937, studies used a calamine- and lanolin-based aloe preparation to treat skin irritations resulting from burns, pruritus vulvae, and poison ivy. The results suggested that aloe stimulated tissue granulation and accelerated wound healing.103 Barnes11 evaluated the effect of 5% aloe ointment on sandpaper-abraded fingertips and found that the wound-healing rate was two to three times that of control subjects, as measured by decreased electrical potential of the wound. Other studies measured tensile strength of the healed surgical wounds of mice. Healing occurred within 9 days, an improvement over the results in control mice.64 Studies of antibacterial activity of aloe extracts have been attempted several times, yielding mixed results. In 1963, studies

Toxicity.  Because of its cathartic effects, oral aloe is not advised if gripping pain is associated with constipation. Aloe taken orally is contraindicated in pregnancy. Otherwise it has no reported toxicity.

PLANTAIN (Plantago major) Description and Habitat.  The common broadleaf plantain (Figure 66-14) is a familiar perennial “weed,” found along roadsides and in meadowlands. Plantain belongs to the family Plantaginaceae, which contains more than 200 species, 25 or 30 of which have a domestic use (Figures 66-14 to 66-17; Figure 66-16,

FIGURE 66-14  Plantain (Plantago major). (Courtesy Cascade Anderson Geller.)

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FIGURE 66-13  Aloe vera with exposed latex gel. (Courtesy Kevin Davison.)

of the antibacterial effect of macerated Aloe vera gel found no activity against S. aureus and E. coli.57 Other studies have determined that Aloe chinensis is effective against S. aureus, E. coli, and Mycobacterium tuberculosis, although Aloe vera showed no inhibitory effect.65 The latex possesses in vitro activity against several pathogenic strains of bacteria, although the whole leaf minus the latex from the leaf epidermis and mesophyll of aloe showed no activity.108 Two commercial preparations of aloe gel were found to exert antimicrobial activity against gram-negative and gram-positive bacteria and C. albicans when used in concentrations greater than 90%.72 The moisturizing effect of aloe may be beneficial in the treatment of burns. The healing process may be related to mucopolysaccharides along with sulfur derivatives and nitrogen compounds in the gel, but this has not been well substantiated.102 In attempts to document the antiinflammatory effects of aloe, a 1976 study found that Aloe vera had bradykinase activity in vitro, but this was not confirmed in vivo.59 Evidence for the internal use of aloe has been limited to studies involving mucous membrane tissue repair. Corneal ulcers treated with aloe extracts had more healing, less cellular reaction, and fewer signs of irritation than did control groups.103 Topical application of Aloe vera gel after periodontal flap surgery reduced postoperative pain more than did the saline control, and swelling of the treated tissue was less marked than with the control.73 Because of easy recognition and administration, use of the aloe plant in the wilderness environment is practical. The wild plant can yield an excellent preparation for dermal abrasions, cuts, and superficial wounds. A leaf cut from the base of a healthy plant can be conveniently carried. This allows the gel to remain intact, protected by the outer skin of the leaf. It can be squeezed from the inside through the cut portion directly onto superficial wounds with or without a gauze dressing. A standardized preparation of Aloe vera may be used as an antibacterial agent and an emollient for superficial wounds or dermatitis. In the event of constipation, the mixture of aloe gel and latex can be scraped or squeezed from the leaf cortex and ingested, 1 tablespoon 3 times daily, or until a mild laxative effect is noted. A gel and latex mixture produces less cathartic effect than does latex alone. Because of the bitterness of the gel and latex, the mixture should be taken with food or a flavored beverage.

PART 7  PLANTS

sitosterol, sorbitol, stachyose, syringic acid, tyrosol, ursolic acid, vanillic acid, and D-xylose.48 Native American and European Medicinal Uses and Folklore.  Historically, plantain has long been used for stings, bites, and irritations from venomous insects and reptiles. The folk medicine of the eastern United States suggests using crushed plantain leaves to stop the itching of poison ivy. It has also been reported to help relieve toothache. Ancient herbalists maintained that plantain had “refrigerant” (imparting a cooling sensation to the mucosa and allaying thirst), diuretic, and astringent properties. When the leaves are applied to a bleeding surface wound, hemorrhage lessens. In the highlands of Scotland, plantain is still called slan-lus, or plant of healing. In the United States, plantain has been known as snake weed, from the belief that it is effective for bites from venomous creatures. Felter54 noted that “the crushed leaves were very effective for the distressing symptoms caused by puncture by the horny appendages of larvae of Lepidoptera and the irritation produced by certain caterpillars, as well as the stings of insects and bites of spiders.” In Native American folklore, the plant was known as “white man’s foot,” in reference to its trait of growing in the settlements of white men. The Shoshoni Indians heated the leaves and applied them in a wet dressing for wounds.166

FIGURE 66-15  Plantago laycedota. (Courtesy Jill Stansbury.)

online). The plant is a small weed with a rosette of ribbed leaves and small projecting seed stalks. Its seeds, known as psyllium seeds in North America, resemble those of another species, Plantago psyllium. The leaves contain 84% water, 2.5% protein, 0.2% fat, and 14% carbohydrate; trace amounts of calcium, phosphorus, iron, sodium, and potassium; and beta-carotene, riboflavin, niacin, and ascorbic acid. Biochemically identified compounds include allantoin, adenine, baicalein, baicalin, benzoic acid, chlorogenic acid, choline, cinnamic acid, ferulic acid, L-fructose, fumaric acid, gentisic acid, D-glucose, p-hydroxybenzoic acid, indicain, lignoceric acid, neochlorogenic acid, oleanolic acid, plantagonine, planteose, saccharose, salicylic acid, scutellarein,

Modern Clinical and Wilderness Applications.  Plantain is readily available in the recreational areas of North America. This plant is extremely useful for various superficial wounds, abrasions, stings, and bites of mildly venomous insects. The constituents in the crushed leaves have an antihistaminic effect and anesthetic quality. In the event of a tooth fracture, a compress or poultice of 0.5 teaspoon of fresh leaves may be used on the tooth’s exposed nerve root. The seeds of the plantago plant are useful for spastic colon, an effect that appears to be related to their mucilaginous properties. Psyllium seeds, known on the Asian continent as flea seed husk, are often used as a bulk laxative. The seeds are collected from the stalk, and 2 teaspoons of fresh seeds in 4 oz of water is taken twice a day for mild constipation. Water should be ingested throughout the day to alleviate the condition and assist the laxative effect. Because of its astringent quality, an infusion of the leaves is recommended to treat diarrhea. The preparer pours 1 pint of boiling water on 1 oz of the herb and leaves it in a warm place for 20 minutes. After straining and cooling, 0.5 cup is ingested 3 or 4 times a day. Toxicity.  No known toxicities are attributed to Plantago.

CHAMOMILE (Matricaria chamomilla) Description and Habitat.  Chamomile (Figure 66-18) is a lowgrowing perennial with a hairy prostrate branching stem. It

FIGURE 66-17  Plantago—flowering plantain. (Courtesy Jill Stansbury.)

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FIGURE 66-18  Chamomile (Matricaria chamomilla).

Pharmacology.  The most important chemicals associated with chamomile are the volatile oils containing tiglic acid esters, chamazulene, farnesene, and α-bisabolol oxide. These volatile oils are destroyed if the herb is boiled.147 Native American and European Medicinal Uses and Folklore.  A distinction should be made between the German and Roman species of chamomile, although they have been used interchangeably for centuries. German chamomile is preferred on the European continent, whereas Roman chamomile has been used widely in Great Britain. In the United States, German chamomile is by far the more widely consumed of the two species.113 German chamomile has a long tradition as a folk or domestic remedy. It has been used as an external compress or fomentation for gout, sciatica, inflammations, lumbago, rheumatism, and skin ailments. Infusions, decoctions, and tinctures have long been used internally to treat colic, convulsions, croup, diarrhea, fever, indigestion, insomnia, teething, toothaches, and bleeding or swollen gums. Historically, Roman chamomile was used similarly.48,107 Chamomile is also a folk remedy for cancer. Modern Clinical and Wilderness Applications.  The principal biochemical constituent of chamomile is chamazulene. It is found in both species of chamomile and is reported to have antihistaminic properties.53 Both histamine release and inhibition of histamine discharge have been considered mechanisms for the potential antiallergic action of chamazulene. In Germany, chamomile products include tinctures, extracts, teas, and salves, widely used as antiinflammatory, antibacterial, antispasmodic, and sedative agents.113 Studies have shown that both chamazulene and α-bisabolol have antiinflammatory activity. Chamazulene may constitute as much as 5% of the essential oil. Other studies have shown that α-bisabolol has a protective effect against peptic ulcer, as well as antibacterial and antifungal effects. α-Bisabolol has also reduced fever and shortened the healing time of skin burns in laboratory animals.45 Most commercial European chamomile preparations have been standardized with regard to the chamazulene and α-bisabolol content.160 According to Rudolph Weiss,165 one action of chamomile is to reduce gastric motility and secretions, which would alleviate colic and painful spasm. About 20 flavones and flavonols, such as apigenin, are found in the aqueous portion of the distillation process. These are three times as effective at spasmolytic activity as is the opium alkaloid papaverine. Chamomile also has a significant calming effect and has traditionally had an application as a mild sedative. Chamomile is a good botanical to have on hand when traveling or camping. For infants experiencing restlessness and discomfort from teething, one-third of the adult dosage may provide relief. For treatment of conditions (intestinal gas, colic, peptic ulcers) that may arise from excessive nervous tension, 2 teaspoons (or one standard teabag) of the flower tops can be added to a cup of boiling water and infused for 5 to 10 minutes; 2 to 3 cups may be taken in 30 minutes for acute intestinal colic.

FIGURE 66-19  Echinacea flower. (Courtesy Jill Stansbury.)

Pharmacology.  The compounds currently identified from Echinacea spp. are inulin, glucose, fructose, betaine, echinacin, echinacoside, 3-(m-trihydroxyphenyl) propionic acid, and nonspecific resins.158 Native American and European Medicinal Uses.  This medicinal herb came to the attention of American herbalists in the late 1800s. Echinacea was originally used by the Indian tribes of Nebraska and the Sioux for treatment of snakebite and as an antiseptic and analgesic. Eclectic practitioners used it externally for the same purposes but used it internally to treat “bad blood” or any condition that manifested signs of local or systemic infection, whether bacterial or viral. Modern Clinical and Wilderness Applications.  Echinacea is probably the most common botanical used and known by the public, especially in relation to its immunomodulating effects. Many have empirically found that it can reduce symptoms and derail the onset of URIs and minor influenza episodes. However, an evaluation of E. angustifolia in experimental rhinovirus infections concluded that extracts of this plant’s root, either alone or in combination, did not have clinically significant effects on infection with the virus or on the clinical illness that results from it.156 Echinacea is also a good systemic adjunct to the treatment of any contusion or laceration. The polysaccharide component echinacin can maintain the structure and integrity of the collagen matrix in connective tissue and ground substance and can accelerate wound healing experimentally.124 Echinacin also has a cortisone-like effect, with intermediate stabilization of inflammation reactions. Inulin, a major component of echinacea, is a powerful activator of the immune system’s alternative

ECHINACEA (Echinacea species) Description and Habitat.  Echinacea (Figures 66-19 to 66-22; Figures 66-20 and 66-21, online) is a perennial herb native to the Midwestern region of North America, from Saskatchewan to Texas. Species include Echinacea angustifolia and Echinacea purpurea. The plant produces a characteristic large, pale purple flower and thick hairy leaves and grows 60 to 90 cm (23.6 to 35.4 inches) high. The dried root is typically used for medicinal purposes.

FIGURE 66-22  Echinacea (Echinacea purpurea).

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blooms late in July through September and is found growing throughout North America and Europe. The name chamomile is derived from the Greek chamos (ground) and melos (apple), which refer to the plant’s low growth and the apple-like scent of its fresh blooms.146 The flower head is about 2.5 cm (1 inch) in diameter, has a conical receptacle, and is covered by yellow disk-like flowers surrounded by 10 or 20 white, down-curving ray flowers.

PART 7  PLANTS

complement pathway. It may increase host defense mechanisms for the neutralization of viruses, destruction of bacteria, and increased action of white blood cells (lymphocytes, neutrophils, monocytes, eosinophils) within areas of infection. Extracts of the root have been shown to possess interferon-like properties. As an immune stimulant early in infection, and for post-trauma rehabilitation, doses are taken orally 3 times a day: tincture (1 : 5), 30 to 60 drops, or solid extract (dry powdered extract, 6 : 1), 250 to 500 mg.

CALENDULA (Calendula officinalis) Description and Habitat.  Calendula, a member of the daisy and dandelion family, is found throughout Asia, North America, and Europe (see Figure 66-1). It is most often known as the pot marigold. The flower is generally used for production of a tincture. Pharmacology.  Calendula’s chemical constituents include flavonoids, carotenes, saponin, resin, and volatile oils. The volatile oil content is responsible for a localized increase in blood circulation and diaphoresis. The resin content is responsible for the antimicrobial and antiinflammatory action of the topical application. Native American and European Medicinal Uses.  Native Americans apparently did not use calendula extensively, and the early European literature mentions only its medicinal role. Calendula, however, is one of the best topical applications for treatment and prevention of infection and skin irritation. Early American surgeons highly regarded its ability to treat and prevent postsurgical infections. Modern Clinical and Wilderness Applications.  A fluid or water extraction, or an oil infusion (prepared as a tincture but using vegetable oil instead of alcohol) of calendula should be used in the initial treatment of lacerations, abrasions, and scalds; immediately after any required debridement and cleaning of a wound; and for generalized inflammation of mucous membranes. It has shown its usefulness in dermatitis and in vaginal, sinus, ophthalmic, and middle and external ear infections. The choice of application mode (ointment, tincture, or fluid extract) depends on the wound. The succus (fluid extract) of the flower should be applied for irrigation of wounds and for ophthalmic uses.

GENTIAN, BITTER GENTIAN, YELLOW GENTIAN (Gentiana L. species) Description and Habitat.  Over 300 species of gentian (Figure 66-23) are found throughout the world, but it is especially common in mountainous regions of southern and central Europe, Eurasia, and western North America. All parts are used, but it is primarily the roots and rhizomes that are medicinal. Because of concern that overharvesting may endanger this genus,

partial root/rhizome collection or leaf-only preparations are recommended. Pharmacology.  The yellow gentian is native to Europe and has been used as a digestive bitter, as an antiinflammatory, and as an aid to treating infection. Secoiridoids, γ-pyrones, and triterpenoids are among the most notable constituents that have been studied. The bitter secoiridoid gentiopicroside (2% to 4% of the root) is known to have antibacterial and smooth muscle–relaxing effects consistent with gentian’s traditional use as a digestive bitter, an antibacterial, and an antiarthralgic.99,135 Native American and European Medicinal Uses.  Gentian’s use is ancient. The genus is named after King Gentius, the king of Illyria (180 to 167 BC), and it was described by Dioscorides in De Materia Medica. Although gentian is native to Europe, it is generally considered one of the very best stomach tonics in the world. In Germany, it is a standard medicinal and is approved by the Commission E for digestive disorders (loss of appetite, fullness, flatulence) Traditionally gentian has been used for chronic dyspepsia, indigestion, and poor digestive function. The root, rhizome, or cut herb is steeped and drunk 15 to 30 minutes before eating, especially in the evening. It stimulates the appetite and disperses the “full” and not hungry sensation. It is very bitter. Modern Clinical and Wilderness Applications.  A tea of the leaf, root, or rhizome is most convenient and readily available in many areas at altitude at or below tree line. It can be very helpful for indigestion and digestive dysfunction brought about by poor food quality, weakness, and overexertion that impairs appetite. This tea can also be very helpful for fever or joint inflammation from infection, fatigue, and overuse. In Chinese herbal medicine, gentian is an essential component of Long dan xie gan wan, an excellent herbal formula for fever, viral infection, headache, iritis, cystitis, urethritis, genital herpes, and liver dysfunction.

DESERT PARSLEY, FERN-LEAFED LOMATIUM (Lomatium dissectum, Nutt.) Description and Habitat.  Lomatium, a perennial herb (Figure 66-24, online), is native to the western United States and grows predominantly at low to mid elevation in temperate to arid regions. The genus Lomatium contains over 80 species, used more or less interchangeably. It is found on wooded or brushy rocky slopes, on alpine meadow steppes, or on dry hillsides. The root is drunk as an infusion, chewed, or pounded for topical application. Pharmacology.  The root extract has been shown to completely inhibit the cytopathic effects of rotaviruses in vitro.116 The active constituent from Lomatium suksdorfii, suksdorfin, is related to coumarin and has been shown to strongly inhibit human immunodeficiency virus (HIV)-1.104 This finding is consistent with its use as an antiinfective. Flavonoids and ichthyotoxic (fish killing) tetronic acids have also been identified.163 Native American and European Medicinal Uses.  Lomatium was highly revered by Native Americans and was used for a wide variety of problems. It gained legendary status in the U.S. Southwest when Native Americans used it during the influenza pandemic of 1917. The Paiutes of Nevada treated sore throats with a decoction of the root. Many Native American groups considered Lomatium important for treatment of tuberculosis, asthma, and other lung diseases. It was also used internally and topically for venereal disease. Naturopathic physicians in the western United States have popularized the use of Lomatium as an antiviral when the root extract is taken internally, for vaginitis when used as a douche, or as an oral rinse to treat periodontal disease.12

FIGURE 66-23  Gentian (Gentiana lutea).

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Modern Clinical and Wilderness Applications.  Because of unconfirmed toxicity, it is probably best to avoid the tops of Lomatium, but the root is very helpful for upper respiratory infections, viral illnesses, sore throats, mouth infections, and

FIGURE 66-27  Devil’s club (Oplopanax horridum). (Courtesy Jill Stansbury.)

topical local infections. In the clinic, specific root isolates (with resins removed) are used; in naturopathic medicine, these are considered specific for herpes infections. These isolates are also thought to reduce the incidence of a benign hive-like rash that appears in individuals sensitive to Lomatium. A pioneer in naturopathic medicine, John Bastyr, said the appearance of the rash is a sign to decrease the dose, not discontinue the medicine.12 In the wilderness, Lomatium may be a significant aid in treating and preventing a wide variety of microbial and viral infections and is easily prepared from fresh or recently dried root as a decoction.

DEVIL’S CLUB (Oplopanax horridums) Description and Habitat.  Native to North America, Oplopanax (Figures 66-25 to 66-27; Figures 66-25 and 66-26, online) is an erect, slightly spreading deciduous shrub present in moist but well-drained forested and river bank ecosystems from coastal Alaska to central Oregon, east to Idaho, Montana, northwestern Alberta, southwestern Yukon, and the Canadian Rockies, with a few populations near northern Lake Superior, the upper peninsula of Michigan, and Ontario. The stems, leaves, and petioles have a dense armor of needle-like yellow spines that can cause injury and irritation. Flowers are small, whitish, and numerous in compact terminal pyramidal clusters. Notably, Oplopanax is an Araliacea, which includes P. ginseng (Asian ginseng), P. quinquefolius (American ginseng), and Aralia nudicauli (sarsaparilla). Pharmacology.  The best-known constituents of devil’s club include saponin triterpenoid glycosides, which have been described primarily in Japanese and Russian Oplopanax. There has been much discussion as to whether these saponins are like the ginsenosides in Panax spp., consistent with devil’s club traditional use among Native Americans as a tonic. Sterols, sesquiterpenes, and polyenes that have been shown to have significant action against mycobacteria, fungi, and common bacteria such as S. aureus, Bacillus subtilis, Pseudomonas aeruginosa, E. coli, and C. albicans.95 These findings are consistent with the primary historical use of devil’s club internally and topically for all varieties of infection, including tuberculosis. Native American and European Medicinal Uses.  It is difficult to overstate the importance of this herb to the native peoples of North America. It is of extreme significance as a spiritual and shamanic herb, including purification and healing, protection against evil spirits, and gaining of supernatural powers, and as an emetic and purgative. Its primary uses as medicinal herb are for infections, fever, arthritis, respiratory ailments, post–childbirth bleeding, pain, broken bones, digestive ailments, stomach complaints, and even dandruff and lice. European medicinal use is mostly in formulas for joint pain, arthritis (especially autoimmune arthritis), and rheumatism. The root is considered to be an effective expectorant and respiratory

Modern Clinical and Wilderness Uses.  Modern clinical use is focused primarily on joint pain, osteoarthritis, and inflammatory arthritides in various formulas or as a single herb. Devil’s club is often found in combination with devil’s claw (Harpagophytum), cat’s claw (Uncaria spp.), or one of its western companions chaparral (Larrea tridentata) and Oregon grape (Berberis aquifolium) as an antiinfective combination. Decoction of the inner bark of the stem is the primary method of preparation, but other parts, such as the inner bark (burned, and the ash used topically), whole stems, berries, leaves, and root, have all been used. In the wilderness, an infusion or decoction of the stem’s inner bark is easily prepared and may help allay fatigue, ease joint or headache pain, or serve as an expectorant. In the practice of traditional medicine, devil’s club appears to be good for everything.

OLD MAN’S BEARD (Usnea species) Description and Habitat.  Usnea spp. (Figures 66-28 to 66-30; Figures 66-29 and 66-30, online) are lichens (composed of fungi and algae in a stable symbiotic relationship) that are ubiquitous in old-growth forests of the Northwest. They can be seen hanging from shrubs or conifers, often lightly tethered to the tree bark, or lying on the forest floor, especially after a storm. It is difficult for any but the expert to distinguish between species of usneas, but they typically have a long, single, unbranched (or sparsely branched) central cord colored from white to yellow with an outer portion that is gray to pale green. Native American and European Medicinal Uses.  This plant has been used since ancient times in the Americas, Europe, and China. Native Americans saw Usnea as representing the male gender and the northerly direction and maintaining the “respiratory” system of the planet (namely the trees); they saw its human uses as secondary to this crucial function.81 Usnea appears in the ancient Chinese herbal, the Shennong Ben Cao Jing (Divine Farmer’s Materia Medica, around 200 BC), and it is presently classified as a phlegm-resolving herb. Among northwestern Native Americans, it has variously been used as bedding, as sanitary napkins, and to wipe slime when cleaning salmon, but most significantly it is used as wound dressing and bandage material.162 This is because of not only its wispy soft form but also its antibacterial properties. In Europe, it has been used predominantly as a topical medication, employing the active constituent usnic acid, present in many lichens, as an antibiotic, antiinflammatory, and

FIGURE 66-28  Old man’s beard (Usnea sp.).

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stimulant. Recently some marketers have played up the adaptogenic potential of Oplopanax, calling it “Alaskan ginseng” or “Pacific ginseng.” Commercial products also emphasize the root, whereas traditional uses and much of the research have focused on the inner bark of the stem.

PART 7  PLANTS

analgesic substance.76 Since its isolation in 1844, usnic acid has been the most studied of lichen constituents and one of the few to be commercially available. In addition to the bacterial inhibition of staphylococci, streptococci, pneumococci, and mycobacteria, usnic acid has been shown to have antiviral, antiprotozoal, and antiproliferative effects consistent with its traditional use.80 Also present in Usnea, but less well studied than usnic acid, are the organic acids usnaric, thamnolic, lobaric, and stictinic. Modern Clinical and Wilderness Uses.  Although pure usnic acid has been used for weight loss in recent times, this use cannot be considered safe and has been associated with liver failure.50 Usnea has been used in several formulas in modern-day China, usually paired with the seaweed Laminaria or Sargassum (or both) for treatment of thyroid cancer,77 and in the treatment of bronchitis with profuse sputum.47 Other current uses include lozenges for oral inflammation and many different salves and creams with antimicrobial and antiinflammatory action. In the wilderness, Usnea is readily available in the regions mentioned earlier, and it makes excellent bandages for wounds, superficial infections, and contact dermatitis. Most herbalists recommend collection from the ground so as not to disturb growth on shrubs or trees. Soft and wispy Usnea is applied directly to the affected area and held in place with whatever means are available. Alternatively, dry Usnea may be powdered and sprinkled directly on wounds, affording antimicrobial wound protection.

First-Aid Kit of Natural Products A natural products first-aid kit should contain a variety of products that are easy to obtain and replace and that have a wide spectrum of use, including herbs (Box 66-1), homeopathic preparations, and vitamin and enzyme supplements (Table 66-1).

HOMEOPATHIC MEDICINES Homeopathy can be an excellent source of relief and treatment for emergencies and general first-aid situations. Homeopathic preparations include powders, tablets, tinctures, lotions, ointments, creams, and sprays. The advantages of homeopathy are ease of administration, lack of toxicity, rapid action, and small volume of material. The disadvantages are the degree of understanding and competence required to become an effective prescriber and the lack of readily available sources of each medicine at most North American pharmacies. A kit made exclusively of homeopathic medicines can cover most first-aid emergency situations. For the acute, straightforward injury or malady without a complex set of symptoms, the correct simillimum and rapid amelioration of symptoms are not difficult to achieve. This section discusses a few indications for use of homeopathic medicines and the preparation most often used. Unless otherwise noted, a 6× to 12× potency in lactose pellet form should be given every 15 to 30 minutes immediately after the injury until noticeable improvement occurs. If no effect is

BOX 66-1  Herbal Medicines Recommended for

a First-Aid Kit

Aloe gel and powder capsules Arnica ointment Calendula gel, ointment, and tincture Chamomile tincture Comfrey gel or ointment Echinacea tincture or freeze-dried powder capsules Ephedra freeze-dried powder capsules Goldenseal tincture or ointment Hypericum ointment or tincture Plantain tincture Witch hazel fluid extract or tincture

1318

noted after the first two doses, the medicine selection should be reconsidered. The personal experience of one of these authors (KJD) exemplifies the relief that can be obtained from an acute injury with the appropriate homeopathic medicine: I was bitten on the lip by a small centipede while sleeping. I instantly experienced swelling and intense burning pain. Local application of ice provided no relief. I chose the homeopathic medicine Apis mellifica in a 6c potency because the wound was shiny and felt hot, and the swelling was increasing. After sublingual ingestion of two pellets, I waited 1 to 2 minutes, still in excruciating pain with no change in symptoms. My next selection was cantharis in a 6c potency, because a key symptom for this remedy is extreme red and hot burning pain of the face. Less than 30 seconds after administration, the pain was almost undetectable. Total relief was obtained within a few minutes after being bitten. As an unintended control, I have had no homeopathic kit available after other centipede bites, and the pain generally lasted for hours and the residual swelling for days. Reactions from different centipedes can cause different sensations and symptoms, however, so cantharis may not work for all bites. Proper selection of the simillimum or indicated homeopathic medicine requires the ability to note the subtle differences in the ways the victim responds to apparently similar traumatic or toxicologic influences. An appropriate homeopathic field guide that lists specific indications and differentiations for each homeopathic remedy should accompany any first-aid kit. It is essential to understand the specific homeopathic indications for each of the remedies (simillima) on hand. Otherwise, the chance of obtaining a successful outcome is small. Practitioners and the homeopathic industry have realized the difficulty of single-remedy prescribing, which involves understanding and memorizing indications for every homeopathic medicine. Therefore medicines have been developed that combine remedies to cover a large number of the symptoms and symptom characteristics that typically accompany most ailments. These medicines, known as complex or combination homeopathic preparations, can be very helpful for the new user.

SINGLE PREPARATIONS AND THEIR INDICATIONS Aconite.  Tincture of the whole plant with its root is derived when monkshood or wolfsbane (Aconitum napellus) begins to flower. Aconite is indicated for acute states of emotional disturbance, including anxiety and intense fear or pain. This is one of the key remedies that should be administered after an acute injury that has dazed, shocked, or frightened the victim. Persons who are fearful or restless, cannot tolerate being touched, and have pain followed by numbness and tingling sensations are most responsive to aconite. Those with sudden onset of fever, nausea, and vomiting and who exhibit symptoms of fear, restlessness, and anxiety may also benefit. Apis.  The original tincture is manufactured from the whole honeybee and from dilutions of its venom (Apis mellifica). Apis is used for insect stings, particularly from bees and related insects, when the wound is swollen, shiny, and hot to the touch. Treatable symptoms from other conditions are histamine reactions (resulting in facial flushing; puffiness or swelling around the mouth, face, and eyes), sunburn, hives, burns, and early stages of abscesses and frostbite. If symptoms include a stinging, burning, or swelling quality and subside by applying cold rather than heat, Apis is the indicated remedy.134 Arnica.  Tincture comes from the whole fresh plant, flowers, and dried roots of leopard’s bane or Fallkraut (A. montana). Arnica is indicated for blunt traumatic wounds (resulting in both deep and superficial hematomas), contusions, swelling, and localized tenderness. It is also effective for sore muscles, as well as sprains,

— —

—

—

—

—

Peppermint

Plantain

Rhus toxicodendron Witch hazel

—

—

—

—

Hypericum

Ephedra Goldenseal

Comfrey Echinacea

Botanical internal, topical — Botanical internal, topical — Botanical internal, topical

— —

— —

Botanical internal, topical — Botanical internal, topical — —

—

Chamomile

Arsenicum album Bromelain Calendula

—

Homeopathic internal Botanical topical —

—

—

Arnica montana

—

—

Aconitum napellus Apis mellifica

Antibiotic

Analgesic

Plant Medicines

TABLE 66-1  Uses for Phytopharmaceuticals

—

—

—

—

—

— Botanical internal, topical — Botanical internal, topical

— Botanical internal, topical —

—

—

—

—

Antifungal

Homeopathic topical, internal —

—

—

—

— Botanical topical

Botanical internal, topical Botanical topical Botanical internal

Botanical internal Botanical topical

—

Homeopathic topical, internal Homeopathic topical, internal

—

Antiinflammatory

Botanical topical Botanical topical Botanical topical

—

— Botanical internal, topical —

— —

— Botanical topical —

—

—

—

—

Astringent

—

—

Botanical topical

Homeopathic topical, internal —

— Botanic homeopathic topical — Botanical topical

Botanical topical

— Botanical topical

—

—

—

—

Antiseptic

—

—

Botanical internal, topical —

—

Botanical internal —

— —

Botanical internal

— —

—

—

—

—

Decongestant

—

—

—

—

Homeopathic internal

— —

Botanical homeopathic internal — —

— —

Homeopathic internal

—

—

Homeopathic internal

Sedative

CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

1319

PART 7  PLANTS

fractures, dislocations, and internal bleeding. The authors recommend taking a 6× to 30× potency every 15 minutes to 3 hours for the first few days after a severe injury. The more severe the injury, the more frequently the dose is taken for the first day. As symptom severity decreases, the medicine is taken less often. Arnica can be helpful in decreasing severity of symptoms and recovery time. Arsenicum.  Derived from arsenic trioxide, arsenicum is used for skin rashes (those that feel warm but are relieved by hot applications), hay fever, asthma (especially when accompanied by notable anxiety), diarrhea, vomiting, and gastroenteritis (especially from food-borne microbes). Hypericum.  The tincture comes from the whole fresh plant and flowers of St John’s wort (Hypericum perforatum). Indications include any pain that affects the peripheral or central nervous system and exhibits shooting pains that travel in a dermatomal pattern (e.g., sciatica). Wounds that affect nerve endings, such as injuries to fingers, toes, or teeth, are improved by hypericum. Pain from dental surgery, toothache, injury to the coccyx, or first- and second-degree dermal burns is another indication. Ledum.  Ledum is made from leaves and stems of the whole fresh plant of wild rosemary (Ledum palustre). Homeopathic indications include puncture wounds from small, sharp objects (e.g., nails, needles) and some mosquito bites when the injured area feels cold, swollen, and numb and pain is relieved by cold application. Rhus.  The homeopathic preparation of Rhus comes from leaves and stems of the whole fresh plant of poison ivy. This is the remedy of choice for the urticaria caused by poison ivy exposure, and it is also helpful for some cases of poison oak. Other skin rashes that are red, weeping, blistered, and swollen with itching can be treated with Rhus. It is also effective for treatment of connective tissue irritations with swelling, stiffness, and tightness. Rhus is often used for overuse injuries (e.g., fasciitis, tendinitis) and some forms of arthritis, especially when the injured area feels better with warm applications and movement. Note that the name of this preparation may change, because Toxicodendron is now the correct name of the genus.

COMBINATION PREPARATIONS FOR ACUTE SPRAINS AND STRAINS Homeopathic companies have created combination remedies for the general public that can be used without the need for in-depth understanding of homeopathic prescribing. These remedies are designed to cover a broad range of symptoms associated with acute ailments and trauma-induced medical conditions. They are sometimes touted to be effective for many disorders on the basis of empirical observations, rather than on the basis of randomized, blinded studies. Practitioners are advised to be aware of the possibility for unsubstantiated claims of clinical efficacy for these and any other medications marketed for profit. Traumeel is a combination homeopathic formula that is effective for treatment of trauma and inflammatory changes affecting skin, connective tissue, and muscle.61 The preparation comes in liquid, tablet, and ointment form. Traumeel includes remedies indicated for traumatic injuries (sprains, strains, contusions) and resulting pain, swelling, and ecchymoses. Many German studies have demonstrated its effectiveness.30 Traumeel may be the primary homeopathic medicine chosen for the first-aid kit because of its wide range of applications and multiple delivery systems. Inflamyar ointment is a uniquely formulated homeopathic medicine that combines eight ingredients to provide treatment of traumatic sports-related injuries, such as sprains, bruises, and muscle strains. This formula developed from a long tradition of German homeopathic salves also is available as a homeopathic tincture. It has been used with great success for immediate relief and resolution of bursitis, sciatica, and acute and chronic 1320

inflammation as well as pain of rheumatic and arthritic conditions, After strenuous exercise, massaging Inflamyar into tender points will help prevent soreness the next day. Routine self-massage with Inflamyar into tender points has been shown to restore flexibility and elasticity to muscles, tendons and ligaments. Herbal Combination Formulas In the tradition of Chinese herbal medicine, many formulas have been developed over the centuries to treat acute ailments. Many of these formulas were kept secret and reserved for the nobility and ruling class. As the field of Chinese herbology has developed and become more accessible to the general populace, some of the secret formulas have been mass produced into convenient pill form, known as patent medicines. Many are extremely useful for acute conditions. Zheng Gu Shui (“Rectify Bones Liquid”) trauma lotion is wonderful for sprains, strains, and bruises. It is also indicated for back pain and arthritis pain. The herbs of which it is composed invigorate circulation, relieve pain, induce a nice warming feeling, and accelerate healing. This formula has long been a mainstay of martial artists, massage therapists, and Chinese herbalists. It should be applied to affected areas 2 to 3 times a day, keeping the liquid away from mucous membranes and open cuts. It accelerates resolution of bruises and connective tissue injuries, reducing swelling, pain, and inflammation. It is produced by Guangxi Yulin Pharmaceutical Factory, which is well known in China and has been honored with awards for quality and effectiveness. This product can be ordered through the Institute for Traditional Medicine (ITM; listed in the resources section of the Appendix) and from most Chinese herbal pharmacies.

NUTRITIONAL SUPPLEMENTS For immune system support, antiinflammatory action, and pain relief, many natural products in the nutritional supplement category have proved to be effective agents. Bromelain.  Bromelain is a naturally occurring proteolytic enzyme found in pineapple that is used to reduce pain and swelling after sprains and strains of soft tissues. Ingested on an empty stomach, the complex proteases in bromelain are absorbed intact and have significant antiedema, antiinflammatory, and coagulation-inhibiting effects. Bromelain exhibits fibrinolytic activity and acts to inhibit fibrinogen synthesis, decreasing kininogen and bradykinins.109 For treatment of injuries and postsurgical recovery, 125 to 400 mg is ingested 3 times daily at 30 minutes before or 90 minutes after a meal. Bromelain is nontoxic even at high dosages and is generally prepared as 100-mg tablets. Papain.  Like bromelain, papain is a naturally occurring plant enzyme (from papaya fruit) that exhibits proteolytic activity. Papain is generally used externally to neutralize bee, ant, or wasp venom. It is available as commercial meat tenderizer (e.g., Adolph’s) or in tablet form. After removal of the stinger, a thick paste is prepared from water and tenderizer (or five or six crushed tablets) and applied to the area as soon as possible. A convenient form that contains bromelain, papain, and pancreas-derived proteolytic enzymes is the product Wobenzym. This product has had decades of use in addition to clinical trials to back its claims as an effective proteolytic antiinflammatory. Suggested use is three tablets three times a day or as directed by the practitioner. Wobenzym-N is taken on an empty stomach at least 45 minutes before meals. Vitamin C.  Ascorbic acid has both wound-healing and antiinflammatory effects. Vitamin C is required for hydroxylation of proline and subsequently for synthesis of effective collagen. Studies have shown that the stress associated with injury and wound healing results in an increased need for vitamin C.115 For acute trauma and acute upper respiratory allergy, vitamin C in larger dosages (2 to 5 g/day in divided doses) has been claimed to reduce anaphylactic reactions and recovery time.71 Therefore,

FOR ACUTE GASTROENTERITIS Pill Curing (Kang Ning Wan, “Healthy Quiet Pill”), botanically called Coix Formula, consists of 16 herbal medicines that are collectively effective for relieving disturbances caused by motion sickness, food poisoning, overeating, excessive alcohol consumption (nausea, headache, vomiting), difficulty passing stool, loose stools, and GI cramping and pain. Coix Formula is currently produced in a convenient globule form. One or two capfuls of globules are swallowed with warm water every hour until symptoms improve. Relief should occur within 4 hours of administration. Pill Curing (or Culing) is also available as a Chinese patent (or prepared) medicine from ITM or from a Chinese herbal pharmacy. The package includes 10 vials; the usual dose is 1 to 2 vials, each containing multiple small pilules to be swallowed all at once. Relief is generally within hours. This is an all-purpose remedy claimed to be useful for everything from traveler’s diarrhea, to hangover, to the common cold.

FOR ACUTE HEMORRHAGIC CONDITIONS The product Yunnan Bai Yao (“Yunnan white medicine”), produced in the western Chinese province of Yunnan, has been used for centuries as a first-line approach to trauma that results in internal or external bleeding. It is prescribed in China for excessive menstrual cramps and bleeding, bleeding ulcers, trauma-induced swelling, bleeding wounds, and allergic reactions to insect bites. It comes in powder (4  g per bottle) and capsule (packets of 20) form and contains one red pellet that is to be ingested only for serious bleeding conditions. Dosage is 1 to 2 capsules 4 times per day. The powder can be applied externally after the wound has been properly cleaned. This product is exclusively produced in China from a proprietary formula and can be obtained from most Chinese herbal pharmacies.

FOR DERMATOLOGIC CONDITIONS SssstingStop Gel.  The Boericke and Tafel SssstingStop gel is for temporary relief of itch, pain, and redness of nonpoisonous insect bites and stings from insects—mosquitoes, bees, wasps. It also soothes fever blisters and cold sores. The London School of Hygiene and Tropical Medicine conducted two double-blind clinical studies using mosquitoes that had not been fed for 24 hours and human volunteers. The tests were reported to prove that the medicines in SssstingStop provide dependable, effective relief. SssstingStop combines three natural homeopathic medicines prepared from botanical sources and listed in the Homeopathic Pharmacopoeia of the United States (HPUS). It contains no hydrocortisone or other steroids, antihistamines, “-caine” anesthetics, or synthetic medicines of any kind. It is applied to the affected skin area, with applications repeated as needed. Ingredients are E. angustifolia (1×, 10%), L. palustre (1×, 10%), Urtica dioica (1×, 10%), and citronella oil and eucalyptus oil in a water gel base. Ching Wang Hun (or Jing Wan Hong) Burn Ointment.  This fast-acting analgesic and burn-healing salve is a remarkable herbal medicine. It is effective for chemical, thermal, electrical, radiation, and solar burns. It can also be used to decrease inflammation and stimulate regeneration of the skin, and for contact dermatitis (poison oak, ivy, sumac), hemorrhoids, and infected skin. The ointment is applied liberally to the affected areas. Ideally, it is covered to prevent accumulation of dirt and grime and to reduce the red stain that occurs if the ointment gets on clothing. It should be reapplied and the dressing changed once or twice a day. This ointment is made by one of the best-known manufacturers in China, and it can be ordered through ITM (see the resource section in the Appendix) and from most Chinese herbal pharmacies.

APPENDIX COMPANIES Boiron Natural Home Health Care LeKit contains 36 single-remedy medicines in distinctive blue tubes, including the commercial flu remedy Oscillococcinum. The home kit also contains four external remedies: tinctures of calendula and hypericum, and ointments of arnica and calendula. Travel LeKit is a more compact collection of single remedies (22 multidose and 16 one-dose tubes) plus the flu remedy. Biological Homeopathic Industries (BHI) BHI is the U.S. distributor of the German line of complex homeopathic remedies manufactured by Heel. http://www.heel.com BioResource Inc. BioResource Inc. is the U.S. distributor of quality German botanical and homepathic medications like Inflamyar ointment. http://www.bioresourceinc.com Institute for Traditional Medicine (ITM) http://www.itmonline.org ITM is a nonprofit resource for Chinese herbal medicines, patent formulas (prepared medicines), and professional herbal formulas for practitioners. Jintu is the nonprescription resource for the products listed here: http://www.itmonline.org/jintu. http://www.pureprescriptions.com is a website to access Wobenzym-N and other products that are generally sold only to health care practitioners.

BOOKS Natural Health and Medicine Lust J, Tierra M: The natural remedy bible, New York, 1990, Pocket Books. Murray M, Pizzorno J: Encyclopedia of natural medicine, Rocklin, Calif, 1991, Prima. Weil A: Health and healing: Understanding conventional and alternative medicine, Boston, 1983, Houghton Mifflin. Herbs and Herbalism Murray M: The healing power of herbs, Rocklin, Calif, 1991, Prima. Weiss RF: Herbal medicine, Beaconsfield, UK, 1988, Beaconsfield. Homeopathy Books Boericke W, Boericke O: Boericke’s materia medica with repertory, New Delhi, 1991, B Jain. Kruzel T: The homeopathic emergency guide, Berkeley, Calif, 1992, North Atlantic Books/Homeopathic Education Services. Reckeweg HH: Homotoxicology: Illness and healing through antihomotoxic therapy, ed 2, Albuquerque, 1984, Menaco. Subotnick S: Sports and exercise injuries: Conventional, homeopathic, and alternative treatments, Berkeley, Calif, 1991, North Atlantic Books.

PRACTITIONERS American Association of Naturopathic Physicians 4435 Wisconsin Ave, NW, Suite 403 Washington, DC 20016 202-237-8150 telephone 866-538-2267 toll-free 202-237-8152 fax http://www.naturopathic.org

HERBAL MEDICINES Herb Research Foundation http://www.herbs.org

NUTRITIONAL PRODUCTS Crane Herb Company 745 Falmouth Rd Mashpee, MA 02649 800-227-4118 http://www.craneherb.com (registration required) 1321

CHAPTER 66  Ethnobotany: Plant-Derived Medical Therapy

for any traumatic event, high-dose vitamin C should be administered as part of the treatment.

PART 7  PLANTS

Thorne Research 25820 Highway 2 W PO Box 25 Dover, ID 83825 800-228-1966 http://www.thorne.com Metagenics 100 Avenida La Pata San Clemente, CA 92673 800-692-9400 http://www.metagenics.com Mountain Peak Nutritionals 3310 SW Vista Dr Portland, OR 97225 877-686-7325

1322

Vital Nutrients 45 Kenneth Dooley Dr Middletown, CT 06457 888-328-9992 http://www.vitalnutrients.net

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 67 

Field Water Disinfection  HOWARD D. BACKER

Waterborne disease is a risk for international travelers who visit countries that have poor hygiene and inadequate sanitation and for wilderness users relying on surface water in any country, including the United States. Natural water may be contaminated with organic or inorganic material from land erosion, dissolution of minerals, decay of organic vegetation, biologic organisms that reside in soil and water, industrial chemical pollutants, and microorganisms from animal or human biologic waste.61,106 The main reason for treating drinking water is to prevent gastrointestinal illness from fecal pollution with enteric pathogens.270 Appearance, odor, and taste are not reliable to estimate water safety. Natural organic and inorganic material may not cause illness but can impart unpleasant turbidity, color, and taste to the water (Box 67-1). Of the 1700 million square miles of water on Earth, less than 0.5% is potable.295 Global warming is accelerating deterioration of the remaining potable supplies,161 and emerging waterborne pathogens create the need to reevaluate detection and disin­ fection methods.270 Chemical contamination of groundwater is increasing at an alarming rate in the United States and worldwide from industrial, agricultural, and individual sources. Except for certain pristine alpine or other remote water sources, virtually none of the surface water in the United States is drinkable without treatment.161 According to the National Water Quality Inventory Report by the U.S. Environmental Protection Agency (EPA), as of 2004, bacterial contamination was the leading cause of river and stream impairment; mercury contamination was the leading cause of impairment in lakes, ponds, and reservoirs. Overall, about 40% of the nation’s surveyed rivers, lakes, and estuaries are too polluted for basic uses such as fishing and swimming.285 Disasters, such as floods and hurricanes, often overwhelm treatment facilities and contaminate ground water, requiring point-of-use disinfection.250 The World Health Organization (WHO) reports that 1.1 billion people lack access to an

BOX 67-1  Chapter Outline and Shortcuts • For summary of each technique, see boxes in specific sections. • For comparison of various techniques, see text and Tables 67-16 to 67-18. • For details of products, see the appendixes. Methods of Water Disinfection That Can Be Applied in the Field Heat Physical Removal   Sedimentation   Coagulation–flocculation   Granular activated carbon Filtration   Reverse osmosis Chemical Disinfectants Chlorine Iodine Chlorine Dioxide Silver Potassium Permanganate Hydrogen Peroxide Citrus Ultraviolet Light and Solar Copper-zinc

1324

Page 1330 1332 1333 1333 1333 1334 1335 1336 1339 1341 1345 1345 1346 1346 1346 1346 1347

improved drinking water supply, and 2.4 billion people lack access to improved sanitation.303

Benefits of Water Treatment Methods for treating water are found in Sanskrit medical lore, and pictures of apparatus used to purify water appear on Egyptian walls from the 15th century BC. Boiling and filtration through porous vessels, sand, and gravel have been known for thousands of years. The Greeks and Romans also understood the importance of pure water.186 Sanitation, including water treatment, is considered one of the ten great public health achievements that helped conquer infectious disease as a main cause of mortality in the United States.43 As the percentage of the U.S. urban population served by water treatment utilities increased after 1900, the annual death rate from typhoid decreased.249 Drinking-water treatment processes provide enormous benefits with minimal risk. Without filtration and disinfection, waterborne disease would spread rapidly in most public water systems served by surface water.69,286 The combined roles of safe water, hygiene, and adequate sanitation in reducing diarrhea and other diseases are clear and well documented. WHO estimates that 94% of diarrheal cases globally are preventable through modifications to the environment, including access to safe water.303 Recent studies of simple water interventions in households of developing countries clearly document improved microbiologic quality of water, 30% to 60% reduced incidence of diarrheal illness, enhanced childhood survival, and reduction of parasitic diseases; much of this progress is independent of other measures to improve sanitation.* Moreover, from a global health perspective, water and sanitation improvements are cost beneficial in all developing world regions.118,135 Although the combination of improved water quality and sanitation has the greatest effect, improvement in water quality alone has a beneficial effect on health and can reduce incidence of diarrheal disease by more than one-third.260,262 In contrast to extensive evidence from developing areas of the world, there are few data to demonstrate benefits of water disinfection in the U.S. wilderness. Boulware27 demonstrated that drinking untreated water correlated with higher rates of diarrhea among Appalachian Trail hikers.

Risk and Etiology Infectious agents with the potential for waterborne transmission include bacteria, viruses, protozoa, and parasites (Box 67-2).101,270 The long list of pathogenic microorganisms capable of waterborne transmission is similar to that of potential etiologic agents of traveler’s diarrhea; almost all enteric pathogens and opportunistic pathogens that are transmissible by the fecal–oral route can be transmitted through water. Separating the contribution of waterborne transmission of these pathogens from food-borne and person-to-person transmission is impossible; the latter two are probably more common. In developing countries, 15% to 20% of diarrhea is estimated to be waterborne. Surprisingly, this is similar in developed countries, where as much as 15% to 30% is attributed to municipal drinking water.

*References 8, 60, 72, 94, 98, 134, 166, 167, 184, 217, 218, 225, 226, 260, 262.

For online-only figures, please go to www.expertconsult.com

TABLE 67-1  Estimated Infectious Dose

of Enteric Organisms

Organism Salmonella Shigella Vibrio Enteric viruses Giardia Cryptosporidium

Infectious Dose 105 102 103 1-10 10-100 10-100

Data from Hurst C, Clark R, Regli S: Estimating the risk of acquiring infectious disease from ingestion of water. In Hurst C, editor: Modeling disease transmission and its prevention by disinfection, Melbourne, 1996, Cambridge University Press, pp. 99-139.

BOX 67-2  Waterborne Enteric Pathogens

CHAPTER 67  Field Water Disinfection

Risk for waterborne illness depends on the number of organisms consumed, which is determined by the volume of water, concentration of organisms, and treatment system efficiency.33,67,133 Additional factors include virulence of the organism and defenses of the host. Infection and illness are not synonymous; the overall likelihood of illness for all three categories of microorganisms (bacterial, viral, protozoan) is 50% to 60%. Death from enteric pathogens is unlikely in healthy, well-nourished persons, except with a few specific organisms (e.g., Escherichia coli O157:H7, E. coli: 0104:H4, or, in pregnant women, hepatitis E). In malnourished individuals, especially young children, many other pathogens, including Vibrio cholerae and Cryptosporidium, can lead to infectious causes of death. Total immunity does not develop for most enteric pathogens, and reinfection may occur.133 Several nonenteric waterborne organisms have high case fatality rates. These include Legionella (respiratory) and Acanthamoeba (neurologic). Waterborne outbreaks do not give a complete picture of the potential for waterborne illness. Most outbreaks of waterborne diseases are not identified because not enough people become ill, providing an insensitive mechanism for detecting water contamination. When an outbreak is identified, it is very difficult to prove conclusively that the source was waterborne. The supply may have been only transiently contaminated, water samples from the time of exposure are seldom available, some organisms are difficult to detect, and almost everyone has some exposure to water.274,305 The data on concentration of microorganisms in surface water show widely varying values, but the testing is insufficient for risk assessment and dose-response models. Instead, infectious dose data and statistical techniques have been used to devise models for determining risk (Table 67-1).133 These models cannot be applied unless the microbial content of water is known. Pathogenic microorganisms clearly exist in most raw source waters, especially in surface waters.286 Most microbiologic testing is done on community water intake sources and sewage treatment effluent. Less information is available for more remote water sources.68,241,300 Detection techniques using enzyme immunoassay and polymerase chain reaction may give a much more accurate picture of the specific microbes and degree of water contamination.270 But testing may not be representative, because excretion and loading of microbial contaminants are dynamic and change over time. Surface water is subject to frequent, dramatic changes in microbial quality as a result of activities on a watershed. Storm water causes deterioration of source water quality by increasing suspended solids, organic materials, and microorganisms. Some of these contaminants are carried by rain from the atmosphere, but most come from ground runoff. In water sources downstream from towns or villages, storms may overload sewage facilities and cause them to discharge directly into the receiving water. The source of fecal contamination in water may be either human or animal. Some bacterial pathogens (Shigella, Salmonella typhosa) occur exclusively in human feces, whereas others (Yersinia, Campylobacter, nontyphoidal Salmonella) may be present in wild or domestic animals. No enteric viruses excreted by animals have been shown to be pathogenic to humans.222 Derlet and colleagues84,85 found that wilderness water sources in

Bacterial Escherichia coli Shigella Campylobacter Vibrio cholerae Salmonella Yersinia enterocolitica Aeromonas Viral Hepatitis A Hepatitis E Norovirus Poliovirus Miscellaneous viruses (more than 100 types: e.g., adenovirus, enterovirus, calicivirus, echovirus, astrovirus, coronavirus) Protozoal Giardia lamblia Entamoeba histolytica Cryptosporidium Blastocystis hominis Isospora belli Balantidium coli Acanthamoeba Cyclospora Parasitic Ascaris lumbricoides Ancylostoma duodenale (hookworm) Taenia spp. (tapeworm) Fasciola hepatica (sheep liver fluke) Dracunculus medinensis Strongyloides stercoralis (pinworm) Trichuris trichiura (whipworm) Clonorchis sinensis (Oriental liver fluke) Paragonimus westermani (lung fluke) Diphyllobothrium latum (fish tapeworm) Echinococcus granulosus (hydatid disease) Data from references 101, 106, 228, 249, and 280.

the California Sierra Nevada with significant amounts of human or animal activity are more likely to be contaminated with bacteria. Some organisms (e.g., Legionella pneumophila and Vibrio cholerae) exist as natural organisms in water.264

DEVELOPING COUNTRIES In tropical areas and developing countries, water has a complex relationship with spread of disease. Table 67-2 presents a useful classification,28 and Steiner and associates265 proposed adding the category “water carried” for infections resulting from accidental ingestion in recreational water. Globally, 88% of the 4 billion annual cases of diarrheal disease are attributed to unsafe water and inadequate sanitation and hygiene. About 2 million people, most children under 5 years of age, die annually from illnesses associated with unsafe drinking water or inadequate sanitation.303 WHO estimates that worldwide 25% of the population (1.5 billion rural and 200 million urban people) lack safe drinking water and 50% lack adequate sanitation. In Africa, about 40% of the population does not have access to an improved water supply, and 52% are without access to improved sanitation. In Asia, 20% are without improved water, and nearly 50% without sanitation. In both Africa and Asia, nearly 20% of rural water supplies are not functioning at any one time. In Latin America, 15% are without improved water and 20% without sanitation.302 1325

PART 8  FOOD AND WATER

TABLE 67-2  Water and Spread of Disease Type

Mechanism

Examples

Prevention

Waterborne

Fecal contamination of drinking water by infectious organisms Person-to-person fecal–oral spread via direct contact, food, water (all these are also waterborne) Organism or agent that lives in water

Typhoid fever, cholera, campylobacteriosis, giardiasis, hepatitis A Shigellosis, amebiasis, ascariasis, eye (trachoma) and skin infections

Sanitation and disinfection of water

Water-washed Water-based Water-related

Spread by insects that breed in water or collecting water

Schistosomiasis, dracunculosis, parasitic worms Malaria, sleeping sickness, yellow fever, dengue

Hand washing and personal hygiene Prevention of exposure from bathing Insect protection and piped water

Data from Bradley D: Health aspects of water supplies in tropical countries. In Feachem R, McGarry M, Mara D, editors: Water, wastes and health in hot climates, New York, 1977, Wiley, p. 3; and Steiner T, Thielman N, Guerrant R: Protozoal agents: What are the dangers for the public water supply? Annu Rev Med 48:329, 1997.

Only 30% of waste from India’s cities is treated before disposal, the rest flowing into surface or ground waters. Eight hundred million Indians lack a household water connection, relying on public taps, wells, or surface sources.58 An estimated 80% of the world’s diseases are linked to inadequate water supply and sanitation. Of the four diseases that may cause the most morbidity and death in developing parts of the world—cholera, hepatitis, malaria, and typhoid—malaria is the only one that is not waterborne.133 In developing countries, these illnesses account for 1 billion cases of diarrhea every year and 95% of deaths in children under 5 years of age.101,121,293 Another estimate puts the disease burden from water-related diseases, sanitation, and hygiene at 4% of all deaths and 5.7% of the total disease burden occurring worldwide.216 In certain tropical countries, the influence of high-density population, rampant pollution, and absence of sanitation systems means that available raw water is virtually wastewater.53 Contamination of tap water in many urban areas should be assumed because of antiquated and inadequately monitored disposal, disinfection, and distribution systems.70 Recent studies of household point-of-use water treatment in developing countries and refugee camps provide evidence of extensive coliform contamination in these settings.55,72,87,225 Water from springs and wells and even commercial bottled water may be contaminated with pathogenic microorganisms.

THE UNITED STATES AND DEVELOPED COUNTRIES Developed countries like the United States still face substantial challenges to ensure potable water in households and to maintain quality of water sources.101,161,249,270 Community water supplies treated by modern methods are responsible for outbreaks of gastrointestinal illness. Based on studies comparing rates of diarrheal illness in households with and without effective water filters, Colford and associates62-64 have estimated that 4 to 11 million cases of acute gastrointestinal illness annually are attributable to public drinking water systems in the United States. The etiology of waterborne disease outbreaks from drinking water is different from untreated sources, with more respiratory disease due to Legionella and a mix of bacterial, virus, and protozoan pathogens resulting in gastroenteritis.305 Waterborne pathogens account for most outbreaks of infectious diarrhea acquired in U.S. wilderness and recreation areas (Box 67-3).69 In both public and surface water supplies there has been an increase in the number of outbreaks caused by protozoan pathogens. Giardia is one of the most common waterborne infections, but Cryptosporidium epidemics have been identified with increasing frequency.69,120,122,238 Enteric bacteria are responsible for a relatively small but consistent proportion of waterborne outbreaks in the United States,122,305 but less commonly than are protozoa. Bacteria linked to water ingestion include Salmonella, Campylobacter, Shigella sonnei, Plesiomonas shigelloides, and E. coli O157:H7.41,42,45,305 In recreational areas, a distinct seasonal variation is seen, with the majority of cases from recreational areas occurring during summer months.69 This is probably a result of both increased contamination and number of persons at risk. 1326

Risk for gastrointestinal disease to wilderness users is determined primarily by indirect evidence based on surveys.27,305 Derlet and colleagues80-85 have performed extensive testing for bacterial contamination of wilderness waters in the California Sierra Nevada. Human pathogenic bacteria were uncommon, and other enteric bacteria as indicators of contamination were associated with animal grazing, pack animals, and high levels of human activity.

RECREATIONAL CONTACT Inadvertent ingestion during recreational activities of water not intended for drinking is a risk for swimmers and white-water boaters. The microorganisms that cause infection are those that require only a small dose. Recreational water activities have resulted in giardiasis, cryptosporidiosis,40,44,48,306 typhoid fever, salmonellosis, shigellosis, E. coli O157 infection,96 viral gastroenteritis, and hepatitis A, as well as in wound infections, septicemia, and aspiration pneumonia due to Legionella.69 Between 2005 and 2006, a total of 78 outbreaks associated with recreational water were reported, involving 4412 persons, resulting in 116 hospitalizations and 5 deaths.306 Most outbreaks occurred in treated water venues such as pools and water parks. Of these, the majority were caused by parasites, predominantly Cryptosporidium, and a only few by Giardia, reflecting Cryptosporidium resistance to chlorine disinfection.48 Bacterial contamination in treated water sources (including hospitals and hotels) most often resulted in respiratory disease caused by Legionella rather than in gastrointestinal illness. In untreated recreational water, most commonly lakes and ponds, bacteria (Shigella and E. coli O157:H7) and norovirus were much more common than were protozoa. These were predominantly small inland water bodies without external

BOX 67-3  Enteric Pathogens in U.S. Wilderness or

Recreational Water

Commonly Reported Giardia Cryptosporidium Occasionally Reported With Firm Evidence for Waterborne Campylobacter Hepatitis A Hepatitis E Enterotoxigenic E. coli E. coli O157:H7 Shigella Enteric viruses (especially norovirus, enteric adenovirus) Unusual Occurrences, Waterborne Suspected Yersinia enterocolitica Aeromonas hydrophila Cyanobacterium (blue-green algae)

SPECIFIC ETIOLOGIC AGENTS Viruses The infectious dose of enteric viruses is only a few infectious units in the most susceptible people.174,292,300 The risk for infections from enteric viruses is estimated to be 10 to 10,000 times higher than bacteria at the same level of exposure.270 Hepatitis A virus (HAV), norovirus, and rotavirus are the main viruses of concern for potable water supplies. Norovirus was the most commonly identified enteric virus in waterborne outbreaks in Finland.173 All serotypes of adenovirus (besides enteric alone) are excreted in feces, so contaminated water could be a source of exposure for any type, either through ingestion, inhalation, or direct contact with the eyes. Outbreaks of adenovirus have been associated with drinking water and contact with recreational water, including swimming pools.180 In addition to HAV, waterborne transmission of hepatitis E is suspected in outbreaks among travelers from Asia.37,144,252 Many other viruses are capable and suspected of waterborne transmission, and more than 100 different virus types are known to be excreted in human feces.112,241The most frequent waterborne illness (acute infectious nonbacterial gastroenteritis of unknown etiology) in the United States may be caused by undetected viruses; estimates of viral waterborne illness are 6.5 million cases annually.69,101,174,256 Enteroviruses have been detected even in finished water from sewage treatment plants with measurable levels of free residual chlorine.113 All surface water supplies in the United States and Canada contain naturally occurring human enteroviruses.295 Even remote surface lakes and streams tested in California showed disturbing levels of viral contamination.112 Widespread enteric viral contamination was found at multiple sites in a popular recreational canyon in Arizona. Viruses included poliovirus, echovirus, coxsackievirus, rotavirus, and other unidentifiable viruses and exceeded the recommended state level for recreational water use in several areas. Virus levels correlated with human activity but not with excess levels of standard coliform indicators.241 In 2002, a series of outbreaks involving more than 130 individuals was reported on 17 different Colorado River rafting trips. Laboratory evaluation of effluent from portable toilets found norovirus, which was also isolated from river water at Lee’s Ferry. No specific risk factors were identified in individuals or trips, and it was concluded that risk was likely from the river water.125 No evidence exists of human immunodeficiency virus (HIV) transmitted via a waterborne route, and no epidemiologic evidence exists of casual transmission by fomites or by any environmentally mediated mode.232 There has never been a documented case of influenza virus infection associated with water exposure. Free chlorine levels of 1 to 3 mg/L are adequate to disinfect avian, H1N1, or other influenza viruses. Protozoa Six protozoa that cause enteric disease and may be passed via waterborne transmission are Giardia lamblia, Cryptosporidium parvum, Entamoeba histolytica, Cyclospora cayetanensis, Isospora belli, and the microsporidia.101,172 The first two are the most important for wilderness travelers. Cryptosporidium is an emerging enteric pathogen that has overtaken Giardia as the most common waterborne protozoa.38,101,306 Many aspects of the epidemiology and transmission appear similar to Giardia; 10 G. lamblia cysts may result in infection, and the infectious dose of Cryptosporidium is also on the order of 102 oocysts.88,227 Waterborne transmission of E. histolytica is common in developing countries. Cyclospora has been epidemiologically linked to waterborne transmission in the United States and in Nepal, but the reservoir and host range are not known. Unlike Giardia and Cryptosporidium, Cyclospora is not infectious when passed in feces and requires up to 2 weeks in the laboratory to sporulate.254Surface water is a common environmental source for

microsporidia; however, the route of infection is unknown. N. fowleri is a waterborne protozoan that enters the body through the nasal epithelia during swimming in contaminated surface water and causes meningoencephalitis. Giardia and Cryptosporidium.  Giardia cysts have been found as frequently in pristine water and protected sources as in unprotected waters.123,136,233,239,240,263 Repeated sampling of “negative” sources invariably produced positive results. A zoonosis with Giardia is known, with at least three different species; the extent of cross-species infection is not clear.15,298 Many of the species apparently capable of passing Giardia cysts to humans, including dogs, cattle, ungulates (deer), and beaver, are present in wilderness areas. Forty percent of beavers in Colorado were infected and shedding 1 × 108 cysts per animal per day. All 386 muskrats found were infected. Up to 20% of cattle examined were infected.123 Beaver have been implicated in multiple municipal outbreaks of giardiasis. Samples from Rocky Mountain National Park154,187 and the California Sierra Nevada263,267 show a direct correlation between numbers of cysts and levels of human use or beaver habitation. In Yukon, Canada, 13 of 61 scat samples from various wild animals yielded Giardia cysts.234 Even with a low infectious dose, environmental cyst recovery data indicate that the risk for ingesting an infectious dose of Giardia cysts is small.308 However, the likely model that poses a risk to campers is pulse contamination—a brief period of high cyst concentration from fecal contamination. Beaver stool and human stool may contain 1 × 106 cysts/g. Stream contamination from a beaver has been calculated to reach 245 cysts/gal.136 This is consistent with outbreaks in recreational water due to human contamination.46,48,209 In this instance, small amounts of water may cause infection, similar to an outbreak among lap swimmers from inadvertent water ingestion in a fecally contaminated pool. Cryptosporidium oocysts are found widespread in surface water, and the cyst is durable in the environment. A large zoonosis is evident. Environmental occurrence appears ubiquitous.159,237,238 Cryptosporidium is now found more frequently than is Giardia in surface water, albeit in smaller numbers; it is the most frequent contaminant in treated recreational water; and it has resulted in large outbreaks in municipal water systems.36,77,120,169,306 Parasitic Organisms Parasitic organisms other than protozoa are seldom considered in discussions of disinfection. Infectious eggs or larvae of many helminths are found in sewage, even in the United States.224,251 The frequency of infection by waterborne transmission is unknown, because food and environmental contamination or skin penetration is more prevalent.301 The most obvious risk is from nematodes, with no intermediate hosts, that are infectious immediately or soon after eggs are passed in stool. Ascaris lumbricoides (roundworm) is transmitted by ingestion of the eggs in contaminated food or drink. In endemic areas, 85% of the population is infected; this leads to daily global environmental contamination by 9 × 1014 eggs.301 Ancylostoma duodenale (hookworm) usually infects as larvae penetrate the skin of the foot, but it also may be acquired by mouth. Oral entry of the larvae causes pulmonary (Wakana) disease. Necator americanus (hookworm) does not appear to be infectious via the oral route. Taenia solium (pork tapeworm) is infectious to humans in cyst or egg form. Eggs passed in stool are ingested in food or water and develop into tissue cysts, often in the brain, resulting in cysticercosis. Echinococcus granulosus (dog tapeworm) can use humans as intermediate hosts. Eggs from the feces of an infected dog or other carnivore are ingested in food and water. Hydatid disease generates cysts in the liver, peritoneum, and other sites. Fasciola hepatica (liver fluke of herbivores and humans) is normally acquired by ingestion of encysted metacercariae on water plants or free organisms in water. Cercariae of schistosomiasis, which live in fresh water and normally enter through skin, can enter through the oral mucosa. The cercariae are killed by stomach acid. 1327

CHAPTER 67  Field Water Disinfection

sources of contamination, suggesting swimmers were the source. At least one case of usually fatal neuroinvasive disease caused by Naegleria fowleri is reported each year from untreated recreational water.

PART 8  FOOD AND WATER

Dracunculus medinensis (guinea tapeworm) is a tissue nematode of humans and causes the only such disease transmitted exclusively through drinking water.293 Dracunculus larvae are released in water from subcutaneous worms on the legs of infected bathers or water-gatherers. Larvae are ingested by a tiny crustacean (Cyclops species), which acts as the intermediate host and releases infectious larvae when ingested by humans. Worldwide eradication of dracunculosis has nearly been accomplished. Bacterial Spores Bacterial spores can cause serious wound and gut infections but are not likely to be waterborne enteric pathogens. Clostridium is ubiquitous in soil, lake sediment, tropical water sources, and the stool of animals and humans.121,247 Clostridium botulinum and Clostridium perfringens type A food poisoning are not waterborne because they require germination of spores in food by inadequate cooking, then production of an enterotoxin, which is ingested. C. perfringens type C causes enteritis necroticans, probably through in vivo production of an enterotoxin, and thus has the potential for waterborne transmission in the tropics. However, the epidemiology of these infections in the United States, as in infant botulism, is related to food-borne sources. Algae Cyanobacterium, also known as blue-green algae, grow rapidly in water rich in organic matter during warm weather and produce toxins that pose a health risk to humans, pets, and wildlife. Effects depend on the type of cyanobacterium and the level of exposure through dermal contact or aspiration, as well as ingestion. Adverse effects include skin and eye irritation or gastrointestinal upset. At higher levels, exposure can result in serious illness, including hepatotoxicity (from microcystin toxins) or neurotoxicity. The algae are readily visible and would dissuade most humans from drinking, so it poses more of a threat to animals or small children due to recreational ingestion.32 Chemical Hazards Chemical hazards are also an alarming source of pollution in surface water. Wilderness users must consider removal of chemical, as well as microbiologic, contaminants. The greatest risks to wilderness travelers are pesticides from agricultural runoff

and heavy metals from old mine tailings. Industrialization proceeds worldwide without adequate environmental protection. A vast array of toxins are sold with little concept of safe use and no means of safe disposal. Inorganic chemicals in drinking water include common salts, heavy metals, asbestos, fluorides, nitrates, radionuclides, and heavy metals (arsenic, copper, iron, lead, selenium). Natural organic chemicals predominate from soil runoff, forest canopy aquatic biota, and human and animal wastes. Synthetic organic matter includes pesticides, herbicides, and chemicals from industrial or human activities.286 Major underground aquifers are becoming contaminated. Streams and rivers in rural areas are contaminated by individual carelessness, leaching landfills, and agricultural runoff. Numerous pesticides have been found in runoff and rivers in agricultural areas of the Midwest.183 Atmospheric spread has resulted in pesticides being found in remote wilderness lakes and in acid rain. Persistence of Enteric Pathogens in the Environment Once environmental contamination has occurred, a natural inactivation or die-off begins. However, enteric pathogens can retain viability for long periods (Table 67-3).240,286 Factors promoting survival of microorganisms are pH near neutral (between 6 and 8) and cold temperatures, which contribute to the risk for transmission in mountain regions. In temperate and warm water, survival is measured in days, with densities of infectious agents decreasing by 90% every 60 minutes. However, tropical water differs from temperate water because it contains nutrients that create a microbiologically rich environment. Coliform bacteria can survive several months in natural tropical river water and may even proliferate. Survival of other bacteria is also prolonged (about 200 hours in tropical compared with 30 hours in temperate water). E. coli and V. cholerae may occur naturally in tropical waters and are capable of surviving indefinitely.70,121,205 As a rule, viruses persist longer than enteric bacteria in water.290 Most enteric organisms, including Shigella, resist freezing.86 S. typhosa (typhi) can survive for up to 5 months in frozen debris and ice.295 HAV survives 6 months at below-freezing temperatures.273 Cryptosporidium may be able to survive a week or more in home freezers.265 Viruses persist well on chilled, acidified, frozen foods and foods packed under modified atmosphere or in dried conditions.10

TABLE 67-3  Viability of Enteric Pathogens in Water Organism

Conditions

Survival

Reference

Vibrio cholerae V. cholerae Campylobacter Campylobacter Escherichia coli E. coli Salmonella Yersinia Shigella Shigella Enteric pathogens Salmonella typhosa Viruses Enteric viruses Enteric viruses Enteric adenovirus Hepatitis A virus Hepatitis A Hepatitis A Giardia Giardia Entamoeba histolytica Microsporidia Cryptosporidium Ascaris eggs Hookworm larvae

Cold Tropical Cold Temperate stream Temperate stream Tropical Temperate stream Temperate stream Temperate stream Freeze/thaw Freeze/thaw Ice/frozen debris Cold 15°-25° C (59°-77° F) water 4° C (39.2° F) water Cold Cold Fresh, sea, wastewater <0° C (32° F) Cold 15° C (59° F) lake, river Cold 4° C (39.2° F) Cold Wet or dry Wet sand

4-5 wk >1 yr 3-5 wk 3-10 days 13 hr >1 yr Half-life 16 hr 540 days Half-life 22 hr Yes Yes 5 mo 17-130 days 6-10 days 30 days Months 1 yr 12 wk 6 mo 2-3 mo 10-28 days 3 mo >1 yr 12 mo 6-9 yr 122 days

Felsenfeld, 196597 Perez-Rosas, 1989205 Blaser, 198025 Singh, 1990253 Singh, 1990253 Perez-Rosas, 1989205 Perez-Rosas, 1989205 Singh, 1990253 Singh, 1990253 DuPont, 19989 Dickens, 198586 White, 1992295 Sattar, 1978246; World Health Organization, 1979300 Rose, 1996240 Rose, 1996240 Mena, 2009180 Biziagos, 198822; Thraenhart, 1991273 Biziagos, 198822 Thraenhart, 1991273 Bingham, 197920; DeReigner, 198979 DeReigner, 198979 Chang, 195352 Marshall, 1997172 Current, 198576 World Health Organization, 1981301 World Health Organization, 1981301

1328

• In general, cloudiness indicates higher risk for contamination; however, in remote wilderness water, most sediment is inorganic and clarity is not an indication of microbiologic purity. • The major factor determining amount of microbe pollution in surface water is human and animal activity in the watershed. • Streams do not purify themselves but may dilute a limited source of contamination. • Settling effect of lakes may make them safer than streams, but care should be taken not to disturb bottom sediments when obtaining water. • Groundwater (springs and protected wells) are generally cleaner than surface water because of the filtration action of overlying sediments.

Natural Purification Mechanisms It is widely believed that streams purify themselves and that certain water sources are reliably safe for drinking. These concepts have some truth but do not preclude the need for disinfection to ensure water quality (Box 67-4). Storms usually deteriorate surface water quality by washing solids, organic materials, and microorganisms into water sources; however, rainwater can also flush streams clean by dilution and by washing microbe-laden bottom sediments downstream.106,121 Every stream, lake, or groundwater aquifer has limited capacity to assimilate waste effluents and storm water runoff entering the drainage basin. Self-purification is a complex process that involves settling of microorganisms after clumping or adherence to particles, sunlight providing ultraviolet (UV) destruction, natural die-off, predators eating bacteria, and dilution. Environmental factors include water volume and temperature, hydrologic effects, acid soil contact, and solar radiation. The process is time dependent and less active during wet periods and winter conditions. Hours needed in flow time downstream to achieve a 90% bacterial kill by natural self-purification vary with pollution inflow and rate of water flow. They have been measured at approximately 50 hours in the Tennessee River in summer, 47 hours in the Ohio River in summer, and 32 hours in the Sacramento River in summer.106 Storage in reservoirs or lakes also improves microbiologic quality, with sedimentation as the primary process. A 100-to 1000-fold increase in fecal coliform bacteria can be found in bottom sediments compared with overlying water. This removal must be considered temporary, influenced by recirculation of organisms trapped in bottom sediments.79,106 In optimal conditions, 10 days of reservoir storage can result in 75% to 99% removal of coliform bacteria, and 30 days can produce safe drinking water. Generally, 80% to 90% of bacteria and viruses are removed by storage, depending on inflow and outflow, temperature, and no further contamination. Cysts, with a larger size and greater weight, should settle even faster than do bacteria and viruses.2 Groundwater is generally cleaner than surface water because of the filtration action of overlying sediments, but wells and aquifers can be polluted from surface runoff. Spring water is generally of higher quality than surface water, provided that the true source is not surface water channeling underground from a short distance above the spring. Drawing conclusions from the preceding factors is difficult. The major factor governing the amount of microbe pollution in surface water is human and animal activity in the watershed. The settling effect of lakes may make them safer than streams, but care should be taken not to disturb bottom sediments when obtaining water.

Standards Because coliforms originate primarily in the intestinal tracts of warm-blooded animals, including humans, they are used as indicators of possible fecal contamination.121 Although compelling

reasons exist for testing other organisms before determining the safety of drinking water, cost and relative difficulty in testing for viruses and protozoa are major obstacles to expanding routine water testing, so coliforms remain the worldwide standard indicator organism. In the United States, bacterial indicators of water quality do not predict vulnerability to an outbreak. Contamination with other organisms has become common, resulting in expansion of U.S. regulations to test for organisms such as Cryptosporidium. In the future, molecular probes should make this process much easier.186,270 The basic federal law pertaining to drinking water is the 1974 Safe Drinking Water Act, which was expanded and strengthened by amendments in 1977, 1986, and 1996.186,305 Additional rules were added in 1989, 1996, 1998, and 2006.45,228 The U.S. Public Health Service recommendations for potable water specify a mean of 1 coliform organism per 100 mL of water, or 10 organisms per liter. Absolute limits are 3 coliform bacteria per 50 mL, 4 per 100 mL, and 13 per 500 mL.288 In 1989, the standards for detection of fecal coliform bacteria in drinking water were relaxed slightly in recognition that coliform bacteria occur in large numbers in many water distribution systems that have no problem with waterborne disease.284 All standards acknowledge the impracticality of trying to eliminate all microorganisms from drinking water, allowing a small risk for enteric infection.33,228,256 Risk models are used to predict levels of illness and desired levels of reduction, with the reality that large numbers of people in the United States have increased susceptibility to enteric infections because of decreased immunologic competency.228 For example, EPA and Canadian guidelines suggest Giardia cyst removal with the goal of ensuring high probability that consumer risk is no more than one infection per 10,000 people per year.33,222,228 Generally, the goal of treatment is to achieve a 3- to 5-log reduction in the level of microorganisms: treatment must reduce Giardia by 99.9% (3 log) and enteric viruses by at least 99.99% (4 log).221 The concept of risk is important for wilderness travelers as well, because it is impossible to know the risk of drinking the water in advance and may not be practical to eliminate all risk with treatment.

STANDARDS FOR PORTABLE DISINFECTION PRODUCTS The EPA and NSF International are the primary agencies that set standards for disinfection products and protocols for testing to meet these standards. NSF, The Public Health and Safety Company, is a not-for-profit, nongovernmental organization and world leader in standards development and product certification. EPA and NSF Protocol P231 (Microbiological Purifiers) were used to create NSF Protocol P248 (Emergency Military Operations Microbiological Water Purifiers) to test individual water purifiers for field military operations. The protocols are applicable to all types of individual water purifiers. EPA Registration Mechanical Filters.  Until recently, no testing criteria were mandated for EPA registration. The EPA does not endorse, test, or approve mechanical filters; it merely assigns registration numbers. However, registration requirements distinguish between two types of filters: those that use mechanical means only and those that use a chemical, designated as a pesticide. Standards were developed to act as a framework for testing and evaluation of water purifiers for EPA registration, as a testing guide for manufacturers, to assist in research and development of new units, and as a guide for consumers.284 Filter Testing.  Current registration of mechanical filters requires only that the product make reasonable claims and that the location of the manufacturer be listed; no disinfection studies are required. However, many companies now use the standards as their testing guidelines. For mechanical filters, the standards should be applied only for those microorganisms against which claims are made, such as protozoa and bacteria, excluding 1329

CHAPTER 67  Field Water Disinfection

BOX 67-4  Water Quality: Key Points

PART 8  FOOD AND WATER

viruses. Despite criticisms of the methodology and inconsistencies and loopholes in the reporting process, EPA standards are currently the best means to compare filters. EPA standards include performance-based microbiologic reduction requirements, chemical health limits for substances that may be discharged, and stability requirements for chemical(s) sufficient for the shelf life of the device. The unit should signal the end of effective lifetime (e.g., by terminating discharge of treated water) or give simple instructions for servicing or replacing within measurable volume, throughput, or time frame. There are currently no national guidelines for removal of chemicals by portable filters. EPA standards require that challenge water seeded with specific amounts of microorganisms be pumped through the filters at given intervals during the claimed volume capacity of the filter. Between bacteriologic challenges, different test waters without organisms are passed through the unit. Water conditions are specified to include average and worst-case conditions; the latter are 5° C (41° F) with high levels of pollution, turbidity, and alkaline pH. Testing must be done with bacteria (Klebsiella), viruses (poliovirus and rotavirus), and protozoa (Cryptosporidium has replaced Giardia). A 3-log reduction (99.9%) is required for cysts, 4-log reduction (99.99%) for viruses, and 5- to 6-log reduction for bacteria. Testing is done or contracted by the manufacturer; the EPA neither tests nor specifies laboratories. To be called a “microbiologic water purifier,” the unit must remove, kill, or inactivate all types of disease-causing microorganisms from the water, including bacteria, viruses, and protozoan cysts, so as to render the processed water safe for drinking. An exception for limited claims may be allowed for units removing specific organisms to serve a definable environmental need, for example, removal of protozoan cysts.

CHEMICAL METHODS Products that are used for treating municipal or private water supplies for drinking are considered pesticides and must be registered by the EPA Office of Pesticide Programs. Registration signifies the following: • The composition is such as to warrant the proposed claims. • The labeling and other material required to be submitted comply with the requirements of the act. • The method will perform its intended function without unreasonable adverse effects on the environment. • When used in accordance with widespread and commonly recognized practice, the method will not generally cause unreasonable adverse effects on the environment. Thus EPA registration implies only that the “pesticide” agent is not released into the water at unsafe levels.4,35 This is less stringent than for filters that contain halogens.

Disinfection Methods DEFINITIONS (Box 67-5) Disinfection, the desired result of field water treatment, means the removal or destruction of harmful microorganisms. Technically it refers only to chemical means such as halogens, but the term is often applied to heat and filtration. Pasteurization is similar to disinfection but specifically refers to the use of heat, usually at temperatures below 100° C (212° F), to kill most pathogenic organisms. Disinfection and pasteurization should not be confused with sterilization, which is the destruction or removal of all life forms.156 The goal of disinfection is to achieve potable water, indicating only that a water source, on average over a period of time, contains a “minimal microbial hazard,” so that the statistical likelihood of illness is acceptable. Water sterilization is not necessary, because not all organisms are enteric human pathogens.128 Purification is the removal of organic or inorganic chemicals and particulate matter to remove offensive color, taste, and odor. It is frequently used interchangeably with disinfection, but purification as used here may not remove or kill enough microorganisms to ensure microbiologic safety.293 1330

BOX 67-5  Definitions of Terms Clarification Coagulation– flocculation Contact time Disinfection

Enteric pathogen

Halogen Halogen demand Potable

Purification

Residual halogen concentration Reverse osmosis

Sterilization

Techniques that reduce turbidity of water. Removes smaller suspended particles and chemical complexes too small to settle by gravity (colloids). The length of time that the halogen is in contact with microorganisms in the water. A process that kills or destroys nearly all disease-producing microorganisms, with the exception of bacterial spores. As applied here, refers to pathogenic waterborne microbes and is the desired result of water treatment. Microorganism capable of causing intestinal infection after ingested; may be transmitted through food, water, or direct fecal–oral contamination. Oxidant chemical (primarily chlorine and iodine) that can be used for disinfection of water. The amount of halogen reacting with impurities in the water. Implies “drinkable” water, but technically means that a water source, on average, over a period of time, contains a “minimal microbial hazard,” so that the statistical likelihood of illness is acceptable. The removal of organic or inorganic chemicals and particulate matter to improve offensive color, taste, and odor. Sometimes used by other sources to indicate microbiologic removal. The amount of active halogen remaining after halogen demand of the water is met. A process of filtration that uses high pressure to force water through a nanopore semipermeable membrane that filters out dissolved ions, molecules, and solids. A process by which all forms of microbial life, including bacteria, viruses, protozoa, and spores, are destroyed.

Heat Heat is the oldest means of water disinfection. It is used worldwide by residents, travelers, and campers to provide safe drinking water. In countries with normally safe drinking water, it is often recommended as backup in emergencies or when water systems have become contaminated by floods or a lapse in water treatment plant efficacy. Fuel availability is the most important limitation to using heat. One kilogram of wood is required to boil 1 L of water.53 For wilderness travelers without access to wood, liquid fuel is heavy (Box 67-6). Heat inactivation of microorganisms is exponential and follows first-order kinetics. Time plotted against temperature yields a straight line when plotted on a logarithmic scale.141 The thermal death point is reached in shorter time at higher temperatures, whereas lower temperatures are effective with a longer contact time. Pasteurization uses this principle to kill enteric food pathogens and spoiling organisms at temperatures between 60° and 74° C (140° and 165.2° F), well below boiling.103 Pasteurization is not intended to kill all pathogenic microorganisms in the food or liquid. Instead, pasteurization aims to reduce the number of viable pathogens so they are unlikely to cause disease; for example, the high temperature–short time pasteurization standard for milk uses 71.7° C (161° F) for 15 to 20 seconds to achieve a 5-log reduction, killing 99.999% of viable microorganisms. Flash pasteurization subjects fruit or vegetable juice to temperatures of 71.5° C (160.7° F) to 74° C (165.2° F) for about 15 to 30 seconds. Therefore the minimum critical temperature is well below the boiling point at any terrestrial elevation. Microorganisms have varying sensitivity to heat; however, all common enteric pathogens are readily inactivated by heat

Advantages Does not impart additional taste or color to water Single-step process that inactivates all enteric pathogens Efficacy is not compromised by contaminants or particles in   the water, as with chemical treatment and filtration Can pasteurize water without sustained boiling

Disadvantages Does not improve the taste, smell, or appearance of poor-quality water Fuel sources may be scarce, expensive, or unavailable Does not prevent recontamination during storage

Relative susceptibility of microorganisms to heat: protozoa > bacteria > viruses.

(Table 67-4). Bacterial spores (e.g., Clostridium spp.) are the most resistant; some can survive 100° C (212° F) for long periods but, as discussed, are not likely to be waterborne enteric pathogens. Boiling does not depend on water quality as does filtration or chemical disinfection. Heat kills or inactivates all enteric waterborne pathogens, regardless of whether they are freely suspended or present in particles.249 Protozoal cysts, including Giardia and E. histolytica, are very susceptible to heat. Cryptosporidium is also inactivated at these lower pasteurization levels. Parasitic eggs, larvae, and cercariae are all susceptible to heat. For most helminth eggs and larvae, which are more resistant than cercariae and Cyclops (the copepod that carries Dracunculus), the critical lethal temperature is 50° to 55° C (122° to 131° F).251 Common bacterial enteric pathogens (E. coli, Salmonella, Shigella) are killed by standard pasteurization temperatures of 55° C (131° F) for 30 minutes or 65° C (149° F) for less than 1 minute.103,194 Recent studies confirmed safety of water

contaminated with V. cholerae and E. coli after 10 minutes at 60° to 62° C (140° to 143.6° F) or after boiling water for 30 seconds.116,230 Viruses are more closely related to vegetative bacteria than to spore-bearing organisms141 and are generally inactivated at 56° to 60° C (132.8° to 140° F) in less than 20 to 40 minutes.1,206,269 Inactivation at higher temperatures is similar to that of vegetative bacteria. Death occurs in less than 1 minute above 70° C (158° F), as confirmed in milk products.268 Given its environmental stability and clinical virulence, HAV is a special concern. Some data indicate that it has greater thermal resistance than do other enteric viruses, but a review of data from food industry studies confirms susceptibility of HAV and other enteric viruses to heat at pasteurization temperatures, even in milk and other products with solids that would shield the virus.10 Widely varying data probably result from different models for virus infectivity and destruction and from the use of various test media.

BOILING TIME The boiling time required is important when fuel is limited. The old recommendation for treating water was to boil for 10 minutes and add 1 minute for every 304.8 m (1000 feet) in elevation. However, available data indicate this is not necessary for disinfection. Evidence indicates that enteric pathogens are killed within seconds by boiling water and rapidly at temperatures above 60° C (140° F). In the wilderness, the time required to heat water from 55° C (131° F) to boiling temperature works toward disinfection. Therefore any water brought to a boil should be adequately disinfected.257 An extra margin of safety can be added by boiling for 1 minute or by keeping the water covered for several more minutes, which will maintain high temperature without using fuel, or allowing it to cool slowly. Although the boiling

TABLE 67-4  Data on Heat Inactivation of Microorganisms Organism

Lethal Temperature/Time

Reference

Giardia

55° C (131° F) for 5 min 100° C (212° F) immediately 50° C (122° F) for 10 min (95% inactivation) 60° C (140° F) for 10 min (98% inactivation) 70° C (158° F) for 10 min (100% inactivation) 55° C (131° F) Similar to Giardia 50°-55° C (122°-131° F) 65° C (149° F) for 1 min, 50° C (122°) for 30 min 45°-55° C (113°-131° F) for 20 min 55° C (131° F) warmed over 20 min 64.2° C (147.6° F) within 2 min 72° C (161.6° F) heated up over 1 min 55° C (131° F) for 30 min 60°-62° C (140°-143.6° F) for 10 min 65° C (149° F) for <1 min 60°-62° C (140°-143.6° F) for 10 min 100° C (212° F) for 30 sec 60° C (140° F) for 3 min (3-log reduction) 65° C (149° F) for 3 min (all but a few Campylobacter) 75° C (167° F) for 3 min (100% kill) 50° C (122° F) for 10 min ineffective 60° C (140° F) for 5 min 70° C (158° F) for 1 min 55°-60° C (131°-140°) within 20-40 min 70° C (158° F) for <1 min 98° C (208.4° F) for 1 min 85° C (185° F) for 1 min 61° C (141.8° F) for 10 min (50% disintegrated) 60° C (140° F) for 19 min (in shellfish) 60° C (140° F) for 10 min; 80° C (176° F) for 3 min; 85° C (185° F) for 1 min or less (in various food products) 60° C (140° F) for 30 min >100° C (212° F)

Jarroll, 1984139 Bingham, 197920 Ongerth,1989201

Entamoeba histolytica Nematode cycsts, helminth eggs, larvae, cercariae Cryptosporidium

E. coli Salmonella and Shigella V. cholerae E. coli, Salmonella, Shigella, Campylobacter Escherichia coli Viruses Hepatitis A

Hepatitis E Bacterial spores

Aukerman, 19896 Shephart, 1977251 Anderson, 19853 Fayer, 199495 Frazier, 1978103 Neumann, 1969194 Rice, 1991230 Bandres, 198811 Groh, 1996116 Alder, 19921 Krugman, 1970153 Thraenhart, 1991273 Peterson, 1978208 Baert,200910 Thraenhart, 1991273 Alder, 19921

1331

CHAPTER 67  Field Water Disinfection

BOX 67-6  Heat

PART 8  FOOD AND WATER

TABLE 67-5  Boiling Temperatures at Various

Altitudes

Altitude (ft)

Altitude (m)

5000 10,000 14,000 19,000

1524 3048 4267 5791

Boiling Point 95° 90° 86° 81°

C C C C

(203° F) (194° F) (186.8° F) (177.8° F)

point decreases with increasing altitude, this is not significant compared with the time required for thermal death at these temperatures (Table 67-5). In recognition of the difference between pasteurizing water for drinking purposes and sterilizing to kill all microbes, for surgical or laboratory purposes, many other sources, including WHO, now agree with this recommendation to simply bring water to a boil. The Centers for Disease Control and Prevention (CDC) and EPA still recommend boiling for 1 minute to add a margin of safety.39 Other sources still suggest 3 minutes of boiling time at high altitude to give a wide margin of safety.12,105,238,281

HOT TAP WATER Although attaining boiling temperature is not necessary, it is the only easily recognizable end point without using a thermometer. Other markers, such as early bubble formation on the bottom of the pot, do not occur at a consistent temperature. When no other means are available, the use of hot tap water may prevent travel­ er’s diarrhea in developing countries. Neumann194,195 cultured samples from the hot water tap of 17 hotels in west Africa with water temperature ranging from 57° to 69° C (134.6° to 156.2° F) and found no coliforms in 15 samples; one sample yielded a single colony and another sample two colonies. As a rule of thumb, water too hot to touch fell within the pasteurization range. Bandres and associates11 also measured hot tap water temperature in 14 hotels in four different countries outside the United States. Most temperatures were 55° to 60° C (131° to 140° F), but one was 44° C (111.2° F), one was 65° C (149° F), and several were 52° C (125.6° F). The authors concluded that hot water from taps would not be safe to drink. Groh and colleagues116 showed that tolerance to touch is too variable to be reliable, because some people found 55° C (131° F) too hot to touch. From these studies, one can conclude that if water has been sitting in a tank near 55° to 60° C (131° to 140° F) for a prolonged period, enteric pathogens will be significantly reduced, likely to potable levels. Neumann’s suggestion is reasonable if no other method of water treatment is available.

SOLAR HEAT Pasteurization has been successfully achieved using solar heating. Bottom temperatures of 65° C (149° F) have been obtained for at least 1 hour in up to three 3.7-L jugs. Exposure to full sunshine in Kenya destroyed E. coli in 2-L clear plastic bottles within 7 hours if the maximum temperature reached 55° C (131° F). No thermal inactivation occurs below 40° C (104° F). Inactivation using solar heat is a combination of thermal and UV irradiation.142,176 A solar cooker constructed from a foil-lined cardboard box with a glass window in the lid can be used for disinfecting large amounts of water by pasteurization. Most commonly, clear plastic bottles are placed on a reflective metal surface. This is a low-cost method for improving water quality, especially in refugee camps and disaster areas179 (see Ultraviolet Light discussion, later).

Physical Removal TURBIDITY AND CLARIFICATION River, lake, or pond water is often cloudy and unappealing. Turbidity (cloudiness) is an optical measurement of light scattering as it passes through water. Visibility in water with turbidity 1332

of 10 nephelometric turbidity units (NTU) is about 30 inches and with 25 NTU is 10 inches. Turbidity is caused by suspended organic and inorganic matter, such as clay, silt, plankton, and other microscopic organisms. High turbidity is often associated with unpleasant odors and tastes, most often caused by organic compounds and metallic hydroxides with a much smaller particle size.61,158 Clay-organic complexes may also carry pesticides or heavy metals. Bacteria, as well as viruses, may be adsorbed to particulate matter or be embedded in it, and in highly contaminated water, microorganisms tend to aggregate and clump. In one study, 17% of turbidity particles contained attached microbes, averaging 10 to 100 bacteria per particle.158 Organisms in the centers of these conglomerates are afforded some protection from disinfectants. Even the flocculate produced by a chlorination– flocculation tablet may harbor viable organisms.212 Therefore removal of turbidity and particulates may be important in preventing chemical or infectious illness. Of 106 samples from various sources in 13 developing countries, 33% exceeded 5 NTU and 64% exceeded 1 NTU, which is the maximum turbidity level set by the EPA before water chlorination.155 As expected, turbidity was lower in improved sources, but only 5 out of 22 of these urban water sources had any detectable free chlorine residual. Household studies in developing countries indicate that most consumers find water with less than 5 NTU esthetically acceptable for drinking. Clarification to remove turbidity is an important first step, before using filtration or chemical disinfection, that greatly improves the efficacy of these techniques (Box 67-7).248 Even if turbidity is caused by benign inorganic particles, such as clay, removal is desirable for improving esthetic quality of the water. Filtration can remove larger particles, but cloudy water can rapidly clog a filter. Sedimentation and coagulation–flocculation are other clarification techniques routinely used in municipal disinfection plants that can be easily applied in the wilderness for pretreatment of cloudy water, which is then disinfected by microfiltration or halogenation. Coagulation–flocculation and filtration are also used to remove Giardia and Cryptosporidium cysts that are more resistant to chlorine. Early experiments with water heavily contaminated with feces containing HAV demonstrated that filtration and sedimentation alone did not prevent infection, but reduced the severity of the illness. Water pretreated with coagulation, settling, and filtration and subsequently disinfected with 0.4 ppm of residual chlorine was noninfectious, whereas water chlorinated to 1 mg/L without pretreatment

BOX 67-7  Summary of Clarification Techniques Technique Sedimentation Coagulation– flocculation

Process Settling by gravity of large particulates Removes suspended particles, most microorganisms, some dissolved substances

Activated carbon (charcoal)

Removes organic and some inorganic chemicals

Filtration

Physical and chemical process

Uses, Advantages Requires only time. Greatly improves water esthetics. Simple process, easily applied in field. Greatly improves water quality. Improves efficacy of filtration and chemical disinfection. Removes toxins such as pesticides and removes chemical disinfectants. Improves taste esthetics of water. Removes microorganisms and particulates. Nanofiltration may remove chemicals and monovalent ions (salt). Charcoal stage may improve taste and remove chemicals.

SEDIMENTATION Sedimentation is the separation of suspended particles large enough to settle rapidly by gravity, such as sand and silt. Water is allowed to sit without agitation. After sediment has formed on the bottom of the container, the clear water is decanted or filtered from the top. The time required depends on the size of the particle. Generally, 1 to 3 hours are adequate for large particles such as inorganic sands and silts. Microorganisms, especially protozoan cysts, eventually settle, hastened by attachment to organic biologic particles; reductions up to 90% may be achieved within 1 to 2 days.53,178 However, the organisms are easily disturbed during pouring or filtering. Reservoirs take advantage of sedimentation to improve microbiologic quality. In conclusion, sedimentation is often effective in reducing water turbidity and will improve microbiologic quality, but is not recommended as the sole means of disinfection.

COAGULATION–FLOCCULATION Smaller suspended particles and chemical complexes too small to settle by gravity are called colloids. Most of these can be removed by chemical precipitation, known as coagulation– flocculation, a technique that has been used to remove unpleasant color, smell, and taste in water since 2000 BC. This technique is used routinely in large municipal disinfection plants, but is simple enough to be used at the household level and in the outdoors72,225,257(Box 67-8). Coagulation is achieved with addition of an appropriate chemical that alters the physical state of dissolved and suspended solids, causing particles to stick together on contact because of electrostatic and ionic forces.61,286Aluminum salts (alum), iron, lime (alkaline chemicals principally containing calcium or magnesium and oxygen) are commonly used, readily available coagulants. Rapid mixing is important to obtain dispersion of the coagulant. The second stage, flocculation, is a purely physical process obtained by prolonged gentle mixing to increase interparticle collisions and promote formation of larger particles. The flocculate particles can be removed by sedimentation and filtration. To clarify water by coagulation–flocculation in the field, add 10 to 30 mg of alum per liter of water. The exact amount is not important, so it can be done with a pinch of alum, lime (calcium oxide), or both for each gallon of water, using more if the water is very cloudy. Next, stir or shake briskly for 1 minute to mix the coagulant, and then agitate gently and frequently for at least 5 minutes to assist flocculation. Settling requires at least 30 minutes, after which the water is carefully decanted or poured

BOX 67-8  Coagulation–Flocculation Advantages Highly effective to clarify water and   remove many microorganisms and   some other contaminants Improves efficacy of filtration and   chemical disinfection Inexpensive and widely available Simple process with no toxicity

Disadvantages Unfamiliar technique to many consumers Adds extra step unless combined flocculentdisinfectant tablet

Relative susceptibility of microorganisms to coagulation–flocculation: protozoa > bacteria = viruses.

through a cloth or paper filter. The process can be repeated, if necessary. Coagulation–flocculation removes most coliform bacteria (60% to 98%),71 viruses (65% to 99%),75,219,256 Giardia (60% to 99%), helminth ova (95%),251 heavy metals, dissolved phosphates, and minerals.61,165,286,300 Organic and inorganic compounds may be removed by forming a precipitate or by adsorbing onto aluminum hydroxide or ferric hydroxide floc particles.286 Coagulation generally removes large molecules that absorb poorly on granular activated carbon (GAC).7 Despite removal of most microorganisms, a subsequent disinfection step is advised. Products combining flocculants with chlorine provide a two-step process that removes turbidity and allows effective disinfection by chlorine.225 Toxicity Questions have been raised concerning the association of aluminum with central nervous system (CNS) toxicity in mammals, but these effects have been observed only after exposures other than ingestion. Most of the aluminum in alum is removed with the floc. A report from the National Academy of Sciences concluded that aluminum in drinking water does not present a significant risk.286 Alum is a common chemical used by the food industry in baking powder and for pickling. It can be found in some food stores or at chemical supply stores. Alternative Agents Many inorganic and organic compounds can be used as a coagulant, including lime (calcium oxide) or potash (from wood ash). In an emergency, baking powder or even the fine white ash from a campfire can be used.5 Other coagulation–flocculation agents used traditionally by native peoples include seed extracts from the nirmali plant in southern India, moringa plants in Sudan, crushed almonds, dried and crushed beans, and rauwaq (a form of bentonite clay).53

ADSORPTION Adsorbents such as charcoal, clay, and other types of organic matter have been used for water treatment since biblical times.157 These processes are often combined with filtration or coagulation, because these substances are used as the filter media and also can act as coagulants.257 Clays can decrease turbidity and microbes in water by about 90% to 95%, but adsorption is not the main action of ceramic or clay filters. Vegetative matter, including burnt rice hulls and activated (burnt) coconut shell, also have adsorptive capacity. Granular Activated Carbon Granular carbon (i.e., charcoal) is widely used for water treatment and for medical detoxification. Activated carbon is a natural material derived from bituminous coal, lignite, wood, coconut shell, and other materials that are activated by steam and other means. When activated, charcoal’s regular array of carbon bonds is disrupted, yielding free valences that are highly reactive and adsorb dissolved chemicals.107,242 GAC is the best means to removing toxic organic and inorganic chemicals from water (including disinfection by-products) and to improve odor and taste.191,286 Thus, it is widely used in municipal disinfection plants and in home undersink devices. GAC also removes radioactive contamination. Many, but not all, viral particles, bacteria, and protozoan cysts are removed by GAC filters, primarily by adherence to GAC,127,191 and some cysts are trapped in the matrix.165 GAC does not kill microorganisms; in fact, bacteria attach to and colonize charcoal, where they are resistant to chlorination because the chlorine is adsorbed by the GAC.157,191,286 This bacterial contamination has not been found to be harmful because the usual heterophilic bacteria are not enteric pathogens. Enteric pathogens have been shown to survive on GAC, but if an active biofilm exists, the pathogens are rapidly displaced by heterophilic bacteria and fail to become established. Therefore nonpathogenic bacterial colonization is encouraged in municipal plants.223 However, these properties of carbon indicate that it will not reduce pathogenic microbes in water over an extended period of time, and an alternative means of disinfection should always be used. 1333

CHAPTER 67  Field Water Disinfection

remained infectious.193,192 A comparison of three locally available clarification techniques (cloth filtration, settling/decanting, and sand filtration) on turbidity and chlorine demand demonstrated that all three mechanisms reduced turbidity: cloth filtration, 1% to 60%; settling/decanting, 78% to 88%; and sand filtration, 57% to 99%. Sand filtration and settling/decanting, but not cloth filtration, were effective at reducing chlorine demand compared with controls.150 Thus removing particulate matter decreases the number of microorganisms and halogen demand.143,191

PART 8  FOOD AND WATER

Eventually the binding sites on the carbon particles become saturated and no longer adsorb; some molecules are released as others preferentially bind.191 Unfortunately, no reliable means are available to determining precisely when saturation is reached. Filters using charcoal in compressed block form as the filter element may clog before the charcoal is fully adsorbed. Presence of unpleasant taste or color in the water can be the first sign that the charcoal is spent. To test the activity of the charcoal, one may filter iodinated water or water tinted with food coloring. With regular use, the lifetime of GAC is probably measured in months; it is substantially longer with infrequent use. GAC can be “recharged,” but this is not practical for small-quantity use. GAC is best used after chemical disinfection to make water more palatable by completely removing the halogen191,295and other chemical impurities that result in bad odor and taste. For point-of-use field filters, activated carbon is used in granular or powder form, or extruded into a block that acts both as a depth filter and an adsorbent. Block carbon is more effective than granular carbon because the passages are smaller, forcing closer contact with the carbon. Ingested particles of charcoal are harmless. With increasing industrial and agricultural contamination of distant groundwater, final treatment of drinking water with GAC may be important for some wilderness users.

TABLE 67-6  Microorganism Susceptibility

to Filtration

Organism Viruses Escherichia coli Campylobacter Microsporidia Cryptosporidium oocyst Giardia cyst Entamoeba histolytica cyst Cyclospora Nematode eggs Schistosome cercariae Dracunculus larvae

Average Size (µm)

Maximum Recommended Filter Rating (µm)

0.03 0.5 × 3-8 0.2-0.4 × 1.5-3.5 1-2 2-6 (mean 5)

N/S 0.2-0.4 Same as above N/S 1

6-10 × 8-15 5-30 (average 10) 8-10 30-40 × 50-80 50 × 100

3-5 Same as Giardia

20 × 500

Coffee filter or fine cloth

Same as Giardia 20 Coffee filter or fine cloth

N/S, Not specified.

FILTRATION Filters are appealing due to their simplicity and suitability for commercial production. Portable water treatment products are the third highest intended purchase of outdoor equipment after backpacks and tents.140 Filtration is a standard step in municipal disinfection and widely used in the food and beverage industry, as well as many other industrial processes. Many different types of media, from sand to vegetable products to fabric, have been used for water treatment throughout history in various parts of the world. Filters have the advantages of being simple and requiring no holding time (Box 67-9). They do not add any unpleasant taste and may improve taste and appearance of water. However, they take space and add weight to baggage. All filters eventually clog from suspended particulate matter, present even in clear streams, requiring cleaning or replacement of the filter. As a filter clogs, it requires increasing pressure to drive the water through, which can force microorganisms through the filter. A crack or eroded channel allows passage of unfiltered water. Filtration is a physical and a chemical process, so many variables influence filter efficiency. The characteristics of the filter

BOX 67-9  Filtration Advantages Simple to operate Mechanical filters require no holding time for treatment (water is treated as it comes out of filter) Large choice of commercial products Adds no unpleasant taste   and often improves   taste and appearance   of water Rationally combined with halogens for removal or destruction of all pathogenic waterborne microbes Different pore sizes available determine removal of microorganisms and smaller particles, including salt Effectiveness not dependent on water temperature

Disadvantages Adds bulk and weight to baggage Most filters not reliable for removal of viruses Expensive relative to chemical treatment Channeling of water or high pressure can force microorganisms through the filter Eventually clog from suspended particulate matter; may require some maintenance or repair in field Smallest pore sizes (nanofilters) require higher pressure, as in reverse osmosis Freezing water within filter element will compromise or destroy some filters

Susceptibility of microorganisms to filtration: protozoa > bacteria > viruses.

1334

media and the water, as well as flow rate, determine the interactions. Filtration can reduce turbidity, bacteria, algae, viruses, color, oxidized iron, manganese, and radioactive particles.75 Many filters constructed with various designs and materials are marketed for field use. Surface, membrane, hollow-fiber, and mesh filters are very thin with a single layer of fairly precise pores, whose size should be equal to or less than the smallest dimension of the organism. These filters provide little volume for holding contaminants and thus clog rapidly, but can be cleaned easily by washing and brushing without destroying the filter. Maze or depth filters depend on a long, irregular labyrinth to trap the organism, so they may have a larger pore or passage size. Contaminants adhere to the walls of the passageway or are trapped in the numerous dead-end tunnels. Granular media, such as sand or charcoal, diatomaceous Earth, or ceramic filters, function as maze filters. A depth filter has a large holding capacity for particles and lasts longer before clogging, but may be difficult to clean effectively, because many particles are trapped deep in the filter. Flow can be partially restored to a clogged filter by back flushing or surface cleaning, which removes the larger particles trapped near the surface. For ceramic filters, surface cleaning is highly effective but removes a tiny layer of the filter medium. Hollow-fiber and pleated filters rely on large surface area to avoid clogging by particles. The size of a microorganism is the primary determinant of its susceptibility to filtration (Table 67-6 and Figure 67-1). Filters are rated by their ability to retain particles of a certain size, which is described by two terms. Absolute rating means that 100% of a certain size of particle is retained. Nominal rating indicates that more than 90% of a given particle size will be retained. Filter efficiency is generally determined with hard particles (beads of known diameter), but microorganisms are soft and compressible under pressure. Waterborne pathogens often adhere to larger particles or clump together, making them easier to remove by physical processes.178 Therefore observed reductions are often greater than expected based on their individual sizes.257 In general, portable filters for water treatment can be divided into microfiltration with pores down to 0.1 µm, ultrafiltration that can remove particles as small as 0.01 µm, and nanofiltration with pores sizes as small as 0.001 or less. Microfilters are effective for removing protozoa and bacteria, algae, most particles, and sediment but allow dissolved material, small colloids, and some viruses to pass through. Ultrafiltration membranes are required for complete removal of viruses, colloids, and some dissolved solids. Nanofilters can remove other dissolved substances, including sodium chloride, from water. All filters require pressure to drive the water through the filter element. The smaller the pore size, the more pressure required.

Ultrafiltration Nanofiltration Reverse osmosis Size (µm) 0.001 0.01

0.1

1.0

10

100

1000

Visible to naked eye Beach sand Protozoan cysts Bacteria Viruses Colloidal clays and particles Organic compounds that add “tea” color to water Pesticides, taste and odor compounds Dissolved salts, metal ions

FIGURE 67-1  Relative size of microorganisms determines susceptibility to mechanical filtration. Mechanical filters span a wide range of pore sizes.

Filters are a reliable means to removing protozoan cysts.18 A membrane with a pore size of 0.2 µm can remove enteric bacteria. Giardia and E. histolytica cysts are easily filtered, requiring a maximum filter size of 5 µm. Cryptosporidium cysts are somewhat smaller than Giardia and more flexible; 57% are able to pass through a 3-µm membrane filter, so a filter with 1- to 2-µm pores is recommended.238 Helminth eggs and larvae, which are much larger, can be removed by a 20-µm filter. Cyclops (the water dwelling copepod that ingests the larva and transmits dracunculosis) can be removed by passage through a fine cloth.251 Adsorption and aggregation during passage through microfilters reduce viruses. Virus particles may adhere to the walls of diatomite (ceramic) or charcoal filters by electrostatic chemical attraction, which can be enhanced by a coating on the filter or a positive charge.93,108,111,223 Viruses in heavily polluted water often aggregate in large clumps and become adsorbed to particles or enmeshed in colloidal materials, making them amenable to filtration.219,286 Thus turbidity (cloudiness from contaminants) may help remove pathogens with filtration, while it inhibits chemical disinfection. In one study, however, only 10% of total virus particles detected were recovered on 3- to 5-µm pore prefilters, suggesting that most were not associated with the suspended sediment.198 Furthermore, adsorbed viral particles can be subsequently dislodged and eluted from a filter because of competitive binding and competing electrostatic forces.108,215,276 Some ceramic filters now remove 99% to 99.9% of viruses, but the fourth log required by water treatment units remains a challenge. First Need filter has been able to meet the EPA standards for water purifiers, including 4-log removal of viruses, apparently through use of a charged media111 (Appendix A). Ultra filters like Sawyer 0.02 µm hollow fiber filter (or reverse osmosis nanofiltration) can mechanically filter viruses. In general, however, microfilters should not be considered adequate for complete removal of viruses, except with special equipment.293 Reverse Osmosis A reverse-osmosis filter uses high pressure (100 to 800 psi) to force water through a semipermeable membrane that filters out dissolved ions, molecules, and solids.286 This process can desalinate water, as well as remove microbiologic contamination. If pressure or degradation causes breakdown of the membrane, treatment effectiveness is lost. Even Giardia cyst passage has been shown to occur in a compromised reverse osmosis unit.73 Small hand-pump reverse-osmosis units have been developed. Their high price and slow output currently prohibit use by landbased wilderness travelers, but they are important survival items

for ocean travelers. Battery- or power-operated units are standard equipment on large boats. The U.S. Department of Defense uses large-scale mobile reverse-osmosis units for water treatment. These are considered the most fuel-efficient mobile units, producing the highest quality water from the greatest variety of raw water qualities, capable of producing potable water from fresh, brackish, or salt water, as well as from water contaminated by nuclear, biologic, or chemical agents. The units use pretreatment, filtration, and desalination, then disinfection for storage.5 Forward Osmosis Osmotic pressure also can be used to draw water through a membrane to create highly purified drinking water from lowquality source water, including brackish water. These products use a double chamber bag or container with the membrane in between. A high-osmotic substance is added to the clean side that draws water from the dirty side. Because some form of sugar and/or salt is often used to create osmotic pressure, this may result in a sweetened solution similar to a sports-electrolyte drink (see Appendix A). Choice of Filter (See Preferred Technique and Appendix A) There are extensive data on the effectiveness of filtration in other settings, but few data are available to compare different filters for field use. Most data are from testing organized by the filter manufacturer, so nearly all filters perform well. The ceramic filters have been tested most extensively and generally perform well for their claims.93,201,276 Gravity ceramic filters for household use have been extensively field tested in developing countries and are generally effective.59,262 As with all types of filters, results depend on the characteristics of the materials (e.g., ceramic), water quality, product engineering, and prior extent of filter use. Schlosser and colleagues248 tested three hand-pump filters (Katadyn Mini Ceramic, First Need Deluxe, and Sweetwater Walkabout), all of which removed 3 log (99.9%) or more of viable bacteria, leaving none in the effluent. Filters and granular charcoal media are sometimes coated with silver to prevent bacterial growth on the surface, but this does not maintain sterility. (See discussion of silver in Miscellaneous Disinfectants, later.) The military preventive medicine group has enumerated the requirements for individual filters for field use.279 Choice should be based on anticipated water quality, number of persons to be served, mode of travel and need for portability, and availability of power source. Hollow microfiber filters, adapted from medicine and industry, are the newest addition to point-of-use field filtration. For domestic use and in pristine protected watersheds where pollution is minimal and the main concerns are bacteria and cysts, microfiltration can be used as the only means of disinfection. For foreign travel and for surface water with high levels of human use or sewage contamination, however, higher levels of filtration or supplemental methods should be used.93 Ultrafilters, now available with hollow-fiber technology or nanofilters (see Reverse Osmosis, earlier) are an alternative. Otherwise, additional treatment with heat or halogens before or after filtration guarantees effective virus removal.223 One rational use of filtration is to clear the water of sediment and organic debris, allowing lower doses of halogens with more predictable residual levels.191 Filters are also useful as a first step to remove parasites and Cryptosporidium organisms that have high resistance to halogens. Improvised Filters Filtration using simple, available products is of interest for use in developing countries and in emergency situations.257 Rice hull ash filters, crushed charcoal, sponges, and various fabrics have all been used. Typically, bacteria and viruses can be reduced by as much as 50% to 85% and larger parasites by 99%, depending on the media. Fine woven cotton fabric is effective at removing larger parasites, such as schistosome cercariae, Fasciola species, and guinea worm larvae. Kozlicic and associates151 tested five commonly available household materials (newspaper, filter paper, cotton, four-layer gauze, and white cotton cloth) for filtration efficiency. Newspaper performed poorly, being too slow. Cotton cloth performed best for both physical and microbiologic 1335

CHAPTER 67  Field Water Disinfection

Microfiltration

PART 8  FOOD AND WATER

parameters of water (although the latter was poorly studied). He incidentally noted that melted snow with the top 4 to 5 cm (1.6 to 2 inches) removed was a better quality water source than rainwater from roof runoff. Biosand Filters Sand filters employ a technology that has been proved over centuries of time and is still used widely in municipal plants. When constructed properly they are very reliable, but with slow flow rates. Sand filters are constructed by forming layers of aggregate increasing in size from the top to the bottom. The top layer is very fine sand and the bottom layer consists of large gravel. The container needs an exit port on the bottom. Water on the top layer forms a biolayer where micro-organisms “eat” the pathogens that pass through them. Over time, the biolayer grows to the point where it will not allow any water to pass through. At this point, the layer needs to be removed by either drying out the layer and then removing it, or stirring it up and removing dirty water from the top. The optimum depth of a sand filter is 2 m (6.6 feet). A column of fine sand 60 to 75 cm (23.6 to 29.5 inches) deep that permits no more than 200 L/m2/hr of water is capable of removing turbidity and greater than 99% of organisms.221 Diameter is determined by the volume of water needed. A family of four adults needs 16 L (4.2 gal) per day, which would require a 0.5-m (1.6-foot)-diameter tank. A sand filter can be improvised with stacked buckets or barrels. An emergency sand filter can be made in a 20-L (5.3-gal) bucket, composed of a 10-cm (3.9-inch) layer of gravel beneath a 23-cm (9.1-inch) layer of sand; a layer of cotton cloth, sandwiched between two layers of wire mesh, separates the sand and gravel layers.150

Chemical Disinfectants HALOGENS (CHLORINE AND IODINE) Worldwide, chemical disinfection is the most widely used method for improving and maintaining microbiologic quality of drinking water. Chemical disinfectants used for water disinfection are strong oxidants. Halogens, chiefly chlorine and iodine, are the most common chemical disinfectants used in the field; however, chlorine dioxide is now available in small-use applications and gaining acceptance. Germicidal activity results from oxidation of essential cellular structures and enzymes.50,156,191,196 Halogenated amines may be synthesized by white blood cells as part of the body’s natural defenses to destroy microorganisms.294 The disinfection process is determined by characteristics of the disinfectant, the microorganism, and environmental factors.52,130,190 Dilute solutions do not sterilize water. The relative potency of common disinfectants to inactivate waterborne microbes is as follows:

ozone > chlorine dioxide > electrochemically generated mixed species oxidant > free chlorine or iodine > chloramine Ozone and chlorine dioxide are discussed under Miscellaneous Disinfectants. Variables With Chemical Agents Understanding the principal factors of chemical disinfection allows intelligent and flexible use (Table 67-7). Concentration and Contact Time.  The major variables in the disinfection reaction are the amount of disinfectant (concentration) and the exposure time of the microorganism to the disinfectant (contact time). Concentration of disinfectant in water is measured in parts per million (ppm) or milligrams per liter (mg/L), which are equivalent. Contact time is usually measured in minutes but ranges from seconds to hours. In field disinfection, halogen (iodine or chlorine) concentrations of 1 to 10 mg/L for 10 to 60 minutes are generally effective. Theoretically, the disinfection reaction follows first-order kinetics. The rate of the reaction is determined by the initial concentration of reactants, and a given proportion of the reaction occurs in any specified interval.130,295 This means that concentration and time are inversely related, and their product results in a constant for specified disinfectant, organism, percent reduction of viable microorganisms, and given conditions of water temperature and pH: concentration × time = constant (Ct = K) (Figure 67-2).295 When concentration and contact time are graphed on logarithmic coordinates, a straight line results. This means that concentration and time can be varied oppositely and still achieve the same result.13 In field disinfection, this can be used to minimize halogen dose and improve taste or, conversely, to minimize the required contact time. In reality, the disinfection reaction deviates from first-order kinetics, and Ct values do not follow the exponential rates described by the empiric equation because microorganisms do not act as chemical reagents (Cnt = K). An initial lag period may be seen before inactivation begins (e.g., because of penetration of the cyst wall), and inactivation declines for more resistant organisms or those shielded by aggregation or other particles (Figure 67-3).117,123,130 Contaminants.  Organic and inorganic nitrogen compounds from decomposition of organisms and their wastes, fecal matter, and urea complicate chemical disinfection and must be considered in field water treatment. Vegetable matter, ferrous ions, nitrites, sulfides, and humic substances also affect oxidizing disinfectants.90,191,295 These contaminants react, especially with chlorine, to form compounds with little or no disinfecting ability, effectively decreasing the concentration of available halogen.

TABLE 67-7  Factors Affecting Halogen Disinfection

Primary Factors Concentration Contact time Secondary Factors Temperature

Water contaminants, cloudy water (turbidity) pH

1336

Effect

Compensation

Measured in milligrams per liter (mg/L) or the equivalent, parts per million (ppm); higher concentration increases rate and proportion of microorganisms killed. Usually measured in minutes; longer contact time ensures higher proportion of organisms killed.

Higher concentration allows shorter contact time for equivalent results. Lower concentration requires increased contact time for equivalent levels of kill. Contact time is inversely related to concentration; longer time allows lower concentration.

Cold slows reaction time.

Some treatment protocols recommend doubling the dose (concentration) of halogen in cold water, but if time allows, exposure time can be increased instead, or the temperature of the water can be increased. Doubling the dose of halogen for cloudy water is a crude means of compensation that often results in a strong disinfectant taste on top of the taste of the contaminants. A more rational approach is to first clarify water to reduce halogen demand. Compensating for pH is not necessary for most surface water.

Halogens reacts with organic nitrogen compounds from decomposition of organisms and their wastes to form compounds with little or no disinfecting ability, effectively decreasing the concentration of available halogen. In general, turbidity increases halogen demand. The optimal pH for disinfection is 6.5-7.5. As water becomes more alkaline, approaching pH 8.0, much higher doses of halogens are required.

E. histolytica cyst

Iodine (mg/L)

10

E. coli 1.0 Poliovirus

0.1 1.0

10

100

Contact time (min) FIGURE 67-2  Relationship of halogen concentration and contact time for a given temperature and pH. The first-order chemical reaction results in a straight line over most values for each microorganism and halogen compound. (Data from Chang SL: The use of active iodine as a water disinfectant, J Am Pharm Assoc 47:417, 1958; and Water and Sanitation for Health [WASH] Project: Report on mobile emergency water treatment and disinfection units, WASH field report No 217, 1980, Arlington, Va.)

Temperature.  Temperature influences the rate of the disinfection reaction.90,156,191 Cold water affects germicidal power and must be offset by longer contact time or higher concentration to achieve comparable disinfection.114 The common rule is a twofold to threefold increase in inactivation rate per 10° C (18° F) increase in temperature. Temperature can be estimated in the field. Some treatment protocols recommend doubling the dose of halogen in cold water, but if there is no urgency, time can be increased instead of dose. Data for killing Giardia in very cold water (5° C [41° F])

2 ppm iodine 100 30° C

80 60 40 20 0

0 15 30 45 60 75 90 105 120 135 150 165 180 195 210 225 240

4 ppm iodine 100 Cyst inactivation (%)

Halogen Demand and Residual Concentration.  Halogen demand is the amount of halogen reacting with impurities. The concept applies to all chemical disinfectant agents. Residual concentration is the amount of active disinfectant remaining after demand of the water is met. To achieve microbial inactivation in aqueous solution with a chemical agent, a residual concentration must be present for a specified contact time. Failure of chlorination in municipal systems to kill cysts or other microorganisms is usually caused by difficulty maintaining adequate residual halogen concentration and contact times, rather than by extreme resistance of the organism.266 Halogen demand and residual concentration in surface water are the greatest uncertainties in field disinfection. Nitrogen appears in most natural waters in varying amounts, which relate directly to the sanitary quality of water. Cysticidal dose of halogens is strongly affected by the level of contamination in otherwise clean water.52,115,266 Scant data are available on halogen demand of surface water (Table 67-8). Clear water is assumed to have minimal demand and cloudy water high demand. Surface water in the wilderness contains 10 times the organic carbon content of aquifer groundwater. The green or brown color in stagnant ponds or lakes or in tropical and lowland rivers is usually caused by organic matter with considerable halogen demand. In some cases, such as runoff after storms and snowmelt, cloudy water may be caused by inorganic sand and clay that exert little halogen demand, but in general, chlorine demand rises with increased turbidity.155,158 In addition, particulate turbidity can shield microorganisms and interfere with disinfection.75,143,158 (See earlier discussion of turbidity.) The initial dose of halogen must consider halogen demand. For clear alpine waters, 1 mg/L demand can be assumed; for cloudy waters, the assumption is 3 to 5 mg/L. If a method is used that adds 4 mg/L to clear water, extra time can compensate for the lower expected residual concentration; however, in cloudy water, an increased dose of halogen, rather than prolonging the contact time, is needed to ensure free residual. The usual field recommendation to compensate for the unknown demand of cloudy water is a double dose of halogen (to achieve 8 to 16 mg/L). This crude means of compensation often results in a strong halogen taste on top of the tastes of the contaminants. If the cause of turbidity is uncertain, the water should be allowed to sit; inorganic clay and sand will sediment, clarifying the water considerably. Other means of clarification, such as

15° C 5° C

30° C 15° C

80

5° C

60 40 20 0 0

15

30

45

60

75

90

105

120

75

90

105

120

8 ppm iodine 15° C 30° C

100 80

5° C

60 40 20 0 0

15

30

45

60

Time (min) FIGURE 67-3  Effect of concentration and temperature on Giardia cyst inactivation by iodine. Low concentrations are effective at cold temperatures with prolonged contact time. (From Fraker LD, Gentile D, Krivoy D, et al: Giardia cyst inactivation by iodine, J Wilderness Med 3:351, 1992.)

1337

CHAPTER 67  Field Water Disinfection

coagulation–flocculation or filtration, significantly reduce halogen demand. (See clarification techniques.) Several simple color strip tests are available for field use, similar to those used for swimming pools and spas to measure the amount of free (residual) halogen in water. Testing in the wilderness for halogen residual may be reasonable for large groups but is not practical for most. Smell of chlorine usually indicates some free residual. Color and taste of iodine can be used as indicators. Above 0.6 ppm, a yellow to brown tint is noted.295

PART 8  FOOD AND WATER

TABLE 67-8  Halogen Demand of Surface Water Halogen Demand (mg/L)

Source Cloudy river water, Portland, Oregon Cloudy water from clay particles Clear water with 10% sewage added Lily pond and turbid river water Colorado River; cloudy from inorganic sand, clay Unspecified surface waters Municipal wastewater High-elevation spring Western river Six watersheds in western Oregon Small stream, Australia Bolivian village (well and collected rain) Spring and well water, Haiti Cloudy surface water (ponds, rivers)— household water sources in western Kenya

Reference

3-4

Jarroll, 1980138

None

Chang, 195352

2

Chang, 195352

5-6

Chang, 195352

0.3

Tunnicliff, 1984277

2-3

Culp, 197474 Culp, 197474 Ongerth, 1989200 Ongerth, 1989200 LeChevallier,1981158

20-30 0.3 0.7 0.4-1.6 1.3 2

Thomson, 1985272 Quick, 1999218

≤1

Colindres, 200765 Crump, 200572

100-150

with both chlorine and iodine indicate that contact time must be prolonged three to four times, not merely doubled, to achieve high levels of inactivation.102,124If feasible, raising the temperature by 10° to 20° C (18° to 36° F) allows a lower dose of halogen and more reliable disinfection at a given dose. pH.  Halogen oxidizes water to form several compounds, each with different disinfection capabilities. The percentage of each

halogen compound is determined by pH. The optimal pH for halogen disinfection is 6.5 to 7.5.52,189As water becomes more alkaline, approaching pH 8.0, much higher doses of halogens are required. Although pH can be measured in the field, the relationship is too complex to allow meaningful use of the information. Most surface water pH is neutral to mildly acidic, which is within the effective range of any chemical agent used. On the alkaline side, some surface water with pH 7.0 to 8.0 begins to affect the chemical species of chlorine, favoring less active forms.130 Certain desert water is so alkaline that halogens would have little activity; however, these waters are usually not palatable. At this time, compensating for pH is not necessary. Tablet formulations of halogen have the advantage of some buffering capacity. Susceptibility of Microorganisms.  The final variable is the target microorganism. Sensitivity to halogen is determined by the diffusion barrier of the cell wall or capsule and the relative susceptibility of proteins and cellular respiration to denaturation and oxidation.50,191 Organisms, in order of increasing resistance to halogen disinfection, are enteric (vegetative) bacteria, viruses, protozoan cysts, bacterial spores, and parasitic ova47 (Tables 67-9 and 67-10); for example, E. histolytica cysts are 160 times as resistant as E. coli and 9 times as resistant as hardier enteroviruses to chlorine (HOCl). Virucidal residuals of I2 and HOCl are 5 to 70 times higher than bactericidal residuals.50,191 Relative resistance between organisms is similar for iodine and chlorine. The physical state of the microbes also determines their susceptibility. Microbes that are aggregated in clumps or embedded in other matter or organisms may be shielded from disinfectants. Bacteria.  All vegetative bacteria are extremely sensitive to halogens. Inactivation involves oxidation of enzymes on the cell membrane and does not require penetration.295 Little modern work has focused on bacterial agents because they are more sensitive than viruses and cysts, and little difference is evident between the bacterial pathogens.130 Although halogens were first used to disinfect water during cholera epidemics in 1850, recent cholera epidemics prompted review of data that reaffirmed the susceptibility of V. cholerae to low levels of chlorine and iodine.70 Campylobacter has susceptibility similar to that of other enteric pathogens.25

TABLE 67-9  Disinfection Data for Chlorine* Halogen†

Organism

HOCl FAC FRC Free Cl FRC Free Cl HOCl FRC Free Cl Free Cl

Free Cl

Escherichia coli Campylobacter 20 enteric virus 6 enteric viruses Hepatitis A virus Hepatitis A virus Amebic cysts Amebic cysts Giardia cysts Giardia lamblia cysts Giardia muris cysts G. muris cysts Giardia Giardia Cryptosporidium Schistosome cercariae Nematodes

Free Cl

Nematodes

FRC

Ascaris eggs

Free Free Free Free Free FRC

Cl Cl Cl Cl Cl

Concentration(mg/L)

Time (min)

pH

Temp

0.1 0.3 0.5 0.5 0.5 0.5 3.5 3.0 2.5 0.85

0.16 0.5 60 4.5 1 5 10 10 60 90

6.0 6.0-8.0 7.8 6.0-8.0 6.0 6.0

3.05 5.87

50 25

7.0 7.0 6.0 6.0

5° C (41° F) 25° C (77° F) 2° C (35.6° F) 5° C (41° F) 25° C (77° F) 5° C (41° F) 25° C (77° F) 30° C (86° F) 5° C (41° F) 2°-3° C (35.6°-37.4° F) 5° C (41° F) 5° C (41° F) 0.5° C (32.9° F) 5° C (41° F)

7.0

28° C (82.4° F)

7.0 6.0-8.0 8.0

Disinfection Constant (Ct) .016 0.15 30 2.5 0.5 2.5‡ 35 30 150 77 153 139 170 120 7200 30

80 1.0

90 30

2-3

120

(Not lethal)

95-100

30

(95% lethal)

200

20

5.0

37° C (98.6° F)

2000

FAC, Free active chlorine; FRC, free residual chlorine; Free Cl, free chlorine; HOCl, hypochlorous acid. *Also see reference 47. † These represent nearly equivalent measurements of the residual concentration of active chlorine disinfectant compounds. ‡ Four-log reduction. Most experiments use 2- to 3-log (99% to 99.9%) reduction as the end point.

1338

Reference White, 1992295 Blaser,198624 Briton,198030 Engelbrecht, 198091 Grabow, 1983115 Sobsey, 1975256 Chang, 197050 Stringer, 1970266 Rice, 1982229 Wallis, 1988291 Rubin, 1989244 Rubin, 1989244 Hibler, 1987124 Hibler, 1987124 Korich,1990149 World Health Organization, 1981301 National Academy of Sciences, 1980191 National Academy of Sciences, 1980191 Krishnaswami, 1968152

Concentration (mg/L)

Halogen*

Organism

FRI

Escherichia coli

1.3

I2 I2 I2 FRI FRI I2 I2 I2 I2 FRI FRI FRI

Amebic cysts Amebic cysts Amebic cysts Poliovirus 1 Poliovirus 1 Poliovirus 1 Coxsackie virus Amebic cysts Bacteria, viruses Giardia cysts Giardia cysts Giardia cysts

3.5 6.0 12.5 1.25 12.7 1 0.5 8 8 4 4 4

Time (min) 1 10 5 2 39 5 6 30 10 20 15 45 120

pH

Temp

6.0-7.0

2°-5° C (35.6°-41° F)

6.0 6.0 7.0 7.0 4.0-8.0 5.0 5.0 5.0

25° C (77° F) 25° C (77° F) 25° C (77° F) 25° C (77° F) 25° C (77° F) 18° C (64.4° F) 5° C (41° F) 23° C (73.4° F) 0°-5° C (32°-41° F) 30° C (86° F) 15° C (59° F) 5° C (41° F)

Disinfection Constant (Ct) 1.3 35 30 25 49 63 6 15 80 160 60† 170† 480†

Reference National Academy of Sciences, 1980191 Chang, 197050 Chang, 197050 Chang, 197050 Berg, 196416 Berg, 196416 Berg, 196416 Berg, 196416 Chang, 195352 Chang, 195352 Fraker, 1992102 Fraker, 1992102 Fraker, 1992102

*FRI (free residual iodine) and I2 (elemental iodine) are nearly equivalent measurements of the residual concentration of active iodine disinfectant compounds. † 100% kill; viability tested only at 15, 30, 45, 60, and 120 minutes.

Bacterial spores, such as Bacillus anthracis, are relatively resistant to halogens, but with chlorine, spores are not much more resistant than are Giardia cysts.13,295 Quantitative data are not available for iodine solutions, but iodine kills spores. Fortunately, sporulating bacteria do not normally cause waterborne enteric disease.128 Viruses.  Enteroviruses are more resistant than are enteric bacteria,191 but they constitute such a large and diverse group of organisms that generalization is especially difficult.51,156,286 Most studies have used poliovirus, a phage virus, or coxsackievirus. The mechanism of action for halogen inactivation of viruses has not been resolved. It is not clear whether the oxidant injures protein on the shell, a process similar to bacterial inactivation,31 or penetrates the protein capsid by chemical transformation and then attacks the nucleic acid core, as in cyst inactivation.295 Most viruses tested against chlorine have shown resistance 10 times greater than that of enteric bacteria, but inactivation is still achieved rapidly (0.3 to 4.5 minutes) with low levels (0.5 mg/L) of chlorine.91,282Current data suggest that HAV is not significantly more resistant than are other enteric viruses.115,207,259,273 In one test using iodine tablets, HAV was inactivated under difficult conditions more readily than was poliovirus or echovirus.258 Norovirus may be more resistant to chlorine than are several other viruses, which may account for its importance in waterborne outbreaks.146 Clumping and association of viruses with cells and particulate matter are thought to be significant factors affecting viral dis­ infection, causing departure from first-order kinetics.91,258,282 Cell-associated HAV was 10 times more resistant than was dispersed HAV. Cysts and Parasites.  Protozoal cysts are considerably more resistant than are enteric bacteria and enteric viruses, probably because of cysts’ physiologically inactive outer shell, which the disinfectant must penetrate to be effective.50,295 Halogens can be used in the field to inactivate Giardia cysts (see Figure 67-3). Testing on G. lamblia indicates similar sensitivity to both iodine and chlorine.139 Lower temperature decreases the effectiveness of halogens on Giardia: longer contact time is required in cold and dirty water.109,123,136,258 Review literature frequently attributes exaggerated resistance of Giardia to halogens.129 Jarrol and colleagues137,138tested two chlorine methods and four iodine methods for effectiveness against Giardia cysts. They found all methods effective in warm water, but only two methods destroyed all cysts in cold water in recommended doses. Higher doses or longer contact times would make all these methods effective. Cryptosporidium oocysts differ greatly from other protozoan cysts and are highly resistant to halogens. The Ct constant for Cryptosporidium in warm water with chlorine has been estimated to be 9600.40 Other data demonstrated 90% inactivation with 80 ppm of chlorine after 90 minutes, 14 times more resistant than Giardia cysts.149 The current recommendation for

decontaminating chlorinated swimming pools is 20 mg for 9 hours (Ct 10,800).34 From 65% to 80% of Cryptosporidium oocysts were inactivated after 4 hours by two iodine tablets in “general case” water.109 This implies that 3-log inactivation could have been achieved after 3 to 4 more hours. Although halogens can achieve disinfection of Cryptosporidium in the field, this is not practical.76,238,249,295 The resistance of Cyclospora and microsporidia is not well studied, but the oocysts are similar to Cryptosporidium and thus may resemble this protozoa more than Giardia. Both Cryptosporidium and Giardia are susceptible to chlorine dioxide.57,149 Schistosome cercariae are susceptible to low concentrations of chlorine.296 Limited data on parasitic helminth larvae and ova indicate the presence of such high levels of resistance that chemical disinfection is not useful.152,191,251However, these are not common waterborne pathogens and can be readily removed or destroyed by heat, filtration, or coagulation–flocculation. Disinfection Constant.  The best comparison of disinfection power is the disinfection constant (Ct). Disparate results may be caused by lack of standardized experimental conditions of pH, temperature, chemical species of halogen, and species of microorganism or by different techniques for concentrating, counting, and determining viability of organisms.130,191 The latter is especially a problem for cysts and viruses, which cannot be cultured easily.246 The end point for disinfection effectiveness is now standardized by the EPA guidelines; most older studies used 99.9% for all organisms, with some using 99% or 99.99%. Differences between laboratory and field conditions also make extrapolation from data to practice inaccurate and suggest the need for a safety factor in the field. Despite variation, Ct remains a useful and widely used concept; values provide a basis for comparing the effectiveness of different disinfectants for inactivation of specific microorganisms.130 To use halogens for disinfection, a consensus organism (the most resistant target) determines the Ct.130,156,295For wilderness water, this has been protozoan cysts. The resistance of Cryptosporidium will not raise the threshold for halogen use; rather, it will force an alternative or a combination of methods to ensure removal and inactivation of all pathogens.

CHLORINE Chlorine has been used as a disinfectant for 200 years. Hypochlorite was first used for water disinfection in 1854 during cholera epidemics in London and was first used continuously for water treatment in Belgium in 1902. It is currently the preferred means of municipal water disinfection worldwide and the preference of CDC and WHO for individual household disinfection of drinking water where there is no community-level treatment, so extensive data support its use (see Table 67-9).47,155,295 1339

CHAPTER 67  Field Water Disinfection

TABLE 67-10  Disinfection Data for Iodine

PART 8  FOOD AND WATER

Toxicity

Chemistry 90,295

Chlorine reacts in water to form the following compounds: Cl 2 + H2O → HOCl + H + Cl +

−

HOCl → OCl − + H + At neutral pH, negligible amounts of diatomic chlorine are present. The major disinfectant is hypochlorous acid (HOCl), which penetrates cell and cyst walls easily. Dissociation of HOCl to the much weaker disinfectant hypochlorite (OCl−) depends on temperature and pH. In pure water at pH 6.0, 97% of chlorine is HOCl; at pH 7.5, the HOCl/OCl− ratio is 1 : 1; and above pH 7.5, OCl− predominates.295 The combination of these two compounds is defined as free available chlorine. Both calcium hypochlorite (Ca[OCl]2) and sodium hypochlorite (NaOCl) readily dissociate in water, allowing the same equilibrium to form as when elemental chlorine is used.156,295 Chloride ion (Cl−, NaCl, or CaCl2) is germicidally inactive. In addition, chlorine readily reacts with ammonia to form monochloramines (NH2Cl), dichloramines, or trichloramines, referred to as combined chlorine. Chloramines have weak disinfecting power and are calculated as a disinfectant in municipal sewage plants130,189,191,295; however, in field disinfection these compounds are not considered, and only free residual chlorine should be measured. However, at doses of a few milligrams per liter and contact times of about 30 minutes, free chlorine generally inactivates greater than 99.99% of enteric bacteria and viruses.260 The CDC-WHO Safe Water System for household disinfection in developing countries provides a dosage of 1.875 or 3.75 mg/L of sodium hypochlorite with a contact time of 30 minutes, sufficient to inactivate most bacteria, viruses, and some protozoa that cause waterborne diseases.150,155 Chlorine bleaches organic matter, making water sparkling blue, as in swimming pools.295

Acute toxicity to chlorine is limited; the main danger is irritation and corrosion of mucous membranes if concentrated solutions (for example, household bleach) are ingested. Numerous cases have been reported of short-term ingestion of very high residuals (50 to 90 ppm) in drinking water; one military study used 32 ppm for several months without adverse effects.295 Animal studies using long-term chlorination of drinking water at 100 to 200 ppm have not shown toxic effects.191 Sodium hypochlorite is not carcinogenic; however, reactions of chlorine with certain organic contaminants yield chlorinated hydrocarbons, chloroform, and other trihalomethanes, which are considered carcinogenic.191,286 Public health regulations limit residual chlorine in public systems to decrease ingestion of trihalomethane. The concern is now fueled more by public fears than by scientific conclusion.295 The risk for death from infectious diseases if disinfection is not used is far greater than any risk from chlorine disinfection by-products.231,286 These compounds are not likely to form in clean wilderness surface water, since the organic precursors are not present. Products and Techniques for Chlorination Free chlorine is the most widely available and affordable of chemical water disinfectants.260 For household or field water treatment, free chlorine can be obtained in liquid, granular, and tablet forms or generated from electrolysis of salt (Appendix B; for dosage information, see Tables 67-11 to 67-13). Tablets have the advantage of easy administration and can be salvaged if the container breaks. However, they lose effectiveness with exposure to heat, air, or moisture. Although no significant loss of potency results from opening a glass bottle intermittently over weeks, activity is rapidly lost after a few days of continuous exposure to air with high heat and

TABLE 67-11  Water Disinfection Techniques and Halogen Doses Add to 1 Liter or Quart of Water Iodination Techniques Iodine tabs   Tetraglycine hydroperiodide   EDWGT   Potable Aqua   Globaline 2% iodine solution (tincture) 10% povidone–iodine solution† Saturated solution: iodine crystals in water Saturated solution: iodine crystals in alcohol Chlorination Techniques§|| Sodium hypochlorite (household bleach 5%) 1% bleach (CDC-WHO Safe Water System)¶ Calcium hypochlorite** (Redi Chlor [0.1-g tab]) Sodium dichloroisocyanurate (NaDCC)†† (Aquatab, Kintab) Chlorine plus flocculating agent (Chlor-Floc)

Amount for 4 ppm

Amount for 8 ppm

0.5 tab

1 tab

0.2 mL 5 gtt* 0.35 mL 8 gtt 13 mL 0.1 mL‡

0.4 mL 10 gtt 0.70 mL 16 gtt 26 mL 0.2 mL

Amount for 5 ppm

Amount for 10 ppm

0.1 mL 2 gtt 8-10 gtt 0.25 tab

0.2 mL 4 gtt 0.5 tab 1 tab (8.5 mg NaDCC) 1 tab‡‡

EDWGT, Emergency drinking water germicidal tablet. *Measure of a drop varies from 16-24 gtt/mL, median 20 gtt/mL is used here. † Povidone–iodine solutions release free iodine in levels adequate for disinfection, but scant data are available. ‡ Measure with dropper or tuberculin syringe. § Recommended concentration of chlorine for emergency point-of-use water treatment varies across health agencies, but generally does not exceed 5 mg/L. For long-term household use in developing areas, CDC Safe Water System establishes a maximum of 2 mg/L, which is the limit of taste tolerance for many people (see reference 155). || For treatment of large volumes, see reference 280 for TB MED 577. ¶ Safe Water System for long-term routine household point-of-use water disinfection recommends a hypochlorite dose of about 2 mg/L in clear water and 4 mg/L in slightly turbid water. This results in a low yet effective target residual concentration with acceptable taste, but requires testing in a particular water source to ensure sufficient residual. **Concentrated source of hypochlorite available as granules or tablets. Useful for treating larger volumes of water. Commonly used to treat swimming pool water. †† Available in different strengths to treat different volumes of water. Check packaging to determine proper dose. ‡‡ Yields 8 ppm.

1340

With Halogenations in the Field

Concentration of Halogen 2 ppm 4 ppm 8 ppm

Contact Time in Minutes at Various Water Temperatures 5° C (41° F)

15° C (59° F)

30° C (86° F)

240 180 60

180 60 30

60 45 15

Note: Data indicate that very cold water requires prolonged contact time with iodine or chlorine to kill Giardia cysts. These contact times have been extended from the usual recommendations in cold water to account for this and for the uncertainty of residual concentration.

humidity. To extend shelf-life, many tablets are individually wrapped in foil. Superchlorination–Dechlorination.  The process of superchlorination–dechlorination with different reagents is used in some large-scale disinfection plants to avoid long contact times and to remove tastes and smells. High doses of chlorine remove or oxidize hydrogen sulfide and some other chemical contaminants that contribute to poor taste and odor. This method of chlorination can readily be adapted to field use. High doses of chlorine are added to the water in the form of calcium hypochlorite crystals to achieve concentrations of 30 to 200 ppm of free chlorine. These extremely high levels are above the margin of safety for field conditions and rapidly kill all bacteria, viruses, and protozoa and could kill Cryptosporidium with overnight contact times. After at least 10 to 15 minutes, several drops of 30% hydrogen peroxide solution are added. This reduces hypochlorite to chloride, forming calcium chloride (a common food additive), which remains in solution, as follows: Ca( OCl )2 + 2H2O → 2HOCl + Ca ++ ( OH − )2 Ca( OCl )2 + 2H2O2 → CaCl 2 + 2H2O + 2O2 Excess hydrogen peroxide reacts with water to form oxygen and water. Chloride has no taste or smell. Hydrogen peroxide is also a weak disinfectant,307 although not in common use.

The minor disadvantage of a two-step process is offset by excellent taste. Measurements to titrate peroxide to the estimated amount of chlorine do not need to be exact, but some experience is needed to balance the two and achieve optimal results. This is a good technique for highly polluted or cloudy water and for disinfecting large quantities. It is the best technique for storing water on boats or for emergency use. A high level of chlorine prevents growth of algae or bacteria during storage; water is then dechlorinated in needed quantities when ready to use. The two reagents must be kept tightly sealed to maintain potency of the reagents. Properly stored, calcium hypochlorite (70% available chlorine) loses only 3% to 5% of available chlorine per year. Thirty-percent hydrogen peroxide is corrosive and burns skin, so it should be used cautiously. There is currently no commercial formulation; however, the ingredients can be easily obtained and packaged in small Nalgene bottles.

IODINE Iodine has been used as a topical and water disinfectant since the beginning of the 20th century.156 Iodine is effective in low concentrations for killing bacteria, viruses, and cysts, and in higher concentrations against fungi and even bacterial spores, but it is a poor algicide52,114,191 (see Table 67-10 and Figure 67-3). Iodine has been used successfully in low concentrations for continuous water disinfection of small communities.148 Despite several advantages over chlorine disinfection, it has not gained general acceptance because of concern for its physiologic activity. Recently the European Union has stopped the sale of iodine products used for water disinfection. Chemistry Iodine is the only halogen that is a solid at room temperature. Of the halogens, it has the highest atomic weight, lowest oxidation potential, and lowest water solubility. Its disinfectant activity in water is quite complex because of formation of various chemical intermediates with variable germicidal efficiencies. Seven different ions or molecules are present in pure aqueous iodine solutions, but only elemental (diatomic) iodine (I2) and hypoiodous acid (HOI) play major roles as germicides. Diatomic iodine reacts in water to form the following compounds:52,114 I2 + H2O → HOI + I− + H +

TABLE 67-13  Chlorine Dose for Large-Volume Water Disinfection Gallons to be Chlorinated

1 mg/L*

2 mg/L

5% Liquid Bleach 5 6 gtt 0.75 mL 10 0.75 mL 1.5 mL 25 2 mL 3.8 mL 36 3 mL 5.5 mL 50 4 mL 1.5 tsp 100 7.7 mL 3 tsp 400 2 tbsp 4.25 tsp 500 3 tbsp 0.33 C 1000 0.33 C 0.67 C 70% Available Chlorine (Calcium Hypochlorite or Solution Concentrate†) 5 0.9 mL 1.7 mL 10 1.7 mL 3.3 mL 25 4.1 mL 8.3 mL 36 6 mL 11.9 mL 50 8.3 mL 16.6 mL 100 16.6 mL 33 mL 400 0.92 mL 1.9 mL 500 1.3 mL 0.5 tsp 1000 0.5 tsp 1 tsp

5 mg/L

10 mg/L

1.9 mL 3.8 mL 2 tsp 2.75 tsp 4 tsp 3 tbsp 0.75 C 1C 1.75 C

3.8 mL 1.5 tsp 4 tsp 2 tbsp 3 tbsp 5 tbsp 1.5 C 1.75 C 3.25 C

4.1 mL 8.3 mL 20.7 mL 29.8 mL 0.6 mL 0.25 tsp 1 tsp 1.25 tsp 2.5 tsp

8.3 mL 16.6 mL 41.4 mL 0.9 mL 0.25 tsp 0.5 tsp 2 tsp 2.5 tsp 5 tsp

100 mg/L 8 tsp 16 tsp 1C 1.25 C 1.75 C 3.25 C 3 qt 1 gal 2 gal 0.25 tsp 0.5 tsp 1.25 tsp 1.75 tsp 2.5 tsp 5 tsp 19 tsp 0.5 C 1C

Data from U.S. Army: Sanitary control and surveillance of field water supplies, Dept. of Army technical bulletin (TB Med 577), Washington, DC, December 15, 2005, Departments of the Army, Navy, and Air Force. *For all chlorine residual concentrations in water, values in parts per million (ppm) are equivalent to values in milligrams per liter (mg/L). † The shaded area of the table indicates the volume of a concentrated solution made from dissolving 1 tsp of 70% calcium hypochlorite (most commonly used for swimming pool chlorination) in water.

1341

CHAPTER 67  Field Water Disinfection

TABLE 67-12  Recommendations for Contact Time

PART 8  FOOD AND WATER

I2 is two to three times as cysticidal and six times as sporicidal as HOI, because it more easily diffuses through the cyst wall. Conversely, HOI is 40 times as virucidal and three to four times as bactericidal as I2, because inactivation of organisms depends directly on oxidation potential, without involving cell wall diffusion.50 Their relative concentrations are determined by pH and concentration of iodine in solution.52 At pH 7.0 and 0.5 ppm of iodine, the concentrations of I2 and HOI are approximately equal, resulting in a broad spectrum of germicidal action. At pH 5.0 to 6.0, most of the iodine is present as I2, whereas at pH 8.0, 12% is present as I2 and 88% as HOI. At higher concentrations of iodine, more HOI is present. Under field conditions, I2 is the major disinfectant for which doses are calculated.52 Iodide is important because it readily forms when reducing substances are added to iodine solution. Iodide ion is without any effect for water disinfection and also has no taste or color, but is still physiologically active. Toxicity The main disadvantage of iodine is its physiologic activity, with effects on thyroid function, potential toxicity, and allergenicity.204 Acute toxic responses generally result from intentional overdoses of iodine, with corrosive effects in the gastrointestinal tract leading to hemorrhagic gastritis. Mean lethal dose is probably about 2 to 4 g (0.07 to 0.14 oz) of free iodine or 29.6 to 59.1 mL (1 to 2 oz) of strong tincture.100 Iodide is absorbed into the bloodstream but has minimal toxicity (thus its use for radiographic imaging). Sensitivity reactions, including rashes and acne, may occur with usual supplementation levels of iodine. Given the physiologic necessity of iodine, it is not clear why some people react to certain forms of the substance, such as iodized salt. As with other sensitivity reactions, these may occur with very low doses. Acute allergy to iodide is rare and manifests as individual hypersensitivity, such as angioneurotic and laryngeal edema.204 Chronic iodide poisoning, or iodism, occurs after prolonged ingestion of sufficiently high doses, but marked individual variation is seen. Symptoms simulate upper respiratory illness, with irritation of mucous membranes, mucus production, and cough. Thyroid Effects of Iodine Ingestion.  Iodine is an essential element for normal thyroid function and health in small amounts of 100 to 300 mcg/day. Excess amounts can result in thyroid dysfunction. Maximum safe level and duration of iodine ingestion are not clearly defined, making it difficult to provide recommendations for prolonged use in water treatment. Most persons can tolerate high doses of iodine without development of thyroid abnormalities,29 because the thyroid gland has an autoregulatory mechanism that effectively manages excessive iodine intake. Initially, excess iodine suppresses production of thyroid hormone, but production usually returns to normal in a few days. Iodine-induced hyperthyroidism can result from iodine ingestion by persons with underlying thyroid disease or when iodine is given to persons with prior iodine deficiency.29,243 During the worldwide campaign to eliminate endemic goiter and cretinism, 1% to 2% of residents developed hyperthyroidism from small amounts of dietary iodine supplementation. Groups at higher risk were older adults, Graves’ disease patients (especially after antithyroid therapy), and patients taking pharmacologic sources of iodine. Hyperthyroidism has been reported from iodine use as a water disinfectant in two travelers. Both were from iodinesufficient areas and had antithyroid antibodies, suggesting underlying thyroiditis; one had a mother and sister with Hashimoto’s thyroiditis.162 Iodine-induced hypothyroidism or goiter is much more common from excessive iodine intake. Hypothyroidism is attributed to prolonged suppression of thyroid hormone production induced by excess iodine levels, but the mechanism through which iodide goiter is produced is not well understood. The incidence of goiter varies and does not correlate well with quantity of iodine or with the level of hypothyroidism. Goiters were discovered among a group of Peace Corps volunteers in Africa and were linked epidemiologically to the use of iodine resin 1342

water filters.102,146a Forty-four (46%) of the volunteers had enlarged thyroids, but 30 of these had normal thyroid function tests. Iodine-induced hypothyroidism or goiter may occur with or without underlying thyroid disease but is more common in several groups:29,243,297 (1) those with underlying thyroid problems, including prior treatment for Graves’ disease or subtotal thyroidectomy; (2) fetuses and infants, from placental transfer of iodide from mothers treated with iodides; (3) persons with subclinical hypothyroidism, especially older adults, in whom the incidence is 5% to 10%; and (4) patients with excessive iodide from medications (formerly potassium iodide; currently amiodarone). Neonatal goiter is especially worrisome because it can lead to asphyxia during birth or hypothyroidism with mental impairment. Daily intakes as small as 12 mg have been reported to produce congenital iodide goiters, but generally much higher doses are required. Dose-Response or Threshold Level.  The reported incidences of goiter, hypothyroid effects, and hyperthyroid response vary so widely that they provide no clear dose limits.204 These data and other controlled trials of high doses have been reviewed.9 The use of iodine for decades as a field water disinfectant by military and civilian populations without reports of associated clinical thyroid problems suggests that the risks are minimal and would be outweighed by the risk for enteric disease. Biochemical assays show that changes in thyroid function tests are common with excess iodine intake; however, changes in thyroid function usually remain subclinical. All changes reverted to normal within weeks to months without persistent thyroid disease. Studying longer duration of ingestion, Freund104 found minimal changes and no clinical problems when water with 1 mg/L of iodine was used to disinfect water at a prison for up to 3 years. Referring to the same project, Thomas and colleagues271 reported that after 15 years of ongoing iodine use at 1 mg/L, iodinated water caused no decrease in serum concentrations of T4 below normal values and no allergic reactions. Patients with prior thyroid disease had no recurrence with iodinated water; four patients with active hyperthyroidism were treated in standard fashion, and their condition remained well controlled despite the extra iodine intake. Also, 177 inmates gave birth to 181 full-term infants, and no neonatal goiters were detected. The military studied long-term toxic effects of iodine, adding sodium iodide to drinking water at a naval base for 6 months.188 The estimated daily dose of iodine per person was 12 mg for the first 16 weeks and 19.2 mg for the next 10 weeks. No evidence of functional changes or damage in the thyroid gland, cardiovascular system, bone marrow, eyes, or kidneys was noted. No increase in skin diseases, no sensitization to iodine, and no impaired wound healing or resolution of infections were evident. Recommendations.  The 2001 U.S. Department of Agriculture (USDA) Recommended Dietary Intake suggested an upper limit of 1.1 mg/day for adults, weight adjusted for children. WHO did not set a guideline value for iodine in drinking water, because of a paucity of data and because it is not recommended for longterm disinfection. The EPA and WHO, supported by the American Water Works Association (AWWA), have recommended iodine use for water disinfection only as an emergency measure for short periods of about 3 weeks. However, this period of short use appears arbitrary. The European Union revoked approval of iodine for water purification on October 25, 2009, and it can no longer be sold for this purpose. Available data suggest the following: • High levels of iodine, such as those produced by recommended doses of iodine tablets, should be limited to periods of 1 month or less. • Iodine treatment that produces a low residual (1 mg/L or less) appears safe, even for long periods in people with normal thyroid function. This would require very low doses of iodine added to the water or an activated charcoal stage to remove residual iodine. • Persons planning to use iodine for a prolonged period should have the thyroid gland examined and thyroid

Preparation

Iodine (%)

Iodide (%)

Type of Solution

2.0

2.4 (sodium)

Aqueous

5.0 2.0 7.0

10.0 (potassium) 2.4 (sodium) 9.0 (potassium)

Aqueous Aqueous-ethanol Ethanol (85%)

Iodine topical solution Lugols solution Iodine tincture Strong iodine solution

function measured to ensure that a state of euthyroidism exists. • The following groups should not use iodine for water treatment because of their increased susceptibility to thyroid problems: • Pregnant women • Persons with known hypersensitivity to iodine • Persons with a history of thyroid disease, even if controlled by medication • Persons with a strong family history of thyroid disease (thyroiditis) • Persons from areas with chronic dietary iodine deficiency

Products and Techniques for Iodination Several formulations of iodine are available for field use. (See Tables 67-10 and 67-15 for efficacy, Tables 67-11 to 67-14 for product dosing, and Appendix B for details on commercial products, including tablets and crystalline iodine.) Resins.  Iodine can be bound to an inert resin to create a disinfectant with unique properties. These are considered demand disinfectants because iodine transfers from the resin to the microorganism on contact, aided by electrostatic forces, but limited amounts of iodine dissolve in the water. Iodine binds to the wall or capsule, penetrates, and kills the organism. This effectively exposes the organisms to high iodine concentrations and allows reduced contact time compared with dilute iodine solutions. Residual iodine concentration in the water depends on the properties of the resin, the temperature of the water, and presence of an activated charcoal stage.

Resins have proved effective against bacteria, viruses, and cysts but not against C. parvum oocysts or bacterial spores.170 When Cryptosporidium oocysts were passed through a triiodide resin column, most were retained in the resin column, probably by electrostatic attraction to the resin. Of those that passed through, only a small percentage were inactivated within 30 minutes by the iodine.278 Data suggest that both contact time and iodine residual are important for optimal results.99,171,170 Fifty percent of Giardia cysts were viable 10 minutes after passage through a triiodine resin. Viable Giardia cysts could be recovered in 4° C (39.2° F) water 40 minutes after passage through an iodine resin.171 A simple resin filter failed to pass the EPA protocol for “worst-case” water unless water was passed through the filter twice. The data implied that a holding (contact) time could have achieved the desired results.110 The Canadian health department, challenging an in-line triiodine resin with highly polluted water, also found that a 15-minute contact time was necessary for warm water and 30-minute contact time for cold water.92 The EPA conducted tests of triiodide resin against E. coli but not against other organisms, for which it relied on independent testing. It concluded that the product depends on a 0.2 ppm residual and that additional testing would be necessary below this level. Resins are chemically and physically stable during conditions of dry storage at room temperature. Aqueous suspensions or resins retain biocidal potential for 15 years. No alteration in activity was observed after dry storage for 1 month at 50° C (122° F).170 Iodine Resin Filters.  Iodine resins have been used for water disinfection in individual or small systems and incorporated into filter designs for field use. Iodine filters are generally designed with two stages in addition to the iodine resin. A microfilter, generally 1 µm, effectively removes Cryptosporidium, Giardia, and other halogen-resistant parasitic eggs or larva. Because iodine resins kill bacteria and viruses rapidly, limited contact time is required for most water.110 Addition of a third stage of activated charcoal removes dissolved residual, which may decrease efficacy.171,275 In the United States, inconsistent results of product testing under variable conditions led to withdrawal of most filter models from the market. It was not clear whether failure to achieve desired results was related to inadequate contact with the resin or insufficient contact time with iodine residual. Resins are now being used in point-of-use household devices in other countries with generally good but variable microbial removal or inactivation. Significant levels of residual iodine are noted without a charcoal stage.58

TABLE 67-15  Data on Efficacy of Iodine Tablets Halogen

Dose

Chlor-Floc

1 tab or 2 tabs

Globaline

1 tab 2 tabs

FRC (mg/L)

Time min

4-7 4-14

5 20 5 20 12 20 45 20 60 40 30-40

AquaPure

2 tabs 1 tab

7-11

Globaline

2 tabs 1 2 1 or 2

10

Iodine tabs

8-16 8 16

20 60 180 120 60 60 60

Temperature 10°-20° C (50°-68° 10°-20° C (50°-68° 10°-20° C (50°-68° 10°-20° C (50°-68° 25° C (77° F) Various 5° C (41° F) 5° C (41° F) 5° C (41° F) 5° C (41° F) 15°-25° C (59°-77° 15°-25° C (59°-77° 15°-25° C (59°-77° 15°-25° C (59°-77° 15° C (59° F) 5° C (41° F) 5° C (41° F) 5°-25° C 5° C (41° F) 5° C (41° F)

Organism

Log reduction

Reference

F) F) F) F)

Bacteria Giardia muris Rotavirus Poliovirus Poliovirus Bacteria G. muris Rotavirus Poliovirus

6 3 4 Inadequate Inadequate 6 3 4 60

Powers, 1994212

F) F) F) F)

Bacteria Rotavirus Poliovirus G. muris Giardia Giardia Giardia Hepatitis A Poliovirus, echovirus Poliovirus, echovirus

6 4 2 2 3 3 3 4 Insufficient 4

Powers, 1992214

Powers, 1991213 Sobsey, 1991261

1343

CHAPTER 67  Field Water Disinfection

TABLE 67-14  Iodine Solutions

PART 8  FOOD AND WATER

Given some of the variability in results and uncertainty of mechanism of action, the U.S. outdoor gear companies have abandoned iodine resin–containing portable hand-pump filters, and only drink-through bottles remain on the U.S. market. Other products may still be available outside the United States or via Internet retailers.

CHLORINE VERSUS IODINE A large body of data proves that both iodine and chlorine are effective disinfectants with adequate concentrations and contact times, except for dealing with Cryptosporidium.128 Under identical water test conditions and using recommended dose and contact time, chlorine and iodine tablets are similar in their biocidal activity211 (see Tables 67-11, 67-12, and 67-15). A few investi­ gators have reported data suggesting ineffectiveness of common halogen preparations. Jarroll and associates138,139tested six methods of field disinfection and found that none achieved high levels of Giardia inactivation at the recommended dose and times. However, this failure simply reflected the need for longer contact times in cold water.163 Ongerth and colleagues201 tested seven chemical treatments for Giardia inactivation in clear and turbid water at 10° C (50° F). None achieved 99.9% reduction in 30 minutes. All iodine-based chemical methods were effective at 8 hours, but none of the chlorine preparations was effective, even after this extended time. Although these results after 30 minutes in cold water are to be expected, the 8-hour results do not conform with other experimental data on chlorine. Unfortunately, the authors did not test for residual halogen, although initial levels achieved should have been effective, and they did not test at regular time intervals to determine when the iodine methods had achieved the target reduction of organisms. Schlosser and co-workers248 found that sodium hypochlorite tablets, sodium dichloroisocyanurate tablets, and iodine in ethanol used according to package instructions removed 2 to 3 log of bacteria in clear water, but less in turbid river water. This suggests the need for clarifying dirty water before halogen use and, if possible, providing extra contact time in any situation. Iodine has some advantages over chlorine. Of the halogens, iodine has the lowest oxidation potential, reacts least readily with organic compounds, is least soluble, is least hydrolyzed by water, and is less affected by pH, all of which indicate that low iodine residuals should be more stable and persistent than corresponding concentrations of chlorine.75,114,148,191 The major disadvantage is its physiologic activity. Taste Objectionable taste and smell are the major problems with acceptance of halogens. Most objectionable taste in treated water is derived from dissolved minerals, such as sulfur, and from chlorine compounds, chloramines, and organic nitrogen compounds, even at extremely low levels. People are familiar with the taste of chlorine compounds; tap water usually contains 0.2 to 0.5 ppm of chlorine, swimming pools 1.5 to 3.0 ppm, and hot tubs 3.0 to 5.0 ppm. Most persons used to the faint taste of chlorine in water note a distinct taste at 5 ppm and a strong, unpleasant taste at 10 to 15 ppm.236 With the promotion of chlorination for household use, focus groups on taste testing have found that the majority of CDC-WHO Safe Water System users are comfortable drinking water with a free chlorine residual of up to 2 mg/L; however, there is significant regional variation in the acceptable maximum residual, and many found the taste objectionable and unsuitable at 3 to 4 mg/L.155 The higher sodium hypochlorite dosages necessary to ensure maintenance of chlorine residual in turbid waters exacerbate the taste and odor concerns.150 Elemental iodine at 1 mg/L is undetectable. Most persons can detect iodine solutions at 1.5 to 2 mg/L but do not find it objectionable.23,75,107 Distinct taste and odor are produced by 8 ppm of iodine; however, tablets yielding these concentrations were preferred by military personnel over tincture of iodine in equivalent doses.52,190 Taste tolerance or preference for iodine over chlorine is individual. Opposite preferences have been documented when direct comparisons are done.199,214Informal taste tests suggest that most 1344

BOX 67-10  Improving the Taste of Halogens • Decrease dose and increase contact time. • Clarify cloudy water, allowing decreased halogen. • Remove halogen. • Use granular activated charcoal. • Chemical reduction techniques • Ascorbic acid • Sodium thiosulfate • Chlorination-dechlorination • Zinc-copper (KDF) media • Alternative techniques: • Heat • Filtration • Chlorine dioxide or mixed species (Miox)

persons prefer the taste of iodine to chlorine at concentrations typically used in the field. In addition, iodine forms fewer organic compounds that produce highly objectionable taste and smell. Taste can be improved by several means (Box 67-10). Minimizing Dose.  The relationship between halogen concentration and time allows use of the minimum necessary dose, with a longer contact time (see Tables 67-11 and 67-12). Theoretically, doubling the contact time allows a 50% reduction of halogen dose at any level. Although this relationship holds true at the higher field doses of halogens, as the levels drop, the reaction departs from mathematical models, and the straight-line graph has a “tail” (see Figure 67-3). This departure from strict first-order kinetics and the uncertainty of halogen demand in field disinfection mean that a margin of safety must be incorporated into contact times at lower doses. Of all standard iodine doses, iodine tablets yield the highest dose (8 mg/L with an intended contact time of 10 minutes in warm water). The tablets cannot be broken in one-half but can be added to 2 qt instead of 1 qt of water to yield concentrations consistent with the other preparations. The recommended doses of the liquid iodine preparations yield 4 mg/L. Because even clear surface water has some halogen demand, this dose of 4 mg/L should generally not be reduced for surface water, but for backing up tap water in developing countries or prefiltered water, the dose may routinely be cut in one-half for an added dose of 2 ppm with a few hours of contact time.102,124,156 A similar approach can be used for chlorination methods. None of these concentrations will destroy Cryptosporidium oocysts. Temperature and organic matter in the water may be manipulated. Increasing the temperature of the water, especially when initially near 5° C (41° F), decreases the Ct constant (see Tables 67-11 and 67-12 and Figure 67-3). Filtering water before adding halogen improves the reliability of a given halogen dose by decreasing halogen demand, allowing a lower dose of halogen.191 Sedimentation or coagulation–flocculation cleans cloudy water and lowers the required halogen dosage considerably, in addition to removing many of the contaminants that contribute to objectionable taste. Dehalogenation.  Halogen can be removed from water after the required contact time. Activated charcoal removes iodine or chlorine, allowing standard or even high doses to be used without residual taste. The relative instability of chlorine in dilute solutions can be used to decrease taste over time. Chlorine residual in an open container decreases 1 mg/L in the first hour, then 0.2 mg/L in the next 5 to 8 hours, for a total of 2.0 to 2.5 mg/L in 24 hours. UV light also depletes free chlorine.295 Alteration of Chemical Species (Reduction).  Several chemical means are available to reduce free iodine or chlorine to iodide or chloride that have no color, smell, or taste. These “ides” have no disinfection action, so the techniques should be used only after the required contact time. In superchlorination– dechlorination, hydrogen peroxide “dechlorinates” water treated with calcium hypochlorite by forming calcium chloride.

Miscellaneous Disinfectants CHLORINE DIOXIDE Chlorine dioxide (ClO2), a potent biocide, has been used for many years to disinfect municipal water and in numerous other large-scale applications. Until recently, the benefits of chlorine dioxide have been limited to large-scale applications, because it is formulated as a volatile gas that must be produced on-site with sophisticated chemical-generation equipment. Newer methods enable cost-effective and portable chlorine dioxide generation and distribution for use in an ever widening array of small-scale applications (Box 67-11). For point-of-use treatment of water, chlorine dioxide is produced on site from the reaction of sodium chlorite with acid.21,257 For example: 5NaClO2 + 4 HCl → 4ClO2 + 5NaCl + 2H2O It is capable of inactivating most waterborne pathogens, including C. parvum oocysts, at practical doses and contact times. It is as least as effective a bactericide as chlorine, and far superior as a virucide.295 Chlorine dioxide is not as unstable as ozone but does not produce a lasting residual. It does not form chlorinated compounds in the presence of organics and is efficacious over a wide pH range. By-products of chlorine dioxide are chlorite (ClO2−) and chlorate (ClO3−). There are several new commercial point-of-use applications using chlorine dioxide in liquid or tablet form (see Appendixes).

MIXED SPECIES DISINFECTION (ELECTROLYSIS) Passing a current through a simple brine salt solution generates free available chlorine, as well as other “mixed species” disinfectants that have been demonstrated effective against bacteria,

BOX 67-11  Chlorine Dioxide Advantages Effective against all microorganisms, including Cryptosporidium Low doses have no taste or   color Portable device now available   for individual and small group field use and simple to use More potent than equivalent doses of chlorine Less affected by nitrogenous wastes

Disadvantages Volatile, so do not expose tablets to air and use generated solutions rapidly No persistent residual, so does not prevent recontamination during storage Sensitive to sunlight, so keep bottle shaded or in pack during treatment

Relative susceptibility of microorganisms to chlorine dioxide: bacteria > viruses > protozoa.

viruses, and bacterial spores.245 The process is well described and can be used on both large and small scales. It is practical and economic enough to be useful in developing areas of the world. The exact composition of the resulting solution is not well delineated because many of the compounds are evanescent and unstable. However, the resulting solution has greater disinfectant ability than a simple solution of sodium hypochlorite. It has even been demonstrated to inactivate Cryptosporidium, suggesting that chlorine dioxide is among the chemicals generated.289 A pointof-use commercial product is now available (Miox, see product appendixes for more information).

SOLAR PHOTOCATALYTIC DISINFECTION Advanced oxidation processes uses sunlight to catalyze production of hydroxyl radicals (OH−) and free electrons, which are potent oxidizers. Various semi-conductor materials can be used, but the most efficacious is titanium dioxide (TiO2). High energy short-wavelength photons from sunlight promote the photochemical reactions. In addition to being an excellent disinfectant for various micro-organisms, this process is unique in its ability to break down complex organic contaminants and most heavy metals into carbon dioxide, water, and inorganics, which is driving considerable research for industrial processes and largescale water treatment. For field water disinfection, nanoparticles coated with TiO2 can be integrated into a plastic bag and remain active for hundreds of uses (see Appendix A).23a

OZONE Ozone is an unstable form of oxygen, with the chemical formula O3. In solution, it decays to O2, producing free hydroxyl radicals. Both ozone and the hydroxyl radicals are two of the most powerful oxidants used in water treatment.21 It is a highly effective disinfectant widely used in municipal water treatment plants.295 Ozone and chlorine dioxide are the only chemical disinfectants that have been demonstrated effective against Cryptosporidium in typical concentrations.18,57,149,203 Advantages of ozone disinfection are that it has high efficacy against all groups of microorganisms and that it produces very few disinfection by-products.18 The main disadvantage is its chemical instability: there is no stable product that can be used in the field. Ozone is a colorless gas manufactured by passing air or oxygen through a high-voltage current discharge. The resulting ozone-rich gas is then dissolved in water. Clearly this is not conducive to small, point-of-use generation, so consumers should be skeptical of techniques claiming to rely on ozone.

SILVER Silver ion has bactericidal effects in low doses. The literature on antimicrobial effects of silver is confusing and contradictory.132,168,191,295,299 Concentrations in water less than 100 parts per billion (ppb) are effective against enteric bacteria. The reaction follows first-order kinetics and is temperature dependent. Calcium, phosphates, and sulfides interfere significantly with silver disinfection. Organic chemicals, amines, and particulate or colloidal matter may also interfere, but no more than with chlorine. Silver is physiologically active. Acute toxicity does not occur from small doses used in disinfection, but argyria, which is permanent discoloration of the skin and mucous membranes, may result from prolonged use. For this reason a maximum limit of 50 ppb of silver ion in potable water is recommended with an upper limit of 10 g per lifetime—NOAEL (no observed adverse effect level). This would be reached only after drinking 3 L/day containing 0.1 mg/L over 70 years. WHO acknowledges that the daily intake of silver when used to maintain the bacteriologic quality of drinking water can constitute the major route of oral exposure but states that “It is unnecessary to recommend a healthbased guideline value because [silver] is not hazardous to human health at concentrations normally found in drinking water.” At the recommended concentration of 50 ppb for water treatment, disinfection requires several hours. Experimental results indicate 18% survival of E. coli at 3 hours at 40 mcg/L. S. typhi 1345

CHAPTER 67  Field Water Disinfection

Two other chemicals that may be safely used with any form of chlorine or iodine are ascorbic acid (vitamin C) and sodium thiosulfate. Ascorbic acid is widely available in the crystalline or powder form. Grinding up tablets that have binders may cloud the water. Ascorbic acid is a common ingredient of flavored drink mixes, which accounts for their effectiveness in covering up the taste of halogens.199,236 Sodium thiosulfate similarly “neutralizes” iodine and chlorine. A few granules in 1 qt of iodinated water decolorizes and removes the taste of iodine by converting it to iodide. In reaction with chlorine, it forms hydrochloric acid, which is not harmful or detectable in such dilute concentration. Thiosulfate salts are inert in vivo and poorly absorbed from the gastrointestinal tract. Sodium thiosulfate is available at chemical supply stores. This is the active ingredient in Katadyn Antichlorine drops. Copper-zinc alloys act as catalysts to reduce free iodine and chlorine through an electrochemical reaction (see Copper and Zinc, later).

PART 8  FOOD AND WATER

was reduced more than 5 log at 50 mcg/L with a 1-hour exposure; poliovirus was not reduced at 50 mcg/L with a 1-hour exposure.14 Bacteria can develop resistance to silver ions through generation of silver reductase. Large-scale use of silver for water disinfection has been limited by cost, difficulty controlling and measuring silver content, and physiologic effects. Short-term field use is limited by its marked tendency to adsorb onto the surface of any container (resulting in unreliable concentrations) and interference by several common substances. Data on silver for disinfection of viruses and cysts indicate limited effect, even at high doses.50,191 Nevertheless, water disinfection systems using silver have been devised for spacecraft, swimming pools, and other settings.295 The advantage is absence of taste, odor, and color. Persistence of residual silver concentration allows reliable storage of disinfected water. Silver can be supplied through a silver nitrate solution, desorption from silver-coated materials, or electrolysis. When coated on surfaces, silver acts as a constant-release disinfectant that produces aqueous silver ion concentrations of 0.006 to 0.5 ppm, which are sufficient to disinfect drinking water.170 Because of this attractive feature, silver-based devices are being designed and tested in developing countries. In Pakistan, a nylon bag with silver-coated sand was designed to be placed in earthenware pitchers that store water. Silver incorporated into alum is also being tested in India.53 The use of silver as a drinking water disinfectant has been much more popular in Europe, where silver tablets (Micropur) are sold widely for field water disinfection. They have not been approved by the EPA for this purpose in the United States, but they were approved as a water preservative to prevent bacterial growth in previously treated and stored water. Micropur Forte tablets release free chlorine for disinfection and silver for prolonged persistence of antimicrobial activity. Silver impregnation of filters may inactivate pathogens that pass through the filter pores or limit bacterial growth in the filter itself (bacteriostatic). Ceramic filters coated with silver have higher removal rates of bacteria, and filters that had been just recoated with silver initially yielded much higher disinfection efficiencies but were not able to sustain them.14,19,107 Filter cartridges impregnated with silver typically become colonized with heterotrophic bacteria, and effluent bacterial populations are about as large as units without silver. These bacteria have not been linked to increased illness.14,93,107,223 Colonization of filters with pathogenic coliforms has not been demonstrated, but protective effect cannot be attributed to silver impregnation.93,223

POTASSIUM PERMANGANATE Potassium permanganate is a strong oxidizing agent with some disinfectant properties. It is used in municipal disinfection to control taste and odor. It has been used in a 1% to 5% solution as a drinking water disinfectant190 and is still used for this purpose in some countries, as well as for washing fruits and vegetables. Bacterial inactivation can be achieved with moderate concentrations and contact times (45 minutes at 2 mg/L, 15 minutes at 8 mg/L). A 1 : 5000 (0.5%) solution controlled V. cholerae and S. typhi contamination of fruits and vegetables. The virucidal action has been tested, but without titrations of virus that remained after various periods of contact time, so the rate of action is not known. In most instances, however, a 1 : 10,000 solution destroyed the infectivity of virus suspensions in 30 minutes at room temperature; 30 mg/L was effective in inactivating HAV within 15 minutes.273 Although potassium permanganate clearly has disinfectant action and is frequently used in some parts of the world, it cannot be recommended for point-of-use water disinfection unless no other means are available, because quantitative data are not available for viruses and no data are available for protozoan cysts. Packets of 1 g to be added to 1 L of water are sold in some countries. A French military guide from 1940 instructed users: “To sterilize water, use a solution of 1 gram of KMnO4 for 100 grams of water. Add this solution drop by drop to the water to sterilize until the water becomes pink. The operation is considered sufficient if the water remains pink for half an hour.”54 The solutions are deep pink to purple and stain surfaces. The 1346

chemical leaves a pink to brown color in water at concentrations above 0.05 mg/L. Small deposits of brown oxides settle to the bottom of the water container. A few drops of alcohol will cause this residual color to disappear.

HYDROGEN PEROXIDE Hydrogen peroxide is a strong oxidizing agent but a weak disinfectant.26,191,307 Small doses (1 mL of 3% H2O2 in 1 L water) are effective for inactivating bacteria within minutes to hours, depending on the level of contamination. Tested against seven bacterial strains, hydrogen peroxide killed 1 × 106 colony-forming units per milliliter overnight, with 80% kill in 1 hour. Viruses require extremely high doses and longer contact times. It is a promising sporicidal agent in high (10% to 25%) concentrations. Hydrogen peroxide is popular today as a wound cleanser; for odor control in sewage, sludges, and landfill leachates; and for many other applications. It is considered safe enough for use in foods, yielding the innocuous end products oxygen and water. It is considered nature’s disinfectant, because it is naturally present in milk and honey, helping to prevent spoilage. Solutions lose potency in time, but stabilizers can be added to prevent decomposition.26 Although hydrogen peroxide can sterilize water, lack of data for protozoal cysts and quantitative data for dilute solutions prevents it from being useful as a field water disinfectant.

PERACETIC ACID Peracetic acid (CH3COOOH) consists of a quaternary mix of acetic acid, hydrogen peroxide, peracetic acid, and water with a pH value close to 2. It has been used with success in water disinfection because of its strong oxidizing properties.

CITRUS Citrus juice has biocidal properties. Lemon or lime juice has been shown to destroy V. cholerae at a concentration of 2% (equivalent of 2 tbsp/L of water) with a contact time of 30 minutes. A pH of less than 3.9 is essential, which depends on the concentration of lemon juice and the initial pH of the water.78 Lime juice also killed 99.9% of V. cholerae on cabbage and lettuce and inhibited growth of V. cholerae in rice foods, suggesting that adding lime juice to water, beverages, and other foods can reduce disease risks.257 More research is needed before this can be recommended as more than an ancillary or emergency measure. Commercial products using citrus cannot be recommended as primary means of water disinfection.

ULTRAVIOLET LIGHT UV lamp disinfection systems are widely used to disinfect drinking water at the community and household levels (Box 67-12). In sufficient doses, all waterborne enteric pathogens are inactivated by UV radiation (UVR). The germicidal effect of UV light is the result of action on the nucleic acids of bacteria and depends on light intensity and exposure time.49 Bacteria and protozoan parasites require lower doses than do enteric viruses

BOX 67-12  Ultraviolet Irradiation Advantages Effective against all microorganisms Imparts no taste Portable device now available for individual and small group field use and simple to use Available from sunlight

Disadvantages Requires clear water Does not improve water esthetics No residual effect—does not prevent recontamination during storage Expensive Require power source Requires direct sunlight, prolonged exposure; dose low and uncontrolled

Relative susceptibility of microorganisms to ultraviolet: protozoa > bacteria > viruses.

Advantages Improves the microbiologic   quality of drinking water; including protozoan cysts Does not change the taste of water Simple in application; can be   used at household level Utilizes sunlight Requires no special equipment   or power; relies on local resources and renewable   energy Can be used in austere environments

Disadvantages Requires clear water No residual effect—does not prevent recontamination during storage Does not improve water esthetics Not useful to treat large volumes of water; use maximum 2-L bottle. Requires strong, direct, abundant sunlight, prolonged exposure; dose low and uncontrolled

Relative susceptibility of microorganisms to SODIS: protozoa > bacteria > viruses.

and bacterial spores. However, all viruses, including hepatitis A and norovirus, are susceptible with relatively minor differences, and follow similar kinetics.126 Bacteria (vegetative cells) are significantly more susceptible to UVR than are viruses. Giardia and Cryptosporidium are susceptible to practical doses of UVR and may be more sensitive because of their relatively large size.18,126,164 UV treatment does not require chemicals and does not affect the taste of the water. It works rapidly, and an overdose to the water presents no danger; in fact, it is a safety factor. UV irradiation with lamps requires a power source and is costly. UV light has no residual disinfection power; water may become recontaminated, or regrowth of bacteria may occur.93 Particulate matter can shield microorganisms from UV rays. A portable field unit, Steri-PEN, is now available (see Appendix A). Solar Irradiation There is now strong evidence that UV irradiation by sunlight in UV-A range can substantially improve microbiologic quality of water and reduce diarrheal illness in developing countries. Recent work has confirmed efficacy and optimal procedures of the solar disinfection (SODIS) technique49,66,197,257(Box 67-13). Transparent bottles (e.g., clear plastic beverage bottles) are exposed to sunlight for a minimum of 4 to 6 hours, but some investigations demonstrate improved benefit from several sequential days. Multiple studies demonstrate reduction of enteric bacteria, viruses, and protozoan cysts, and some data exist for reduction of bacterial spores.147,176,177,262 With a water temperature of 30° C (86° F), 6 hours of mid-latitude midday summer sunshine are required to achieve a 3-log reduction of fecal coliforms.179 UV and thermal inactivation were strongly synergistic for solar disinfection of drinking water in transparent plastic bottles that was heavily contaminated with E. coli for temperatures above 45° C (113° F). Above 55° C (131° F), thermal inactivation is of primary importance.175 Whereas thermal inactivation is effective in turbid water, UV effects are inhibited.142 If cloudiness is greater than 50%, the plastic bottles need to be exposed for 2 consecutive days in order to produce water safe for consumption. However, if water temperatures exceed 50° C (122° F), 1 hour of exposure is sufficient to obtain safe drinking water. The treatment efficiency can be improved if the plastic bottles are exposed on sunlight-reflecting surfaces such as aluminum or corrugated iron sheets. Use of a simple reflector or solar cooker can achieve pasteurization temperatures of 65° C (149° F). Oxygenation induces greater reductions of bacteria, so agitation is recommended before solar treatment in bottles. Various types of transparent plastic materials are good transmitters of light in the UV-A and visible range of the solar spectrum. Plastic bottles are made of either polyethylene terephtalate (PET) or polyvinylchloride (PVC). The use of bottles made from PET instead of PVC is recommended because PET contains fewer

additives than do bottles made from PVC. Glass bottles are not used for SODIS because the transmission of UVR through glass is determined by its content of iron oxide; ordinary window glass of 2-mm thickness transmits almost no UVA light. Because UVR is reduced at increasing water depth, the containers used for SODIS should not exceed a water depth of 10 cm (3.9 inches). Aged or heavily scratched plastic bottles show reduced UV transmittance, which in turn can result in less efficient inactivation of microorganisms.179 In summary, where strong sunshine and clear water are available, solar disinfection of drinking water is an effective, low-cost method for improving water quality and may be of particular use in refugee camps and disaster areas.179

COPPER AND ZINC Kinetic degradation fluxion (KDF) is a high-purity copper-zinc formulation that uses a basic chemical process known as redox (oxidation-reduction) to remove chlorine, heavy metals such as lead and mercury, iron, and hydrogen sulfide from water supplies. Its main actions are through its strong redox potential of 500 mV due to the propensity to exchange electrons with other substances. The redox reactions change contaminants into harmless components: chlorine into chloride (removing the taste of chlorine or iodine from treated water), soluble ferrous cations into insoluble ferric hydroxide, and hydrogen sulfide into insoluble copper sulfide. Up to 98% of lead, mercury, nickel, chromium, and other dissolved metals are removed by KDF simply by bonding to the media. KDF controls the buildup of bacteria, algae, and fungi and is used for this purpose in GAC beds and carbon block filters, extending the life of carbon and improving its effectiveness. KDF or copper alone has bacteriostatic with some bactericidal activity; microorganisms may be killed by the electrolytic field, and by formation of hydroxyl radicals and peroxide water molecules.168 Although KDF has been ruled a “pesticidal device” by the EPA, it should not be used as the sole means of water treatment and is best combined with filtration or chlorination. KDF media can be manufactured as granules, fine steel wool– like media, or brushes with wire bristles. Currently, this technique is mostly applied in industrial settings and household in-line filters. No portable products are currently targeting the outdoor market.

Comparative Studies and Preferred Techniques Presumably, standard protocols for product testing in experienced laboratories would provide comparable and reproducible results. However, studies that directly compare techniques or products often yield results that vary widely from the individual product testing. Data for the effectiveness of water disinfection techniques for wilderness travelers are essentially all done in the laboratory and not in field settings during actual use. On the other hand, many studies have recently been done on point-of-use devices in households and refugee settings in developing countries, where contamination and the risk for illness are many times higher, so techniques can be evaluated for both microbiologic reduction under real use and reduction of illness attributable to water treatment (Table 67-16). Moreover, these techniques are necessarily low cost, simple to use, and include some improvised methods, which make them particularly valuable for survival, disaster, or other austere situations characterized by suboptional conditions and supplies. Furthermore, the need for household point-of-use water treatment in developing countries is stimulating innovative approaches to disinfection that combine multiple treatment steps in series, as is done in municipal plants. For those tasked with engineering water solutions for communities or populations in austere environments, point-of-use methods were found to be more effective than were source solutions.60,155 Several studies comparing halogens are noted in the Iodine Versus Chlorine section.128,137,139,211,248 Lee and Lee160 compared iodine, chlorine dioxide, mixed oxidants, and UV radiation (UVR) 1347

CHAPTER 67  Field Water Disinfection

BOX 67-13  Solar Disinfection (SODIS)

PART 8  FOOD AND WATER

TABLE 67-16  Efficacy and Effectiveness of Point-of-Use Technologies for Developing World Households Treatment Process

Pathogen

Ceramic filters

Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa Bacteria Viruses Protozoa

Free chlorine Coagulation/chlorination Biosand filtration SODIS

Optimal Log Reduction*

Expected Log Reduction†

Diarrheal Disease Reduction‡

2 0.5 4 3 3 3 7 2-4.5 3 1 0.5 2 3 2 1

63% (51%-72%) for candle filters 46% (29%-59%) for bowl filters 37% (25%-48%)

6 4 6 6 6 5 9 6 5 3 3 4 5.5 4 3

31% (18%-42%) 47% (21%-64%) 31% (26%-37%)

Data from multiple studies, analyzed and summarized by Sobsey and colleagues.262 SODIS, Solar disinfection. *Skilled operators using optimal conditions and practices (efficacy); log reduction: pretreatment minus post-treatment concentration of organisms (e.g., 6 log = 99.999% removal). † Actual field practice by unskilled persons (effectiveness). Depends on water quality, quality and age of filter or materials, following proper procedure, and other factors. ‡ Summary estimates from published data. Vary with consistency and correct use of technique, integrity of techniques (e.g., cracked filter), and other household sanitation measures.

contamination, methods of disinfection available, and tolerance of risk.

for disinfection of coccidian oocysts to represent Cryptosporidium and found that only UVR consistently inhibited sporulation. Iodine in recommended contact times was little better than controls, and chlorine dioxide left nearly one-quarter of oocysts viable in moderately contaminated water and was similar to controls in highly contaminated water. One important factor may have been the large number of organisms added to the water, which greatly exceeded likely levels encountered in surface water. Betancourt and Rose reviewed methods for removal of Cryptosporidium and found UVR and filtration effective.18 Sobsey and colleagues262 reviewed data for point-of-use methods for household disinfection in developing countries. All methods had high levels of optimal effectiveness, but their actual efficacy was much less over time, likely impacted by inconsistent use. Verma and Arankalle290 evaluated eight different higher-technology household disinfection units sold in India that each used some combination of filtration, iodine resin, chlorination, and UVR. Average removal of hepatitis E virus was 1 to 3 log, except for a hollow-fiber membrane unit that achieved 6.5-log removal. This study highlights the incorporation of common disinfection techniques into household appliances for point-of-use water treatment and the discrepancy between optimal and actual efficacy for these devices, which would certainly apply to field units as well. Similarly, another study compared ceramic filters and iodine resin household devices and found high levels of bacterial removal, but that reduction of viruses and microspheres did not meet standards of EPA protocols.59 One recently developed household device that does not require power and combines the complementary methods of filtration and disinfection did meet EPA criteria for microbiologic reduction.59 Although the gap between optimal and actual efficacy is disturbing, it is reassuring that in actual field conditions, all point-of-use techniques will markedly decrease the number of microorganisms and risk for illness.60,262 As in any wilderness medical situation, some basic assessment must be done of the likely level and type of

PREFERRED TECHNIQUE Field disinfection techniques and their effects on microorganisms are summarized in Table 67-17. The optimal technique for an individual or group in the wilderness or traveling in developing countries depends on the number of persons to be served, space and weight available, quality of source water (Table 67-18), personal taste preferences, and availability of fuel. The most effective technique may not always be available, but all methods will greatly reduce the load of microorganisms and reduce the risk for illness. A multibarrier approach for drinking water treatment in which a combination of various disinfectants and filtration technologies are applied for removal and inactivation of different microbial pathogens will provide a lower risk for microbial contamination.18 A combination of clarification using coagulation–flocculation and filtration followed by chlorination remains the standard for water treatment worldwide. The CDC and WHO also promote chlorine for household level point-of-use disinfection in the developing world.155 In austere situations such as disasters or refugee camps, hypochlorite (household bleach) or chlorination– flocculation packets may be available. If not, the SODIS technique or sand filters can be used with improvised materials. For environments with a high-quality, low-risk source water, any of the primary techniques is adequate, understanding that the limitation for halogens is Cryptosporidium oocysts, and that microfilters may not remove all viruses. Surface water, even if clear, in undeveloped countries where there is human and animal activity should be considered highly contaminated with enteric pathogens. Optimal protection requires heat, ultrafiltration, UVR, or a two-stage process of filtration and halogens. Chlorine dioxide or mixed species techniques are currently the only one-step

TABLE 67-17  Summary of Field Water Disinfection Techniques

Heat Filtration Halogens Chlorine dioxide

Bacteria

Viruses

Giardia/Amebae

Cryptosporidium

Nematodes/Cercaria

+ + + +

+ +/−* + +

+ + + +

+ + − +

+ + +/−† +/− †

Most filters make no claims for viruses. Reverse osmosis and Sawyer 0.02 µm hollow-fiber filter technology can be effective. General Ecology claims virus removal. Eggs are not very susceptible to halogens but are very low risk for waterborne transmission.

*

†

1348

“Pristine” Wilderness Water With Little Human or Domestic Animal Activity Primary concern

Giardia, enteric bacteria

Effective methods

Any single-step method† Low-risk water; many would choose to drink untreated

Developed or Developing Country Tap Water in Developing Country

Clear Surface Water Near Human and Animal Activity*

Bacteria, Giardia, small numbers of viruses Any single-step method†

All enteric pathogens, including Cryptosporidium 1. Heat 2. Filtration plus halogen (can be done in either order) 3. Hollow-fiber ultrafiltration 4. Chlorine dioxide 5. Ultraviolet (commercial product, not sunlight)

Risk varies depending on country; judgment required for decision to treat

Cloudy Water All enteric pathogens plus microorganisms CF followed by second step (heat, filtration, or chemical)

CF, Coagulation–flocculation. *Includes agricultural run-off with cattle grazing or sewage treatment effluent from upstream villages or towns. † Includes heat, filtration, halogens, chlorine dioxide, ultraviolet irradiation.

chemical processes available. Even in the United States, water with agricultural runoff or sewage plant discharge from upstream towns or cities must be treated to remove Cryptosporidium and viruses. In addition, water receiving agricultural, industrial, or mining runoff may contain chemical contamination from pesticides, other chemicals, and heavy metals. A filter containing a charcoal element is the best method for removing most chemicals. Water from cloudy low-elevation rivers, ponds, and lakes in developed or developing countries that does not clear with sedimentation should be pretreated with coagulation–flocculation and then disinfected with heat or halogens. Tablets combining coagulation–flocculation and chlorination are readily available and have extensive testing to demonstrate effectiveness.72,87,211,225 Filters can be used but will clog rapidly with silted or cloudy water. A sand filtration unit can be improvised.150 Coagulation– flocculation will also remove some chemical contamination. The preferred method of treatment for the military, when large-scale equipment can be brought to the site, is a reverse osmosis water purification unit, because it can produce highquality water from a low-quality source. For smaller groups, the military relies mainly on monitored chlorine. Individual means include iodine tablets, Chlor-Floc tablets, and chlorine liquid bleach.280 Chemical agents need to be used when water will be stored, such as on a boat, in a large camp, or for disaster relief. When only heat or filtration is used before storage, recontamination and bacterial growth can occur. Hypochlorite still has many advantages for stored water, including cost, ease of handling, and minimal volatilization in tightly covered containers.185 A minimum residual of 3 to 5 mg/L should be maintained in the water. Superchlorination–dechlorination is especially useful in this situation because high levels of chlorination can be maintained for long periods, and when ready for use, the water can be poured into a smaller container and dechlorinated. Iodine works for short-term but not prolonged storage, because it is a poor algicide. Silver has been approved by the EPA for preservation of stored water. Chlorine dioxide does not maintain a residual concentration. On ocean-going vessels where water must be desalinated during the voyage, only reverse-osmosis membrane filters are adequate. Halogens should then be added to the water in the storage tanks.

Prevention and Sanitation Studies in developing countries have demonstrated a clear benefit in the reduction of diarrheal illness and other infections from safe drinking water, hygiene, and adequate sanitation.* Although

*References 60, 134, 166, 182, 217-218, 226, 260.

a benefit can be demonstrated for these interventions independently, the benefit is greater when all are applied together, especially with appropriate education.53 Wilderness travelers essentially live in conditions similar to the developing world, without running water or sanitation. Unfortunately, many wilderness travelers confuse the continuing need for hygiene with the need to relax their standard of cleanliness.

HAND WASHING Personal hygiene, mainly hand washing, prevents spread of infection from food contamination during preparation of meals.181 A widely publicized study in the United States demonstrated that only 67% of Americans wash hands after using a public toilet. No one with a diarrheal illness should prepare food. A study of Appalachian Trail hikers showed that water disinfection, routine hand washing, and proper cookware cleaning were all associated with decreased diarrhea.27 A Shigella outbreak among river rafters on the Colorado River was investigated and assumed to be waterborne from adjacent Native American communities, but was finally traced to infected guides who were shedding organisms in the stool and contaminating food through poor hygiene.181 Simple hand washing with soap and water purified with hypochlorite (bleach) significantly reduced fecal contamination of market-vended beverages in Guatemala.255 Extensive research in the developing world has demonstrated that water is often recontaminated before use, and proper storage techniques can decrease this risk for contamination.260,304 In a refugee camp, using only a simple improved bucket that did not allow dirty hands or a ladle to touch the water, there was a 69% reduction in mean fecal coliform levels in the household water and 31% less diarrheal disease in children under 5 years of age among the group.235 For water access, narrow-mouth jars or containers with water spigots prevent contamination from repeated contact with hands or utensils.225,235,255

KITCHEN AND FOOD SANITATION Sanitation should extend to the kitchen or food preparation area.166 In addition to hand washing, dishes and utensils should be disinfected by rinsing in chlorinated water, prepared by adding enough household bleach to achieve a distinct chlorine odor. Hargreaves tested various combinations of wash and rinse water in three-bowl systems to determine what worked best for cleanliness, bacterial disinfection, and residual smell or taste of disinfectant. The optimal combination was water plus detergent in bowl 1 to remove the majority of food residue and grease; water with 10 mL added bleach in bowl 2 to remove the remaining food residue and provide disinfection; and plain water in bowl 3 to remove residue of disinfectant. This is a variation of the most commonly used method that adds the disinfectant to bowl 3 instead of bowl 2. If there is insufficient water or containers to provide a three-bowl system, omit bowl 3.119 1349

CHAPTER 67  Field Water Disinfection

TABLE 67-18  Choice of Method for Various Source Water

PART 8  FOOD AND WATER

Washing fruits and vegetables in purified water is a common practice. Washing has a mechanical action of removing dirt and microorganisms while the disinfectant kills microorganisms on the surface. However, neither reaches the organisms that are embedded in surface crevices or protected by biofilms or other particulate matter, which is why it is safer to peel most fruits and vegetables with rough skins.145 When lettuce was seeded with oocysts, then washed and the supernatant examined for cysts, only 25% to 36% of C. parvum and 13% to 15% of C. cayetanensis oocysts were recovered in the washes. Scanning electron microscopy detected oocysts on the surface of the vegetables after washing.202 A review of washing lettuce with various disinfectant solutions shows that high concentrations usually reduce level of viruses by 1 to 3 log.10 Chlorine, iodine, or potassium permanganate are often used for this purpose in higher concentrations than would normally be palatable for drinking water. In the United States, chlorine wash at 20 to 200 ppm is the most commonly used sanitizing treatment by the fresh produce industry. The ultimate responsibility for wilderness travelers is proper sanitation to prevent contamination of water supplies from human waste. Some suggest that campers smear feces on rocks. Desiccation occurs, and UV rays in sunlight eventually inactivate most microorganisms, but rain may first wash pathogens into a water source.56 Moreover, it will be repulsive to other campers. In the Sierras, feces left on the ground generally disappeared within 1 month, but it was not known whether disinfection occurred before decomposition or whether the feces washed away, dried, or were blown in the wind.220 Despite more rapid decomposition in sunlight rather than underground, burying feces is still preferable in areas that receive regular use. In the soil, microorganisms can survive for months.283 A Sierra Club study found more prolonged survival in alpine environments.220 The investigator marked group latrines in alpine terrain and returned 1 to 2 years later to dig test trenches. He found a thin crust of decomposition covering unaltered raw waste with high coliform bacteria counts. Microorganisms may percolate through the soil. Most bacteria are retained within 50.8 cm (20 inches) of the surface, but in sandy soil this increases to 22.9 to 30.5 m (75 to 100 feet)5; viruses can move laterally 22. 9 to 92 m (75 to 302 feet).246 When organisms reach groundwater, their survival is prolonged, and they often reappear in surface water or wells.283 The U.S. military and U.S. Forest Service recommend burial of human waste 20.3 to 30.5 cm (8 to 12 inches) deep and a

minimum of 30.5 m (100 feet) from any water.5,287Decomposition is hastened by mixing in some dirt before burial. Shallow burying is not recommended because animals are more likely to find and overturn the feces. Judgment should be used to determine a location that is not likely to allow water runoff to wash organisms into nearby water sources. Groups larger than three persons should dig a common latrine to avoid numerous individual potholes and inadequate disposal. To minimize latrine odor and improve its function, it should not be used for disposal of wastewater. In some areas the number of individual and group latrines is so great that the entire area becomes contaminated. Therefore sanitary facilities (outhouses) are becoming common in high-use wilderness areas. Popular river canyons require camp toilets, and all waste must be carried out in sealed containers.

APPENDIX A 

WATER DISINFECTION DEVICES AND PRODUCTS FOR FIELD USE Product lines are continuously evolving, and prices change frequently and vary widely. For most of these products, claims are substantiated only by company sponsored and designed testing. Some results have been extrapolated to similar products. Products are tested using a standardized Environmental Protection Agency (EPA) protocol: depending on claims, filters must demonstrate removal or inactivation of 103 cysts (99.9%), 104 viruses (99.99%), and 106 bacteria under varying water conditions of temperature and turbidity. Objective, comparable test results for these products are not available. Filter capacity is highly variable, depending on clarity of water. Numbers cited for capacity are usually based on clear water; testing using slightly turbid river water and following manufacturer instructions for cleaning reveals markedly different values. For all filters, it is recommended to pump dilute bleach solution through the unit after each trip and dry thoroughly before storage to decrease bacterial growth in the filter.

APPENDIX A Katadyn Endurance Series Product

http://www.katadyn.com Price

Pocket Filter (Figure 67-4, online)

$250-290

Combi (Figure 67-5, online) Accessories: prefilter bottle adaptor, carrying bag

$130

Expedition (Figure 67-6, online)

$1200

Ceradyn (Figure 67-7, online) and Gravidyn

$200-250

Siphon filter (Figure 67-8, online)

$65

1350

Structure/Function Endurance filters contain a 0.2-µm ceramic candle filter, silver impregnated to decrease bacterial growth. Large units also contain silver quartz in center of filter. Hand pump; 40-inch intake hose and strainer, zipper case; in-line carbon cartridge available; size: 10 × 2.4 inches; weight: 20 oz; flow: 0.75-1 L /min; capacity: 50,000 L. Small hand pump with ceramic filter and activated charcoal granule stage; with the optional “PLUS” package, the Combi can be connected to a water faucet for use in campers, cottages, or boats. Size: 2.4 × 10.4 inches; weight: 21 oz; flow: 1.0 L/min; capacity: up to 50,000 L; charcoal capacity: 200 L. Large hand pump with steel stand for medium to large groups; size (packed in case): 23 × 6 × 8 inches; weight: 12 lb; flow: 4 L/min; capacity (per filter element): up to 100,000 L. Gravity drip from one plastic bucket to another with three ceramic candle filter elements. Ceradyn uses ceramic candle filters, whereas Gravidyn filter candles combine ceramic and activated carbon elements; size: 18 inches × 11 inches diameter (26 inches high when assembled), 10 L water container; weight: 7 lb; flow: 4 L/hr; capacity: up to 150,000 L. Gravity 0.2-µm ceramic siphon filter element without reservoir bag that can be used to make a gravity system out of any water container. Place one or more Siphon filter elements into a container, and let the water run through the hose into a lowerpositioned vessel. Size: 6.3 × 2.6 inches; weight: 16 oz; flow: 5 L/hr; capacity: about 20,000 L.

Katadyn Backcountry Series Product

Price

Vario (Figure 67-9, online)

$90

Hiker and Hiker Pro (Figure 67-10, online)

$60-80

Base Camp (Figure 67-11, online)

$70

Structure/Function Hand pump; 0.3-µm pleated glass fiber filter with 143 inches2 surface area, ceramic prefilter, and activated charcoal stage; attaches directly to water bottle; size: 7.5 × 4.0 inches; weight: 15 oz; max flow: 2 L/min (36 stokes/L); capacity: 2000 L. Hand pump; 0.3-µm pleated glass fiber with 107-square-inch surface and activated carbon core; size: 6.5 × 2.4 × 3 inches; weight: 11 oz; flow: 1 L/min (48 strokes/L); capacity: 750 L. Gravity filter with a 0.3-µm glass fiber filter (Hiker filter cartridge) plus granular charcoal; includes dirty water reservoir bag and tubing; size: 3 × 6.5 × 2.4 inches; weight: 11 oz; flow: 1 L/hr; capacity: 750 L.

Katadyn Ultralight Series Product Mini (Figure 67-12, online)

Price $90

Water bottles Exstream MyBottle (Figure 67-13, online)

$50

Microfilter

$40

Structure/Function Smaller, lighter hand pump; 0.2-µm ceramic filter with activated carbon; 31-inch intake hose and strainer, hard plastic enclosure and pump; size: 3.2 × 7 × 2 inches; weight: 8 oz; flow: 0.5 L/min; capacity: approx 7000 L. Drink-through bottle with three-stage water filter: 1-µm plastic membrane cyst filter for protozoa, pentaiodide iodine resin(ViruStat), and activated carbon; weight: 7 oz, size: Exstream 21 oz (bike bottle size), XR 28 oz; cartridge capacity: 26 gal. Drink-through bottle with 0.3-µm glass fiber filter and activated charcoal (optional iodine resin); weight: 8 oz; size: 10 inches high, 24 oz; capacity: up to 26 gal.

Katadyn Claims Endurance series and mini with ceramic and carbon filter elements remove bacterial pathogens, protozoan cysts, parasites, nuclear debris. Clarifies cloudy water. If filter clogs, brushing the filter element (which can be done hundreds of times before needing to replace the filter element) can restore flow, or filter elements can be replaced. Claims for removal of viruses by ceramic filters not made in the United States. Pocket Filter has a lifetime warranty. Vario and Hiker are microfilters designed for high-quality surface water. They will eliminate Giardia, Cryptosporidium, and most bacteria; activated carbon core “reduces chemicals and pesticides, plus improves taste of water.” Filters with large surface area are “guaranteed not to clog for 1 year.” Exstream with iodine resin filter passed EPA tests to remove 3-log cysts, 4-log viruses, and 6-log bacteria. Patented ion-release technology and carbon scrubber dramatically reduce residual iodine. I5 is 1000 times more effective than I3 resin. Comments Well-designed, durable products that are effective for claims. However, high filter volume capacity is optimistic and not likely to be achieved filtering average surface water. Backpacker magazine field tests found the flow comparatively slow, requiring more energy to pump and frequent cleaning. Abrading the outer surface can effectively clean ceramic filters; after multiple cleanings, it is necessary to use the gauge to indicate when filter thickness becomes too thin. Pocket Filter is the original individual or small group filter design. Metal parts make it durable, but the heaviest for its size. Expedition filter is popular for larger groups, especially river trips, where weight is not a factor. Complete virus removal cannot be expected, although most viruses clump or adhere to larger particles and bacteria that can be filtered. Silver impregnation does not prevent bacterial growth in filters. Vario and Hiker were designed for the domestic backpacking market with higher water quality, where cysts and bacteria are threats, but viruses are less of a problem. The Hiker received top ratings by Backpacker magazine for field tests evaluating user-friendliness. These filters may be used with a halogen disinfectant for international travel or conditions, where high levels of contamination are possible. Bottle filter with iodine resin is currently the only water bottle or filter product available with iodine resin (see text). Drink-through design limits to single-person day use. The filter design with charcoal removing residual iodine and ingestion directly from the filter allows no contact time and may not provide complete viral protection in all situations. Katadyn Desalinators Reverse Osmosis Filters Desalinator Survivor 06 (Figure 67-14, online) Survivor 35 (Figure 67-15, online)

$1425

Powersurvivor 40E

$2499

$550

Hand-operated pump, reverse osmosis membrane filter with prefilter on intake line; size: 2.5 × 5 × 8 inches; weight: 2.5 lb; flow: 40 strokes/min yields 0.9 L /hr. Hand-operated pump, reverse osmosis membrane filter with prefilter on intake line; size: 3.5 × 5.5 × 22 inches; weight: 7 lb; flow: 30 strokes/min yields 4.5 L/hr. Smallest power-operated model in this line of reverse osmosis filters; uses only 4 amps, so can run for extended periods on 12-volt power source; converts to manual operation in emergencies; contains 40% fewer parts than its predecessor; pump size: 6.75 × 16.5 × 15.5 inches; prefilter 12 × 6 inches; Weight: 11.33 kg (25 lb); flow: 5.7 L/hr.

Reverse Osmosis Filters Claims Reverse osmosis units desalinate, removing 98% of salt from seawater by forcing water through a semipermeable membrane at 800 psi. In the process, microorganisms are filtered out. The manual operation of these units makes them unique and useful for survival at sea or for use in small craft without power source. Comments Reverse osmosis units are nanofilters capable of removing sodium molecules, as well as all microorganisms, including viruses. They are included here for sea kayaking and small boat journeys in open water. These units can obviate the need for relying solely on stored water or can be carried for emergency survival. Reverse osmosis filters currently are not practical for land travel because of cost, weight, and flow rates; however, the U.S. military uses truck-mounted reverse osmosis filters on land for their ability to handle brackish water and remove all types of microorganisms. Note that the company does not make claims for viral removal because they assume that the membrane is imperfect and some pores will be imprecise, perhaps allowing viral passage. Higher-flow power models are available from the company (Model 80E, 160E). Continued

CHAPTER 67  Field Water Disinfection

APPENDIX A—cont’d

PART 8  FOOD AND WATER

APPENDIX A—cont’d British Berkfeld

U.S. distributor: James Filter http://www.jamesfilter.com/

Product

Price

Berkey Filters Models include: Travel, Big Berkey, Royal, Imperial, Berkey Light (Lexan, not stainless steel) SS-4

Structure/Function A line of stainless steel stacked bucket filters that operate by gravity drip and can accommodate variable numbers of candle filter elements. There are two types of filter elements: (1) ceramic with carbon core and silver impregnation, and (2) compressed carbon impregnated with silver (Black Berkey). The size of the lower reservoir varies from 1.5-6 gal. Price varies by size and number of filter elements. Flow depends on number of filters elements. Stacked stainless steel containers with four 7-inch ceramic filters with activated carbon core; gravity flow; size: 20 × 8.5 inches (15 inches when nested); weight: 6.0 lb; flow: 24 gal/day; 2 gal capacity of lower container, capacity: 6,000 gal.

$220

British Berkfeld Claims and Comments Ceramic filter is 0.9 µm absolute, but filters >99.99% of particles larger than 0.5 µm. Removes 100% cysts and 4-5 log bacteria. Complete protection requires chlorine treatment as the first step. Black (compressed carbon) filters remove 4- to 5-log cysts and bacteria. The bucket filters are excellent for stationary base camps or expatriate homes. Ceramic candle filters will perform better than the carbon ones. AquaRain Filter Systems AquaRain 200 (Figure 67-16, online) AquaRain 400 (Figure 67-17, online)

$160-200 $240-320

http://www.aquarain.com Stainless steel containers (3 gal each) with one to four silver impregnated ceramic filters with carbon core; gravity flow; size: 22 × 10.25 inches; weight: 10 lb; flow: 1 gal/hr with four elements, 16 gal/day with two; capacity: 30,000-60,000 gal. Price depends on size and number of filter elements.

AquaRain Claims and Comments Filter has 0.2-µm absolute pore size, removes 100% cysts and 4-log reduction of bacteria. Ceramic elements can be cleaned 200 times before replacement. Similar design as Berkfeld and Katadyn bucket drip filters, although ceramic elements differ slightly. No claims for viruses. General Ecology, Inc Product

http://www.generalecology.com Price

Structure/Function

All filters contain 0.1-µm (0.4-µm absolute) Structured Matrix filter in removable canister. Hand pump with intake strainer; outflow end connects directly to common water bottle and adaptors available for Platypus bottles; self-cleaning prefilter float; size: 6 × 6 inches; weight: 15 oz; flow: 2 L/min; capacity: 600 L. Trav-L-Pure (Figure 67-19, $198 Filter and hand pump in rectangular housing (1.5-pt capacity); pour water into housing, then online) pump through prefilter and microfilter; size: 4.5 × 3.5 × 6.75 inches; weight: 22 oz; flow: 1-2 pt/ (Carrying case included.) min; capacity: 100-400 L. Trav-L-Pure Camper (Figure $88 Trav-L-Pur canister with attachment to hose bib for recreational vehicles and trailers requires 67-20, online) water pressure of 20 psi; flow: 0.5 gal/min (1.9 L/min); capacity: 570 L Base Camp (see Figure 67-11, $650 Stainless steel casing and hand pump connected by tubing; size: canister 4.1 × 8.8 inches, pump online) 1.5 × 10.5 inches; weight: 3 lb; flow: 2 L/min; capacity: 500 gal. Also available with electric pump and can be hooked up in series to provide higher capacity and flow. General Ecology has an extensive product line of larger-capacity filters for use on cars, boats, aircraft, and other situations requiring high-volume output where power is available. These use the Seagull IV purifier cartridge with a pump that pushes water through the system and a prefilter that can be cleaned. They can be operated off regular current or vehicle battery. General Ecology Filters Claims First Need Filter is a proprietary blend of materials including activated charcoal. “Microfiltration” with 0.1 µm retention (0.4 µm absolute) “removes bacteria and larger pathogens” (cysts, parasites). “Adsorption and molecular sieving:” carbon absorbers remove chemicals and organic pollutants that cause color and taste; cavities in surface of adsorption material draw particles in deeper. Does not remove all dissolved minerals or desalinate. Proprietary process also creates ionic surface charge that removes colloids and ultra-small particles through “electrokinetic attraction.” Has passed laboratory tests as a purifier under single-pass conditions without added chemicals or hold time, reducing test virus by 104 as well as bacteria by 106 and Cryptosporidium by 103. Comments Reasonable design, cost, and effectiveness. All units use the same basic filter design. Most testing with Escherichia coli and Giardia cysts show excellent removal. Although they have not tested with hepatitis virus, testing with rotavirus and poliovirus indicate effectiveness against viruses. Charcoal matrix will remove chemical pollutants. Despite viral claims, recommend caution in highly polluted water; prior disinfection with halogen or clarification with coagulation–flocculation would provide additional security, and coagulation–flocculation would extend filter life, whereas filter carbon would subsequently remove halogen. The filter cannot be removed to clean, although it can potentially be back-flushed; so it must be replaced when clogged. First Need XL Portable Water Filter (Figure 67-18, online)

$109

Cascade Designs and MSR Product

http://www.cascadedesigns.com/MSR Price

Miniworks EX (Figure 67-21, online)

$90

SweetWater Microfilter (Figure 67-22, online) Purifier Kit with Microfilter, purifier solution and Platypus water bag Purifier solution

$90 $90

$10

Structure/Function Hand pump with cylindric ceramic filter with block carbon core, porous foam intake filter, and 10-µm stainless steel wire mesh screen; pressure-relief valve releases at 90-95 psi; storage bag (2 or 4 L) attaches directly to outlet of pump; size: 2.75 × 7.5 inches; weight: 16 oz; flow rate: 1 L/min (85 strokes/L); capacity: 400-2000 L (400 L under average conditions). Lexan body and pump handle; 80-µm metal prefilter; in-line 4-µm secondary filter; labyrinth filter cylinder of borosilicate fibers removes pathogens to 0.2 µm; granular activated carbon; safety pressure-relief valve; end-of-life indicator; outflow tubing has universal adapter that fits all water bottles; optional input adapter that attaches to sink faucet while traveling; size: 7.75 × 2 inches; weight: 11 oz; flow: 1.25 L/min (new filter); capacity: 750 L. A chlorine-based purifier solution containing 3.5% sodium hypochlorite; add 5 drops to each liter of filtered water, mix for at least 10 seconds, and wait 5 minutes

Product

Price

Structure/Function

HyperFlow (Figure 67-23, online)

$100

Hand pump using 0.2-µm hollow-fiber filter; attaches directly to top of water bottle for pumping; maintenance kit and replacement cartridges available; size: 7 × 3.5 inches; weight: 7.4 oz; flow: 3 L/min (1 L/20 strokes); capacity: about 1000 L.

AutoFlow (Figure 67-24, online) Platypus CleanStream Gravity Filter (Figure 67-25, online) Miox Purifier (Figure 67-26, online)

$100

Gravity drip filter using hollow-fiber filter cartridge; size: 4 × 6 inches; reservoir capacity: 4 L; weight: 10.5oz; flow: 1.75 L/min; capacity: about 1500 L/cartridge. 0.2-µm hollow-fiber filter cartridge gravity drip in-line system or can be used in personal hydration pack system; size: 1.8 × 5.7 inches; weight: 13.7 oz; flow: 4 L in under 2.5 min; capacity: about 1500 L. New technology created by military, uses salt, water, and electrical current generated from camera batteries to produce mixed-species disinfectant solution that is added to water; kit comes with pen, batteries, salt packet, indicator strips, instructions, storage sack; refills of salt cartridge are available; size: 7 × 1 inches; weight: pen 3.5 oz, kit 8 oz; battery life: about 200 L.

$90 $140

Cascade Designs and MSR Claims Miniworks EX Fully field-maintainable, meaning that all elements can be removed, cleaned, and replaced. Removes protozoa (including Giardia and Cryptosporidium), bacteria, pesticides, herbicides, chlorine, and discoloration. Meets EPA standards for removal of cysts and bacteria. Ceramic filters reduced turbidity from 68.8 NTU to 0.01 NTU. Carbon has been shown to reduce levels of iodine from 16 mg/L to <0.01 mg/L for at least 150 L. SweetWater Filter Eliminates Giardia, Cryptosporidium, and other critical bacterial and protozoan pathogens, pollutants, heavy metals, pesticides, and flavors. Cartridge accessory. Lighter, more compact and durable than comparable models, and easiest to clean or replace. The company recycles filter cartridges. HyperFlow and AutoFlow Effective against bacteria, particles, and protozoa, but not against viruses, chemicals, or toxins. Miox Just add water, shake, and press a button. Solution generated is then added to drinking water. Inactivates all bacteria, viruses, and protozoa. Viruses and bacteria require dwell time of 15 min, Giardia 30 min, Cryptosporidium 4 hr. Can be used for individuals or groups. LED lights indicate if low battery or if inadequate reagents (salt and water). Test strips are used to test water for adequate chemical residual. Cascade Designs and MSR Comments Miniworks EX Excellent filter design and function. Prefilters protect more-expensive microfilter. Effective for claims; high quality control and extensive testing. No claims are made for viruses, although clumping and adherence remove the majority (currently 2- to 3-log removal, but not 4-log required for purifiers). Reservoir bag that attaches to outflow for filtered water storage is convenient. Filter can be easily maintained in the field; maintenance kit and all replacement parts available. Ceramic filters can be cleaned by abrading outer surface many times without compromising the filter. A simple caliper gauge indicates when filter has become too thin for reliable function. SweetWater Well-designed filter at a reasonable price. Pressure-release valve indicates when filter needs cleaning, but this can be a problem as the filter clogs. A brush is provided for cleaning, and cartridges are replaceable. HyperFlow and AutoFlow These use microtubule, hollow-fiber technology that can provide higher flow rates with less pressure, which makes them amenable to gravity systems. HyperFlow is the first hand pump with microtubules, but others are likely to follow. Miox The science has been known for some time and is used in large commercial processes (http://www.miox.com), but previously was not available in a portable design. Although difficult to measure various disinfectant species generated, testing has confirmed that disinfectant activity is greater than with comparable concentrations of sodium hypochlorite. The active oxidant disinfectant that kills Cryptosporidium is assumed to be chlorine dioxide. The extended dwell time indicates low concentrations of this disinfectant and the need to plan for prolonged contact time, if Cryptosporidium is a strong concern. High-technology approach will appeal to some but be intimidating to others. The indicator lights and test strips add reassurance that process is proceeding effectively. Although this technique can be used for large volumes, this instrument generates enough for only 1 L at a time and may be difficult to use for larger-volume containers. Sawyer Products

http://www.sawyerproducts.com/

Product

Price

Structure/Function

PointOne Filter Water Treatment System (Figure 67-27, online) (includes 2-L dirty water bag, in-line filter, faucet adaptor) Complete System (includes above plus clean water bag), available in 2 L, 4 L, 8 L 4-L Purifier system Filter Bucket Adaptor 0.1 Filter Bucket Adaptor 0.02 (Figure 67-28, online) Squeeze Water Filter (includes 12, 16, and 32 oz pouches, water filter, and pop-up drinking spout) Point One 10˝ Filter Unit

$60 $100

0.1-µm (absolute) hollow-fiber membrane filter, composed of a cluster of microtubules. Purifier filter has 0.02-µm fiber filter. Water is drawn through the walls of the tubules by suction, gravity, or pressure applied by squeezing a bottle; both filter cartridges can be adapted as in-line cartridge for backpack water systems, gravity drip, faucet in-line systems, or polycarbonate drinking bottle with filter. Activated charcoal prefilter cartridge included for optional use; flow: depends on method used, about 1.5 L/min, 5 gallons/30 min via gravity feed system; 30 mL/sec from drink-through; capacity: 1 million gal, but depends on clarity of source water. Kit to attach filter cartridge to a plastic bucket or barrel for gravity drip; comes with hole cutter, adapter, and tubing to construct system. Either 0.1- or 0.02-µm cartridge can be used; flow: up to 540 gal/day. 0.1 micron hollow fiber filter cartridge attaches to bags that can be squeezed to maximize flow. Squeeze water into water bottle or drink directly from the filter; weight: 3 oz; capacity: 1 million gal Filter cartridge and regulator with 0.1 absolute hollow fiber membrane that attaches in-line to water line or plumbing; for school, hospital, and other settings with highvolume needs; regulator allows safe cleaning of the filter by backwashing at an exact pressure; size: 10˝ long; flow: 5000 gal/day.

$130 $236 $62 $145 $60 $700

Continued

CHAPTER 67  Field Water Disinfection

APPENDIX A—cont’d

PART 8  FOOD AND WATER

APPENDIX A—cont’d Claims Microtubule technology (Figure 67-29, online) allows unprecedented flow rates and 0.1- or 0.02-µm absolute filtration. Highest level of biological filtration available on the market today; exceeds EPA standards. GAV prefilter removes lead, chlorine, odors, and taste sediment, whereas the microfilter removes bacteria, protozoa, and cysts. Biologic filters 0.1-µm filter removes 7-log (99.9999%) bacteria and 6-log protozoa, but makes no claims for viruses; add chlorine to kill viruses. The Zero Point Two absolute purifier removes 99.99999% of bacteria, 99.9999% of protozoa and cysts, and 99.9997% of viruses from the water. It is impossible for any bacteria, protozoa, cysts, and viruses to pass through the filter. Filters can be back-washed and are able to handle 40 psi, so they can be attached to faucets. Comments This technology has been used in industrial and medical processes, but only recently adapted to field water treatment. These filters were carefully designed and tested. They are highly versatile, because designed as a cartridge that can be used in various systems from drinking bottles, to gravity drip systems, to in-line household systems. They offer a potential advantage over other water bottle filters because the hollow-fiber technology provides faster filtration with less pressure. The charcoal cartridge compromises some of this low-pressure flow, so is supplied separately for use only when needed. This is the first low-pressure ultrafilter to claim viral removal through mechanical filtration alone. The million-gallon guarantee is based on the large surface area of the tubules. Bucket filter is a particularly creative application to these filters with many applications in rural or developing countries. Hydro-Photon Inc

http://www.steripen.com/

Product

Price

Structure/Function

Steri-Pen Classic Traveler (Figure 67-30, online) (Comes with a thermoformed nylon carrying case)

$60

Adventurer Journey (LCD display) (Figure 67-31, online) Freedom

$90 $100

Portable, battery-operated (4 AA-lithium) ultraviolet water disinfection system. Disinfects up to 16 oz of clear water in less than 1 minute and 32 oz in 90 sec by stirring UV element in water. Weight: 8 oz, with batteries; size: 7.6 × 1.5 × 1.5 inches; capacity: lamp lasts 8,000 treatments, lithium batteries, 200 treatments. Other models use 2 CR123 batteries and are significantly smaller and lighter. Lamp life is 8000 cycles and can expect up to 100 uses from batteries. Weight: 3.6 oz; size 6.1 × 1.5 × 1 inches. Weight: 4.5 oz; size: 7.3 × 1.6 × 1.3 inches.

Sidewinder

$100

$120

Smallest and lightest unit, rechargeable battery through computer USB, AC outlet, or solar charger. Weight: 2.6 oz; size: 5.1 × 1.4 × 0.8 inches; capacity: 40 treatments/charge; battery and UV lamp life: 8000 16 oz (0.5 L) treatments (1 L volumes disinfected by treating twice.) 1 L bottle fits into unit with hand crank that generates UV light without batteries. Weight: 16.6 oz; size: 8.6 × 5.5 × 3.8 inches; capacity: 8000 1 L treatments

Steri-PEN Claims Highly effective against bacteria, viruses, and protozoa, including Cryptosporidium oocysts. Ultraviolet light delivered destroys viruses, bacteria, and protozoa in 0.5 L (16 oz) of water in 48 seconds or 1 L (32 oz) in 90 seconds. Unit automatically turns off lamp after UV dose is delivered. Dose counter indicates when lamp replacement is necessary. Testing demonstrates that Steri-PEN meets the EPA standards as a microbiological water purifier. Steri-Pen Comments In general, UV light for water disinfection is well established with extensive science and widely used for water treatment in many large and varied applications, most of which require a fixed power and light source. The use of this portable technology is currently limited to small volumes of clear water; however the potential is great for further advances that will increase its uses in the field. The price of some units has already decreased. Currently, one can do slightly larger volumes with multiple cycles. The testing for this device can be found on the website. Since particulates block the UV rays and shield micro-organisms, testing was only successful in clear water, not in EPA “worst case scenario” water unless pre-filtered with microfiltration. Users must pre-filter or clarify cloudy water. The simplicity and rapidity of this technique is appealing. In units that run on AA batteries, the recommendation is to use lithium, not alkaline batteries. Puralytics

http://www.puralytics.com

Product

Price

Structure/Function

SolarBag

$80

Shield 500

$9500

3 L food grade clear plastic bag with clear top and black backing and a coating of titanium dioxide nanoparticles inside. Bag is filled with water and placed in sunlight, which activates the TiO2 to catalyze a reaction to form active disinfectants (see text). The bag has backpack and handle straps to carry to and from water source; inlet debris filter; can be hung for water storage and water can be dispensed by a valve into canteen or pot as required. For disinfection, bag is placed flat or hanging in direct sunlight; disinfection requires 1-2 hr on sunny day and 2-4 hr on cloudy day; for unknown water sources, a food-safe dye can be used as a tracer and timer—when the color has cleared, the water has been purified. Dry weight: 100 g; size: 3 L; capacity: 250 L; shelf life: > 2 yr. High volume unit that uses UV LEDs; size: 28 × 8 × 19 inches; weight: 89 lb; flow: 200-500 gal/day; power: 640 watts; pressure 15-60 psi; life span: 10 yr.

Claims Works through multiple photo-chemical processes. Selected wavelengths of UV light generate hydroxyl radicals (OH−) without any chemical additives. Disassociates and eliminates organic compounds from the water. Reduces heavy metal to less toxic, more elemental state and irreversibly adsorbs heavy metals, including mercury, lead, chromium, and arsenic. Disinfects pathogens more effectively than standard UV irradiation. After 2 hours in the sun on an 80° F sunny day, process will reduce 7-log bacteria, 5-log viruses, 90% heavy metals, and 90% organics. Comments This is a new and promising technology for field water disinfection and purification. Significant testing and literature is available because it has multiple applications in industry and community level water treatment. Testing according to the EPA protocol is currently being done, and the field product is expected to be commercially available soon. Blue food dye can also be used to assure continued function of bag.

Hydration Technology Innovations (HTI)

http://www.htiwater.com/hti.html

Product

Price

Structure/Function

X-Pack Ten 2-oz sports drink syrup charges and dye tabs

$64 $16.50

SeaPack Includes eight 4-oz. syrup charges Expedition Includes ten 120-mL syrup pouches, cleaning kit

$75

A plastic pouch with two compartments separated by a semipermeable membrane that provides ultrafiltration to 0.0005 µm (5 angstroms); fill one side with dirty or contaminated suspect water; add to the other side a specially formulated syrup supplied with the kit that contains salts and sugars. Volume: 1.8 L; weight: 3 lb, includes syrup charges; flow: 1 L/4 hr, can produce a total of over 5 L of hydration drink per day; capacity: good for a total of 10 days of use after first use. Dual-chamber pouch, 1.8 L capacity each, separated by semipermeable membrane with nominal pore size of 3-5 angstroms; flow: 0.5 L/ 5 hr at 20° C (68° F); capacity: 4 L from seawater, or up to 24 L from freshwater; filter life: 10 days. Dual-reservoir water bladder for use with clean or contaminated water; uses osmotic filter cartridge that works by forward osmosis from osmotic syrup; one 4-oz. (0.12 L) syrup pouch will filter about 2.5 L of water; capable of filtering fresh to brackish water; clean reservoir volume: 3.0 L, dirty reservoir volume: 2.5 L; flow: about 1 L/hr; filter life: 30-90 days (clean weekly). Dual 20-L cans with osmotic filter built into a standard water can cap; forward osmosis driven by one sports syrup pouch that fits into the cap; one syrup pouch will filter one 20-L can of fresh to brackish water; flow: about 1.7 L/hr; filter life: 30-90 days (clean weekly)

$299

HydroWell $389 Includes twenty 410-mL syrup pouches, cleaning kit Claims Forward osmosis—water is driven across the membrane, not by hydraulic pressure, but by osmotic pressure created by a standard sport drink powder on the clean side of the membrane. This syrup is formulated much like the concentrate for a typical sports drink containing about 4% sugar (this compares with some other sports drinks at 6% and soda at 12%). Capable of filtering highly turbid water (tested to 800 NTU). Minimum 3 yr shelf life when stored below 90° F. Comments Forward osmosis is based on sound technology, and these products provide a good solution for disaster supplies or survival cache with long shelf life. Less optimal when on the move, although the bags could be primed and carried throughout the day while filtering. For those who prefer fresh water, the resulting sweetened solution is a major disadvantage. Simple filters or chemical solutions are lighter and faster for fresh water but cannot handle brackish water like some of the HTI products can. Household and Large-Scale Field Products The following are included as examples of multistage products that are available for household or large-volume field water treatment. This is not a comprehensive list of products, and many others are available, including trailer-mounted reverse osmosis systems. These products require a power source and may require truck or trailer for transportation. Most chemical systems can be scaled up through using large containers or water bladders and multistation distribution systems. Hindustan Lever Limited

http://www.pureitwater.com/IN

Product

Structure/Function

Pureit

Microfiber mesh, carbon block prefilter, chlorination, granular activated carbon (GAC) final stage; designed to operate without fixed power source (but does require batteries) and without a piped-in water supply; weight: 4.1 kg; chamber capacity: 9 L; flow: 9 L/2-3 hr; disinfection capacity: 1500 L.

Claims By combining filtration with disinfection, the treatment unit has overcome some of the shortcomings of other household-based water treatment systems intended for low-income populations. Provides the protection-meeting criteria established by the U.S. EPA for water purifiers (6-log reduction of bacteria, 4-log reduction of viruses, and 3-log reduction of protozoan cysts) while being affordable ($0.01/L) and capable of achieving scaled-up and sustained adoption by vulnerable populations. Comments Rational combination of filtration, chlorination, and charcoal and an example of technology being developed for developing countries with poor water quality that is available to expatriates or base camps. Published test results. Global Hydration Water Treatment Systems Inc Can Pure Water Purification System Various models available

http://www.globalhydration.com/canpure-water-purification-system.htm

First Water Systems, Inc Responder, Outpost, Villager

http://firstwaterinc.com/Suwanee, Ga All units use high-strength UV bulb for disinfection with in-line prefilter for large particulates, a sediment filter to reduce turbidity, a carbon block for improving taste and smell; all units can be supplemented with residual chlorination system; run off variety of power sources, including solar, battery, or generator. Water bladder and distribution system available; filling station enables either four or six lines of people to obtain water at any given time. Aqua Bags for transport of clean water are 3-gal heavy-gauge food-grade plastic bags that weigh about 20 lb when full. Portable model with canister configuration that runs on solar, on-board 12-volt battery, AC or DC power; size: briefcase size, 20 × 17 × 9 inches; 45 lb, including wheeled case; flow: 4 gal (16 L)/min, or about 600 gal (2500 L)/day per battery. Semiportable model water purification system runs exclusively off integrated solar system and an on-board battery; size: fits in the back of a pickup truck, SUV, minivan, mounted on wheeled frame; weight: 160 lb; flow: 4 gal (16 L)/min, or about 600 gal (2500 L)/day per battery (enough water for a thousand persons per day with multiple batteries)

Dual-process purification system incorporating six-stage microfiltration system and UV disinfection; optional residual chlorination using NaDCC tablets; size: 58 × 58 × 74 cm; weight: 41 kg; output: 19,000 L/day, 13 L/min, up to 50,000 L/day; power requirements: small generator (130 watts), can also be run on 12-volt DC. Complete stand-alone water treatment system designed to produce potable water in remote field conditions, emergency and disaster situations. Compact, portable, capable of running off gas or diesel generator without electricity or gravity.

Responder Outpost-4

Comments The UV system forces the water to circulate around the UV bulb twice, providing significantly greater “contact time” and greater ability to neutralize biologic contamination. Cigarette lighter plug adapters for additional battery power and AC power. Using multiple batteries 1355 extends the usable time and the amount of water produced. All filters easily detach for rapid cleaning or replacement.

CHAPTER 67  Field Water Disinfection

APPENDIX A—cont’d

PART 8  FOOD AND WATER

APPENDIX B 

CHEMICAL DISINFECTION PRODUCTS See text for further discussion of halogens, chlorine dioxide, and silver.

IODINATION Iodine Solutions Iodine solutions commercially sold as topical disinfectants contain iodine, potassium or sodium iodide in water, and ethyl alcohol or glycerol (see Table 67-14). Iodide improves stability and solubility but has no germicidal activity and adds to the total amount of iodine ingested and absorbed into the body. “Decolorized” iodine solution contains iodide and should not be used for water disinfection.

IODOPHORS (POVIDONE–IODINE) These solutions bind diatomic iodine to a neutral polymer of high molecular weight, giving the iodine greater solubility and stability with less toxicity and corrosive effect.52,114 Povidone– iodine is a 1-vinyl-2-pyrrolidinone polymer with 9% to 12% available iodine. The iodophors are routinely used for topical disinfection, because they have less tissue toxicity than iodine solutions. Povidone is nontoxic. In aqueous solution, povidone–iodine provides a sustainedrelease reservoir of halogen; free iodine is released in water solution depending on the concentration (normally, 2 to 10 ppm is present in solution). Data indicate persistence of about 2 ppm of free iodine at a 1 : 10,000 dilution,114 equivalent to 0.1 mL (2 drops) added to 1 L of water. One report found these compounds similar in germicidal efficiency to other iodine-iodide solutions.52 Conflicting values for available iodine and free iodine in dilute solutions result from the complex chemistry of povidone–iodine.17,131

CRYSTALS (SATURATED SOLUTION) Because of limited solubility in water, iodine crystals may be used to generate an iodine solution for disinfection. A small amount of elemental iodine goes into solution (no significant iodide is present); the saturated solution is used to disinfect drinking water. Water can be added to the crystals hundreds of times before they are completely dissolved. To formulate this solution at home, put 4 to 8 g (exact amount does not matter) of crystalline iodine in a 1- or 2-oz bottle, and fill with water. Because iodine crystals evaporate in air, always keep covered with water. An alternative technique is to add 8 g of iodine crystals to 100 mL of 95% ethanol. Increased solubility of iodine in alcohol makes the solution less temperature dependent and allows much smaller volumes to be used (8 mg/0.1 mL), which can be measured with a 1-mL syringe or dropper (2 drops). Residual iodine can be removed with granular activated carbon. Product Polar Pure http://www.polarequipment.com/ Price: $16.00 Widely available through suppliers of outdoor products Formulation Eight grams of iodine crystals in a 3-oz glass bottle filled with water; 30 to 50 µm fabric prefilter provided; "trap" in bottle to catch crystals when pouring off water; capacity: 2000 qt; weight: 5 oz Instructions The bottle cap is used to measure iodine solution: one capful is approximately 6.5 mL. Directions and color-dot thermometer are printed on the bottle. Recommended dose: 2 capfuls if iodine solution is 20° C (68° F) yields 4 ppm iodine when added to 1 qt of clean water. To shorten contact time, warm water to 20° C (68° F) before adding iodine. Comments Saturated aqueous solution of crystalline iodine is an excellent and stable source of iodine. Recommendations are adequate for clear, warm water; but, because it is not feasible to warm all 1356

water, extend contact time to 1 to 2 hours for very cold water. Temperature of the iodine bottle also affects the concentration of iodine in the saturated solution (200 ppm at 10° C [50° F), 300 ppm at 20° C [68° F], 400 ppm at 30° C [86° F]),52,114 which is the reason for the color-dot thermometer on the bottle. In the field, it may be easier to warm the bottle in an inner pocket than to estimate temperature and adjust the dose. The supernatant should be carefully decanted or filtered to avoid ingestion of the crystals309; this is aided by the weight of the crystals, which causes them to sink. Many people prefer crystalline iodine because of its large disinfectant capacity, small size, and light weight. The absence of iodide decreases total amount of iodine ingested. The glass bottle can break, and there are anecdotal reports of freezing in very cold temperatures. Iodine in alcohol is a viable option that allows for much smaller doses because of higher solubility of iodine in alcohol. Currently there is no commercial product, but it can easily be formulated at home.

IODINE TABLETS The tablets contain tetraglycine hydroperiodide, which is 40% I2 and 20% iodide.52,190 They were originally developed by the military for individual field use because of their broad-spectrum disinfection effect, ease of handling, rapid dissolution, stability, and acceptable taste.199,210,236 One tablet contains 20  mg tetraglycine hydroperiodide that releases 8  mg/L of elemental iodine into water; both diatomic iodine (I2) and hypoiodous acid (HIO) are released. An acidic buffer provides a pH of 5.5 to 6.5, which supports better cysticidal than virucidal capacity but should be adequate for both. Tablets have the advantages of easy handling and no danger of staining or corroding if spilled. They are stable for 4 to 5 years under sealed storage conditions and for 2 weeks with frequent opening under field conditions, but they lose 30% of the active iodine if bottles are left open for 4 days in high heat or humidity. Products Potable Aqua (Wisconsin Pharmacal Co, Jackson, Wis) http://potableaqua.com/ Price: 50 tablets, $5.00; with PA Plus Neutralizing tablets, $8.00 Widely available through suppliers of outdoor products Also sold as Globaline and EDWGT (emergency drinking water germicidal tablets) Instructions One tablet is added to 1 qt of water. In cloudy or cold water, add two tablets. Contact time is only 10 to 15 minutes in clear, warm water; much more in cold, cloudy water (see Tables 67-10 to 67-12). To remove taste and color of iodine, add one tablet of Potable Aqua PA Plus, mix, and wait 3 minutes. PA Plus should be used after the 30-minute waiting period for Potable Aqua. If the tablets are gray or dark brown in color, they are still likely to be effective. If they are light green or yellow, it means they are probably no longer effective. An opened bottle should not be kept for more than 1 year. Comments This method was developed by the military for troops in the field. Advantages are unit dose and short contact time, but these concentrations create strong taste that is not acceptable to many wilderness users. The military requirements dictated a short contact time (10 minutes in clear, warm water), thus the relatively high concentration of iodine (8 to 16 ppm). With adequate contact time and moderate temperatures, one tablet can be added to 2 qt of water to yield 4 ppm of free iodine (see Table 67-15). Rather than use two tablets in cloudy water, clarify the water first. PA Plus “neutralizing” tablet contains approximately 45 mg of ascorbic acid (vitamin C), which converts iodine to iodide and removes the taste and color of iodine but has no disinfecting action. However, iodide is physiologically active, so concerns about toxicity or physiologic activity remain. For short-term use, iodine is safe and removing the taste is a major benefit. Ascorbic acid powder can be purchased at many health food stores and used to neutralize any iodine disinfecting solution.

Free chlorine is available from several compounds and widely available in liquid and tablet formulations. (See text discussion and Tables 67-11 and 67-12.) Chlorine test strips or meters are widely available for large groups or disaster/community situations where testing for adequate chlorine residual is desired. Simple field test kits or swimming pool test kits with color strips are widely available to ensure adequate residual chlorine, for example: SenSafe Free Chlorine Water Check http://sensafe-test-kits.com/ Detection Ranges for 0, 0.05, 0.1, 0.2, 0.4, 0.6, 0.8, 1.2, 1.5, 2, 2.6, 4, 6 ppm (mg/L) http://www.serim.com Serim Residual Chlorine Test Strips measure free chlorine concentrations of 0 to 10 ppm with color block increments at 0, 0.5, 1, 2, 5, and 10 ppm. Price: $30.00 for 100 strips

SODIUM HYPOCHLORITE Household Bleach Liquid household bleach is a sodium hypochlorite solution, most often 5.25%. It has the convenience of wide availability, low cost, and high stability. Sodium hypochlorite solutions are vulnerable to significant loss of available chlorine over time. Stability is greatly affected by heat and light. Five percent solution loses about 10% available chlorine over 6 months at 21.1° C (70° F) and freezes at 4.4° C (40° F). The liquid is corrosive and stains clothing if the bleach container breaks or leaks in a pack. Sodium hypochlorite solution in a squeeze dropper bottle is paired with several portable microfilter products to ensure viral disinfection, for example, SweetWater Viral Stop 2-oz squeeze dropper bottle. The Centers for Disease Control and Prevention (CDC)–World Health Organization (WHO) Safe Water System promotes products worldwide with 1% sodium hypochlorite for water disinfection.155

CALCIUM HYPOCHLORITE (DRY CHLORINE) Calcium hypochlorite is a stable, concentrated, dry source of hypochlorite that is commonly used for chlorination of swimming pools. The usual formulation contains 70% concentration of chlorine. Calcium hypochlorite is available in tablets or tubs of granules through chemical supply or swimming pool supply stores; one common brand is HTH, but there are many commercial products. Redi-Chlor (Gripo Laboratories, New Delhi, India) http://www.gripolabs.com 50 tablets in blister packs Price: $9.95 Multiple strengths, including: 0.5 g, 1.0 g, 2.0 g, 2.5 g, for treating 20, 80, 200, 240 L, respectively Available from multiple suppliers Formulation Redi-Chlor tablets come in different sizes and can be broken in half or fourths to treat different quantities of water. Recommended dose results in 2 to 5 mg/L residual chlorine. Add more for very cold water or if faint chlorine smell is not detected after contact time. Available in blister packs of 50 0.1-g tablets that treat 1 gal per tablet or 0.25-g tablets that treat 5 gal per tablet. Instructions For situations where many water containers are to be disinfected, it is easier to use a concentrated disinfecting solution. U.S. Environmental Protection Agency (EPA) instructions: Add and dissolve one heaping teaspoon of high-test granular calcium hypochlorite (approximately 0.25 oz) for each 2 gal of water. The mixture will produce a stock chlorine solution of approximately 500 mg/L (100 to 200 times desired strength for drinking). To disinfect water, add the chlorine solution in the ratio of one part of chlorine solution to each 100 parts of water to be treated. This is roughly equal to adding 1 pt (16 oz) of the stock chlorine solution to each 12.5 gal of water or (approximately 0.5 L to 50 L of water) to be disinfected. U.S. military instructions: See Table 67-13 for more details for dosing calcium hypochlorite for various strengths of chlorine and volume of water.

Comments This is a convenient source of concentrated hypochlorite, which can also be used for superchlorination (see text).

HALAZONE TABLETS Aquazone (Gripo Laboratories, New Delhi, India) www.gripolabs.com 100/250/500/1000 tablets in plastic container or 50/60 tablets in blister packs Tablets contain a mixture of monochloraminobenzoic and dichloraminobenzoic acids.90 Each tablet releases 2.3 to 2.5 ppm of titratable chlorine.199 These tablets have been criticized because the alkaline buffer necessary to improve halazone dissolution decreases disinfectant efficiency, requiring unacceptably high concentrations and contact times (6 tablets yield 15 mg/L with recommended contact time of 60 minutes) for reliable disinfection under all conditions.236 The shelf life is 6 months; potency decreases 50% when stored at 40° to 50° C (104° to 122° F). A new bottle should be taken on each major trip or changed every 3 to 6 months. Halazone has mainly been replaced by newer tablet formulations of chlorine.

SODIUM DICHLOROISOCYANURATE Sodium dichloroisocyanurate (NaDCC) is a stable, nontoxic chlorine compound that releases free active chlorine and forms a mildly acidic solution, which is optimal for hypochlorous acid, the most active disinfectant of the free chlorine compounds. Free chlorine is in equilibrium with available chlorine that remains in compound, providing greater biocidal capacity. NaDCC is more stable and provides more free, active chlorine than other available chlorine products for water disinfection. Manufacturers and Product Formulations Gripo Laboratories (New Delhi, India) http://www.gripolabs.com/nadcc_tablets.html Tablets available in sizes to treat 1 L to 100,000 L Kintab (Bioman Products) (Mottram, Hyde, Cheshire, UK) http://www.bioman.co.uk Aquatabs (Medentech, Wexford, Ireland) Six tablet strengths: 3.5 mg; 8.5 mg; 17 mg; 33 mg; 67 mg; 167 mg, depending on the volume to be treated, in individual foil-wrapped packets or strips. Larger quantities are available in tubs. Also available through Global Hydration Water Treatment Systems (Kakabeka Falls, Ontario, Canada) http://www.globalhydration.com/aquatabs-water-purificationtablets.htm Packs of 24 or 50 tablets to treat 1 L/tab or 30 tablets to treat 20 L (5 gal)/tab Formulation/Instructions When dissolved in 1 L of water, each effervescent tablet releases 10 mg of free chlorine; 50% of the available chlorine remains in compound and released as free chlorine is used up by halogen demand. Aquatab also makes slow-dissolving tablets for larger quantities of water that contain trichloroisocynuric acid (TCCA), which acts similarly to NaDCC. Disinfection of clear surface water is accomplished at 10 mg/L in 10 minutes, 1 mg/L for tap water and 2 to 5 mg/L for well water. NaDCC is also used to wash fruits and vegetables in concentrations of at least 20 mg/L. The tablets have a 3- to 5-year shelf life. Comments This is a good source of chlorine available in multiple doses and formulations, including individually wrapped tablet form; higherconcentration tablets allow for disinfection of large volumes of water or for shock chlorination of tanks and other storage systems.

CHLORINATION–FLOCCULATION Tablets contain alum and 1.4% available chlorine in the form of sodium dichloro-s-triazinetrione with proprietary flocculating agents. Bicarbonate in the tablets promotes rapid dissolution and acts as a buffer. One 600-mg tablet yields 8 mg/L of free chlorine. 1357

CHAPTER 67  Field Water Disinfection

CHLORINATION

PART 8  FOOD AND WATER

Testing by the U.S. military demonstrated biocidal effectiveness similar to iodine tablets under most conditions.211,212,214 Extended contact time was necessary for complete viral removal in some of the tests. Because of the ability to flocculate turbid water, the action was superior to iodine in some poor-quality water. The method is optimal for humanitarian disasters where available surface water is often highly turbid.87 Testing in households in developing countries demonstrates reduction of diarrhea episodes with proper use.55,72,225 Chlor-Floc (Deatrick & Associates, Alexandria, Va) 30 tablets individually sealed in foil packets; weight 1.6 oz.; capacity: 30 L (8 gal); Price: $8.00 Widely available through camping, military surplus, and survival websites Formulation/Instructions One tablet for the clarification and disinfection of 1 L of water from polluted sources at temperatures of 25° C (77° F). At 5° C (41° F) use two 600-mg tablets to provide 2.8% available chlorine. To strain the sediment, pour the water through the cloth provided. The tablets are stable for 3 years if stored out of the heat in their packaging. At 25° C (77° F), add 1 tablet; wait 7 minutes. At 15° C (59° F), add 1 tablet; wait 15 minutes. At 10° C (50° F), add 1 tablet; wait 15 minutes. At 5° C (41° F), add 2 tablets; wait 15 minutes. (1) Add 1 or 2 tablets (600 mg) to 1 L (1.1 qt) of water. (2) Shake for 1 minute to make sure that the tablets dissolve completely. (3) Wait for 7 to 10 minutes (or the necessary time), then strain through a piece of broadly woven cloth (e.g., T-shirt material) into clean container. (4) The clarified water is now ready for drinking. (5) If water is still murky, add an additional 0.5 tablet and repeat steps 2 and 3. After decanting, the water looks markedly clearer and is left with a free chlorine residual that produces microbiologically safer water without pronounced chlorine taste or odor.55 PUR Purifier of Water (Proctor and Gamble) www.pghsi.com Sachet of powder containing ferric sulfate as a coagulant and calcium hypochlorite as a disinfectant. Add one sachet to 10 L of water, and agitate vigorously. After the floc has settled to the bottom, filter through a clean cotton cloth and wait 20 minutes to drink. This product is available to large relief organizations for use outside the United States in disaster and conflict situations. They will also begin distribution for individual users in the developing countries. Comments This is one of the individual field methods for U.S. military troops and suggested for potential use in developing countries by the World Health Organization. It is an excellent one-step technique for cloudy and highly polluted water (see Table 67-15.). PUR has been used at the household level in many developing world communities and disasters.55,65,71,72,225 Alum and ferric sulfate are widely used flocculants that cause suspended sediment, colloids, and many microorganisms to clump, settle to the bottom, and readily be filtered or strained. Most Cryptosporidium oocysts would be removed by the flocculation. Some chlorine reacts with contaminants and is inactivated. It is important to confirm some chlorine taste and smell at the end of the contact time. For added safety, prolong the contact times up to 1 hour contact time in cold polluted and dirty water. In clear water without enough impurities to flocculate, the alum causes some cloudiness and leaves a strong chlorine residual. After treatment, water should be poured through a special cloth to remove floc and decrease turbidity. Both products have undergone extensive testing in field situations.

CHLORINE DIOXIDE Until recently, chlorine dioxide could be used only in large-scale water treatment applications, as a volatile gas that must be generated on site. Chemical methods for generating chlorine dioxide 1358

using either tablet or liquid formulations are now available for point of use in the field. Advantages of chlorine dioxide are greater effectiveness than chlorine at equivalent doses and the ability to inactivate Cryptosporidium oocysts with reasonable doses and contact times.

TABLETS Katadyn Micropur MP-1 http://www.katadyn.com/usen/katadyn-products/ Price: 20 tablets, $9.95; 30 tablets, $13.95 Available through many suppliers of outdoor products Potable Aqua Chlorine Dioxide Water Purification Tablets (Wisconsin Pharmacal Co, Jackson, Wis) Price: 20 tablets, $9.00; 30 tablets, $13.00 Available from many outdoor suppliers Aquamira (McNett Corp) http://www.aquamira.com/ Pristine (Advanced Chemicals Ltd, Port Coquitlam, BC, Canada) http://www.pristine.ca/ Tablets in blister packs Price: 12 tablets, $8.00; 24 tablets, $14.00; 50 tablets, $24.00 Formulation/Instructions The primary chemistry reaction that produces chlorine dioxide (ClO2) in Katadyn MP-1 tablets is the acid–chlorite reaction using sodium acid sulfate as the acid, a well-known reaction for ClO2. 5NaClO2 + 4 NaHSO4 → 4ClO2 + NaCl + 2H2O + 4 Na 2SO4 A small amount of chlorine in the tablet also catalyzes the otherwise sluggish reaction. These tablets generate chlorine dioxide only when coming into contact with water. Shortly after a tablet is immersed into water, a saturated solution of the soluble solid constituents forms within the matrix of the tablet. ClO2 is rapidly formed within the pores and then carried into the bulk solution by CO2 effervescence, which ensures that the resultant solution is well mixed without the user having to agitate the container. After the chlorine dioxide gas is released, the material reduces into common salts. Katadyn company product testing shows killing of bacteria and viruses within 15 minutes in any water conditions, and inactivation of Giardia and Cryptosporidium within 30 minutes in clear warm water and 4 hours in cold and dirty water. One tablet is used for treating 1 qt of water. Instructions are to insert rapidly into water after removing from package and avoid exposure to sunlight during disinfection contact time. Wisconsin Pharmacal would not provide information or testing data for their chlorine dioxide product. Comments This is an important addition to chemical methods for field disinfection. Several products have met the criteria for EPA registration as an antimicrobial water purifier. The extended contact time in cold, dirty water ensures that sufficient chlorine dioxide is generated and adequate residual remains for sufficient time to treat water in all conditions. Where possible, clarify the water to improve taste and esthetics and warm the water to reduce contact time. Available tests appear well designed with multiple controls. There is also documentation that residual concentrations of chlorine dioxide were well maintained during the recommended contact times. Chlorine dioxide does not have extended persistence in water, so it should not be used to maintain microbiologic purity of stored water. Sunlight breaks down chlorine dioxide, so for optimal effect, keep the water bottle in a dark location, such as inside a pack or bag, during disinfection time.

LIQUID CHLORINE DIOXIDE PRODUCTS Aquamira (McNett Corp) http://www.aquamira.com/ Pristine (Advanced Chemicals Ltd, Port Coquitlam, BC, Canada) http://www.pristine.ca/ Personal size: Two 1- oz plastic bottles; Capacity: up to 120 L (30 gal) of water; $15.00

Aquarius Bulk Water Treatment http://www.advancechemicals.ca/Aquarius-Bulk-WaterTreatment-System Includes 10 kits of Pristine solution to treat 50,000 L Available as a system with Terra Tank water bladders (5,000to 10,000-L capacity), Honda pump to fill the bladders, mixing and injection units, and six- to eight-spigot water-dispensing system. The system is packed in metal chests and weighs 200 lb. Formulation/Instructions A stabilized solution of chlorine dioxide is mixed with phosphoric acid, which activates the chemical and is then mixed with water for disinfection. Contact times for inactivation of Cryptosporidium by Pristine range from 15 minutes in warm water using a triple dose to 7 hours using a single dose in very cold water. The two solutions are mixed together in a mixing cap and added to the water for treatment. Comments The chemistry of generating chlorine dioxide through a similar method is well described. Aquamira solution was not able to meet EPA purifier standards in cold, dirty water. Currently claims for the solution include “kills odor causing bacteria and enhances taste of stored water.” The Canadian liquid product makes full claims, including Cryptosporidium. Given the volatility of chlorine dioxide and slow reaction times, concentrations may be variable due to mixing process and time delay. Cold and dirty “worst-case” test water may be an issue in disaster situations but is not often encountered by wilderness users. Aquamira tablets are registered as an EPA purifier, suggesting that tablets are the more stable and reliable form of chlorine dioxide.

MIXED SPECIES DISINFECTION (WITH CHLORINE DIOXIDE) Miox Purifier, Cascade Designs/MSR (Seattle, Wash) http://www.cascadedesigns.com/MSR/Water-Treatment-AndHydration/Expedition-Water-Treatment-And-Hydration/MIOXPurifier/product See Appendix A for more information on this product, which uses salt and an electrical current from camera batteries to generate chlorine dioxide, free chlorine species, and perhaps other disinfectants such as ozone. Electrolysis of salt to produce chlorine has been used for more than a century. Passing a current through a simple brine salt solution generates free available chlorine, as well as other “mixed species” disinfectants that have been demonstrated effective against bacteria, viruses, and bacterial spores.245 The process is well described and can be used on both large and small scale (http://www.miox.com/). Mixed oxidants behave like chlorine dioxide and ozone, although these disinfectants have not been detected in finished water treated with the Miox mixedoxidant solutions using classical analytical methods. The only residual, measurable species is hypochlorite; however, the resulting solution has greater disinfectant ability than a simple solution of sodium hypochlorite, including inactivation of Cryptosporidium.289 Additional testing is available on the Miox website.

SILVER Micropur Forte Tablets from Katadyn http://www.katadyn.com/chen/katadyn-products/ Widely available in Europe, but not marketed in the United States, these tablets contain silver chloride 0.1% and NaDCC 2.5%. The chlorine kills viruses, bacteria, and Giardia. The silver adds to the disinfection capacity, as well as preventing recontamination if water is stored for up to 6 months. Contact time is 20 to 120 minutes, depending on the temperature of the water. Shelf life is 5 years, stored in cool, dry conditions. Available as tablets, liquid, or powder and in various quantities for individual or large-scale use. One tablet treats 1 L of clear water. Claims Eliminates bacteria and viruses in 30 minutes and Giardia in 120 minutes. Conserves drinking water for up to 6 months. Can

be used in plastic or glass but not all metal containers. Shelf life: 5 years in original packaging and if stored under 25° C (77° F). Cloudy water can weaken the effect of chlorine and silver ions. Use filter for cloudy water. Micropur Classic from Katadyn This product releases silver ions. Available in two sizes of tablets (for 1 qt or 5 qt), liquid (10 drops/gal), or crystals for treating larger quantities of water. Claims Conserves clear water for up to 6 months. Deactivates bacteria after 2 hours of contact. The silver ions cling to the cell walls of microorganisms, thus hindering their growth. Affected by some metal containers. Shelf life: tablets, powder: 10 years from manufacture date, liquid: 5 years. Comments Although having proved antibacterial effects, silver tablets are not licensed as a water purifier in the United States; however, they are widely used in Europe for this purpose. In addition to poorly documented effects on many different types of microorganisms, there is some difficulty controlling the residual concentration and concern over chronic effects. This product makes no claims for viruses and protozoa, because concentrations may not be adequate to kill these organisms. Silver has the advantage of having no taste, color, or odor. It has been approved by the EPA to be marketed in the United States as a “water preservative” to maintain bacteria-free water for up to 6 months.

MISCELLANEOUS PRODUCTS The following products cannot be recommended because of insufficient effectiveness data. Traveler’s Friend (NutriBiotic) Description Extract from citrus seeds in 10-mL plastic dropper bottle. Price: $6.00 Claims “All natural treatment for drinking water.” Nontoxic, noncorrosive, proved effective as disinfectant for bacteria, viruses, protozoa. Recommended dose (drops/qt): 5 to 10 for filtered water, 10 to 15 for ice water, 10 to 20 for tap water, 15 to 25 for untreated water. Allow 30 minutes contact time. Comments Citrus extract is known to have some bacteriostatic effect (see text). This product was introduced into the health food market and is now looking for a broader market. Company data from independent laboratories support bacteriocidal and virucidal effects. However, protozoal tests were done with trophozoites, not cysts. The data have gaps, and too much of the marketing is testimonial to allow a recommendation at this time. Aerobic Oxygen and Aquagen These products claim to contain other forms of oxygen electrolytes that kill harmful bacteria in stored water and to have multiple health benefits when ingested in water or used topically. Aerobic Oxygen was initially introduced into the health food market but is now being offered to the general travel market. It is advertised not only as a water disinfectant, but for qualities from strengthening the immune system and energizing to curing headaches and tropical fish diseases. Company literature implies that the active disinfectants are chlorine dioxide, ozone, and free-oxygen radicals, but this is not credible because these are not chemically stable. Company-sponsored testing demonstrates activity against bacteria and viruses, but not against cysts. No dose-time response has been developed to compare the product with other disinfectants.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

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CHAPTER 67  Field Water Disinfection

Pristine also makes 2-oz bottles ($17.00) and larger packages for relief agencies to disinfect large quantities.

CHAPTER 68 

Infectious Diarrhea From Wilderness and Foreign Travel JAVIER A. ADACHI, HOWARD D. BACKER, AND HERBERT L. DUPONT

Acute infectious diarrhea is one of the most common and significant medical problems in any population, second only to acute upper respiratory diseases. Worldwide, diarrheal diseases were reported to cause nearly 1 billion episodes of illness in 1996.182 The rates of illness among children in developing areas of the world range from 5 to 15 bouts per child per year, with diarrhea being the most important cause of morbidity and mortality in many regions. Readily available oral rehydration solutions prevent great numbers of dehydration-associated deaths related to acute diarrhea, especially in developing areas, but invasive bacterial enterocolitis (caused by Shigella species and Campylobacter spp.), persistent diarrhea (defined as illness lasting 14 days or longer), malnutrition, and increased susceptibility to other infections still cause significant morbidity and mortality.182 Specific groups of U.S. populations, including international travelers to developing regions, gay males practicing unsafe sex, non-toilet-trained toddlers in some day care centers, and mentally impaired residents of custodial institutions, can have rates of diarrhea approximating those seen in the developing world. This chapter provides information to help to decrease exposure to risk factors and enteric pathogens, reducing the chance of acquiring diarrheal illness. The clinical features of acute diarrheal illnesses often do not permit differentiation of the specific etiologic agent, but fortunately, the majority of these infections do not require specific treatment. We formulate a clinical approach to self-therapy that is likely to minimize the complications and suffering caused by these illnesses. For the purpose of this discussion, “travelers” includes business or pleasure travelers as well as wilderness venturers.

General Principles of Enteric Disease EPIDEMIOLOGY

Fecal–oral contamination through ingestion of contaminated water and food (waterborne or foodborne) is the usual route of transmission of the enteric pathogens causing acute infectious diarrhea. The relative importance of food and water depends mainly on location and precautions taken. The majority of pathogens that cause traveler’s diarrhea (TD) or wilderness-acquired diarrhea can be either foodborne or waterborne; however, waterborne pathogens from drinking untreated surface water or from an inadvertent ingestion during water recreational activity probably account for most infectious diarrhea acquired in the U.S. wilderness. Prevention of infection from all these pathogens includes proper sanitation and water disinfection. Person-toperson transmission is seen with pathogens that have small infectious doses, such as Shigella species, hepatitis A virus, Giardia, and noroviruses. These infections are most common in select populations whose habits expose them to high levels of pathogens (e.g., infants in day care centers, homosexuals, persons with minimal access to water); prevention of these illnesses includes adequate hand washing and personal hygiene. Other, less common routes of fecal–oral transmission are through aerosols (some viruses), contaminated hands or surfaces, and sexual activity. In areas of Africa, Asia, and Latin America, where satisfactory sanitation is lacking, diarrhea is still the leading cause of infant morbidity and mortality. Good sanitation is related to a much 1360

lower incidence of infectious diarrhea in industrialized areas of the world. Travelers to foreign countries and wilderness areas often leave behind sanitation in the forms of flush toilets and safe tap water and do not have proximity to advanced medical care. Similar hygiene conditions are created in many other settings. Outbreaks of infectious diarrhea in day care centers among non-toilet-trained toddlers are associated with low inoculum organisms, including Shigella, Cryptosporidium, Giardia and the viral pathogens. Hospitals, especially intensive care units and pediatric wards, institutions for mentally handicapped patients, and nursing homes are also locations with a high incidence of diarrheal diseases. Clostridium difficile is the most important definable pathogen in those settings.160 Salmonella species, rotavirus, and enteropathogenic Escherichia coli (EPEC) may on occasion cause nosocomial outbreaks. Antimicrobial therapy is indicated for moderate to severe TD. When a specific bacterial or parasitic pathogen is identified (see later details), C. difficile infection (CDI) is frequently related to recent use of an antimicrobial agent (or cytotoxic agent) in debilitated hospitalized patients with a high rate of CDI recurrence.75 In developing areas of the world, children under 5 years of age have the highest morbidity of diarrhea, and infants under 1 year of age experience the highest mortality rates.40 The enteropathogens more common in infectious diarrhea during childhood are rotavirus, enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroaggregative E. coli (EAEC), Campylobacter spp., and Giardia. Residents in industrialized countries, such as the United States, have only one to two bouts of diarrhea per person per year, with no difference between age groups. Complications, including death, are more common in elderly persons.122 Organisms are shed in the stools during asymptomatic and symptomatic infection and for a period after illness. Long-term fecal shedding or chronic carrier states are reported to be important only for typhoid fever, whereas in other intestinal protozoal infections, the parasite may be persistently shed, as is seen in amebiasis, giardiasis and cryptosporidiosis. These cases may act as reservoirs for spreading infection, even in areas with low risk for infection. A few enteric pathogens have animal reservoirs and are spread to exposed persons. These zoonotic organisms include Salmonella spp., Yersinia, Campylobacter, Giardia, Balantidium coli, Sarcocystis, and Cryptosporidium. Food intoxication, caused by ingestion of preformed toxins from Staphylococcus aureus or Bacillus cereus, typically has a short incubation period (2 to 7 hours) and causes common source outbreaks involving multiple persons.41 Infection and diarrhea caused by a living enteropathogen must first traverse the stomach and infect the small bowel or colon, explaining a longer incubation period of 14 or more hours, usually more than 1 day. Immunocompromised patients, including those with advanced infection by the human immunodeficiency virus (HIV), and persons with metastatic cancer are prone to acquire infection by a wide variety of enteropathogens, to develop infectious diarrhea, and to experience recurrent infections. Advanced AIDS is associated with chronic diarrhea secondary to ultrastructural changes in gut morphology and malabsorption, or because of reduced immunity and coinfection with enteropathogens. The agents responsible for diarrheal diseases in advanced AIDS include Mycobacterium avium-intracellulare complex, Cryptosporidium, Giardia, Isospora, Cyclospora, Microsporidium,

PATHOPHYSIOLOGY Three intestinal mechanisms lead to acute diarrhea. The most common pathophysiologic mechanism in acute infectious diarrhea is alteration of fluid and electrolyte movement from the serosal to the mucosal surface of the gut (secretory diarrhea). This alteration may occur as a result of cyclic nucleotide stimulation (as a second messenger) or by an inflammatory process that is associated with release of proinflammatory cytokines. The second mechanism is malabsorption or presence of nonabsorbable substances in the lumen of the bowel, including lactase deficiency and AIDS-associated malabsorption. The third mechanism of diarrhea is altered intestinal motility. Secretory mechanisms best explain acute infectious diarrhea, while malabsorption and altered motility are more important in chronic

TABLE 68-1  Enteropathogens Found in Tropical

and Wilderness Travel

Agents Bacteria Enterotoxigenic Escherichia coli Enteroinvasive E. coli Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter spp. Vibrio cholerae Yersinia enterocolitica Aeromonas spp. Plesiomonas shigelloides Viruses Norovirus Rotavirus Hepatitis A Protozoa Giardia lamblia Entamoeba histolytica Cryptosporidium parvum Isospora belli Cyclospora cayetanensis Microsporidia Balantidium coli Sarcocystis Blastocystis hominis

Travel to Developing Tropical Regions

Wilderness Travel in Industrialized Regions

Yes

Rarely

Rarely Yes

Rarely Rarely

Yes Yes Yes Limited Rare Yes Yes

Yes Yes Yes Not currently Limited Yes Rarely

Yes Yes Yes

Yes Rarely Yes

Yes Yes Yes

Yes Rarely Yes

Limited Limited

Rarely Rarely

Limited Limited Limited Limited

Rarely Rarely Rarely Rarely

TABLE 68-2  Bacterial Enteropathogens: Virulence

Properties

Pathogen

Virulence Properties

Vibrio cholerae Vibrio parahemolyticus

Heat-labile enterotoxin Invasiveness (?), enterotoxin, hemolytic toxin Heat-stable and heat-labile enterotoxins, colonization factor antigens Shigella-like invasiveness Enteroadherence Cholera-like toxin, invasiveness Shiga-like toxin, invasiveness Cholera-like toxin, invasiveness Hemolysin, cytotoxin, enterotoxin Heat-stable enterotoxiin, invasiveness Toxins A and B Preformed toxin Preformed toxin Preformed toxin

Enterotoxigenic Escherichia coli Enteroinvasive E. coli Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter jejuni Aeromonas spp. Yersinia enterocolitica Clostridium difficile Clostridium perfringens Bacillus cereus Staphylococcus aureus

forms of diarrhea, such as tropical and nontropical sprue, Whipple’s disease, intestinal scleroderma, irritable bowel syndrome and inflammatory bowel disease. Table 68-2 shows the virulence factors of the most important enteric pathogens related to infectious diarrhea. In secretory diarrhea, the unformed stools are usually of large volume and small in number (characteristically less than six bowel movements per day). Stools do not contain blood and fever is unusual. Examples of pathogens in this group are Vibrio cholerae, ETEC, preformed enterotoxins, noroviruses, rotavirus, Giardia, and Cryptosporidium. Dehydration is the major complication, especially in the extremes of age. Without adequate therapy, secretory diarrhea can be followed by renal insufficiency. Invasive pathogens involving the distal ileum and colon damage the mucosa and elicit an inflammatory response that is associated with secretory diarrhea and colitis. In this form of colitis, stools are typically liquid, small-volume, and may contain blood and many leukocytes. The common microorganisms in this group are Shigella, Salmonella, EIEC, Shiga-toxin producing E. coli (STEC), Yersinia enterocolitica, Campylobacter spp., Aeromonas, Vibrio parahaemolyticus, and E. histolytica. Complications include dehydration and systemic involvement, especially in children with malnutrition.151

Traveler’s Diarrhea Traveler’s diarrhea is the most important travel-related illness in terms of frequency and economic impact. Point of origin, destination, and host factors are the main risk determinants.42 Inter­ national travel is more often associated with enteric infection and diarrhea, particularly when the destination is a developing tropical region, although the same infections can be contracted domestically. The 2% to 4% rate of diarrhea for people who take short-term trips to low-endemic areas (e.g., United States, Canada, Northwestern Europe, Australia, Japan) may be related to more frequent consumption of food in public restaurants, increased intake of alcohol, or stress. This rate of diarrhea increases to about 10% for travelers from these low-endemic areas to northern Mediterranean areas, China, Russia, or some Caribbean islands. This incidence increases as high as 40% to 50% for short-term travelers from low-risk countries to high-risk countries (developing tropical and subtropical regions of Latin America, Southeast Asia, or Africa). More than 100 million persons travel each year from industrialized countries to high-risk areas, resulting in more than 30 million travelers with diarrhea.42 Multiple episodes of diarrhea may occur on the same trip. Attack rates remain high for the first 4 weeks in a country of risk,54 then decrease, but not to the levels of local inhabitants. Immunity to ETEC infection, 1361

CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

cytomegalovirus, herpes simplex virus, and HIV itself (so called “AIDS enteropathy”). Treatment of HIV with highly active antiretroviral therapy and treatment of the enteric infection(s) are associated with improved symptomatology and decreased rates of infection. Most cases of acute diarrhea are caused by infectious microorganisms, including bacteria, viruses, and protozoa. Fungal agents have been reported rarely. Table 68-1 lists the etiologic agents often associated with travel to developing tropical areas or with wilderness travel in an industrialized region. Foodborne illness may consist of food “poisoning” or food “infection.” In food poisoning, an intoxication results when toxins produced by bacteria are found in food in sufficient concentrations to produce symptoms. A rare cause of food poisoning that results in paralysis is botulism, caused when the neurotoxin of Clostridium botulinum is ingested. Other foodborne pathogens are viruses, including rotavirus and small round viruses (noroviruses, astrovirus, etc.), and intestinal protozoal agents, including Giardia, Entamoeba histolytica, and Cryptosporidium.

PART 8 FOOD AND WATER

either asymptomatic or symptomatic, occurs after repeated or chronic exposure, which supports the feasibility of developing a vaccine.72 Although any waterborne or foodborne enteropathogen can cause TD, bacteria are the most common etiologic agents among persons traveling to high-risk areas. The bacterial flora of the bowel changes rapidly after arrival in a country with high rates of TD. At least 15% of travelers remain asymptomatic despite the occurrence of infection by pathogenic organisms, including ETEC and Shigella.155

TABLE 68-4  Clinical Syndromes in Enteric Disease

DEFINITION

Vomiting (predominant symptom) Persistent diarrhea (>14 days) Chronic diarrhea (>30 days)

TD refers to an illness contracted while traveling, although in 15% of sufferers symptoms first become ill after returning home. Most clinical studies define TD as passage of three or more unformed stools in a 24-hour period in association with one or more enteric symptoms, such as abdominal cramps, fever, fecal urgency, tenesmus, bloody–mucoid stools, nausea, and vomiting.45

Syndrome

Agent

Acute watery diarrhea

Any agent, especially with toxin-mediated diseases (e.g., enterotoxogenic Escherichia coli, Vibrio cholerae) Shigella, Campylobacter jejuni, Salmonella, Enteroinvasive E. coli, Aeromonas spp., Vibrio spp., Yersinia enterocolitica, Entamoeba histolytica, inflammatory bowel disease Viral agents, particularly noroviruses, preformed toxins of S. aureus or B. cereus

Febrile dysentery

Protozoa, small bowel bacterial overgrowth, inflammatory or invasive enteropathogens (Shigella, enteroaggregative E. coli) Small bowel injury, inflammatory bowel disease, irritable bowel syndrome (postinfectious), Brainerd diarrhea

ETIOLOGY Because the incidence of TD reflects in part the extent of environmental contamination with feces, the etiologic agents are pathogens causing illness in local children. A list of etiologic agents important in TD is provided in Table 68-3). Twenty years ago, specific pathogens were found in only 20% of cases. Currently, etiologic agents can be identified in up to 80% of TD episodes.103 In most studies, however, causative pathogens are not identified in 20% to 40% of cases. In most of these cases, antimicrobial therapy shortens illness, suggesting that this subset of diarrhea is caused by undetected bacterial pathogens.53 Overall,

TABLE 68-3  Major Pathogens in Traveler’s Diarrhea

(Travel to Developing Tropical Regions)

Agent Bacteria Enterotoxigenic Escherichia coli

Frequency (%) 50-80 5-50

Enteroaggregative E. coli Salmonella spp. Shigella spp. Campylobacter jejuni Aeromonas spp.

5-30

Plesiomonas shigelloides Other Viruses Rotavirus

0-5 0-5 0-20 0-20

Norovirus

1-20

Protozoa Giardia lamblia

1-5 0-5

Entamoeba hystolitica

0-5

Cryptosporidium parvum

0-5

Unknown

1-15 1-15 1-30 0-10

10-40

For details on published studies see reference 177.

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Distribution Developing countries, tropical areas, infants, travelers Infants, worldwide Worldwide Worldwide Worldwide Worldwide, especially Thailand, Australia, Canada Worldwide

Worldwide, children 6-24 mo Worldwide, cruise ships Worldwide, zoonosis, alpine areas Developing and tropical countries, especially Mexico, India, western and South Africa, parts of South America Worldwide, including cooler developed countries

the major etiologic agents and their frequency of isolation are remarkably similar worldwide. ETEC is the most common cause of TD worldwide,177 accounting for about one-third to one-half of cases. Since the last edition of this book, EAEC has been identified as the second most common bacterial cause of TD, causing up to 30% of TD cases in some areas of the world.3 One study has shown that the source of both types of E. coli is food. Viable ETEC and EAEC were found in hot sauces served on the table in popular restaurants in Guadalajara, Mexico.4 Shigella and Campylobacter species cause around 20% of illness. Other causes of TD include Salmonella (4% to 5% of cases), Vibrio, Aeromonas, Plesiomonas, viruses (10%), and parasites.177 Specific pathogens may predominate at a particular time or location.

CLINICAL SYNDROMES Table 68-4 outlines the major syndromes in patients with enteric infection. The typical clinical syndrome experienced by travelers with diarrhea secondary to the major infectious causes (e.g., ETEC) begins abruptly with abdominal cramping and watery diarrhea. Most cases are mild, consisting of passage of one to two unformed stools per day associated with symptoms that are tolerable and do not interfere with normal activities. Approximately 30% of affected persons experience moderately severe illness, with three to five unformed stools per day and distressing symptoms that force a change in activities or itinerary. Only 1% to 3% of persons with TD occurring in Latin America or Africa experience febrile dysenteric illness,64,129 whereas approximately 9% of travelers with diarrhea acquired in Asia (Indian subcontinent) develop this more serious form of illness.187 TD may lead to a chronic illness43 and postinfectious irritable bowel syndrome (PI-IBS).147,190 TD should be considered a self-limited nonfatal condition. An illness associated with vomiting without important diarrhea is commonly seen in travelers and is characteristically due to noroviruses.6,113 Symptoms lasting more than 1 to 2 weeks suggest a protozoan etiology such as Giardia, E. histolytica, Cryptosporidium or other parasite.43 An important part of the initial assessment is to measure the level of hydration, which includes a determination of vital signs, orthostatic pulse and blood pressure, mental status, skin turgor, hydration of mucous membranes, and urine output. Dehydration is most common in pediatric and elder populations. Fever is a reaction to an intestinal inflammatory process. High fever suggests a pathogen invasive to the intestinal mucosa, which classically includes bacterial enteropathogens such as Shigella, Salmonella, and Campylobacter spp. Fever can also be produced by strains of EIEC, V. parahaemolyticus, Aeromonas, C. difficile, and viral pathogens. Vomiting as the predominant symptom in a traveler usually suggests norovirus infection. Vomiting is also seen in “food poisoning” secondary to consumption of pre-formed enterotoxin produced by S. aureus or B. cereus.

PERSISTENT AND CHRONIC DIARRHEA Diarrhea may persist after the traveler returns home. Up to 3% of persons with TD in high-risk areas will develop persistent diarrhea.43 Persistent diarrhea is defined as illness lasting 14 days or longer, whereas diarrhea is considered chronic when the illness has lasted 30 days or longer. The etiology of persistent or chronic diarrhea often differs from that of acute diarrhea. Important causes of persistent diarrhea include (1) protozoal parasitic agents (Giardia, Cryptosporidium, Cyclospora, and E. histolytica), (2) bacterial infection (Salmonella, Shigella, Campylobacter, and Y. enterocolitica), (3) lactase deficiency induced by a small bowel pathogen (Giardia, rotavirus, or norovirus), and (4) a small bowel bacterial overgrowth syndrome secondary to small bowel motility inhibition (as a result of enteric infection) or secondary to antimicrobial use. Occasionally, other parasitic enteric infections can cause more persistent illness. These include Strongyloides stercoralis, Trichuris trichiura, and severe infection by Necator americanus or Ancylostoma duodenale. In rare cases, more protracted diarrhea may be a prominent symptom in persons with schistosomiasis, Plasmodium falciparum malaria, leishmaniasis, or African trypanosomiasis. When chronic diarrhea follows a bout of TD, a pathogen is not identified and the patient fails to respond to empiric antimicrobial therapy, PI-IBS, or activation of an underlying condition such as inflammatory bowel disease or celiac or tropical sprue should be considered. Even with eradication of microbial pathogens with antimicrobial therapy, bowel habits may not return to normal for several weeks. This represents slow repair of the damage to the intestinal mucosa. Small bowel bacterial overgrowth has been identified in patients with persistent diarrhea after a bout of TD. Finally, there first occurred in the 1980s an idiopathic form of chronic diarrhea called Brainerd diarrhea after the name of the city in Minnesota where the first outbreak was identified.150 The known vehicles of transmission of Brainerd diarrhea are raw (unpasteurized) milk150 and untreated water, such as well water.152 There is no diagnostic test or therapy, and the diagnosis is suspected based on the epidemiologic history (exposure to

FIGURE 68-1  Methylene blue stain of a fecal smear from a patient with bacillary dysentery (×400). Numerous polymorphonuclear leukocytes are present. This indicates the presence of diffuse colonic inflammation.

unpasteurized milk or untreated water just before onset of illness). Although the average duration of Brainerd diarrhea is 2 years, persons with this condition invariably become totally well. The approach to evaluate persistent or chronic diarrhea in travelers should begin with diagnostic tests for conventional bacterial pathogens in stools and at least three parasitologic evaluations of freshly passed stools. Dietary modification in all cases should initially include avoidance of milk and dairy products because of the possibility of lactase deficiency. Treatment should be specific, following the results of the microbiologic tests. Because most of these chronic forms of diarrhea are selflimited, it is unwise to employ empiric antibiotics in these patients. A single, limited empiric trial with metronidazole for possible Giardia infection is considered an option by some experts if all tests are negative.

LABORATORY TESTS AND PROCEDURES Several laboratory tests are useful in evaluating patients with diarrheal disease (Table 68-5). In clinical practice, laboratory testing is reserved for illness continuing after the patient returns home or when empiric treatment is unsuccessful. Persons with milder forms of diarrhea usually need only clinical evaluation; etiologic assessment is unnecessary. Laboratory tests are reserved for persons with moderate to severe diarrhea and those with persistent illness. The presence of fecal leukocytes is a reliable indicator of diffuse colonic inflammation. For moderate to severe illness, this is the most rapid, useful test and the ideal screening procedure. A large number of polymorphonuclear leukocytes (PMNs) per high-power field using dilute methylene blue stain or trichrome stain (which also helps with identification of parasites) can be helpful in making an etiologic diagnosis (Figure 68-1) of Shigella, Salmonella, or Campylobacter spp.88 Other

TABLE 68-5  Indications for Laboratory Test in Diarrheal Diseases and Possible Diagnoses Laboratory Test

Indication

Diagnosis/Agent

Fecal leukocytes or fecal lactoferrin Stool culture

Moderate to severe cases

Diffuse colonic inflammation, invasive bacterial enteropathogen Any bacterial enteric pathogen

Blood culture Parasite examination Parasite enzyme immunoassay Amebic serology Rotavirus antigen Clostridium difficile toxin by EIA or PCR

Moderate to severe diarrhea, fever, persistent diarrhea, fecal leukocytes or lactoferrin (+), male homosexual Enteric fever, sepsis Persistent diarrhea, travel to specific areas, day-care centers, male homosexuals Persistent diarrhea, travel to specific areas, day-care centers, male homosexuals Persistent diarrhea, liver abscess Hospitalized infants (<3 years old). Antibiotic associated diarrhea, especially occurring in the hospital

Salmonella, less likely Campylobacter, Shigella, Yersinia Any protozoan parasite Giardia, Entamoeba histolytica, Cryptosporidium Entamoeba histolytica Rotavirus C. difficile

EIA, Enzyme immunoassay; PCR, polymerase chain reaction

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Dysentery is defined as the passage of small-volume stools with gross blood and mucus. Common causes include Shigella, C. jejuni, Salmonella, Aeromonas, V. parahaemolyticus, Y. enterocolitica, EIEC, STEC, E. histolytica, and preexistent inflammatory bowel disease. The abdominal examination in persons with TD often shows mild tenderness but should not demonstrate signs of peritoneal irritation. A rectal examination may reveal tenderness in enterocolitis, and the victim may have painful external hemorrhoids, a result of the excessive rate of stooling. Some enteric pathogens produce both diarrheal and systemic diseases, such as hemolytic–uremic syndrome related to infection with shigellosis or STEC, Reiter’s syndrome, or glomerulonephritis related to Y. enterocolitica, and sepsis seen with bacteremic salmonellosis caused by Salmonella typhi, Salmonella paratyphi, and nontyphoid strains of Salmonella.

PART 8 FOOD AND WATER

organisms and conditions that may lead to presence of fecal leukocytes in the stools are C. difficile, Aeromonas, Y. enterocolitica, V. parahaemolyticus, EIEC, idiopathic ulcerative colitis, and allergic colitis. Lactoferrin is found in granules of neutrophils and can be identified in fecal samples by commercial immunoassay method (Leukotest, TechLab). This test does not require a freshly collected stool sample or an experienced technician, and is more sensitive than is microscopic examination of fecal leukocytes.21 Bacterial infection is specifically diagnosed by stool culture, although routine stool testing identifies few pathogens. A routine laboratory should be able to recover Shigella, Salmonella, and Campylobacter from a stool culture and, if specifically requested, V. cholerae, V. parahaemolyticus, Aeromonas, Y. enterocolitica, and C. difficile. The major indication for performing a stool culture is the presence of febrile and dysenteric disease. Blood culture(s) should be performed in all patients who are hospitalized with gastrointestinal (GI) illness or those with significant fever, especially when combined with degrees of systemic toxicity. Systemic infections by S. typhi and non-typhi Salmonella, Shigella, Campylobacter fetus, and Y. enterocolitica may be diagnosed by blood culture. Patients with persistent TD should be studied for presence of parasitic infection. Immunologic techniques to detect antigens of protozoan parasites are more efficient than are stool examinations for ova and parasites and are in common use for parasites that inhabit the duodenum (e.g., Giardia, Cryptosporidium, E. histolytica, Microsporidia).86,128 At times, intestinal parasites are better detected using a sample from duodenal aspiration or intestinal biopsy.86,128 In select cases, particularly clinical colitis and diarrhea persisting for 14 days or longer, flexible sigmoidoscopy or colonoscopy should be considered to study colonic lesions and collect samples for culture and microscopy. Lower GI tract endoscopy is particularly useful when stools contain many leukocytes per high-power field. Colonic mucosal changes may not be specific, except when pseudomembranes are sought in CDI. In homosexual male patients with acute diarrhea, examination of the distal colon may show evidence of proctitis (mucosal inflammation in the distal 15 cm of the colon), proctocolitis (inflammation beyond 15 cm), or enteritis. If there are no leukocytes in stool exam or if colonoscopy is negative, esophagogastroduodenoscopy (EGD) should be considered, looking at duodenal mucus for Giardia lamblia. Tests for malabsorption and biopsy of the small bowel mucosa may be useful in making a diagnosis.

TREATMENT In all cases of diarrhea, fluid and electrolyte replacement should be the primary therapy. This is particularly important in persons with cholera-like diarrhea or when diarrhea is seen in extremes of age (infants and the elderly). Outpatient treatment with instructions for oral rehydration can be used in the vast majority of adults and children. Significant dehydration from diarrhea in travelers is unusual. Treatment with intravenous (IV) fluids is indicated for • patients with hypotension, • inability to retain oral fluids, • systemic compromise (high fever and toxicity), • moderate toxicity or dehydration and a severe underlying disease, or • severe diarrhea at extremes of age. Supplemental nutrition is beneficial (essential in undernourished populations) and can be given as soon as fluid deficit losses are replaced, usually after the first 4 hours. In the face of more severe forms of acute diarrheal disease, the intestinal tract may not be able to process complex dietary products, so patients are often told to avoid solid foods and eat easily digested foods. As stooling decreases and appetite improves, staple foods, such as cereals, bananas, crackers, toasts, lentils, potatoes, and other cooked vegetables, are well tolerated and can be gradually added to the diet to facilitate enterocyte renewal, with subsequent progression to white meats, fruits, and vegetables. Dairy products and red meat are recommended only after diarrhea has resolved, usually after 2 to 3 days. Only foods and drinks that prolong 1364

diarrhea or increase intestinal motility should be avoided, such as those that contain lactose, caffeine, alcohol, high fiber, and fats. Breastfeeding of infants should be continued or should be resumed as soon as possible. Patients with TD should avoid excessive physical activity to reduce the risk of fluid loss and dehydration. The major cause of morbidity and mortality from acute diarrheal disease is depletion of body water and electrolytes. Rehydration is an essential part of therapy, especially in the extremes of age and during pregnancy. Most patients with TD do not become dehydrated, and hydration can be maintained by ingesting fluids such as sodas, juices, soup, and potable water in conjunction with a source of electrolytes (e.g., salted crackers). Fluid status in the field must be guided by physical signs related to hydration, including pulse, mucous membranes, skin turgor, and urine output. Urine color and volume are excellent measures. For travelers in the wilderness or tropics, fluid replacement must equal basic needs plus volume of diarrhea plus estimated sweat loss. Symptomatic Therapy Symptomatic medications are useful for treatment of milder forms of diarrhea, because they decrease symptoms and allow patients to return more quickly to normal activities. Lactobacillus preparations and yogurt are safe, but evidence is insufficient to establish their value in the therapy of TD. Adsorbent agents bind nonspecifically to water and other intraluminal material and make stools more formed. They have limited value in the treatment of acute diarrhea. The most useful drug for symptomatic therapy is the antimotility drug loperamide. In addition to slowing intestinal motility, these drugs alter water and electrolyte transport, probably affecting both secretion and absorption. Compared with placebo, antimotility drugs reduce the number of stools passed and the duration of illness by about 80%.46,51 The usual dose of loperamide is 4 mg initially. If diarrhea continues, the drug can be given in additional doses of 2 mg after each unformed stool, not to exceed 8 mg/day. Loperamide is not given for more than 2 days. Diphenoxylate with atropine is less expensive than loperamide, but has greater central opiate effects, a danger in case of accidental overdose by a child, and more side effects without antidiarrheal benefits because of the atropine, which is added only to prevent drug overdose. Tincture of opium or paregoric opium preparations are rapidly and equally effective and offer modest relief of symptoms. A major problem with this class of drugs is postdiarrhea constipation, so we recommend that only the loading dose be employed in most cases of diarrhea. Antimotility drugs should never be used alone in patients who have dysenteric or febrile diarrhea, because inhibition of gut motility may facilitate intestinal infection by invasive bacterial enteropathogens.55 However, this theoretic deleterious effect does not appear to be an issue when loperamide is used concurrently with an effective antimicrobial agent.62,63,193 Antimotility drugs should not be given to children younger than 3 years of age. Probiotics have been tested for both treatment and prevention of infectious diarrhea. Several meta-analyses of randomized controlled trails have noted a modest effect on frequency and duration of diarrhea. They may also be of value for antibiotic induced diarrhea and PI-IBS. Different types of probiotic bacteria are available in capsules, powder, therapeutic yogurts, and other modalities. Effective dosage is not well delineated and the number of live microorganisms is unreliable. Probiotics are generally benign and could be beneficial adjuncts to other more effective measures. Because increased secretion of water and electrolytes is the major physiologic derangement in acute watery diarrhea, therapy aimed at this effect is appealing. Although aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) inhibit secretion,159 their safety is a concern because of gastric mucosal toxicity. The salicylate moiety of bismuth subsalicylate reduces the number of stools passed and duration of diarrhea by about 50%, altering secretion in the intestine. Bismuth subsalicylate also has antimicrobial and antiinflammatory properties. New compounds are being developed that have antisecretory properties without motility effects.37,50 Table 68-6 summarizes the recommended dosages of available symptomatic treatments.

Adults

Agent

Therapeutic Dose

Attapulgite

3 g initially, then 3 g after each loose stool or every 2 hr (not to exceed 9 g/day); should be safe during pregnancy and childhood. (available in 600-mg tablets or liquid 600 mg/ tsp) 4 mg initially; this is usually sufficient. If nonresponsive, can give 2 mg (one capsule) after each loose stool not to exceed 8 mg (four capsules)/day; do not use in dysenteric or febrile diarrhea. 30 mL or two 262-mg tablets every 30 min for eight doses; may repeat on day 2 Dose according to package, because products and formulations vary. Daily dose may make diarrhea less severe and shorten its duration; consider in postinfectious or postantibiotic diarrhea.

Loperamide

Bismuth subsalicylate Probiotics

Antimicrobial Therapy Although most enteric infections do not require antibiotics, empiric antimicrobial therapy is indicated in acute TD and febrile, dysenteric illness, because of the importance of Shigella and Campylobacter as etiologic agents of this syndrome. Travelers with acute diarrhea and mild symptomatology usually do not need empiric antimicrobial therapy and can be treated with oral fluids and saltine crackers. Travelers with acute diarrhea and moderate symptoms, serious enough to change an itinerary, should be treated with antimicrobial empiric therapy or

symptomatic therapy with loperamide or bismuth subsalicylate. Finally, travelers with more severe symptoms with any degree of incapacitation, or with dysentery, should be treated with empiric antimicrobial therapy, immediately after the first passage of the first unformed stool (Table 68-7).45 Loperamide can be given with the antibacterial drug for faster clinical response.57 Therapy for specific infections is discussed in the corresponding sections (Table 68-8). Fluoroquinolones, azithromycin, and the rifaximin have adequate activity against most of the bacterial enteric pathogens to be considered useful for empiric therapy of TD.47 Ciprofloxacin is often the least expensive drug known to be effective. Problems196,201 with this drug are ineffectiveness for the common fluoroquinolone-resistant Campylobacter strains,196 depletion of gut flora,106 predisposing to CDI,142 and damage to articular cartilage.132 Azithromycin has been found to be a good alternative for treatment of acute TD. It is given in a dose of 1 g in a single dose for TD.196 Its main use is treatment of dysenteric and febrile TD. Azithromycin has the advantage of being useful and approved for pediatric TD (5 mg/kg/day for 3 days). Rifaximin (200 mg three times a day) was approved in 2004 by the U.S. Food and Drug Administration (FDA) for the treatment of TD caused by noninvasive E. coli in patients ≥12 years of age. Rifaximin is as effective as ciprofloxacin against noninvasive bacterial causes of TD.58 Travelers to high-risk regions should carry with them an antibacterial drug for treatment of bacterial diarrhea.47 A symptomatic drug, such as loperamide, may also be included for immediate relief of symptoms. If both drugs are employed in acute TD, persons should be instructed to take loperamide only if they have no fever and are not passing grossly bloody stools. The duration of antimicrobials needed in TD appears to be short for the absorbed drugs, fluoroquinolones or azithromycin. For rifaximin therapy, a full 3 days of treatment should be undertaken.

TABLE 68-7  Empiric Treatment and Evaluation of Traveler’s Diarrhea in Adults Clinical Manifestations

Recommendations*

Watery diarrhea with mild symptoms (no change in itinerary) Watery diarrhea with moderate symptoms (change in itinerary but able to function) Watery diarrhea with severe symptoms (incapacitating) Dysentery or fever Persistent diarrhea (>14 days) Vomiting, minimal diarrhea Diarrhea in pregnant women

Oral fluids and symptomatic therapy (can give antibiotics† or loperamide) Symptomatic treatment with loperamide and antibiotics† after passage of first unformed stool Antibiotic† after passage of first unformed stool Azithromycin, 1000 mg in single dose; loperamide is not recommended Parasite examination and stool culture; consider gastrointestinal evaluation Oral fluids and consider using bismuth subsalicylate Fluids and electrolytes; if severely ill, treat with azithromycin 500 mg once a day for 3 days.

*Treatment should be self initiated during travel without evaluation. † Antibiotic options include: norfloxacin 400 mg twice a day for 1-3 days, ciprofloxacin 500 mg twice a day for 1-3 days, ofloxacin 300 mg twice a day for 1-3 days, or levofloxacin 500 mg once a day for 1-3 days; or rifaximin 200 mg three times a day for 3 days; or azithromycin 1000 mg in a single dose.

TABLE 68-8  Antimicrobial Therapy for Organism-Specific Diarrhea in Adults Diagnosis

Recommendation

Enterotoxigenic and enteroaggregative Escherichia coli diarrhea

Rifaximin 200 mg three times a day for 3 days; or ciprofloxacin 500 mg twice a day for 1-3 days; or norfloxacin 400 mg twice a day for 1 to 3 days; or levofloxacin 500 mg once a day for 1-3 days; or azithromycin 1000-mg single dose Ciprofloxacin 1000-mg single dose; norfloxacin 400 mg twice a day or levofloxacin 500 mg once a day for 3 days; or doxycycline 300-mg single dose Norfloxacin 400 mg twice a day for 5 days, or ciprofloxacin 500 mg twice a day for 5-7 days, or levofloxacin 500 mg once a day for 7-10 days Antimicrobial therapy controversial if systemically ill (high fever and toxicity) or in a high risk group: sickle cell anemia, age <3 mo or >64 yr, on corticosteroids, undergoing dialysis, those with inflammatory bowel disease (if decision to treat, use regimen like systemic salmonellosis above) Norfloxacin 400 mg twice a day for 3 days, or ciprofloxacin 500 mg twice a day for 3 days, or levofloxacin 500 mg twice a day for 3 days Erythromycin 500 mg four times a day for 5 days; azithromycin 500 mg once a day for 3 days or 1000 mg in single dose

Cholera Systemic salmonellosis (typhoid fever or bacteremic infection) Salmonellosis (intestinal nontyphoid salmonellosis without systemic infection) Shigellosis Campylobacteriosis

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

TABLE 68-6  Nonspecific Drugs for Therapy in

PART 8 FOOD AND WATER

PREVENTION AND PROPHYLAXIS Care in Food and Beverages Consumed During Travel Food and water transmit the pathogens that cause infectious diarrhea and TD.4,195,206 When diarrhea occurs, however, the exact source cannot be determined. Being careful about what is eaten is recommended and may be helpful in reducing the occurrence of illness,115 but dietary habits usually cannot be rigidly controlled.179 Food in developing countries is often contaminated with fecal coliforms and enteropathogens.206 V. cholerae remains viable for 1 to 3 weeks in food,68 and Salmonella can survive 2 to 14 days in water or in the environment in a desiccated state. Risk of illness is lowest when most of the meals are selfprepared and eaten in a private home, intermediate when food is consumed at public restaurants, and highest when food is obtained from street vendors.16 The following standard dietary recommendations for prevention are based more on known potential vehicles for transmission of illness than on strong evidence. 1. Avoid tap water, ice made from untreated water, and suspect bottled water. Bottled and carbonated drinks, beer, and wine are probably safe. Boiled or otherwise disinfected water is safe. Tap water in high-risk countries is difficult to implicate in TD, but has been shown to contain enteric bacteria and pathogenic viruses and parasites.11 Bottled carbonated beverages are considered safe because of the antibacterial effects of the low acidity. Alcohol in mixed drinks does not disinfect contaminated ice cubes unless the alcohol content is at very high and potentially unsafe concentrations.38 2. Avoid unpasteurized dairy products. These may be the source of infection with Salmonella, Campylobacter, Brucella, Listeria monocytogenes, Mycobacterium spp., and others.158 3. Avoid raw meat and vegetables. Raw vegetables in salads may be contaminated by fertilization with human waste or by washing in contaminated water. Anything that can be peeled or have the surface removed is safe. Fruits and leafy vegetables can also be disinfected by immersion and washing in iodinated water or by exposure to boiling water for 30 seconds. Raw seafood, including that in traditional dishes such as ceviche and sashimi, has been associated with increased risk of TD. Shellfish concentrate enteric organisms from contaminated water and can carry hepatitis A, noroviruses, Aeromonas hydrophila, Y. enterocolitica, V. cholerae, and V. parahaemolyticus. Raw fish can carry parasites such as Anisakis simplex, Clonorchis sinensis, and Metagonimus yokogawai. Raw meat is a source of Salmonella and Campylobacter and the vehicle for Trichinella, Taenia saginata and Taenia solium (beef or pork tapeworm), and Sarcocystis. Although adequate cooking kills all microorganisms and parasites, if food is left at room temperature and recontaminated before serving, it can transmit Salmonella, Shigella, ETEC, or EAEC. Food served on an airplane, train, boat, or bus probably has been catered in the country of origin. Problems of food hygiene pertaining to these forms of public transportation may be related to employee handling of food, even in the United States.

Generally safe foods are those served steaming hot, dry items such as bread, freshly cooked food, foods that have high sugar content (e.g., syrups, jellies, jam and honey), and fruits that have been peeled. Chemoprophylaxis Chemoprophylaxis with antibiotics was shown in the 1950s and 1960s to effectively prevent TD among international travelers.111 This was the first evidence that bacterial pathogens were the most important causes of TD. Preventive antibiotics are generally recommended to be used for trips of 2 weeks or less and will require a prescription from a physician (Table 68-9). Because of safety and efficacy, rifaximin is the optimal drug when prophylaxis is employed: the dose is one 200 mg tablet twice a day with major daily meals for trips up to 2 weeks in length. Another effective dosage formulation of rifaximin is a 550 mg tablet taken once for breakfast each day of the trip to high-risk regions. The medication should be started the day of arrival to a high-risk region and can be stopped once leaving the area. Most wilderness travelers taking their own food or preparing their own food are not at high enough risk for TD to justify chemoprophylaxis with antibiotics. Several non-antimicrobial agents have been studied for prevention of TD, with some found to be minimally effective. Lactobacilli have been tested on the assumption that they are safe and favorably modify intestinal flora, but they did not invariably reduce the incidence of TD and provided protective efficacy only up to 47%.90 Of the non-antibiotic drugs, only bismuth subsalicylate (BSS), the active ingredient of Pepto-Bismol, has been shown by controlled studies to offer reasonable protection and safety.49,61 The currently recommended dose of BSS is two tablets with each meal and two tablets at bedtime or two tablets four times a day (2.1 g/day) while in a high-risk region for trips of 2 weeks or less. Mild side effects include constipation, tinnitus, and temporarily blackened tongue or stools. BSS should not be used by someone with a history of aspirin allergy or in young children. The precise mechanism by which BSS prevents diarrhea is still unknown. Salicylate released during dissociation in the stomach exhibits antisecretory activity after exposure to bacterial enterotoxin on intestinal mucosa, and bismuth salts have antimicrobial activity.83 Indications for recommending antimicrobial chemoprophylaxis in TD prevention are as follows:45,59,67,81 1. An underlying illness that increases the risk of enteric infection or morbidity, such as gastric achlorhydria (from surgery or taking proton pump inhibitors), AIDS, inflammatory bowel disease, diabetes with insulin treatment, or a cardiac, renal, or CNS disorder. 2. An itinerary that is so rigid and critical to the overall mission that travelers would not tolerate even minor schedule changes caused by illness. 3. Travelers who prefer prophylaxis after hearing the pros and cons of the approach. An evidence-based analysis of the available data on chemoprophylaxis in the prevention of TD was published by the International Society of Travel Medicine.48 Immunoprophylaxis Spurred by the emergence of in vitro resistance among enteropathogens to antimicrobial agents, including the fluoroquinolones, and with the knowledge that persons develop natural

TABLE 68-9  Prophylactic Medications for Prevention of Traveler’s Diarrhea* Agent Bismuth subsalicylate Fluoroquinolones Rifaximin

Protective Efficacy 65% 90% 70-80%

Prophylactic Dose

Comment

30 mL or two 262-mg tablets before meals and at bedtime Norfloxacin 400 mg, ciprofloxacin 500 mg, or levofloxacin 500 mg once a day Rifaximin 200 mg twice a day with meals

Safe, temporary darkening of stools and tongue Side effects and toxicity unacceptable, concern with development of antibiotic resistance Safe, nonabsorbable, no increased resistance, should be considered the standard agent for prophylaxis during high-risk travel

*Not generally recommended for healthy travelers able to carry out preventive measures, to be used in special situations (see text) and for no longer than 2 weeks.

1366

Bacterial Enteropathogens ESCHERICHIA COLI The diarrheagenic E. coli represent a heterogenous group of organisms that belong to one taxonomic species, but have different virulence properties, epidemiologic characteristics, and clinical features. At least six groups have been characterized, based on genotypic or phenotypic markers.140 We will discuss207 here the pathotypes of diarrheagenic E. coli important in TD. Enterotoxigenic E. coli.  ETEC strains were first identified in the 1970s and shown to produce one or two enterotoxins that act on the small intestine through different cyclic nucleotide pathways showing different time responses in the gut.140 One of these toxins is a heat-labile cholera-like toxin (LT), a highmolecular-weight protein immunologically and physiologically similar to cholera toxin. Human ETEC strains also have a lowmolecular-weight, poorly antigenic toxin that is heat stable (ST).165 One common method for the diagnosis of ETEC is identification of specific DNA plasmid sequences, using a hybridization technique.140 More recently, polymerase chain reaction (PCR) has been used to improve the level of detection.* ETEC has worldwide distribution and is the major cause of TD, accounting for 30% to 40% of cases in series from Latin America, Africa and south Asia (Indian subcontinent).177 It also accounts for a large percentage and is frequently the majority of enteritis in local pediatric populations of developing countries, where contaminated food and water are the primary sources of infection. Person-to-person spread is infrequent because of the large infectious dose (106 to 1010 organisms).52 Enteroinvasive E. coli.  As with Shigella, EIEC strains possess the property of bowel mucosa invasion, resulting in microabscesses and ulcer formation. Because of the presence of the same invasive plasmid and other antigens of Shigella,118,166 EIEC must be considered in the differential diagnosis of febrile dysenteric diarrhea. EIEC strains cause a small fraction of TD cases.203 Enteroaggregative E. coli.  EAEC strains are an important cause of TD in all regions of the world.3 These strains adhere to HEp-2 cells in a typical aggregative, “stacked brick” pattern. Several bacterial markers have been studied as possible diagnostic aids, but no single marker is present in all strains. 94,96,102 Some studies

*References 8, 14, 73, 197, 199, 207.

suggest that EAEC should be considered a phenotypically and genotypically heterogeneous group.* Although the pathophysiology of EAEC is not completely understood, presence of multiple virulence factors and stimulation of inflammatory cytokines/ chemokines have been described.† EAEC has been associated with acute and persistent diarrhea in children living in developing countries.30,94,143,174,209 Diffusely Adherent E. coli.  These strains show a diffuse, nonaggregative, adherence pattern to HEp-2 cells. There is limited evidence that these strains are causes of TD134,198 and diarrhea in children in developing countries.77 Laboratory culture cannot differentiate the various diarrheagenic strains of E. coli from normal bowel flora or from one another. Specialized assays such as DNA probing and HEp-2 adherence technique are specifically used for research purposes.139 New serologic and molecular diagnostic techniques under investigation may become available in the future to differentiate these organisms.‡ Most cases of E. coli diarrhea are brief and self-limited and treatment is with rifaximin, ciprofloxacin, or azithromycin. EIEC should be treated as for shigellosis with 3 days of therapy with a fluoroquinolone or 1000 mg azithromycin in a single dose.

SALMONELLA Salmonella infections may result in four different clinical syndromes: gastroenterocolitis, enteric (typhoid) fever, bacteremia with focal extraintestinal infection, and asymptomatic carriage.19,173 Gastroenterocolitis and typhoid fever are the two most important forms for travelers. Although the incubation period for typhoid fever is usually 1 to 2 weeks, it is only 8 to 48 hours for intestinal infections with nontyphoid Salmonella.156 Nausea, vomiting, malaise, headache, and low-grade fever may precede abdominal cramps and diarrhea. Stools are usually foul and green-brown to watery, with variable amounts of mucus, blood, and leukocytes. Cholera-like fluid loss or dysentery with grossly bloody and mucoid stools occurs less often. The acute phase lasts only a few days. Asymptomatic excretion of organisms in the stool continues for 4 to 8 weeks, and chronic carriers are rare. Infants younger than age 3 months experience longer illnesses (average 8 days) with more complications. Among all ages, transient bacteremia is common, accounting for significant isolation of Salmonella types from blood. Fever and malaise occurring more than a week after resolution of diarrhea suggest a complication or another diagnosis.107,156 In healthy adults, Salmonella bacteremia occurs in 5% to 8% of infections and is not distinguishable from other causes of sepsis. Diagnosis is made by isolation of Salmonella from stool or blood cultured onto selective media (MacConkey or SalmonellaShigella agar). Supportive treatment with fluids is sufficient therapy for most cases of uncomplicated Salmonella enterocolitis. Antimicrobial therapy is indicated for persons who have symptomatic Salmonella infection with fever, systemic toxicity, or bloody stools. Fluoroquinolones are the treatment of choice for most forms of systemic salmonellosis because they shorten the duration of illness. Doses are the same as those recommended to treat shigellosis, although treatment is continued for 7 days (14 days if the patient is immunosuppressed). For known intestinal salmonellosis, antibiotics are used only in the more severely ill or when bacteremia is suspected. Immunity to Salmonella is serotype specific. Vaccines have not been successful for nontyphoid Salmonella because of the number of serotypes. For typhoid fever, immunoprophylaxis is available with two licensed, protective vaccines. The first is a live attenuated strain Ty21a that is given as one oral dose every other day for four doses.9,76 The second is an inactivated Vi polysaccharide

*References 22, 34, 96, 119, 139, 140. † References 21, 84, 95-97, 102, 104, 138, 209. ‡ References 8, 11, 15, 73, 124, 141, 162, 184, 199.

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

protection against TD as they remain in a high-risk area, vaccines are being developed to prevent TD. Several vaccines are being or have been developed for protection against rotavirus, Shigella, V. cholerae, and ETEC. The vaccine most relevant to TD is ETEC. ETEC is the most important cause of TD and typically occurs during the first 2 weeks in a country of risk.2 An orally administered ETEC vaccine is marketed as Dukoral in many European countries. The vaccine uses a recombinant form of the binding subunit of cholera toxin that resembles the heat-labile toxin of ETEC (LT). The vaccine was successfully employed in a study of Finish travelers to Morocco.153 The vaccine fails to immunize against the nonantigenic heat stable toxin of ETEC (ST). Adding whole cells containing gut attachment fimbriae of ETEC has been one approach to increase the spectrum of activity of this oral vaccine. Making sure the correct fimbrial adhesin is included in the vaccine is a challenge of this approach.170 An exciting new vaccine in development is a LT skin patch vaccine. When LT is applied to the skin after minimal abrasion of the stratum corneum, a brisk antibody develops.78 The vaccine has prevented moresevere forms of ETEC diarrhea in volunteers131 and in a phase II trial among international travelers to Mexico and Guatemala, the patch vaccine had a protection rate against moderate and severe diarrhea of 75%.72 At the time of this writing, this vaccine is in a phase III trial in Mexico, Guatemala, and India.

PART 8 FOOD AND WATER

preparation given as a single parenteral immunization.1 Both preparations are of approximately equal cost and effectiveness.

SHIGELLA Shigellae are nonmotile, nonsporulating, and gram-negative rods in the Enterobacteriaceae family. There are four species or groups: A (Shigella dysenteriae), B (Shigella flexneri), C (Shigella boydii), and D (Shigella sonnei); the first three contain numerous serotypes. Fecal–oral contamination is the mode of spread, most commonly from contaminated food in the case of TD. With an infectious dose as low as 10 to 200 organisms, person-to-person spread also occurs.60 The essential virulence factor of Shigella is invasiveness associated with a large (120- to 140-megadalton) plasmid. As with most enteric pathogens, infection with Shigella may be asymptomatic, mild, or severe. In the classic form of shigellosis, after 1 to 3 days of small bowel disease, colonic involvement causes progression to clinical dysentery. In the dysenteric form, the volume of stools decreases and the frequency increases, with passage of up to 20 to 30 movements a day, containing gross blood and associated with fecal urgency and often tenesmus. Fever is common in dysenteric cases, found in up to one-half of cases of shigellosis overall. Mild abdominal tenderness is also common, but without peritoneal signs. Laboratory tests often show a mild leukocytosis with a shift to the left (increase in number of immature granulocytes). If colitis is present, microscopic examination of the stool shows countless white blood cells. Diagnosis is made by stool culture on selective media (MacConkey or Salmonella-Shigella agar), which is positive in most infected patients.56 Patients with fever and dysentery should be treated with absorbed antimicrobial agents, including fluoroquinolones or azithromycin. The current dosage recommendations for fluoroquinolones are norfloxacin 400 mg twice a day, ciprofloxacin 500 mg twice a day, or levofloxacin 500 mg once daily, for a total of 3 days. Single-dose therapy is probably effective in milder forms of illness. For children, azithromycin (10 mg/kg/day for 3 days) or a 3-day course of a fluoroquinolone can safely be used, even though this class of drugs is not approved for use in children.

CAMPYLOBACTER The organism is a small, curved, and gram-negative rod, formerly classified as Vibrio. Campylobacter jejuni/coli strains are widespread in the environment, most often spread from contaminated food. The most important source for human illness is poultry, but epidemics have also been associated with ingestion of raw milk.17,18 C. jejuni has been isolated from surface water and can survive up to 5 weeks in cold water, ensuring its potential for wilderness waterborne spread. Person-to-person spread occurs but is uncommon. The prevalence of C. jejuni as a cause of TD varies with geographic area and time of year. TD secondary to C. jejuni is more prevalent in Southeast Asia and accounts for about 3% of cases in rainy summertime and in up to 15% of cases during drier wintertime.17,130,172 All segments of the small and large intestine may be affected in intestinal campylobacteriosis.  The incubation period of C. jejuni enteritis is 2 to 7 days. Clinical symptoms are extremely variable and nonspecific. Victims often have a 1-day prodrome of general malaise and fever, followed by abdominal cramps and pain that herald the onset of diarrhea, with up to eight bowel movements a day. The diarrhea is initially watery, followed by passage of stools that are bile stained or bloody. C. jejuni infection has been associated with occurrence of Guillain-Barré syndrome.17,98,136,164 The mechanism of development of this postinfectious complication relates to molecular mimicry with development of antiganglioside antibodies stimulated by infection by specific strains of Campylobacter.79 Definitive diagnosis is made by stool culture on a selective medium (e.g., Skirrow, Butzler, Campy-BAP), with isolation rates directly related to the severity of the disease. C. fetus may be grown from the blood in patients with systemic illness. Treatment is primarily supportive with oral fluids; dehydration is usually mild. Early antibiotic therapy appears to be effective in intestinal campylobacteriosis.17 The antibiotic of choice is erythromycin or azithromycin.82,116 1368

VIBRIOS Cholera is a severe form of watery diarrhea often associated with dehydration. The disease is caused by V. cholerae O group 1 (O1), a motile, curved, gram-negative rod. These microorganisms have two major biotypes, classic and El Tor, which produce similar clinical illness, and each one contains two main serotypes, Ogawa and Inaba.169 Non-O1 V. cholerae strains also produce diarrheal illness, but they show less potential for epidemic disease.108,117 Most cases of gastroenteritis caused by noncholera vibrios have been associated with ingestion of raw seafood. Cases have been reported from travelers, particularly after visits to coastal areas of Southeast Asia and Latin America. V. parahaemolyticus causes 70% of cases of foodborne gastroenteritis in Japan (where large amounts of raw seafood are eaten), leads to sporadic outbreaks in the United States, and is a common cause of TD in Thailand.20 After passing through the stomach, the organism multiplies and colonizes the small bowel. The local effects of enterotoxin account for the pathophysiology of cholera. No pathologic changes are noted in the intestinal wall. Some cholera infections are asymptomatic, and 60% to 80% of clinical cases are presented as mild diarrhea that never raise suspicion for cholera.93 After an incubation period of 2 days (range 1-5 days), fluid accumulates in the gut, causing intestinal distention and diarrhea. Diarrhea may begin as passage of brown stools but soon assumes the translucent gray watery appearance known as “rice water” stools. In serious cases, stool volume may reach 1 L/ hr, leading to severe dehydration, acidosis, shock, and death. Vomiting may occur as a result of gut distention or acidosis.108,169 The clinical syndrome caused by noncholera vibrios is not characteristic. Intestinal illness is associated with diarrhea, abdominal cramps, and fever, with nausea and vomiting in about 20% of cases. Diarrhea may be severe, with up to 20 to 30 watery stools per day. In outbreaks of V. parahaemolyticus infection, explosive diarrhea associated with abdominal cramps and nausea is often described, with vomiting in about 50% and fever in about 30% of cases. A dysentery-like syndrome with mucoid bloody diarrhea is often seen in disease outbreaks.20 Infections are usually brief, lasting an average of 3 days, with spontaneous resolution. Diagnosis for any of the Vibrio strains can be made by stool culture on suitable media (e.g., thiosulfate–citrate–bile salts–sucrose, or TCBS, agar). Vibrios can survive for 1 week on a stool-saturated piece of filter paper sealed in a plastic bag, before placing it in the culture media.108 In the case of V. cholerae, another way to diagnose infection is using a darkfield microscopic examination of fresh stools, which may reveal the characteristic helical vibrio in motion. Aggressive replacement of fluid and electrolytes is the cornerstone of therapy for cholera, especially in severe cases. Severe untreated cholera has a 50% mortality, which may be reduced to 1% with appropriate treatment. Children are at higher risk for complications and death. Antibiotics shorten the duration of diarrhea and excretion of organisms in severe cholera and reduce fluid losses, but they are not as important as fluid therapy. Oral antibiotics can be started within a few hours of initial rehydration. The drug of choice is doxycycline, 300-mg single dose in adults or 50  mg/kg/day in four divided doses for children. Treatment of patients infected with noncholera vibrios should also focus on fluid replacement. Little information exists on the benefit of antibiotic therapy for GI disease, but antimicrobials may be reasonable in dysentery-like cases or prolonged illness. The same antimicrobial agents used in cholera could be used against this infection. The current parenteral cholera vaccine has no antitoxin activity and is only about 50% effective in reducing attack rates over a 3- to 6-month period for those living in endemic areas. It is not recommended for travelers to endemic areas.108 Outside the United States, two additional vaccines are available: an oral killed whole cellcholera toxin recombinant B subunit (WC-rBS) and an oral live attenuated V. cholerae vaccine (CVD 103-HgR), both with 60% to 100% rate of protection against V. cholerae O1 for at least 6 months. They are not active against V. cholerae O139.168 Finally, a bivalent (CVD103-HgR plus CVD 111) oral vaccine has been shown to be more effective than is the monovalent one.10,12,87,194

Intestinal Protozoa

GIARDIA LAMBLIA

Protozoal infections may be pathogenic or commensal (having little or no effect) for the human host. Although acute self-limited diarrheal illness may occur, only a small proportion of cases of acute TD are caused by parasites. Symptoms are nonspecific, and diagnosis is often made on stool examination. Most protozoal infections are suspected on the basis of subacute or chronic GI symptoms, which may fluctuate over time. Several factors have increased the prevalence of intestinal parasites in the United States and worldwide: an increase in

G. lamblia (also known as Giardia intestinalis or Giardia duodenalis) is a flagellate protozoan. Classification of Giardia species remains controversial, but there are at least six species and other genotypes, primarily distinguished by host. G. duodenalis is the species of major concern for human infection.5 Giardia is the most common protozoal intestinal parasite isolated worldwide, including the United States. Prevalence ranges from 3% to 7% in the United States to 30% or more in developing areas with poor sanitation. All age groups are affected.

Aeromonas species and P. shigelloides are gram-negative, facultative anaerobic, nonsporulating rods. Their normal habitats are water and soil, and these bacteria have been implicated in a variety of human illnesses, most often gastroenteritis.91,92,101,202 Clinical illness associated with enteric infection by A. hydrophila varies from acute to chronic diarrhea and from passage of watery stools to dysentery with colitis.101,175,200 Aeromonas strains are susceptible to antibiotics used to treat TD. P. shigelloides has been associated with recent travel and ingestion of raw or inadequately cooked shellfish. Plesiomonas may cause dysenteric illness suggestive of an invasive organism, but its pathogenic mechanisms remain poorly defined.92 Plesiomonas is susceptible to anti-TD antibiotics.

VIRAL ENTERIC PATHOGENS

TABLE 68-10  Antiparasitic Therapy for Giardiasis* Adult Treatment

Pediatric Treatment and Other Drugs

Tinidazole 2000 mg single dose, or Nitazoxanide 500 mg twice a day for 3 days, or Metronidazole 250 mg three times a day for 5-7 days or 2 g/day in a single dose for 3 days (high dose has more side effects), or Albendazole 400 mg single dose or once a day for 5-7 days (single dose less effective), or Diloxanide (Furamide), adults and children aged 12 yr and older: 500 mg three times a day for 5-10 days

Tinidazole 50 mg/kg single dose Children aged 1-4 yr: nitazoxanide 100 mg twice a day for 3 days; Children aged 4-11 yr: nitazoxanide 200 mg twice a day for 3 days Metronidazole 15 mg/kg/day divided three times a day for 5-7 days Albendazole 10 to 15 mg/kg once a day for 5-7 days Children up to age 12 yr: diloxanide 20 mg/kg/day in three divided doses for 5-10 days

*References 23, 24, 31, 66, 70, 74, 85, 125, 137, 145, 148, 154, 157, 167, 176, 181, 183, and 204.

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Noroviruses have been shown to be important causes of approximately 10% of TD cases.6,28,99,113 These viruses are highly infective (10 to 100 organisms per inoculum), and infection is spread by common-source vehicles with a propensity for secondary personto-person spread (high secondary attack rate).89 Humans are the only known carriers of these viruses. Norovirus is known as the “cruise ship virus” based on its importance in that setting. Between 20% and 67% of outbreaks of noroviruses have been associated with food.26,144 After a cruise ship has experienced a norovirus outbreak, this viral infection can continue to be a problem in future trips with the involved ship, despite extensive sanitization.99 Transmission is followed by an incubation period of 24 to 48 hours, and illness begins abruptly with vomiting, abdominal cramps, and diarrhea. Stools are watery without blood or leukocytes. Other common symptoms include low-grade fever, malaise, myalgias, respiratory symptoms, and headache. Illness is almost always mild and self-limited, lasting 1 to 2 days. Complications and mortality are extremely rare and usually involve elderly and debilitated patients. Currently, there are immunoassays and molecular techniques (reverse-transcription PCR) available for detection of these small round RNA viruses in stool.6,27 Vaccine development is being explored for the noroviruses, but the studies are in a very early stage.114

immunocompromised patients, who frequently become infected by these organisms; improvement in diagnostic techniques; increase in group settings (day care centers and nursing homes); more frequent international travel; and in the United States, increased immigration of people from developing countries.110,128 All intestinal protozoa are transmitted by the fecal–oral route, so infection rates are highest in areas and groups with poor sanitation, close contact, or particular customs favoring transmission. These reemerging infections have been related to large outbreaks of communicable diseases in the United States, often secondary to water contamination.208 In addition to spread by food, water, and person-to-person contact, mechanical vectors, such as flies, may spread these organisms. Transmission of intestinal protozoa is favored by a hardy cyst, which is passed in the feces of an infected host. In addition to an infective cyst, the life cycle for most intestinal protozoa includes a trophozoite, which is responsible for reproduction and pathogenicity. Only a single host is required, except for Sarcocystis, which requires ingestion of raw meat from an intermediate host. Zoonotic spread to humans has been documented for Giardia, Cryptosporidium, Entamoeba polecki, and B. coli. As with enteric bacteria, symptoms from infection by intestinal protozoa depend on the level of bowel colonized. Those colonizing the small intestine, such as Giardia and coccidia (see Cryptosporidium, later), cause a wide spectrum of GI complaints, including malabsorption (resulting in foul stools and flatulence) and weight loss in persistent infections. Although many protozoa are capable of superficial mucosal invasion, only E. histolytica and B. coli, which colonize the colon, can ulcerate the bowel wall, cause dysentery, and spread to other tissues.86 Most infections are asymptomatic and self-limited in immunocompetent persons but can be persistent and severe in immunocompromised hosts. Treatment of intestinal protozoal infections is summarized in Table 68-10. Prevention of infection is focused on interruption of fecal–oral transmission and is similar to other bacterial and viral causes of traveler’s diarrhea, including personal hygiene, water disinfection, basic food precautions, and care in food preparation. Currently, no vaccines are available for enteric protozoan infections, although there are efforts to develop a vaccine for E. histolytica.

AEROMONAS SPECIES AND PLESIOMONAS SHIGELLOIDES

PART 8 FOOD AND WATER

In the United States, a seasonal peak in case reports coincides with the summer recreational water season and likely reflects increased outdoor activities and exposures, such as camping and use of communal swimming venues (e.g., lakes, rivers, swimming pools, and water parks).208 Persons at increased risk for infection reflect the fecal–oral transmission through food, water, and person to person and a low infectious dose, including (1) travelers to disease-endemic areas; (2) children in child care settings; (3) close contacts of infected persons (family or household contacts); (4) persons who ingest contaminated drinking water, contaminated recreational water (lakes, rivers, and pools), or untreated surface water (backpacking or camping); (5) persons who have contact with infected animals; and (6) men who have sex with men. Giardia accounts for a small percentage of TD. Because of the relatively long incubation period and persistent symptoms, Giardia is more likely to be found as the cause of diarrhea that occurs or persists after returning home from travel to a developing region. Epidemiologic studies suggest acquired resistance, with lower rates of infection and illness (1) among residents of endemically infected areas, compared with visitors and (2) among adults compared with children; however, reinfection occurs. Reservoir Giardiasis usually represents a zoonosis and has been detected in nearly all classes of vertebrates, including domestic animals and wildlife, including beavers, cattle, dogs, cats, rodents, and sheep. Although G. intestinalis infects both humans and animals with cross-infectivity, molecular epidemiology suggests that the role of zoonotic transmission to humans and the importance of animal contamination of food and water may be less than previously thought.208 Transmission and Infectious Dose Giardia infection is transmitted by the fecal–oral route and results from the ingestion of Giardia cysts through consumption of fecally contaminated food or water or through person-to-person (or, to a lesser extent, animal-to-person) transmission. The cysts are infectious immediately on being excreted in feces. Infected persons have been reported to shed 108 to 109 cysts in the stool per day and to excrete cysts for months. The infective dose of Giardia for humans is low; 10 to 25 cysts caused infection in eight of 25 subjects; more than 25 cysts caused infection in 100%. Infectivity apparently depends on both host and parasite factors.148 Person-to-person spread may be the most common means of transmission for humans. Areas and populations with poor hygiene and close physical contact have higher rates of infection, and infection of other household members is common. Venereal transmission occurs between homosexuals through direct fecal– oral contamination. Water is a major vehicle of infection in community outbreaks, from small water systems that use untreated or inadequately treated surface water, and may play a significant role in U.S. wilderness travelers who develop intestinal illness.109,208 Cysts retain viability in cold water for as long as 2 to 3 months. Giardiasis has been called backpacker’s diarrhea, because of the common association with alpine mountain waters. Pathophysiology and Clinical Presentation The pathophysiologic mechanisms of diarrhea and malabsorption in giardiasis are poorly understood, and more than one mechanism, including altered gut motility and hypersecretion of fluids, is probably involved. Most small bowel biopsies in human patients demonstrate minimal or no changes. Enterotoxins have not been found.148,157 Most infections are asymptomatic, but carriers can excrete high numbers of cysts in stools. Giardia is found in healthy people. The attack rate for symptomatic infection in the natural setting varies from 5% to 70%. Correlation between inoculum size and infection rates has been noted, but not with numbers of cysts passed or severity of symptoms. The incubation period averages 1 to 2 weeks, with a mean of 9 days. A few people experience abrupt onset of explosive watery diarrhea accompanied by abdominal cramps, foul flatus, vomiting, 1370

low-grade fever, and malaise. This typically lasts 3 to 4 days before transition into the more common subacute syndrome. In most patients, onset is more insidious and symptoms are persistent or recurrent. Stools become mushy, greasy, and malodorous. Watery diarrhea may alternate with soft stools and even constipation. Upper GI tract symptoms, typically exacerbated postprandially, accompany stool changes, but they may be present in the absence of soft stool. These include midabdominal and upper abdominal cramping, substernal burning, acid indigestion, sulfurous belching, nausea, distention, early satiety, and foul flatus. Constitutional symptoms of anorexia, fatigue, and weight loss are common. Unusual presentations include allergic manifestations, such as urticaria, erythema multiforme, and bronchospasm. Some Giardia infections are associated with chronic illness. Adults may have a longstanding malabsorption syndrome and marked weight loss, and children may have failure-to-thrive syndrome.65,86 Immunologic responses are effective in the majority of infections because spontaneous clinical recovery is common with or without the disappearance of organisms. The average duration of symptoms in all ages ranges from 3 to 10 weeks. Both cellular and humoral responses to Giardia have been demonstrated. Diagnosis Direct stool examination may be used when newer immunologic tests are not available. Cyst passage is extremely variable and not related to clinical symptoms, so multiple stool collections (i.e., three stool specimens collected every other day) increase test sensitivity. One stool sample will allow detection of 60% to 80% of infections, two stool samples will allow detection of 80% to 90%, and three stool samples will allow detection of more than 90%. Trophozoites may be found in fresh, watery stools (Figure 68-2) but disintegrate rapidly. Stools should be preserved in a fixative, such as polyvinyl alcohol, or a formalin preparation if not immediately examined. In the office, fresh stool can be mixed with an iodine solution (e.g., Gram’s iodine) or methylene blue and examined for cysts on a wet mount. Many antibiotics, enemas, laxatives, and barium studies mask or eliminate parasites from stools, so examinations should be delayed for 5 to 10 days after these interventions. Trichrome stain is better than the formalin–ether concentration technique for identification of protozoal cysts and trophozoites. Another noninvasive office test is duodenal mucus sampling, using a string test (Enterotest), which has a reported sensitivity of 10% to 80%. Duodenal biopsy is a sensitive test, but should rarely be necessary.128 Direct fluorescent antibody (DFA) testing is an extremely sensitive and specific detection method and is considered the “gold standard” by many laboratorians. Immunoassays using ELISA or enzyme immunoassay (EIA) on stool approach 100% sensitivity and specificity. Moreover, EIA is much easier and requires less experience than does microscopy. Other molecular techniques are available but not commonly used in clinical settings.

FIGURE 68-2  Giardia lamblia trophozoite seen by methylene blue wet mount staining under oil (×1000). The finding of cysts or trophozoites in a patient with diarrhea is sufficient to make a tentative diagnosis of giardiasis.

Pathophysiology and Clinical Course

Because of the difficulty and expense of confirming the diagnosis in some patients, a therapeutic trial of drugs may be attempted when suspicion is high. In the field, it is reasonable to initiate presumptive treatment for Giardia for secretory diarrhea (nondysentery) lasting more than 1 week that does not respond to a trial of antibiotic therapy. Symptomatic patients should be treated for comfort and to prevent development of chronic illness. Asymptomatic carriers in nonendemic areas should be treated when identified because they may transmit the infection or develop symptomatic illness. No drug is effective in all cases. In resistant cases, a longer course of two drugs taken concurrently has been suggested. Relapses occur up to several weeks after treatment, necessitating a second course of the same medication or an alternative drug. Malabsorption usually resolves with treatment, but persistent diarrhea may result from lactose intolerance or a syndrome resembling celiac disease, rather than from treatment failure. The three groups of drugs currently being used are nitroimidazoles (metronidazole, tinidazole, albendazole, ornidazole, nimorazole), nitrofuran derivatives (furazolidone), and acridine compounds (mepacrine, quinacrine).24,74 Tinidazole and nitazo­ xanide (Alinia) have similar or better effectiveness (average 85 to 90%) than does metronidazole and have been approved by the FDA for this use in the United States. Tinidazole is licensed for children older than age 3 years, and nitazoxanide is available in suspension for children as young as age 1 year. Albendazole has comparable effectiveness with metronidazole and is used commonly outside the United States because of its broad activity against other parasitic worms.183 Other alternatives include furazolidone, which results in cure rates between 80% and 96% and is also available as a pediatric suspension. Paromomycin (Humatin) is a nonabsorbable drug that is recommended for pregnant women or for use in severely symptomatic individuals. Quinacrine (Atabrine) achieves high cure rates, but it is no longer available in the United States because it produces more frequent side effects, especially in children. Mebendazole and ornidazole are two other nitroimidazoles that have been used successfully, but less data are available for these drugs. Treatment of giardiasis has been extensively reviewed by Gardner and Hill.74

The pathogenicity of E. histolytica is still not well understood. Invasion may be a function of motility, soluble toxins, cysteine protease, or lytic enzymes.171,185 The cecum and ascending colon are most frequently involved, followed by the rectum and sigmoid colon, with lesions of increasing severity and depth of inflammation and ulceration. Extraintestinal spread is hematogenous. Abscesses containing acellular debris develop primarily in the liver but may involve the brain and lung. The incubation period ranges from 1 to 4 months. Although 80% to 99% of infections result in asymptomatic carriers, a spectrum of GI diseases may result, with considerable variation in severity. Most often, colonic inflammation without dysentery causes lower abdominal cramping and altered stools, sometimes containing mucus and blood.100 Weight loss, anorexia, and nausea may be present. Symptoms commonly fluctuate and continue for months. The subacute infection may evolve into a chronic, nondysenteric bowel syndrome, with intermittent diarrhea, abdominal pain, weight loss, and flatulence. Dysentery may develop suddenly after an incubation period of 8 to 10 days or after a period of mild symptoms. Affected persons may have frequent passage of bloody stools, tenesmus, moderate to severe abdominal pain and tenderness, and fever.163,185 Amebic liver abscess is the most common and serious complication from hematogenous spread. Individuals can present with liver abscess months to years after travel or residency in an area of endemicity. The disease should be suspected in anyone with an appropriate exposure history (residency or travel in an area of endemicity) presenting with fever, right upper quadrant pain, and substantial hepatic tenderness. The fatality rate for amebic dysentery and its complications is about 2%. Complications of intestinal involvement develop in 2% to 20% of cases and include perforation, toxic megacolon, and ameboma—an annular inflammatory lesion of the ascending colon containing live trophozoites. A postdysenteric syndrome can occur in patients with acute amebic dysentery and can be confused with ulcerative colitis. Asymptomatic carriers of E. histolytica can develop invasive disease, but more often the infection resolves spontaneously. Humoral antibodies increase with invasive disease and persist for long periods. Although they do not protect against reinfection or bowel invasion, they may prevent recurrent liver infection. Mucosal immunity may provide some protection against recurrent intestinal infection with E. histolytica; once the infection is cleared, recurrence is unusual. But asymptomatic cyst shedding and active GI illness may persist for years, indicating lack of consistent immune response in the intestinal lumen. Oral vaccines and DNA-based vaccines have been successfully tested in animal models, but human testing has not been done and no vaccine is currently available.185,186

ENTAMOEBA The genus Entamoeba contains many species. Six that can reside in the human intestinal lumen are E. histolytica, Entamoeba dispar, Entamoeba moshkovskii, E. polecki, Entamoeba coli, and Entamoeba hartmanni. E. histolytica is the only species definitely associated with clinical pathology in humans. The others are considered commensal; however, E. polecki and E. moshkovskii have been suspected of causing lower intestinal symptoms in cases involving heavy infection.69 In addition, isoenzyme analysis has recognized 22 different zymodemes of E. histolytica, which may explain geographic differences in rates of invasive disease.161 Epidemiology and Risk E. histolytica is found worldwide. Similar to Giardia, transmission is fecal–oral through person-to-person contact or contaminated food or water. Cysts remain viable outside the body for weeks to months, as opposed to the fragile trophozoites. Unlike Giardia, there is no zoonosis, and the reservoir of infection is human. Approximately 12% of the world’s population is infected. The higher prevalence (30% to 50%) in tropical countries is related to increased risk of fecal–oral contamination, which depends on sanitation, cultural habits, crowding, and socioeconomic status.185 E. histolytica is a leading cause of death by parasitic infection worldwide. The WHO estimates that E. histolytica infects 500 million people per year, causes disease in 50 million, and kills 100,000 individuals annually. Importation of infections by travelers and immigrants accounts for most cases in the United States and other temperate countries. Amebiasis accounts for less than 1% of TD.

Diagnosis Routine screening of asymptomatic persons of high-risk groups is not cost-effective, except perhaps for food handlers and persons returning from extended stay in endemic countries. The diagnosis of invasive amebiasis is most commonly attempted by a combination of microscopy of a fecal specimen, serological testing, and, where indicated, colonoscopy and biopsy of intestinal amebic lesions or drainage of a liver abscess. Where available, detection of E. histolytica–specific antigen and DNA in stool and other clinical samples (enzyme-linked immunosorbent assay [ELISA]) may replace microscopic stool exam, which is complicated by morphologically similar nonpathogenic species. Antigen detection using ELISA is both rapid and technically simple to perform and can be used in laboratories that do not have molecular facilities, making it appropriate for use in the developing world where amebiasis is most prevalent.192 Serologic tests are not useful for identifying asymptomatic carriers but are positive in 85% to 95% of patients with dysentery and 90% to 100% of patients with liver abscess. In combination with ultrasound or other abdominal imaging, serology is helpful for diagnosis where PCR is not routinely available. Because they also do not distinguish between current and prior infections, serologic tests are more useful in developed countries with low 1371

CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Treatment

PART 8 FOOD AND WATER

incidence of infection. The combination of serological tests with detection of the parasite (by antigen detection or PCR) offers the best approach to diagnosis.69 New antigen detection techniques can differentiate between E. histolytica and E. dispar. PCR techniques have been developed and show greater than 95% sensitivity and specificity. Diagnosis of intestinal amebiasis by microscopic identification of cysts or trophozoites in stool still plays a significant role where other techniques are not available. Mucus from fresh stools or sigmoidoscopic scrapings and aspirates mixed with a drop of saline may show trophozoites if examined within an hour. For delayed examination, stool must be preserved in polyvinyl alcohol or other fixative and may be examined later with trichrome stain. Fecal shedding of cysts is irregular, but three stools on alternate days identify most infections. Sigmoidoscopy or colonoscopy is useful for viewing the pathologic lesions and obtaining selective samples of mucus and biopsies of mucosal ulcers, which usually contain organisms. Finding cysts does not confirm the diagnosis of symptomatic intestinal amebiasis. The key to establishing the diagnosis is finding motile trophozoites with ingested red blood cells. It is rare to identify E. histolytica in stool samples from patients with liver abscesses. Culture techniques are available, but not generally used in clinical laboratories because they are expensive and time consuming. Treatment There are multiple benefits to treatment, including reducing the infectious period, length of illness, risks of transmission to others, rates of severe illness, and preventing complications of invasive disease.35 U.S. guidelines suggest that asymptomatic carriers should be treated, because a cyst passer represents a potential health hazard to others, and reinfection in the United States is uncommon. Moreover, asymptomatic colonization with E. histolytica, if left untreated, can lead to invasive disease. Treatment of amebiasis is based on the location of infection and the degree of symptoms. Medications are divided into tissue amebicides (e.g., metronidazole, tinidazole, emetine, dehydroemetine, chloroquine), which are well-absorbed drugs that combat invasive amebiasis in the bowel and liver, and poorly absorbed drugs (e.g., iodoquinol, paromomycin, diloxanide furoate) for luminal infections. In general, treatment is effective for invasive infections but disappointing for intestinal colonization. The current drug of choice for asymptomatic carriers is iodoquinol. Side effects are mild and consist of abdominal pain, diarrhea, and rash. Diloxanide furoate (Furamide) is another drug of choice, but in the United States it is classified as an investigational drug, available only through the Centers for Disease Control and Prevention. Paromomycin is also effective. Although metronidazole has been used in asymptomatic carriers with 90% success, most reserve this drug for invasive and symptomatic infections.13,161 Invasive disease is treated with a tissue-active drug, followed by a luminal agent (in the same dosages as for asymptomatic infection). Tinidazole or metronidazole are the drugs of choice for oral therapy of amebic dysentery or liver abscess. Tinidazole has slightly better effectiveness and fewer side effects than does metronidazole. Other nitroimidazoles that have been tested include ornidazole, nitazoxanide, and secnidazole. Emetine and dehydroemetine are used parenterally in severe cases of amebiasis, primarily extraintestinal, followed by iodoquinol for 20 days. These two drugs have frequent systemic side effects, including development of cardiac arrhythmias requiring hospitalization for cardiac monitoring. Because this class of drugs is related to ipecac, the drugs also cause vomiting. Successful resolution of symptoms from E. polecki has been reported with metronidazole followed by diloxanide furoate in the same dosages as for amebiasis.

CRYPTOSPORIDIUM* Cryptosporidium is a coccidian parasite related to Toxoplasma and Plasmodium. Other coccidia capable of causing human intestinal infection include Microsporidia, Cyclosporidia, and Isospora. In *References 25, 29, 32, 33, 36, 85, 112, 133, 146, 167, 181.

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the environment, Cryptosporidium exists as a hearty, 5-mm-­ diameter oocyst containing four sporozoites. As with Giardia, the cysts are infectious when excreted. Humans and animals are infected by ingesting these oocysts, which travel through the gut lumen to the small intestine, where they release the sporozoites. Epidemiology and Risk for Wilderness and International Travelers The epidemiology and transmission of Giardia and Cryptosporidium parvum are similar. C. parvum causes a ubiquitous zoonosis with worldwide distribution. Cryptosporidium infects a wide variety of domestic and wild animals. Molecular analysis has revealed at least 14 species of Cryptosporidium that are distinguished primarily, but not solely, by host and cannot be distinguished by morphology. It is a reemergent enteric pathogen in humans. The prevalence of infection in human populations varies from 0.1% to 3% in cooler, developed countries (in Europe, North America) to 0.5% to 10% in warmer countries (Africa, Asia). The infection has been described in persons who have contact with animals, such as veterinarians and farmers; infants in day care centers; travelers to endemic areas; and patients who have AIDS or who are otherwise immunocompromised. It has infected large numbers of individuals in community-wide waterborne outbreaks.208 Cryptosporidium poses a risk to wilderness users because oocysts are found widely in surface water and have high degree of resistance to chlorine.120,121 (see Chapter 67) The infective dose of Cryptosporidium for humans is low (mean 132 cysts in a human challenge trial), similar to that seen with Giardia species.44 Fecal–oral contamination is the mode of transmission. The different routes of transmission are waterborne, especially in large community outbreaks; person to person, especially in day care centers, custodial institutions, and hospitals; food-borne; sexual, with no association with specific behavior; and zoonotic. Pathophysiology and Clinical Course The pathophysiologic mechanisms of diarrhea and malabsorption are not completely understood. The parasites may activate cellular and humoral immune and inflammatory responses, leading to cell damage and ultimately producing malabsorption and osmotic diarrhea. Clinical manifestations depend on the patient’s immune status, but asymptomatic infection occurs in both normal and immunocompromised hosts. In immunocompetent persons, the usual incubation period of Cryptosporidium is from 5 to 28 days. Symptoms consist of watery diarrhea associated with cramps, nausea, flatulence, and, at times, vomiting and low-grade fever. The syndrome is generally mild and self-limited, lasting 5 to 6 days in some groups (range, 2 to 26 days). In contrast, immunocompromised hosts experience more frequent and prolonged infections, with profuse chronic watery diarrhea, malabsorption, and weight loss lasting months to years. Fluid losses can be overwhelming in a fulminant cholera-like illness, with high mortality. Cyst passage in stool usually ends within 1 week of resolution of symptoms, but may persist for up to two months after recovery. Reinfection of an immunocompetent person has been documented. Rarely, Cryptosporidium can infect other organ systems, include the respiratory system, liver and biliary system, and stomach, particularly in immunocompromised persons. Diagnosis Oocysts can be found in the stools routinely in intestinal infections, even though shedding may be intermittent. Concentration techniques and staining with modified acid-fast, Giemsa, or Ziehl–Neelsen techniques facilitate identification of Cryptosporidium oocysts. The Enterotest (string test to sample duodenal mucus) is also useful in the diagnosis of cryptosporidiosis. Newer immunologic techniques (immunofluorescence and enzyme immunoassay) to detect antigen in stools are faster and have adequate sensitivity and excellent specificity. Several other molecular diagnostic methods have been developed, but their efficacy in the clinical setting is not yet known.

No clearly effective treatment has been found for cryptosporidiosis. Because this disease is usually mild and self-limited in immunocompetent hosts, only supportive care is needed. Treatment is indicated for immunocompetent persons with persistent infection and in immunocompromised patients. Some effectiveness with paromomycin, azithromycin, and nitazoxanide has been found against Cryptosporidium. Paromomycin, roxithromycin, ionophores, sulfonamides, and mefloquine have also been tested against cryptosporidiosis, especially in patients with AIDS and chronic diarrheal disease, with variable but generally positive effects. The most effective prevention in HIV patients is antiretroviral therapy (HAART) that supports the immune system.

ISOSPORA BELLI* Isospora belli is a coccidian protozoal parasite. It is an uncommon cause of diarrhea in humans, but its prevalence, like that of Cryptosporidium, has been increasing in immunocompromised patients. Ingested oocysts release sporocytes in the small intestine that develop into trophozoites. Epidemiology and the Risk for Wilderness and International Travelers Humans are the only host (although there are a few reports in dogs), and infections are transmitted by fecal–oral contamination through direct contact of food and water, so rates are typically higher in settings with high density of people, close contact, or poor hygiene. I. belli is endemic in areas of South America, Africa, and Asia. The prevalence is not precisely known, but ranges from 0.2% to 3% in U.S. patients with AIDS and from 8% to 20% in Haitian and African patients with AIDS. Infection rates in otherwise healthy persons with diarrhea are usually low. Most cases have been identified in tropical regions among natives, travelers, and the military. Pathophysiology and Clinical Course The life cycle and pathogenesis of I. belli are similar to those of Cryptosporidium. The organism invades mucosal cells of the small intestine, causing an inflammatory response in the submucosa and variable destruction of the brush border. In immunocompetent persons, I. belli infection may be asymptomatic or cause mild transient diarrhea and abdominal cramps. Other symptoms include profuse watery diarrhea, flatulence, anorexia, weight loss, low-grade fever, and malabsorption. Generally, infection is self-limited, ending in 2 to 3 weeks, but some persons have symptoms lasting months to years. Infections in immunocompromised patients tend to be more severe and follow a more protracted course. Rarely, acalculous cholecystitis or reactive arthritis has been reported. Recurrences are common. Diagnosis Diagnosis can be made by identification of immature oocysts in fresh stool. However, excretion may occur sporadically and in small numbers, so concentration techniques are usually required. Staining with modified Ziehl-Neelsen can also be useful. When stools are negative, the organism can be recovered from the jejunum through a biopsy or string test. Unlike the other intestinal protozoa, I. belli may cause eosinophilia. Treatment Successful treatment has been reported with trimethoprim– sulfamethoxazole (TMP-SMX). Other options are pyrimethamine with folinic acid, metronidazole, and nitazoxanide (for patients *References 33, 80, 125, 128, 157, 204.

allergic to sulfonamides). In patients with HIV infection, chronic lifetime suppression therapy is indicated with either TMP-SMX or pyrimethamine plus folinic acid daily.

CYCLOSPORA CAYETANENSIS* Cyclospora species were initially thought to be blue-green algae (cyanobacteria-like organisms). The life cycle and pathogenesis of Cyclospora cayetanensis are not completely understood. Oocysts need about 7 to 15 days to sporulate and become infectious, so they are not immediately infectious on passage. Epidemiology and the Risk for Wilderness and International Travelers C. cayetanensis has been shown to be an important cause of acute and protracted diarrhea. Fecal–oral transmission occurs through food, water, and soil. The organism is endemic in many developing countries in all continents. There are numerous reports of Cyclospora infection with diarrhea in travelers to Nepal, Haiti, Peru, and Guatemala. In the United States, most of the outbreaks have been food-borne, associated with ingestion of contaminated imported raspberries. Humans are the only known reservoir; there is conflicting evidence for a zoonosis. Pathophysiology and Clinical Course The onset of diarrhea is usually abrupt, with symptoms lasting 7 weeks or even longer. Other symptoms include anorexia, nausea, flatulence, fatigue, abdominal cramping, and weight loss. In patients with AIDS, the duration may be longer and severity greater. This is a familiar clinical picture from intestinal protozoa. Diagnosis Small spheric organisms can be detected in fresh or concentrated stool. They show variable staining with acid-fast methods, but stain best with carbolfuchsin. Phase-contrast microscopy and autofluorescence are also useful in the diagnosis. A PCR method is used primarily for research. Treatment The treatment of choice is TMP-SMX. This treatment provides rapid clinical and parasitologic cure, with few recurrences. In patients with AIDS, chronic suppression with TMP-SMX may be required. Ciprofloxacin has been used successfully in persons with sulfa allergy.

MISCELLANEOUS PARASITIC AGENTS Microsporidia† More than 100 genera and 1000 species of microsporidia exist in the phylum Microspora. Most species infect insects, birds, and fish. Only 12 species have been reported to infect humans, and of these, only two, Enterocytozoon bieneusi and Encephalitozoon intestinalis, have been found to cause diarrhea in humans. Microsporidia are obligate intracellular protozoa. Transmission is thought to be fecal–oral or urinary–oral and the infection zoonotic. Spores are environmentally resistant, so waterborne transmission also occurs. Prevalence of microsporidiosis in patients who have AIDS and chronic diarrhea is 7% to 50%. Diarrhea from microsporidia has been reported in travelers to the tropics. Clinical manifestations of intestinal microsporidiosis are chronic diarrhea, loss of appetite, weight loss, malabsorption, and fever. Acute self-limited diarrhea has been reported in immunocompetent hosts. Other infections include keratoconjunctivitis, hepatitis, peritonitis, myositis, CNS infection, urinary tract infections, sinusitis, and disseminated disease. Diagnosis involves trichrome staining of concentrated stools or intestinal biopsy sampling. Electron microscopy is considered the gold standard. Immunologic and molecular biologic techniques are still under evaluation.

*References 7, 33, 80, 126, 149, 157, 178, 189. † References 31, 33, 39, 71, 80, 123, 128, 135, 180, 204, 205.

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CHAPTER 68  Infectious Diarrhea From Wilderness and Foreign Travel

Treatment

The most effective drug against most species is albendazole (400 mg twice a day for 2 to 4 weeks). Other drugs that show different efficacies include atovaquone, metronidazole, furazolidone, azithromycin, itraconazole, and sulfonamides. Sarcocystis* Few human infections with Sarcocystis have been reported. Infection may be asymptomatic or associated with diarrhea, abdominal pain, nausea, and bloating. Symptoms typically improve within 48 hours of onset of illness. Diagnosis is based on identification of cysts in concentrated feces. No specific treatment has been established, but TMP-SMX and furazolidone have had variable efficacy. Balantidium  B. coli is a rare pathogen in humans.176,204 It is the largest and only ciliated protozoa that infects humans. The life cycle involves only trophozoite and cyst stages. Many aspects of the epidemiology are unclear. Pigs appear to be the primary reservoir, although other animals have been implicated. There is no intermediate host. Transmission is fecal–oral, and water is the most common vehicle. Infection is most common in tropical and subtropical regions with poor hygiene. Clinical features resemble those of amebiasis, with a spectrum including asymptomatic infection, chronic intermittent diarrhea of variable intensity, acute dysentery with mucosal invasion, and, rarely, metastatic abscesses. Diagnosis is made by observing the organism in a stool wet mount. Trophozoites are seen much more often than are cysts. Recommended treatment is tetracycline or metronidazole. Nitazoxanide is an alternative. *References 33, 80, 176, 204.

Blastocystis* The role of Blastocystis hominis in diarrheal disease is still controversial. The life cycle of B. hominis continues to be debated. The organism is frequently identified in stool samples by its characteristic appearance, but has not been directly correlated with symptoms, which might be caused by other undetected pathogens. Treatment is not warranted in asymptomatic infections. When found in large numbers as the sole pathogen, B. hominis is suspected as the potential etiologic agent of diarrheal illness. The few treatment trials yield mixed reports and are supported by in vitro studies. Dientamoeba† Dientamoeba fragilis occasionally causes diarrhea, occurring characteristically in residents of or visitors to developing tropical regions. It may be found in stools of persons without enteric symptoms. Because cyst forms have not been identified, the mode of transmission remains unknown. Illness caused by the parasite typically resembles giardiasis. Identification can be done from stool samples, a fixative, and nearly any type of stain. Treatment of D. fragilis is effective with iodoquinol and tetracyclines. There are also reports of successful treatment with metronidazole, paramomycin, and secnidazole.176,204

*References 127, 188, 191, 204. † References 105, 176, 204.

REFERENCES Complete references used in this text are available online at www.expertconsult.com.

CHAPTER 69 

Nutrition, Malnutrition, and Starvation  E. WAYNE ASKEW

How does it feel to starve? I am hungry. I am always hungry. … At times I can almost forget about it but there is nothing that can hold my interest for long. … I am cold. … My body flame is burning as low as possible to conserve precious fuel and still maintain my life processes. … I am weak. I can walk miles at my own pace in order to satisfy laboratory requirements, but often I trip on cracks in the sidewalk. To open a heavy door, it is necessary to brace myself and push or pull with all my might. I wouldn’t think of throwing a baseball and I couldn’t jump over a twelve inch railing if I tried. This lack of strength is a great frustration. It is often a greater frustration than the hunger … and now I have edema. When I wake up in the morning my face is puffy. … Sometimes my ankles swell and my knees are puffy. … Social graces, interests, spontaneous activity and responsibility take second place to concerns about food. … I lick my plate unashamedly at each meal even when guests are present. … I can talk intellectually, my mental ability has not decreased, but my will to use my ability has. OBSERVATIONS BY A TEST SUBJECT, MINNESOTA STARVATION STUDY, AFTER 24 WEEKS OF SEMI-STARVATION (1570  KCAL/DAY, 24% WEIGHT 58 LOSS) (IN THE BIOLOGY OF HUMAN STARVATION, VOL. II ) 1374

Importance of Nutrition in Stressful Environments Nutrition has a profound underlying importance to human physiologic homeostasis and functioning on a day-to-day basis in everyday life; it becomes even more important when humans work or recreate in particularly challenging or “extreme” environments.10 The central role of nutrition is often underappreciated in wilderness expedition planning and may even be thought by some to be of minor importance. Many enthusiasts do not consider food as critical as gear and equipment, medical supplies, physical fitness, and other logistical considerations. In temperate environments, where food and water are plentiful and re-supply is feasible, the importance of nutrition may seem to diminish compared with other aspects of wilderness medicine. However, when a stressful physical environment is superimposed on the physically demanding tasks associated with wilderness activities, the role of nutrition rapidly becomes of prime importance for maintenance of performance and for prevention of disease and injury, as evidenced from the description of Napoleon’s disastrous 1812 winter retreat from Moscow: The ice and deep snow with which the plains of Russia were covered, impeded … calorification in the capillaries and

For online-only figures, please go to www.expertconsult.com

Fortunately, situations encountered in wilderness activities are usually less grim than those faced by Napoleon’s army. There is usually some food available, and few enter these environments unprepared. However, misfortune, combined with suboptimal or haphazard nutritional planning, can spell disaster for even the best-prepared adventurer. A wrong turn on the trail, an injury, unanticipated terrain, an unexpected storm, or a downed airplane can deplete or isolate a victim from anticipated food sources. Food becomes an overriding consideration in a survival situation, particularly as the supply is exhausted. Although a shortage of food is certainly of concern, it does not necessarily imply impending disaster. Humans are remarkably adaptable and can subsist on nonideal dietary patterns for prolonged periods without dis­ astrous effects on health and performance. As long as some baseline level of energy intake is present, at least a minimal intake of vitamins and minerals will be ensured, forestalling the eventual onset of malnutrition and clinical nutrient deficiency states. Hunger is not comfortable; optimism wanes, weight loss results, and performance may suffer, but a food-deprived individual can still function for an extended period of time. One purpose of this chapter is to review some of the physical and mental consequences of suboptimal nutrition that might be anticipated under varying degrees of food restriction. The medical planner can use this information to anticipate limitations in expedition progress or capabilities and to recognize the state of health of rescued victims of starvation or food restriction. Equally important is the proper way to re-aliment a victim after a prolonged period of unintentional starvation. This can be critically important in a rescue situation, where transport of a victim to a medical facility requires several days of refeeding en route. Although the goal of expedition food planning is to meet daily energy and micronutrient requirements, it is not always possible to provide optimal nutrition because of logistic or situational constraints. Three nutritional states or situations may be anticipated or encountered in the wilderness: (1) optimal nutrition for effective functioning in environmental extremes, (2) suboptimal nutrition or malnutrition, and (3) lack of nutrition or starvation. Dietary planning for both wilderness expeditions and emergencies will be discussed, along with some specific food or nutrient items that may be particularly useful in wilderness expeditions.

ENVIRONMENTAL STRESS AND NUTRIENT REQUIREMENTS The physical and physiologic conditions of an individual (e.g., body weight, strength, coordination, fluid and electrolyte balance, and core temperature) play a significant role in determining nutritional requirements to maintain homeostasis. These conditions also directly influence survival time, especially when humans are deprived of food or water. In the short run, the most important nutrient is water.9 If an adequate supply of water is not available, all discourse on the physiology of starvation and malnutrition is pointless, because death from dehydration will occur prior to depletion of energy stores. Humans can survive food deprivation for extended periods of time—weeks or even months—depending on their level of body fat. A nonobese adult may live as long as 60 to 70 days while fasting in clinical setting.52 At the end of this time, almost all body fat and one-third of the lean body mass would be lost.51 James Scott, a victim of unintentional situational starvation, was marooned in a snow cave in the Himalayas with water but no food. He survived 43 days without food while losing one-third of his body weight, although he was near death at the time of rescue.104 Death from starvation in nonobese individuals is imminent if approximately 50% of body weight has been lost.

This usually corresponds to a body mass index (BMI) of 12 kg/ m2, although under some circumstances, a BMI of as low as 11 may be encountered prior to death.31 Time to death after complete water deprivation is measured in days—estimates run from 6 to 14 days, depending on the rate of body water loss, which is influenced by the temperature, humidity, and activity level.51 Water is critical because it, more so than any other nutrient, is responsible for maintaining homeostasis of the internal environment.9 It provides an aqueous medium to transport heat from cells to blood, to solvate and pass nutrients between blood and cells, to serve as a medium for intracellular reactions, and to transfer metabolic products for redistribution or excretion via urine. Both the quantity of reactants and the volume of fluid in which they are dissolved influence cellular chemical reaction rates; hence, imbalances in hydration status can alter cellular and tissue function, such as the body’s ability to regulate temperature. Muscle contraction depends on transformation of chemical energy (ATP) to mechanical energy. Nearly three-fourths of the energy used for muscle contraction is released as heat. Unless localized heat production from metabolism and muscle contraction is dissipated, the heat burden can be structurally damaging to enzymes or other proteins. Water absorbs heat produced at the cellular level and transfers it to the surface of the skin, where it can be dissipated to the external environment. The importance of water is discussed in greater detail in Chapter 70. The focus of this discussion is on energy restriction and assumes an adequate supply of water. For planning purposes, most wilderness expeditions require 3 to 5  L (about 3 to 5  qt) of potable water per person per day. Advances in food processing, preservation, and nutrient fortification have resulted in modern camping foods and the military equivalent, field rations, that can support health and performance in a variety of temperate environments, even if they are not consumed to complete caloric adequacy.73 However, nutrition that was marginally adequate in a temperate environment may rapidly become inadequate in wilderness environments characterized by extreme temperatures, terrain, and physical demands.72,74 Rodahl and Issekutz100 observed, “While short-term nutritional deficiencies in men at room temperature appear to have little or no detrimental effect on the capacity to do short-term, heavy work, there is a marked reduction in physical work capacity when a nutritional deficiency or nutritional stress is superimposed on a cold stress.” Superimposed stressors, such as extreme heat, cold, altitude, sleep deprivation, physical exertion, and food restriction, influence nutrient requirements7 and can jeopardize performance.* The complex interrelationship between environment and nutrition, and its effect on human physiology and performance, is depicted in Figure 69-1. Stressors in the form of environmental extremes can have serious consequences on health and performance. Proper nutrition can help counter detrimental environmental influences on physical and mental performance.2-7 Energy and fluid deficits arising from the interaction of environment and nutrition can negatively impact both physical39 and mental77 performance. Volitional physical activity as well as mood can suffer under caloric deprivation, depending on the magnitude and duration of the restriction. Motivation may be more acutely influenced by undernutrition than is actual physical performance.77 Nutritional deficits may have a greater effect on what individuals are willing to do (i.e., on their perceived mood, symptoms, and self-motivation) than on what they can do (psychomotor performance).108 Nutritional Considerations in Planning for Wilderness Activities Current national nutritional recommendations are revised periodically and can be found in the most recent dietary reference intakes published by the Institute of Medicine, National Academies.54 The dietary reference intakes (DRIs)88 are reference values for nutrient intakes that can be used to assess and plan diets for healthy people. Publications that list DRIs can be

*References 10, 39, 68, 72, 74, 77.

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CHAPTER 69  Nutrition, Malnutrition, and Starvation

pulmonary organs. The snow and cold water, which the soldiers swallowed for the purpose of allaying their hunger or satisfying their thirst … contributed greatly to the destruction of these individuals by absorbing the small portion of heat remaining in the viscera. The agents produced the death of those particularly who had been deprived of nutriment. BARON D. J. LARREY, INSPECTOR GENERAL, NAPOLEON’s MILITARY MEDICAL STAFF (IN HYPOTHERMIA AND WARFARE, 90 NAPOLEON’s RETREAT FROM MOSCOW, 1812 )

PART 8  FOOD AND WATER

Increased energy requirements

Increased water requirements

Inappropriate appetite response Decreased availability of food

Inappropriate thirst response Extreme environments (heat, cold, altitude)

Negative energy balance

Decreased availability of water Dehydration

Impaired thermoregulation Depleted muscle glycogen Deterioration of fine motor coordination Impaired effectiveness Diminished work capacity

FIGURE 69-1  The influence of extreme wilderness environments on food and fluid intake and on physical and mental performance. (Redrawn from Askew EW: In Hickson JF Jr, Wolinski I, editors: Nutrition in exercise and sport, Boca Raton, Fla, 1989, CRC Press, pp 367-384.)

clothing ensemble, and level of physical exertion.74 Work in cold environments can be adequately supported by various combinations of fat, carbohydrate, and protein, although certain combinations of macronutrients may be more beneficial than others in helping a person withstand cold exposure.4 As an example, Mitchell and colleagues81 demonstrated that cold tolerance (the length of time body core temperature could be defended during a controlled cold challenge) was favored by previous diets high in fat as opposed to diets higher in carbohydrate or protein. Subsequent research has indicated that the macronutrient source is less important in the cold than consuming enough total calories to support activity and thermogenesis.4,45

obtained through the National Academies website (http:// www.nap.edu/catalog.php?record_id=11767) and the National Institutes of Health website (http://ods.od.nih.gov/Health_ Information/Dietary_Reference_Intakes.aspx). The DRIs include four categories: estimated average requirement (EAR), recommended dietary allowance (RDA), adequate intake (AI), and tolerable upper limit (UL). EAR is the nutrient intake level estimated to meet the needs of 50% of the individuals in a population group. RDA is the nutrient intake level sufficient to meet the needs of 97% to 98% of individuals in a population group. AI is an estimate of adequate intake when an EAR cannot be established. AI and RDA are similar but not identical. The UL is the highest daily consumption level of a nutrient; when UL is exceeded, the nutrient poses a risk of adverse health effects. In general, for nutritional planning for wilderness expeditions, the basic daily diet should meet or exceed the DRI recommendations, especially if the traveler plans to subsist on them for prolonged periods of time (greater than 10 days). In the short run (less than 10 days), adequate energy provision is likely to be the predominant dietary concern. In the short run, certain nutrients may assume more critical or primary roles in environmental extremes than they might normally fulfill in everyday life. Cold, heat, and altitude stressors and their influences on macronutrient vitamin and mineral requirements have been a focus of considerable military and civilian research.8 Research conducted primarily in the era since World War II (WWII) and the Korean conflict has established that vitamin and mineral requirements are not significantly increased by cold exposure, although caloric requirements for thermogenesis and work may be elevated to varying degrees, depending on the cold challenge,

Oxidation of energy substrates from the diet or body stores

ATP

Utilization

UCP1

HEAT ~35%

Synthesis

Food and Adaptive Thermogenesis.  Mild cold exposure, even without increased physical activity, elevates energy expenditure in mammals, including humans.59,70,127 This process is called adaptive thermogenesis. Adaptive thermogenesis, or regulated production of heat by the body, is influenced by environmental temperature and diet.70 Figure 69-2 depicts the major sources of metabolic heat production in mammals. Heat can be generated from synthetic, oxidative, and/or uncoupling processes. Mitochondria, the organelles that convert food to carbon dioxide, water, and ATP, are fundamental in mediating effects on energy dissipation in response to an energy demand stimulus.48 Adaptive thermogenesis is a complex cascade of cell signaling events and primarily regulated by two major hormonal effectors: β-adrenergic agents and thyroid hormone. Thyroid hormones are major endocrine controllers of energy expenditure.48 Thyroid hormones are critical in providing a vigorous response to cold exposure and to sustaining that response by providing glucose and fatty acids

Biologic work. Muscular contraction, metabolic processes

HEAT ~60%

Brown adipose tissue. Up-coupling oxidation from phosphorylation

HEAT ~100%

FIGURE 69-2  Energy transforming pathways and heat production.

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Coffee

Green tea

Caffeine

Catechins (−)

(+)

(−) COMT

NFκ-β

(+) Phosphodiesterase

Norepinephrine (+)

(−)

Adenyl cyclase (+)

(+) Cold

cAMP

ATP

(+)

(+)

PGC1-α

Lipolysis

AMP (+) UCPs

(+) PPARs (+)

Fatty acid oxidation

(+)

(+) Energy expenditure/thermogenesis

FIGURE 69-3  Cell signaling , activation of thermogenesis and mecha­ nism of green tea and coffee stimulation of thermogenesis. Abbre­ viations: NFκB, nuclear factor kappa B; COMT, catechol O-methyl transferase; PC1-α, peroxisome proliferator-activated receptor gamma coactivator-1α; PPAR, peroxisome proliferator activated receptors; UCP, uncoupling protein; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; AMP, adenosine monophosphate. (Modified from Hursel R, Westerterp-Plantenga MS: Thermogenic ingredients and body weight regulation. Int J Obes 34:659, 2010.)

little attention in recent years, possibly because of the current focus of thermogenic research on obesity and perhaps because of the perception that advances in clothing and equipment make internal heat generation somewhat less critical as a mechanism to prevent hypothermia. Based mostly on older research, we know that dietary approaches incorporating frequent small meals, fat, caffeine/ephedra, or capsaicin seem to be the most practical and proven approaches to augmenting diet-induced thermogenesis. Other Potential Thermogenic Nutrients.  Recent research on the thermogenic properties of green tea seem to provide support for tea as a historically favored hot beverage for cold weather and high-altitude expeditions. In research directed at the possible role of green tea in stimulating thermogenesis in conjunction with weight loss diets to combat obesity, it has been found that green tea stimulates thermogenesis in a manner that cannot be completely attributed to its relatively low caffeine content.35,36 Green tea contains catechins that inhibit the enzyme catechol O-methyltransferase (COMT), which degrades catecholic compounds such as norepinephrine. Diminishing COMT’s net effect would be to permit higher and more sustained levels of norepinephrine, which in turn would permit a more sustained lipolytic response to support increased energy expenditure. Besides the catechin inhibition of COMT, green tea, as well as coffee, contains caffeine, which enhances thermogenesis by inhibiting the enzyme phosphodiesterase. Inhibition of phosphodiesterase prevents degradation of cyclic AMP, permitting lipolysis to continue and provide additional fatty acids for eventual oxidation.53 1377

CHAPTER 69  Nutrition, Malnutrition, and Starvation

to fuel energy production and thermogenesis.109 Thyroid hormone acts synergistically with catecholamines of the sympathoadrenal system during cold adaptation, times of high energy output and, conversely, when energy demands should be reduced, such as during starvation.109 Physiologic stimuli, such as cold exposure, elicit these thermogenic hormones, which in turn interact with specific cellular tissue ligand-activated nuclear receptors called peroxisome proliferator activated receptors (PPARs) in brown and white adipose tissue, liver, heart, and skeletal muscle. PPARs act as fatty acid sensors to control many metabolic pathways essential for energy homeostasis.125 PPARs are mainly expressed in white and brown adipose tissue, where they control expression of several proteins involved in upregulation of lipid metabolism, subsequent energy generation and thermogenesis. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a tissue-specific transcriptional coactivator protein that interacts with the nuclear receptor PPAR-γ. This permits interaction of this protein with multiple transcription factors, thus serving as a coactivator that enhances the activity of many nuclear receptors and coordinates cellular transcriptional programs important for energy metabolism and energy homeostasis. PGC-1α can interact with, and regulate the activities of, cAMP response element binding protein and nuclear respiratory factors that are involved in energy metabolism and thermogenesis. Uncoupling protein-1 (UCP1) is an uncoupling protein found in the mitochondria of brown adipose tissue (BAT). It is used to generate heat by non-shivering thermogenesis. Adrenergic and thyroid hormones have an impact on energy dissipation and subsequent heat production by the mitochondria in brown fat and skeletal muscle via a complex signaling mechanism involving PGC-1α, PPARγ, and UCP1.96 PPARγ is a nuclear receptor, subject to transcriptional coactivation by PGC-1α. PGC-1α is a transcription coactivator that plays a central role in regulation of cellular energy metabolism. It is induced by cold exposure, linking this environmental stimulus to adaptive thermogenesis.66 Induction of increased mitochondrial activity through activation of PGC-1α results in an increase in oxidative-type muscle fibers that in turn leads to enhanced resistance to muscle fatigue and increased tolerance to cold.63 PGC-1α is expressed at high levels in tissues where mitochondria are abundant and oxidative metabolism is active, such as BAT, heart, and skeletal muscle.96 The schematic relationship of these cell signaling and response elements and their potential interaction with cold, caffeine, and catechins is depicted in Figure 69-3. Although considerable research has been accomplished recently on basic cell signaling mechanisms influencing gene activity in response to thermogenic stimuli, less applied research has been conducted on nutrients and whole-body cold tolerance. Older studies of food and cold tolerance have largely used core temperature responses to actual cold exposure along with a dietary intervention; more recent cold tolerance research has incorporated aspects of basic cell signaling research described above in response to other food-derived components. Most notably, resveratrol, a plant polyphenol found in abundance in sources such as grapes and Japanese knotweed, has been shown to induce mitochondrial activity via activation of PGC-1α, which in turn increases oxidative-type muscle fibers, enhanced resistance to fatigue, and increased tolerance to the cold in a rat model.63 Assuming the rat model research has applicability to human cold tolerance, these effects are all potentially beneficial attributes for facilitating strenuous cold weather activities. Human resveratrol cold tolerance studies are lacking. It is unlikely that the food products containing resveratrol could be consumed in quantities adequate to exert a similar effect to that seen in the supplemented rat model. However, numerous concentrated resveratrol supplements and even food bars containing as much resveratrol as 50 glasses of wine are commercially available, making a comparable dose level of resveratrol perhaps feasible for human ingestion. Predicting significant effects of nutrients on cold tolerance based on the thermic effect of food (specific dynamic action of dietary component carbohydrate, fat, and protein) has not proved to be a reliable indicator of the ability of the body to resist cold exposure. Human cold tolerance thermogenic research, quite active in the World War II/Korean conflict, has received relatively

PART 8  FOOD AND WATER

In addition to inhibition of key enzyme responders in the body’s “braking system” of the stimulatory effect of norepinephrineactivated lipolysis, catechins also inhibit nuclear factor kappa B (NFκB), a transcription factor that normally regulates PPARs. Upregulation of key enzymes involved in fatty acid oxidation by PPARs increases energy expenditure along with enhanced stimulation of fatty acid release afforded by elevated cAMP. Finally, catechins have a direct effect on expression of several uncoupling proteins that also can influence thermogenesis via uncoupling or decreasing the efficiency of oxidative phosphorlyation.61,70 The role of green tea and coffee in enhancing energy expenditure (thermogenesis) is shown schematically in Figure 69-3. Other thermogenic “nutrients” may also have application in cold tolerance. Capsaicin is the major pungent compound found in certain pepper species and a common spice in many food products. It has been studied with mixed results for its thermogenic properties and influence on increasing fat oxidation.111 Capsaicin is believed to increase thermogenesis by enhancing catecholamine secretion from the adrenal medulla through activation of the central nervous system, resulting in β-adrenergic stimulation.53 It possibly upregulates certain uncoupling proteins in response to the catecholamine release.76 Polymorphisms in the receptor and promoter regions of genes of individuals may explain the variability in efficacy of capsaicin stimulation between individuals53 and some of the differences in capsaicin study results reported in the literature.46,50,111 Brown adipose tissue has been extensively studied in infants and animals under a variety of conditions. It helps maintain body temperature. It was formerly thought that this energy-rich and heat-generating tissue regresses with age.64,65 The recent discovery that humans contain more BAT than previously thought33,124 and that cold exposure activates BAT thermogenic activity in humans123 has stimulated BAT research in adult humans. In human cold exposure studies, BAT activity was inversely correlated with changes in distal skin temperature, suggesting a role for BAT in maintaining core body temperature.123 The unique uncoupling properties of BAT that make it such an efficient heatproducing organ may also be shared by other tissues, such as skeletal muscle. Wijers and colleagues127 have found that mitochondrial uncoupling in skeletal muscle during cold exposure may be one mechanism facilitating cold adaptive thermogenesis in humans. Dietary or pharmacologic approaches to stimulating BAT activity may be a promising way to turn on heat production during cold exposure. Future research on the metabolic and dietary control of adaptive thermogenesis may have particular relevance to diverse metabolic outcomes, such as obesity and weight loss research, as well as human cold tolerance. Fat, Carbohydrate, and Protein Content of the Diet May Be Tailored to Different Environments.  Although the most important nutritional concern in challenging environments, aside from water, is total energy intake, when wilderness activities shift from a sea-level, cold-weather environment to a moderateor high-altitude, cold-weather environment, the macronutrient balance in the diet should be reconsidered. Although fat is an efficient and well-tolerated energy source during relatively lowpower-output, cold-weather activities at sea level, it is not as well tolerated at high altitude.5 Substituting carbohydrate for fat and, to a certain degree, for protein can theoretically provide metabolic advantages to the individual’s critical oxygen economy when working at altitude.3 This is because carbohydrate is a more efficiently metabolized fuel at altitude than is fat, because it is already partially oxidized (i.e., it contains a higher ratio of oxygen atoms to carbon atoms) and therefore requires less oxygen to combust its carbon skeleton to CO2, H2O, and energy. Metabolizing carbohydrate for energy requires approximately 8% to 10% less inspired oxygen than is required to obtain a similar amount of calories from fat. A high-carbohydrate diet can reduce the symptoms of acute mountain sickness, enhance short-term highintensity work as well as long-term submaximal efforts, and lower the effective “felt” elevation by as much as 300 to 600 m (984 to 1969 feet) by requiring less oxygen for metabolism. Initial altitude exposure frequently results in anorexia and subsequently reduces energy and carbohydrate intake.25 Anorexia 1378

(and thus food intake) usually improves with time and acclimatization (3 to 7 days at altitude), but, depending on the altitude, may never match that at sea level. Weight loss and performance decrements are quite common under these conditions. Carbohydrate supplementation of the diet at elevations exceeding 2200 m (7218 feet), particularly with carbohydrate-containing beverages, is usually an effective method to increase carbohydrate and total energy intakes.3,25,37 Some,32 but not all,117 studies of carbohydrate supplementation at altitude have demonstrated a decrease in the adverse symptoms resulting from acute altitude exposure. Enhancement of short-term, high-intensity performance,26 as well as long-term, submaximal performance,3,14 by carbohydrate supplementation has also been noted in some studies involving altitude exposure. The beneficial effects of carbohydrate at altitude most likely depend on the type of exercise performed (intensity and duration) and the degree of prior muscle glycogen depletion experienced by the test subject, because of varying degrees of anorexia. Muscle glycogen is related to the caloric adequacy of an individual’s prior diet; carbohydrate intake usually parallels the overall dietary intake of the antecedent diet.3 It is a good plan to consume a mixed diet with snacks high in carbohydrate. The most effective form of carbohydrate supplementation in environmental extremes is usually liquid beverages; people will drink even when they are reluctant to eat.3,14,25,37 Increasing fluid intake along with carbohydrate intake is also beneficial at altitude, where increased fluid losses occur as the result of diuresis and of respiration in the dry (low-relative-humidity) atmosphere.9 The “Right” Macronutrient Mix for Work at Altitude.  There are two schools of thought regarding the most advantageous mixture of dietary macronutrients for work at altitude. Some believe that food preferences change markedly as elevation increases during the climb, and that carbohydrate becomes more palatable to the anorexic appetite. Others believe that once appetite recovers from the initial period of altitude acclimatization, the relative proportions of carbohydrate and fat in the diet are not as important as eating to energy demands to prevent loss of lean body mass. Early work published by Teasdale119 and later advocated by Pugh97 and Consolazio32 favored carbohydrate for work at altitude largely because of its structural oxygen content; carbohydrate is more highly oxidized than is fat or protein and therefore theoretically should require less atmospheric oxygen (which is, in effect, reduced at the reduced barometric pressure at altitude) for its metabolism to CO2 and ATP. This line of reasoning also agrees with what we know about the need for glycogen replenishment. Glycogen stores would be important energy providers for intense physical climbing work at altitude if one was working at a high percentage of V˙ O2max. However, as Teasdale119 aptly pointed out in his writings on “The Diet Problem for Mountaineers in the Himalayas,” the actual amount of work in foot-pounds done at altitude is usually self-limited and may be relatively low compared with that at sea level; the real problem is not the amount of energy that is expended but rather oxygen availability. Teasdale119 recommended that climbers should seek a diet “demanding as little oxygen as possible” and his recommendation for accomplishing this was the ingestion of carbohydrate at frequent intervals. He also was one of the first to point out the oft-encountered “vicious” cycle of human physical deterioration at altitude: loss of appetite– partial starvation–metabolism of climbers’ fat stores for energy– ketoacidosis–further anorexia and loss of appetite–loss of weight–deteriorated physical performance. This cycle of events, along with dehydration, is depicted schematically in Figure 69-1. Many of these situational/physiologic turning points leading to physical performance decrements can happen in other extreme environments, but the climber at high altitude seems to experience these adverse factors sooner and to a more significant degree than do workers in other environments. Washburn126 emphasizes that dietary carbohydrate becomes particularly more critical as altitude increases above 10,000 feet, and Consolazio32 identified carbohydrate as an important factor in lessening the initial severity of altitude illness. Although early observations by Pugh97 and subsequent research by other investigators seem to indicate that carbohydrate is better “tolerated” or preferred at

ENERGY: HOW CRITICAL IS IT? When planning for a prolonged wilderness outing, the following question should be asked: “If we run short on food, will we suffer severe consequences in our progress along our route and experience difficulty carrying our heavy packs?” For optimal performance, it is total energy intake, especially carbohydrate intake, that is the key for sustaining high-level work capacity for extended periods. However, performance across a broad spectrum of backcountry tasks, including load-bearing work, is not always severely degraded by short periods of suboptimal energy and carbohydrate intake. A review of the effect of energy restriction on military work performance indicated that soldiers can maintain relatively normal work capacities for short time periods (<10 days) of food restriction.39 The Minnesota starvation studies conducted during World War II demonstrated that energy deficits resulting in a loss of less than 10% of body weight did not greatly impair physical performance; however, underconsumption of calories for longer periods producing continued loss of body weight created significant deficits in physical performance,118 as evidenced by the observations of one test subject who participated in the 1570-kcal/day, 24-week semi-starvation study, resulting in 24% body weight loss: “Then came February twelfth, the starting date of semi-starvation … only two meals a day from now on. For the first two weeks the new life was fun. I was losing weight, of course, but I still had lots of energy. Then came the day when I lost my ‘will to activity’—I no longer cared to do anything that required energy.” The degree of reduction of work capacity depends on the degree of caloric restriction, the carbohydrate content of the food available, and the power output the work demanded. Studies of food restriction in military scenarios have revealed that restricted energy and dietary carbohydrate content over a 30-day period supported light to moderate activity level without evidence of greatly impaired physical performance capabilities.15 On the other hand, longer periods (8 weeks) of caloric restriction coupled with higher levels of energy expenditure (U.S. Army Ranger training) have been associated with significantly reduced physical performance capacity.86 Because studies have varied with regard to experimental conditions and performance measures, it is difficult to draw conclusions about the relationship between energy deficit and performance. Some indicators of performance, such as grip strength, appear to be well preserved until nutritional status is severely compromised. Other measures, such as maximal lift test, maximal jump height, isometric leg extension, and maximal oxygen uptake, appear to be more sensitive predictors of impaired performance.56 In general, in nonobese individuals, strength seems to be rather well maintained at a body weight loss of up to 5%. This may be good news for wilderness travelers who are concurrently on a gradual weight loss program. Shedding fat actually “lightens the load” without diminishing strength.

However, when dieting or restricting food results in loss of lean body mass, performance decrements result. Aerobic capacity and strength are reduced when loss of body weight exceeds 10%. Friedl39 reviewed the influence of reduction in body weight resulting from reduced food intake on muscle strength and aerobic capacity and concluded that changes in maximum oxygen consumption (V˙O2max) in response to modest caloric restriction generally influence performance to a lesser degree than do reductions in muscle strength in response to weight loss. The primary concern of weight loss due to inadequate energy consumption occurring during extended wilderness activities appears to be loss of muscle strength. Significant loss of muscle strength can be expected to occur following 5% to 10% body weight loss.39 Significant declines in aerobic capacity can also occur following weight losses of this magnitude, but the decline in aerobic capacity appears to have relatively little effect on individual performance at moderate (<50% V˙O2max) sustainable workload levels.39 In practical terms, this may mean that a gradual trek to the summit may not be precluded by a prior food restriction accompanied by significant loss of body weight, but that a short-term, all-out push for the summit to avoid impending bad weather would most likely be compromised. Factors other than strength and aerobic capacity should also be considered when evaluating the effects of energy restriction on performance. Although weight losses of 6% or less over periods of 10 to 45 days generally do not produce significant degradations in cognitive performance,108 mood may be adversely affected by caloric restriction.30,79 However, long-term reduced consumption resulting in 50% loss of energy requirements may significantly degrade cognitive performance.77 Reduced food intake, when coupled with other stressors such as high rates of energy expenditure and sleep deprivation, can also impair immune function.54,62,68 Carbohydrates: Critical for High Work Output Performance Both the length of time provided for dietary adaptation to carbohydrate restriction and the amount of carbohydrates in the diet can influence the level of aerobic endurance performance.2 Aerobic endurance performance can be reduced by 40% after only 4 days on a total-calorie-adequate but low-carbohydrate diet (i.e., with carbohydrates providing 10% of the kilocalories).42 When a diet that was similarly adequate in total calories, but with carbohydrates providing only 5% of the kilocalories, was fed for 2 weeks, performance was also reduced, but only by approximately 15%, presumably because of metabolic adaptations to the shift in energy sources that occur with time.95 Carbohydrate is important to performance, but the impact of any reduction in dietary carbohydrate intake depends on (1) the period of time over which it is reduced, (2) the absolute level of carbohydrate in the diet, and (3) the power output (P = F × D /T) needed to accomplish the task at hand. The latter point regarding power output requirements is an important consideration in the provision of food for wilderness activities. Since much wilderness activity is usually recreational and not competitive, self-paced work and the lowering of power requirements by increasing the time over which the work is accomplished is a feasible approach that can result in less reliance on carbohydrates and more reliance on a “slower burning” fuel, such as fat. Reduced carbohydrate intake, more than the reduction of any other macronutrient (with the exception of water), has the potential to negatively influence muscle glycogen levels and endurance.2 There is abundant evidence in the sports medicine literature to permit extrapolation to similar wilderness activities and to conclude that certain types of performance, such as backpacking, cross-country skiing, and climbing, may be influenced by an acute shortage of carbohydrates in the diet, depending on the intensity of the workload (% V˙O2max) in which the individual is engaged. Inadequate carbohydrates in the diet, coupled with successive days of intense prolonged exercise, results in a gradual reduction of glycogen stores, deterioration of performance, and increased perception of fatigue. Perceived or “felt” exertion for certain wilderness activities, such as load-bearing work, may reasonably be assumed to be a function of the dietary carbohydrate intake and its subsequent effect on muscle 1379

CHAPTER 69  Nutrition, Malnutrition, and Starvation

altitude, other more recent studies in normobaric101 and hypobaric hypoxic conditions99 have failed to show a carbohydrate “preference” at altitude.12 Reynolds and co-workers99 expected carbohydrate consumption to increase with increasing altitude in a study of climbers on Everest, but surprisingly found that retort pouch packages of high fat sausages seemed to be preferred under cold, high-altitude conditions. This preference could be due to a true preference for fat or simply the ease of utilization of the heat in a pouched food product. However, just because high fat foods gain some acceptance in the cold and perhaps even at altitude does not necessarily mean that carbohydrate loses its importance for glycogen repletion and maintenance of blood glucose levels for periods of high-power energy output. The most important consideration regarding fueling heavy physical work in the cold or in combination of cold and altitude is as Washburn126 puts it, “plenty of good food is of vital importance.” “Good food” that is appetizing served warm is likely to be consumed and therefore subsequently beneficial. Perhaps the real advantage of carbohydrate at altitude is more evident early in the ascent and, as climbers become more acclimated to the altitude, the exact macronutrient composition of the diet may be of lesser importance than individual climber food preferences.

PART 8  FOOD AND WATER

glycogen levels. To avoid fatigue and extend or enhance performance, carbohydrates may be ingested before, during, and after moderate to heavy intensity aerobic exercise.55 This requires daily consumption of approximately 500 to 600g of carbohydrate (about 60% of the kilocalories in a day’s food). The actual amount of carbohydrates required depends on the individual’s body size and energy needs. To put this into perspective, a review of typical dietary carbohydrate intakes of male soldiers fed a variety of rations during 18 field studies in temperate, hot, and cold environments revealed intakes ranging from 244 to 467 g/day.18 Similar data are not as well documented for nonmilitary wilderness activities, but it is probable that daily carbohydrate intakes would be similar and considerably less than the 500 to 600 g/ day recommended for optimal physical performance, because total caloric intake during work in the outdoor environments is often less than that required to maintain energy balance.73 Most people do not selectively consume low-carbohydrate diets during wilderness activities, but total carbohydrate intake is often low because of its relationship to total energy intake and because of limited high-carbohydrate food choices. Some backpackers seek to maximize food and caloric density because of the weight of, and space available in, their packs. Calorie-dense food item choices that achieve this goal are often high in fat and relatively low in carbohydrates. Inadequate food consumption in military field exercises has been ascribed to poor ration palatability and variety, menu boredom, not enough time to eat or prepare meals, anxiety, and intentional dieting to lose weight.73 Similar factors may be operative in wilderness expeditions. Countermeasures to reduce the effect of these factors should be taken into consideration during ration planning. To sustain short-term performance, a shortfall of energy (calories) is not as significant a concern as the lack of carbohydrate.39 Field studies of carbohydrate intake and performance are difficult to conduct because of the many uncontrolled variables encountered outside the laboratory. Therefore, definitive field studies demonstrating a positive effect of dietary carbohydrate supplements on wilderness performance are lacking.6 However, when field conditions can be imitated in well-controlled laboratory settings, the results suggest that carbohydrate supplementation benefits performance. In a study84 conducted using 18 physically fit U.S. Army Special Operation Forces soldiers as test subjects designed to test the concept that soldier performance would benefit from carbohydrate supplementation under conditions simulating field operations, subjects were fed a diet controlled to simulate a “typical” daily dietary intake of carbohydrate and protein encountered during field operations (327 g carbohydrate per day, 201 g fat per day, and 118 g protein per day, furnishing 3657 kcal/day). The soldiers exercised daily (11 days total) under conditions designed to simulate field energy expenditure patterns (intermittent- as well as sustained-activity patterns of varying intensity levels). Each test subject received one of three beverage supplements during the program: placebo (0 g carbohydrate), carbohydrates once a day immediately after exercise (180 g carbohydrate), or carbohydrates divided into several doses taken after the morning exercise session and at intervals during the afternoon exercise session (180 g carbohydrate in divided doses). A drop in the respiratory exchange ratio in all treatments was observed, indicating that the soldiers were experiencing a carbohydrate shortage in response to the field simulation and were switching to fat energy sources to sustain energy expenditure. However, the provision of supplemental carbohydrates permitted a higher level of physical performance or aerobic power to be attained. Run times to exhaustion were increased approximately 6% with the single carbohydrate feeding and 17% with the divided-dose administration. The ingestion pattern of the carbohydrate supplement as well as the carbohydrate itself appeared to influence performance, indicating that a supply of easily consumed carbohydrates (supplement or food) ingested before, during, and after field activities is an effective method to sustain or boost physical performance. Fat: A Special Place in Wilderness Exploration? Historically, wilderness explorers and expeditions have relied heavily on foods higher in fat content than current sports nutrition and healthy dietary guidelines recommend. One early 1380

20th-century explorer, Vilhjalmur Stefansson, became such a strong advocate of meat-based high-fat diets that he volunteered himself for an unusual experiment in 1928.67,113 Stefansson consumed an all-meat diet for a year with no detectable adverse medical consequences. Stefansson’s championing of high-fat diets for work in cold regions led to a World War II–era U.S. Army and Canadian test of a high-protein and high-fat pemmican diet (low in carbohydrate) for work in the cold, with less-thanencouraging results.57 Predictable fatigue occurred when the high-fat, low-carbohydrate diet was abruptly thrust on the soldiers. At the time, this study was offered as an argument against including pemmican in the cold-weather military diet. Notwithstanding the military’s lack of enthusiasm for high-fat food, recent arctic explorers such as Will Steger have relied on pemmican for nutritional support during cold-weather polar expeditions.114 Although we now know that a period of time is required for metabolic adaptation to a high-fat diet,92,93 the dispute concerning the suitability of high-fat diets continues. A review of numerous studies and the composition of the diets and experimental conditions under which they were conducted indicates that two factors are critical to the satisfactory utilization of high-fat diets: prior adaptation to fat in the diet and the power or exertion level at which the subjects were required to work.91 Humans permitted to adapt gradually to increasing levels of fat in the diet for approximately 3 weeks can function much better than if the dietary change is abrupt. High-power outputs require the capacity for repeated bursts of anaerobic metabolism, which is best fueled by carbohydrates (i.e., via glucose and glycolysis). Efficient fat metabolism depends on the ready availability of oxygen. The ability to take up oxygen necessary for fat oxidation becomes limiting at high power outputs. Military studies of fat content of the diet confirms that a subcaloric, relatively high-fat diet (1976 kcal/day; 46% fat) can maintain a moderate physical performance (including load-bearing work) for periods of up to 30 days.15,68 Practical physical and situational constraints such as caloric density, weight-per-volume considerations, prior experience, work level intensity, and local availability of food seem to affect the usefulness of relatively high-fat provisions used in support of wilderness expeditions.3,38 Fat, although not an ideal energy source for high power output competitive sporting events, can serve admirably as a concentrated energy source for outdoor activities requiring low power but sustained work performance over longer periods of time. This is because low power but sustained work such a carrying a loaded backpack along a trail at a comfortable pace, can usually be accomplished aerobically at a moderate % V˙O2max effort that can be energetically powered largely by fat oxidation without dipping deeply into glycogen reserves. Although fat has received a somewhat “tarnished” health image over the past 40 years via an imperfectly understood relationship with atherosclerosis and coronary heart disease, we have gradually come to understand that there is a significant interaction between the type of fat (fatty acid composition) and the individual’s habitual level of physical exertion. Simply put (although a bit oversimplified), fat intake becomes particularly problematic when highly saturated fat (e.g., C-16:0 palmitic acid) is consumed habitually without accompanying daily high rates of energy expenditure. Anthropologic support for this concept can be found by examining cardiovascular disease in early Arctic populations that subsisted on a largely meat diet, where fat was a highly prized commodity in comparison. No one would consider classically made pemmican a “health” food, because of its high saturated fat content. Although pemmican is historically considered to be an ideal “trail” food for cold-weather expeditions because of its caloric density and resistance to spoilage, no one advocates a long-term habitual diet based on pemmican. Pemmican consumption is largely self-limited—acceptable for its purpose in the backcountry for defined lengths of time but not acceptable as a staple in daily everyday life. There is little scientific evidence that short periods (usually less than 1 month) of a high-fat diet has an irreversible effect on cardiovascular health, although a single high-fat meal can acutely influence endothelial response to the meal ingestion, causing a narrowing of the arteries supplying blood to the extremities.85 We project from observations such as this and epidemiologic studies linking long-term high dietary fat

Protein and Maintenance of Lean Body Mass and Performance Considerable discussion of the proper amount of protein to maintain muscle mass, prevent wasting, and sustain performance under conditions of physical stress exists in the literature. However, despite all the controversies, recommendations concerning the amount of protein in the diet have changed little since the World War I era, as evidenced by the 1919 report by Murlin and Miller:83 “The amount of protein … sufficient to repair all of the wastes of the body and to supply an adequate reserve is 13% of the total energy intake. It seems a matter of indifference to the muscles whether they receive their energy from carbohydrate or from fat … . Hard muscular work therefore can be done on a diet high in carbohydrate or on a high fat diet. It is of general experience, however, that muscular work is done with less effort if there is a plentiful supply of carbohydrate.” Thirteen percent of the energy intake translates to an intake of 65 g of protein per day on a modest energy intake of 2000 kcal/ day, or 130 g of protein per day on a more strenuous 4000 kcal/ day energy intake. Quantities of dietary protein in the range of 65 to 135 g/day are rather easy to obtain, even for the most casual ration planner (e.g., one stick of beef jerky or one serving of peanut butter contains 6 to 8 g of protein). Protein and the Maintenance of Muscle Mass When Energy Intake Is Inadequate.  Approximately 40 g of dietary protein per day seems to be the minimum required to prevent excessive nitrogen loss under food restriction.27 Although this amount is easily achieved, even with a suboptimal intake of 1500 kcal/day of a mixed diet containing 15% protein, ration planners should strive to achieve 100 to 150 g protein per day (15% of the daily kilocalories) for most individuals consuming food in proportion to their energy expenditure. Protein considerations seem to take a bit of a “backseat” to the metabolic “jockeying” of fat and carbohydrate for prominence in energy provision during coldweather and high-altitude operations. Protein is generally assumed to be of less nutritional importance from an energetic standpoint. However, protein becomes of greater metabolic importance when energy demands are not being met (caloric restriction). Such situations often encountered in wilderness settings in physically challenging environments. Classically, the quantity of carbohydrate, rather than the amount of protein, in a food-restricted diet has been considered critical to maintenance of nitrogen balance and preservation of lean body mass.27 This is attributed to carbohydrate’s amino acid-sparing action (e.g., amino acids from dietary protein are spared from subsequent deamination, gluconeogenesis, and oxidation for energy by carbohydrate). This reciprocal relationship between carbohydrate and protein has recently come under scrutiny.80 Recent studies of maintaining lean body mass during caloric restriction suggest that protein intakes in amounts approximately double the RDA may be helpful in maintaining muscle protein synthesis and muscle mass despite low energy and relatively low carbohydrate intakes.19,89,94 Diets providing 80% of the energy actually expended (20% caloric shortfall) for time periods up to 10 days have been shown to decrease muscle protein synthesis by 19% and, perhaps

TABLE 69-1  Nutrient Contents of Some Common Grains to Add to a Pemmican “Hoosh”* Grain Quinoa Amaranth Rice (white) Rice (wild) Oats (oatmeal) Wheat (couscous) Corn (grits)

Energy (kcal)

Protein (g)

CHO (g)

Fat (g)

Fiber (g)

374 374 379 357 375 376 347

13 14 8 15 10 13 9

69 66 84 75 78 77 79

6 7 0 1 4 1 1

6 15 2 6 7 5 5

Values from http://www.elook.org/nutrition/grains/. *Note: Serving size = 100 g = 3.5 oz = approximately 1/2 cup.

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CHAPTER 69  Nutrition, Malnutrition, and Starvation

intakes to increased incidence of heart disease that repeated insults of this nature may ultimately lead to increased deposition of lipid in the intima of arteries.22,110 All indications, however, lead to the conclusion that we really do not know the time course required for high-fat diets to take a toll on our arteries, particularly if the periods of high fat consumption are intermittently imposed and further complicated by the level of caloric expenditure during the periods of high fat consumption, as well as the type of fat consumed. The amount and type of fat in wilderness provisions remains largely a personal choice balanced against logistic constraints and the requirement for caloric density. Washburn126 stated that diets consisting of high levels of fat can be tolerated well by individuals doing heavy exercise in extreme, cold environments. He also wrote that diets for work in cold weather at low altitude can rely heavily on fats for energy. Because the usual diet of most humans now is generally higher in carbohydrates than fats, it is advisable that a gradual transition to a higher proportion of calories in the diet from fat be accomplished over a period of a few weeks prior to embarking on an expedition. Enzymic adaptation to a higher-fat diet can help prepare the individual to optimally metabolize and utilize increased fat in the diet. Drury and associates34 studied the metabolic effects of a diet high in fat and protein under cold weather field conditions and found that there is distinct adaptation to diets of this nature. Initially, blood glucose levels drop sharply because of the low amount of carbohydrate in the diet, but level out in the low normal range after 2 to 3 days. Ketone excretion rises over the same time period in response to the high levels of fat being oxidized for energy, peaking about the same time (3 days) as when glucose decrease levels out, and returns to normal levels after about 9 days. Two weeks should be considered the minimum amount of time to adapt to a high fat–low carbohydrate diet prior to utilizing it as the main daily food routine during expeditions.92 Early explorers utilized pemmican and other high fat–high protein foods as staples for their expeditions, partially from observations of the dietary patterns of native people and partially from logistic considerations of weight/volume and perishabilty. Evidence that pemmican is not just an “antiquated dietary anachronism” has been demonstrated by the modern day use of pemmican by Arctic adventurers Several food supply houses still manufacture and supply various versions of pemmican to out­ door enthusiasts. Those desiring to prepare their own pemmican can do so quite easily using common kitchen food processor and readily available supermarket products. Numerous Internet guides to pemmican making can be easily accessed, such as http://www.traditionaltx.us/images/PEMMICAN.pdf. Pemmican is energy dense, well preserved without refrigeration, and can be a versatile energy source, especially on long days on the trail when there is not a large amount of time or daylight for leisurely food preparation. It lends itself well as a cold snack on the trail. When added to a pot of hot water and mixed with a nutritious grain such as quinoa or brown rice, it becomes a hot filling meal (generically referred to by Arctic explorers as “hoosh”) that can provide protein, fat, and some carbohydrate at the end of a hard day. Table 69-1 lists some nutritious carbohydrate grains that compliment a meal of pemmican “hoosh.”

PART 8  FOOD AND WATER

TABLE 69-2  Pemmican Fortified With Unflavored Whey Hydrolysate Powder Food Item

Grams

Energy (kcal)

Pemmican Standard Recipe Without Whey Protein Beef jerky 255 390 Beef tallow 60 2232 Cranberries, dried 115 354 Total 430 2976 Per 1000 kcal meal 144 1000 Pemmican Modified Recipe With Whey Protein Beef jerky 255 390 Beef tallow 60 2232 Cranberries, dried 115 354 Whey protein powder 56 220 Total 486 3196 Per 1000 kcal meal 152 1000

CHO (g)

Saturated Fat Content (g)

Total Fat Content (g)

Protein (g)

Leucine (g)

7 0 95 102 34.3

2.4 26.9 0.1 29 9.7

5 59.1 1.6 65.7 22.1

79 0 0.1 79.1 34.4

5.8 0 0 5.8 1.95

7 0 95 4 106 33.2

2.4 26.9 0.1 2 31.4 9.8

5 59.1 1.6 4 69.7 21.8

79 0 0.1 42 121 37.9

5.8 0 0 4.6 10.4 3.25

more importantly, to reduce levels of cell signaling proteins specific to protein synthesis.89 Current research indicates that if prolonged energy deficits cannot be avoided (such as during a period of several days of inadequate food intake), nitrogen retention and maintenance of lean body mass is better preserved with accompanying protein intakes approximately twice the usually recommended RDA of 0.8 g/kg body weight. In this manner, even though protein synthesis will not be maintained, lean body mass will be better preserved and nitrogen balance will be better maintained. This adds some retrospective credibility to the customary use of high-protein food items such as pemmican and jerky as ration staples by early wilderness explorers, who often found themselves in situations where it was not possible to eat a full day’s ration (adequate kcal) for extended periods of time. Branched-chain amino acids (BCAAs), in particular leucine, are important for muscle protein synthesis and may be good nutritional “tools” to help preserve lean body mass under energy restriction.19 Leucine serves both as a substrate for protein synthesis and as an important signaling nutrient for regulating protein metabolism. Leucine has been suggested to stimulate protein synthesis and, at the same time, decrease protein degradation.43 The unique metabolic property of leucine to prevent muscle protein loss under catabolic situations suggests that whey protein products that are high in leucine and other BCAAs may have application in wilderness nutrition food preparation. The efficacy and human tolerance of leucine-rich proteins, such as whey, in support of maintaining or increasing muscle mass suggest that the efficacy of leucine depends in part on the presence of other BCAAs. Indeed, leucine-rich proteins have been shown to be more efficient than leucine supplementation alone.19 Extension of the beneficial leucine-specific effects reported in the literature involving exercise, malnutrition, weight management, and prevention of the sarcopenia of aging to the situation of inadequate energy intakes in wilderness activities requires further research. However, as a practical matter, a powdered whey protein supplement rich in leucine would take up little room in the pack and might be useful to incorporate into the diet on days that eating to caloric demand is not possible. Excess leucine and other BCAAs ingested beyond those required for protein synthesis and cell signaling roles would also serve a beneficial role as an alternate supply of glucose through their conversion via gluconeogenesis to glucose. Natural sources of leucine include brown rice, beans, meat, nuts, soy flour, milk, and whole wheat, although these food products might not elevate plasma leucine levels efficiently if consumed in small quantities. Whey protein supplements high in leucine are more practical and are commercially available in powdered (flavored and unflavored) and food bar form. Food bars containing whey protein are particularly convenient items to increase protein and leucine intakes throughout the day. Unflavored powdered whey protein can be added to other food preparations, such as stews, or soups or pemmican, to arrive at a high protein, high leucine food product. Recommended supplemental 1382

doses of leucine generally range from 2 to 3  g leucine per day. Balage and Dardevet19 have summarized human clinical trials involving as much as 7.9  g leucine supplement/day for time periods of up to 4 months without untoward effects. Gleeson44 observed that acute intakes of BCAA supplements of as much as 10 to 30  g of BCAA were without ill effect. A recipe and nutrient content for whey-fortified pemmican containing approximately 3  g of leucine per 1000  kcal compared with pemmican prepared without whey powder is given in Table 69-2. The consistency of the pemmican can be varied as desired by adjusting the amount of melted fat added to the pemmican. The unflavored whey protein flavor is largely masked by the customary pemmican ingredients. It should be noted that pemmican itself, by virtue of its endogenous leucine content from the dried meat (jerky), is an excellent dietary source of leucine even prior to whey protein supplementation. Pemmican, aside from its concentrated calorie source and adaptability to various nutritional modifications, also has the added advantage of a favorable weight/volume consideration for packing for extended backpacking trips. Figure 69-4, online shows a visual comparison of the volume of a day’s ration of 4000  kcal from pemmican versus typical dehydrated outdoor store backpacking food products.

VITAMINS AND THEIR RELATIONSHIP TO HEALTH AND PHYSICAL PERFORMANCE Vitamins are complex essential organic micronutrients that function in growth, maintenance, and metabolism. Vitamins act as coenzymes in metabolic reactions, and vitamins E and C and β-carotene (the precursor of vitamin A) act as protective anti­ oxidants. Considerable oxidative stress may be experienced while working in environmental extremes.7,11 High rates of energy expenditure, ultraviolet light exposure, and reduced dietary availability of foods containing antioxidants can cause excessive oxidative stress. Supplementing the diet with a vitamin and mineral mixture containing antioxidants to combat these stresses is perhaps a more immediate concern than supplementation to prevent vitamin deficiencies (e.g., scurvy), which take a relatively long time to develop. Prevention of vitamin deficiencies is among the most misunderstood aspect of short- and long-range nutrition planning. Body stores of some vitamins (primarily the water-soluble vitamins) are limited, and under prolonged periods (i.e., weeks, not days) of dietary restriction, vitamin deficiencies can be manifested. This is rarely the case, however, for individuals consuming a mixed diet supplying close to the daily energy requirement. Although it is not routinely encountered, it is possible to develop a state of tissue depletion of thiamin, riboflavin, and pyridoxine in as short a time as 11 weeks by consuming a calorie-adequate, but vitamin-deficient, experimental diet composed of common food products.122 Deficiencies of this nature do not develop over the short term; they are not caused by a few days of suboptimal vitamin intake. Van der Beek and colleagues121,122 have studied

Maximal workload (watts)

Vitamin Deficiency

300

1.  Preliminary Stage • Inadequate amount because of poor dietary patterns or altered availability in the diet • Commonly encountered after short-duration (<30 days) wilderness activities with poor nutritional planning • Consequence: None except danger of progressing to stage 2

250 200 150 100 50 0 Control

Deficient Baseline Week 4 Week 8

FIGURE 69-5  Impact of restricted vitamin intake on functional perfor­ mance in humans. Experimental conditions: diet, 3070 kcal; thiamin, 28% RDA; riboflavin, 31% RDA; vitamin B6, 16% RDA; vitamin C, 10% RDA. Performance test is workload achieved during incremental cycle ergometer testing. (Data from van derBeek EJ, van Dokkum W, Schrijver J, et al: Thiamin, riboflavin, and vitamins B-6 and C: Impact of combined restricted intake on functional performance in man, Am J Clin Nutr 48:1451, 1988; and van derBeek EJ, van Dokkum W, Wedel M, et al: Thiamin, riboflavin and vitamin B-6: Impact of restricted intake on physical performance in man, J Am Coll Nutr 13:629, 1994.)

the maintenance of human physical performance with varying degrees of vitamin restriction. Dietary vitamin deficiencies in subjects consuming restricted vitamin intakes significantly less than the RDAs were manifested slowly, particularly in terms of physical performance impairments. Diets containing restricted intakes of thiamin (28% RDA), riboflavin (31% RDA), pyridoxal phosphate (16% RDA), and ascorbate (10% RDA) resulted in less than a 20% decrement in cycle ergometer performance (maximal work load) after 8 weeks at this level of restriction (Figure 69-5). The relatively small change in performance decrements in response to vitamin restriction can be contrasted with the more immediate effects of acute or long-term dietary carbohydrate restriction on physical performance. The manifestation of physical performance impairment is much more sensitive to the amount of carbohydrates in the diet in the short term (1 to 3 days) than it is to the vitamin, protein, or fat content of the diet (6 to 8 weeks).2 It can be generalized that the development of a vitamin deficiency has four stages (Box 69-1), which involve a continuum of physiologic manifestations. The possibility that certain nutrients (in particular, vitamins) might help people adapt to, or function more efficiently in, stressful environments has intrigued explorers and scientists for years. Perhaps the most thorough study of the interaction between nutrients and the environment was conducted in 1953 in a field study titled the “Medical Nutrition Laboratory Army Winter Project: Vitamin Supplementation of Army Rations under Stress Conditions in a Cold Environment—The Pole Mountain Wyoming Study.” The objective of this study was to determine if supplementation with large quantities of ascorbic acid and B-complex vitamins would influence the physical performance of soldiers engaged in high levels of physical activity in a cold environment, both with and without caloric restriction.8 The investigators concluded that supplementing the mixed diet of men engaged in high levels of physical activity in the cold, with or without caloric restriction, did not result in significantly better physical performance. Thus, it appears reasonable to conclude (at least from a performance standpoint) that vitamin supplementation in the wilderness environment is not nearly as critical as total energy and carbohydrate provision. This does not mean, however, that dietary vitamin intakes should be ignored. Including a

2.  Biochemical Deficiency Stage • The body’s pool of the vitamin is decreased • May be encountered after long-term (>30 days) wilderness activities accompanied by suboptimal daily nutrient intakes • Consequence: Rates of enzyme catalyzed reactions may be slightly altered 3.  Physiologic or Subclinical Deficiency Stage • Can be detected by functional tests • May be encountered after extended periods of consuming foods low in vitamins or periods of food restriction • Consequence: Performance may be impaired slightly 4.  Clinical Deficiency Stage • Specific symptoms manifested, physical signs clinically detectable • May be encountered after starvation or extended periods of food deprivation • Consequence: Possible impairments of both health and performance

multivitamin and mineral supplement is a practical preventive measure. Conditions under which vitamin supplementation may be recommended are summarized in Box 69-2. Certain vitamins, such as vitamins E and C, may have important functions beyond their conventional essential roles, such as preventing degradation of the immune response and maintaining red blood cell flexibility and oxygen delivery under conditions of increased oxidative stress. Because oxidative stressors may be encountered during wilderness activities, and because the quantity and quality of food are often uncertain, it seems prudent to include a multivitamin supplement with the food supplies. This nutritional insurance is inexpensive and takes up little space. The composition of a typical antioxidant vitamin and mineral supplement is shown in Figure 69-6. A popular alternative to the typical antioxidant supplement is a food (fruit and/or vegetable)–based extract. Two examples of this type of supplement are shown in Figure 69-7.

MINERAL SUPPLEMENTS—ELECTROLYTES, HEMATOPOIESIS, AND BONE HEALTH The mineral content of the diet is usually not a primary concern, provided that a mixed diet that meets energy requirements is consumed daily. Supplemental calcium and iron are considerations for female travelers, as discussed in the next paragraph. Sodium in hot environments is an exception, because it is lost

BOX 69-2  Conditions That Might Warrant Vitamin

Supplementation

• When energy intake is below 1200 to 1600 kcal/day • When meals are routinely missed • When extremely poor or bizarre eating habits are practiced • When oxidative stressors (ultraviolet light exposure, high rates of energy expenditure, lack of fruits and vegetables in the diet) are high • When unusual physiologic conditions, such as pregnancy or lactation, are present

1383

CHAPTER 69  Nutrition, Malnutrition, and Starvation

BOX 69-1  Four Stages in the Development of a

350

rare when regular meals are consumed. Hyponatremia as a complication of overhydration in wilderness environments where food is neglected has been described for hot16,17 and cold128 environments. Calorie deprivation can alter sodium intake. In addition to reduced intake of sodium via food, severe caloric restriction leads to marked natriuresis.91 Increased loss of sodium in turn leads to depletion of fluid volume, impaired cardiovascular function, and reduced work capacity, further exacerbating the effects of energy restriction. Accompanying increased aldos­ terone levels in response to reduced plasma volume can also lead to accelerated potassium wasting.91 For insurance and safety considerations, include 5 g (about two typical restaurant serving packets) of table salt for every day in the field packed with the food supplies. If necessary for fluid replacement after excessive sweating, this extra salt can be used to make a dilute electrolyte beverage by adding 0.5 tsp salt (2 to 3 g) to one quart of water. Excess sodium should be avoided because its excretion increases metabolic water demands.5

PART 8  FOOD AND WATER

Supplement Facts Serving Size 1 softgel

Amount Per Softgel

% Daily Value

Vitamin A 10,000 I.U. 100% as Beta Carotene

200%

Vitamin C 250 mg

417%

Vitamin E 200 I.U.

667%

Zinc 7.5 mg

50%

Selenium 15 mcg

21%

Copper 1 mg

50%

Manganese 1.5 mg

75%

FIGURE 69-6  Antioxidant supplements can contain a variety of nutri­ ent components designed to act as sacrificial antioxidants (e.g., vitamin C) or as cofactors in antioxidant enzyme systems (e.g., selenium). The supplement shown is typical of many basic antioxidant formulations containing vitamin and mineral antioxidant components. (Copyright 2007 by Mosby, Inc., an affiliate of Elsevier Inc.)

during activities producing excessive sweating (see Chapter 70). Hyponatremia can also be occasionally encountered in unanticipated scenarios such as a cold environment.128 With appropriate acclimatization to the heat (and resultant sodium conservation by the kidneys), the amount of sodium required in the diet for work in the heat is reduced. Laboratory studies have shown that heat acclimatization can occur when as little as 4 to 8 g of salt (NaCl) is ingested per day.1 The amount of NaCl required for safe work in the heat depends on the degree of prior heat acclimatization and the amount of sweat loss. Altered dietary patterns or excessive sweating can influence sodium balance. Starvation can lead to plasma volume depletion when sodium in the circulation is insufficient to allow osmotic forces to retain water.51 When nonacclimatized humans are exposed simultaneously to acute food restriction and high sweat rates, the resulting excessive loss of sodium can lead to dizziness, syncope, and even collapse. These problems can be avoided by ensuring that extra salt is included in the food provisions for wilderness expeditions and that salt is available to vigorously season food during and after high sweat losses. Another form of sodium deficit is dilutional hyponatremia caused by overhydration with fluids in conjunction with lowerthan-normal sodium intake or excessive sodium loss in the sweat. Hyponatremia caused by overconsumption of fluids is extremely

Supplement Facts

Supplement Facts

Serving Size 1 Capsule

Serving Size 1 Tablet Amount Per % Daily Serving Value

Acai Berry Extract 125 mg (Euterpe oleracea) (standardized to 10% phenolic acid)

Amount Per % Daily Tablet Value

-

Vitamin C (as ascorbic acid)

100 mg

167%

Noni Fruit Extract 8:1 (Morinda citrifolia)

125 mg

-

16 mg Resveratrol (from 200 mg Polygonum cuspidatum 8% total resveratrols) (Tiger cane)

Pomegranate Fruit Extract 5:1 (Punica granatum)

125 mg

-

Grape Seed Extract (Vitis vinifera) 50 mg (95% polyphenols)

-

125 mg Wolfberry (goji) Fruit (Lycium barbarum) (freeze-dried concentrate typically containing 60% polysaccharides)

-

100 mg Grape Skin Extract (Ancellota lambrusco) (30% polyphenols)

-

Mangosteen 125 mg (Garcinia mangostana) (fruit)

-

Green Tea 5:1 Extract 200 mg (Carmellia sinensis) (45% polyphenolics)

-

*Daily Value not established.

*Daily Value not established.

FIGURE 69-7  Examples of phytochemical antioxidant supplements containing naturally occurring polyphenols that can be effective free radical quenchers. Many of these fruit or vegetable extract antioxidant formulations can have higher ORAC (oxygen radical absorption capac­ ity) values than conventional vitamin mineral antioxidant supplements.

1384

Special Nutritional Requirements for Female Wilderness Travelers Although our understanding of the differences between male and female nutritional requirements is incomplete, gender differences exist for certain nutrients, such as iron, calcium, folate, and vitamin B6 under normal environmental living conditions.82 Differences are particularly notable for women using oral contraceptives75 and those who are pregnant or lactating.28 The health implications for pregnant travelers planning a trip to altitude are beyond the scope of this chapter; these individuals should consult a knowledgeable pediatrician or obstetrician. Investigations of nutritional requirements at environmental extremes have been conducted on men, but comparatively little research has been directed toward women. The few studies that have been done suggest that dietary nutrient intakes of women at moderate altitude are similar to those at sea level,60 implying that specific gender requirements that exist at sea level may be even more important at altitude, particularly if there is scarcity of nutrient-dense foods or if appetite is blunted. Some genderspecific nutrient requirements are known. For example, research conducted in the late 1960s identified that female service members deployed to places at moderate to high altitude required supplemental dietary iron to optimally support the hematopoietic response to hypoxia.47 Subsequently, research on iron requirements and the thermogenic response to cold have also identified iron as a key micronutrient for women in a cold environment.21,71 Women, because of their reduced body size, usually consume fewer total food calories than do men. They are therefore at increased risk for reduced vitamin and mineral intake. Fortunately, the need for these vitamins and minerals (with the exception of iron) is related to lean body mass, and women usually have a lower lean body mass than do men. Because the choice of available foods may be limited during expeditions into the wilderness, female travelers should include a multivitamin supplement in their provisions. It should contain at least 50% of the female RDA for iron, zinc, folate, vitamin B6, and calcium. Antioxidant nutrients (see Vitamins and Their Relationship to Health and Physical Performance, earlier), including extra vitamins C and E and perhaps certain carotenoids, such as lutein and zeaxanthan, provide additional insurance against oxidative stress. The composition of a typical multivitamin and mineral supplement is shown in Figure 69-8. The values shown reflect the daily value (DV) of the nutrients—that is, the recommended daily amount for most adults needing 2000 to 2500 kcal/day. Multivitamins often contain relatively low amounts of calcium compared with the female RDA of 1000 to 1300 mg/day, so it may be beneficial for female travelers to include an additional bioavailable calcium supplement containing 250 to 500 mg of calcium per dose. Commercially available chocolate- or caramelflavored calcium “chews” are convenient and contain a small amount of carbohydrate, as well as “bone-friendly” nutrients such as vitamins D and K. The U.S. RDA for calcium intake for adults younger than age 50 years is 1000 mg daily, and people older than age 50 years should ingest 1200 mg daily. Calcium supplements are best taken in small (no more than 500 mg) divided doses throughout the day. If an iron supplement is being taken

Serving Size 1 tablet

Amount Per Tablet

100%

Iodine 150 mcg

Vitamin C 120 mg

200%

Magnesium 100 mg

Vitamin D 400 I.U.

100%

Zinc 15 mg

Vitamin E 50 I.U.

167%

Selenium 25 mcg

Vitamin K 100 mcg

31%

% Daily Value 100% 25% 100% 36%

Copper 2 mg

100%

Thiamin 1.5 mg

100%

Maganese 2 mg

100%

Riboflavin 1.7 mg

100%

Chromium 120 mcg

100%

Niacin 20 mg

100%

Molybdenum 25 mcg

33%

Vitamin B6 2 mg

100%

Chloride 36 mg

1%

Folic Acid 400 mcg

100%

Potassium 40 mg

1%

Vitamin B12 6 mcg

100%

Boron 150 mcg

*

10%

Nickel 5 mcg

*

Biotin 30 mcg Pantothenic Acid 10 mg

4

100%

Silicon 2 mg

Calcium 250 mg

10%

Tin 10 mcg

*

Iron 18 mg

50%

Vanadium 10 mcg

*

Lutein 250 mcg

*

Phosphorus 77 mg

8%

5 10-02

% Daily Value

Vitamin A 3,000 I.U.

KK10386N

Amount Per Tablet

3

1

6

*

*Daily Value (DV) not established

7

1. % of the Daily Value: The amount of the nutrient recommended for one person for one day based upon a daily energy requirement of 2000-2500 kcal. The DV is a simplification of the RDA; it doesn’t take into account age and gender. 2. Serving size: The number of tablets needed to reach the % DV on the label. 3. Scientific units: Quantitative amount of the nutrient per tablet. May be in international units (IU), mg, or mcg. For example, 1 IU of Vitamin A activity would be equivalent to 0.3 g retinol or 6 mcg of beta carotene. 4. *(no DV available): Necessary (essential) nutrients for which quantitative guidelines have not been established. 5. Expiration date: After this date the supplement may contain somewhat less than the amount shown on the label. 6. Lot number: For tracking specific supplement batches. 7. Suggested use: Directions for usage. 8. Warning alerts: Potential adverse effects. 9. Quality statements: Consumer assurance that product meets quality standards. 10. Dietary Supplement Verification Program: The United States Pharmacopeia (USP) assurance that product contains what is stated on the label.

CHAPTER 69  Nutrition, Malnutrition, and Starvation

2

Supplement Facts

No Artificial Colors * No Artificial Flavors * No Preservatives * No Chemical Solvents or Yeast SUGGESTED USE: Take one tablet daily with a meal. Keep bottle tightly closed. Store in a cool, dry place. Do not use if imprinted seal under cap is broken or missing.

8

A

M

ER

ICAN MEDIC

A

ACCEPTED VE RIFIED

9

L

SUPPLE RY M TA

T EN

10

DI E

WARNING: Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children under 6. Keep this product out of reach of children. In case of accidental overdose, call a doctor or poison control center immediately.

Essential Balance tablets made to Nature Made’s guaranteed purity and potency standards.

FIGURE 69-8  An annotated multivitamin and mineral supplement label showing some key components and pertinent information. Nutrients are expressed as a percentage of the daily value (DV), the amount of nutrients recommended for daily consumption by most adults needing 2000 to 2500 kcal/day.

in a multivitamin or by itself, it is best not to take it at the same time as the calcium supplement, because the absorption of each is unpredictable and may be less than optimal in the presence of the other.98 The nutrients in a vitamin–mineral supplement should be present at close to the DV level (100% or less). This ensures adequate intake of major micronutrients with minimal risk of adverse nutrient interactions. To avoid unpredictable absorption conflicts, such as between iron and calcium, the recommended dose should not be exceeded. Synthetic vitamins are structurally the same as, and cost less than, so-called natural vitamins. Generic brands are also generally less expensive and equally effective. The addition of herbs, enzymes, or amino acids accomplishes little but adds cost. Some supplements containing phytonutrients extracted from plants may be appropriate when the logistics of the trip offer little or no chance to secure fresh fruits and vegetables. A source of information on vitamin and mineral supplements is ConsumerLab, which provides independent test results and information to help consumers and health care professionals evaluate health, wellness, and nutrition products. The results of its tests, including brands that have passed testing, are available at www.consumerlab.com. Supplements can lose potency over time, so check the expiration date on the label. Figure 69-8 provides guidance for reading and interpreting supplement labels. The initials USP (for the testing organization U.S. Pharmacopeia) or words such as “release assured” or “proven release” indicate that the supplement is easily dissolved and absorbed.

Nutritional Deprivation: Malnutrition and Starvation DEFINITIONS There is little uniformity in the terminology used to describe the physiology of human starvation. Hoffer51 has suggested the following definitions: Fasting: The total absence of food intake. Starvation: The physiologic condition that develops when macronutrient content is inadequate for a prolonged period. Semi-starvation or food restriction: The more commonly encountered condition of some food, but of insufficient energy and protein provision. Malnutrition: A general term for the condition resulting from longstanding inadequate consumption of nutrients, abnormal absorption of nutrients, or unusual demands on certain nutrients; usually involves suboptimal food intake or the consumption of food of poor nutrient density, resulting in micronutrient and macronutrient deficiencies. Protein–energy malnutrition (PEM): The result of inadequate intake of energy, protein, or both for prolonged periods. Two related types of PEM are marasmus (primarily an energy deficiency) and kwashiorkor (primarily a protein deficiency). Both forms occur across a spectrum of situational and environmental conditions and exhibit many of the same symptoms. PEM is frequently a consequence of starvation, but all starvation does not necessarily lead to PEM. 1385

PART 8  FOOD AND WATER

Development of PEM depends on body energy reserves, length of the fast, age, and presence or absence of disease. PEM is unlikely to be encountered by most wilderness travelers—a possible exception being within indigenous populations in certain Third World locations. When malnourished indigenous people are encountered in wilderness travels, caution should be exercised about sharing food. These individuals may not be accustomed to ingesting large quantities of food replete with sodium, and there may be consequences to overeating (see Feeding Victims of Starvation, later). Cachexia: This more specific term refers to the wasting that results from metabolic stress and loss of appetite. It is sometimes called cytokine-induced malnutrition to distinguish it from simple food deprivation in the absence of stress. The inanition of advanced-stage cancer patients is an example of cachexia. Malnutrition in a Wilderness Setting This discussion will be limited to the metabolic and physiologic consequences of starvation or energy restriction that might be encountered in wilderness settings, including unplanned emergencies that result in shortage of food, and wilderness rescue operations of victims of unintentional starvation. In these settings, the duration of food restriction is usually, but not always,104 of shorter duration than that associated with the hunger encountered during famine, war, crop failure, and disease. Solomons112 has stated that malnutrition simply means “bad” nutrition and has listed six possible causes of nutrient deficiencies leading to malnutrition: reduced intake, decreased absorption, decreased utilization, increased destruction, increased wastage, and increased requirement. Primary malnutrition is caused by reduced intake of food. This is the most commonly encountered cause of malnutrition in wilderness settings. Reduced intake, along with an increased requirement, can contribute to development of nutrient deficiencies during expeditions under extreme environmental conditions. Secondary causes of nutrient deficiencies are less commonly encountered but can contribute significantly if disease or illness strikes the wilderness traveler. Malnutrition develops in stages that usually require a considerable length of time to manifest. As seen in cases of vitamin deficiency, the first changes reflect diminished dietary intake, with resultant reduced blood and tissue levels of nutrients, followed by intracellular changes in biochemical functions. Eventually, if the malnutrition is unrelieved, physical symptoms develop. These effects can include oral lesions, rashes, petechial hemorrhages, ecchymoses, pigmentation changes, and edema. People who undergo prolonged semistarvation experience hunger, weakness, lack of drive, mood changes, osteoporosis, hypoalbuminemia, edema, decreased muscle mass, alopecia, hypotension, and poor wound healing. Impaired immune function, decreased resistance to infection, and prolonged recovery from injury are all consequences of long-term food restriction.* Starvation Starvation is the physical condition brought about by inadequate consumption, absorption, or retention of protein and dietary energy from carbohydrate and fat.52 Starvation can be acute or chronic as well as total or partial. Different forms of starvation are similar but not identical. Starvation can result from a disease or simply from a lack of food. It can ultimately manifest as a disease (PEM) or, if not prolonged, as nonpathologic weight reduction. The metabolic adaptations that occur in the progression of starvation depend on whether there is acute energy restriction or chronic undernourishment as a result of long-term low-energy intake.105 Acute Energy Restriction.  The rapid progression of events that occur in response to acute energy inadequacy (e.g., a 50% shortfall of food during the second week of a 2-week backpacking trip) is shown in the first three steps in Figure 69-9. The body

*References 29, 40, 62, 106, 107.

1386

Cessation of food consumption

Depletion of body fuel stores

Metabolic adaptations

“Decompensation”

Death

FIGURE 69-9  Sequence of events during prolonged starvation. If the fast is not terminated and energy reserves are depleted, internal organ systems ultimately used for energy will fail (decompensation), resulting in death. (Copyright 2007 by Mosby, Inc., an affiliate of Elsevier Inc.)

reacts quickly to an energy shortage by utilizing readily available muscle and liver glycogen stores. Progression to the final steps of organ decompensation and death would be encountered only after complete starvation for several weeks. Following food restriction when the body’s carbohydrate stores have been depleted, glucagon level rises, insulin level falls, and the process of gluconeogenesis accelerates, converting noncarbohydrate precursors such as lactate, glycerol, and amino acids to glucose to maintain the blood glucose level and prevent hypoglycemia (Figure 69-10). These metabolic principles are expressed in more detail in Figures 69-11 and 69-12. Data used to prepare this classic scheme of carbon flux during starvation are based largely on the work of Cahill,26 who studied metabolic aspects of starvation in humans. Reduction in carbohydrate intake and resultant reduced glucose provision during food restriction is in large part compensated for by accelerated gluconeogenesis. The carbon skeletons of 100 g of protein from endogenous tissue sources can ultimately provide approximately 55 g of carbohydrate after metabolic transformations. The glycerol from 100 g of mobilized fat can yield 10 to 15 g of carbohydrate via gluconeogenesis.24 As glycogen is depleted, catecholamine production rises simultaneously, facilitating fatty acid mobilization from adipose depots. Once mobilized, fatty acids are taken up by muscle in proportion to their concentration in the blood and oxidized for energy. The metabolic events of a short-term fast are shown in Figure 69-11. The major difference between short- and long-term fasts is in the shift

Refeeding

Energy balance

Restriction

Energy surfeit Insulin Equilibrium

() Blood glucose ()

Equilibrium Glucagon Epinephrine Energy Cortisol deficit

FIGURE 69-10  Influence of energy balance on hormonal control of blood glucose. When food is consumed after ingestion, insulin is released, lowering blood glucose. When no food is consumed and blood glucose drops, gluconeogenic hormones are released, and endogenous sources are used to raise blood glucose levels. (Copyright 2007 by Mosby, Inc., an affiliate of Elsevier Inc.)

CHAPTER 69  Nutrition, Malnutrition, and Starvation

Energy utilization

Energy source

O2

Adipose tissue Triglycerides 135

Glycogen

30 g

Glycerol 14 g 40 g

E–

H2O

36 g

RBC, WBC, etc.

Lactate + pyruvate

Urea O2 Heart, kidneys, muscle, etc.

Ketone bodies 60 g

Fatty acids 129 g

CO2 + H2O

E–

Gluconeogenesis O2

E–

94 g Glucose 130 g 36 g

g

75 g

Amino acids

10 0

Muscle protein

CO2, H2O, urea

Liver E–

O2

Nervous system

10 g

50 g Fatty acids 89 g

E– CO2 + H2O 30 g Glycogen

FIGURE 69-11  Fuel utilization in short-term starvation. Metabolic rates in grams per day after a 24-hour fast. Energy expenditure, 1800 kcal/day (7.53 MJ/day); respiratory quotient, 0.76. E−, Oxidative formation of energy (ATP). (Original data from Cahill GF Jr: Starvation in man, N Engl J Med 282:668, 1970. Algorithm redrawn from Bursztein S, Elwyn DH, Askanazi J, Kinney JM: Energy metabolism, indirect calorimetry, and nutrition, Baltimore, 1989, Lippincott Williams & Wilkins.)

of carbon source for energy production. As the length of the fast increases, the amount of glucose oxidized decreases and the amount of ketone bodies oxidized increases. Long-Term Energy Restriction.  Prolonged fasting is characterized initially by increased protein catabolism for gluconeogenesis, followed by increased production of ketone bodies as a consequence of fat mobilization for energy demands. A fast longer than 2 to 3 days exhausts liver glycogen and uses up about half the muscle glycogen stores.51 Thereafter, glucose utilized by the body (in the absence of food consumption) must be synthesized from endogenous precursors via gluconeogenesis. The appearance of large amounts of ketone bodies in the blood, breath, and urine is the result of the low insulin-to-glucagon ratio accompanying a prolonged fast, and of massive fatty acid mobilization from adipose tissue. Ketone bodies are a metabolic consequence of vigorous fatty acid oxidation engendered by starvation in the absence of significant carbohydrate intake. Production of acetoacetate and β-hydroxybutyrate increases significantly during the first 7 to 10 days of fasting and stabilizes after 2 to 3 weeks.23 Ketone bodies can be increasingly used for energy by muscle and brain as energy restriction becomes prolonged. Even a short-term fast elicits a significant production of ketone bodies (see Figure 69-11); however, ketone body production may be virtually abolished if a minimum of 150 g of carbohydrate is ingested daily to supply the brain with glucose for energy.24,51 Normally, in the fed state, ketone body oxidation accounts for the provision of less than 3% of the total energy requirement. Longer periods (7 to 10 days) of fasting are accompanied by a large elevation of the level of circulating ketone bodies, which can provide as much as 40% of the total energy expenditure and greater than 50% of the brain’s energy requirement.24,51 The switch to using ketone bodies for energy in the brain is believed to be controlled by the concentration of ketone bodies in the blood rather than being a direct hormonal effect on the brain.23 Metabolic changes during a long-term (e.g., a 30-day) fast are depicted in Figure 69-12. With increasing duration of the fast and depletion of muscle and liver glycogen, ketones and glucose derived from gluconeogenesis from amino acid carbon skeletons contribute to energy requirements of the brain. As starvation is prolonged and ketone bodies become the predominant fuel, less and less glucose is

used, thereby reducing the amount of protein that must be catabolized to support gluconeogenesis. Blood levels of BCAAs (leucine, isoleucine, valine) are preferred amino acid substrates for muscle energy metabolism and double by 3 to 5 days of fasting, but they fall during prolonged fasting. These BCAAs are believed to augment gluconeogenesis until fat metabolism has adapted to fasting.23 The amino acid glutamine has special importance during fasting, assuming several roles—as an energy source as a precursor of glucose, and as a transporter of amino acid nitrogen in the form of ammonia (NH3) from tissues to the kidneys for excretion. Urea is the major nitrogen excretory product in the urine during the fed state, but it becomes much reduced as the fast progresses and ammonia nitrogen increases. The increase in ammonia nitrogen serves to buffer ketoacids during their excretion via the urine, as well as to provide an excretory route for nitrogen. Glutamine is released from muscle during fasting (NH3 formed from amino acid deamination by muscle is subsequently transaminated to glutamate to form glutamine) and serves as both a special energy source for the gut and a gluconeogenic substrate for the kidney. With increasing ketone body production, the liver reduces its rate of gluconeogenesis and the kidney becomes the major organ of gluconeogenesis, producing more than one-half the body’s glucose requirement.23 Glutamine is the predominant substrate for kidney gluconeogenesis and provides the NH3 required to buffer ketoacid excretion produced by ketogenesis from fat oxidation.23 Fortunately, muscle proteolysis does not continue at the typically high initial rate of negative nitrogen balances (10 to 12 g/ day during the first 7 to 10 days of fasting). After 7 to 10 days of fasting, adaptation in the nitrogen economy of the body reduces nitrogen loss in the urine to less than one-half the initial rate.51 Although the signal that causes muscle to reduce its catabolic rate is not well understood, it is probably related to the shift to ketone body utilization in the brain and the shift to fatty acid oxidation in muscle during this same period. When adaptation to food restriction is not successful or food restriction is too severe, nitrogen can be lost from both central (visceral) and peripheral (skeletal muscle) sites. Development of central protein deficiency can lead to anergy and hypoalbuminemia. Reduced plasma albumin lowers plasma oncotic pressure, which permits fluid to migrate out of the vessels into the extracellular space, resulting in edema of the extremities. Edema is not present in all 1387

PART 8  FOOD AND WATER

Energy source

Energy utilization O2

Muscle protein 20 g

Adipose tissue Triglycerides 150

Amino acids

Glycerol 16 g 67 g

CO2, H2O, urea

Liver E–

O2

H2O

CO2 + H2O

RBC, WBC, etc. E–

Gluconeogenesis E–

50 g

14 g

Lactate + pyruvate

Urea O2 Heart, kidneys, muscle, etc.

Ketone bodies 100 g

Fatty acids 143 g

E–

44 g Glucose 80 g 36 g

Glycogen

O2

Nervous system

60 g

39 g

E– CO2 + H2O

Fatty acids 76 g

Glycogen

Urine Ketone bodies 10 g FIGURE 69-12  Fuel utilization in long-term starvation. Metabolic rates in g/day after a prolonged fast of 5 to 6 weeks. Energy expenditure, 1450kcal/day (6.07MJ/day); respiratory quotient, 0.74. E−, Oxidative formation of energy (ATP). (Original data from Cahill GF Jr: Starvation in man, N Engl J Med 282:668, 1970. Algorithm redrawn from Bursztein S, Elwyn DH, Askanazi J, Kinney JM: Energy metabolism, indirect calorimetry, and nutrition, Baltimore, 1989, Lippincott Williams & Wilkins.)

instances of starvation, but the presence of edema indicates severe metabolic stress and central protein deficiency and is a potentially dangerous condition.51 The net result of short- and long-term metabolic adaptations in energy restriction is increased efficiency of the body’s metabolism. When body weight decreases 8% to 10% over a 14-day period, the basal metabolic rate (BMR) can decrease about 21%. This short-term decrease in BMR is greater than would be predicted if it were caused solely by the loss of metabolically active lean tissue mass. Reduction in BMR during energy restriction occurs in two different phases.23 Initially, there is a decrease in BMR that is not attributable to changes in body weight or body composition. This is presumably an attempt by the body to conserve energy by increasing its metabolic efficiency despite reduced energy intake. Then, with continued energy restriction, further lowering of BMR occurs because of the loss of metabolically active tissue. Several physiologic mechanisms operate to downregulate metabolic activity in the active tissue mass and to increase its metabolic efficiency. The decreased energy flux reduces activity of the sympathetic nervous system and lowers secretion and activity of three thermogenic hormones: catecholamines, T3 (triiodothyronine), and insulin. Other energy-requiring activities, such as the sodium–potassium pump and futile metabolic cycling (e.g., phosphorylating and dephosphorylating metabolic intermediates), may also be reduced during starvation, further conserving energy.

cell mass decreases linearly with the severity and duration of a fast.105 Adipose mass decreases along with muscle, but not as rapidly initially, because of the caloric density of the energy of the fat depot and the low amount of associated water. Hoffer52 has estimated that during a typical 3-week fast that elicits a weight loss of 350 g/day, the shed tissues are composed of approximately 125 g of lean tissue and 200 g of adipose tissue. The body defends a certain amount of body fat as essential for nerve sheath insulation, brain neurolipids, cell membrane integrity, and hormone synthesis. The general hierarchy of energy-source utilization during progressive starvation is shown in Figure 69-13. The largest energy reserves are found in the largest organs of the body—muscle (about 28 kg) and adipose tissue (about 15 kg). Critical internal organs, such as the liver, brain, heart, and kidneys, have a collective mass of less than 9 kg and are

Late stages

Adipose tissue

Intermediate stages Muscle protein

HIERARCHY OF TISSUE UTILIZATION DURING STARVATION There is a hierarchy of fuel source utilization during starvation. During an extended period of fasting, the mass of muscle and adipose tissue is more likely to be reduced than that of the viscera.105 Important internal organs, such as the liver, show no evidence of dysfunction after 7 days of fasting,103 whereas muscle 1388

Internal organs

Early stages

Liver and muscle glycogen

FIGURE 69-13  Energy sources during progressive stages of starvation. Note the hierarchy of the progression of utilization of energy sources.

70-kg Man

Energy Source Fat Protein (muscle) Glycogen (muscle) Glycogen (liver) Plasma glucose Plasma free fatty acids Plasma triglycerides

Mass (kg)

Energy (kJ)

15 6 0.15 0.075 0.020 0.0003 0.003

590 100 2.51 1.25 0.33 0.012 0.125

Data from Cahill GF Jr: Starvation in man, N Engl J Med 282:668, 1970.

not good fuel-source candidates, because they begin to lose critical functions when they become energy sources during starvation (decompensation). The body reserves that can be drawn on for energy during fasting are shown in Table 69-3 for a sedentary 70-kg man.

SEQUENCE OF EVENTS DURING STARVATION Sex hormone synthesis is depressed during extended periods of food restriction,40,41 because reproduction is not a high priority during starvation. As the fast progresses, eventually even visceral organs begin to be used for energy as the body decompensates or “feeds on itself.” During a prolonged fast, the body initially undergoes the series of events depicted in Figure 69-14.23 The initial steps are similar to those of short-term energy deficiency (see Figure 69-9), but if the starvation continues metabolic adaptations ultimately fail, leading to a grim conclusion: the body has expended its reserves and enters the decomposition or final stages of metabolic self-destruction. Organ failure and death are the ultimate outcomes of starvation unless nutritional intervention occurs prior to decompensation (internal organ catabolism, loss of integration of function of bodily systems, and deterioration of homeostasis).

THE LIMITS OF HUMAN STARVATION AND FACTORS INFLUENCING SURVIVAL There were horrific changes in my body. My buttocks were bones jutting against skin. I could no longer warm my hands by nestling them between my thighs. Now I could push a clenched fist between my legs without touching either thigh. I continually felt nauseated. The nausea became so severe I retched uncontrollably. This went on night after night. Death was closing in. My body was conceding defeat. JAMES SCOTT’s OBSERVATIONS NEAR THE END OF A 43-DAY PERIOD OF 104 STARVATION WHILE LOST IN THE HIMALAYAS.

Restriction of food consumption

Depletion of body glycogen stores

Hormonal changes

Metabolic adaptations

Increased metabolic efficiency

FIGURE 69-14  Sequence of metabolic events during short-term energy restriction or starvation. In the short term, metabolic efficiency increases to compensate for an energy deficit.

Loss of Fat and Lean Body Mass The body fat of humans can be considered beneficial when viewed in the context of surviving starvation.87 A decreasing level of body fat approaching 6% loss is a harbinger of impending lean body mass deterioration in the fasting individual.3,87 Essential fat stores (in bone marrow, heart, lungs, liver, kidneys, intestine, muscle, cell membranes, and the central nervous system) are necessary for maintenance of life and prevention of decompensation. Essential fat stores constitute 3% to 4% of body weight.87 Total body fat depletion in previously nonobese individuals occurs at approximately 50% body weight loss. In fasting uncomplicated by disease, the time until death is largely determined by the size of fat stores and the time to reach the 3% level of essential fat. Fat stores protect function.87 Low fat stores per se are not the cause of death, but their diminution contributes to breakdown of homeostasis and impairment of physiologic function. Typical fat stores in humans vary but are typically between 10 and 15  kg (including 2.1  kg of essential fat), or approximately 27% of body weight. In a well-nourished adult, there are sufficient fat energy stores to sustain life for 60 to 70 days. Death has been reported sooner in voluntary hunger strikers and may be related to simultaneous fluid restriction and the intangible lack of the will to live. A loss of greater than 50% of the lean body mass is also predictive of death. From a practical standpoint, the remaining body fat and protein reserves in a starving individual are difficult to measure accurately. A more practical measurement is the BMI—weight in kilograms divided by height in meters squared. BMI is easy to obtain and a convenient method to assess risk of mortality in severely starved individuals. Prior to the war and famine in Somalia, the lowest BMI compatible with life was thought to be 13 in males and 11 in females.49 Collins31 collected data at Baidoa, Somalia, in 1992 at the Concern Worldwide Adult Therapeutic Centre, where many victims of starvation were treated. He found that a BMI of 10 could be compatible with life under conditions of specialized hospital care, possibly explained by somatotype and the warm climate; however, other races in colder climates may face death prior to reaching the low BMI level noted in Somalia.31 Age and Gender Differences in Survival from Starvation Persons possessing the most limited body reserves, such as older adults and the very young, are at increased risk for early mortality during extended periods of starvation. Children have increased nutrient requirements for growth and develop deficiency symptoms rapidly when faced with severe food restriction. Starving women have not been studied in the same controlled manner as have men. However, observational evidence of unintentional situational starvation involving both men and women seems to indicate that women may possess certain metabolic or cultural advantages over men, which may lead to a reduced incidence of mortality from severe starvation. Such evidence comes from wartime and famine, when there has been a disproportionate survival of women over men.39,87 Although situational circumstances have been suggested to account for these differences, studies of the Mormon handcart trek20 and the Donner party115 support the conclusion that women are at lower risk for mortality under nutritionally stressful situations. McCurdy78 examined the mortality pattern in the Donner party, which became trapped with inadequate food supplies in the Sierra Nevada Mountains during the winter of 1846-1847. The demographic mortality data derived by McCurdy (Table 69-4) indicate that very young children and males, in general, had the highest risk for mortality during starvation. The influence of gender on starvation may be attributable, at least in part, to certain metabolic advantages possessed by women, such as a higher initial level of body fat and subsequent reduced loss of protein and lean body mass during fasting. Lowell and Goodman69 proposed that protein sparing in skeletal muscle during prolonged starvation depends on availability of lipid fuels that may provide energy and attenuate the rise in catabolic hormones during starvation. They also suggest that fatty acids may specifically modulate the breakdown of myofibrillar protein, 1389

CHAPTER 69  Nutrition, Malnutrition, and Starvation

TABLE 69-3  Utilizable Energy Stores in a Sedentary

PART 8  FOOD AND WATER

TABLE 69-4  Demographics and Mortality Rates in

the Donner Party, 1846-1847

Total party Age (yr)   <5   6-14   15-34   >35 Gender   Male   Female

Frequency N (%)

Mortality Rate: n/N (%)

90 (100)

42/90 (47)

19 21 34 14

11/19 2/21 16/34 11/14

(21) (23) (38) (16)

55 (61) 35 (39)

(58) (10) (47) (79)

32/55 (58) 10/35 (29)

Data from McCurdy SA: Epidemiology of disaster: The Donner party, West J Med 160:338, 1994.

independent of their oxidation as a fuel, thus causing a direct muscle-sparing effect during prolonged starvation. Other factors may also contribute. Women generally have lower body mass and less lean body mass to maintain than men, as well as more subcutaneous fat, which may have insulation value during cold exposure. Gender-related cultural behavior, such as the performance of strenuous and high-risk tasks (e.g., the men usually pulled the handcarts during the Mormon pioneer trek west from Missouri to Utah), may also play an important role.

FEEDING VICTIMS OF STARVATION With modern sophisticated means of communication, highly trained search-and-rescue teams, and air evacuation resources, rescue of a lost or injured person in a wilderness environment is usually relatively rapid. Whereas the rescue of the starving Donner party from the Sierra Mountains in 184778 took 4 months, the evacuation of recent polar explorers, such as the nutritionally depleted Mike Stroud and Ranulph Fiennes116 from Antarctica in 1993, took 1 day. Although Stroud and Fiennes voluntarily prolonged their period of starvation before requesting evacuation, most individuals do not have to spend longer than a weekend or, at most, a few days longer than anticipated in uncomfortable circumstances. It is likely that some food will be available to the stranded person, as most people do not enter the wilderness totally unprepared. The individual may have consumed the initial food supply and then fasted for several days before rescue or, if disciplined, may have restricted or rationed food intake for several days. Helicopter evacuation can place the rescued individual in a hospital within hours of rescue. The worst-case scenario might be the rescue of a severely injured or ill person who could not or would not eat for an extended period and could not be evacuated by helicopter. Refeeding victims of short-term starvation is less complicated and dangerous than refeeding victims of prolonged starvation (e.g., James Scott, who was stranded in the Himalayas for 43 days without food104). Victims of prolonged starvation have dramatically altered blood mineral and protein levels, which can be rapidly perturbed by rapid refeeding large quantities of a normal mixed diet. The flood of nutrients with osmotic properties can lead to dangerous fluid compartment shifts. Cardiovascular and pulmonary overload caused by a rapid increase in plasma volume after fluid and nutrient ingestion can result in pulmonary edema. The specific physiologic and metabolic effects induced by refeeding (the refeeding syndrome) depend on the individual’s existing metabolic state and body composition, as well as on the composition of the refeeding diet.51 Refeeding syndrome must be avoided in severely wasted individuals, particularly during the first week of nutritional repletion.52 The rescuer need not be reluctant to offer normal food to most victims of shortterm (3- to 5-day) starvation. The most commonly encountered problem may be that the individual wants to eat too much too soon. This problem is usually self-correcting. The individual may be very hungry, weak, and dehydrated. The victim should first be reassured and then checked for injuries, illness, and 1390

dehydration. Juices, soups, instant oatmeal, granola bars, and small pieces of jerky slowly chewed along with the fruit juice are all good choices to get the digestive system back to processing food while simultaneously supplying fluid, sodium, potassium, protein, and carbohydrate. Frequent small feedings are best. Sports drinks (if available) are a good choice for simultaneous rehydration, because they provide carbohydrates for energy and electrolytes that may be needed for plasma volume expansion. The priority for re-alimentation of individuals lost in the wilderness for an extended time is to first correct fluid and electrolyte imbalance and arrest ongoing protein catabolism. It is not uncommon to encounter waterborne or foodborne illness in a backcountry scenario.16 Rescued victims may be suffering from diarrheal disease as well as starvation. Oral rehydration solutions similar to those used to treat diarrheal disease can be used in wilderness rescue for extremely dehydrated individuals.16 Intravenous saline and dextrose may be needed for those unable to eat because of shock, injury, or vomiting. The composition of the World Health Organization’s oral rehydration solution is shown in Table 69-5. It is important to ensure that the kidneys are capable of normal functioning. Fluids should continue to be offered until the victim is able to urinate every 2 to 3 hours, and then a more aggressive re-alimentation program can be followed. If the individual does not seem to be especially dehydrated, dilute fruit juices or sports drinks containing 5% to 10% carbohydrate and about 20  mEq (about 1.2  g) Na++ per liter are reasonable rehydration fluids. Water is always appropriate, and additional sodium can be provided by liberally salting the solid food offered. A simple rehydration solution can be made by adding 1 teaspoon of table salt and 8 teaspoons of sugar to a liter of boiled water (http://rehydrate.org/solutions/homemade.htm). Sports drinks usually contain 10 to 25  mEq of Na++ and 2 to 5  mEq K++/L. Bouillon cubes are a good source of sodium and convenient to carry. One bouillon cube contains about 1000  mg of Na++ (about 44  mEq). While providing sodium to a moderately depleted individual is beneficial and desirable for restoring plasma volume, this should be approached much more cautiously in victims of prolonged and severe malnutrition to avoid an overly rapid expansion of plasma volume that could lead to congestive heart failure.51 Bananas are excellent sources of K++ (450  mg per banana), but because they are perishable, they are seldom available to a rescue party. Dried banana chips are a good alternative (152  mg K++/oz), easily included in the rescue provisions. After being corrected for hydration status and electrolyte balance, the victim should be placed on a high-protein, highenergy diet as soon as ingesting solid food is comfortable. Some diets are more appropriate than others for re-alimenting starvation victims.52 For example, a diet high in sodium and carbohydrate fed to a severely malnourished individual may cause a rapid and large increase in extracellular volume, resulting in peripheral edema as well as fluid accumulation in the heart and lungs. A low-protein, high-energy diet may make sense initially, but, if continued, may bring about an increase in fat mass without the desired increase

TABLE 69-5  Composition of WHO Oral

Rehydration Solution*

Solution World Health Organization (WHO) oral rehydration

Glucose (g/L)

NaCl (g/L)

KCl (g/L)

Trisodium Citrate† (g/L)

Osmolality

20.0

3.5

1.5

2.9

310

*Preparation information available at http://rehydrate.org/ors/the_salts_of_ life.htm#ORS%20Formula (commercially available from Jianas Brothers Packaging Co., 2533 SW Blvd, Kansas City, MO 64108). † If trisodium citrate is not available, 2.5 g of common baking soda can be substituted.16

1. Normalize and maintain fluid and electrolyte parameters. 2. Provide a mixed diet at the maintenance level to establish tolerance and avoid the refeeding syndrome. 3. Slowly increase energy intake to achieve a positive energy balance and promote fat and protein gain. 4. Provide protein intakes of 1.5 to 2.0 g/kg to promote rapid repletion of body protein at any refeeding energy level. From Hoffer LJ: In Shils ME, Ross AC, Shike M, et al, editors: Modern nutrition in health and disease, ed 10, Philadelphia, 2006, Lippincott Williams & Wilkins, pp 730-748.

in lean tissue mass. A high-protein diet may arrest nitrogen loss, but it will not lead to simultaneous replenishment of fat stores. High-protein diets are also not appropriate (at least initially) for severely starved individuals encountered during relief work in famine-stricken areas. Collins31 has reported that under the famine circumstances in Somalia, a protein-to-energy (P : E) ratio of 5 g protein per MJ of energy in the diet reduced refeeding complications compared to a P : E ratio of 9.5/MJ. Torun and Chew120 have provided the following easy recipe for a high-protein, high-energy liquid food for initial refeeding of severely malnourished and starving individuals: powdered cow’s milk, 140 g; sucrose, 100 g; cooking oil, 40 g; water, 900 mL. This mixture provides 3 to 4 g of protein and 0.6 MJ (135-145 kcal)/100 mL. Victims of prolonged starvation may suffer from hypona­ tremia, hypocalcemia, hypomagnesemia, severe anemia, and impaired membrane and cardiovascular function. These victims should be re-alimented cautiously to avoid sudden expansion of intravascular fluid volume. Cardiac failure may develop if highprotein or high-energy feedings are instituted too vigorously too soon.52 Increased sodium and albumin resulting from refeeding can cause a large expansion of the circulatory volume leading to pulmonary edema, congestive heart failure, and possibly secondary pulmonary infection. Hoffer52 listed four steps to follow in refeeding severely malnourished persons (Box 69-3). Further guidance regarding the homeostatic restoration of nutritional status in severely malnourished individuals (Box 69-4), along with appropriate diets, is discussed in detail by Torun and Chew.120

BOX 69-4  Homeostatic Restoration of Nutritional

Status in the Severely Malnourished Individual

1. Resolve life-threatening conditions first. 2. Begin restoration of nutrition as soon as possible. 3. Replace nutrient tissue deficits as rapidly and as safely as possible, but 4. Begin slowly, to avoid deleterious metabolic disruptions. 5. Schedule frequent feedings of small amounts (e.g., every 4 hours). 6. Diets that derive 60% to 75% of their energy from fat are usually well tolerated. 7. The protein source should be of high biologic value (i.e., high protein quality: milk, eggs, meat, fish, soy isolates). 8. Supplement the diet to provide K++, Mg2++, Zn++, and Cu2++. Fe2++ supplementation begins 1 week after the start of diet therapy. Sodium should be kept low until peripheral edema has disappeared. 9. Introduce a normal diet gradually when edema has disappeared, skin lesions have improved, and appetite is restored. From Shils ME, Olson JA, Shike M, Ross AC editors: Modern nutrition in health and disease, ed 9, Baltimore, 1999, Lippincott Williams & Wilkins, pp 963-988.

Nutritional Planning for Wilderness Activities PRACTICAL CONSIDERATIONS Nutritional planning is an important aspect of wilderness logistics, and one difficulty is that the amount of food carried is often constrained by the space it occupies and its weight. A daily food ration of 4000 kcal for men and 3500 kcal for women will adequately encompass most energy expenditure situations. If it is known that the task at hand will be hard physical work in the cold, 4000 to 6000 kcal/day may be needed. Generally, an energy allowance of 45 to 55 kcal/kg body weight/day will cover energy needs for most moderate to moderately heavy levels of exertion (e.g., for a 70-kg individual anticipating moderate work levels, 50 kcal/kg/day × 70 kg body weight =